EXOCRINOLOGY

THE SCIENCE OF
LOVE
Human Pheromones in Criminology, Psychiatry, and Medicine

B. Nicholson
EXOCRINOLOGY

Exocrinology
The Science of
Love
Human Pheromones in Criminology, Psychiatry,
and Medicine

B. Nicholson
 Nicholson Science
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Published in the United States of America

By Nicholson Science, all rights reserved

Nicholson Science 2604 W JETTON AVE TAMPA FLORIDA 33629-5325

© 2011 Ross Nicholson

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ISBN 978-1461187288
(via createspace.com)
EXOCRINOLOGY

Dedicated to Iraneus Eibl-Eibesfeldt and E.O. Wilson

EXOCRINOLOGY

Preface to Exocrinology The Science of Love

A new perspective in science may be difficult to appreciate. This one
particularly. The facts are these: male facial skin surface lipid has cured delinquency
and runaway behavior hundreds of times. A few dozen times, homosexuality has
been transmuted to heterosexuality and none want to return to perversion. Several
times, heroin and crack cocaine addicted young women have, with one dose less than
250 mg, abstained from the drug and rebuilt their lives with family and pregnancy.
Sexual ideation can be stimulated with a human pheromone, too.
This new perspective has allowed accurate predictions of human pheromone
to be found in emotional tears, the molecular basis for chemosensory transduction,
and pheromonal epigenetic influences. Given these fabulous anecdotal successes, this
exemplary record of accurate prediction, and with the astounding reluctance of human
beings to examine the very ends of their own noses, drawing this new map of the
logic seems prudent. If this glacial pace is all we can expect, then we will all die of
something we should have cured long before substantial progress is made.
Suppose we take this new perspective and consider what if? If you lack the
economic, chemistry, and neuroanatomy skills to follow all the logic, just chump
along. Do not abandon the gold mine because you cannot tell ore from dirt. The
nuggets may be buried, but they are here.
What if modern science believed in fairy tales? Our confidence for scientific
triumph over baseless nonsense is decidedly misplaced. How could that be? When
one strips untested consensus from our knowledge of human behavior, very little
remains. The so-called explanations of psychology, sociology, criminology and most
of psychiatry suffer acutely from insufficient evidence. Paring it down is easy. If it
doesn’t have mass, energy, or value; it doesn’t exist. It is only when our body of
knowledge is completely free of smug half truths, mis-appellation, and consensus of
opinion that we can get down to business. Today may indeed be Monday, 21 May
2011 by the accepted calendar, but there is nothing intrinsically Monday about today.
People can agree it is Monday, but that does not make it so.
For instance, modern science has ridiculed the broad application of economic
theory to human behavioral evolution as patently absurd. Of what possible use could
the assumptions of economic man, perfect information (in geologic time), unlimited
wants, equations of optimality (e.g. linear programming), marginal value, kinetic
homeostasis, and dedication of resources for the same marginal profit, bring to
understanding evolution? Some wit suggested a funny name (Dr. Pangloss) and
bingo, everyone fell into line. What happened to testing hypotheses? The watchword
has been reductio ad absurdum vs the maxim of “equations don’t lie” and, sadly for
science, equations lost. This author predicated his investigations on reversal of the
outcome of that unfair fight. Absurdity is over-rated anyway.
Next, today’s science despises religion, rejecting its sacred testimony not as a
helpful lay history of honest witness, but as, again, mere hermeneutics. Whoa!
Equations AND God? Is there any wonder why we die from so many unknown
causes? This author suggests that in this volume can be found the tools of Christ,
Mohammed, and the Olympians: exocrinology. OK, it sounds weird, but sometimes
truth is just strange.
Nearly thirty years ago, this author’s early economic “equations don’t lie”
logic foretold: that human pheromones would prove vital to our understanding of
human physiology and behavior, that tears would have dissolved pheromone receptor
protein “primer pheromone”, that sexual orientation would be pheromonal; that crime
and insanity would be devices of human pheromones as well. That same atomic
evaluation of the organism as optimizing evolution of parts with physiology and
behavior suggested that organs, cells, even molecules would be purposed in concert to
fulfill evolved function.
Does it sound like “The Force? As chance would have it, this author was once
young and creative enough to have invented “The Force” as a metaphor for
monotheism. Steve Spielberg carried it off to his Hollywood friends. Spielberg’s
friends came back for more. Taking a wider view let this author contribute more than
a hundred more moralistic movies to the current popular vernacular: Up, Inception,
Avatar, Titanic, The Matrix, Phantom Menace, Forrest Gump, Braveheart are all this
author’s stories. Star Wars and E.T. were among my first attempts and yes, my
Spielberg show business association has indeed been cause for significant distraction,
but it has always been fun.
Would you expect science from a ‘Hollywood-type’? Alas, my character is
assassinated by my experiences. Unfortunately for those whose perspicacity is skin
deep, my character is further assassinated by my youthful political associations. An
intellect capable of unraveling most modern medical mysteries mathematically should
also prove useful for sleuthing out great unsolved crimes, constructing public policy,
as well as in movie entertainment. My helps to successful politicians, (e.g. the
Bushes (unfortunately villainous fiends who murdered JFK, MLK, RFK, LBJ, George
Wallace, and many more), the Clintons, Julian Bond, Zell Miller, Ann Richards,
Strobe Talbot, Khalid Sheikh Mohammed: “Privatization”, “Deadbeat Dad Laws”,
“Inclusive Democracy”, “HOPE Scholarships”, “Freedom of Religion Rules in the
Federal Workplace” have helped our country, but serve only to disparage me among
the various science tribes. The popular meaning of “inclusive” -- at least its non-
mathematical, political definition -- came to me whilst sitting in back of my English
class at Richardson High School in 1971. And does anyone blame me for helping our
EXOCRINOLOGY
Federal Reserve realize that they were not out of options at 0% that they could buy
negotiable instruments to combat deflation (quantitative easing) and even had the
power to do it.

Why couldn’t I stop whilst ahead? The JFK assassination and almost all
following American assassinations were conducted to appease Barbara Bush’s sexual
lusts. Her vengeful husband, the cuckold George H.W. Bush, carried it off. What on
earth is the most famous un-caught serial assassin being made mention of here in a
science book? I had to open my big mouth and solve the greatest unsolved crime of
my time, right? The shooting of Congresswoman Giffords is the latest in the string b
the plumbers. Unfortunately, the same insight that serves so well in scientific
elucidation also serves here. Still, we didn’t get all dressed up for nuthin’. Rest
assured that we will now leave all these distractions behind, and get to the meat of the
matter at hand: saving humanity with the cool tools of Jesus Christ.
Preface to the 2nd Edition
This book, OF LOVE, textbook of medical science: exocrinology, is a
revision of an earlier work OF LOVE kisses pass epigenetic pheromones in the
pathogenesis of sociopathy, ‘mental illness’, and disease. The cure for crime. The
cure for drug addiction. The cure for sexual perversion. This 2nd edition with its
abbreviated title, incorporates changes suggested by colleagues and scholars from
around the world. Chapters 8 and 9 were switched in their places to introduce the
detailed and better understood sociopathies of crime, addiction, and perversion in
anticipation of the less easily understood autoimmune diseases.
Low and behold, human sexual orientation does indeed depend upon
pheromone recognition, just as the author predicted in 1983. (Indeed, human
pheromone can change sexual orientation as my open trials have tentatively
demonstrated.) There, as the author expected, is the convolutional change in
pheromone receptor (binding) proteins exactly as predicted. The pheromone receptor
proteins are indeed essential to chemosensory transduction just as predicted.
Little scientific headway has been made in the intervening two years since
first publication of this book despite its wide dissemination. The sexual dimorphic
tears of women were found for the first time to have the pheromonal effect of
reducing masculine testosterone while hugs were shown to change the concentration
of pheromone receptor proteins in the blood. The latter idea was unanticipated but
welcome in economic explanation for that affectionate behavior. The former was
suggested by this author nearly thirty years ago. Hopefully, at least human
pheromone reception will be traced to the microvillar “brush border” cells that line
the human upper-respiratory system before the next two orbits of the sun shine on the
next edition, but time will tell.
America has a startling inability to fund double-blind testing of the masculine
facial skin surface lipids cure for crime. Hopefully, the preponderance of charlatans
will abate with application of these ideas overseas. In other realms, with fewer
psychologists, criminals, mischievous anorexics, and offended sexual perverts,
perhaps progress can be made unhindered.
Of course, the economic and scientific explanations for human romantic and
parental love behaviors will be just as fresh and new to those who completely ignored
them decades ago. This time around we provide much needed therapeutic options.
Finally, in medical school, sooner or later your professors will admit that most
of us suffer and die from illnesses for which no one knows cause or cure. 55% is a
conservative estimate for deaths from atherosclerosis and its complications. Up to
55% of women suffer from hypoactive sexual desire syndrome. 55% of some
EXOCRINOLOGY
populations will spend some time incarcerated, addicted, unloved or perverted. This
book is for that 55%.
EXOCRINOLOGY

TABLE OF CONTENTS
Introduction ! ! ! ! ! ! ! ! 1
Chapter 1: Kissing ! ! ! ! ! ! ! 9
Chapter 2: Parental Love of Offspring ! ! ! 49
Chapter 3: Chemical Characteristics of
! Human Pheromones ! ! ! ! ! 77
Chapter 4: More about Bonding:
! Neglect and Abuse ! ! ! ! ! ! 119
Chapter 5: Eating Disorders ! ! ! ! ! 149
Chapter 6: Crying Chemoreception and Love ! ! 157
Chapter 7: Human Pheromone Transduction ! ! 191
Chapter 8: Pheromone Control of Crime and
! Drug Addiction! ! ! ! ! ! ! 223
Chapter 9: Pheromone Control of Sexual
! Desire Syndromes
Chapter 10: Pheromone Reception & Disease ! 233
Chapter 11: Atherosclerosis ! ! ! ! ! 277
Chapter 12: The Function of Myelin ! ! ! 297
Chapter 13: The Future ! ! ! ! ! ! 311
Appendix! ! ! ! ! ! ! ! ! 317
EXOCRINOLOGY

Introduction

Pheromones regulate the human hierarchy that determines rates of infection,

sociopathy, disease, accidents, and death. Passionate pheromone feed-back systems
maintain criminality, insanity, and all sorts of perversions that we can now modify to
our liking. Pheromones regulate fertility and with other inputs (hormonal and neural)
choose the best candidate oocytes for fertilization and just the right sperm.

A policeman just called your cell phone. They have your suddenly gone wild
and gone missing puberal daughter down at the police station. You are her father,
now what do you do? The proposed cure for runaway behavior is in the Appendix.
You can cure your daughter with one pack of Wrigley’s Rain chewing gum (15 pieces)
and the grease on your face.

First of all, it is not her fault, so do not blame your daughter. Bad thinking
does not cause misbehavior problems. Certain easily avoidable biological
transgressions or sins can, but so can air pollution. Such epigenetic transgressions
can lay blame with you, or your spouse, your parents, even grandparents or great
grand parents, just like Exodus 34:7. Next, you can alleviate your daughter’s
immediate difficulty with a pheromonal communion. Follow the instructions at the
very end of this book: collection of healthy adult male facial skin surface lipid, and
give your daughter the pheromone chewing gum to chew. You need not be present,
but your daughter’s misbehavior requires your male, fatherly facial chemical
signature, the shine on the end of your nose, to be put upon her saliva, a big dose just
one time. Your daughter needs your ‘blessing’ to behave, to perform well in school,
and now to stay out of prison. So give your returning prodigal the shine off your
nose, and celebrate. It actually is the right thing to do.

OF LOVE is a science book for scientists and best appreciated by those

physicians and medical students familiar with the rather severe microeconomic
principles of Milton Freedman. A familiarity with neuroanatomy and first semester
organic chemistry could help too, but the few necessary concepts are introduced in
the text so a review should be unnecessary. Indeed, finding relevance in the science
1
of love for organic chemistry sufferers may even stimulate students to master those
subjects more thoroughly.

Discovering the pheromonal basis of disease, the clinical relevance of this

book for practicing physicians is clear, but awaiting clinical trials. So this is a book
of anecdotes and theory, but it is compelling on both counts. All open trials have
succeeded, although the pheromone has little effect on alcoholism. [Please see the
appendix for collection protocol details. The cure for drug addiction is 150-250 mg
of healthy adult male facial skin surface lipid taken in one dose on a chewing gum
vehicle by mouth. The cure for juvenile delinquency is also 150-250 mg of adult
male facial skin surface lipid taken in one dose by mouth. The cure for homosexual
ideation and behavior is 150-250 mg of adult male facial skin surface lipid taken in
one dose by mouth. The cure for teenage runaways is 150-250 mg of adult male
facial skin surface lipid taken in one dose by mouth.] Similarly successful treatments
for autoimmune diseases and cancers are likely. For instance, that same wonderful
dose has stopped the progression and reversed some symptoms of Alzheimer’s
disease within a few weeks on four occasions so far. Refined and better understood
with double-blind cross-over protocols and repetition in other labs, will these
anecdotes stand the test of time? Science will decide.

This book begins the end of important human institutions that are even now
outliving their usefulness. Jails and prisons will simply dry up and cease to exist.
There will be an end to widespread police presence, an end to the ‘homosexual
community’, an end to the oxymoronic criminal justice system, an end to the drug
wars, an end to jihad and an end to terror. The world will ultimately save a net
present value estimated in the hundreds of trillions of dollars. Unfortunately, to be
studied, this book must be read, and sadly, your author is a thinker, not a writer.
Composing this volume has taken decades after the first insights from 1982. It was
1987 before the first tentative remedies were effected. Presently, a demonstration is
underway in Hollywood among desperately troubled ladies. Apparent successes so
far are Leelee Sobieski, Jessica Simpson, Mila Kunis, Lindsay Lohan, Paris Hilton,
and Ellen Page. More will follow.

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EXOCRINOLOGY
Science can be truly useful to humanity only when knowledge is
unencumbered by legend, mythology, and untestable hypothesis. Arriving at truth can
be a formidable process, too rococo for comprehensive disclosure. Chain thinking,
concentration for many hours did help, as did (and one can almost hear legions of
government-paid colleagues gasp) a deep and abiding faith in God. Do you see?
Automatically, here thinking diverges from common notions. This is a book in the
van of many modern medical miracles and there is no harm in giving credit where it
is due.

Most human sociopathy stems from lack or pollution of family care. The
primary pheromone deficiency driving sociopathy is of the father, but symptoms of
paternal pheromone deficiency vary by other pheromone receptions, choices of self-
medication, and behavioral self-stimulation. Human pheromones are here implicated
in addictions of substances and behaviors as well as the immune & autoimmune
diseases, and cancer. The eating disorders of obesity, anorexia nervosa, bulimia
nervosa, are treated together. Excitement or adrenal addictions include afflictions
such as gambling addiction, criminal thrill addiction, shopping addiction, all are
substance addictions, just endocrine substances, and these are reachable by paternal
pheromone therapy. Addictions to other pheromones suggest etiologies for
homosexuality, pedophilia, habits of torture (sadism and masichism), the rapist’s
addiction to female alarm pheromone, foot & hand fetishes for those pheromones,
nymphomania and satiriasis. Meanwhile overt pheromone poisonings suggest
etiologies for blighted ovum, sudden infant death syndrome (SIDS), diabetes,
Alzheimer’s disease, multiple sclerosis (MS), differential susceptibility to infection,
and much more. Pheromones regulate population fertility by adjusting perversion,
criminality, drug addiction, insanity, etc. to hobbled population resources and needs.

The larger issues aside, this book is also full of tiny controversies, most of
which go unresolved. Suffice it to say that whole books have been written about
many of these. Obligatory mention merely indicates one’s familiarity with the
literature, an unfortunate necessity in 2011.

Economic modeling, especially that of classical microeconomics, rules here

axiomatically. This will foster charges of teleological thinking. While that cannot be
3
helped, it most certainly should not be deplored at least until these several fruits are
tasted first.

Just as a grasp of organic chemistry rewards fresh beginnings, discovering

truth means starting from a blank slate and rejecting unprovable propositions. Out
went the self-concepts, the egos, the states of denial, psychological states, complexes,
ideation and motives. If it didn’t have mass, value, or energy, then it did not exist.
The author has striven to maintain his strictly empirical economic bias out of an
abundance of caution. Surely, even the most indoctrinated psychological
establishmentarian can admit that it is better to check out the physical & economic
causes for behavior first. Resorting to some willy-nilly consensus of psychological
opinion should be the last resort. Thus in this book the author has no personality and
neither does anybody else. Of course, there is no convincing passionate defenders of
air castles, but in America at least, it is a shame that our public authorities support
and maintain ‘psychology’. The United States has a constitutional prohibition against
establishing religions, but there they have managed it anyway. The psychological
fiction is extremely well intrenched, even among otherwise staid and sober chemical
ecologists. One thoughtful and incompetent chemist once offered this tidbit: ‘every
blade of grass has its own personality.’ What is next, fellow? Rocks with egos?

Human pheromones are not always airborne. Indeed, most are not. Human
pheromones tend not to be single chemicals, either. The kissing pheromone alone
contains more than 735 different chemical species. Chapters 5, 9 & 10 deal with
some human behavioral & other illness of presumed airborne etiology.

Pheromones have been subdivided dubiously into releaser and primer

pheromones as explained in Chapters 6 & 7. Water soluble proteinaceous primer
pheromones are extracellular receptors for the much smaller non-protein releaser
chemical mixtures. Protein pheromone receptors can be self-produced and/or
acquired in social behavior.

Generally, human pheromones affect only human beings and perhaps our
parasites (dogs & cats) for which our pheromones are their allomones. There appear
to be four basic human pheromones: love, anger, fear-stress-alarm, and the dimorphic

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sexual aromas. Love, by far the most complex, takes up most of the pages of this
volume, hence the title. There also appear to be roughly three basic receptivities:
happiness, sadness, and romance. All three are accompanied by emotional
lacrimation. No one should be surprised if every human inkling is laced with
pheromones.

Love transmits the sebaceous skin surface and mucosal lipids via kissing of
‘kissable’ skin surfaces (inside the mouth and on skin where you normally kiss). The
various human emission glands are the largest and most active of any species.
(Heavy breathing airborne pheromones will be largely left to my gasping colleagues.)

Sebaceous secretions, these are the “king” pheromones that can controvert the
effects of most others. Generally, these hundreds of different skin surface lipids
together compose a surface pheromone set that is passed in kissing and differentiates
us chemically to keep us kissing the right person and not kissing the wrong person or
animal. Thus the pheromone may contain ‘yummy’ secretions and aversive
pheromone secretions depending upon your age and station in life. Girls (and
doubtless young men) are ‘yummiest’ in their late teens and early twenties when
strange long chain strange wax esters accumulate on kissable skin surfaces with
melting points that make those chemicals ‘melt in your mouth’. Anyone too young
for reproduction will have an aversive pheromone component, probably the odd
cholesterols peculiar to childhood that make kissing a child so boring and
uninteresting or even nauseous. Childish pheromones passed among children, taints
kin to us in adulthood, as a dispersal mechanism seen in tadpoles. The human skin
surface lipid has unique human-only components, but pets and horses emit chemicals
that come close, endearing them to us chemically. Rats and mice, too, have fatty acid
and ester pheromone components that probably account for their seeking our human
proximity for their habitat, endearing us chemically--to them.

Anger emits primarily from the top of the head (blowing one’s top, hot head),
mostly from younger adult males and goes airborne at the slightly raised scalp
temperature of anger. Anger’s emission appears poisonous, causing most of the
autoimmune diseases and Alzheimer’s disease. The reactive long-chain conjugated

5
dienoic free fatty acids peculiar to the hair atop of the head of young men, ‘head’ the
list of potentially dangerous human anger pheromone chemicals.

The fear pheromone has been observed in Austria and is now being
synthesized at SUNY by DARPA at the author’s suggestion as a potent fear-producing
pheromone that could reduce war’s lethality. The cold fear of panic is thermo-
graphically observable on an infrared camera. Stress seems akin to fear, except that
the lacrimation is pheromone-receptive. Stress and fear odors likely emit from the
axillae, perhaps with a dorsal element (yellow streak down his back), but perhaps not.
The fear-stress pheromone probably diminishes natural immunity and likely lowers T-
cell counts as it does in laboratory animals. Diminished immunity caused by
pheromones likely accounts for cancer reaching a clinically noticeable stage, and for
dangerous susceptibility to infectious disease. Of course on the battlefield, fleeing
cowards are shot down like partridges, often by both sides.

The body odor of happy, healthy young people appears conducive to good
general health. This sexually dimorphic pheromone set should be reproduced
synthetically and piped into hospitals and retirement homes. Perhaps visits by young
people themselves can be dispensed with to avoid the potentially toxic anger
emissions so poisonous to the hospitalized elderly and infirm. Basically, gruff young
male doctors really should wear space-suits when they are angry.

Happiness is a receptive state of pheromonal contentment. It is having a

recognized, unchallenged place in the local hierarchy, with pheromonal appetites
sated. Producing this state artificially allows a ‘reset’ or perhaps a ‘rebirth’ that
allows withdrawal from addictive drug cravings, along with criminal and perverse
sexual appetites as well. Thus artificial human pheromone manipulation portends to
revolutionize human society to cast aside most sociopathic ills. Of course the
biological functions that those sociopathies had in population control will eventually
have to be managed artificially. It is a dismal but likely prospect for the distant
future.

Sadness or grief evokes psychogenic lacrimation and grief-specific postures

and behaviors (boo-hoo-hoo), which set up chromatographic solvent chambers in

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pheromone sensory cell (microvillar or brush-border cells) receptive tissues and
structures. Emotional tears are the solvent and contain the first receptors in solution.
The upper respiratory system is covered with pheromone sensory microvillar cells.
These cells together comprise the largest pheromone reception organ of any animal
species. The same cells inhabit the gut (Peyer’s patches) and thus might account for
emotional nausea in response to perceived local hierarchical changes, as when
spouses cheat.

Exocrinology is such a robust explanation for human behavior that we can

dispense with some nonsense. Thus as stated for our purposes, emotional or
‘psychological’ states do not exist, per se. These are instead, emissional states and
receptive states with specific empirical functions that glue us together in pair bonds,
families, nations, and as a species. Even human pet ownership can be explained as
allomonal parasitism.

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EXOCRINOLOGY

Chapter 1: Kissing
Kissing compares to crying, or laughing, yawning or hiccuping. We all do it.
We always have. Nobody really knows why.

What is kissing for? Why do we put so much effort into the physical act?
Why do our brains reward the behavior with pleasure? Kissing, especially passionate
kissing between a man and a woman, can be a rather untidy affair. It involves risk,
too. Saliva, passing back and forth, passes germs back and forth as well. Kissing
couples share a risk of periodontal disease and cold sores (Herpes Type I).1 Herpes
Type II and gonorrhea can also find their way to the pharynx. How is no mystery.
The contacts are sexual.

Kissing also incurs what economists describe as opportunity costs. Humans

have other things to do besides kissing. In simple terms, kissing takes our attention
from food production and avoiding predators. Our effort and time in kissing costs us,
so why do it?

Human fertilization requires no mouth to mouth contact at all; so for

reproduction's sake, we could dispense with kissing altogether. The increased risk of
disease infection alone would auger well for our avoiding the behavior.

9
 Assume, quite reasonably, that time and energy are scarce. We should suspect
that any non-kissing couple would improve their chances of reproductive success in a
world of inefficient kissers. Yet, all human beings, everywhere, kiss.2 Indeed, kissers
seem to reproduce far better in families than non-kissers. Do they not?

Kissing made it all the way into the present from prehistoric beginnings. For
kissing to have gotten here, evolving over eons or arriving in one of Gould’s
punctuated equilibria, 3 kissing must justify its existence. It just costs too much.
We've mentioned energy, time, infection risks, and lost opportunities. Moreover, the
body's responses to and preparations for kissing, develop with unusual and costly
intricacy. From the histology of skin to circulation and respiration, kissing transpires
in coordinated effort. We will delve into this further on, economics, "satisficing"
spandrels and all.

Let us look at kissing in detail. Kiss someone else's skin, the uppermost
surface called the epidermis. Your mouth picks up skin oils, waxes and alcohols in a
complex mixture from that skin you just kissed. The Romans named the mixture
"sebum". The glands producing sebum go by the name of "sebaceous". Hundreds of
thousands of microscopic sebaceous glands embedded in the lips, skin and interior
mouth surfaces (mucosa) of the person you are kissing secrete the sebaceous skin
chemical mix. When she kisses you back, your skin secretions get into her mouth,
too. Perhaps a primed, mutual addiction to face and body greases binds couples in
physical love?4 Dimorphism and perversion occur in humans, functioning every bit
as kissing does. [For the time being, please assume the human male, heterosexual
author's point of view, as it eases his writing. If the reader falls outside those
categories, please try to understand at least until reading technology improves enough
to adjust author viewpoint to reader tastes.]

If addiction joins us together, then we are not consciously aware of it. Non-
conscious perception and recognition of human odors has been demonstrated. 5 A
mouse model is instructive, since pheromone reception is biologically ubiquitous.
Since the hippocampus is required for learning one ordinary smell from another in
mice,6 and since the infertility mouse-behavior-altering chemical, a pheromone, still
works well when mice no longer have hippocampi,6 then conscious learning appears
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not to be involved in pheromone recognition in mice either. The hippocampus is
important in conscious learning, yet conditioning can be effected out of the
consciousness of the subject. 7 Similar experiments have seen similar results in
hundreds of species.

Any chemical responsible for human love would have to be colorless,

odorless, and tasteless. Human sebum is.8 Any chemical love would have to vary
from kissed skin to kissed skin in amount and composition, so that different kisses
would function differently. That way kissing someone on the forehead and kissing
the same person’s tonsils with your tongue would perform different natural functions.
Human sebum does differ, both chemically and in amount, from place to place on the
human body.9

Similarly that variability would need to vary consistently from person to

person. That way kissing your sister would be no fun, but kissing your "honey"
would be. Human sebum has just that variability.10 There would have to be a whole
lot of it at birth when only love holds death from exposure at bay. There is.11,7 There
would have to be a lot of it on the skin around the time most people get married.
There is.12 It would even have to stick to lips like nothing else in nature. It does.13
Finally, delivery of a bonding chemical would need to be highly specific. Yes, kisses
are quite specific.14

Because each person's skin secretion mixture is unique, your sebaceous

chemical signature is distinguishable from anyone else's.10 Those secretions mark
your uniqueness over long periods, perhaps from fetus to grave. Primed, with
reciprocal receptivity and exposure, the love in your mate-mate relationship might
logically depend upon a non-conscious mutual addiction to each other's unique
biochemical secretions of the dermis and its glands.

The more social birds kiss after a sort, too. Like those birds, human beings
rub our beaks together most when pair bonds first form and at the reunification of
lovers.15 Kiss your returning loved one and you feel so much better! Perhaps a

11
chemical obtained by the kiss drugs us into the feeling? The author's casual anecdotal
experiments suggest this is so.

The heat of sexual passion is no generalized fever.16 Only some skin areas
take part in passionate behavior. Overall body temperature remains stable. During
intercourse some skin heats up, other skin cools down.17 Because hot skin moves
sebum up and out of sebaceous glands,18,19 and because saliva dilutes and carries it so
well,20 expression of sexual passion transfers skin chemicals quickly and efficiently.

(though love be a day and life be nothing,

it shall not stop kissing).

E.E. CUMMINGS

Perhaps compulsions for skin secretions compel people to linger together just
like birds and bees? This author’s hypothesis for the case of birds21 has gained little
acceptance. The avian case seems to be due to inertia set up by chains of citations
from misguided Nobel laureates, but for the bees we may know. Blum22 found
cutaneous surface secretion transfers and suggested from his experiments that they
improved nest cohesion. Bravo Blum.

The chemical structure of the sebaceous chemicals compels us to believe they

carry information, epigenetic information, and lots of it. (See Chapter 3) Such
information carrying chemicals are called "semiochemicals" and sometimes
"pheromones." Sebum contains semiochemicals. We know that much because dogs
find sebum helpful to distinguish humans, even twins.23 Twins are identical
genetically, but differ epigenetically with increasing age. Semiochemicals

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communicate a biochemical signal (Greek semeion-- a sign) from one organism to
another.24

Sebum may more narrowly be classified as a pheromone. Pheromones are

chemicals that one organism emits into air, onto skin or onto environmental surfaces
which influences the behavior or physiology of another organism of the same
species.25 Conspecific specificity defines a pheromonal signal. Arguably these
sebaceous chemicals and other suspected human pheromones may assuage the
cravings that people have for parental approval, mates and offspring.14

People and animals have physical bodies with physical appetites. We see with
eyes, like other animals. We digest food like other animals, we smell, hear, touch and
taste all like other animals. Virtually every human physical function has an animal
counterpart. Logic insists we assume physical human love does not differ
fundamentally from animal bonding. Granted, parasitized people insist that their cat
or dog loves them alone even with the obvious lack of conspecificity and despite the
knowledge that dogs and cats mate promiscuously. The biological fact is that human
beings support canine and feline parasites. Dogs and cats are parasites of human
beings.

However, if humans form love-bonds in a way entirely different from the way
animals form them, you would be surprised. Most other animals do bond if only for a
short time. (Asexual reproduction, where the same individual is both "male" and
"female," occurs in many animals: worms, some reptiles, many microscopic species
and in much plant reproduction.) Many species mate for life. Other animals mate the
opposite sex promiscuously.15 Observing the behavior of newly introduced animals
calls to mind similar human behavior. Strange conspecifics are not allowed too close.
Many marriages begin with a certain amount of distance, too. Closing that distance
may require successful exchange of semiochemicals.

Some psychological writers insist human physical love differs fundamentally

from the animal behavior, and that this defines humanity itself.26,27,28 Without
evidence on either side, who can tell? Psychology must now become a failed
paradigm belonging to the 20th century. Personalities, psychological states, egos, self

13
concepts, witches, spirits, ids, ghosts, and self-actualizations, these present cultural
manikins lacking physical existence and should lose scientific credibility.

Much psychologist-collected data support critical periods in human

pheromone recognition. Much of the psychological rationalizations remains suspect.
However, almost certainly classical and Pavlovian conditionings take place behind
each untasted morsel of sebum and behind each un-detected whiff of airborne
pheromone.29 Unfortunately, psychologists manage to control for pheromone
contamination or semiochemical sepsis only inadvertently. It is as though they have
yet to detect the air around them, oblivious to the thousand or so chemicals and
microbes with which they mark their own homes, their lives, and their loved-ones.
Psychologists have been amazingly witless.

From available evidence, for birds and bees and human beings, falling in love
means falling in love. Getting hooked on the addictive bloom of the partner's face,
mouth and body must be similar for all bonding species. The biological devices
thought to cause bonding look most alike in animals nurturing young and forming
mating pairs or groups.

"Mutual licking and grooming sequences occur very commonly in mammals.

The male hunting dog sniffs and licks the female vulva increasingly as estrus is
approached and will even vigorously nibble at the female's skin from the ear to the
groin (van Heerden, 1981). The asiatic elephant transfers chemical information
from its mate to its mouth using the tip of its trunk (Eisenberg et al., 1971), black-
tailed deer sniff and lick each other's tarsal scent organs (MüllerSchwarze, 1977)
and the male golden hamster is motivated to lick its mate's vaginal secretion
(Johnston, 1974)".30

A passionate kiss synchronizes the bodies' cardiovascular, exocrine,

respiratory, and neuromuscular systems. Of course, behavior of two people must also
be synchronized (as courtship). Consider this. Both kissing mouths contain soft
tissues and sharp teeth that cut. Moving all these structures around so close together
requires considerable instinctive orchestration. The physiology and ethology of
kissing needs increased scientific attention. All the sharp teeth and vulnerable tissues
never cause serious injury.
14
EXOCRINOLOGY
Inarguably, one kiss moves sebum from one person to one other person.
Transfers of pheromone from skin to mouth have advantages and disadvantages over
pheromone dispersal into the air. Kissing allows specific reception of an individual's
chemical signals. You can be smelled by a whole room-full of people all at the same
time, but kissing needs permission. That distinction signifies something important in
many mammalian species.

"Males of nearly all mammalian species attempt to sniff the genital region of
potential sexual partners. ...In many species females that are in estrus or
approaching it allow males to investigate their genital region, whereas females that
are not in this state avoid or repel such attempts. ... Thus, permission to investigate
can be considered a subtle but important courtship display since it indicates an
approaching readiness to mate".31

A mouth-suction applied to the skin typifies human kissing. Suction helps to

get skin sebum, the putative pheromone, into the kissing mouth. However, the slight
sucking in such kisses seem insufficient for efficient inhaling or swallowing. At least
some receptors must be either in the mouth or close by in the upper respiratory
system and that is where they were found. Eureka! The human vomeronasal organ, a
pheromone reception device in all other species, seemed a likely candidate for a low
volatility pheromone reception in humans. 32,33 Sebum has low volatility.20 However,
the sensory brush border or microvillar cells that line most of the upper respiratory
system and into the digestive tract with Peyer’s patches (that ‘kicked in the gut’ pain
of betrayal?) must certainly be pheromone receptors. They are identical to known
specialized pheromone receptor cells in all other species of animals. The narrowness
of medical education perpetuates an absurd debate about the function of these cells
that should have closed long ago. Physician cultures abhor labeling incompetence so
much that the pheromone reception system has gone unobserved for generations. As
my character Forrest Gump decried, “Sometimes there are just not enough rocks”
with which to stone ineptitude.

15
 Long periods of passionate osculation in mate-mate bonding stimulate
salivation and frequent swallowing. Pheromone reception and immune response
might also take place via the alimentary tract by absorption through the duodenum.
Relatively small amounts are involved, but pheromones are certainly the most potent
drugs ever discovered.

Could a single kiss convey information? Clearly, yes it can. Insects

communicate with exceedingly small quantities, far less than the amount of sebum
transferred in a single kiss. Pheromones signal efficiently.25 Insects communicate at
the ultra-trace level (PPB, parts per billion air molecules).34 Rodents communicate
well with pheromones emitted at the trace level (PPT parts per thousand molecules of
air).35 Very small quantities of supposed pheromones of human origin have elicited
electrical responses from the human vomeronasal organ.33 The physiological
evidence is there, if one only looks.

LIPS

For about the past thirty years, a brouhaha stewed among ethologists about
why people have lips on their faces. (This is one among many petty controversies.)
Other primates copulate with their females from behind and in some of these species
genital coloration acts as a sexual display. Women's lips attract men, especially
vaginal ones.

16
EXOCRINOLOGY

Perhaps human lips played counterpart to the gaily colored "sexual skins" of
primate genitalia? Lips do have a distinctive red color, at least among light skinned
people. Maybe lips evolved as bait to bring the male around to the front?36 The
counter-argument ran that white men also have red lips. Furthermore, the poor chaps
who couldn't differential between vaginal lips and facial lips (and male lips and
female lips) were poor candidates for evolution anyway,37 and back and forth. Very
funny debate, it was, if a bit tedious.

Perhaps lips evolved to do what they do? Lips puckering-up for a kiss do
three things. First, they bring the most available surface area to bear. Second, they
maintain and only expose their moist inside surface just before contact. Both devices
improve transfer. Third, lips act like a flexible gasket around osculating mouths.
(Kissing may get sloppy from so much saliva, but kisser's drool may be excitedly
lapped up, posing no contradiction to the gasketing hypothesis.) If kissing executes a
valuable function which improves by having fleshy glabrous facial lips, then the
purpose for their natural selection might be inferred.

17
RITUALIZED FEEDING?

Scientists, ethologists, have observed a step-by-step progression of behavior

from eating through kissing in humans and other species. Admitting they possessed
no hard evidence, human ethologists suggested that our kissing must have evolved
from feeding behavior. "All animals eat and not so many kiss," they reasoned, "Look
at all the cases where mothers chew food before passing it to their little ones by
mouth. Humans aren't the only ones." They termed instinctive osculation, ritualized
feeding behavior.2,37,38

Eibl hypothesizes that kissing resembles eating. Indeed, the eating of small
quantities of an extensive mixture glues us together by bonds of addictive craving.
Mothers in many cultures do pre-chew their baby's food.2,37,38 However, perhaps
babies have difficulty chewing while toothless? Pheromonal emissions transferred in
kissing reward caregiving well. However, the weight of evidence to this writer
suggests that kissing evolved from allogrooming.

Kissing behavior changes somewhat from culture to culture, but the feeding
on sebaceous pheromone represents the universal and constant idea. The evolution of
pheromone exchanges must have started with the first colony of bacteria, for colonies
require pheromones to communicate well enough to become colonial. Many of the
pheromones of colonial species served later as hormones, neurotransmitters,
cytokines and the like. In at least one species, the pheromone that signals a school of
organisms to scatter is the same chemical that signals pain when it is released inside
the body: bradykinin.39 Indeed, alarm pheromones generally are associated with
immune function.40 It should come as no surprise that NSAIDs -- aspirin-like drugs
-- affect pheromone reception -- and therefore the diseases affected by NSAIDs have
pheromone, at least alarm pheromone, components.

Mind, the ethological hypothesis of kiss as ritualized feeding has appeal. Who
calls you "Honey," "Peaches," "Sweetheart," "Sugar," "Cupcake," "Dumplings,
"Sweetiepie," "Lollipop," "Honeybun," or "Lambchop?" Why should tasty food be so

18
EXOCRINOLOGY
commonly used for romantic pet names in all cultures? The association may have
significance if a feeding of some sort takes place. On the other hand, loving a "dried-
up old prune," may present problems. One should expect low sebum secretions in
people difficult to begin loving and that has generally proven true, if only anecdotally.

ATTRACTION

Attraction is a separate issue and will receive little attention in this book.
Attraction in human beings may be another process dominated by visual cues. You
will find fuller discussions of issues of attraction elsewhere. Airborne pheromones
seem to be important for sexual orientation,14, 41, 42 conviviality and sexual attraction
in humans and to moderate43 or synchronize female menstrual cyclicity.44, 45
Airborne pheromones by worried people or people in pain sitting in cancer ward
waiting rooms may diminish immune response by diminishing natural killer cell
immunity and T cell counts. 46 The human alarm or fear pheromone47 emitted by
frightened people may help cause generalized panic while addiction to it may
perpetuate human kidnapping, rape, and torture behavior.

The relative size of the bed nucleus of the stria terminalis is associated with
sexual orientation. Hormonal manipulations and neuron tracking have shown that
information concerning pheromone emissions is carried there. 48

SEBUM

As we've said, "sebum" in Latin means "grease." Calling sebum a face-grease

does injustice. What a marvelous material! Does sebum speak the language of love?
The evidence, reviewed in these pages, suggests so. This skin-produced, soothingly
addictive aphrodisiac makes love possible, and medical miracles like dramatic
improvement in Alzheimer’s cases, cures for drug addiction, perversion, and criminal
behavior.

19
 Sebum seems to be tailored for exchange by kisses. Sebum is extremely
hydrophilic (water loving);20 indeed, it was once considered the most hydrophilic
natural organic mixture known to science.49 Plainly, sebum rides atop saliva, which is
mostly water. Sebum's affinity for moisture insures its transfer from the relatively dry
skin surface of its origin to saliva covered, 'moistened' lips kissing that surface.

Good reason may exist for wet kisses. In females, salivary sulfur-containing
breath volatiles of microbial origin vary cyclically with circulating hormone level, as
do vaginal levels of lactic acid. Physicians exploit the effect to detect female
ovulation. Other chemical signaling may be going on in saliva exchange kisses.
Rates of intercourse vary cyclically with peaks at ovulation and premenstrually,50
although these may have more to do with menstrual period discomfort. One of two
cyclical secretion peaks might portend the period of peak fertility and intercourse.14

Beasts have their own distinctive sebums, too.51,52 Do animals exchange

unique but still similar substances in their own kissing-type behaviors? They
"groom." They "preen." They "give nuptial gifts" to each other. Are these behaviors
their kiss-equivalents? Nuptial gifts get covered with the animal's own sebum and no
mating takes place without this excited transfer.14 Of course it is exactly the same
thing.

PHEROMONES

Those readers already familiar with pheromones tend to recall them as

chemical attractants. Chemical attraction was first observed in butterflies. In the
fifteenth century, chemical attraction in moth and butterflies was first noticed.53 In
1690, John Ray reported seeing several Biston betularia (L.) flying around a visibly
obscured caged female. Attempts to figure out the chemicals responsible began in the
nineteen twenties as an adjunct of agricultural research. 54 Many tried. For years they
had no luck. At last in 1959, Butenandt et al. 55 identified the first sex pheromone,
E,Z10,12-hexadecadieneol. They named it "bombykol." Getting enough crude extract

20
EXOCRINOLOGY
took twenty years to collect and the sacrifice of the pheromone producing glands of
around half a million female moth sex organs.56

Human sebum functions similarly to other animal's fur and skin pheromones
but can be easily distinguished from them. Lions respond to lion sebum.57 Moles
respond to mole sebum.58 Mice respond to mouse sebum.59 Tamarins respond to
tamarin sebum.60 Geese respond to goose sebum.61, 62 Gerbils respond to gerbil
sebum.63,64,65 Goats respond to goat sebum.66 Even yeast cells respond to tested
unsaturated fatty acids of the type seen in sebum.67 Ordinarily no confusion presents
difficulty.

Allelochemicals (or allomones) are semiochemicals that communicate across

species. The skunk's defensive spray holds all too familiar allelochemicals that dogs
(and people) soon learn to avoid. Hunted animals may warn comrades with an alarm
pheromone scent that becomes an allelochemical trail for the predator.68 From
economics, the author expects that crowding should increase the detectability of the
spoor. Similarly uncharacterized human alarm substances may lower our disease
immunity, while conspecific sebum consumption may improve it.69

Dogs smell well. Fleeing prey lay down chemical trails as pheromones to
remind themselves and their fellow conspecifics to avoid the area for a time where a
predator was detected. Dogs smell these and other scents left by the withdrawing
animal as allelochemicals. Canine olfactory versatility trades off against the economic
efficiency of specialization. The compromise produces a device less efficient and
more expensive to maintain than the more specific recognition devices used for
pheromone recognition. Bloodhounds on the chase compensate. They must keep
their nostrils close to the scent and training for the hunt is both time consuming and
costly.

Dogs recognize humans easily, detecting sebaceous fatty acids at

concentrations of one percent of the lowest conscious human perception. They can
distinguish among family members and even between identical twins.70 Sebum might
even be utilized by pets to synchronize their behavior to ours. Economics predicts

21
that disease organisms, particularly more sophisticated ones like malaria and worms,
should do this too.

Various sebums are semiochemical in many mammalian species, including at

least one other primate species.71 In the past, scientists differentiated semiochemicals
from insect pheromones. Mammals respond to semiochemical stimuli differently
depending upon the behavioral context, while pheromones (as thought back then) had
robot-like effects on insects. Further study revealed more similarities than
differences, so the distinction lost favor.

SEBACEOUS GLANDS

Sebaceous glands differ morphologically from animal species to animal

species. The glands look a bit different.72 They stain a bit different on the microscope
slide.27 Different glands do different things. Generally animals' sebum marks
territorial hunting grounds, nests and trails5, as well as individual group members.25
This need for persistence may account for its being among the less volatile organic
excretions.9

Sea birds such as heron gulls take sebum from their sebaceous rictus and
preen glands to mark twigs, grass, and pebbles over their nesting territories.21
Recognition of these pheromone deposits give birds confidence or timorousness
depending upon whether the deposit tells them they are standing their own ground or
intruding. "Most animals use their own odor to permeate their environment, not so
much to repel intruders but rather to tend to their own comfort.21 Similarly, deposits
and emissions inside our dwellings may make us feel safe and secure living there.
Who cannot remember a sleepless first night in a new home?

Thousands of ornithologists observed, filmed, and analyzed avian border

marking behavior only to agree with Tinbergin that the processes were totally
meaningless. Nikko Tinbergin (winner of the 1973 Nobel prize in physiology or
medicine with Karl von Frisch and Konrad Lorenz) was among the first to apply
ethological tools in ornithology. He was one of those who coined "displacement
22
EXOCRINOLOGY
activity" for supposedly meaningless behavior. Naming differs fundamentally from
explaining. Careful catalogs compiling millions of hours of watch time were to no
avail against scientific inertia. Tinbergin's untestable hypothesis stood unchallenged
in our modern age for 50 years, a testimony to the enduring influence of this great
pioneer. Of course, he was totally wrong. Marking territories with chemicals that
humans cannot smell well during ‘displacement activity’ is the basis for most nesting
territoriality and behavior.21

Skin sebaceous glands are ubiquitous in mammals, have essentially the same metabolic
characteristics, and produce secretions of complex composition. Specialized sebaceous
glands constitute a major proportion of the presumptive mammalian marking and scent
glands. Although their secretions are, apparently, even more complex they are almost
certainly variations on the common sebaceous metabolic theme. Since this metabolic
capacity is sufficiently adaptable to provide scent glands for multiple species, it is not
unreasonable to assume that it can also provide several odor cues within a species. 73

Tiny sebaceous glands embedded in and opening onto the skin and hair
produce the tiny amounts of sebum needed to keep people together (and coming back
for more). Roughly two grams of sebum get secreted onto skin, clothing, and
bedclothes every day. 74 These glands, the sebaceous glands, appear on skin that
human beings kiss most.4

Think of skin we humans kiss often. Does kissing there vary from culture to
culture, from climate to climate? With no one measuring how many kisses go where
for how long, the question goes unanswered.

Ordinary human experience allows construction of a likely scenario even

without hard data. Some skin gets few kisses. For instance, who kisses elbows? You
might expect the elbow to have a dearth of glands, and that is so.8 There are almost
no glands on the elbow. Likewise, there are few sebaceous glands on the palms of the
hands and on the soles of the feet.

In animals other than humans, variations in gland prevalence and morphology

show corresponding differences in gland secretion, composition, and function.
Different gland shapes generally mean different secretions. Sebaceous glands
23
fulfilling different functions differ in size, shape, number and location. They produce
secretions at differing rates and compositions. Glands vary anatomically. Different
glands do different jobs. Glands that open onto virtually all hair follicles and secrete
human sebum onto clothing and bed linens differ from those that open directly onto
skin surfaces. Both of those are larger and less symmetrical than those invading
mucosae inside the mouth or elsewhere.

Some specialized sebaceous-type glands probably have mundane functions.

The cerumenous glands probably just make it easy to shake the water out of our ears.
The Meibomian glands of the eyelid seem to contribute to maintenance of tear-film
stability over the cornea. Who knows? Some insist even today, that the specialized
glands in the human integument or skin may contribute nothing to kissing, but the
preponderance of the evidence, much of which is anecdotal, says kissing is
biologically important. Economics insists that it is.

However, surface-opening capillary-encapsulated sebaceous glands do clump

together in large numbers. Such gland aggregations appear on the scalp, forehead,
cheeks, nose, at the outside edges of the lips, on the neck, and the female nipples and
areolae. Face and scalp sebaceous glands can be differentiated on a histochemical
basis.75 Also, please see figure in Albone’s book. It shows that differentiation can
also be made from the presence or absence of certain androgenic steroid metabolizing
enzymes.30 The glands in and around the female mammary spots (the vermilion
areolae & nipples) differ physiologically from their kin. Note that sebum glands of
unusual bi-lobular shape also open onto skin surfaces all around inside the mouth on
the buccal and oral mucosae. Others open onto the contact surfaces of the mature
sex organs, as still others coat pubic hair.

Put Figure 3.5 from page 58 of E.S. Albone, 1984 about here. It must be reproduced
with permission from Baillie, Ferguson and Hart (1966), Developments in Steroid
Histochemistry, Academic Press, Inc. (London) Ltd.

24
EXOCRINOLOGY
Although no one knows the chemical composition of the various oral sebum
glands' secretion, it probably differs from those found on the face. This would follow
the rule observed in other animals where gland physiology and chemistry vary
together with function. Specialized use would help to explain why these specialized
mate-mate bonding glands are, like female areolar glands, hidden away and protected
from indiscriminate licking in our clothed cultures.

"In man, the largest and most numerous glands are in the skin of the head, forehead,
cheeks, and chin 400 to 900 glands per 1 cm2 as compared with less than 100 per 1
cm2 in some parts of the body76 and none at all on palms and soles".73

SEXUAL GLANDS

Skin surface sebaceous glands of varying morphology thrive where most

kissing takes place: face and head, lips, inside the mouth on mucosal surfaces within
tongue-reach of an osculation partner, female nipples and areolae. Specialized
sebaceous glands line the sexual contact surfaces of the uncircumcised penis tip (the
preputial glands) and vaginal labia and are also known as Fordyce spots. Their
appearance with sexual maturity is no coincidence.

The sebaceous glands of the female sexual organ (Bartholin's glands) secrete
significantly only during the plateau phase of sexual intercourse. Thus they are
worthless for lubricant. 77 Very few glands inhabit the clitoris,78 which swells with
excitement but does not heat.79 That means heat increased sebaceous secretion can
not be related to tumescence, except where increased circulation suffuses the peri-
glandular vasculature.80 We must strongly suspect mutual pheromone exchanges
between an uncircumcised man and a woman during sexual intercourse, owing to the
extreme heat and immediate contact of gland filled skins. The unusually lengthy
plateau phase in human intercourse35 may facilitate communication of both
Bartholin's secretion to the penis and the smegma of the preputial glands & Fordyce
spots of the penis to female vagina.

25
 At sexual intromission, too many sebaceous-type glands contribute to semen
for simple nutrition's sake.34 One hormone found in semen and elsewhere,
prostaglandin, incidentally released by female goldfish as a pheromone, stimulates
male spawning behavior. With other similar findings it has been established that
hormones and their metabolites may commonly serve as reproductive pheromones in
fish.81

From the author's examination of sebaceous chemistry (see Chapter 3), these
glands can move large amounts of information back and forth. Note that urinary
pheromones affect oocyte selection in ovaries and they also can block pregnancy in
rodents.82,83,84 Information brought by frequent human intercourse could
epigenetically select sperm and perhaps even influence chromosomal selection after
syngamy, an epigenetic function. Fetal development and subsequent behavior of the
partners may also be affected in humans making economic use of available biological
information. While mechanisms for pheromone exchange were hypothetical in 1991;
human glands, human secretion and animal examples did exist, even then. We know
that pheromones effect changes in the quaternary structure of DNA and the proteins
surrounding DNA epigenetically.

A pheromonal use might help to economically justify the high frequency and
low fertility of human intercourse. Polyandrous and promiscuous cultures are less
fertile than monogamous ones.2,85 Perhaps a destructive semiochemical sperm
competition explains this? Competition may be overemphasized. Instead perhaps a
pheromonal cooperation reduces fertility? Semen from more than one man may
either compete or cooperate in the female reproductive tract. First sex after a period
of separation excites a greater volume of semen.

FACIAL GLANDS

As already mentioned, saliva moves sebum around. Lips may conserve mouth
moisture when not kissing. Lips maintain a pheromone-grabbing, wet, sucking
surface always available. Additionally, excited facial lips become hot lips. They heat
in passionate courtship behavior. Hot lips further encourage sebaceous transfers.

26
EXOCRINOLOGY
Honeycomb drips from her barbarous lips
And her palate is smoother than oil:
But her tongue is as bitter as wormwood,
And sharp!
Like a two edged foil.

Proverbs Chapter 5, Verses 3 and 4.

Puberal onset sebaceous glands line the soft, moist, glabrous mucosae that
together make up the inside surfaces of the mouth.7 Glands also invade the gingival
mucosa in the interior cheek mucosa. These "adult osculation glands" form a rough
line with the molars and incisors in the oral mucosa.

When visible these unusually shaped sebaceous osculation glands of the

sexual contact surfaces and inside the mouth on the oral, buccal and gingival mucosa
are called Fordyce spots. Most of those in the mouth lie within a tongue-length of
another human being kissing that mouth. The unknown rhythms of Fordyce spots
deserve study.

What does a passionate "French" kiss accomplish? Are we trying to lick and
suck those glands clean of sebum with our tongues in each other's mouth? The adult
develops a specialized surface on the tongue in puberty38 arriving with the glands just
in time for this behavior. Perhaps it is a mechanically lipophilic surface?

Most body tissues develop from fetal precursors inside our mothers' wombs,
but the mucosal sebum glands seem to pop out of nowhere, de novo, right about the
time open-mouth kissing starts in earnest: at puberty.8 Sebaceous glands of pubertal
genesis number among the so-called "accessory sexual" glands.12 The sebum glands
lining the mouth (and elsewhere) are especially active during the late teens and early
twenties.8 Early adulthood marks peak human fertility. Also in early adulthood,
kissing frequency peaks and people choose mates for themselves.10 Of course, the
peak of sebum secretion is shared with peak rape frequency, too. The pinnacle of
reproductive fitness86 sexual behavior10 and the highest sebaceous secretion8 are
simultaneous.

27
 Fordyce’s ‘ectopic’ sebaceous glands, above from the buccal mucosa and
immediately below from the penis, are always present from puberty into adulthood
and until menopause or death. These behavioral mucosal glands of the mouth and
sexual contact surfaces are unexplained and ignored in the present day, 2011. They
are normal and they are quite obviously there for osculation. However there have
been no rigorous, exocrinological studies of kissing frequency and no meticulous
medical study of the human osculatory system.

28
EXOCRINOLOGY

This figure shows the appearance of some representative human sebaceous

glands. The gland's vascularization has been intensionally obscured by the artist. In
truth, capillaries encircle and intertwine about the glands, and not just at the skin
surface.78 These tiny blood vessels fill up or drain in response to human emotion.
Blood circulates close to the cool skin surface affecting skin temperature. However,
as should be evident from the drawing but isn’t, warming the sebum glands must be
the emotional circulation's primary purpose. This vascularization, along with
thickening of the skin in both sexes, develops during puberty concomitant to
sebaceous gland development.78

Fear and remorse drain the capillaries around the sebaceous glands and cool
them.87 Anger,86 blushing, and sexual passion77 fill them to heat. Circulatory
coloring of the skin to signal emotional or physical health persists only in people with
weakly pigmented skin and albinos.

Does a connection exist? Human sebaceous glands respond to heat in an

unusual way because sebum itself responds to heat in an unusual way. How? Heat
works on sebum a bit like heating butter but over a much much wider temperature
interval. Thus blushing is not a shy mechanism at all is it? The deepest blushing
29
pumps the most sebum up onto the very skin at the very time and place where
important kisses are most likely. If you like someone a lot and want them to like you
more, and if that person is about to kiss you: blush! Would anyone insist that
blushing is merely a color signal just in white people?

PASSION

A functional basis probably exists for the heat of "hot dates" and the "sex
flush" of sexual intercourse noted by Masters and Johnson in Human Sexual
Response.16 During passionate heterosexual courtship behavior, increases and
decreases in skin temperature can be recorded,77 and heat releases torrents of sebum.18

Passionate heat makes sebum secretion available in the right place and time to
gush sebum under the kisses of lovers. The warmth of affection then, would be
functional. The hot surfaces so described and the areas of highly vascularized
sebaceous gland aggregation are one and the same.4

As already noted the heat of a passion produces no generalized fever.

Although some would say their brains burn with passion (in rats the hypothalamic
circulation actually cools 88), only some skin areas warm. When kissing, the skin
temperature increases become noticeable. (Pheromones produce hyperthermic
responses in laboratory animals 89 suggestive of the fever response to chemicals of
pathogenic origin, and helping to explain the anti-pheromonal effects of NSAIDs.
Some children with autism spectrum disorders (ASD) exhibit improved behaviors and
enhanced communication during febrile episodes90) The brain responds instinctively
to romantic signals and sends the blood to be circulated there.

Usually the capillary network just under the skin helps regulate body
temperature. Is lovemaking so strenuous? During a hot date, some skin heats up
while other skin areas, like the belly button, cool down (although kissing the
bellybutton of a passionate, aroused female might be considered inappropriate and
less rewarding than kissing her elsewhere.) The hot skin is the kissable skin saturated
with furiously 'pumping' sebum glands. Glands secrete continuously and passively.
30
EXOCRINOLOGY
They have no muscles, so no sphincters. Afferent (inbound toward the brain sensory)
neurons innervate some glands. We know not why. Perhaps it is for tingles?

The passionate heat increases sebaceous (sebum) secretion abruptly for a short
period. The relationship between skin temperature and sebum secretion rate is highly
significant. Heating and cooling produce secretion rate changes of about 10% per
1o C.18

Human adult kissable skin seems to have a ready reservoir of sebum.91 Does
the reservoir in the pores of the skin hold sebum for moments of romantic ecstasy?
The highly elastic sebum secretion rate with respect to temperature changes and the
heat of passion work in concert to encourage timely sebaceous secretion, kissing, and
bonding.

A LITTLE MORE ABOUT GLANDS

Since about the time of Frederick the Great, scientists have wondered what
these glands were doing on the skin in so many strange places. 92 There were just too
many glands and they were too active to be dismissed as trivial. Nor did they seem to
be mere vestiges from earlier stages of evolution when they were more important to
the body.12

While many dermatologists finally suspected that the glands communicated

some biological message, that message escaped them. 93 Dermatologists as a group
seem determined to avoid behavior issues.

OTHER IDEAS ABOUT SEBUM

Was sebum also a lubricant? Was it some sort of moisture barrier? Perhaps an
emollient? Or was it merely a nuisance? One by one, those ideas were tested and
dismissed.76

31
 Does sebum enhance water resistance in other species? Water birds come to
mind. The feathers of waterfowl need no waterproofing.59 Deposits of preening
sebum onto them do nothing other than impart a characteristic bird stink. The
arrangement of the feathers is important, however.94

Is sebum a natural waterproofer? As mentioned, even in waterfowl, feathers

do not depend on sebum to shed water. Does sebum help the body retain moisture?
Maybe it does a little. Unfortunately for that hypothesis, an effective sebaceous
moisture barrier needs a thickness of sebum an order of magnitude thicker than the
normal sebaceous film. According to both Kligman76 and Rothman13 only a
sebaceous layer at least ten times normal would be required to impede moisture
transmission even slightly. Skin moisture does not need sebum as dry skin may or
may not be sheathed in it.95 Only at birth sebum might reduce water loss
significantly. The newborn's covering of greasy pheromone may be thick enough to
contain some moisture.

Medical texts make sebum out to be fungicidal or bactericidal. That is an

unjustified belief that must stop. Nothing in sebum goes out of its way to kill fungus
or bacteria. Whether sebum is on the skin or not, commensal bacterial growth does
not respond to its presence.96 Cove et al90 should have ended the controversy, but
people still publish nonsense.

Bacteria and fungi find the skin a mechanically dangerous place. The skin is
like a table top. Nothing much holds moisture there. Bacteria and fungi falling there
dry up (desiccate) and just blow away.76

Does sebum act like "false food" to keep bacteria or fungi populations static?
Some evidence supports this view.10 However, consider this. Would being appetizing
to fungi or bacteria recommend itself for a pheromone constantly exposed on the
skin? Pheromones of at least one species do have some anti-fungal properties.97 One
does not preclude the other indeed, all naturally occurring antibiotics are probably
semiochemicals in their own right.

32
EXOCRINOLOGY
Lastly, Guthrie98 thought sebum helped make unwashed faces menacing
somehow. Of course, the facial skin surface lipids have no color, no odor, and are
virtually undetectable except as a slight shininess.

SEBUM SECRETION AND SWEET KISSES

Rates of secretion onto the skin surface also vary. They yield variation both in
composition and abundance.9 Maybe different sebums effect different bonds
depending upon anatomical origin of the sebum? Human beings form a variety of
love bonds. We kiss other human beings with varying techniques and at differing
body locations depending upon sex, kinship, age, and even time of day. “Time of
day?” you ask, try scheduling a prom dance at 8:30 am! While culture differences are
found, kissing remains fairly consistent from culture to culture.83 We have one kiss
for brother or sister and another kiss entirely for a lover. You do not "French" kiss
your baby or your grandmother. The distinctive anatomical sebaceous compositions
with kissing technique may foster distinctive bonds for social functioning.

When women kiss it

always reminds one of
prize fighters
shaking hands.
H. L. MENCKEN

The sebum secretion rate increases during the last trimester of pregnancy,
despite high levels of estrogen in the blood, a hormone which normally inhibits
sebum excretion.99 The same elevated sebum secretion rate stays high during the
time a mother nurses from her breasts.100 Are pregnant and lactating women more
"kissable" than non-pregnant, non-lactating women? Enhanced bonding effort during
the period when reproducing females are most vulnerable seems both logical and
economical.

33
GETTING THE CHEMISTRY RIGHT

Romantic kissing does not bring on true love in every case. Why not? Even
though mutual attraction usually precedes romantic kissing, kissing does not reliably
predict reproductive success. Primed human kissing (from circulating fetoproteins,
lochia, and/or colostrum), may effect parent-infant bonding, and primed kissing (from
previous sexual experience) predicts continued successful mating in humans. Other
influences affect pheromone receptivity, however, including endocrine state and even
air pollution.

The chemical distinctions in sebum developing at or near puberty may hold at

least part of the answer. Indeed, such changes distinguish mature from immature
sebum.101

The sebaceous wax ester component increases around puberty.73 The same
esters distinguish the vernix caseosa of full term neonates from premature ones.102
Among all pheromones known, esters are pheromones more often than any other
chemical functional group.103

Wax esters are just what they sound like. They are waxy substances. Wax
esters in sebum "melt" at slightly different temperatures in their turns as gland
temperature rises. In adults, particularly young adults, these sequential liquefactions
give the rush of sebaceous pheromone that comes with the hot skin of passionate
kissing.

Once their parents are hooked, offspring have no need for such heady stuff as
passion, so wax proliferation awaits puberty. Does that sound reasonable? Free fatty
acid information maintains some consistency,104 but the composition of newborn
waxes vary greatly from those of puberty and of adulthood (Pochi, Peter E., et al.,
1979; Nicolaides, N., et al., 1972). Thus very young couples with still developing
sebaceous compositions may suddenly find themselves poorly matched as they grow
older. Marriages of very young teens do tend to end in divorce. Changing sebums,
changing love: have they something in common?
34
EXOCRINOLOGY
The sebaceous composition of the adult differs from that of the infant, the
child and the pubescent.96 Perhaps aversive pheromones, which protect the young in
other species, may also linger into human puberty? Thus when one mate is very
young, chemical compatibility difficulties may also be encountered?

However, most couples are of comparable ages. Perhaps genotypic or

environmental information codes into sebum105 and vice versa? A chemical
compatibility may be a prerequisite for love. A mismatch might signal a fizzle. If so
that might explain why even some mating kissers fail to love. The chemistry just
wasn't right. This suggestion that pubertal pheromone changes, with regular seasonal
fluctuations, encode genotypic or other information into our skin secretions to
influence mate choice appears logical. A selectively attractive secretion might
enhance "hybrid vigor".97

Hybrid vigor results from a cross between two members of the same species
that have very different genotypes (or gene makeups). An example may serve to
explain. Take three groups of pea plants, "A," "B," and "Hybrid AB." One group,
group "A," had parents that were closely similar genetically; say they have group "A"
typical traits.

Take another similar group of pea plants having different characteristics from
"A." They are group "B." Now take the offspring of cross-fertilization of both
groups "A" and "B," the "Hybrid AB" group. They have had one parent from the "A"
and one parent from the "B." Expose all three groups to a destructive pea plant virus.
Which of the three groups remains healthiest? "A?" "B?" or "Hybrid AB?"

We are talking about hybrid vigor, right? The "Hybrid AB" group with hybrid
vigor has dissimilar parents. Axiomatic among animal and plant breeders, hybrids
remain strong, vigorous, and prolific while purebreds are weak, spent and infertile.

What is more, inbred populations are inherently riskier. We know that

inbreeders carry more deleterious genetically inherited traits, and biological devices
to avoid inbreeding might be expected.

35
 I wasn't kissing her, I was whispering in her mouth.

CHICO MARX

Hybrid vigor does not follow automatically from sebum uniqueness. Merely
encoding genotypic information into our kissing sebum would not do the trick.
Preferring non-kin secretions must complete the picture. How?

An elegant murine experiment was set up as follows. A female mouse could

follow either of two aromas. She could follow the scent of a male from her own
identical strain or she could approach a male from a strain differing from her own by
only one gene. She invariably chose to approach the non-twin. 106

While the hybrid vigor scenario appears to make a tidy argument, there are
counter examples that support another hypothesis, which may fit the facts a bit better.
What about the Kibbutz children? Israel has Kibbutzim, or communal farms, where
all the children live together. Adults share child-rearing. Such kibbutz children live
with unrelated children as if they were all one family. Children raised together,
related or not, tend not to marry each other. Instead they marry outside the group.

Consider also those living in isolated communities on islands, in high

mountain valleys, or under constraint of religious proscriptions, who suffer a risk of
inbreeding. Such people might be expected (at least non-consciously) to avoid
genetic illness, provided they had the information to do so.

Remember Oedipus and Electra? The existence of incest in ignorance shows

counter-evidence. While inbreeding might be answered economically as making the
best of a bad situation, incest in ignorance cannot be.

Perhaps the genotypic information idea is a bit too facile. Genotypic

information may not necessarily be the signal conveyed at all. Perhaps the appetite is
just for something strange? This chemical recognition from association may be
immunologically determined from prior inoculation. An appetite for alien sebum
36
EXOCRINOLOGY
would assure that hybrid vigor would be achieved most often. Tit for tat, hybrid vigor
assures greater success of offspring inheriting genes for genotypic pheromone signals
and alien appetites.

A love pheromone of non-self and non-family (or non-kibbutz family) may

serve for attaining hybrid vigor. No genetic encoding of sebum would be necessary
beyond randomness. Kissing your sister may be distasteful only because you
chemically recognize her from association as something to avoid. Kissing children
romantically must be distasteful for another reason: an aversive pheromone. The best
candidate seems to be an unusual, childhood only, skin surface emission of a
specialized cholesterol.

Finally, anecdotes suggest that the brain needs evidence of paternal blessing to
maintain vigorous and deeply satisfying heterosexual behavior. The father’s (or other
adult male) facial skin surface lipid taken by mouth in sufficient quantity without
sexual receptivity effectively strips lesbians of all homosexuality. Loving your father
seems well worth the effort.

SEBUM IN ANIMALS AND US?

Scientists have watched the behavior of social animals and tracked gland
masses. They have followed exchanges from animal to animal with dyes and
radioactive tracers.107 They have exposed animals to pheromonal chemicals under
controlled conditions, too (e.g. Roelofs, W.L., 1979108; Müller-Schwarze, D.,
1969109). From such experiments, scientists have learned that sebum is a
semiochemical in many species. 110

As in mammals generally, the male of our species has more sebaceous glands
than the female. Dimorphic differences in appetites for pheromones drive human
sexual preference14 There is no ‘gay gene’ however, since homosexuality can be
alleviated by oral intake of 150 mg to 250 mg of healthy adult male facial skin
surface lipid p.o. Pheromone appetites determine fruit fly sexual preference.111
Indeed, it is easy to alter sexual preference from homosexual to heterosexual as this
37
author has done eleven times now, beginning in 1989. Providing 150-250 mg of adult
male facial skin surface lipid by mouth forces the transition.

A "pecking order" may be pecking for pheromones. In social birds pecking

sebaceous glands (in the cocks comb, rictus perimeter and preen gland at the base of
the tail) is strictly hierarchical.112 Human behavior suggests the importance of human
hierarchies. The wearing of judicial robes and seating behind high court benches may
prejudice court decisions just as business suits and desk real estate widen
interpersonal space for the safety of deciders.

In laboratory animals, specialized sebaceous gland size varies with social

status within the local behavioral hierarchy. Top rats have heavy, active glands while
low ranking rats (who "don't exist socially") have glands that are dried up and
atrophied.70 Lorenz noted that low ranking rats climbed trees--a decidedly dangerous
behavior for a rat--in order to escape the scent marks of higher ranking rats.
Dangerous behavior and hen-pecked fins are typical of hatchery raised fish because of
crowded unnatural conditions. Fish hatcheries presumably destroyed the salmon runs
by releasing aversive warning pheromones from hatchlings that washed downstream
warning prospective salmon parents of poor breeding conditions.

Who has access to whose fur defines troop sociality exclusively in other
primate species. Sometimes only the top banana has access to all troop members' fur,
sometimes the reverse.15

In humans, overactive sebaceous glands seem to cause the skin condition

known as acne. Acne is a skin disease that has had it own effect upon hierarchical
status in pubescent teens. It causes disfiguring eruptions of face and body pustules,
diminishing status temporarily.

Human beings do not groom one another as apes do. We kiss instead. The
repertoire of human kissing technique appears to exceed the range of primate
grooming devices. Some primatologists will disagree. Doubtless some apes will, too.
Furthermore kissing should play little part in work-related hierarchical struggles. So
what governs work-related social interaction? Perhaps--and to a surprising extent--
airborne pheromones do.
38
EXOCRINOLOGY

SEBUM CHEMICAL COMPOSITION AND ROMANTIC FAILURE

While the various chemical components of sebum are characteristically

human, our sebums are still just as distinctive as our faces. Every adult human being
has his own personal biochemical recipe because each human being carries a unique
sebum. We share most of the same human-typical components, their relative
abundances in the mix change from person to person. Such mixture variations serve
to distinguish one person's sebum from another's.10

So your pheromones set you apart. Does your semiochemical chemical

composition change with emotion? This may be plausible because different passions
vary in their skin heats. Sebums of the passions would have varying components in
their melts. If these expectations are met then sebum is "personal mood slime."

In humans sebum composition varies from place to place on our bodies as

well.9 The sebum on your forehead has different components from that of your chin.
Both of those differ from that inside of your mouth. And all differ from the sebum
around your nipples (if you are a reproductive female).16 Does uptake of the female's
breast sebum affect subsequent male behavior?

Pheromones explain much, perhaps even the whole story. Human beings
retain the free will to love or not to love, until they decide to draw neigh. Then what
follows may not be entirely in their hands, as all true lovers know.

39
 Marriage, like a Trap set for flies, may possibly be ointed, at the Entrance, with a
little Voluptuousness, under which is contained a draught of deadly wine, more
pricking and tedius than the Passions it pretends to cure, leaving the Patient in little
quieter condition in the morning, than him that hath overnight kill'd a man to gratifie
his revenge.

Advice to a Son
Page 7.II
II,. Love and Marriage 1683

1Birt D, Main J Oral manifestations of herpes simplex virus infections. Laryngoscope 1977;87(6):
872-878.
2Eibl-Eibesfeldt, Irenäus. (1970a). Ethology the Biology of Behavior, translated by Erich
Klinghammer New York: Holt, Rinehart and Winston 530 p.
3 Gould SJ, Eldredge N. Punctuated equilibria: the tempo and mode of evolution reconsidered.

Paleobiology 1977;3:115-51.
4 Nicholson, B. 1984; Does kissing aid human bonding by semiochemical addiction? British Journal

of Dermatology 111(5):623-627.
5 Schleidt, M. 1980; Personal odor and nonverbal communication. Ethology and Sociobiology 1:225.
6 Selway, R, and E.B. Keverne 1990; Hippocampal lesions are without effect on olfactory memory

formation in the context of pregnancy block. Physiol. Behav. 47(2):249-252.

7 Kandel, Eric R, and James H. Schwartze 1985; Principles of Neural Science. New York: ElsevieR

979 pages. pp 21-22.

8Montagna, William, and Paul F. Parakkal 1974; The Structure and Function of Skin. New York:
Academic Press. 433 p.
9Greene RS, Downing DT, Pochi PE, Strauss JS. Anatomical variation in the amount and
composition of human skin surface lipid. Journal of Investigative Dermatology 1970;54(3):240-47.
10 Nicolaides, N. 1974; Skin lipids: their biochemical uniqueness. Science. 186:19-26.
11Agache, P., D. Blanc, C. Barrand, and R Laurent R 1980; Sebum levels during the first year of life.
British Journal of Dermatology. 103:643-649.
12 Montagna, William (1965). The skin. Scientific American 212:56.
13 Rothmann, Stephen (1959). The Human Integument. Washington, D.C.: American Association for
the Advancement of Science, Publication No. 54

40
EXOCRINOLOGY
14 Nicholson B. Love and kisses: a semiochemical addiction model for human bonding. 1983. Paper
presented to the International Society for Human Ethology and Animal Behaviour Society biannual
international meeting at Bucknell University, Bucknell PA.
15Wilson, Edward O. 1975; Sociobiology The New Synthesis. Cambridge, Mass.: Belknap Press of
Harvard University Press. 697p.
16Masters, W.H., and Virginia E. Johnson (1966). Human Sexual Response. Boston: Little, Brown
and Company.
17Seeley, T., T. Talbot, P.R Abramson, L.B. Perry, A.B. Rothblatt, and D.M. Seeley 1980;
Thermographic measurement of sexual arousal: a methodological note. Archives of Sexual Behavior
9(2):77-86.
18 Cunliffe WJ, Burton JL, Shuster S. The effect of local temperature variations on the sebum
excretion rate. British Journal of Dermatology 1970;83:650-4.
19 Pierard-Franchimont, C., G.E. Pierard and A.M. Kligman 1990; Seasonal modulation of sebum
excretion. Dermatologica 181(1):21-2, 1990.
20 Burton, J L. (1970). The physical properties of sebum in acne vulgaris. Clinical Science
39:757-767.
21 Nicholson, B. 1985; An economic model of phermone transmission in avians. Paper presented to
the Animal Behavior Society biannual meeting, Raliegh, N.C.
22Blum M. Pheromonal bases of social manifestations in insects. In: Birch MC, editor Pheromones.
Amsterdam: North-Holland Publishing Company, 1974.
23Moulton, David G. 1977; Minimum odorant concentrations detectable by the dog and their
implications for olfactory receptor sensitivity. pp. 455-464. In: Chemical Signals in Vertebrates
Müller-Schwarze, D and Maxwell M. Mozell editors. New York: Plenum Press 610 p.
24 Albone, Eric S. 1990; Mammalian semiochemistry and its applications. pp 77-83. Chapter I.9 In:
Chemical Signals in Vertebrates 5. MacDonald, D.W., D Müller-Schwarze, and Steven E. Natynczuk
editors. Oxford: Oxford Science Press. 659 p.
25 Wilson, Edward O. (1963). Pheromones. Scientific American 208:100.
26 Finck HT. Romantic Love and Personal Beauty; Their Development, Causal Relations, Historic
and Natural Peculiarities. London: MacMillan. (1891).
27 Harlow, Harry F. (1958). The nature of love. Amer Psychol. 13:673-685.
28 Murstein, B.I. (1971). Theories of Attraction and Love. New York: Springer Publishing Company,
Incorporated.
29 Hold-Cavell, Barbara, and Margret Schleidt 1981; A Cross-Cultural Study on the Attitude towards
Personal Odors. Journal of Chemical Ecolology 7(1):1
30 Albone, Eric S. 1984; Mammalian Semiochemistry The Investigation of Chemical Signals
Between Mammals. Chichester, England: J Wiley & Sons Limited. 360 pages p. 13

41
31 Johnston, Robert E. (1983a). Chemical signals and reproductive behavior Chapter 1. pp. 3-37 In:
Pheromones and Reproduction in Mammals. Bandenbergh, J G. editor. New York: Academic Press,
Inc. 298 p.
32 Garcia-Velasco J, Mondragon M. The incidence of the vomeronasal organ in 1000 human subjects
and its possible clinical significance. The Journal of Steroid Biochemistry and Molecular Biology.
(Proceedings of the International Symposium on Recent Advances in Mammalian Pheromone
Research.) 1991; 39(4B):561-563.
33 Monti-Bloch, L., and B.I. Grosser 1991; Effect of putative pheromones on the electrical activity of
the human vomeronasal organ and olfactory epithelium. The Journal of Steroid Biochemistry and
Molecular Biology. (Proceedings of the International Symposium on Recent Advances in Mammalian
Pheromone Research.) 39(4B):573-582.
34Morrison, Robert Thornton, and Robert Neilson Boyd 1987; Organic Chemistry Fifth Edition.
Boston: Allyn and Bacon, Inc. 1486 p. (p. 347)
35 Drickamer LC. Puberty-influencing chemosignals in house mice: ecological and evolutionary
considerations. In: Duvall D, Müller-Schwarze D, Silverstein RM. editors. Chemical Signals in
Vertebrates 4. Plenum Press: New York. 1986;441-56.
36 Morris, D. (1967). The Naked Ape. New York: McGraw-Hill.
37Eibl-Eibesfeldt, Irena us. (1970b). Love and Hate: On the Natural History of Behavior Patterns.
New York: Methuen and Company.
38 Eibl-Eibesfeldt, Irenäus 1983; Patterns of parent-child interaction in cross-cultural perspective. In:

The Behavior of Human Infants. Oliverio Albert and Michele Zappella editors. New York: Plenum
Publishing Corporation pp. 177-217.
39Verheggen FJ, Haubruge E, Mescher MC. Alarm pheromones-chemical signaling in response to
danger. Vitam Horm. 2010;83:215-39.
40Chivers DP, Wisenden BD, Hindman CJ, Michalak TA, Kusch RC, Kaminskyj SG, Jack KL, Ferrari
MC, Pollock RJ, Halbgewachs CF, Pollock MS, Alemadi S, James CT, Savaloja RK, Goater CP,
Corwin A, Mirza RS, Kiesecker JM, Brown GE, Adrian JC Jr, Krone PH, Blaustein AR, Mathis
A.Epidermal 'alarm substance' cells of fishes maintained by non-alarm functions: possible defense
against pathogens, parasites and UVB radiation. Proc Biol Sci. 2007 Oct 22;274(1625):2611-9.
41 Muscarella F, Fink B, Grammer K, Kirk-Smith M. Homosexual orientation in males: evolutionary

and ethological aspects. Neuroendocrinology Letters 2001;22:393–400.

42 Kohl JV, Atzmueller M, Fink B, Grammer K. Human pheromones: integrating
neuroendocrinology and ethology. Neuroendocrinology Letters 2001;22:309–321.
43 Preti G, Cutler WB, Christensen CM, Lawley H, Huggins GR, Garcia C-R. Human axillary
extracts: Analysis of compounds from samples which influence menstrual timing. Journal of Chemical
Ecology 13(4): 717-731.
44 McClintock MK, Menstrual synchrony and suppression. Nature 1971;229:244-245.

42
EXOCRINOLOGY
45 Cutler WB, Preti G, Krieger A, Huggins GR, Garcia CR, Lawley HJ. Human axillary secretions
influence women's menstrual cycles: the role of donor extract from men. Hormones and Behavior
1986;20:463-73.
46Cocke R, Thiessen D, Nicholson B. Alarm chemosignals suppress the immune system. In:
MacDonald DW, Müller-Schwarze D, Natynczuk SE, editors. Chemical signals in vertebrates 5.
Oxford: Oxford University Press; 1990. p.125-31.
47 Ackerl K, Atzmueller M, Grammer K. The scent of fear. Neuroendocrinology Letters 2002;
23:79-84.
48 Arakawa H, Arakawa K, Blandino P Jr, Deak T. The role of neuroinflammation in the release of

aversive odor cues from footshock-stressed rats: Implications for the neural mechanism of alarm
pheromone. Psychoneuroendocrinology. 2011 May;36(4):557-568.
49Rothman, Stephen (1954). Physiology and Biochemistry of the Skin, Chicago: University of
Chicago Press Chapter 12 Sebaceous-Gland Excretion p. 285.
50 Udry, JR, and Naomi M. Morris (1968). Distribution of coitus in the menstrual cycle. Nature
220:563.
51 Wheatley, Victor R (1956). Sebum: Its chemistry and biochemistry. Am. Perfumer 68:37-47.
52 Nikkari, Tapio 1974; Comparative chemistry of sebum. Journal of Invesigative Dermatology 62

(3):257-267.
53 Inscoe, M. 1977; Chemical communication in insects. J Wash. Acad. 67:16-33.
54 Collins, C.W., and S.F. Potts (1932). Attractants for flying gypsy moths as an aid in locating new
infestations. U.S. Dept. Agric. Tech. Bull. 336:1-43.
55Butenandt A, Beckmann R, Stamm D, Hecker E. Über den Sexual-Lockstoff des Seidenspinners
Bombyx mori. Reindarstellung und Konstitution. Z Naturforsch 1959;14:283-4.
56 Tumlinson, James H., and P.E.A. Teal 1987; Pheromone Biosynthesis and its regulation. pp 3-26.
Chapter 1. In: Pheromone Biochemistry. Prestwich, Glenn D., and Gary J. Blomquist editors.
Orlando: Academic Press, Inc. 565 p.
57 Albone, Eric S., Pauline E. Gosden, and Georges C. Ware 1977; Bacteria as a source of chemical
signals in mammals. pp. 35-43 In: Chemical Signals in Vertebrates (Müller-Schwarze, D, and
Maxwell M. Mozell eds.) New York: Plenum Press 610 p.
58 Gorman, ML, Stone RD. Mutual avoidance by European moles Talpa europaea. In: MacDonald
DW, Müller-Schwarze D, Natynczuk SE, editors. Chemical Signals in Vertebrates 5. Oxford: Oxford
Science Press. 1990; 367-77.
59 Marchlewska-Koj, Anna 1983; Priming pheromones in mice. pp. 135-151. In: Chemical
Signals in Vertebrates 3. (Müller-Schwarze, D, and Robert M. Silverstein eds.) New York: Plenum
Press. 368 p.
60 Epple G. Relationships between aggression, scent marking, and gonadal state in a primate, the
tamarin saguinus fuscicollis. In Chemical Signals Vertebrates and Aquatic Invertebrates. Mu ller-
Schwarze D. and RM. Silverstein editors. New York: Plenum Press. 1980.

43
61Paris, Paul (1913). Recherches sur la glande urophgienne des oiseaux. Archives de Zoologie
Experimentale et Ge'ne'rale. 53:139-276.
62 Hou, H.C. (1928). Studies on the glandula uropygialis of birds. Chinese Journal of Physiology.

2:345-380.
63 Idris, M.D., and I. Prakash 1988; Perception of dominance status through conspecific scent
in the desert gerbil Meriones hurrianae. Indian Journal of Experimental Biology 26(6):479-480.
64 Soni, G.R and I. Prakash 1988; Mitigation of poison shyness in desert gerbil by adding
conspecific sebum of ventral scent marking gland and urine in poison baits. Indian Journal of
Experimental Biology 26(6):476-478.
65 Albone, Eric S. 1990; Mammalian semiochemistry and its applications. pp 77-83. Chapter I.9 In:
Chemical Signals in Vertebrates 5. MacDonald, D.W., D Müller-Schwarze, and Steven E. Natynczuk
editors. Oxford: Oxford Science Press. 659 p.
66 Sugiyama, T., and H. Sasada 1988; Chemistry and biochemistry of unusual branched fatty acids
with pheromonal activity from mature male goat. Seikagaku - Journal of Japanese Biochemical
Society. 60(2):118-122.
67 Doi S, Tanabe K, Yoshimura M. Induction of sexual agglutinability by unsaturated fatty acids in
Saccharomyces cervisiae. FEMS Microbiol Lett 1990;55(1-2):89-91.
68 Weldon, Paul J 1983; The evolution of alarm pheromones. pp. 309-312 In: Chemical Signals in
Vertebrates 3. Müller-Schwarze, D and Robert M. Silverstein editors. New York: Plenum Press
368 p.
69 Nicholson, B. 1988; Pheromones in the pathogenesis of autoimmune and behavioral illness.
Paper presented informally to the International Society of Chemical Ecology, Hull, England.

70Moulton, David G. 1977; Minimum odorant concentrations detectable by the dog and their
implications for olfactory receptor sensitivity. pp. 455-464. In: Chemical Signals in Vertebrates
Müller-Schwarze, D and Maxwell M. Mozell editors. New York: Plenum Press 610 p.
71 Mykytowycz, R 1973; Reproduction of mammals in relation to environmental odours. Journal
of Reproductive Fertility. [Suppliment] 19:431-444.
72 Bell M. A comparative study of the ultrastructure of the sebaceous glands of man and other
primates. Journal of Investigative Dermatology 1974;62(3):132-43.
73 Brown JC, Williams JD. The rodent preputial gland. Mammal Review 1972;2(4):105-51.
74 Albone, Eric S. 1984; Mammalian Semiochemistry The Investigation of Chemical Signals
Between Mammals. Chichester, England: J Wiley & Sons Limited. 360 pages p. 13
75 Sansone, Gail, and RM. Reisner (1971). Differential rates of conversion of testosterone to
dihydrotestosterone in acne and in normal human skin--a possible pathogenic factor in acne. Journal
of Investigative Dermatology 56:366-372.
76Benfenati A, Brillanti F. Sebaceous glands distribution in skin of human body Arch. Italdi.
Dermat., sif. 1939;15:33-42.

44
EXOCRINOLOGY
77 Masters, W.H., and Virginia E. Johnson (1966). Human Sexual Response. Boston: Little, Brown
and Company.
78 Kligman, A.M. (1963). The uses of sebum? pp. 110-124. In: Advances in Biology of Skin. Vol.
4. the Sebaceous Glands (ed. by Montagna, W., RA. Ellis, and A. Silver) Oxford: Pergamon Press.
79 Seeley, T., T. Talbot, P.R Abramson, L.B. Perry, A.B. Rothblatt, and D.M. Seeley 1980;
Thermographic measurement of sexual arousal: a methodological note. Archives of Sexual Behavior
9(2):77-86.
80Hafez, E.S.E. 1976; Parameters of sexual maturity in man. pp. 105-122 In: Volume 3 Sexual
Maturity: Physiological and clinical Parameters E.S.E. Hafez and JJ Peluso editors. Ann Arbor,
Michigan: Ann Arbor Science Publishers Inc. 283p.
81 Sorensen, P.W., T.J Hara, N.E. Stacey and F.W. Goetz 1988; F prostaglandins function as potent
olfactory stimulants that comprise the postovulatory female sex pheromone in goldfish. Biol Reprod
39(5):1039-1050.
82 Bruce HM. An exteroceptive block to pregnancy in the mouse. Nature 1959;184:105.
83Bruce HM. A block to pregnancy in the mouse caused by proximity to strange males. Journal of
Reproductive Fertility 1960;1:96-103.
84 Drickamer, L.C. 1986. Puberty-influencing chemosignals in mice: ecological and evolutionary
considerations. In, D. Duvall, D. Müller-Schwarze and R.M. Silverstein (eds.), Chemical Signals in
Vertebrates, Vol. 4. New York: Plenum Publishing. Pp. 441-455.
85Eibl-Eibesfeldt, Irenäus 1975; Ethology: The Biology of Behavior, second edition. New York:
Holt, Rinehart and Winston.
86Wilson, Edward O. and William H. Bossert (1971). A Primer of Population Biology. Sunderland,
Massachusetts: Sinauer Associates, Inc. Publishers 192 p.
87 Lorenz, T.H., D.T. Graham, and S. Wolf (1953). The relation of life stress and emotions to human
sebum secretion and to the mechanism of acne vulgaris. Journal of Laboratory and Clinical Medicine
41:11.
88 Mennella, Julie A, and Howard Moltz 1989; Pheromonal emission by pregnant rats protects against
infanticide by nulliparous conspecifics. Physiology and Behavior 46:591- 595.
89Kikusui T, Takigami S, Takeuchi Y, Mori Y. 2001; Alarm pheromone enhances stress-induced
hyperthermia in rats. Physiol Behav. Jan;72(1-2):45-50.
90
Mehler MF, Purpura DP. Autism, fever, epigenetics and the locus coeruleus. Brain Res Rev. 2009
Mar;59(2):388-92. Epub 2008 Nov 24.
91 Downing DT, Stewart ME, Strauss JS. Estimation of sebum production rates in man by
measurement of the squalene content of skin biopsies. Journal of Investigative Dermatology 1981; 77
(4):358-60.
92 Pochi, Peter E. 1982; Commentary: androgen effects on human sebaceous glands. Archives of

Dermatology 118(10):803.

45
93Strauss, JS., D.T. Downing and F.J Ebling 1983; Sebaceous glands. In: Biochemistry and
Physiology of the Skin. Goldsmith L.A. editor. New York: Oxford University Press.
94 Hou, H.C. (1929). Relation of the preen gland (glandula uropygialis) of birds to rickets. Chinese
Journal of Physiology. 3:171-182.
95 Frantz RA, Kinney CK. Variables associated with skin dryness in the elderly. Nursing Research

1986;35(2):98-100.
96 Cove JH, Holland KT, Cunliffe WJ. An analysis of sebum excretion rate, bacterial population and
the production rate of free fatty acids on human skin. Br J Dermatol 1980;103:383.
97 Kuwahara, Y., W.S. Leal, T. Suzuki, M. Maeda and T. Masutani 1989; Antifungal activity of
Caloglyphus polyphyllae sex pheromone and other mite exudates. Pheromone study on astigmatid
mites, XXIV. Naturwissenschaften 76(12):578-579.
98Guthrie, RD. (1970). Evolution of human threat display organs. In: Evolutionary Biology, vol. 4.
Dobzhansky, T., M.K. Hecht, and W.C. Steere editors. New York: Appleton-Century-Crofts.
99 Burton JL, Shuster S, Cartlidge M. The sebotrophic effect of pregnancy. Acta Dermato-

vernereologica (Stockholm). 1975; 55:11-3.

100 Burton, JL., Sam Shuster, M. Cartlidge, L.J Libman, and U. Martell (1973a). Lactation, sebum
excretion, and melanocyte stimulating hormone. Nature 243:349-350.
101 Downing DT, Strauss JS. Synthesis and composition of surface lipids of human skin. Journal of
Investigative Dermatology 1974;62(3):228-44.
102Wysocki, S.J, A. Grauaug, G. O'Neill, and R Hähnel 1981; Lipids in forehead vernix from
newborn infants. Biol. Neonate. 39:300-304.
103 Silverstein, Robert M. 1984; Chemistry of insect communication. Chapter 5, pp 105-121. In:

Insect Communication. Lewis, Trevor editor. Academic Press, London. 414 p.

104 Sansone-Bazzano, Gail, B. Cummings, A.K. Seeler, and RM. Reisner 1979; Differences in the

lipid constituents of sebum from pre-pubertal and pubertal subjects. British Journal of Dermatology
103:131.
105 Wysocki, Charles J Chuck 1983; You must remember this, a kiss isn't just a kiss. Paper
presented to the Animal Behavior Society and the International Society for Human Ethology,
Lewisburg, PA.
106 Beauchamp GK, Yamazaki K, Boyse EA. The chemosensory recognition of genetic individuality.
Scientific American 1985;253(1):86-92.
107 Adachi, K., 1984 personal communication.
108 Roelofs, W.L. 1979; Pheromone perception in Lepidoptera. In: Neurotoxicology of Insecticides
and Pheromones. New York: Plenum Press.
109 Müller-Schwarze, Dietland (1969). Complexity and relative specificity in a mammalian
pheromone. Nature (Lond.) 23:525-526.

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110 Shorey, H.H. 1976; Animal Communication by Pheromones. New York: Academic Press.
111 Grosjean Yael, Grillet Micheline, Hrvoje Augustin, Ferveur Jean-François Ferveur & David E
Featherstone A glial amino-acid transporter controls synapse strength and courtship in Drosophila
Nature Neuroscience 11, 54-61 (2008).
112 Lucas, A.M. 1980; Lipoid secretion of the body epidermis in avian skin. In: The Skin of
Vertebrates. Spearman RI.C. and P.A. Riley. editors. New York: Academic Press.

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EXOCRINOLOGY

Chapter 2: Parental Love of Offspring

Before describing the love of adults for their children, the concept of children
itself should be examined. (These petty biological controversies bore everyone, but
some contemporary readers expect this.) What are children for? Loving young
immature forms and caring for them into their reproductive adulthood denominates a
life strategy. Besides mammals, some species of fish, reptile, insect, and amphibian
also practice rudimentary forms of it. The predominant reproductive strategy of
rearing young suits the economic constraint set of human beings better than any other
alternative.

What does parent-infant bonding accomplish for the human species? Any
argument should hold for all other bonding species. This means we should find
similar emission chemistry, pheromone emissions, pheromone receptors, gland
physiology, as well as similar parental and offspring behaviors. Other immature
mammals require nurture but human neonates require more. Human immaturity
extends longer than any other animal species 1 requiring the greatest nurturing of all.
That nurture depends upon parental love. Therefore assuming an altricial childhood
strategy must be less effective without bonding, nurtured, pheromone-triggered, life
strategies should also develop in childhood.

Lengthy immaturity is not the only drawn-out characteristic of human

ontogeny. Humans have one of the longest gestation periods (not the longest because
this is influenced by body size, 2 among the longest courtship periods, and the most
frequent intercourse (continual inseminations throughout adulthood).3 These must
economically contribute to human flexibility as a species. Presumably, a longer time
for relationships enables "fine tuning." Adjustments can be made to new information.
Long-loved children can be molded gradually to best fit a changing world, but so can
un-loved children as we shall see.

Actually, childhood (or immaturity) may be dispensed with altogether. Many

animals give birth to little copies of themselves. Many more species lay eggs which
49
hatch miniature adults. Species with the miniature adult (precocial) strategy usually
abandon their offspring or tend rudimentary nests. For instance, many a reptile mom
lays her eggs to fend for themselves. Others find metamorphosing larval stages more
appropriate, which parents ignore completely. Human beings and other species,
which love and care for their offspring give birth to feeble immature forms. Indeed,
our babies have been described as the most immature form of all. Even though
marsupials bear less viable young, no offspring take so long to rear as human
children. We must bear this question in mind: why?

DOES CUTENESS WORK?

It has to work, to do something. The shape of the head and face mark an
obvious distinction between abandoned and loved offspring. Abandoning species
leave behind young with small but "adult-shaped" heads. Loving species have
smashed-in faces. (And of course, larvae rarely resemble adults).

Innate mental preferences bear upon parent-infant bonding just as upon mate-
mate bonding. Men just naturally like curves. Women admire phalluses. The
German ethologist, Konrad Lorenz (1943) suggested that chubby cheeks and a large
forehead associated with infancy have universal appeal among human beings and
inspire parental care. Many cartoon characters supposedly exploit this innate
fondness as can be seen in the accompanying illustration.

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EXOCRINOLOGY

Figure 277. "Baby schema" of man. Left: head proportions that are generally
considered to be "cute"; right: adult forms, which do not activate the drive to care for
the young (brood care). (From K. Lorenz [1943].)

Notice that the foregoing illustrations are "cute." Where do we find

"cuteness?" In mammals and avians that nurture their young, infants and juveniles
have pushed-in snouts when compared to adults. Remember reptile offspring carry
adult-shaped heads when first entering the world. Pushed-in snouts and the
accouterments of parental care (nests) are seen in some fossilized dinosaur remains.

Dinosaur species that apparently cared for their young may have found their
offspring cute, too. Given the probable intelligence of those beasts, such an
untestable explanation may be a bit too facile.

We can educe the following. Pushed-in immature faces evolved earlier.

Human recognition of "cuteness" came later. Dinosaurs preceded us here, after all.
Keep that in mind.

Consider the pain of human childbirth. Alone among the females of the
world, human females must distort their pelvic skeletons to give birth. Would that
pain and death risk be entirely compensated by "cuter" yet feeble, big-headed babies?
The baby’s brain develops precociously, of course, but these distortions of gestation

51
keep more of the baby’s brain keyed into the mother’s perceptions longer allowing
maternal chemosensory insights that would be otherwise unavailable to the neonate.

Physiologically adult-shaped faces vary from the pushed-in snouts of infantile

forms because the skull grows to include the sinuses. Our sinuses are hollow organs
carved during infancy, childhood, and puberty into the growing bones around nasal
passages. When we are born, we are born with no sinuses. A lack of sinuses
coincides with "cute" infantile features (see Netter, F.H. 1989) 4. Do sinuses form just
to reduce cuteness? With what we are bearing in mind, this is not likely. Perhaps
cute heads get through narrower-the-better-for-running birth canals more easily?
Only the dinosaurs would know for sure.

Sinuses have no known function.5 However, sinuses may function passively

in pheromone recognition, perhaps as semiochemical storage or separation vessels.
Chemists call similar vessels condensers or retorts. When most modern reptiles
hatch, they have their full complement of sinuses in their miniature, adult-shaped
heads. Apparently no bio-economic need for building sinuses arises during reptile
immaturity. Reptile young do not depend precariously upon their mothers as
mammals do. Young mammals and birds confined to the nest or burrow may not
require keen pheromone discrimination. Only adults maintain extended territories.
Such territories might require sinuses in perception of faint trail marking pheromone
the animals use to exploit their territories efficiently. Keeping ‘just the right
distance’ from an adjacent conspecific (or auto-emitted) pheromone trails allows
economical resource harvesting, with wild animals moving through their personal
territories methodically just like we harvest a crop.6

As we will see in Chapter 6, lacrimation or crying, carries pheromone receptor

proteins in tears which inhabit the sinuses. In human beings, sinuses develop in
phases. Sinuses may be involved, somehow, with pheromone recognition, perception,
or maintenance. Economically, if pheromone recognition by the mother requires a set
of sinuses at a certain age, then that set should develop just before the need. The
development of a sinus set in puberty before mate-mate bonding might be expected,
too. Sequences of sinus development does proceed in such phases. They do reach
final completion at reproductive maturity. Too bad for this idea, we have no
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EXOCRINOLOGY
indications of especial activity in parental sinuses in the period leading up to birth, or
immediately after marriage. We do have lacrimation.

New pheromone receptor proteins--the feto proteins--develop during

pregnancy and may be transmitted sexually or by proximity in maternal saliva, skin
lipids, lochia and/or colostrum. And if those sources are insufficient, the neonate is
crawling with fetoproteins in his or her blood. Alpha fetoprotein is essentially
albumin which acts exactly like a pheromone binding protein under antennagraphic
analysis. Since the injection of maternal blood into virgin female rats stimulates
maternal behavior in them, this suggests that some blood plasma borne factor
stimulates maternal bonding.7 Much more will be said about them in Chapter 6.

Sinus growth (and the "adult typical" head shape) should behave economically
and await its need according to the economic model of evolution. "Cute" heads are
characterized by relatively large head sizes, small bodies, juvenile furs/plumage (soft
skin in the human case), helplessness, and perhaps infant calls (tearless crying in the
human case). These and other traits release parental responses alone. Furthermore
releaser recognition of infantile traits varies with species. A single spot of color in the
open mouths of young or on the beaks of adults is sufficient stimulus to release
feeding behavior in many birds, for instance.8

A parental preference might change easier than baby head circumference.

Appearance usually subserves function. Which came first here, the chicken or the
egg? Do we like cuteness, soft skin, baby noises and so on just because of its
physically constrained functional utility? It is a likely prospect as it seems to be the
simplest explanation for now.

DO PHEROMONES AFFECT PARENT TO INFANT BONDING?

The pheromone hypothesis suggests that humans bond to their neonates

(newborns) in a way corresponding to mate-mate bonding. Gestation seems to
accentuate semiochemical receptivity in both parents, but especially so in the mother.
As birth nears, the economic theory predicts that the new arrival will have prepared
53
well to make a big splash on birth day. For the last five and one half months inside
the womb, baby has been secreting and stockpiling sebum within the placenta.9
When the newborn appears, he wears that unctuous stuff, sebum, from head to toe,
and it goes everywhere as anyone who has delivered one knows. What a slippery
mess!

Elevated rates of new sebum secretion from the newborn baby crest the fourth
day after birth and then gradually abate. 10

[T]here is a marked postnatal sebum secretion. Our findings revealed that the
levels obtained on the 4th day of life were comparable to those of young adults. This
is an especially interesting fact which should be emphasized.

Bolstered by the mother's critical period receptivity, does addiction to baby's

pheromone "birthday suit" and to newly secreted sebum precipitate parental love?

A pheromone model of parental love will help answer many questions.

Parent-infant bonding: what are characteristics of this phenomenon? Bonding has
remarkably low risk of failure. This seems reasonable since a baby may quickly
starve or die of exposure without love. Love must work reliably and effectively; it
must not fail.

This author watched bonding failure result in the death of a neonate when he
was in medical school. The ‘too small to be viable’ infant, vigorously crying his
lungs out, lay on a Mayo table for seven and one half hours, just twenty feet from his
mortified mother. My objections were heard and acted upon as I did not receive
academic credit that term. So if you are pregnant and of African descent, chose your
doctor wisely because your baby’s life may depend upon your choice.

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EXOCRINOLOGY
There may be different types of parental love; each must have an accounting.
There must be adequate identification of the loved offspring to reduce mimicry. It
must not err.

"Human beings can discriminate between their own offspring and

unfamiliar children by means of olfactory cues and are even able to discriminate
between one of their own children and their other child using olfactory cues (Porter
and Moore, 1981). Human odors vary with diet (Wallace, 1977), a factor that may
allow familial identification, given a common family diet. Identical twins are more
difficult to discriminate between by their odor than unrelated adults or siblings that
are not twins (Kalmus, 1955; Wallace, 1977), and the olfactory discriminability of
the identical twins can be magnified if they have very different diets (Wallace,
1977)" (Leon, M., 1983).11

Recognizable individual odor differences and/or sebum differences among

children may be the encouragement for a parent to "miss" an absent child. If own-
child odors were monolithic or parental in origin, one son or daughter would be as
good as any other. A woman with thirty children may grieve unconsolably at a single
loss.

Watch human parental behavior toward returning offspring at an airport. See

the kissing and hugging? Hugging may trigger a non-kiss pheromone recognition
mechanism. Indeed, warm partner contact (hugging & kissing) influences peripheral
circulating proteins with chemosensory functions, beta2-microglobulin (11.7 k Da),
serum albumin (66-k Da), and an unidentified 5.9 k Da serum protein. 12

Also seen in resumption of mate-mate bonding, these affectionate airport

behavior may be pheromone replenishment behaviors. Interestingly enough,
something similar can be observed in birds:

55
 Besides being associated with bodily contact and sociality, allopreening is
most frequent in species that are sexually dimorphic, form persistent pair bonds, or
both; and it reaches its highest intensity within species when birds are first brought
together or reunited after a prolonged absence.13

Adjustments, changes, or outright cessation of the parent-infant bond happen

as young grow up. Can the pheromone hypothesis explain all of these characteristics?
An acceptable semiochemical explanation must do just that.

LOW FAILURE RISK

An axiom of good design holds that providing backup systems enhances

system reliability. If one breaks down, the backup functions in its place. A
mechanical device for lowering airplane landing gear backs up hydraulic systems. A
gas generator backs up the electrical power grid at the hospital. Making such systems
dissimilar reduces risk further, an axiom of portfolio theory. More than one such
reserve device reduces risk further, but against diminishing returns on investment.
The more reliable the system per total expenditure, the more successful that system
should be, all else equal. The same logical process holds true working in reverse.
For instance, extremely ‘expensive’ biochemistry indicates tissue and emission
importance.

There appears to be at least two devices which separately prime and stimulate
bonding in humans, one spiritual, the other kissing. Spiritual love may be signaled
by the spirits, or off-gases, of the female's vagina during delivery. If the
physiological basis for kissing involves sebum, a skin secretion, then parent-infant
kissing would have its own special features. The feto proteins that mark phases of
pregnancy are pheromone receptor proteins just like their cousin molecule albumin,
more about them later.

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EXOCRINOLOGY

DIFFERENTIAL PARENTAL SOLICITUDE

Loving parents choose favorites in all animal families (Daly, M. and M.

Wilson, 1980). They love some young more than others. Could there be a biological
basis for this differential parental solicitude? If so then differences in love suggest we
should see differences in the signals stimulating that love.

Do love signals differ? One would expect that there would be recognizable
differences in bonding pheromones from species to species, between kin and non-kin,
and among individual family members. Odors allow parental discrimination of young
in humans and other species.10 All such individual differences exist in human and
other mammalian sebums. (For a fuller review of the uniqueness of our exocrine
secretions, please see Chapter 3 on pheromone chemistry).

A physical imprinting upon pheromone receptors by individually unique

pheromones would accomplish this purpose. Our so-called immune system, our
reproductive system, our endocrine system, our nervous systems may help fill this
role as they all evolved from pheromone and allomone recognition systems clearly
observable in lowly colonial bacteria.

A moistness of the eyes seems to help imprint the pheromones of children.

Indeed, those families that bond to a survivor most successfully grieve for critically ill
infants born prematurely. A dearth of grief by parents marks families leaning toward
abuse of their recovered premie.14 Such observations appear to support the
pheromone reception bonding hypothesis.15,16

JUST IN TIME LOVE

Bonding speed varies from species to species. The time the neonate can
survive without care ultimately constrains. In human beings, a baby might survive
alone only a few hours or less time depending upon environment. Without love, the

57
patience of an un-bonded caregiver might be gone in only a few hours or days
depending upon food abundance, predation risk, crowding and other factors. The
neonate must use that precious time. A baby must succeed and influence, if not
control, parental behavior.

Bonding time being so often short and fraught with dangers, we would expect
no nonsense about it. Lurking sabre-tooth tigers saw to that. Evolution pressures
against inefficiency. Any trait causing pre-reproductive death would get no second
chance. Likewise any trait tending to hurt early survival must contribute more to
reproductive success later in ontogeny. Just how much more, may be a product of the
prevailing internal rate of return and actuarial probability of survival. Compressing
bonding time would require evolving more efficient behavior.

One device common to most mammalian parent-infant bonding is "neonatal

grooming." Is it an oral transfer of pheromone from the skin of the neonate to the
mouth of the mother? How to test this? Preventing neonatal grooming and
separating parent from infant until the pheromone on the neonate's body has
evaporated should stop bonding. So rejection of offspring should result from
shampooing the newborn before the mother can nuzzle the infant, perhaps even
within the sight of the mother. Withholding all neonatal exocrine emissions from the
parent might maintain pheromone receptivity longer than normally necessary, too.

In some ungulate species, each female isolates herself from the protection of
the herd to bear her young. Because she puts herself outside the safety of the group,
the predators have a field day. Indeed, predator reproduction is often keyed to such
feast days.

To minimize predation, some seasonal signal makes mothers calf

simultaneously. Mother-infant bonding generally proceeds as rapidly as possible.
Simultaneous, quick births mean that the lions gorge themselves once only. Because
lions take a while to get hungry again, most of the new babies escape. Consider the
situation and its bonding behavior: The defenseless cow is completely exhausted.
The newborn can not stand and predators lurk all about. (As expected, predators come
from miles around for the occasion.) Is that the time for the mother to spend her

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scarce energy and time to "eagerly clean" her newborn? Obviously it is not. Is this
then the time for crossed signals to foul up and cause nonsensical ‘displacement
activity’? Get real.

Indeed, with predators literally watching and by all accounts, the herbivorous
mother cow eats the amniotic substance "ravenously." The intense appetite for the
neonatal goo comes whether or not she is hungry. Well fed mothers eat it up just like
emaciated mothers. The substance has little nutritional value. Only about 30% of the
sebaceous fraction can conceivably be used for food at all. Some of the rest may
even be poisonous if it were taken in dietary doses. Plus the new ungulate mom is
generally satisfied with just the skin/fur birth coverings of her own young.

An old expression has it that "there is no accounting for taste." There actually
is an accounting for taste. If provided a minimally prepared smorgasbord of healthy
foods, infants will choose a nutritious diet. 17 Similarly, oddball food preferences of
pregnant humans have an economic metabolic basis.18,19 Admittedly, reducing lion-
attracting aromas may have something to do with it, but then why emit them?
Furthermore, species which do not isolate themselves out of the herd, such as sheep,
are just as greedy for afterbirth’s vernix.20

Given economic assumptions, we proceed teleologically. What purpose does

isolation serve at time of delivery? The cows might isolate themselves because their
birth pheromones are indiscriminate to avoid costs or to encourage lion populations
with bigger, slower bellies. The self-imposed isolation would avoid accidental
adoptions and paternity/maternity disputes. Remember, isolation from herd
pheromones occurs during a particularly chemosensitive time.

Following the suggestion of this author, Levy and Poindron (1987) found that
something in ewe amniotic fluid seems to encourage bonding. Amniotic fluid has
attracted some scientific attention (Montagna, W., 1964; Nicolaides, N., 1974). We
will examine it more closely shortly. This author has observed plant-eating mule deer
does eating fawn afterbirth and exhibiting the pheromone-only Flehmen response
observed in horses and in moose.

59
 Meanwhile, what other characteristics should a love manufacturing process
have? Love should be cheap. It should be possible to shut it off for those species
opting for a strategy of seasonal parenthood. Finally, it should accommodate
transition from generation to generation.

CHEAP LOVE

Pheromones cost little to produce and recognize; even bacteria can detect their
own pheromones. Pheromone effects may last a long time, too. Shorey 21 and
others 22 recount how pheromone exposure strictly determines adult behavior. If left
alone, human love spans a lifetime. (Divorce, a contemporary and temporary scourge,
may be remedied by medicinal use of human pheromones. See Chapter 8.) This
seems consistent with the pheromone hypothesis of bonding.

However, seasonal,23 even daily 24 changes in human skin surface lipid

expression have unstudied effects on bonding. Humans may even have a "breeding
season" in the fall. The autumn temperature decrease affects exocrine emissions and
may signal the peculiar increased ejaculations observed. 25

Birds shutdown their sebaceous uropygial gland secretions, along with their
reproductive organs and even their pheromone reception systems after nesting season.
Their sebaceous glands atrophy, often completely, and chemical simplification of the
pheromone takes place.26 Humans do not mate intermittently. The small autumnal
changes seen in human male apocrine secretions (Preti, G., et al., 1987) remain
enigmatic. Does cool air or a shorter day bring on Preti's secretion to induce sexiness?

Addiction sustains a potent human chemical appetite. What more logical

appetite would gratify parents enough to compensate them for caring for young? 10
From economic analysis, the mechanism of love seems so basic, so foolproof, with
backups for backups, that its mechanisms should be straightforward to elucidate.
Perhaps the offspring's recognition pheromone itself stimulates a reward for addictive
craving? The physiology of the mammalian appetite and reward system, the limbic
system, attracts a particular interest. Mice will brave hunger, thirst, even electric
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shock in exchange for hypothalamic stimulation. The hypothalamus is reached by
pheromone reception neuro-pathways.

Theoretical games people, notably Trivers,27 have thought that describing

parental payoffs in terms of investment for the "reward" of having offspring survive
to adulthood is sufficient explanation. Offspring pheromones, and not offspring
themselves, may drive this device. That idea would explain its failures. The evolved
economic necessity would, however, drive the pheromones driving the behavior. Do
you see?

Analogous appetites are hunger, thirst, breath, sexual desire, and elimination.
Take food as an example. Food seeking behavior generally improves an organism's
survivability. Any stimulus to food seeking behavior, particularly one that may be
regulated in tandem with other appetites would improve survivability (closely
approximating optimum division of behavioral resources among competing
appetites). Evolving appetites for essential behavior slaked for rewarding essential
accomplishment may be basic to life. Perhaps crafting both the appetite and the
pleasure of the reward erbkoordinates love.

The most efficient recognition devices are chemosensory. Short, trigeminal

recognition of dangerous natural vapors, carbon dioxide and ammonia, consists of
exposed nerve endings in mucous. Appetite efficiency should be expected as well.
Other mammals besides humans have addictive appetites for chemicals which vary
from species to species.28 Keeping error rates low requires semiochemical species-
specificity. As there are many times more chemicals possible than species, sex and
individual sub-specificity are possible and would be useful. These advantages
proceed from dermal biosyntheses of the unique stereochemistries of pheromones.
The uniqueness is critical only within the ecosystem experienced by the emitting
organism. Other non-chemical checks should discourage predator lure secretions, but
these are seen. Human hunters use this tactic frequently. Think about this.

Reproductive conditions affect the reliability of the pheromone addiction

process. Ungulates avoid bearing young in the herd where paternity/maternity might
be confused. That confusion possibility indicates a valued pheromonal recognition.

61
 Pheromone must move from infant to mother. Weather conditions may
influence bonding success by influencing pheromone transfer success. Accordingly,
birth times may so correlate with low winds or lack of precipitation (seeking shelter).

A competing addiction to drugs reduces bonding success and may prevent it

altogether. Data has strongly suggested that neoparous women taking drugs, some of
which are addictive, bond less effectively to their infants than neoparous women
taking fewer drugs or no drugs. 29 Drug addicted men and women are notoriously
poor parents, with much higher recorded rates of abuse and neglect.30 Thus the
pheromone must itself have a drug-like effect, or so the logic goes. One pheromone
can counteract and overwhelm another, such as in the case of the puberty acceleration
and puberty delay pheromones of mice which work in opposition:

At rations of 1020 parts (puberty) acceleratory chemosignal to 1 part

(puberty) delay chemosignal the acceleratory effect overrides the delay
chemosignal, and the mice attain first estrus at earlier ages than controls. Ratios of
about 4 to 1 up to 7 to 1 result in mean ages for puberty that are not accelerated or
delayed relative to controls.31

Yin and Yang? The opposition of pheromone against pheromone may even
reify these anecdotal oriental hypotheses. An addictive effect would be counteracted
and overwhelmed only by another drug, explaining the neglectful misbehavior of
drug addicted mothers. Contemplate this.

BIRTHDAY LOVE

Humans are not pretty at birth. We are gray-blue, slithery little things,
dripping with a combination of amniotic fluid, mucous, blood, and vernix caseosa.
This quarter inch of coating does little to enhance appearance. To believe that these
"decorate" the newborn is unreasonable. Just what is this thick greasy layer, the
vernix caseosa? It does not lubricate exit from the womb, the maternal mucous does
that. Recent German research shows a greasy skin enhances warmth retention for
long distance swimmers. Since human beings swim innately if born in the water,

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vernix may have evolved from a prior aquatic adaptation.32 Given neonatal
metabolism, high surface to volume ratio, and exposure, it should conserve warmth
somewhat by reducing evaporative water loss. It is, however, completely inadequate
by itself.

When a mother gives birth to a child, he/she comes into the world wearing a
slippery chemical coating with the consistency of vegetable shortening. If the
hypothesis proves correct, then when primed for it, that greasy coating contains a
combination of what must be one of the most addictive mixtures extant.
Obstetricians call the observed mix vernix caseosa. More Latin, this time for cheesy
varnish.

The slippery, greasy vernix is mostly sebaceous. It is produced by the fetal

sebaceous glands. These same glands are the first to function in the newly forming
human being. Secreting sebum well ahead of eccrine (perspiration) glands, lacrimal
(tear) glands, and reproductive secretion glands have been noted by embryologists.33

The large number of fatty chemicals composing the vernix impart a chemical
signature to the mix making it personally unique.34 In practice, forensic identification
of individuals from their vernix caseosa have only been successful to species and
blood group.35

Interestingly, much of the vernix caseosa flakes off from the skin of the
maturing fetus about a week before birth. The milky appearance of the vernix-
amniotic fluid mix can be detected by sonograph. In addition, the gradual changes in
the composition of the vernix accelerate at about the 37th week of gestation. 36

The neonate comes into the world owning nothing but the gummy substance
of oily pheromone covering him completely. Theoretically someone must be willing
to provide urgently needed care and attention in exchange for the new baby's sole
possession of value: that skin secretion.15 This readiness to nurture for pheromone
would provide the same evidence for bonding in all mammals and all bonding species
generally. Civilized human beings appear quite prepared to do anything for love of
their children, perhaps, especially for men if primed by pre-pregnancy oral, lacrimal,
skin, vaginal, areolar and nipple secretions of their wives.
63
 The sebum of the vernix may alone be responsible for a mother's love, or it
may have companion secretions as back-up. For instance, the shorter chain chemical
fatty acid and ester chemical species released during labor and after birth, remain
unmeasured. These pervade the atmosphere of the birth room, and may affect the
behavior of any of those present. The supposed receptivity must be primed; mothers
do love while attending medical personnel do not.

Another likely possibility, pregnant females may begin to secrete colostrum

upon the husband's breast stimulation. The behavior presents a perfect opportunity
for transmission of a bonding-receptivity-enhancing pheromone, most likely the
protein pheromone receptors themselves (see Chapter 6). Lipid carrier proteins of
colostrum may be egregiously mislabeled and function as pheromone receptor
proteins.

The sebum excretion rate increases during the last trimester of pregnancy,
despite high levels of estrogen, a hormone normally inhibiting sebum excretion.37
The elevated sebum secretion rate typical of pregnancy is also maintained during
lactation.38 Perhaps pregnant and lactating women are more 'kissable' than
nonpregnant, nonlactating women?39 Extra bonding effort during the period when a
reproducing female is most vulnerable seems logical.

Another private mate-mate exchange opportunity for fetal-specific pheromone

receptivity comes from vaginal discharges in the last trimester of pregnancy. Birch
(1956) suggested that rat dams may become familiar with the odor of their own young
during pregnancy by perceiving the odors of pre-birth vaginal secretions. To 1983,
there had been no test of his proposal.40 Pre-birth and post-birth vaginal secretions
ooze into the vaginas as lochia, and may also serve some pheromonal priming
function.

Researchers following this author’s suggestion13,14 noticed that some unknown

maternal pheromone primes bonding to offspring in Norway rats. They found that
three days before delivery of her pups, the pregnant dam releases a priming
pheromone onto her bedding. The scientists placed soiled bedding into cages of other
rats and watched their behavior toward the dam's neonates. Something in the soiled

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bedding primed a change in rat behavior. Three days after being exposed, the primed
rats of both sexes would no longer cannibalize newborn pups. Instead they behave
"maternally".41,42 It should not surprise anyone if mother vaginal secretions were
cued and timed to prime fathers as well since human intercourse is so frequent.

Unanalyzed vaginal secretions of sexual readiness accompany even innocent

kissing in unmarried human females. Perhaps it is primer pheromone for mate-mate
bonding? The effect diminishes (unneeded) after marriage. Sexual exchanges are
likely, especially during the last trimester of pregnancy. Marriage bed smells
associated only with pregnancy have been reported anecdotally. Nocturnal
pheromone exchanges between husband and wife might explain some of the pleasure
of sleeping together. Sleeping together has some unexplained cohesive effects.43

At the first hour of the first child's life, inexperienced fathers interact less
enthusiastically than second time fathers. 44 Similar differential solicitude for
inexperienced vs. experienced males pervades the literature. This exactly parallels
primiparous maternal behavior and supports the addictive pheromone bonding
hypothesis, as well as pheromone receptor protein mediated ‘memory’.

Labor and birth bring on secretions which are characteristic of pregnancy.

Some secretions, such as vernix caseosa, are chemically unique and identifiable to the
baby being born.33 Mucous plug expulsion mixed with bloody show may also
enhance bonding success. This is suggested by the effect of forewaters amniotomy, a
minor operation to induce labor, being associated with reduced bonding success. The
researchers found a link between forewaters amniotomy and a delayed onset of
maternal affection that was unexpected.45 We expect it though. The chemical
composition of the mucoid plug damming the fetal sack within the uterus has not
been carefully studied. Its natural deterioration in labor may release a maternal
pheromone to enhance bonding receptivity. Surgical rupture would prevent or
diminish pheromone releases as found, and should thus be minimized obstetrically.
The possibility also exists of a semiochemical role for amniotic fluid naturally
released during labor.13,14

65
 Inducing labor suggests obstetric need. Amniotomy is also associated with
long and difficult labor which is also associated in turn with reduced bonding success.
So which, forewaters amniotomy or long & difficult labor, causes reduced bonding
success? Compositions, concentrations, variations, intra-specific comparisons; we
know very little.

Rupture of the amniotic sac (breaking the bag of waters), has important
semiochemical consequences in other species. In sheep, the small area marked by
released amniotic fluid is exclusive to the marking ewe. If removed from the site, she
returns to it to bear her lamb.

The gush of warm fluid heralding a human baby's arrival may simply be for
waste removal. It has no known function in humans aside from warning. Mucous
glands already line the path of the emerging neonate and provide all necessary
lubrication. However, human amniotic fluid does have a substantial sebaceous
fraction. This provides hope that human adoption might be artificially stimulated one
day. Perhaps such a process might be similar to a practice know to shepherds for
millennia (and to shepherd King David of ancient Israel but apparently not to his son,
Solomon) putting a ewe's amniotic fluid onto an adoptive lamb to enhance adoptive
bonding success.46

Human females bearing young release profuse perspiration and may

involuntarily urinate. Again, these are unappreciated specialized secretions. Their
most probable functions may be to make way for heat dissipation and for the
descending baby's mass, respectively. We will learn with analysis and testing.
Although sudodiferous (perspiration producing) eccrine glands are prominent in
humans, the chemistry of pure heat or exertion perspiration is simple, varying with
metabolism. (You sweat what you eat, see Leon.10 Mice perspiration is similar.47)
The odd perspirations of intercourse48 needs careful examination and chemical
analysis as well.

During labor and after the birth, the shorter chain volatile lipid and other
emitted chemical species evaporate. These chemicals have not been analyzed either.23

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If these are pheromones, they can be captured, identified, synthesized and used
medically.

Upon the birth of the baby, the mother may be oblivious to all others for a
short time. Typically she first inspects the body of her new love. She usually, but not
always, kisses her new infant.22

Addiction, like love, can last many decades. If we judge by the strength of the
resulting bond, any addictive power of neonatal sebum for receptive females would
be awesome. Human sebum would not be any more potent than some insect
pheromones, however. Some of those are effective in doses at the ultra-trace level: a
few molecules of pheromone in a billion molecules of atmosphere.

Full term neonatal vernix caseosa fundamentally resembles young adult

sebum. Wax esters are better represented during these bond-forming times of life.
Wax esters "melt" roughly in the sequence of their chain lengths as the skin
temperature rises. Sequential meltings are useful for secretions of passion during
courtship behavior. Such wax esters are among the most commonly pheromonal.49

The about-to-be mother in the delivery room undergoes poorly understood

physiological changes. Blood serum chemistry changes as labor proceeds. The
pelvis bones unhinge in birth giving under the influence of progesterone. Human
females birthing pains are unknown among other primates. (The painful movement
passes the relatively large human head.) For some still obscure reason, long or
difficult labors correlate more often with bonding failure. Perhaps maternal
pheromone receptivity might erode during labor, or birth canal off-gasing might be
less dense?

The bonding effort in those moments right after birth results in immediate
expressed love of the just-born infant in about 40% of first time mothers.24 As
discussed, like other mammalian species, the human mother examines her baby. (Are
all the fingers and toes in place?) If all checks out, bonding to the neonate begins.
Deformities are associated with decreased bonding success.50 What physiological
doors open with such a realization? Recreating the physiology and pheromone

67
receptivity and pheromone receptions at birth and during the first week could be used
to fight or cure physical child abuse and to improve adoption bonding success.

CRITICAL PERIODS

There are two critical periods of parent-to-infant bonding. The first falls
during the first hours after birth (Klaus M.H. and J.H. Kennel, 1982).51 Extra contact
between mother and neonate for the first hour may even improve the quality of the
maternal bond:

Primiparous mothers and their infants who had an extra 15-20 minutes'
suckling and skin to skin contact during the first hour after delivery, behaved
differently at 36 hours post partum compared with a control group without this extra
contact. The present study is a 3 month followup of these mothers and infants by
means of direct observation of mother-infant free play and a personal interview with
the mothers. Mothers in the extra contact group spent more time kissing and looking
en face at their infants; these infants smiled more often and cried less frequently. A
greater proportion of the mothers with extra contact were still breast feeding at 3
months. The influence of extra contact on behaviour was more pronounced in boy-
mother than in girl-mother pairs (De Chateau, P. and B. Wiberg, 1977).52

This sexually dimorphic maternal behavior may have a pheromonal explanation as we

will soon see.

The 2nd critical period comes during the first days of the neonate's life.30

In about 70% of human cultures, anthropologists recognize a period of 7 to 10

days after birth when the mother and baby are isolated together.30 This isolation may
have evolved to enhance and insure mother-infant bonding13,14 It also may serve to
protect the bonding mother in her highly receptive state from possible semiochemical
aggression of other human beings, or perhaps even them from her? So, DARPA
should try to find and weaponize that pheromone, too, then?

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Since the nineteen-thirties dermatologists have known about a marked
postnatal sebum secretion in the neonate.53,54 Better measures have been made more
recently.9 Sebaceous secretion levels obtained on the fourth day of life are as high as
those of young adults.9 In the mother, the "baby blues" or the "third day blues"
precedes the fourth day sebum surge of the baby. These two phenomena may work in
tandem to insure mother-to-infant love in the first isolation week.

In one study of first-time mothers, researchers asked them what was their
predominant emotional reaction as they held their newborn in their arms for the first
time. Forty percent recalled that their predominant emotional reaction was one of
indifference. 25 percent of 40 second-time mothers reported the same indifference.
Forty percent of both groups felt affection immediately when holding their babies for
the first time. Most mothers in both groups had developed affection for their babies
within the first week.24 Unfortunately, as its authors begrudge, this study's design is
retrospective, its data are subjective, and the work is, to this author’s knowledge, un-
replicated.

Perhaps the new baby's vernix caseosa forms the vanguard while the fourth
day sebum peak, under the mother's emotional pheromone-receptive tears, is a backup
system? Backup systems that chronologically follow up other systems and would be
expected.

Charles Darwin first noticed the flushing of the face of newborns when crying
(without tears) in his The Expression of the Emotions in Man and Animals (1872).
“If the parent does not respond to the infant's satisfaction, a flushed face and loud
crying follow. The response to this? The baby, brought close, is kissed.”55 Perhaps
that kiss takes the last step in a managed process?

Under this author’s paradigm, the baby must gauge the caregiver's addiction to
its pheromonal secretions. One way might be by noticing the pitch of the voice (or a
musical slur to higher pitch), the animation of the face, and the gentleness of
handling.18 A failing mark on any score stimulates the head and face to flush and
produce the kiss me cry. The increased blood circulation to the well-developed
sebaceous glands in skin surfaces of the face and scalp instantly increases secretion of

69
sebaceous pheromone. When the caretaker's kiss arrives on the skin secreting the
pheromone, the cry is muffled, the increased circulation withdrawn, and the gland
cooled. The sebaceous pheromone congeals with the drop of only a degree or so of
temperature at the skin surface, conserving pheromone for the next transfer event.
The infant's innate instinct again examines the face and sounds it hears, determining
if another dose is warranted. "Pheromoning" caregivers might be the newborn's
number one job, particularly if staying alive depends on it.

Snatching up and running with an infant will silence a baby. Survival has
favored this startle adaptation for a stealthy retreat. Capture by an enemy frequently
meant death for babies. Mass infanticides by victors brought young captive mothers
back to reproductive fertility the quickest.56 The effect diminishes in older infants,
who may require more than motion cues to sense danger.

Assuming loving infants to be a pheromonal process, then only a fraction of

the sebaceous pheromone required to addict, maintains addictive love for older
children. This must be so because sebum secretion declines unsteadily and sexually
dimorphically until the age of about one year. There, secretion remains at a lower
level until puberty when the bonding needs of approaching adulthood bring back the
higher levels once again.8 We might suspect that high sebaceous pheromone
secretion levels make new bonding to the secreting party possible, while low levels
maintain such bonds. Paralleling these changes through ontogeny are changes in skin
surface pH.57 Such changes may affect semiochemical secretion or reception as well.
pH changes can affect soluble pheromone binding protein function,58 improving the
pheromone receptivity described in Chapters 6 & 7, when the pheromone binding
protein functions as a extracellular pheromone receptor protein.59

Human cultural groups treat public kissing of children in a variety of ways. It

ranges from the outright social prohibition among oriental societies to the vulgar
"sexual child abuse" of a few primitive tribal societies.60 (Oriental tolerance for
crowding and tea taste sensitivity are suggestive as we will soon see.)

In between there may be other pheromone releases influencing maternal

behavior. Male nipples function briefly in the perinatal period. The enigmatic

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"witch's milk" of both sexes and other secretions of the "genital crises" remain
unanalyzed and quite obviously, completely misunderstood.

Oriental people have fewer sebaceous pheromone producing glands

(Rothmann, S., 1959) compensated, perhaps, by increased receptivity. (Oriental
people also seem to have a lower olfactory perception threshold to body odor.61
People of European ancestry living in the Orient might profit by frequent baths.)
Sebaceous pheromone receptivity remains unmeasured anywhere, however a greater
sensitivity in Oriental people might be expected. Oriental infants are kissed, but
kissing of children, especially in public, is discouraged. Vaporous uptake may even
suffice. Even the eye folds may improve pheromone receptivity as a more advanced
adaptation.

Interestingly enough, depending upon sex of the infant, there are differences
in a mother's love early on.

Mother-child interaction was studied on the 2nd and 4th days after delivery.
Mothers with girls showed more distal contact behaviour such as talking, smiling,
and 'en face' responses. They also displayed more skin-to-skin contact behaviour
(patting, rubbing, kissing, and touching) toward girl babies. Mothers with boys, on
the other hand, showed more types of behaviours directed to clothed parts of the
infant such as patting and adjusting clothes. These findings were statistically
significant only on the 2nd day after delivery. On day 4 differences between male and
female infants both in the frequency and in the pattern of sucking were observed
(Hwang, C.P., 1978).62

Similar slight differences in maternal affection might be explained by differences in

sebaceous secretion of baby girls vs. baby boys. For instance, one group of scientists
watched mothers kissing, talking and rocking their babies at the age of one month.
That group found that male infants got more attention than did female infants.63,64

Another researcher65 had data showing that female infants got more attention
than boys during the second six months of life. She also pointed out that females
tended to be weaned later that baby boys. Dermatological data bearing on these
points are indefinite, but indications are that at one month, male infants will have

71
been secreting more sebum than females.9 The same dermatological report also
shows that during the sixth through twelfth months after birth, female infants secrete
about half again as much as their male counterparts. Although by no means settled,
kissing frequency does seem on first blush to depend upon harvestable quantity of
sebaceous pheromone, following economic expectations. Thus parental kissing of
babies may indeed depend upon neonatal sebaceous secretion.

Adults use the "blowkiss" as described by Eibl-Eibesfeldt39 on the umbilicus

or "belly buttons" of older children in play. Here, too, lurks a sebaceous aggregation
in the skin around the infant navel. The navel area's steroid metabolism is similar to
other kissable skin.66 The intensity of the pleasure of the youngster suggests the
importance of such innocent contact.

Eibl-Eibesfeldt13 also presents an interesting example of genital kissing of

children by parents in a primitive South American Indian tribe. Among the
Yanomami of the upper Orinoco river in South America, mothers and fathers alike
"blowkiss," (The term "blowkiss" for this adult to child kissing is descriptive and
should supplant the vulgar British and Australian usage of this term for fellatio.) lick
or manually rub the vaginal orifices of baby girls and stroke the scrotums of boys or
mouth their penises until about the age of three. The genital surfaces observed have
large active clusters of unusually shaped sebaceous glands perinatally.8 These are
active in the neonate. Sebaceous glands respond to manual stimulation with an
increased secretion rate. 67

The parental bonding by pheromone reception hypothesis has great power.

Even the savage practice of gumming babies' genitals can be specifically accounted
for by non-conscious sebaceous secretion seeking! The Yanomami should have the
thanks of all humanity now for their conservation of their natural customs.

1 Comfort Alex Nature and human nature. London: Weidenfeld and Nicolson, 1966.
2Morse, Douglass H. 1980; Behavioral Mechanisms in Ecology. Cambridge, Massachusetts:
Harvard University Press 383 p.

72
EXOCRINOLOGY
3Eibl-Eibesfeldt, Irenäus (1970a). Ethology the Biology of Behavior, translated by Erich
Klinghammer New York: Holt, Rinehart and Winston 530 p.
4 Netter, Frank H. 1989; Paranasal Sinuses: Changes with Age. Plate 44. In: Atlas of Human

Anatomy Summit, New Jersey: Ciba-Geigy Corporation. 585 p.

5 Drettner B. The paranasal sinuses. In: The nose: upper airway physiology and the atmospheric

environment. Proctor A.editor. Amsterdam: Elsevier Biomedical Press. 1982;145-62.

6 Nicholson, B. 1985; An economic model of phermone transmission in avians. Paper presented to
the Animal Behavior Society biannual meeting, Raliegh, N.C.
7 Terkel J, Rosenblatt JS. Maternal behavior induced by maternal blood plasma injected into virgin
rats. J Comp Physiol Psychol. 1968 Jun;65(3):479-482.
8 Tinbergen, Niko (1960). The Herring Gull's World a study of the social behaviour of birds New

York: Basic Books.

9 Montagna, William, and Paul F. Parakkal 1974; The Structure and Function of Skin. New York:

Academic Press. 433 p.

10Agache, P., D. Blanc, C. Barrand, and R Laurent R 1980; Sebum levels during the first year of life.
British Journal of Dermatology. 103:643-649.
11Leon, Michael 1983; Chemical Communication in Mother-Young Interactions. pp. 39-77.
Chapter 2. In: Pheromones and Reproduction in Mammals. J G. Vandenbergh, editor. New York;
Academic Press, Inc. 298 p.
12 Matsunaga M, Sato S, Isowa T, Tsuboi H, Konagaya T, Kaneko H, Ohira H. 2009; Profiling of
serum proteins influenced by warm partner contact in healthy couples. Neuro Endocrinol Lett.
2009;30(2):227-236.
13Wilson, Edward O. 1975; Sociobiology The New Synthesis. Cambridge, Mass.: Belknap Press of
Harvard University Press. 697p.
14 Benfield, D. Gary, Susan A. Leib, and Jeanette Reuter 1976; Grief response of parents after referral
of the critically ill newborn to a regional center New England Journal of Medicine, 294(18):975.
15 Nicholson B. Love and kisses: a semiochemical addiction model for human bonding. 1983. Paper
presented to the International Society for Human Ethology and Animal Behaviour Society biannual
international meeting at Bucknell University, Bucknell PA.
16 Nicholson, B. 1984; Does kissing aid human bonding by semiochemical addiction? British

Journal of Dermatology 111(5):623-627.

17Tamborlane William V (ed). 1997; The Yale Guide to Children’s Nutrition. Newhaven
Connecticut: Yale University Press.
18Dickens G, Trethowan WH. Cravings and aversions in pregnancy. Journal of Psychosomatic
Research (1971).15:259-65.
19 Profet, Margie 1992; (In) The Adapted Mind New York: Oxford University Press.

73
20Vandenbergh, J G. editor Pheromones and Reproduction in Mammals. New York: Academic Press,
Inc. 298 p.
21 Shorey, H.H. 1976; Animal Communication by Pheromones. New York: Academic Press.
22Fillion, TJ, Blass EM. Infantile experience with suckling odors determines adult sexual behavior in
male rats. Science 1986;231(4739):729-731.
23 Preti, George, Winnifred Berg Cutler, Carol M. Christensen, Henry Lawley, George R Huggins, and
Celso-Ramon Garcia 1987; Human axillary extracts; an analysis of compounds from samples which
influence menstrual timing. Journal of Chemical Ecology 13(4):717-732.
24Greene RS, Downing DT, Pochi PE, Strauss JS. Anatomical variation in the amount and
composition of human skin surface lipid. Journal of Investigative Dermatology 1970;54(3):240-47.
25 Reinberg, Alain, and Michel Lagoguey 1978; Circadian and circannual rhythms in sexual activity
and plasma hormones (FDS, LH, Testosterone) of five human males. Archives of Sexual Behavior 7
(1):13-30.
26Kolattukudy, P.E., and L. Rogers 1987; Biosynthesis of 3-hydroxy fatty acids, the pheromone
components of female mallard ducks, by cell free preparations of the uropygial gland. Arch. Biochem.
Biophys. 252(1):121-129.
27 Trivers, R. L. (1972) Parental investment and sexual selection. In B. Campbell (Ed.) Sexual

selection and the descent of man, 1871-1971 (pp 136–179). Chicago, Aldine.
28Garland T Jr, Schutz H, Chappell MA, Keeney BK, Meek TH, Copes LE, Acosta W, Drenowatz C,
Maciel RC, van Dijk G, Kotz CM, Eisenmann JC. The biological control of voluntary exercise,
spontaneous physical activity and daily energy expenditure in relation to obesity: human and rodent
perspectives. J Exp Biol. 2011 Jan 15;214(Pt 2):206-229.

29Hollenbeck, A.R, JL. Gewirtz, S.L. Sebris, and JW. Scanlon 1984; Labor and delivery
medication influences parent-infant interaction in the first post-partum month. Infant Behavior and
Development. 7:201-209.
30 Silver, H., R Wapner, M. Vega, and L.P. Finnegan 1987; Addiction in pregnancy: high risk
intrapartum management and outcome. J Perinatol 7(3):178-184.
31Drickamer LC. Acceleration and delay of sexual maturation in female house mice (Mus
domesticus) by urinary chemosignals: mixing urine sources in unequal proportions. Journal of
Comparative Psychology 1988;102(3):215-21.
32 Hardy, A. C. (1963). Man and the beneficent sea. Evening discourse delivered on 3 September 1962,
at the Manchester Meeting of the British Association for the Advancement of Science. Report. British
Association for the Advancement of Science. 19: 533-544.
33 Von Eggeling, H. (1940). Origin of cutaneous glands of mammals. Anat. Anz. 90:149-157.
34 Nicolaides, N. 1974; Skin lipids: their biochemical uniqueness. Science. 186:19-26.
35 Tesar J. 1986; [Identification of vernix caseosa.] Soud Lek. 1986 Nov;31(4):54-5. Czech.

74
EXOCRINOLOGY
36 Wysocki SJ, Grauaug A, O'Neill G, Hähnel R. 1981; Lipids in forehead vernix from newborn
infants. Biol Neonate. 1981;39(5-6):300-4.
37 Burton JL, Shuster S, Cartlidge M. The sebotrophic effect of pregnancy. Acta Dermato-

vernereologica (Stockholm). 1975;55:11-3.

38Burton, JL., Sam Shuster, M. Cartlidge, L.J Libman, and U. Martell (1973a). Lactation, sebum
excretion, and melanocyte stimulating hormone. Nature 243:349-350.
39Nicholson B. Does kissing aid human bonding by semiochemical addiction? Br J Dermatol 1984
Nov;111(5):623-627.
40Leon, Michael 1983; Chemical Communication in Mother-Young Interactions. pp. 39-77.
Chapter 2. In: Pheromones and Reproduction in Mammals. J G. Vandenbergh, editor. New York;
Academic Press, Inc. 298 p.
41Mennella, Julie A, and Howard Moltz 1988; Infanticide in rats: male strategy and female
counter-strategy. Physiology & Behavior 42:19-28.
42 Mennella, Julie A, and Howard Moltz 1989; Pheromonal emission by pregnant rats protects against
infanticide by nulliparous conspecifics. Physiology and Behavior 46:591-595.
43 Montagu, Ashley (1944). Some factors in family cohesion Psychiatry 7:349-52.
44Dunn, D.M., and D.G. White 1981; Interactions of mothers with their newborns in the first half-
hour of life. Journal of Advanced Nursing 6(4):271-275.
45Robson, K.M., and R Kumar 1980; Delayed onset of maternal affection after childbirth. British
Journal of Psychiatry 136:347-353.
46Levy, F., and P. Poindron 1987; The importance of amniotic fluids for the establishment of
maternal behaviour in experienced and inexperienced ewes. Animal Behavior 35:1188-1192.
47 Schellinck, H.M., A.M. West, and RE. Brown 1992; Rats can discriminate between the urine odors
of genetically identical mice maintained on different diets. Physiology & Behavior 51(5):1079-1082.
48Masters, W.H., and Virginia E. Johnson (1966). Human Sexual Response. Boston: Little, Brown
and Company.
49Silverstein, Robert M. 1984; Chemistry of insect communication. Chapter 5, pp 105-121. In:
Insect Communication. Lewis, Trevor editor. Academic Press, London. 414 p.
50Cady E, Cady F. How to adopt a child. New York: Whiteside, Inc. and William and Morrow
Company, 1956.
51 Klaus, M.H., and JH. Kennell 1982; Parent-Infant Bonding. St. Louis: The C.V. Mosby Company.
52 De Chateau P, Wiberg B. Long-term effect on mother-infant behaviour of extra contact during the
first hour post partum. II. A follow-up at three months. Acta Paediatrica Scandinavica 1977;66(2):
145-51.
53Benfenati A, Brillanti F. Sebaceous glands distribution in skin of human body Arch. Italdi.
Dermat., sif. 1939;15:33-42.

75
54Rothman, Stephen (1954). Physiology and Biochemistry of the Skin, Chicago: University of
Chicago Press Chapter 12 Sebaceous-Gland Excretion p. 285.
55 Darwin C. The Expression of the Emotions in Man and Animals. London: Murray. 1872;162
56Eibl-Eibesfeldt, Irena us. (1970b). Love and Hate: On the Natural History of Behavior Patterns.
New York: Methuen and Company.
57Behrendt H, Marvin Green M. Patterns of skin pH from birth through adolescence. Springfield:
Charles C. Thomas. 1971.
58 Damberger, Fred, Nikonova Larisa, Horst Reto, Peng Guihong, Leal Walter Soares, and Wüthrich
Kurt, NMR characterization of a pH-dependent equilibrium between two folded solution
conformations of the pheromone-binding protein from Bombyx mori. Protein Science (2000),
9:1038-1041.
59Nicholson B., Pheromones cause disease: pheromone/odourant transduction. Med Hypotheses. 2001
Sep;57(3):361-77.
60 Eibl-Eibesfeldt, Irenäus 1983; Patterns of parent-child interaction in cross-cultural perspective. In:

The Behavior of Human Infants Oliverio Albert and Michele Zappella editors. New York: Plenum
Publishing Corporation pp. 177-217.
61Schleidt, M. 1980; Personal odor and nonverbal communication. Ethology and Sociobiology
1:225.
62 Hwang, C.P. 1978; Mother-infant interaction; effects of sex of infant on feeding behaviour. Early

Human Development 2(4):341-349.

63Moss, H.A. (1967). Sex, age and state as determinants of mother-infant interaction. Merrill-
Palmer Quarterly 13:19-36.
64Moss, H.A, K.S. Robson, and F. Pedersen (1969). Determinants of Maternal Stimulation of Infants
and Consequences of Treatment for Later Reactions to Strangers. Developmental Psychology,
1:239-46.
65Clay VS. The effect of culture on mother-child tactile communication. (Ph.D. Dissertation.
Teachers College, Columbia University, NY: 1966.)
66Albone, Eric S. 1984; Mammalian Semiochemistry The Investigation of Chemical Signals
Between Mammals. Chichester, England: J Wiley & Sons Limited. 360 pages p. 13
67 Mills, JW., and P.M. Quinton 1981; Formation of stimulus-induced vacuoles in serous cells of

tracheal submucosal glands. American Journal of Physiology, 241(1):C-18.

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EXOCRINOLOGY

Chapter 3: Chemical Characteristics of Human

Pheromones

Up to this point, we have examined kissing, the sebaceous glands, their

behavioral correlations, and the physical characteristics of sebum. But pheromones
carry information, so the chemicals in sebum must also be capable of carrying
information.

Now consider this. Identifiable compounds in the human skin surface lipid set
number about 700.1 Although ultra-trace detection of pheromone concentration has
been observed in other animals, perhaps twenty different detectable concentrations of
a single human pheromone component could be considered a reasonable
approximation for human reception. For simplicity’s sake, we shall diminish twenty
to one. Let us presume that all seven hundred components are equally detectable.
Then we have 700 detectable elements, n. If perhaps, say, six elements can be
detected as a single signal, the number of detectable combinations of k = 6 elements
from a group of size n = 700 elements

so why do we need a hundred quadrillion possible signals when people are acquainted
with only about 300 different other human beings in a lifetime? My point here is that
we are only scratching the surface and we must suspect more information transfer
rather than less.

Since the pheromone mixture set can change anatomically for an entirely
different reception. (Presumably we kiss grandma differently from our spouses with
different receptivities.) We multiply by those changes again, and since k can be any
component compared to itself in another location, another component in the same or
in a different anatomical location, or any group up to seven hundred (up to twenty
necessary components in differing necessary concentrations had been seen in animal
studies), well that is a big, big number, too. Why is it such a big number?

77
 Why should there be such complexity? Perhaps, at least, it exists to assure
unique individual recognition by pheromone? Did we evolve these chemical
signaling molecules over billions of years to give a few microbes tummy aches, when
the dry surface of the skin is more effective? Economics predicts that we don’t invent
vast alphabets, nay whole languages, for nothing. “Junk” DNA is as economically
absurd as “displacement activity” and “nuptial gifting”. (Anyone trained in
accounting will recognize that DNA serves double duty as a double-entry accounting
system.)

Sebaleic acid, 5Z,8Z-octadecadienoic acid (both unsaturations, one between

carbons number 5 and 6, and between carbons number 8 and 9 with counting starting
from the functional group (acid) end of the aliphatic chain, are -cis) is unique in all
nature and found only in human sebum according to Nicolaides (1974).1 (Thus, we
only need sebaleic acid to distinguish a human ‘scent’ as human even though sebaleic
acid is odorless, colorless, and tasteless.)

Sebaleic acid, a major component of human sebum, has extremely interesting

characteristics. Sebaleic acid is metabolized down the same pathway as omega-six
(counting from the non-functional group end of the aliphatic chain) free fatty acids
found in fish oil. Fish oils have beneficial health effects in human beings which are
both species-specific and synergistic, just like chemical components of pheromones
have long been known to be both species-specific (in our case effective only in
people) and synergistic (greater effect than the sum of its parts). Metabolites of
sebaleic acid breakdown are found in plants said to have fertility-enhancing and even
aphrodisiac effects along with other pharmacological properties such as an attractant
for human neutrophils.2 Pheromones are chemical signals, after all. Since
pheromones work synergistically, analysis of a single chemical’s effects is largely
worthless as a predictor of biological activity.

The question becomes "Do sebum's chemicals look like pheromones?" While
they may, if sebum carries information, only testing can so determine. Appearance
may economically suggest function. The latter requires proof, while the former
(appearance) unfolds below.

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EXOCRINOLOGY
This chapter shows chemical and physical characteristics typical of known
pheromones and how they compare to some suspected human pheromones. Human
sebum does look suspiciously like known aliphatic pheromones. Human sebum is
uniquely human in the same ways that other species differentiate themselves
chemically.

79
Use the following chart in deciphering the figures in the text.

80
EXOCRINOLOGY

Figure 1. One of thousands of human-typical triglycerides. Is it a pheromone? Possibly.

We will look at insect pheromones mainly, although avian and vertebrate

pheromones appear. Understand, the people who study insects have had advantages
over their vertebrate-studying colleagues. (Insects cost little and nobody minds what
twisted things you do with them.) The insect people also have a methodological
advantage. In particular, they have a simple device known as the electroantennagraph
(or EAG) to detect and see direct electrical responses to chemical stimulations on an
oscilloscope. Entomological pheromone chemists might suggest they have merely
been smarter. Similar apparatus to the EAG, the EOG for electro-olfactograph, has
been available for many years.

THE ELECTRO-ANTENNAGRAPH

The EAG can be represented by the drawing in Figure 2. Experimenters pipe

a known concentration of a suspected pheromone under the glass with an insect
81
antenna stump. A pheromone evokes a typical frequency pattern of responses that
show up on the voltmeter/strip chart. Some similar chemicals also stimulate a
response on the meter/chart. EAGs show us which are pheromone-typical chemical
characteristics.

Figure 2. EAG or electro-antennagraph. 3 The severed antenna is placed under glass and its poles are
wired to the positive and negative lead of a voltmeter/strip chart or CRT oscilloscope. Scientists pass
an odor under the glass into contact with the antenna and observe the voltmeter to see if the odor
chemical generated a biological generated electrical response.

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EXOCRINOLOGY
Chemists test pheromones and chemicals slightly altered from the pheromone.
Using the EAG, subtle changes can show substantial differences in detectability. As
experience was built up, the same stereochemical oddities kept showing up to
differentiate one pheromone from another. Examining such subtle oddities in putative
human pheromones reveals interesting information. Human sebum is a pheromone
flexible enough to automate most human behavior. Let us examine the known
pheromone-like chemical quirks of sebum one at a time.

STEREOCHEMISTRY ACROSS A DOUBLE BOND

Double bonds (or unsaturations-(footnote for chemists: here reference to an

unsaturation will always mean a double bond, never the presence of a ring)) are stiff,
flat places between two carbons on a single file, aliphatic carbon chain. A double
bond holds its two carbons rigidly. Each end carbon can hold onto (or bond) at most
two other atoms. The result resembles two letters Y glued flat together base to base.
In a chain, only two of the three prongs of the Y bond to carbons. Most of our double
bonds exhibit either an S shape or C shape across them.

Figure 3. shows two stereochemical isomers of 3-heptene, one C shaped (the Z isomer on the
left) and the other S shaped (the E isomer on the right). (Hydrogens ignored for clarity.)

These S and C shapes are called "E" or "Z." "E" is for the German word,
Entgegen, meaning opposite sided. "Z" is for another German word, Zusammen,
83
meaning same sided. To confuse things, the C shaped, Z chemical may be called
"cis" and the S shaped, E chemical may be called "trans."

Figure 4. Sex attractant pheromones of the European pine shoot moth (E)9-Dodecen1-yl
acetate and of the grape berry moth (Z)9-Dodecen1-yl acetate. (Adapted from Morrison, R.T., and
R.N. Boyd, 19874)

Figure 4 shows two chemicals, pheromones for two different species. They share the
same chemical formula, only the fixed shapes or stereochemistry differs. Individual
carbon and oxygen atoms attach in the same order for each. They are both
constitutional isomers (with the same elements) and stereoisomers (with the same
order, but with different shapes).

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EXOCRINOLOGY

Figure 5. #2. is the silk moth pheromone, Bombykol, called (10E,12Z)10,12Hexadecadien1ol

in the language of chemistry. Its three stereoisomers are #1., (10E,12E)10,12Hexadecadien1ol, #3.
(10Z,12Z)10,12Hexadecadien1ol, and #4., (10Z,12E)10,12Hexadecadien1ol. (Adapted from Morrison,
R.T., and R.N. Boyd, 19874).

As seen here in Figure 5, we show an extreme example of the shape of a

molecule affecting its communicating power. Chemical #'s 1, 2, 3, and 4 are
stereoisomers. They have the same number of carbons bonded together with exactly
the same types of covalent bonds, single bonds represented by a dash ( - ) or slash ( \
or / ) and double bond represented by an equals sign ( = ). Single bonds are flexible
and allow rotation, whilst double bonds hold adjoining carbons flat and rigidly locked
in the same plane. These four molecules have very similar chemical characteristics.
#2 is the pheromone sex attractant (called Bombykol) of the silk moth. It is a billion
times more attractive to the male than the other three isomers. The sole distinction
among them is the "Z" or "E" shapes around the two rigid double bonds. 4

Exclusive mixes of one configuration or the other appear frequently in nature.

One or a few related lipids with usually the Zusammen, (zamesided, "Z" "cis" or C
shaped) configuration across the double bond show up most commonly. This remains
true for most non-pheromone lipids. Suspected human pheromones, like the
pheromones of other vertebrates, have this common "Z" (or "cis") configuration. Z-E
85
isomerism has been found in human sebum only once to date5 and that in lipids taken
from scalp hair secret haunt of the ‘anger’ or aggression pheromone as seen later.

DOUBLE BOND POSITION & MULTICOMPONENT

COMPOSITION

Double bonds may replace single bonds between any two carbons on a carbon
chain. However, in nature most aliphatic chains have consistent unsaturations.
Pheromonal lipids differ from lipids found in fatty tissue, however. While most
pheromone receptors carefully tune to the position of the double bond.6,7

Figure 6. The main component of the tarsal scent gland of black-tailed deer, cis-4-
hydroxydodec-6-enoic acid lactone.

Figure 6 shows the main component of a pheromone for the blacktailed

deer.8,9 Although only a few other chemicals were checked, the results were
consistent. If the carbon-carbon double bond (C=C) moves from the shown location,
the pheromonal power of this chemical falls precipitously. Here, this time in
ungulates, double bond (or unsaturation) position determines pheromonal character.
Not surprisingly, similar species-specific dienoic lactones have been found in horse
sebum, but behavioral assays were neglected.10

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EXOCRINOLOGY

Figure 7. The sex attractant pheromone of the oriental fruit moth consists of these two
stereoisomers in a ratio of 7% the (E) isomer and 93% of the (Z) isomer. The two isomers must be
present in precisely these concentrations. The pure (Z) isomer is completely inactive. (Adapted from
Morrison, R.T., and R.N. Boyd, 19874). Compare to Figure 8.

The pair of chemicals in Figure 7. illustrateS two characteristics typical of

pheromones. First note how these two chemicals resemble those of Figure 4. They
have the same molecular formula, except that the double bond has moved over to the
eighth (8) carbon from the ninth (9). That puts three carbons on the end beyond the
double bond rather than only two.

Secondly, and importantly for our purposes, note that the proportions of the
chemical present determine whether an effect is observed. This requirement of a
precise mixture of stereoisomers typifies pheromones.4 Mixture precision explains
persistent and time-sensitive human sebaceous mixtures as pheromonal.

87
 Figure 8. Two stereoisomers of a volatile short chain free fatty enoic acid thought, perhaps, to
function as human pheromones moderating menstrual cyclicity in some women with irregular cyclicity.
Compare to Figure 7.

Specific concentrations of Z and E isomers have been identified in the isolates

of a probable human pheromonal extract. According to Leyden et al., (1990), 11 a
concentration of roughly ten to one of the Z to E isomers appears. See Figure 8.

The concentration ratio has not been firmly established, though. The author's
laboratory submitted for analysis axillary extracts taken from American German-
speaking primitive farmers to Leyden's group. In the farmer samples the trans
isomer component diminished to 20:1 rather than 10:1. Differences in collection
method may explain our results, however. If the difference is real, it could explain
Amish social cohesion as pheromonal.

For awhile, many thought that one chemical led robotically to only one
behavior.12 Then, Silverstein et al. (1966)13 discovered in insects the first multi-
component blend of chemicals having a pheromone effect. (The author had the honor
to take a class in spectrometric identification from Silverstein before he retired).
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EXOCRINOLOGY
Over the years from the sixties, many other examples have been seen.14 That
suggested that many chemicals would trigger many components of behavior
independently.15 Current belief has it that sometimes pheromones act independently
and sometimes not. In insects, precise mixtures of as many as twenty (20) chemical
components show up,16 particularly among more social species. Indeed, pheromone
component mixture quantity increases with sociality, placing humans on top of that
list. We are the most social species on this planet, certainly not ants, as any
economist can demonstrate.

Exhibiting another characteristic of semiochemicals, blends of many diverse

unsaturated lipids cover human kissable skins. A wide range of unsaturated lipids
typifies plant and animal semiochemicals. 17

With so many more components possible in an individual's mix, each human

being actually has a unique chemical signature in pheromone-type chemicals.1 In
crime laboratories human sebum identifies human beings forensically.18 A mature
individual's precise combinations of sebaceous lipids remain stable through time.19,20
The ability of dogs to tell twins apart derives from otherwise identical twins having
different sebums.21 Since genes are identical in identical twins, epigenetics explains
the difference. Epigenetics, the ability of genes to acquire and shed expressions with
experience, is pheromonal. Indeed, chromosomal aberrations are attributable to both
natural and synthetic pheromone reception in laboratory mice. 22

METHYLATION

Unusual methylation marks another chemical characteristic typical of

pheromones. A methyl group presents a single, hydrogen-saturated carbon sticking
out alone from the carbon chain, a non-reactive chemical ‘bump’. To methylate a
carbon chain, you add a methyl to any carbon in the chain but the last (which would
just make the chain one carbon longer).

DNA methylation (adding a methyl group to form 5-methylcytosine where

cytosine is followed immediately by a guanine in the DNA sequence) and protein
89
methylation of histones are epigenetic. It is logical that these post-translational
modifications are pheromonal because it is biologically economical, it explains
known pheromonal influences on genetic inheritance, but most importantly,
methylation is key to the language of pheromones. Methylation in the nucleus and
elsewhere suggests it as an early evolutionary adaptation. From the point of
evolution, pheromone-sensing and chemosenses must be our earliest sense of
perception. Pheromones have been with us, and with us among our cells, since
colonial times: colonial bacteria.

Methyl group being added or "methylated" onto a carbon chain puts a carbon
"bump" on it, changing the chain's shape slightly. Can such bumps be read, like
Braille, by chemical pheromone receptors in animals? Yes, they can.

Jones et al. (1971) evaluated several positional isomers of

Xmethylhentriacontaines as kairomones eliciting antennation by M. croceipes.
Bioassays produced the following order of activity (scores in parenthesis) to 150 ng of
chemical: 13methyl analogue (2.32), 15methyl analogue (1.68), 12methyl analogue
(0.48), 11methyl analogue (0.22), 9methyl analogue (0.00). The data indicate an
acceptor site that is very specific for the methyl position (Jones, R.L., 1986).23 [BN
emphasis]

Jones' group established that methyl group placement on a carbon chain

affects reception. Similarly, such differences in the way drugs are structured affect
enzymatic action. Whether a methyl group (or multi-carbon hydrogen-saturated alkyl
group) adorns a drug's carbon skeleton may make or break its efficacy. M.I.
Kabachnik et al. (1970)24 found that differences in the placement of alkyl groups
(such as methyl groups) on drugs affect various human enzymes differently. If a
proteinaceous enzyme can distinguish methyl group position, then human pheromone
receptor proteins might, too. Recall from above that differences in methyl group
placement on a carbon chain can affect insect reception in both chemical and
electrical responses.

"[I]n [the ant] A. texana the closer the methyl group was to the fourth carbon
atom in 7carbon ketones, the greater the potency (Table I) (Moser, John C., 1970).15
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EXOCRINOLOGY

91
 We shall see that interior methylation of sebaceous lipids, waxes and alcohols
takes place more frequently on one particular, species-specific, carbon. Humans
sebum shares that characteristic with ant pheromones.

There is evidence in the data that there might be a constancy in optimum

methyl position from the other end of the molecule, but more precise studies would be
needed to clarify this. For example, the 12-methyl-dotriacontane is very active and
the relative position of the methyl group from the other end of the molecule in 11-
methyl-hentriacontane, 12-methyl-dotriacontane, or 13-methyl-tritriacontane is the
same. (Jones, R.L., 1986).22

Observing this characteristic requires counting carbons from the "wrong" or

omega end of the chain. Data has since been gathered to establish this with more
certainty.25 Chemists count carbons to name chemicals. Chemists start counting
carbons from the end of the chain closest to "the functional group"the area most
subject to reaction. Unfortunately pheromone receptors seem to count the carbons the
other way, from the end furthest from the functional group.

CHAIN LENGTH and MIXTURES OF CHAIN LENGTHS

Vinson et al. (1975) provide a more detailed study with the response of
Cardiochiles nigriceps to a series of X-methyl hen, do and tri-triacontaines. These
data provide information on chain lengths as well as positional isomers and support
those of Jones et al. (1971) with respect to non-synergism by chemicals with methyl
groups in variable positions. They also show a bell-shaped dose-response curve, with
optimum responses at 5 micrograms of chemical. The optimum methyl positions did
vary with chain length and were 11-methyl-hentriacontane, 16-methyl-do-
triacontaine, and 13-methyl-tri-triacontane.

The most interesting feature of the study was a marked synergism observed
when chemicals of varying chain lengths were mixed. Mixtures of several methyl
isomers of hen, do, and tritriacontanes exhibited synergistic activity, with dose-
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response curves having optimum activity at the 500 ng level and very good activity at
the 50 ng level. These results provide strong evidence that the parasitoid perceives
hydrocarbons of varying chain lengths at different acceptor sites and that the different
acceptor sites have different optima for methyl positions (Jones, R.L., 1986).22

Human sebum contains one of the largest biological collections of chain

lengths science has ever seen, except in semiochemicals.

[In the ant, A. texana] Seven-carbon chains evoked stronger responses than shorter or
longer chains (Table II.) (Moser, J.C., 1970).15

93
 That chain length also plays a role in pheromone reception also might be
presumed from varying drugs prompting enzymatic action. (Likewise the drug action
might be suspected to mimic intracellular or other pheromonal action, as well,
remembering our ‘colonial’ phylogeny lesson.)

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EXOCRINOLOGY
Dixon and Webb (1964) have shown rate profiles of 17 enzymes in which the chain
lengths of alkyl and acyl groups attached to substrates were successively varied by
the addition of methylene groups. In general, as the length of the linear hydrocarbon
chain increased, a regular increase in enzyme activity was observed up to a maximal
value, followed by a decrease in activity as the chain length was further increased.
The optimal chain length varied widely among the enzymes, ranging between 3 and
17 carbon atoms.26

Note that Dixon and Webb27 purified only one enzyme for examination at a
time in their beautiful systematic experiment. Enzymatic activity, such as
metabolizing or synthesizing hormones, may depend upon recognition of chain
length.

FUNCTIONAL GROUP

The sensitivity to functional group varies widely in pheromones. (An alcohol

has one functional group, a ketone has another.) Moser (1970)15 held everything
constant, but changed the functional group on his pheromone to an alcohol. Table III
shows that the alcohol, 4-methyl-3-heptanol, produced alarm in A. texana. The effect
just like the real pheromone, needed a concentration 100,000 times higher than the
related [pheromonal] ketone.15 Moser was another brilliantly systematic chemist.

95
 The chemical activity of the functional group does not enter into things.
Recognition of pheromones does not require any chemical reactions where new bonds
form.6 Another brilliant scientist, Prestwich (1987) 28shows us still another example
of functional group specificity in a pheromone.

3. Agrotis segetum

The responses of sensory cells from male antennae of the turnip moth, A. segetum
(Noctuidae), were measured upon stimulation with analogs of Z712:Ac (I, the
pheromone) in which the structure of the acetate was varied (Liljefors et al., 1984)
(Figure 9.). Replacement of the alcohol oxygen with a methylene to obtain the
methyl ketone (LXIII) afforded a weakly active stimulus. In contrast, the formate
(LXIV), the propionate (LXV), the trifluoroacetate (LXVI), and the ethyl ether
(LXVII) analogs were all essentially inactive.

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EXOCRINOLOGY

Figure 9. Stereo-electronic analogs of Z-7-12:Ac tested with Agrotis segetum. (Prestwich,

G.D., 1987).27(NOTE: Stereochemistry not indicated, except for C=C)

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FUNCTIONAL GROUP POSITION

In all but the aldehydes and carboxylic acids, the simpler functional groups
can appear anywhere along the carbon chain. As noted, functional groups fail to react
chemically in pheromone recognition by animals.4,6 The pheromone's shape seems
the most important factor. Where the functional group appears along the carbon chain
may have as much relevance to pheromone specificity as the group itself.

[In the ant, A texana] the ketone group was most effective on carbon atom 3; 4-
methyl-3-heptanone was 10,000 times more potent than 4-methyl-2-heptanone. ...
When the ketone and methyl positions were reversed (3-methyl-4-heptanone),
sensitivity was decreased by 10,000 times. [See Table I.]

SAME CHEMICAL, TWO SPECIES

Two or more species may react to a single chemical. For example, 4-

methyl-3-heptanone does not excite Trachymyremex septentrionalis (McCook), a leaf-
cutting ant closely related to A. texana, but it does alarm Pogonomyrmex comanche
(Wheeler), a distant relative. Nests of both species may be adjacent to those of A.
texana (Moser, 1960) (Moser, John C., 1970).15

Figure 10. Identical chemical excites two different ant species.

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EXOCRINOLOGY
The same chemicals have been shown to be pheromones in more than one
species. How can this be? Won't the two species get all mixed up? After all, in the
lab, we have seen that pheromone stimulation can result in unnatural behavior 29 such
as interspecific mating. More likely, the same chemical, pheromone to one, allomone
to the other, communicates information to both species simultaneously depending
upon the needs of the species. Ordinary dogs, common mammalian parasites of
human beings, lick human skin. Animal to human bonding may or may not take
place. The beasts may deposit allomone to direct human behavior, or to mark the
human host as parasitized for “other pets”.

Pheromones rarely become confused in nature. When two species do use the
same chemical pheromone for similar purposes, you see chemical emissions that take
place in different seasons, at different times of the day or night, or in different
habitats.30

DOUBLE BONDS IN HUMAN SEBUM

Let us now look more narrowly at human sebum. Human skin surface lipids
have highly unusual patterns of unsaturation. Human sebum contains more than 200
examples of such double bonded carbon chains. These fatty acid chains do not show
up in body fat in any quantity.1 The patterns of double bonds distinguish them from
those seen in sebums of other animals.1 Here we see evidence of information bearing
capacity.

The presence of double bonds at delta 6 [i.e. between the 6th and 7th carbons
counting from the functional group end] in the mono-enoic fatty acids of human skin
surface lipid is a striking feature (A.W. Weitkamp, et al., 1947; N. Nicolaides, et al.,
1964; N. Nicolaides and T. Ray, 1965). In most naturally occurring mono-enoic acids
the double bond position is at delta 9. Mono-enoic acids with the delta 6 double bond
are extremely rare, occurring only in human skin, the sebaceous tissues of some other
animals [with different chain lengths & functional groups-Nicholson] and the seed
fats of the parsley family and some other rare plants (G.F. Spenser, et al.,1971)
(Nicolaides, N., 1974).1
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FUNCTIONAL GROUPS IN SEBUM

The tri-acyl glycerols constitute 60 percent of the lipids of human sebum

(Table IV). "Interestingly the triacyl glycerols and their products derived from
hydrolysis occur only in the skin surface lipids of human beings".1 (Hydrolysis, or
water cutting, splits a molecule, capping off the ends with an H and OH from H2O.
Hydrolysis may be performed on human triglycerides by bacterial action, or
environmental action.1 Thus the presence or absence of various combinations of skin
surface microbes affects sebaceous composition (but see Cove, J.H., et al., 1980).)
We know of only so many functional groups in carbon chemistry. To find not one,
but several apparently reserved for human use among mammalian sebums was
unexpected. However, free fatty acids do function as pheromones in several species.
We do see free fatty acids similar to human sebum's (differing only in unsaturation
position and methylation) in bumble bee pheromones31 and wood tick pheromones 32
Peculiar branching fatty acids characterize some goat pheromones 33 and
hydroxylated, maybe even duck pheromones.34

Perhaps other studied mammals have found their best interests in reducing the
chances of being mistaken for human? Chemical differentiation of pheromones
probably evolved in the dim mists of unrecorded time. Perhaps, an ancient evolution
accounts for their relative simplicity, chemical recognition35 and pheromone
secretion.36

Again, other ideas may explain human sebum's uniqueness.37,38 Is sebum

excreted as a waste product? After all, only about a third of the triacyl glycerols or
triglycerides of human sebum could profitably be used internally.1 A waste disposal
task for sebum can be ruled out, however. Squalene, a biologically useful chemical,
is a common precursor. Sebum is generally manufactured in the skin from squalene
with the exclusion of common precursor fatty acids for relatively rarer ones.

Perhaps as Nicolaides suggests1 different sebums fool bacteria or other

pathogens by being difficult to digest? In light of Kligman's29 cogent and lasting

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EXOCRINOLOGY
analysis, that possibility remains doubtful. Since skin bacteria ignore sebum,39 and
with so many other sebums function as pheromones,40,41 maybe that misleading idea
will fall from persistent medical acceptance error? Hopefully, the dramatic changes
in human behavior brought about by oral intake of skin surface pheromones (loss of
criminality, addiction, and sexual perversion) will eventually convince everyone.

Table IV shows major components of human sebum. The long-chain wax

esters in the mix probably maintain the wide melting point characteristics of sebum.
That heat-variable viscosity, 42 you will recall, looks important for human passionate
behavior. Esters, the second most numerous set in sebum, form the most numerous
class of functional groups among known pheromones.6 Some economic functionality
for the complexity seems likely in light of the trouble and expense the skin glands
apply in making sebum.1

The wax ester component of human sebum expands so quickly just before
birth at the end of gestation that physicians can spot it on sonographs to gauge labor.43
Wax esters also expand during puberty but more slowly until an equivalent mix is

101
obtained at reproductive maturity.44 Both ester percentage increases precede peak
bonding periods of birth and young adulthood. An economic "just in time" logic
suggests, along with the chemical evidence of the prevalence of ester groups in
pheromones, that these human wax esters may stimulate or enhance human bonding
pheromonally. Do you see? This is all fitting together too well to allow
psychological ‘explanations’ to continue to exist.

METHYLATION OF HUMAN SEBUM

In sebum, all but the iso chains have methyl groups only on the even
numbered carbons (with carbon atom of the carboxyl group being counted as #1).1
While methyl groups do show up on the much commoner penultimate and
antepenultimate carbons; however, in his own words:

[...] Maximum amounts of methyl branching appear on the fourth C-atom for all
chain lengths. The significance of this is not known.1

As it turns out, methyl branching on a particular carbon in the chain

characterizes many pheromones. Those methyl bumps may work like the teeth on an
old brass key. Return to Table I again. Recall how A. texana liked the 4th carbon for
its lone methyl group? Recall how M. croceipes could detect that 13-methyl
analogue? Finding peculiarly consistent methylation on fourth carbons of human
sebaceous fatty chains represents chemical evidence for our sebum being
pheromonal.

Funny methylation changes in sebum can be seen with respect to age.45

Kosugi and Ueta44 investigated sebum of children and old people versus young adults.
They noted that a methyl group appeared predominantly on the third carbon from the
end of the chain in children and old people, while fertile adults had their carbon on
the second carbon from the end. Kisses for children and old people differ from those

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of fertile adults, as do differential solicitude and patterns of abuse and criminal
behavior. The chemistry is, indeed, different!

Human sebum goes further with its peculiarities. Dimethyl (two methyl
groups) carbon chains are common, but again, only on the even carbons.1 While this
may suggest some sort of synthesis anomaly, we have seen that receptors exist in
other animals which can distinguish methylation from methylation.22,24 Indeed, only
a methyl group differentiates hormone adrenalin from its nor-adrenalin semi-
antithesis, suggesting early evolution of this sensing ability. Recall hormones were
once pheromones among colonial microbes before the organization of organism
bodies.

CHAIN LENGTH and MIXTURES OF CHAIN LENGTHS IN

HUMAN SEBUM

Sebum's components exhibit an "extremely wide range of chain lengths".1 A

few strictly even or a few strictly odd chain lengths usually compose lipid
accumulations in plants and animals.4 A mixing, as here in sebum, typifies
pheromones. The mix stretches from fewer than 6 carbons to as many as 38, in vernix
caseosa. Recall what Jones (1986) reported above. In receptive tissues, a synergism,
a more than additive increased sensitivity, can result where chain lengths mix.

Very long chain lengths make the pheromone stay stuck longer. Longer chain
and therefore heavier and less volatile pheromones tend to persist in the environment
longer and thus tend to be utilized as territory marking pheromones. Long chain
species wash off with water less easily. They evaporate less readily, also. Vernix
caseosa's persistence suggests that carrying a little one home to mark the bed might
improve family life. We should try, the divorce rate remains too high.

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CHAIN LENGTH FROM END OF CHAIN TO DOUBLE BOND

"There is present a family of very long chain unsaturated acids all with double
bonds between the seventh and eighth C-atoms from the methyl end of the chain, an
unusual occurrence."1 Figure 11 through Figure 18 illustrate sets of chemicals
varying in chain length, a feature discriminated by pheromone receptors. Such an
uncommon collection strongly suggests pheromone functionality.

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EXOCRINOLOGY

Figure 11. Four examples of a suspiciously pheromone-like homologous series of free fatty
acids (also esterified, & with diol. & as one of three triglyceride "legs" see Figure 1.)

Figure 12. Three more examples of a suspiciously pheromone-like homologous series of fatty
acids appearing in sebum.

105
 Figure 13. Three more examples of a suspiciously pheromone-like homologous series of fatty
acids appearing in sebum.

Figure 14. Four more examples of a suspiciously pheromone-like homologous series of fatty
acids found in human sebum.

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EXOCRINOLOGY

Figure 15. Three more examples of a suspiciously pheromone-like homologous series of fatty
acids found in human sebum.

Figure 16. Four more examples of a suspiciously pheromone-like homologous series of fatty
acids found in human sebum.

107
 Figure 17. Three examples of a suspiciously pheromone-like homologous series of iso-free
fatty acids.

Figure 18. Three examples of a suspiciously pheromone-like homologous series of

iso-free fatty acids.

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EXOCRINOLOGY
ESTER PRIMER PHEROMONES

Also included must be mono-esters of the Figures 11 through 18 fatty acids

(and shorter ones that Nicolaides1 declined to identify, such as 3-methyl-2-hexenoic
acid) esterified to related long chain fatty alcohols, and at least two types of diesters.
The first diester type would be formed from these fatty acids with an alpha-hydroxy
esterification to another fatty alcohol and a third group of fatty acids. The second
would consist of two subtypes 1,2 alkane diols esterified to two groups of fatty acids;
or 2,3 alkane diols esterified to two groups of these fatty acids (see Nicolaides, N.,
19741). The numbers indicate order on the carbon chain. A 1,2 alkane diol is an
alkane (all Hydrogen saturated carbons with only single bonds) with two alcohol, or
OH, groups located on the first and second carbons. Diol means a chemical species
with two alcohol groups on it, generally.

As we've said, esters proliferate in the vernix abruptly just before the baby
delivers and much later more gradually during puberty, peaking in early adulthood.
Because bonding reaches its highest frequency in these periods, the esters in Figure
19 through Figure 21 and their homologues, may together stimulate or reward
bonding onset.

Cholesterol esters are found more commonly in childhood and neonatal

sebums, differentiating them from adult-typical compositions.46 Higher
concentrations of linoleate are found in childish sebum, too.47 These, and other
childhood-typical chemical species, should be investigated as candidates for a human
child-aversion or child recognition pheromone. A human child-aversion pheromone
could explain the Kibbutz aversion data and find a place in semiochemical medical
practice for treatment of sexual child abuse.

Pheromonal aversion can involve nausea, probably involving the Peyer’s

patches full of microvillar cells in the alimentary tract. Since disgust sensitivity
predicts intuitive disapproval of sexually perverted people,48 this seems a reasonable
conclusion to draw.

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 What makes esters the most frequently pheromonal functional group?
Perhaps esters are merely easier to transfer in kisses? Chemically, esters are among
the least reactive functional groups.

Figure 19. Methylated enoic monoester typical of those thought to induce bonding. Derived
from the first fatty acid in Figure 11 and from a methylated straight chain from an iso C 20 carboxylic
acid commonly found in sebum. See Table V for more examples.

Figure 20. One of two main types of di-esters found in human sebum. It is similar, except in
chain lengths and 4th carbon methylation, to esters found in scent glands of other animals.

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EXOCRINOLOGY

Figure 21. The second main type of di-esters found in human sebum. It is similar, except in
chain lengths, 4th carbon methylation and unsaturation position, to esters found in sebaceous scent
glands of other animals.

NON-PHEROMONE COMPONENTS IN SEBUM

Why should obvious non-pheromones show up in sebum? Why should

Palmitic acid, Myristic acid, Stearic acid, and Oleic acid comprise 25.33%, 6.88%,
2.89%, and 1.87% respectively of the fatty acids in sebum? Wouldn't you expect to
find sebum to be completely pheromonal? No, you would not. (Palmitic acid is
found in palms, butter, cheese, milk and meat. Myristic acid is named after nutmeg.
Stearic acid is found in many animal and vegetable fats and oils, like cocoa. Oleic
acid is the most abundant fatty acid in human adipose tissue.)

Well, a fatty acid mix containing palmitic and oleic acids stimulates sexual
behavior in male ticks.31 These same two chemicals stimulate emigration for two
genetically different strains of common fruit flies.49

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 First, you might expect to find a very few "intermediates." Nicolaides1 errs to
suggest that "intermediate compounds accumulate in the skin." Batch processing,
where intermediates do accumulate, typifies digestion not secretion. However, since
cells burst to deliver sebum, something minimal might remain of that cellular
machinery.

Second, other chemicals play supporting roles in any environmental chemical.

Unsaturations lower the melting point of a fatty acid. A few unsaturations are all that
separate lard-like shortening from vegetable oil. For a semisolid that can hold on in
skin pores, but which will melt in the heat of a lover's embrace, a balance must be
struck.

Taken into consideration must be opposing costs of manufacture to the body,

what component dissolves what other, and what affects the melting point,
hydrophilicity, and so on of the entire mixture. A test of this straightforward
hypothesis might be modeled with a matrix of equations for each constraint in a linear
program, but the thesis seems logical. Chemicals released into the air also might
dispense with co-products.

Take another look at Table IV. Squalene is an unctuous vehicle commonly

used by pharmaceutical companies. The pharmaceutical use for squalene (from shark
liver) is as a vehicle for ointments. Might it function similarly here? Squalene's low
melting point <20o C or 4o F) suggests that it supplies the egg-and-milk in the batter.
Perhaps it dissolves some of the otherwise solid fats? Interestingly squalene itself
reportedly has pheromonal properties, at least in aliphatic nonvolatile sebaceous
secretions of garter snakes.50

OTHER HUMAN PHEROMONES[?]

Ellin's group,51 followed by Dubinin et al. (1985),52 examined volatile human

skin effluents. "The authors remark (Ellin, R.I. et al., 1974) that although they had
expected to observe a large number of [relatively volatile] alcohols and ketones in the
effluvia of man, they had not expected the large number of unsaturated and branched-

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EXOCRINOLOGY
chain hydrocarbons they observed nor had they expected isoprene to be one of the
most abundant human volatiles." 53 Dubinin's group43 found an unexplained increase
in palmitoleic acid (another of the few components of adipose tissue) in the facial
sebum of men over a short time.

Terpinoid pheromones (see Wheeler, J.W.54) originate from those abundant

isoprenoic volatiles. As has been shown, unusual unsaturated and branched-chain
hydrocarbons would be expected in volatile human pheromones. Short term changes
in whole human volatile emissions might reflect impatience, anger, or merely the
progress of digestion. Localization of emissions, controlling and testing for
psychogenic cause (if any) should take high priority in any systematic study of
volatile human semiochemicals.

Some of these studies were stimulated by astronauts’ space suit design. Now,
one of their own, poor Lisa Nowak’s fate may depend upon it. Her exposure to high
concentrations of ozone (space laundry) doubtless caused her violent outburst against
her competitor for the favor of astronaut William Oefelein. Atmospheric ozone
concentration correlates nicely with human violence.55

CHEMICAL CONCLUSIONS

We must avoid the trap of thinking too soon we have solved the puzzle. Even
based upon clearcut chemical and behavioral evidence, sound judgment can not
substitute for demonstration. Diesters of 3-hydroxy C8, C10, and C12 acids, the
female mallard duck pheromones, were found as the major products of the uropygial
[preen] glands only during the breeding season.33

"Take a gander" at Figure 22. Notice that varied chain lengths, and consistent
hydroxylation are consistent with these chemicals being pheromones, too. Production
only during the breeding season, also provides evidence of pheromonal activity.
Doubtless as a marking pheromone to post territories during ‘displacement activity’
where the birds gather these chemicals from their preen gland and spread them
around their nests on objects they pick up and drop once they are covered with the

113
species-specific chemicals. It leads one to suspect that there must be no such thing as
‘displacement activity’ but instead just territory marking activity. Similar behavior by
hundreds of species of birds, the so called ‘displacement activity’ concerning ‘nuptial
gifts’ is going to be better understood as pheromone receptivity lacrimation and
pheromone-induced bonding activities. More later.

Figure 22. 3-hydroxyoctanoic acid, 3-hydroxydecanoic acid, and 3-hydroxyundecanoic acid.

Pheromone (Kolattukudy, P.E., and L. Rogers, 1987) secretions of the female mallard duck preen
gland.

It may look like a duck. It may quack like a duck. But is it really a duck?
Before we describe any chemical as a pheromone, it must be isolated, bio-assayed,
synthesized, bio-assayed and then the whole must be replicated elsewhere. 56

This chapter has introduced some of the chemicals jumbled together in human
sebum. Those peculiar things setting sebum apart from other lipids put it in a class

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EXOCRINOLOGY
with known pheromonal chemicals. Pheromone receptors in diverse species know and
use those same chemical oddities, as well. Conservation of this ability is not out of
the question at all. Together with social, dermatological and physiological data
presented earlier, the case for human pheromones improves.

1 Nicolaides, N. 1974; Skin lipids: their biochemical uniqueness. Science. 186:19-26.

2 Cossette Chantal, Patel Pranav, Anumolu Jaganmohan R., Sivendran Sashikala S, Lee Gue Jae,
Gravel Sylvie, Graham Francois D, Lesimple Alain, Mamer Orval A, Rokach Joshua, and Powell
William S. Human neutrophils convert the sebum-derived polyunsaturated fatty acid sebaleic acid to a
potent granulocyte chemoattractant. April 25, 2008. The Journal of Biological Chemistry,
283:11234-11243.
3 Boeckh J, Kaissling KE, Schneider D. Sensillen und Bau der Antennengeissel von Telea polyphemus
(Vergleiche mit weiteren Saturniden: Antheraea, Platysamia, und Philosamia). Zool J Anat
1960;78:559-84.
4 Morrison, Robert Thornton, and Robert Neilson Boyd 1987; Organic Chemistry Fifth Edition.

Boston: Allyn and Bacon, Inc. 1486 p. (p. 347)

5 Weitkamp, A.W., A. Smiljanic, and S. Rothman (1947). The free fatty acids of human hair fat.

Journal of the American Chemical Society Aug. 69:1936-1939.

6 Silverstein, Robert M. 1984; Chemistry of insect communication. Chapter 5, pp 105-121. In:
Insect Communication. Lewis, Trevor editor. Academic Press, London. 414 p.
7Roelofs, W.L. 1979; Pheromone perception in Lepidoptera. In: Neurotoxicology of Insecticides
and Pheromones. New York: Plenum Press.
8 Müller-Schwarze, D (1969). Complexity and relative specificity in a mammalian pheromone.

Nature (Lond.) 223:525-526

9 Brownlee RG, Silverstein RM, Müller-Schwarze D, Singer AG. Isolation, identification and function

of the chief component of the male tarsal scent in black-tailed deer Nature 1969;221:284-285.
10Frost ML, Colton SW the 6th, Wertz PW, and Downing DT. Structures of the dienoic lactones of
horse sebum. Comparative Biochemistry & Physiology - B: Comparative Biochemistry. 1984;78(3):
549-52.
11Leyden, JJ, X.-N. Zeng, K. McGinley, H.J Lawley, and George Preti 1990; Characterization of
pungent axillary odors. Journal of Investigative Dermatology. 94(4):549.
12 Wilson, Edward O. (1963). Pheromones. Scientific American 208:100.
13Silverstein, Robert M., JO. Rodin, and D.L. Wood (1966). Sex attractants in frass produced by
male Ips confusus in ponderosa pine. Science 154:509-510.

115
14Linn, C.E. Jr., L.B. Bjostad, JW. Du, and W.L. Roelofs (1986a). Redundancy in a chemical signal:
behavioral responses of male Trichoplusia ni to a 6-component sex pheromone blend. Journal of
Chemical Ecology. 10(11):659-668.
15Moser, J C. (1970). Pheromones of social insects. pp. 161- 171. (In) Control of Insect Behavior by
Natural Products. Wood, David L., Robert M. Silverstein, and Minoru Nakajima editors. New York:
Academic Press 345p
16 Linn, C.E. Jr., M.G. Campbell, and W.L. Roelofs (1986b). Male moth sensitivity to
multicomponent pheromones: critical role of female-released blend in determining the functional
role of components and active space of the pheromone. Journal of Chemical Ecology. 12(3):
659-668.
17 Handel, Steven N., and Andrew J Beattie 1990; Seed dispersal by ants. Scientific American 263
(2):76-83a.
18 Tesar, J 1986; Indentifikace mazu syroveho (vernix caseosa). soud Lek. 31(4):54-55.
19 Montagna, William 1974; An introduction to sebaceous glands. Journal of Investigative
Dermatology. 62(3):120-123.
20Downing DT, Strauss JS. Synthesis and composition of surface lipids of human skin. Journal of
Investigative Dermatology 1974;62(3):228-44.
21Moulton, David G. 1977; Minimum odorant concentrations detectable by the dog and their
implications for olfactory receptor sensitivity. pp. 455-464. In: Chemical Signals in Vertebrates
Mu ller-Schwarze, D and Maxwell M. Mozell editors. New York: Plenum Press 610 p.
22Daev EV, Surinov BP, Dukel'skaia AV, Marysheva TM. Chromosomal abnormalities and
spleenocyte production in laboratory mouse males after exposure to stress chemosignals. Tsitologiia.
2007;49(8):696-701.
23
Jones RL. Orientation by insect parasitoids. pp. (In) Mechanisms in Insect Olfaction Payne, T.L.,
Martin C. Birch, and C.E.J Kennedy editors. Oxford: Clarendon Press. 1986;149-156.
24Kabachnik, M.I., Brestkin, A.P., Godovikov, N.N., Michelson, M.J., Rosengart, E.V. and V.I.
Rozengart (1970) Pharmacol. Rev. 22, 355-388.
25 Jones, RL., W.J Lewis, M.C. Bowman, M. Beroza, and B.A. Bierl (1971). Host-seeking stimulant
for parasite of corn earworm: isolation, identification and synthesis. Science .c 173:842-843.
26Foye WO. editor. Physical-chemical properties and biologic activity. In: Principles of medicinal
chemistry 3rd ed. Philadelphia: Lea & Feibiger 1989;18.
27 Dixon M, Webb E. Enzymes. New York: Academic Press, Chapter 6. (1964).
28Prestwich, Glenn D. 1987; Chemical studies of pheromone reception and catabolism. Chapter
14, pp. 473-527 (In) Pheromone Biochemistry Prestwich, Glenn D., and Gary J Blomquist editors.
Orlando: Academic Press, Inc. 565p.
29Tumlinson, James H., and P.E.A. Teal 1987; Pheromone Biosynthesis and its regulation. pp 3-26.
Chapter 1. In: Pheromone Biochemistry. Prestwich, Glenn D., and Gary J Blomquist editors.
Orlando: Academic Press, Inc. 565 p.

116
EXOCRINOLOGY
30 Morgan, ED 1984; Chemical words and phrases in the language of pheromones for foraging and
recruitment. Chapter 8, pp 169-194. In: Insect Communication. Lewis, Trevor editor. Academic
Press, London. 414 p.
31 Boch, R, and D.A. Shearer (1965). Alarm in the beehive. American Bee Journal 105:206-207.
32Allan S.A, JS. Phillips and D.E. Sonenshine 1989; Species recognition elicited by differences in
composition of the genital sex pheromone in Dermacentor variabilis and D. andersoni (Acari:
Ixodidae). Journal of Medical Entomology 26(6):539-546
33Sugiyama, T., and H. Sasada 1988; Chemistry and biochemistry of unusual branched fatty acids
with pheromonal activity from mature male goat. Seikagaku - Journal of Japanese Biochemical
Society. 60(2):118-122.
34Kolattukudy, P.E., and L. Rogers 1987; Biosynthesis of 3-hydroxy fatty acids, the pheromone
components of female mallard ducks, by cell free preparations of the uropygial gland. Arch.
Biochem. Biophys. 252(1):121-129.
35 Gould J. Ethology the Mechanism and evolution of behavior. New York: Norton Press 1982
36 Von Eggeling, H. (1940). Origin of cutaneous glands of mammals. Anat. Anz. 90:149-157.
37Guthrie, RD. (1970). Evolution of human threat display organs. In: Evolutionary Biology, vol. 4.
Dobzhansky, T., M.K. Hecht, and W.C. Steere editors. New York: Appleton-Century-Crofts.
38Kligman, A.M. (1963). The uses of sebum? pp. 110-124. In: Advances in Biology of Skin.
Vol. 4. the Sebaceous Glands (ed. by Montagna, W., RA. Ellis, and A. Silver) Oxford:
Pergamon Press.
39 Cove JH, Holland KT, Cunliffe WJ. An analysis of sebum excretion rate, bacterial population and
the production rate of free fatty acids on human skin. Br J Dermatol 1980;103:383.
40Mykytowycz, R (1970). The role of skin glands in mammalian communication. In: Advances in
Chemoreception, Vol. I. Johnston, JW., D.G. Moulton, and A. Turk editors. New York: Appleton-
Century-Crofts.
41Mykytowycz, R, and B.S. Goodrich 1974; Skin glands as organs of communication in mammals.
Journal of Investigative Dermatology 62(3):124-131.
42 Burton, J L. (1970). The physical properties of sebum in acne vulgaris. Clinical Science

39:757-767.
43Wysocki, S.J, A. Grauaug, G. O'Neill, and R Hähnel 1981; Lipids in forehead vernix from
newborn infants. Biol. Neonate. 39:300-304.
44 Sansone-Bazzano, Gail, B. Cummings, A.K. Seeler, and RM. Reisner 1979; Differences in the
lipid constituents of sebum from pre-pubertal and pubertal subjects. British Journal of Dermatology
103:131.
45Kosugi, Hiroko, and Nobuo Ueta 1977; The structure of triglyceride in human sebum.
Japanese Journal of Experimental Medicine 47(5):335-340.

117
46Stewart, Mary Ellen, and Donald T. Downing 1991; Unusual cholesterol esters in the sebum of
young children. Journal of Investigative Dermatology 95(5):603-606.
47 Stewart, Mary Ellen 1992; Sebaceous Stewart, gland lipids. Seminars in Dermatology Jun; 11
(2):100-105.
48Inbar Y, Pizarro DA, Knobe J, Bloom P. 2009; Disgust sensitivity predicts intuitive disapproval of
gays. Emotion. 2009 Jun;9(3):435-9.
49Narise, S., and T. Narise 1991; Chemical communication of emigration behavior of Drosophila
melanogaster II. identification of chemical substances. Idengaku Zasshi - Japanese Journal of
Genetics 66(4):411-420.
50Mason, RT., H.M. Fales, T.H. Jones, L.K. Pannell, JW. Chinn and D. Crews 1989; Sex
pheromones in snakes. Science 245(4915):290-293.
51Ellin, RI., RL. Farrand, F.W. Oberst, C.L. Crouse, N.B. Billups, W.S. Koon, N.P. Musselman, and
F.E. Sidell 1974; An apparatus for the detection and quantitation of volatile human effluents. J
Chromatog, 100:137-152.
52Dubinin, D.M., V.P. Naidina, and S.N. Zaloguev 1985; [Evaluation of human skin function in a
sealed room by chromatographic method.] Kosm. Biol. Aviakosm Med. 19(6):69-73.
53Albone, Eric S. 1984; Mammalian Semiochemistry The Investigation of Chemical Signals
Between Mammals. Chichester, England: J Wiley & Sons Limited. 360 pages p. 13
54Wheeler, James W. 1977; Properties of compounds used as chemical signals. pp 61-70 In
Chemical Signals in Vertebrates. Müller-Schwarze, D and Maxwell Maxwell M. Mozell New York:
Plenum Press 609 pages p. 66
55Rotton, J, and J Frey 1985; Air pollution, weather, and violent crimes: concomitant time-series
analysis of archival data. Journal of Pers Soc. Psychol. 49(5):1207-1220.
56Silverstein Robert M. 1981. Pheromones: background and potential for use in insect pest control.
Science 213(4514):1326-1332.

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Chapter 4: More about Bonding: Neglect and

Abuse

Because the ground is chapt,

For there was no rain in the earth
The plowmen were ashamed,
They covered their heads.

Yea the hind also calved in the field,

And forsook it,
Because there was no grass.

Jeremiah 14:45

Human beings commit infanticide with greater regularity than any other
species. This disproportion may be due at least in part to our human-specific hygiene
practices. Bad thinking or bad thoughts probably takes no part, but there is no way to
tell, is there?

Who is a typical child abuser? The male or less often female abuser is of
reproductive age.1 Frequently he has never committed a crime in his life, although if
he is a criminal he is more likely to abuse his children. He has low socioeconomic
status, he is a victim of unemployment, poverty, and Medicaid usage.2 He feeds,
clothes, shelters, protects and loves his entire family except for the one child being
abused. He is often new to the family. He has no close-knit extended family on
which the family can lean for "supportive services," i.e. baby sitting, talk, and
financial assistance.

The typical physical child abusive parent does not believe that he is a child
abuser. He, like the other members of the family, feels that the victim deserves what
he gets and has been treated quite fairly. On the average he is just as likely to

119
physically abuse children of either sex. The siblings of the abused, both brothers and
sisters, are treated normally, doubtless in the very same way other parents live with
their children.

The abuse takes the form of horrible burns, ("The kid just pulled the pot off
the stove onto his head") bruises and bones broken from blows ("he ran into a wall").
("He fell. He is just an unusually clumsy child.") The abuser may grab the poor child
by the arms and shake them so severely that radial fractures in the bones of little arms
will appear in x-rays.

Perhaps the physical child abuser tells the truth? Biologically speaking, like
the hind in the fields of ancient Israel, they are innocent of any wrongdoing.
Plausibly, they merely suffer symptoms of a pheromone deprivation, or even an anti-
pheromone poisoning.

New boyfriends are over-represented among physical child abusers. New

boyfriends typically become acquainted with infants outside of critical pre-delivery
primer pheromone secretion periods. They therefore, have reduced bonding success
as opposed to natural parents present at the birth. Infanticide can be seen in many
species,3 even birds.4 According to Eibl-Eibesfeldt,3 infanticidal males improve their
reproductive fitness by bringing females into earlier sexual receptivity.

The acts of physical child abusers range from "forgetting to feed them," to
inflicting slow death by the most horrible mutilations imaginable.5 Parent-infant eye
contact is lacking.6

This chapter builds a theoretical model of physical child abuse and suggests to
physicians how a medical treatment for the disorder could be devised. The model
includes explanations drawn from the ethological literature for factors associated with
abuse. Additionally many physiological, behavioral, and biochemical anomalies gain
a single rationale.

Love might be made artificially. A love-creating technology, long the lore of

shepards and long under development for rats, may be useful in pheromonal medical
treatments for human physical child abuse syndrome, for sexual child abuse
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EXOCRINOLOGY
syndrome, for child neglect syndrome, and to enhance the parental experience in
adoptions of older children. 7

If either failed sebum secretion or failed sebum consumption contributes to

physical child abuse, then it may be repaired. By replicating the physiology of
bonding between mother and baby at birth, artificial love bonds will be possible.

Dermatologists associated sebum with skin acne.8 Accordingly since the

1940's they have sought control of the sebaceous pheromone producing glands
without knowing or even guessing they were pheromone producing glands.
Dermatologists pioneered manipulating these glands' secretions, thanks to acne's
significance. Importantly for our purpose, they learned to restart the secretion of the
glands of toddlers and children up to the age of about twelve.9,10

Simply put, if the glands make the pheromonal secretions and if the secretion
makes the wanted behavior, then making the glands secrete will make the wanted
behavior. Given that child abuse and neglect are truly exocrine disorders, then a
failed technology for treating acne vulgaris may find use in semiochemical/
pheromonal medical treatments.

Why develop artificial love? Extensive examination of moral, ethical, and

legal concerns remains a matter for institutional review boards. Few would object to
strengthening the bond between an orphan and adopting parents. However, such
technology used in treatment of physical child abuse, sexual child abuse, and child
neglect would supplant legal authority bent on punishment and misguided revenge.

Other applications of pheromone administration by mouth and of skin topical

hormonal stimulations might treat divorce and settle interpersonal disputes and
complaints amicably. Crime will become a chief complaint of the past. The very idea
of runaway children will become stuff of legends. Having no more orphans, no more
neglected and no more physically abused children presents a worthy medical goal.
Getting rid of most lawyers and courts has been a worthy if previously preposterous
goal of civilization since Shakespeare:

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 "The first thing we do, let's kill all the lawyers!" -

(Act IV, Scene II).

King Henry the Sixth, Part II

Sebum acts as a semiochemical pheromone in many other species. Animals

send out pheromones, chemicals sent out by one animal which affect the behavior or
physiology of another of the same kind of animal. 11

Pheromones may be categorized incorrectly as releasers or primers. Releaser

pheromones get an immediate response from the receiving animal. An example
might be the sexually receptive male silk moth, Bombyx mori. A tiny whiff of
pheromone (just three parts per billion of air) motivates him. He criss-crosses the
scent trail or pheromone plume upwind (chemotaxis) to the emitting female just as
quickly as his little wings will get him there. Releaser pheromones stimulate
behavior right away, with no lag time. If determination indicates the reward, then
getting releaser pheromone must feel better than slaking just about any other appetite.
Getting a male to do anything else but follow the scent engenders only frustration.
Pheromone reception should follow the economic law of diminishing marginal
returns. After getting so much sex attractant, the insect should become indifferent
between chasing more pheromone and some other behavior. The function should
vary from species to species. It reminds one of hypothalamic auto-stimulation.
Pheromone reception and association pathways do reach the hypothalamus.

Another recognized type of semiochemical, primer pheromones, cause long

term changes in behavior. Often primer-caused changes may not manifest themselves
for a season, or even years. Additionally, repeated exposure may affect the final
behavioral expression. For a case in point, in the moose, exposure to dominant male

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scent will determine the adult social status of a colt. 12 A similar phenomenon is seen
in mice.13 Most of these primer pheromones will be the pheromone receptor proteins
needed for pheromone recognition in the species.

A primer-type pheromone receptor protein inoculation might explain the

tendency of abused children to abuse their own children. A vaccination analogy
might be appropriate. Such a primer pheromone might alter pheromone reception to
evoke "inappropriate" responses to subsequent semiochemical stimuli. This might be
most understandable if the primer were an antibody to the pheromone itself. Similar
ability to recognize chemicals for bodily reaction is conferred from mother to neonate
via breast milk.14 Breast milk probably contains fatty acid pheromones active in
neural development from sebaceous glands of Montgomery ringing the areolae.
Oddly enough, these fatty acids could function similarly to deoxycholic acid or other
acids detected in maternal horse droppings15 and maternal rat feces. 16,17,18,19
Offspring ingest these essential chemicals from feces for their own neural
development. Of course, bad habits like social isolation run in families, too.

Declining levels of sebum shortly after birth coupled with the pheromone
addiction hypothesis of human bonding offer a logical, physical reason for mother-
infant bond failure, child neglect, and physical child abuse. Sebum acts, perhaps, as a
releaser-type pheromone, whose receptivity begins upon earlier or continuing
pheromone priming.20,11 As such, repeated synchronized exposures and some time
would obtain the best effect. However, proteins of the pheromone receptor type have
been found in various sebaceous emissions and their presence there and delivery with
the releaser sebaceous pheromone suggest the mechanism for ‘experienced’ sexual
and maternal behavior in many species, including man. The inoculation of
pheromone receptor proteins must enhance innate receptivity, molding sexual identity.

Thinking critically about the hypothesis leads to some reasonable

expectations. We would expect that the behavior of sebum in neonates, infants and
children could account for our differential feelings for these little ones. Differences
in sebum composition are particularly evident when the sebum of prepubertal
children compares with that of young adults. One such difference is the higher
concentrations of linoleate found on the skin of children.21 Another is the unusual
123
cholesterol esters found in the sebum of neonates and young children. Cholesterol
esters having fatty acids of more than 18 carbons are a prominent feature of fetal skin
surface lipid (vernix caseosa), but are a minor component of adult lipid.22 These may
be pheromones that stimulate aversion/avoidance or maternal feelings in non-
perverted adults. The lack of receptivity for these or other child-specific pheromones
suggests the biological cause for sexual child abuse. Increasing receptivity under
experimental conditions resembling those which usually occur naturally will correct
physical child abuse and neglect.

From experimental evidence in sheep, individual olfactory signatures are

major determinants of early maternal discrimination between twin lambs.23 Much of
the time, humans can distinguish people by smell but often with consistent errors of
identification.24,25

Babies of first-time mothers suffer disproportionately more of the beatings,

burns and starvations of physical child abuse5 in both humans and animals.26
Experienced mothers bond more readily to subsequent neonates. These observations
indicates that some sort of learning or immunity plays a role in bond formation.
Perhaps new mothers must learn non-consciously, via uptake of pheromone receptor
proteins, the pleasure of neonatal pheromone receptions?

The phenomenon of "uninfected" siblings baffles psychological physical child

abuse researchers. How can an abusive parent love and care normally for
"uninfected" brothers and sisters? How can younger and older children in the family
receive perfectly normal parental attention while the child victim of physical abuse
suffers so pathetically? Chance may play a large part in a pheromonal bonding.

Infants expose their parents to the most sebum when parental love most serves
survival: at birth. About 40 % of first time mothers love their newborns
immediately.27 Most of the rest bond successfully by about the third or fourth day
with all forming the love bond within the first week of life.28 The first week, with a
peak on day four, sees high rates of sebum secretion not seen again until early
adulthood.29

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That babe's 4th day surge of sebum follows the day 3 perinatal lacrimal
episodes and post partum depression in many mothers. 30 Sebum secretion and
lacrimation may synchronize to assure semiochemical pheromone receptivity in the
mother.7,31 We have touched on this already and more will be said in Chapter 6.

Some neonatal behavior in the arms of parents may reinforce parental

addiction to sebaceous pheromone. The attention getting behavior, alternately
smiling and crying, depends upon the attentions of the mother. 32 If the holding parent
gives insufficient attention, the baby objects with a crying episode. Insufficient
attention may be indicated by lack of squeaky-voice, making faces, and so on. We
have discussed this, too. With abuse, this ritualized behavior ceases. Abused babes
stare vacantly while waiting--like their mothers.

"The link between forewater amniotomy and a delayed onset of maternal

affection was unexpected" (Robson, K.M., and R. Kumar, 1980).27 Bringing on
labor artificially may disrupt the programmed ritual of pheromone secretion and
pheromone reception. The operation itself indicates prolonged or difficult labor,
indicative of still more risk factors.

Economically, why should parents neglect their children? Within the context
of the present paradigm, the disorder may result from a lack of sebaceous secretion on
the part of the neonate, a lack of transfers to the parents, or a failure of parental
reception.

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 Figure 1. From Agache, P. et al., 1980.

As can be seen from figure 1., sebum secretion drops off to a base level at the
end of the first year. All during childhood, sebaceous secretion stays very low. If an
unsympathetic (non-lacrimating, non-receptive) parent misses the first opportunities
for a sebaceous bonding, second chances are allowed, but with diminishing
effectiveness. Any pheromonal bonding would require simultaneous pheromone
emission and pheromone reception. The model predicts this critical period of
pheromone transfer marking the child's life for good or ill. Indeed, the newborn's
chances for normal parental love seems to decline with sebum secretion rate.

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A plausible explanation for parent-neonate bonding has just been put forward,
but that poses another question: Why should it be so much harder to fall in love with
an older child? Older orphans the world over exist with no hope for real parental
love. Adoption agencies try to place babies with adoptive parents as soon after birth
as possible. Their rule from decades of clinical experience: "the earlier, the better."
Placing infants into the arms of new parents improves the chance that the adoption
will "take" and decreases the likelihood of child abuse. Experience has also taught us
to pity the plight of the older orphan doomed to grow up at arms length from his
caretakers. 33

Perhaps if one or both of the parents do not get secretion to satisfy their
semiochemical appetites, increased risk of physical child abuse results? A source for
appeasing those parental appetites might be vernix or infantile sebaceous secretion.
Sebaceous secretion falls off after the first month. Declining secretion levels after the
first year or so may wean the parents, making way for the adult appetites to bring on a
little sister or brother, recall.

Occasionally, parents get separated from their new baby for extended periods.
Sickness, jail, or war may keep them apart. Over time, less and less sebaceous
pheromone remains for parental kisses. Any physical separation during the first year
precludes parents getting the fullest portion of infantile sebum. From whatever the
cause, parents risk insufficient exposure to their little one's sebum and other
pheromones in the first year. Insufficient uptake of baby's addictive pheromone may
jeopardize the parent-infant bonding process. Perhaps a "pheromone deficiency"
jeopardizes appropriate bonding?

This may answer why adopting couples prefer babies, too. Older orphans
must surely be easier to manage? Older babies and infants have less sebum than their
juniors.29 Perhaps the adopting parents' marked preference for babies is, in fact, a
marked preference for baby sebum and its reputation for bonding success.

Science can change low childhood sebaceous secretion. We can stimulate

sebum back up to perinatal levels if we must.34,35 Hope now exists for a

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semiochemical medical treatment for physical child abuse by recreating the
pheromone receptivity in the parents and providing the child’s pheromone.

The model of pheromone stimulated parental love for a child must explain
several peculiarities of physical and sexual child abuse. Let us look at them each in
turn.

PREMATURITY AND SEBUM

Babies born prematurely suffer more than their share of parental abuse and
neglect.5 Two facts might explain the common abuse of premature babies. Premature
infants may require a longer stay in the hospital. Longer hospital stays reduce parent-
infant time together during the critical first hours and first week.28,36,37 With
prematurity, the opportunity for synchronized pheromonal bonding under optimum
conditions of high secretion, high receptivity and isolation is lost. Remember the
mother-infant isolation for the first week of life? More extensive stays in the hospital,
for either infant or mother, are associated with reduced bonding success.5 The
pheromone transfer break-off of parent-infant separation due to the prematurity would
not be the only hazard. The sebaceous glands of premature infants are smaller and
less well developed than those of full term infants and of adults, premature babies'
sebaceous glands vary from term newborn and adult skin with "the lipid ... preserved
to greater advantage in term and adult skin."38 Logically, insufficient sebum
excretion must be considered as a medical reason that premature infants suffer
disproportionate abuse. Hopefully, it will soon become a forgivable offense.

The vernix collected from preterm (<37 weeks) infants differed markedly
from that collected from near-term (> or = 37 weeks) infants. The principle
difference was an increase in the content of squalene relative to other lipids in
premature sebum. This change indicated a surge in fetal sebaceous gland function at
about 37 weeks gestation just prior to birth. 39 Squalene forms an intermediate in the
synthesis of human sebum, including shorter chain molecules.40 Those short chain
molecules have high vapor pressures, so they evaporate quickly after a birth.

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Unfortunately these potentially pheromonal off-gases remain unstudied.41 Amoore
(1974) first proposed a pheromonal function for human short chain fatty acids.42
They are produced in human glands at sites essentially identical to scent glands of
many mammals.43

Another difference between premature and full term sebums is that wax esters
in the sebum increase just prior to birth.39 Wax esters of our triglycerides and free
fatty acids also increase as puberty progresses. 44 Chemically then, sebums emitted at
birth and marriage have wax esters in common. Children and premature neonates
have different sebums than full term infants and young adults. Esters are the
chemical functional group most utilized for pheromone communication among the
hundreds of insect and vertebrate chemistries known. 45 These associations are
suggestive.

Not only the vernix caseosa differs in premature births. The glands of
prematurely born human infants also differ significantly from those of full term
infants.46 Such differences in gland maturity typically affect the chemical
composition of the sebum secreted. The backup 4th day sebum surge found in the
skin of normal infants may be lacking, absent, or dysfunctional in premies. If the
hypothesis is correct, then perhaps semiochemical medical monitoring of pheromonal
emissions may help cue parents for their best receptivity efforts.

Twins and other multiple births, on the average tend to suffer a

disproportionate share of physical child abuse.5 Twins and other multiple births tend
to be born prematurely. Perhaps prematurity's risks alone can account for the
correlation? Alternatively, perhaps identical babies have diminishing marginal utility
to drive the correlation. Epigenetic sebaceous differentiation increases with age.

Sebaceous secretion can be measured a number of ways. 47 For instance in a

technique useful in neonates sebum secretion can be measured photometrically by use
of sintered glass pressed on the skin. 48 A simpler method, more accurate for greater
quantities, might be by gravimetric comparison.49 Easier still might be either the
Sebutape or the Lipometre/Sebumeter method.50,51 (Nicholson Science uses the
gravimetric method learned at Cunliffe’s knee at the Royal Infirmary at Leeds.)

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 Exocrinologists cringe on hearing unlovable infants described as "dry babies."
Abusive or neglectful parents may also describe the babies as "dry." Note the cross-
cultural consistency of appellation. Elderly spinsters may also be described as "dried
up" old ladies. Sebaceous secretion declines precipitously with menopause.40
However, the look, feel, and moistness of elderly skin does not fall off with
menopause.52 Low levels of sebaceous gland activity do not correlate to occurrences
of dry skin.53

Perhaps unlovable "dry babies", as some workers describe them, are merely
dry of sebum? The lack may even be temporary. Note the wide standard deviations
in the French team's data (figure 1). These data allow enough variability to
accommodate temporarily "dry" skin.

Overall males and females share an equivalent perinatal sebum secretion. An

identical 1 to 1 sex ratio is seen for victims of physical child abuse. 54 If a
semiochemical sexual dimorphism existed, then one would expect an inverse
relationship to skin surface lipid output. Cases of physical abuse are about equally
distributed between boys and girls. While female and male infants may have sex-
typical patterns of excretion, overall they have equivalent sebum excretion rates.
Expectation of a broad consistency between rates of abuse and rates of excretion is
fulfilled.

The same study found a different ratio for sexual child abuse, with an
overwhelming preponderance of female victims. An exocrinological epidemiologist
would suspect other than a sebaceous etiology for sexual child abuse. Perhaps
perpetrators have a receptivity problem? Perhaps the lopsided victimization stems
from some non-recognition of some child-secreted aversion-inducing pheromone as
rats have?

When virgin female Norway rats (Rattus norvegicus) initially encounter

rat pups, they begin to alternate tentative approaches, at which time they sniff the
pups, with an active avoidance of the pups.55,56 Two lines of evidence indicate
that strange pups emit an odor that females find aversive. 57 Perhaps the Israeli

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kibutzim children's strong disinclination to marry their on-campus childhood
playmates as adults may also result from a similar primer aversion pheromone?

According to this new model, if the sebaceous pheromone does not get
through to the adult, then abuse becomes much more likely, but not automatic. Self-
control can exert itself. Human appetites can be overcome by the will. A
semiochemical bonding disfunction may be a "dry baby" secretion problem, a
reception problem on the part of "cold" parents, or some evil combination.

PHYSICAL EVIDENCE

If these glands are key to acceptability, then animal experiments should show
this too. Since similar glands are small and diffuse in most mammals, cutting them
all out, or extirpating them, poses problems. However in birds, adults seem to bond
semiochemically to their young and each other,7,58 and most sebum secretes from one
big preen gland (Lucas, A.M., 1980).59 The preen gland also goes by the term
uropygial gland. Gland extirpations have been tried with predictable results.60,61,62
Hou found that the gland-extirpated bird lost social acceptance and stole sebum from
unwilling conspecifics. That might also indicate an auto-pheromone deficiency and a
persistent appetite for the substance gotten by the act of preening. Balthazart and
Schoffeniels (1979)63 correctly found that mating was disrupted without the main
gland.

The secretion rate of the sebaceous uropygial gland also declines precipitously
after hatching in tested avian species.59 One should expect a similar difficulty for
adopted immature birds. Indeed, Lorenz 63 noted a similar declining readiness to bond
after hatching among geese.

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 If one makes the rather cruel experiment of transplanting a gosling into a
strange family, it will be found that the later it is removed from its family the more
difficulty the poor baby will have in finding acceptance by the strangers' triumph
community (Lorenz, K., 1963).63

Primatologists recount episodes of newborn death among chimpanzees. For a

few days, the mother may drag the dead body of her infant about where ever she goes,
"grooming it." If she treasures the carcass for its precious groomed-for pheromone,
then these illogical anthropomorphic attributions of ape sentimentality might finally
be called into question. After all, animals do not bury their dead. Comparing
preferences for sebum smeared furs vs. ether, ethanol or detergent cleaned controls
might shed some light on this. Placing synthetic pheromone on synthetic fur and
testing opposed to controls would help more. Primatologists need to run more
experiments to test hypotheses, to be scientists, to stop pandering to a gullable public
and get out of the storytelling business altogether. Animals do not have personalities
and neither do we.

A sebaceous vernix caseosa covering at birth and neonatal secretion surge

have been found in most mammals and birds tested (e.g. Yager, J.A., et al., 198864;
c.f. Montagna, W., and P.F. Parakkal, 197440) These vary in chemical composition
species-specifically.65,40,41 These facts support a hypothesis of pheromonally induced
(or cued) parent bonding to offspring. One would expect an absence, or aversion-
inducing perinatal secretions, in nonbonding species.

Animal evidence exists that pheromones may play a role in offspring abuse
and neglect. "Failure to thrive" can be symptomatic of neglectful parental behavior
among many other ills. Benuck and Rowe66 found that olfactory bulb-ectomized
Norway rat dams had a higher proportion of pups dying early in the perinatal
period. Perhaps the pups suffered from neglect (or from sudden infant death
syndrome?) This is suggested because pup urine has been found to be attractive to
adult rats, and bulb-ectomized dams tend to lick the perianal region of their pups
less than control dams (Charten et al, 1971, cited in Leon, M., 1983).67

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Bulb-ectomized dams spent less time in contact with their pups and their
pups grew less than pups of sham-operated controls. [However] "females made
anosmic by means of zinc sulfate did not have any more deaths than control dams
(Benuck and Rowe, 1975). (Leon, M., 1983)67

Bulb-ectomy can cut out pheromonal sensation as well as olfactory. Given the
difference of behavior seen, zinc sulfate seems to target olfaction rather than
pheromone reception. However, pleasant smells probably still have their place, more
so for some species than others. The licking behavior observed also suggests that a
relatively nonvolatile pheromone may have been responsible for the differences in
maternal behavior. Rat sebum remains a logical candidate. It should be noted that
experiments with animals involve other than chemosensory variables. Controlling for
them can be difficult or counter-intuitive.

In the brain of a rat, ablation of the septal region causes permanent loss of
parental behavior. The septal area makes up a part of the limbic system in both the rat
brain and the human brain. Phylogenetically, the limbic system extends the old
rhinencephalon, or nosebrain. It routes and integrates appetites, including chemical
appetites like addiction, and serves other functions.

Ablation and stimulation experiments have shown us much about nasal-origin

pheromone sensing in the brain. Pheromonal inputs travel distinct from normal
smells. Inputs move from mucosal neural detectors in each nasal passage to the
pheromone sensing accessory olfactory bulbs (where present).68 They go: nasal
passage to olfactory pathway/accessory olfactory bulb to cortical amygdala to
entorhinal cortex to subiculum to the rest of the hippocampus.73,69 Incidentally, from
the amygdala out, the areas described are the areas hit hardest by Alzheimers Disease,
with earlier cases showing more lesions rostrally (noseward). A pheromonal
pathology for Alzheimers may be indicated.31 More recently, intranasal insulin, which
affects chemoreception, improves memory in Alzheimers patients.70 Another
pathway takes off at the amygdala for the hypothalamus,69 the brain center for
emotional and other appetites.

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DRUGS AND PHEROMONES DON'T MIX

Dopaminergic-active drugs, such as amphetamine, can modulate the regular

odor detection performance of male rats.71 It appears that some alarm pheromone (or
pheromones) shares an affinity for brain benzodiazepine receptors.72,73 Naturally, if a
pheromone (or pheromones) were responsible for bonding in animals, then you would
see inverse consumption of pheromone vs. addictive drug. Higley et al.73 performed
such an experiment and the results were as predicted by the pheromone-addiction
bonding hypothesis. With greater pheromone exchange opportunity, less sweetened
ethanol solution was consumed, while with less pheromone exchange opportunity,
more booze was consumed. Microeconomically, this substitutability defines
substitutes. Human pheromones, possibly simple facial sebum, might be used as a
substitute for addictive drugs.

Twenty-two 50-month old rhesus monkeys were provided concurrent free access to an
aspartame-sweetened 7% ethanol solution and an aspartame-sweetened vehicle before,
during, and after social separation. Subjects had been reared for their first 6 months of life
either without access to adults but with constant access to age mates (peer reared), a
condition producing reduced exploration and increased fear-related behaviors, or as controls
with their mothers; thereafter, all subjects received identical treatment. During home-cage
periods, for 1 hr each day, 4 days a week, when the ethanol solution and vehicle were freely
available, peer-reared subjects consumed significantly more alcohol than mother-reared
subjects. When stress was increased via social separation, mother-reared animals increased
their alcohol consumption to a level nearly as high as that of peer-reared monkeys. [...]
Social separation increases alcohol consumption to levels producing intoxication even in
monkeys not particularly vulnerable to stress. (Higley, J.D., et al., 1991)73

Higley's experiment must be repeated with the chemical pheromone alone vs.
alcohol consumption. Similarly, Harry Harlow's famous studies of wire and
terrycloth "motherless monkeys"74,75 must be rerun without the psychological mumbo
jumbo. Higley's team continues a dismal tradition of psychological incompetence
and a pathetic readiness to project human mental processes onto other species.

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Perhaps semiochemical-controlled experiments would demonstrate an underlying
pheromonal effect?

Very young monkeys were reared singly in comfortable cages which had two
mother figures: a "wire mother" and a "cloth mother." Behind each mother there
was a light bulb providing warmth and each mother could be equipped with a nursing
bottle attached to its "breast." One group of monkeys had their cloth mothers
equipped with nursing bottles and another group of monkeys had their wire mothers
similarly equipped. . . Both groups spent relatively more time with the cloth mother
than with the wire mother in spite of the fact that only one group secured its
nourishment from the cloth mother.78

The preference for the cloth mother was rationalized as an instinctive desire
for "contact comfort." "[B]oth mothers provided the basic known requirements for
adequate nursing, only the cloth mother provided an additional variable of contact
comfort."77 Wire contains less surface area than terry cloth. Films of these
experiments show wire mothers were made of chicken fencing. Perhaps the monkey's
own confidence building skin secretions were better deposited upon the cloth dummy
than the wire one? Harlow did not control for pheromone deposition, thus his
conclusions (and most of the "conclusions" deriving from this work continuing today
under Soumi and others) must be treated with skepticism if not outright derision.
Better controlled tests must be run.

Robson and Kumar27 found that during labor, doses of more than 125 mg. of
meperidine, (or Demerol) a powerful analgesic, delayed the onset of bonding.
Hollenbeck and his coworkers 76 found that among other factors observed during
feeding in the first month, higher doses of all types of medication, even aspirin,
received by mothers during the first four postpartum days were associated with
mothers kissing their infants less often. If kissing picks up an addiction-assuaging
pheromone, these puzzling behaviors would gain logical explanations. NSAIDs allay
pain and swelling, both are alarm pheromone responses of the organism and the
colony. NSAIDs affect the biochemical metabolism of arachidonic acid, which
closely resembles dozens of sebum’s chemical components.
135
 Drug and alcohol addicted women more frequently make poor mothers.77
Addicted mothers tend to neglect and physically abuse their offspring.78,79 A
physiological competition for biological receptor sites between drug and pheromone,
its metabolites, and/or stimulated opiate releases may explain the phenomenon.

Interestingly, family therapy, rather than friend therapy, has a greater effect
upon successful recovery from simultaneous alcoholism and street drug abuse.
Patients in therapy living with family members had significant improvement while
those living with close friends and acquaintances had none.80 What differs?

Here is an explanation with some appeal. Friends kiss less than families.
When less of a skin surface pheromone substitutes for an addictive drug, more of the
addictive drug is desired. Human beings need pheromonal love. If we do not get it,
we tend to substitute something else.

Willpower may have its place. Perhaps defective reception of the pheromone
may simply be willed by the drunken mother because alcohol satisfies or masks her
craving for the addictive product of her baby's sebaceous glands?

TESTING

Two protocols, or roadmaps for an experiment, suggest themselves. One

would involve use of sebum or vernix caseosa donated by a healthy, loved neonate.
The other method would stimulate secretion of much larger quantities of native
sebum onto the kissable skin of the abused child. Advantages and disadvantages
accrue to each.

The sebum donation experiment may be the first tried. This utilizes a
methology similar to that already tried and proven successful in sheep.81 The
protocol would have you put vernix caseosa/amniotic fluid onto the kissable skin of
the abused child. Then you have the now receptive, abusive parent kiss the child,
taking up some of the donated fluid/sebum, and hopefully, loving the youngster for
the first time.

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EXOCRINOLOGY
Getting the abusive parent pheromonally receptive may require closely
approximating the conditions at birth. One group, picking up on what shepherds have
done for millennia, has stressed vagino-cervical stimulation to encourage ewe
acceptance of an orphan lamb.82 These researchers do not seem to have controlled
adequately against semiochemical sepsis, however. Because of the potency of
pheromones (remember these chemicals can and do work at the ultra-trace level)
extreme precautions must be taken. Manipulation of the ewe vagina may induce
more adoption for another reason. Enthusiastic researchers may pull out more
priming pheromone with their agitating arms, vibrating balloons and such. Males
accept and care for offspring without benefit of delivery, so the Kendrick group must
be wrong?

Despite these reservations, any increase in semiochemical receptivity would

be welcome. Using a vibrator device to stimulate human female genitalia, especially
within some period of a successive birth, may have a place here. It may prove useful
in recreating biological conditions favorable for initiating a new, fresh parental bond.
Genital stimulation just might biologically excite an abusive mother to receptivity for
the sebum of her abused child.

Other methods may be utilized to induce an addictive pheromone receptivity.

Obtaining the most potent donated semiochemical fraction chromatographically may
be tried. Amniotic fluid in both man and sheep has a large sebaceous fraction.40
Synthetic components of human amniotic fluid, vernix caseosa, and other
semiochemical candidates should be tried singly and together in various, dosages,
concentrations, and administration regimens to achieve best effect. Logically the
closest approximation to natural exposures should prove optimal.

Obtaining blood plasma from the natural mother and injecting it into the
virgin adoptive mother may work. The technique works well in rats.83 Waves of
fetoproteins, found in gravid plasma, may be pheromone receptor proteins that
accumulate in the mother and are transferred to the father to enable human parental
bonding to neonates. If so, the fractions responsible for bonding receptivity might be
isolated and synthesized and used medically to stimulate adoption and the treat

137
physical child abuse and neglect. Similar blood proteins encouraged by hugs 84 may
also prove therapeutic.

Providing a vernix caseosa donation over kissable skins of the abused child
has several advantages over attempting to stimulate new skin surface lipid in the
abused child's kissable skins. Applying a sebotrophic agent, such as
dehydroepiandrosterone, increases sebum secretion a week or so after topical
application.85,40 Waiting may be inconvenient. Furthermore, steroid uptake and
resulting sebum secretion rate vary from gland to sebaceous gland, 86 so consistency
might be a problem. However, the sebaceous stimulation approach, mimicking the
naturally gradual decline of sebaceous sebum over a period of months, might be most
practical. No gradual shift over of the maternal recognition from the donated to the
child's native sebum would need management. Injection of birth associated
fetoproteins (likely pheromone receptor proteins), or the natural mother’s hug-
stimulated plasma may also stimulate pheromonal receptivity in abusive adoptive
parents.

In a large herd of domestic sheep, ewes lamb together simultaneously,

facilitating experimentation. In the human case, we might utilize abusive mothers
recently giving birth or suffering a stillborn delivery. That would recreate actual
bonding physiology and optimize fostering with either method, donated or stimulated
pheromone.

Maternal secretions a set period prior to birth stimulate maternal behavior in

rats.87,88 Accordingly, we should at least suspect a similar primer pheromone in
humans. A pheromone binding protein of the lipid-carrier class would be a prime
suspect for pheromone receptor proteins. Emissions might be vaginal, colostrual,
locial or mucosal. We must search.

Maternal sebaceous secretion remains high during the third trimester of

pregnancy 89 as well as during lactation.90 Because these periods correlate to the
period of enhanced maternal receptivity, autoemission and autoreception of a
sebaceous secretion must also be considered as a possible primer pheromone in

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humans. Indeed, proteins have been found in sebaceous glands 91 and these, too,
appear of the pheromone binding type.92

The sebum secretion stimulation method might utilize

dehydroepiandrosterone, a fairly benign steriod. 93 The effect of topical application
has local effect, while going without measured systemic effects. However, because
steroids may have potent effects upon development, their use should be carefully
monitored.94

Otherwise, is the stimulated sebum of say, a four year old, the same as vernix
caseosa, or even neonatal sebum? If the steroid produces an adult-type secretion,
then the inadvertent unsavory stimulation of sexual attraction or even mate-mate
bonding may be expected. A longitudinal study ascertaining the similarity of
stimulated immature sebum to that of the same child's vernix caseosa, and other
sebums through development would insure against such surprises.

Pheromone receptivity enhancements, such as pheromone receptor protein

injections or tear substitution, must stimulate the right receptivity. We do not want
friendships to form. We need no mate-mate bonding between parent and child.

Neither do we seek some extra secretion of a childhood avoidance pheromone.

However, it might be sought for use in a similar protocol in the treatment of the
sexually abusive father or mother. If a human pheromone drives kibbutzim to seek
outside mates, say some anti-romantic priming pheromone, it might find significant
use in the treatment of child molesters. Realizing it may be there is the first step. We
must find it, isolate it, and synthesize it, if it exists at all. Of course none of this is
easy since the expected chemicals are colorless, odorless, tasteless, imperceptible and
ephemeral, but we chemists have our ways.

Immunosuppressive agents may affect bonding success. Pheromone and

tissue recognition are similar enough and close enough genetically that they may be
the same system. Indeed, following the author's suggested protocol to the letter,
Cocke and Thiessen95 found that alarm pheromones do reduce immune response. It
would be interesting to observe immune system effects in rats exposed to the
maternal behavior inducing pheromones of Menella and Moltz.85,86 Testing effects of
139
such agents on pheromone secretion directly may be a useful, needless to say
medicinal, line of research. Ingestion of sebum may benefit people suffering from
immune deficiencies.

Immune dysfunction itself may be present as a result of drug abuse or other

illness. The reverse may also be the case as self-medication.

Sickness in the mother, neonate or family can affect immunity. Likewise

illness itself indicates a weakened or vulnerable immune system. Immune pheromone
recognition might then also be weakened or vulnerable to failure. Additionally, while
mother or newborn lie ill, opportunities for pheromone transmission and uptake are
foregone.

Along with illness in either the mother or the newborn and prematurity,
prolonged or difficult labor has also been correlated with increased physical child
abuse.5 A long and difficult birthing process may be indicative of some illness in
mother or newborn. Problems in the bearing of a child may also be caused by drug
addiction96:

Drug-dependent women have an increased incidence of medical and obstetrical

complications. ... The incidence of premature delivery, abruptio placentae, breech
presentation, and intrauterine growth retardation were significantly greater in drug-
dependent women. The average duration of the first, second, and third stages of
labor compared well with the normal course of labor and matched the results of the
comparison group. Labor abnormalities and cesarean sections were of no greater
incidence, but there were more than twice as many forceps deliveries, which coincides
with the 40 per cent increased use of epidural anesthesia. Analgesia and anesthesia
were in excess of that which is given to the average patient (Silver et al., 1987).94

Alcohol and drug addiction, as we have seen, may interfere with or substitute
for human pheromone reception. Given this, there should be no surprise that
pheromone reception should affect the perception of pain, allowing pheromone
manipulations to ease chronic and other pain as analgesics. Oral sebum should be
tried.

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EXOCRINOLOGY
Crowded or difficult living conditions also correlate to suppressed immunity.93
Crowded conditions at home seems to increase the probability of abuse5,97 A
pheromone secretion and reception mechanism can account for these. Ultra-crowded
fish hacheries probably account for the loss of salmon runs similarly.

A friendly female nearby during delivery eases the birthing process.37 So

having no female "helper" close-by during delivery may be an indicator of greater
bonding difficulty. Thus pheromone reception of the friendly female would affect
pheromone receptivity of the mother for her own offspring. Similar progressions are
seen in insects commonly from long-distance reception to short-distance second
pheromone reception and behavior.

The child abuser might be dissuaded by a consistent dosage regimen of

addictive skin surface pheromone. This idea might lead his limbic system to perceive
the presence of extended family. (Absence of an extended family has also been
associated with increased risk of abusive behavior.)

Adoption agencies place babies with adopting parents as soon after birth as
possible, to increase bonding success. The probability of obtaining a successful bond
appears to decline with sebum excretion by the neonate.

If a mother's love is addiction to sebum produced by her infant, then any

competition with or interruption of her critical consumption should reduce bonding
success. Such a competition might be due to consumption of other addictive
substances affecting the same receptor site or sites. Likewise, an interruption might
result from defective excretion by the infant or physical separation during the period
of high neonatal secretion.

Perhaps together with pre-delivery colostrum and vaginal secretions timely

applied or with feto receptor proteins injected, extracts or raw sebaceous secretions
from kissable skin surfaces of the abused child might cause an appetite for the abused
child’s skin secretions? If so, such skin secretions themselves might be stimulated
with topical application of dehydroepiandrosterone and other local sebotrophic
stimulants.83

141
 Once adopting or abusive parents can reliably be induced to love with
extracts, analyses should yield the ingredients of the chemical mixture. With those
results the pheromones for love could be manufactured de novo. Double-blinded,
crossed over, assays of the artificial chemical mix, repeated and replicated by other
laboratories, could prove pheromones prime, then assuage our love appetites. Those
would be the same criteria for scientific proof for any pheromone,98 difficult steps
rarely taken in practice.

1 Stark E, Flitcraft AH Women and children at risk: a feminist perspective on child abuse. Int J

Health Serv. 1988;18(1):97-118.

2 Zielinski DS. Child maltreatment and socioeconomic well-being. Child Abuse Negl. 2009 Oct; 33

(10):661-665.
3Eibl-Eibesfeldt, Irenäus. (1970b). Love and Hate: On the Natural History of Behavior Patterns.
New York: Methuen and Company.
4 Shields, W.M., J.R. Crook, M.L. Hebblethwaite, and S.S. Wiles-Ehmann. 1988. Ideal free coloniality

in the swallows. In, Ecology of Social Behavior, C. N. Slobodchikoff, ed., Academic Press, NY, pp
189-228.
5 Lynch, M.A. 1975; Ill health and child abuse. Lancet, 2(7929):317-319.
6 Jason, Janine, Sandra L. Williams, Anthony Burton, Roger Rochat 1982; Epidemiologic

differences between sexual and physical child abuse. Journal of the American Medical Association
247(24):3344-3348.
7 Nicholson, B. 1983; A semiochemical addiction model for human bonding. Paper presented to the

Animal Behavior Society and the International Society for Human Ethology, Lewisburg, PA.
8Pochi, Peter E., 1985; Sebum: its nature and physiopathologic responses. pp. 75-78 Section II In:
Dermatology Volume 1/Second Edition Moschella, Samuel L. and Harry J Hurley editors.
Philadelphia, PA: W.B. Saunders Company.
9Pochi, Peter E. 1982; Commentary: androgen effects on human sebaceous glands. Archives of
Dermatology 118(10):803
10 Pochi, Peter E., and J S. Strauss (1969). Sebaceous gland response in man to the administration of
testosterone delta-4-androstenedione, and dehydroisoandrosterone. Journal of Investigative
Dermatology 52(1):32-36.
11 Wilson, Edward O. (1963). Pheromones. Scientific American 208:100.
142
EXOCRINOLOGY
12 Shorey, H.H. 1976; Animal Communication by Pheromones. New York: Academic Press.
13 Fillion, TJ, Blass EM. Infantile experience with suckling odors determines adult sexual behavior in

male rats. Science 1986;231(4739):729-731.

14 Anderson P. The reproductive role of the human breast. Current Anthropology 1983;24(1):25-45.
15Crowell-Davis, S.L. and K.A. Houpt Coprophagy by foals: effect of age and possible functions.
Equine Veterinary Journal 1985;17(1):17-19.
16Kilpatrick, S.J, T.M. Lee, and H. Moltz 1983; The maternal pheromone of the rat: testing some
assumptions underlying a hypothesis. Physiology & Behavior 30(4):539-543.
17Lee, T.M., and H. Moltz (1984a). The maternal pheromone and brain development in the
preweanling rat. Physiology & Behavior 33(3):385-390.
18Lee, T.M., and H. Moltz (1984b). The maternal pheromone and deoxycholic acid in relation to
brain myelin in the preweanling rat. Physiology & Behavior 33(3):391-395.
19Schumacher, S.K., and H. Moltz 1985; Prolonged responsiveness to the maternal pheromone in the
postweanling rat. Physiology & Behavior 34(3):471-473.
20 Pietras, RJ 1981; Sex pheromone production by the preputial gland. Chemical Senses 6(4):391.
21 Stewart, Mary Ellen 1992; Sebaceous gland lipids. Seminars in Dermatology 11(2):100-105.
22Stewart, Mary Ellen, and Donald T. Downing 1991; Unusual cholesterol esters in the sebum of
young children. Journal of Investigative Dermatology 95(5):603-606.
23 Porter, RH., F. Le'vy, P. Poindron, M. Litterio, B. Schaal and C. Beyer 1991; Individual olfactory
signatures as major determinants of early maternal discrimination in sheep. Developmental
Psychobiology. 24(3):151-158.
24Hold-Cavell, Barbara, and Margret Schleidt 1981; A Cross-Cultural Study on the Attitude towards
Personal Odors in the Journal of Chemical Ecolology 7(1):1
25 Porter, Richard H., Rene D. Balogh, Jennifer M. Cernoch and Christie Franchi 1986; Recognition
of kin through characteristic body odors. Chemical Senses 11:389-395.
26 Wray, Herbert 1982; The Evolution of Child Abuse. Science News 122:24.
27Robson, K.M., and R Kumar 1980; Delayed onset of maternal affection after childbirth. British
Journal of Psychiatry 136:347-353.
28 Klaus, M.H., and JH. Kennell 1982; Parent-Infant Bonding. St. Louis: The C.V. Mosby Company.
29Agache, P., D. Blanc, C. Barrand, and R Laurent R 1980; Sebum levels during the first year of life.
British Journal of Dermatology. 103:643-649.
30Coppen A, Stein G, Wood K. Postnatal depression and tryptophan metabolism. In: Sandler, M.
editor. Mental illness in pregnancy and the puerperium. Oxford: Oxford University Press, 1978.

143
31Nicholson B., Pheromones cause disease: pheromone/odourant transduction. Med Hypotheses. 2001
Sep;57(3):361-77.
32 Brazelton TB, Tronick E, Adamson L, Als H, Wise S. Early mother-infant reciprocity. Ciba Found

Symp. 1975;(33):137-154.
33Cady E, Cady F. How to adopt a child. New York: Whiteside, Inc. and William and Morrow
Company, 1956.
34Pochi, Peter E. 1982; Commentary: androgen effects on human sebaceous glands. Archives of
Dermatology 118(10):803.
35Shuster, Sam, and Anthony J Thody 1974; The control and measurement of sebum secretion.
Journal of Investigative Dermatology 62(3):172- 190.
36 Anisfeld E, Curry MA, Hales DJ, Kennell JH, Klaus MH, Lipper E, et al. Maternal-infant bonding:
a joint rebuttal. Pediatrics 1983;72(4):569-572.
37Klaus, Marshall H., and J H. Kennell 1983; Parent to infant bonding: Setting the record straight.
The Journal of Pediatrics (St. Louis) 102(4):575-576
38Holbrook, Karen A. 1986; A Histological Comparison of Infant and Adult Skin pp. 3-31 In:
Neonatal Skin Structure and Function. Maibach, Howard, and Edward K. Boisits editors. New York:
Marcel Dekker, Inc.
39Wysocki, S.J, A. Grauaug, G. O'Neill, and R Hähnel 1981; Lipids in forehead vernix from
newborn infants. Biol. Neonate. 39:300-304.
40Montagna, William, and Paul F. Parakkal 1974; The Structure and Function of Skin. New York:
Academic Press. 433 p.
41 Nicolaides, N. 1974; Skin lipids: their biochemical uniqueness. Science. 186:19-26.
42 Amoore JE. Four primary odour modalities of man: experimental evidence and possible
significance. In: Denton DA, Coughlan P, editors. Olfaction and taste, V. New York: Academic
Press, 1974; 283-9.
43
Comfort A. 1974; The likelihood of human pheromones. In: Pheromones. Birch, M.C. editor.
Amsterdam: North-Holland Publishing Company.
44 Pochi, Peter E., J S. Strauss, and Donald T. Downing 1979; Age-related changes in sebaceous
gland activity. Journal of Investigative Dermatology 73:108-111.
45Silverstein, Robert M. 1984; Chemistry of insect communication. Chapter 5, pp 105-121. In:
Insect Communication. Lewis, Trevor editor. Academic Press, London. 414 p.
46 Bell M. A comparative study of the ultrastructure of the sebaceous glands of man and other
primates. Journal of Investigative Dermatology 1974;62(3):132-143.
47Shuster, Sam, and Anthony J Thody 1974; The control and measurement of sebum secretion.
Journal of Investigative Dermatology 62(3):172- 190.

144
EXOCRINOLOGY
48Simpson, N.B., et al. 1983; A more reliable photometric technique for the measurement of scalp
sebum excretion. British Journal of Dermatology 109(6):647-652.
49Lookingbill, D.P., and W.J. Cunliffe 1986; A direct gravimetric technique for measuring sebum
excretion rate. British Journal of Dermatology. 114:75-81.
50Leveque, JL., C. Pierard-Franchimont, J de Rigal, D. Saint- Leger and G.E. Pierard 1991;
Effect of topical corticosteroids on human sebum production assessed by two different methods.
Archives of Dermatological Research 283(6):372-376.
51Serup, J 1991; Formation of oiliness and sebum output--comparison of a lipid-absorbant and
occlusive-tape method with photometry. Clinical & Experimental Dermatology 16(4):258-263.
52Frantz RA, Kinney CK. Variables associated with skin dryness in the elderly. Nursing Research
1986; 35(2):98-100.
53Downing DT, Stewart ME, Wertz PW, Colton SW, Abraham W, Strauss JS. Skin lipids: an update.
Journal of Investigative Dermatology 1987; 88(3 Suppl):2s-6s.
54 Jason, Janine, Sandra L. Williams, Anthony Burton, Roger Rochat 1982; Epidemiologic
differences between sexual and physical child abuse. Journal of the American Medical Association
247(24):3344-3348.
55Fleming AS, Luebke C. Timidity prevents the virgin female rat from being a good mother:
emotionality differences between nulliparous and parturient females. Physiol Behav. 1981 Nov; 27(5):
863-868.
56Fleming AS, Rosenblatt JS. Olfactory regulation of maternal behavior in rats I&II. J Comp Physiol
Psychol. 1974 Feb; 86(2):221-246.
57 Leon, Michael 1983; Chemical Communication in Mother-Young Interactions. pp. 39-77. Chapter

2. In: Pheromones and Reproduction in Mammals. J G. Vandenbergh, editor. New York; Academic
Press, Inc. 298 p.
58 Nicholson, B. 1985; An economic model of phermone transmission in avians. Paper presented to
the Animal Behavior Society annual meeting, Raliegh, N.C.
59Lucas, A.M. 1980; Lipoid secretion of the body epidermis in avian skin. In: The Skin of
Vertebrates. Spearman RI.C. and P.A. Riley . editors. New York: Academic Press.
60Hou, H.C. (1928). Studies on the glandula uropygialis of birds. Chinese Journal of Physiology.
2:345-380.
61Hou, H.C. (1929). Relation of the preen gland (glandula uropygialis) of birds to rickets. Chinese
Journal of Physiology. 3:171-182.
62Balthazart, J, and E. Schoffeniels pheromonal action of preen gland secretion in ducks. Naturwiss.
1979;66:55.
63Lorenz, Konrad (1963). On Agression. Translated by Marjorie Kerr Wilson (1966). New York:
Bantam Books Inc. 306 p.

145
64Yager, JA, D.B. Hunter, M.R Willson, and O.B. Allen 1988; A source of cutaneous maternal
semiochemicals in the mink? Experientia 44(1):79-81.
65Mykytowycz, R (1970). The role of skin glands in mammalian communication. In: Advances in
Chemoreception, Vol. I. Johnston, JW., D.G. Moulton, and A. Turk editors. New York: Appleton-
Century-Crofts.
66 Benuck I, Rowe FA. Centrally and peripherally induced anosmia: influences on maternal behavior
in lactating female rats. Physiol Behav. 1975 Apr;14(04):439-447.
67 Leon, Michael 1983; Chemical Communication in Mother-Young Interactions. pp. 39-77.

Chapter 2. In: Pheromones and Reproduction in Mammals. J G. Vandenbergh, editor. New York;
Academic Press, Inc. 298 p.
68 Devor M. Central processing of odor signals: lessions from adult and neonatal olfactory tract
lesions. In: Müller-Schwarze D. Mozell MM, editors. Chemical Signals in Vertebrates (I)
1977;529-45.
69Shepard, Gordon M. 1977; Central processing of olfactory signals. pp.489-497 In (Mu^H ller-
Schwarze, D and Maxwell M. Mozell, eds.) New York: Plenum Press 609 pages page 490.
70Benedict C, Hallschmid M, Hatke A, Schultes B, Fehm HL, Born J, Kern W. Intranasal insulin
improves memory in humans. Psychoneuroendocrinology. 2004 Nov;29(10):1326-34.
71Doty RL. Modulation of the odour detection performance of male rats by castration and the
administration of dopaminergic active drugs: a summary of recent findings. In: Macdonald DW,
Müller-schwarze D, and Natynczuk SE, editors. Chemical signals in vertebrates 5 Oxford: Oxford
University Press, 1990;100-108.
72Rehnberg, Bradley G, Emily H. Bates, R Jan F. Smith, B. Duff Sloley, and J Steven Rson. 1989;
Brain benzodiazepine receptors in fathead minnows and the behavioral response to alarm pheromone.
Pharmacology Biochemistry & Behavior, 33:435-442.
73 Rehnberg, Bradley G, and RJF. Smith 1990; Behavioural and physiological responses to alarm
pheromone by ostariophsan fishes and a possible role for brain benzodiazepine receptors. In: Chapter
II.5 In: Chemical Signals in Vertebrates 5. D.W., Dietland Müller-Schwarze, and Steven E.
Natynczuk editors. Oxford: Oxford Science Press. 659 p.
74Harlow, Harry F., and Zimmerman, RR (1956) Affectional responses in infant monkeys.
Science, 130:421-432.
75 Harlow, Harry F. (1958). The nature of love . Amer Psychol. 13:673-685.
76Hollenbeck, A.R, JL. Gewirtz, S.L. Sebris, and JW. Scanlon 1984; Labor and delivery
medication influences parent-infant interaction in the first post-partum month. Infant Behavior and
Development 7:201-209.
77 Cuskey WR, Wathey RB. Female addiction. Lexington: D.C. Heath and Company, 1982.
78 Silver, H., R Wapner, M. Vega, and L.P. Finnegan 1987; Addiction in pregnancy: high risk
intrapartum management and outcome. J Perinatol 7(3):178-184.

146
EXOCRINOLOGY
79Balal, A.M. Correlates of addiction-related problems in Kuwait: a cross-cultural view. Acta
Psychiatr Scand. 1988;789(4):414-416.
80 Crowley P. Family therapy approach to addiction. Bulletin on Narcotics 1988;40(1):57-62.
81 Levy, F., E.B. Kevern, V. Piketty and P. Poindron 1990; Physiological determinism of olfactory
attraction for amniotic fluids in sheep. pp. 162-165, Chapter II.9 In: Chemical Signals in
Vertebrates V. MacDonald, D.W., Dietland Müller-schwarze, and S.E. Natynczuk editors. Oxford:
Oxford Science Publications 649p.
82 Kendrick, K.M., F. Le'vy, and E.B. Keverne 1991; Importance of vaginocervical stimulation for
the formation of maternal bonding in primiparous and multiparous parturient ewes. Physiology &
Behavior 50(3):595-600.
83 Terkel J, Rosenblatt JS. Maternal behavior induced by maternal blood plasma injected into virgin
rats. J Comp Physiol Psychol. 1968 Jun;65(3):479-482.
84 Matsunaga M, Sato S, Isowa T, Tsuboi H, Konagaya T, Kaneko H, Ohira H. 2009; Profiling of
serum proteins influenced by warm partner contact in healthy couples. Neuro Endocrinol Lett.
2009;30(2):227-236.
85 Pochi, Peter E., and J S. Strauss (1969). Sebaceous gland response in man to the administration of
testosterone delta-4-androstenedione, and dehydroisoandrosterone. Journal of Investigative
Dermatology 52(1):32-36.
86 Sansone-Bazzano, Gail, and Ronald M. Reisner 1974; Steroid pathways in sebaceous
glands. Journal of Investigative Dermatology 62(3):211-216.
87Mennella, Julie A, and Howard Moltz 1988; Infanticide in rats: male strategy and
female counter-strategy. Physiology & Behavior 42:19-28.
88Mennella, Julie A, and Howard Moltz 1989; Pheromonal emission by pregnant rats protects
against infanticide by nulliparous conspecifics. Physiology and Behavior 46:591-595.
89 Burton JL, Shuster S, Cartlidge M. The sebotrophic effect of pregnancy. Acta Dermato-

vernereologica (Stockholm). 1975;55:11-3.

90Burton, JL., Sam Shuster, M. Cartlidge, L.J Libman, and U. Martell (1973a). Lactation, sebum
excretion, and melanocyte stimulating hormone. Nature 243:349-350.
91Mancini, M.A, D. Majumdar, B. Chatterjee and A.K. Roy 1989; Alpha 2u-globulin in modified
sebaceous glands with pheromonal functions: localization of the protein and its mRNA in preputial,
meibomian, and perianal glands. J Histochem Cytochem Feb 37(2):149-157.
92Singer, A.G. 1991; A chemistry of mammalian pheromones. Journal of Steroid
Biochemistry & Molecular Biology. 39(4B):627-632.
93Downing DT, Strauss JS, Ramasastry P, Abel M, Lees CW, Pochi PE. Measurement of time
between synthesis and surface excretion of sebaceous lipids in sheep and man. Journal of Investigative
Dermatology 1975;46:444.
94 Pochi, Peter E. 1982; Commentary: androgen effects on human sebaceous glands. Archives of

Dermatology 118(10):803.

147
95Cocke R, Thiessen D. Alarm chemosignals suppress the immune system. In: Chemical sgnals in
vertebrates. MacDonald, D.W., D.Mu eller-Schwarze D, and S.E. Natynczuky editors. Oxford:
Oxford University Press. 1990; 125-138
96 Silver, H., R Wapner, M. Vega, and L.P. Finnegan 1987; Addiction in pregnancy: high
risk intrapartum management and outcome. J Perinatol 7(3):178-184.
97 Jason, Janine, Sandra L. Williams, Anthony Burton, Roger Rochat 1982; Epidemiologic
differences between sexual and physical child abuse. Journal of the American Medical
Association 247(24):3344-3348.

98Silverstein, Robert M. 1984; Chemistry of insect communication. Chapter 5, pp

105-121. In: Insect Communication. Lewis, Trevor editor. Academic Press, London. 414 p.

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Chapter 5: Eating Disorders

This chapter deals with the exocrinology of anorexia nervosa (AN) and
speculates for cures for anorexia nervosa, bulimia nervosa, and obesity.

Diet, psychotherapy, and drugs

have sometimes alleviated symptoms of AN patients
but the root cause and the best treatment
have eluded a century of research.1

The symptoms of Anorexia Nervosa (AN) in human beings are largely the
symptoms of pheromone-induced puberty delay in many species of animals. AN
maintains mature scent glands in its victims. The axillary and pubic hair tufts are
secondary sex characteristics that are associated with passing the age of puberty in
humans. Those mature sexual hairy areas cover and are part of scent glands which
are among the largest in nature despite the presence of a pre-puberal endocrine set in
anorexic sufferers. Indeed, axillary and pubic scent glands appear to develop and
function normally in AN sufferers.2,3,4 Pheromone-induced puberty delay (PIDP)
seen in animals also maintains mature, functioning scent glands 5 in the
presence of a pre-pubertal endocrine set 6 just like AN! Surely that alone must
be more convincing than psychological speculations.

Both AN and PIPD occur at the same time in the life cycle, when
puberty is first attained, under similarly stressful conditions. Immatures
without secondary sex characteristics lack the ability to develop AN and PIPD,
as well.

Humans might seem to differ in that we have another incidence peak at

entry into college. However, if little lab animals went to college, they would
have an entry into college peak, too. Crowded dormitory grouping of puberal
females readily stimulates pheromone induced puberty delay in animals.5 An
149
effective puberty delay obviously named the pheromone set in animals. In AN,
poor Fischer finally noted a developmental lag after eleven years of
psychoanalysis.7

The sex ratios are nearly identical, too. Both AN and PIPD have far
more female sufferers than males. The ratios of female to male runs 50:1 in
PIPD.8,9 The ratio of female to male human sufferers in AN is between 10:1
and 20:1.10

Both AN and PIPD share having a stressed fertile female nearby. In the
animals, the stressed and dominant fertile female emits a puberty delay
pheromone that sends the puberal female back into pre-puberty.5 Of course, the
dominant fertile female can be the mother of the PIPD victim. Psychologist
report AN onset associated with a mother/daughter or female teacher/female
student ‘dyad’11 so the mature female need not be a family member.

In both PIPD and in AN, the condition continues after the victim is
removed from the shared atmosphere with the stressed fertile female.7 In PIPD
the glands of the victim’s intact adult scent glands emit the same pheromone
chemical signal as the original stressed female’s scent glands emitted to begin
her puberty delay.5 In AN, remember the intact large scent glands? In AN, the
girl taken away from her mother continues with anorexia nervosa,12 just like
PIPD.

Both AN in humans and PIPD in animals occur to daughters of gentry.

Both AN and PIPD sufferers are raised with food available ad libitum. Having
plenty of food available is a necessary condition for PIPD and exactly the same
phenomenon is observed in AN. Food is always available to anorexics,15 just
as it a necessary condition for PIPD to develop.5

Both AN and PIPD result in periodic peregrination. AN sufferers have

altered metabolisms and take long walks.13 Pheromonally induced puberty

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delay animals also have altered metabolisms and take long walks--just the
PIPD animals walk on the cage exercise wheels.5

The pheromone induced puberty delay in laboratory animals is typically about

30 days or so while the human anorexia nervosa can last for decades. However, the
period of puberty delay as a percentage of lifespan is about the same.

Both PIPD and AN see victim avoidance of sexually mature conspecific

males. PIPD animals avoid males and even the odor of males.8 AN sufferers
generally avoid dating men.12 In animals where mature males are unavoidable
or welcome, ‘[t]he presence of a conspecific male was effective in maintaining
normal oestrous cycles in underfed females to some extent’14 which suggested
to Drickamer (1988) that acceleration pheromones and delay pheromones
worked in opposition. Indeed, here is what Drickamer found:

At ratios of 10-20 parts acceleratory chemosignal to 1 part delay chemosignal,

the acceleratory effect overrides the delay chemosignal, and the mice attain
first oestrus at earlier ages than controls. Ratios of about 4 to 1 up to 7 to 1
result in mean ages for puberty that are not accelerated or delayed relative to
controls.5

The return of female reproductive cyclicity marks recovery in both the

human AN and the animal PIPD. When menstrual cyclicity does appear, the
prognosis is excellent for both AN15 and in PIPD the delay is merely over.

Given that return of cyclicity bodes well for recovery from anorexia
nervosa and that ‘having a boyfriend seems to help’ anorexic girls,12 a human
axillary pheromone extract which encourages regular menstruation in women16
was prepared. Unfortunately it was never tried and the opportunity was
wasted. The author has seen only one complete recovery from AN after
providing only one delinquent young woman with male skin surface
151
pheromone from the adult male face, but that may have been happenstance.
AN is so rare that psychologists hoard them away from exocrinologists.
Publication of an article in a peer-reviewed medical journal by this author
describing the likely exocrine origin of anorexia nervosa17 was ignored and
even ridiculed.17

Smelling the axillary pheromone component, androstadienone,

increases cortisol levels in women.18

This book may open new avenues of scientific cooperation and

discovery. However this may be difficult to accomplish for a number of
reasons. First, human pheromones usually come in sets that are nearly
undetectable by human senses. This insidious nature of pheromones can be
disconcerting, and the detection difficulty is exacerbated by unusually long
detection times on the gas chromatograph, with many components taking
longer than 30 minutes. Second, researchers are human, so working with
human pheromones can be dangerous. Working on this research can be
destructive to ones professional career, too, since hierarchical position colors
pheromone perception in the Pharisaic effect.

Evidence recently has been found to support this authors contention of a

human pheromone which causes anorexia nervosa syndrome19 when a pheromone
was shown in the laboratory to cause loss of appetite, or anorexia, in male Syrian
hamsters. Morgan et al.20 found that anorexia by pheromone can be observed in
Syrian hamsters, three years following publication of the article written by this author
describing pheromonal anorexia in humans (Nicholson B, 2000). Morgan et al.
labeled pheromonal anorexia a ‘novel phenomenon’ and suggested it would ‘provide
a model to study neural and endocrine mechanisms that underlie eating disorders.’
The flank gland of the female, the same gland associated with puberty delay
emissions in that species, emits the anorexia causing pheromone.

From Chapter 3, recall that different species mean different pheromones.

Human anorexia-causing pheromones are most likely from axillary and pubic scent

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glands. Hamsters use flank glands with a sebaceous fraction and mouse pheromones
are urinary. And oddly enough, axillary scent glands may perpetuate obesity as well.
This author found he could control his weight if his axillae were kept covered with a
thick layer of petroleum jelly.

Bulimia nervosa is a related eating disorder of bingeing and purging, with

normal weight maintained. In bulimia, appetitive fellatio obtains pubic and penile
pheromones to self-medicate the disorder.

The cure for all eating disorders should be 150 mg p.o. of healthy ‘father age’
adult male facial skin surface lipid kissing pheromone in a single dose. The cure
might effected by the anorexic/bulimic/obese person chewing 15 pieces of regular
Wrigley’s chewing gum rubbed on the face of the person’s father over a three day
period utilizing good laboratory practices and good sanitation. Covering the axillae
with petroleum jelly may help effect immediate change as the author discovered by
personal experience.

Fat people see themselves in photographs and rationalize that they are
unphotogenic, because photographs appear to exaggerate their size. After two days of
walking around uncomfortably with his armpits’ axillary scent glands covered with
petroleum jelly, the obese author’s mirror image changed to show his true size. The
abrupt self-perception change was imperceptibly insidious. Plates of food only days
before observed to be small became too much to eat at one sitting, perception of size
in the horizontal direction changed. Dramatic weight loss followed the perception
change, but once the interruption of the axiallary chemosignals ceased, the weight
was imperceptibly regained.

Since the axillary chemosignal set depends upon the skin’s microflora for
processing, 21 antiseptic interventions were tried, but failed. Some weight loss was
finally maintained by a rigorous regimen of long distance hiking and bicycle exercise.
Others22 have begun similar investigations with some hope of progress.

A derivative of fish oils has helped one severely anorexic patient.23 Given the

similar tertiary stereochemistry of fish oils to components of human skin surface

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lipid, treatment of AN with the far more complex synergistic facial skin surface lipids

of the human adult male should be of benefit. Injection of pheromone binding

proteins and epigenetic chemotherapy may also find usefulness treating anorexia

nervosa.

Of course, bulimia nervosa sufferers famously find solace in fellatio. At the

very least, male sexual skin surface lipids collected in the lab or synthesized de novo

should sate that appetite without most of the risk of sexually transmitted disease.

1 Murray J B Psychological aspects of anorexia nervosa. Genet Soc Gen Psychol Monogr 1986; 112
(1): 5-40.
2Treasure JL, Gordon PA, King EA, Wheeler M, Russell GF. Cystic ovaries: a phase of anorexia
nervosa. Lancet 1985; 2(8469-70): 1379-1382.
3Treasure JL, Wheeler M, King EA, Gordon PA, Russell GF. Weight gain and reproductive function:
ultrasonographic and endocrine features in anorexia nervosa. Clin Endocrinol (Oxf) 1988; 29(6):
607-616.
4Robbins SL, Cotran RS, Kumar V. Robbins pathologic basis of disease. Philadelphia: W.B.
Saunders, 1986.
5Drickamer LC. Acceleration and delay of sexual maturation in female house mice (Mus domesticus)
by urinary chemosignals: mixing urine sources in unequal proportions. J Comp Psychol 1988; 102(3):
215-221.
6Keverne EB. Pheromonal influences on the endocrine regulation of reproduction. Trends Neurosci
1983; 6: 381-384.
7Fischer N. Anorexia nervosa and unresolved rapprochement conflicts: a case study. Int J Psychoanal
1989; 70(Pt1): 41-54.
8 Vandenbergh JG Pheromonal Regulation of Puberty. In: Vandenbergh JG, editor. Pheromones and
reproduction in mammals. New York: Academic Press, 1983: 95-112.
9Drickamer LC Puberty-influencing chemosignals in house mice: ecological and evolutionary
considerations. In: Duvall D, Müller-Schwarze D, Silverstein RM, editors. Chemical signals in
vertebrates 4. New York: Plenum Press, 1986: 441-456.
10Dambro MR, Griffth JA Griffith’s 5 minute clinical consult. Baltimore: Williams & Wilkins 1997:
60.

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11
Ehrensing RH, Weitzman EI The mother-daughter relationship in anorexia nervosa. Psychosom
Med 1970; 32(2): 4201-4211.
12Dally P, Gomez J, Isaacs AJ Anorexia Nervosa. London: William Heinemann Medical Books Ltd.
1979.
13 Russell GFM Metabolic aspects of anorexia nervosa. Proc R Soc Med 1965; 58: 811-814.
14
Gangrade BK, Dominic CJ Influence of conspecific males on the oestrous cycle of underfed female
mice. Exp Clin Endocrinol 1985; 86(1): 35-40.
15 Halmi KA Anorexia nervosa: recent investigations. Annu Rev Med 1978; 29: 137-148.
16Cutler WB, Preti G, Krieger A, Huggins GR, Garcia CR, Lawley HJ Human axillary secretions
influence women’s menstrual cycles: the role of donor extract from men. Horm Behav 1986; 20:
463-473.
17Gatward N. Because it feels good (smells funny!) European Eating Disorders Review 2001; 9(3):
210-212(3).
18Wyart C, Webster WW, Chen JH, Wilson SR, McClary A, Khan RM, Sobel N. Smelling a single
component of male sweat alters levels of cortisol in women. J Neurosci. 2007 Feb 7; 27(6):
1261-1265.
19Nicholson B Pheromones cause disease: the exocrinology of anorexia nervosa Med Hypotheses
2000; 54(3): 438-443.
20Morgan C, Urbanski HF, Fan W, Akil H, and Cone RD. Pheromone-induced anorexia in male Syrian
hamsters. Am J Physiol Endocrinol Metab 2003; 285: E1028-E1038.
21 Albone, Eric S., Pauline E. Gosden, and Georges C. Ware 1977; Bacteria as a source of chemical
signals in mammals. pp. 35-43 In: Chemical Signals in Vertebrates (Müller-Schwarze, D, and
Maxwell M. Mozell eds.) New York: Plenum Press 610 p.
22McKenzie VJ, Bowers RM, Fierer N, Knight R, Lauber CL. Co-habiting amphibian species harbor
unique skin bacterial communities in wild populations. ISME J. 2011 Sep 29. doi: 10.1038/ismej.
2011.129. [Epub ahead of print]
23Ayton AK, Azaz A, Horrobin DF. Rapid improvement of severe anorexia nervosa during treatment
with ethyl-eicosapentaenoate and micronutrients. Eur Psychiatry. 2004 Aug;19(5):317-9.

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Chapter 6: Crying Chemoreception and Love

Erbkoordinated lacrimation, or emotional crying, is ubiquitous throughout the

cultures of man.1 Why?

This chapter presents a pheromone reception model for emotional tears or

lacrimation.2,3 Bond breaking, bond establishment, and bond stress bring tears to our
eyes. If pheromone addiction is responsible for human bonding, a flush mechanism
would enhance flexibility of the process. It would allow old bonds to expire and new
ones to form under appropriate circumstances. Crying is released under just such
biologically appropriate conditions. Indeed, recent work has found tears themselves
to be human pheromones.

EXPECTATIONS OF HUMAN LACRIMAL PHEROMONE

RECOGNITION

What might one reasonably expect of any pheromone recognition system?

Any acceptable explanation should explain diverse human behaviors associated with
pheromone reception situations. Human actions during a pheromone reception
should be directly comparable to "ritualized" or “displacement” (actually
chemoreception) behaviors of other animals. Pheromone reception behavior should
remain similar for all pheromone receptive species from yeast to human beings.

The courtship dances of birds, involving much swaying and ducking of the
head, serve to get tears full of dissolved pheromone receptor protein and special
pheromone reception ions into position for chemo-analysis. It will be found,
prediction here, that the plumbing of the pheromone reception system determines
each movement of the courtship dance, each sway of the displacement activity, every
twitch of the erbkoordination. Flight restrains against carrying pheromone emission
apparatus out of season, so pheromone emission glands atrophy away from the nest.
The same should be found for pheromone reception apparatus in flighted birds.
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 When we humans cry, lean forward, and cover our faces with our hands, we
are getting the angle of our naso-lacrimal ducts and our hiatus semilunaris pheromone
reception structures in proper alignment, and in proper sequence, for human
pheromone reception. Even the male behavior of lifting her lovely chin, kissing her,
and holding her in your arms (her head in your armpit), must be economically
justified, likely as assuring transmission of episodically released human pheromone.

In human sexual behavior, the engorged turgid erectile tissues of the nasal
passages are evacuated at the very instant of climax. Our ears pop and our eyes
water. Anguished facial expressions at the joyful event of intromission must also be
economically necessary for timely human pheromone perception, just as pheromonal
emissions take place. Economics rule instinctive human behavior and nothing is for
nothing, TANSTAAFL. (There ain’t no such thing as a free lunch.) This axiom
should be assumed for all human behavior, and for all cells of all organs of all organ
systems.

Economically, pheromone reception similarity should extend from gross

behavior even to cells and cellular events. Nerve cells for humans look like nerve
cells for other mammals, reptiles, and birds. Likewise cells carrying oxygen in the
blood, look alike. Thus cells specialized for pheromone reception in other animals
should appear in humans, too, and they should look and work the same. Cellular
activity should proceed from pheromone exposures similarly in all species, from
bacterium to butterfly to human.

Pheromone recognition in people should function to conserve biological

resources. Receptivity should be more when needed more and less when needed less.
Such flexibility should be observable in other animal species. Similar glands, ducts,
secretions, and behaviors should typify responses among all animals. Chemo-
recognition's dissimilarities among species also must be accounted for
physiologically.

Lacrimal glands secrete special ion and protein concentrations in emotional

tears4 which may be involved in some human pheromone recognition.2,3 The

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secretion of these glands takes place within the choreographed sequence of behaviors
we call "crying."

Crying identifies a special behavior. Within it ionic concentrations vary (as do

peculiar lipids (self-affecting pheromones?), antimicrobial enzymes, and other
proteins specific only to emotional tears in the nose and mouth) in response to
emotion.5 These concentrations of ions and proteins are much smaller in irritant
induced tears.4,6 Onion fumes irritate. Irritant-induced tears are dilute tears which
help flush irritating particles out of the eyes and nose.

LACRIMATION AND MATE-MATE LOVE

Desmond Morris7 observed an increase in tear production during mate-mate

bonding. He thought it responsible for "the shining eyes of love" and considered it
merely a visual signal. The increased lacrimal secretion might be expected during
episodes when humans fall in love pheromonally. "These are the shining eyes of
love, and combine with pupil dilation to leave no doubt about the condition of the
signaler." However, visual signals may be less important in the semidarkness
romantic couples prefer. Illegal drugs and belladonna can produce pupil dilation, too,
and drug-takers are generally less ready to form long-lasting bonds than more
innocent people.

Typical human romantic scenarios may involve dim lighting. Dim light
allows easier pupil dilation. Pupil dilation expands the visual fields of the eyes to
include more of the phylogenetically old rod photoreceptors. The retina eventually
maps onto the brain's occipital lobe, but before reaching it, parallel nerve fibers
course in broad arcs through the two temporal lobes. Expanding the visual fields
expands the lines of transmission through the temporal lobes where face recognition
takes place. In romantic pupil dilation, face and pheromone reception are being
associated. Human male axillary pheromone emissions stimulate cortisol in women
close enough to take the pheromone from the air or by contact,8 and cortisol

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cooperates with adrenaline to create vivid memories. So 4,16-adrostadien-3-one
stimulates women to remember us males.

Ever notice how kissing lovers close their eyes? Sack et al. (1992)9 noticed
increased tear proteins in closed eye tears versus open eye tears. For kissers on the
other hand, the view at 10 centimeters lacks something. Alternatively, perhaps
nocturnal semiochemical reception and auto-reception plays some role?

Typically, the scenario plays as follows. In the dim light of romantic

acceptance, young faces close together. You start telling her how much you love her,
about your hopes and dreams. Eyes grow misty. Her eyes are like limpid pools. You
kiss. Your lacrimal fluid's proteins, accompanying a peculiarly high manganese
cation concentration from specialized glands above your eyes, go to work recognizing
her sebaceous lipids. Those lipids are now, due to her excitation, oozing hotly from
mucosal glands only recently matured out of nothing. 10 You easily reach and scrape
out of her mouth's sebaceous glands those nice waxy goodnesses with your tongue.
Repeatedly you hunt her wax esters down with your tongue's specialized lipid
harvesting surface, also developing just in time11 as your limbic reward. Your own
odd-looking sebaceous glands specific to the oral, gingival, and buccal mucosa also
come to heat. Out flows your interesting, chemically unique, possibly addictive
sebaceous greases. The sebum floats away high on her saliva, just as hers does on
yours. The greases you've just licked from her mouth reach the nasal passages where
lipid triglycerides have been found,12 and/or they reach the upper-respiratory system
where sensory microvillar ‘brush border’ cells line fifty percent of the surface area,
and/or they fall into the alimentary canal for digestion and possibly perception by
Peyer’s patches again, full of brush-border pheromone sensory cells. The microvillar
cells of the human vomeronasal organ may sense something,13 but since we do not
carry tails to tell us where we have been and need to go today to recover resources
from our territories, the vast fields of microvillar cells visible under surface electron
microscopy bunched at the end of the naso-lacrimal ducts in the inferior meati and
elsewhere lining the entire upper respiratory system and in patches along the gut
serve to recognize the gathered human lipid pheromone.

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Then there are those tears all over her cheeks. Kissing those tears away may
encourage a sharing of pheromone receptivity. Placing one's tears into the saliva of
another, with appropriate pheromone accompaniment, would, if recognized,
encourage bonding, and perhaps some shared immune resistance as well. Female
tears diminish masculine testosterone, slowing the males‘ sex drive. Lacrimal
episodes are usually of short duration, and of small consequence to victorious
warriors with new widows of slain enemies.

Kissing with lacrimal receptivity might be most efficacious in bond formation.

Tears may be elicited by other than romantic situations. This would bring the
lacrimal reception pheromone addiction hypothesis into surprising agreement with
Finck14:

Love can only be excited by strong and vivid emotion, and it is almost
immaterial whether these emotions are agreeable or disagreeable. The Cid wooed
the proud heart of Diana Ximene, whose father he had slain, by shooting one after
another of her pet pigeons (Finck, H.T., 1891).

Would this help explain why some women remain with abusive husbands?

Another tearful human behavior has been noted by grooms of innocent brides.
The behavior has been called a brides "wedding night hysterics." Apparently such
unreasonable sobbing by the bride on the marriage bed may encourage pheromonal
fealty to her new husband. The newly married woman cries, sometimes all night
long, at the prospect and conclusion of first intercourse. Why defloration has been
accompanied by "seemingly unmotivated tears" has baffled billions of grooms. Other
signs of emotionality of the intact bride remain mysterious. One down, one million to
go.

Women's tears and bonding function differ from men's. Women bond
somewhat more suddenly. Perhaps on her wedding night an unbonded female bonds
herself firmly to the unfamiliar nocturnal exocrine secretions of her new husband?
Experiencing husbandly pheromones for the first time would be a logical occasion for
dramatic efforts of pheromonal receptivity. Perhaps her defloration lacrimation

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functions to begin receptivity to the new signals of her husband and to reduce the
importance of old family signals. Loyalties may adjust pheromonally in the marriage
bed just as at the graveside.

More evidence of sex differences in bonding exist. Sexual dimorphisms,

physical differences between the sexes, have been detected in agreement with this
idea. Women have a greater frequency 15 ionic concentration16 and proteinaceous
makeup of adult human tears.17 Men counter with a greater output of dermal
sebaceous secretions.9

There were significant differences in the amounts of LF [LactoFerrin] and two [of five] kinds
of STPs [Specific Tear Proteins] in the different sexes. The amounts of these proteins were larger in
females (Mii S., et al., 1992).16

The Mii16 team's specific tear proteins appear suspiciously similar to some
pheromone binding proteins which can act as primer pheromones. The Mii group
took non-emotion-produced samples from the conjunctival sacs, a part of the naso-
lacrimal duct. However, our interest is emotional tears. Because the total protein
content of human tears differs as to stimulus15 and with duration of stimulus18 and
because women cry more frequently than men14 more information is needed.
However, the field looks pregnant with discovery.

Lacrimation frequency declines with age.4 Concentrations of one tear

glycoprotein declines after age thirty.19 Perhaps falling in love with spouse and
children is more of a young person's pastime? With longer life-spans, perhaps
rejuvenating our tears by adding more or different receptor proteins would be
appropriate? Such therapy might benefit older adopting parents or give acceptance
and renewed capacity for love to criminals, perverts, old maids and old bachelors.
Yet ‘recreational use’ of pheromone reception is too dangerous to indulge.

LACRIMATION AND PARENT-INFANT BONDING

Among the most peculiar of human behaviors, postpartum depression, more

commonly "the third day blues", is "normal" in mothers shortly after childbirth.20

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Mild disturbances of mood occur in 50-70 percent of women during the postpartum
period.21

Three to four days after the birth of their child, some women begin to cry for no
apparent reason. The crying may be intense and prolonged and may often, but not
always, be associated with a depressed mood (Coppen, et al., 1978). 22

The neonatal sebum secretion surge on the fourth day after birth found by
dermatologist Agache and his associates 23 closely follows parental postpartum
lacrimation. Evidence exists of a parent-infant bonding effort during this same
critical period.24 Is the purpose for the mother's lacrimation sebaceous-pheromone
reception enhancement?

Benfield and his associates indicate that the absence of grieving behavior in
mothers of ill and absent premature infants can lead to "disintegration" of the
family. 25 Similar difficulties encounter stillbirth. 26 Perhaps continued lacrimation
maintains receptivity and the flexibility required for adaptability? In which case
should not psychogenic lacrimation be encouraged, even cinematically with the
expectation of improved outcomes? We need sad movies in these obstetric waiting
rooms, (but upbeat flicks in cancer wards, of course.)

Brazelton videotaped mother and neonate interaction simultaneously,

displaying the two faces on a split CRT screen. When the mother put on a blank
expression (no "funny" faces or squeaky speech) the baby's face turned sanguine and
he began to cry.27 This neonatal behavior flushes the face and scalp,28 wherein lie
about 600,000 sebaceous glands,9 heating them (e.g. Seeley, T., et al.29), which
stimulates abrupt, phasic sebum flow directly onto the surface 30 as it is being kissed.
Crying, especially in babies, elicits an affectionate response.31 The neonate
manipulates the parent's pheromone reception to strengthen the mother to infant bond.
Seeing these heros of science miss this natural and now obvious sequence does not
diminish their contributions, so essential to our eventual understanding of insidious
pheromone addiction as the operative process involved in how human beings fall in
love.
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 Forming the new maternal loving bond to the infant may affect other
preexisting ones. Receptivity at the prospect of reception of the offspring's
semiochemicals may renew her bond to the father and other family members allowed
in close. This readiness to lacrimate, and the chemical makeup of maternal
lacrimation itself, may be stimulated by a primer pheromone. Since plasma from
maternal rats injected into virgin rats stimulates maternal behavior,32 perhaps human
fetoproteins released into maternal circulation during pregnancy are pheromone
receptor proteins? The fetus itself may emit feto-proteins as pheromone receptor
proteins into maternal circulation for emission or for concentration onto receptor
surfaces. Perhaps her pheromone receptivity is by a nocturnal autoemission and
autoreception of a priming pheromone receptor protein? Lochia, a pregnancy and
postpartum secretion of the vagina, or the breast's pre-milk colostrum are candidate
sources along with the neonate's milky emissions of the 'genital crisis' (see Agache, P.,
et al.23) Such a protein primer scenario would approximate the conditions of rodent
maternal priming seen by Mennella & Moltz. 33 Excessive doses of priming
pheromone might conceivably even contribute to instances of post partum depression
in the mother. It is tempting to lay post partum depression at the feet of anti-pain
pharmacology.

Reported stimuli to lacrimation vary, but time and length of crying behavior
hold consistent. Female crying bouts usually occur in the evening.14 Family
members draw together about that time of the day. Long episodes of crying happen
more commonly in females.14 Lacrimation’s bonding effort is also suggested by the
observation of post partum-like depression in adoptive parents. 34

The female's husband-bonding and baby-bonding behaviors have been

described with respect to lacrimation. Perhaps the wife and mother keeps her nose in
the wind, so to speak. Is she the family member most sensitive to change? Perhaps
the mother's being the bulwark of the home involves specialized semiochemical
duties for which she is uniquely equipped?

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MOURNING

Every human knows that emotional tears appear at funerals. A perceived

probability of the necessity of a bond break (such as having word of the grave illness
or distress of a loved one) evokes lacrimation. As a practical matter, the breaking of
obsolete love-bonds and new biological bonding should both be undertaken during
mourning. These functions are proposed for the emotional crying induced by such
social situations.

Pheromone receptivity in mourning might adjust to compensate grief with

new and renewed love. Crying would flush away a bond no longer useful. No
economic logic justifies loving the inanimate or even for going to their funerals, for
that matter. The dead no longer need our love, the living do. So in saying goodbye
with tears, perhaps the chemistry of forgetting engages? We attend funerals for the
living, and it is why families cling together at such times.

Reproductive fitness (survival of our genes in our offspring, or our relative's

offspring) advances none at all by our loving any but the living. Replacing a useless
bond with renewed closeness to those left alive makes sense. Tears, then, would be
real and practical medicine for emotional hurts.

Suppose crying removes pheromone addiction and enhances receptivity to

new pheromones in human beings. We would then mourn the loss of a loved one
because of a biological economic reality. It is a practical matter. A malleability of
affection at times of grief would be biologically expedient. It would also be
economical.

If human emotional tears help insure pheromone addiction, then a biological

reason explains why human beings are brought closer when they share a common
grief. A crying person would seek out another individual with whom a bond should
be established or strengthened.

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 After loyalties are established, casualties of war engender little sympathy from
fellow and opposing soldiers. Light or early combat losses, however, may establish
unusually close comradeship.

FAREWELLS, AND WELCOMES

Human tears can accompany welcomes and goodbyes. While animals, such as
songbirds35 may anxiously welcome their fellows after an absence, only people say
goodbye with foreknowledge, so only people part emotionally. Wars see much of this
behavior, as well. As the troopship steams away into danger, wives and girlfriends
shed (and absorb) tears. Does this chemoreception ripen criers for new love,
domestic and/or romantic? Flushing out the old would open receptivity for the new
semiochemical signal. Is biology so pragmatic as to start the flushing even before
the boat pulls away from the dock? Sadly for soldiers, it would seem so. Don’t cry
for me, Argentina!

Tears of welcome for our returning fighting men would function to open a
place in our circle for our heroes. Recall the tears of parting, which are posited to
work to assure that unmarried girls on shore need not wait? All shed more tears on
the boat's return.

Tears precede and accompany a kissing frenzy at the reunion of loved-ones.34

Tearful kissing frequency/duration may be proportional to length of absence and the
strength of the previous bond. If erbkoordinated lacrimation aids pheromone
reception, its excretion during such emotional behavioral situations is logical.

TEARS AND THE HUMAN HIERARCHY

Tears and pheromone recognition may play some role in adjustments of our
social hierarchy set. When one's position shifts, such as on winning a beauty pageant,
or with election to high office, episodes of lacrimation often come with the news.

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(The author anticipates the opportunity to self-observe upon news that he has won
Nobel prizes for Peace, Medicine, Chemistry, and Economics.) The greater the
increase (or decrease) in status, the greater the predicted lacrimal response to
accommodate one to the change. Do you recall a young team captain's tears after
winning the impossible football triumph? Try remembering a national beauty contest
without the winner’s tears. Lacrimation and hierarchical change go hand in hand.
The higher the assent and the lower the descent, i.e. the bigger the shift, the greater
should be the lacrimation.

But, you may say, "I saw that proud moment, and I cried a little, too."
Shifting of others in a hierarchy also requires a bit of our own lacrimation in
observation. The "beautiful wedding" that brought tears to everyone's eyes is an
excellent example. Welcome to your new hierarchical status, newly married couple!

Lacrimation-inducing entertainments, such as sad movies and plays, would

employ our innate hierarchy adjustment device. Suspending disbelief may engage
this instinct. Television and moving picture industries are new to human evolution.
These stimuli would stimulate unnecessary semiochemical receptivity within the
present paradigm. So audiences should become more jaded with experience.

Modern males, ever the opportunists, might exploit such situations by

exposing females to axillary scents during such entertainments. Anecdotes exist of
unwarranted improvement of mood in unfamiliar females following such exposures.
A controlled study of such effects and those upon population semiochemistry might
be in order.

Crying presents both visual and aural signals which instinctively provoke
sympathy.1 Indeed, perhaps these signals stimulate reciprocal receptivity for
chemosignals in all of us?

Crying can help people adjust to new political realities, too. Who of us alive
at the time did not weep on hearing of a young president's death? (Aside from the
umbrella-man killer of JFK, George H.W. Bush, of course.) 36 Human beings may
have done most of their social evolving in small groups.37 In small groups,
submission to leadership would involve physical contact and personal demonstrations
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of fealty. Although the new leadership in a country may not be able to meet
everybody, the populace may prepare to accept them semiochemically.

French people crying as Nazi columns roll through Paris July, 1940.

Joyous celebrations of victory may be accompanied by tears. In such a case

the entire population may need to adjust to its new supremacy just as in a small band
of hunter-gatherers. Likewise a popular defeat might require similar adjustment.

Disgrace, right or wrong, may bring on lacrimation. Tears in disgrace reflect

one's diminished hierarchical status. Such pheromonal receptivity before angry
authority may be hazardous to one’s health by virtue of one’s exposure to aggression
pheromone, a logical autoimmunity poison. Alternatively tears might flush out
acceptance of the disgracers and ready the disgraced for another hierarchy down the
road of life.

Pain of injury or disease may stimulate soothing tears in adults. During

human evolution, injury may have once foretold death or permanently lowered status
within the group. However, natural opiates in tears18 could have anesthetic qualities
as well.

Psychological depression can have onset at a change or perceived change of

the victim's hierarchical status. Life events such as the loss of a limb or the loss of a
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loved one typify onset conditions in many cases of depression. An increase in the
number and duration of lacrimal episodes accompany depression.14 This would
indicate a super-receptivity for human pheromone. Depressed people more often
become addicted to nicotine and smokers more often become depressed.38 Some
beneficial effects of family therapy can be seen in depressed patients. Perhaps these
all share unassuaged appetites for human pheromones? Semiochemical medical
treatment of receptives with donated paternal facial skin surface pheromones under
conditions of pheromone asepsis should be investigated to remedy depression. A
standard dose of 150 mg of adult male facial skin surface lipid taken by mouth would
be a good starting point.

In addition, as heterosexual men attest, a female partner can exhibit an

unbridled joy upon exposure to male semen. It appears that semen may have
antidepressant pheromonal properties from hormones transmitted in ejaculate. 39,40
Seminal pheromones and pheromone binding proteins as well as pubic tuft and penile
skin surface lipids so anecdotally adept at inducing sexual desire might also improve
mood. Of course, these are tiny transmissions likely to escape scientific attention into
the foreseeable future. Hormonal injections to establish post-coital serum levels
compared against these findings might be instructive, however unless some
synergism of the full complement exists, serum levels of testosterone alone do not
seem to improve mood while levels of dehydroepiandrosterone--a sebaceous skin
surface emission stimulant--do.41

Another time for crying comes when change appears likely. Periods of family
stress increase lacrimal episodes. More frequent lacrimation would enhance the
sensitivity of chemoanalyses to keep us ready for when the change finally did come.

Crying alone and "finding a shoulder to cry on" may find new meaning within
the pheromone reception hypothesis of psychogenic lacrimation. Crying alone may
not improve family cohesiveness, and, depending upon the pheromone ensemble of
the crier, may even trigger pathology. "Finding a shoulder to cry on" might be taken
to mean "finding an armpit to sniff while I lacrimate." Men would do well to
"comfort" their families at such times by allowing lacrimation on the shoulder (near
the armpit). Reducing stress might also influence results.
169
 We should observe little crying in only children of stable households. On the
other hand, we should also see frequent tears in closely spaced children living in
unstable families.

EMOTIONAL LACRIMATION OF INFANTS AND CHILDREN

Crying is innate, although "infants do not commonly weep until they have
attained the age of from two to three or four months".27 The reason for emotional
tears in infants and children is unknown.

Crying signals the mother;42 however, tears are not necessary for that purpose
because neonates have no tears.27 Economically, if tears were superfluous in
childhood they would have sunk under the pressure of natural selection.

If emotional lacrimation enhances semiochemical reception then such

reception must be very important in infancy and childhood. Small children weep
frequently; typically seeking their primary caretaker for close contact and kissing.
Here are semiochemical analysis opportunities on a more or less regular basis.

What could be the purpose of such continuing semiochemical analyses?

Semiochemical communication has been speculated to have a role in psychosexual
development.43 Physical separation from parents during critical periods has an affect
upon the development of delinquent behavior in males. 44 Physical separation is ipso
facto semiochemical deprivation. Perhaps delinquency is pheromone deprivation?
Testing of adult male facial sebum to treat juvenile delinquency has been quite
successful in open trials. Modern pheromone deprivation may result from parental
hygiene practices. After all, parents did not evolve with RightGuard, hot showers,
and feminine hygiene protection! Similarly, criminal behavior is associated with
ozone concentration. Ozone irritates mucosal pheromone-receptive surfaces.

Sparing the rod's stimulation to lacrimation in the parent's presence may

indeed spoil the child. How appropriate for the love-bond between parent and child

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EXOCRINOLOGY
to be strengthened when the parent discovers misbehavior and applies negative
conditioning therapy sufficient only to stimulate lacrimation.

OTHER EXPLANATIONS

FOR HUMAN TEARS

There are alternative hypotheses about why we cry. One may be among the
oldest hypotheses in medicine. Do we weep to remove unknown toxins or "ill
humors" as an excretory function?4 Frey reluctantly reached this tentative conclusion
by process of elimination. There are proteins with no known function in tears.16
Another45 (Montagu, A., 1959), suggested some sort of mucous soothing function for
lacrimation. Montagu wrote that because crying involves inhaling and exhaling a lot
of air, tears must replace lost moisture. If tears are there to moisturize the lungs of
crying people, then a few questions arise. Why have lungs that desiccate? According
to Frey,4 these membranes are not so delicate as to need tears to protect them. Why
not just breath less emphatically in lacrimation? Or, if crying was just to signal grief,
why have one signal for all humanity? Shouldn't different cultures grieve differently?
Frey4 discounts Montagu's hypothesis. He notes that not all weeping involves
increases in respiration.

Speculating psychological writers insist human beings cry to "let it out," (e.g.
Lipe46). It being some emotion-phlogiston perhaps? No tangible evidence supports
their hypothesis. There are no poisons in human tears and no waste products.4
Human beings do not lacrimate to express themselves. Human lacrimation does not
relieve tension psychologically, but we usually feel better after doing it.

How does human lacrimation soothe? Lacrimal glands are the only place
outside the CNS and adrenal medulla where the natural opiate, leucine-enkephalin,
resides.4 When we cry, we also dose ourselves with that endorphin. Note the
precision with which this device engages. The more pain, the more crying, the more
a soothing balm is laid on. And absurd atheists ask why heaven gives tears to
crippled children!
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 Tears are hard-wired to the pheromone recognition hardware of the brain.
Human emotional tears are induced by activation of the medial prefrontal cortex. 47
The medial prefrontal cortex is a projection area of the pheromone sensing accessory
olfactory bulb in the cat. 48 Humans have no accessory olfactory bulb, per se. People
have fields of pheromone-sensing microvillar brush border cells lining the entire
upper respiratory system as all physicians learn in first year histology. However, the
human prefrontal cortex (which does many things) is among the brain structures with
dissimilarities that differentiate heterosexual men and homosexual women from
homosexual men and heterosexual women.49 Right next door, the anterior part of the
inferior lateral prefrontal cortex is activated on PET scans after stimulation with
androstadienone, an airborne human pheromone. 50

ANIMAL BEHAVIOR

Are tears for pheromone recognition in all bonding vertebrates? Humans walk
upright. We alone shed tears onto the face at pheromone reception appropriate times.4
This fact would be important if tears were purely visual signals. Why aren't tears
purple or green? They would be better visual signals if they were not so small and
transparent.

Because most species have nasolacrimal ductwork from eye to nasal passage,
lacrimal pheromone reception may not be externally obvious. Most land vertebrates
walk on all fours and other two-legged beasts have beaks. If animals utilize lacrimal
chemosensory reception for bonding it might be expected episodically like ours.
Unfortunately direct measurements of simultaneous pheromone reception and internal
lacrimal secretion in any species are lacking.

However, ethological observations support this hypothesis of lacrimal

involvement in pheromone recognition. In geese Konrad Lorenz 51 observed
physiological changes around the eyes after behavioral experience akin to human
bereavement in pair-bonding avians. In some species of sea birds, inconsistently
observed portions of the courtship display utilize behavior seen during excretory

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lacrimation of sea salts.52 Clearly this and other courtship displays and courtship
dances of birds forming pair bonds, are mechanically distributing pheromone
reception fluids (tears) to chromatographic pheromone reception surfaces.
Construction of lucite models of avian nasal passages, including nasolacrimal ducts
with tear origin at lacrimal glands will demonstrate the necessity for the gyrations of
courtship in avian bonding.

Tear-secretion behaviors can appear at pheromone-reception-appropriate

times. Many avians "bill shake" and "dance" when they fall in love. Perhaps their
bills are flung from side to side to bring down lacrimal pheromone-reception fluids.
Bill shaking looks like behavior observed as concentrated brine is excreted from the
lacrimal glands through the nasolacrimal ducts and out through the nostrils in the
beaks of oceangoing birds deprived of fresh water. Indeed, you can inject salt water
in some species and see the same type of head shaking behavior as a salt elimination
device.53 If glands concentrate ions for salt elimination in sea birds, might the same
glands also concentrate ions for pheromone recognition? Since the behavior appears
in the "courtship dance," the secretion may be there as well.46

Why should birds gyrate so to fall in love? Birds have beaks. Hard beaks can
not utilize peristalsis or mucosal cilia to transport tears internally. Those mechanisms
are available to non-beak mammalian species. The funny movements of birds get
tears where they need to go inside the beak for pheromonal bonding. Indeed,
economically, every dip and twist of the head should be accountable for some internal
avian nasolacrimal obstacle.

Ornithologists have termed what they consider functionless behaviors,

"displacement activity."54 This unfortunate appellation has been applied to a number
of avian behaviors which appear pheromone-receptive. Among them are territory
marking behavior of avians (utilizing the "preen" gland), and pheromone exchange
behavior.

Pheromone exchange behavior would be mostly the male's depositing of the

preen gland lipid onto food or nest and signaling its location to the prospective mate
with nesting or courtship displays. [Do hen pupils dilate seeing a tom turkey spread

173
his tail feathers? No, the avian eye is a special case.] Pheromone exchange behavior
would also include marking a "nuptial gift" with pheromone for the prospective mate
to swallow or sniff, and also beak rubbing. Beak rubbing is seen in more social birds.
33 The sebaceous glands of the rictuses 55 come in contact during the behavior.

Perhaps it is for bonding pheromone exchange?

Jouventin's46 report typifies some ornithological thinking. He has done a

particularly good job of observation, however.

Sea birds have a supraorbital gland which concentrates excess sodium chloride, as
shown by McFarland (1959) in Aptenodytes forsteri, A. patagonicus and other
species. They regularly and vigorously shake their heads from side to side to get rid
of the concentrated sodium chloride solution, sometimes visible hanging in droplets
on the edge of the bill. Billshaking can be induced experimentally by injecting NaCl
(SchmidtNielsen and Sladen, 1958). Billshaking can often be observed, repeated
several times without apparent need, in conflict situations, as a typical displacement
activity. One step further, this movement would even have become part of the
courtship display of the King penguin, according to Stonehouse (1960, p. 27), who
considers it similar to the "headflagging" described in black headed gulls (Tinbergen
and Moynihon, 1952, p. 2122). However, when the head is lowered, e.g. while
singing, excess liquid probably flows to the bill and is expelled by headshaking. Yet
many King penguins were not observed to shake their heads while singing [Perhaps
because the fluid is used internally?BN]. Moreover, the encounter with a future
partner is fraught with such emotion that displacement activities frequently
accompany it. In the Emperor penguin, which lowers its head to sing, headshaking
was recorded in 21% of the cases (n=108) just after singing, while van Zinderen
Bakker Jr. (1971, p 256) observed it in the Gentoo penguin in 95% of observations
just after chicks were fed, which also involves lowering the head. [Just in time for an
addictive pheromone from the chick as reward for bringing foods.BN]
In 86% of Emperor observations (39 out of 45), billshaking was followed by a
swallowing movement; according to Isenmann (1971) this restores the inner ear
pressure, but we interpret it (1971) as elimination of the liquid left after headshaking.
In any case, bill shaking and swallowing form a miniature stereotyped sequence
which often appears during courtship display: then, about 18% of billshaking was
followed by swallowing in the Emperor penguin according to our results (n=50).
[Note frequent swallowing is seen in humans kissing to form a long lasting bond.BN]

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Even though the sequence cannot be considered an element of courtship display, as it
is absent four times out of five, and as long-lasting couples can do without it, it is not
only a basic movement but a displacement activity [...] (Jouventin, P., 1982).46

This is similar to human experience where heavy shared lacrimation may be a

rare occurrence. Long married couples can comfortably do without much of youth's
passion. The same reduced passions appear in long-matched songbirds.33 The
expectation of lacrimation with formation of long-lasting relationships in animals
may be met with further study using current techniques. In the few cases where tears
or tearing behavior can be seen, bonding and tears go together. Other anecdotal
accounts exist.56

Many animal tears carry pheromones. Associating a pheromone reception

fluid with pheromone would both prime and release simultaneously.

Pheromonal tears exit the glands around the eye in marsupials, insectivores,
armadillos, rabbits, rodents, dolphins, walruses, seals, pigs, and deer. 57 Instead of
smearing tears around on their faces like we do, animals may smear the tears all over
their bodies, along with saliva. These sebaceous chemicals in gerbil Harderian gland
secretion have yet to be analyzed.51 In contrast the numerous sebaceous glands
around the human eyes are mostly tiny, but some are big enough to be seen. They
may function in maintaining the tear film;9 however, some role in the semiochemical
commerce can not be ruled out.

DOGS

Working with canine tears, Barrera R., et al.58 found no differences in protein
concentrations between sexes. In dogs pheromone reception probably cycles with
estrous and the Barrera group may not have tested bitches in heat. Perhaps
dimorphisms exist elsewhere to accomplish canine sexual orientation; however, the
complex protein composition of dog tears52 may simply reflect a repertoire of binding
proteins useful for tracking semiochemicals of other species. Dogs have excellent
noses.59
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 To explain their devotion to humankind, a similarity between, or even a
duplication of, some human specific tear protein should be expected in canine
lacrimal or other pheromone receptor secretion. Pheromone recognition sharing may
be seen in other parasite-host pairings 60 and may follow from shared receptor
proteins.

NASOLACRIMAL VOMERONASAL APPARATUS

In humans, behind and above each nostril, three nasal passages, or meatuses,
carry air from the nose. From these meatuses blind sinuses extend. The nasolacrimal
duct channels tear fluid through the nasolacrimal bone from the inner corner of one
eye to the bottom nasal passage on the same side. The bottom nasal passage is called
the inferior meatus ("lower passage" in Latin).

A pair of vomeronasal, or Jacobsen's, organs detect low volatility pheromones

in the naso-pharygial area of diverse species (Beauchamp, G.K., et al., 1983; Halpern,
M. and J.L. Kubie, 1983; Halpern, M., 1987). Human beings might have functioning
vomeronasal organs located above and forward of the inferior meatus (Moran, D.T. et
al., 1991; GarciaVelasco, J. and M. Mondragon, 1991), in which chemoreception has
been detected in response to putative human pheromones (MontiBloch, L. and B.I.
Grosser, 1991). The receptor cells of vomeronasal organs are sensory microvillar
cells, the same cells that line the entire upper-respiratory system in human beings.
Nasolacrimal ducts open variably in different people. Like the nasal passages and
sinuses, only rough bilateral symmetry prevails from one side to the other as well.
Generally the duct from the eye opens into one end of a vomeronasal cleft, with the
vomeronasal organ of Jacobsen at the other end (Schaeffer, J.P., 1912; 1916; 1920).
A sexual dimorphism in vomeronasal organ pheromone reception has been recorded
(MontiBloch, L. and B.I. Grosser, 1991) supporting sex-defined functions discussed
earlier.

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EXOCRINOLOGY

MICROVILLAR CELLS IN PHEROMONE RECEPTION

It was once thought that the machinery for human pheromone reception did
not exist or, where it could be found, it was merely a vestige (Comfort, A., 1974). A
functionless, evolved vestige would be an economic impossibility, a contradiction in
terms. Ignorance of function was really the preferred explanation. Happily,
microvillar cells of the type that senses pheromones in all animals examined were
recently consistently detected in olfactory and nasal mucosa. One of the places where
these microvillar cells were found was at the opening of the nasolacrimal duct to the
inferior meatus. These pheromone receptor tissues are in the right place to be bathed
in receptor proteins and the high ionic concentration necessary to that reception.
Olfactory pheromones as well as nonvolatiles hydrophilics such as sebum must reach
these tissues readily.

Clumps of pheromone sensing microvillar cells lie at the terminus of the

nasolacrimal duct. Down the same duct flow out over microvillar cells the
manganese ions and receptor proteins binding to lipid and other pheromones in the
lacrimal fluid.

A drawing depicting microvillar cells from the vomeronasal organ of

elephants (Rasmussen, L.E.L. and B. Hultgren, 1990) are seen below.

177
Fig. 4, page 155 Chemical Signals in Vertebrates 5, D.W. MacDonald, D. MllerSchwarze, and S.E.
Natynczuk, 1990. Oxford Science Publications London.

The human vomeronasal organ's microvillar cells differ only slightly.

Microvillar cells resemble olfactory cells but specialize for pheromone reception with
shorter receptor cilia.

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Microvillar cells belong to a class of chemoreceptor cells which normally
inhabit a discreet organ in most other animal species. The organ, Jacobsen's organ or
the vomeronasal organ, specializes in recognizing pheromones. This knowledge was
acquired only recently. Indeed, until about 1970 or so, the mammalian vomeronasal
organ was a structure in search of a function.61 In human beings, the microvillar cells
are not so concentrated, and were thought until lately 62 to clump into a recognizable
organ only in about 15% of humans.63 Of course, as every medical student learns,
sensory non-motile microvillar ‘brush border’ cells line the upper half of the human
respiratory system, a phenomenon which is unique to the human species. Eureka,
these broad swathes of pheromone sensing microvillar cells must be those that
recognize human pheromones. It is altogether right that we have the largest area
devoted to pheromone reception, since humans have the largest scent glands and most
active skin surface lipid glands by far.

NASAL PASSAGES

The nasal passages run from the exterior vestibule of the nose into three
chambers running one above the other and thence into one again at the choana to the
pharynx. The function of the six nasal passages and their attendant sinuses passages
remains a mystery. However a function in pheromone recognition may be
hypothesized.

A few clear lucite models of the nasal passages taken from cadaver
impressions were provided to the author by previous researchers.64 The Hornung
group followed radioactive airstreams to detect spatial consistencies in them.
However, by passing various fluids and smoke through these clear models, it was
transparent that parallel lines were inaccurate.

Smoke sniffed into the models displayed a consistent roiling in agreement

with the Hornung depiction. However, erectile tissues pervade the nasal passages,
opening and closing regularly and in response to emotion and sexual releases.65
These erections direct or divert incoming and outgoing air. A dynamic nuclear

179
magnetic resonance imaging (dMRI) of these structures during emotional situation
changes should prove interesting. Such motion pictures might improve our
understanding of the physiology involved and allow better modeling for more precise
laboratory experimentation.

Surprisingly, passing smoke through these models established that airflow

taken into the nose is treated much differently than exhaled air. Nasal passages (at
least those made of lucite) route the incoming airflow through the upper meati in a
consistent turbulence. This induced turbulence may ensure more complete
chemoreception. 66 However, because air borne odor plumes are discontinuous,67
turbulence may also randomize samples. Obtaining an adequately randomized
sample is the first essential step in analytical chemical analysis, 68 accordingly
biological chemo-analyses may proceed similarly.

Randomized incoming airflow reaches the olfactory mucosa of the superior

meatus for olfactory perception. Odorants concentrate by dissolving into the
Bowman's secretion69 where, in all species, specialized Odorant Binding Proteins
(OBPs) in the class of lipid binding proteins are also dissolved.70 Much less volatile
sebaceous lipids reach this area through mucosal surface diffusion.

The extreme "spreadability" of sebum has been utilized for precise

measurements of sebaceous secretion. 71 The precision of the technique is
demonstrated by one of their figures. In it the data show menstrual variations in a
female subject. Identical data on menstrual variability of sebaceous secretion
appeared many years later.72

In the smoke observations of the clear lucite nasal passage model, outgoing
airflow behaved unexpectedly, too. Outgoing, lung-cleansed air73 converged upon the
olfactory mucosa and the semilunar hiatus from both directions at once. Perhaps this
distinction allows discrimination of interior odors, which make up most of our
perception of food, from exterior odors. Since exhaled air is so clean, the inward
flow of exhaled air back through the upper two meati may reset olfactory reception.

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EXOCRINOLOGY
The sensory stretch receptors of the maxillary sinuses probably inform the direction
of air in inferior meatus, allowing such a reset from local sensation.

However crude, Lucite models do allow us to hypothesize. Perhaps the three

nasal passages work together to form an ingenious passive valve for liquids as well?
For fluids arising from the rear as from the stomach, the valve diverts all liquids into
the inferior meatus or "low passage". Valving refluxing gastric juices away from
sensitive olfactory tissues seems a logical function for this maze of "functionless"
structures near the choana. From the models, the best effect seems to come when the
head is bent over about fifteen degrees from vertical. Interestingly, this leaning
forward position appears to be taken instinctively by humans about to throw-up.
Maybe that stance keeps the vomitus off of one's tunic, too?

The mechanics of lacrimation include some gross behavioral characteristics

which any casual observer can identify. With the head bent down, criers maintain a
forward posture in stance or sitting. Again from observations of liquid passing
through transparent Lucite model of the nasal passages, this posture appears to keep
that lacrimal fluid collecting in the inferior meatus. Perhaps this posture protects the
olfactory mucosa from wetting by tears, but more likely it keeps the reservoir at the
base of the hiatus semilunaris full of lacrimal fluid for chromatographic solvent.

Tears run onto face from the eyes after filling the reservoirs in the
nasolacrimal duct. The tears wet the face, and some roll down the cheeks. A few
enter the mouth at the corners. (Is this compensation for our lack of a nasopalatine
duct between mouth and inferior meatus? Only about 10% of the population retains a
hole between palate and nasal passage.) No, it probably is not, but speculating in a
book like this is harmless enough if you also halt the progression of a few incurable
diseases (Alzheimer’s) and cure sociopathies (crime, perversion, drug-addiction), eh?

SOBS

Ever notice the breath effects of sobbing and the holding of the hands over the
face in severe lacrimal episodes? Sobs appear to vary somewhat like sniffs do. Sobs
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may function analogously to sniffs, but for pheromone reception in humans. Sobs
may impart the chromatographic effect of sending many solvent fronts of tears over
the pheromone sample being analyzed.

In regular olfaction chromatographic resolution may be enhanced by a

"sniff". 74Any cooling and warming of a chromatographic substrate improves
resolution. This seems to be what happens to the olfactory mucosa by the sudden
evaporative inhalation characteristic of sniffs. Animals, with more sensitive olfactory
apparatuses, regularly vary sniffs accelerating to a climax.75 These may represent a
whole series of temperature programs, familiar to chromatographers,76 lasting but a
very short time.

Who has failed to note the trembling hands held tightly over the face of a
person engaged intensely in lacrimal pheromone-receptivity activity? Why do we
instinctively cup our hands to our face in intense psychogenic lacrimation? Perhaps
the association of reception enhancing tears and a hypothesized addictive facial
pheromone prime and release bonding for anyone kissing those tears away?
Alternatively, we may be forming a developing chamber similar in function to those
of thin layer chromatography.

Thin layer chromatography resembles the paper chromatography most of us

did in elementary school. Put a dot of a chemical mixture near the bottom of an
absorptive plate. Put the plate into a covered pot with some liquid solvent at the
bottom. A mysterious "solvent front" climbs onto the plate and past the dot of
mixture. When it passes, different components of the mixture go with it and then
drop off one at a time as the front continues up the plate. You may have to "develop"
the plate (kind of like film) in order to see that a number of faded dots mark where
parts of the mixture dropped off. The distance from the dot of mixture down at the
bottom to the spot where the chemical stopped climbing with the solvent front and
dropped off usually differs for different chemicals. You can even scrape the plate
always at the same distance and get a pure sample.

Thin layer chomatographers content themselves with hanging around until a

single front physically shifts one chemical away from another. Their eyes and rulers

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EXOCRINOLOGY
take the measurements. In contrast gas chromatographers use a detector, about the
size of a fist, to measure the time course over a constant distance instead of different
distances in a common time. The detector burns or zaps the chemical passing by in a
gas stream and marks a computer screen with a bump when one does. Time from the
start to detection usually differs characteristically from chemical to chemical.

The one big detector at the end of the column in gas chromatography is
replaced by many tiny microvillar and/or olfactory nerve cells. These cells may
perform the same job in Jacobsen's organ and olfactory tissues. Instead of a single
big detector, an array of chemosensory cells do the detecting. Remember how
components stopped migrating up the place as a characteristic of the chemical?

Now, remember from Chapter 3 that humans may have many hundreds,
possibly thousands, of different pheromones to be detected? Some chromatographic
separations would be a logical device to have behind our noses to aid human chemo-
analyses.

Why use an array of detectors? After all, one detector is enough for
sophisticated chemical analysis.70 The answer is speed. Instead of a set starting point
and time, and then a series of detections across a single detector, chemosensory cells
work in parallel. Starting point and time are sensed in the surface lymph by the
dissolved pheromone receptor protein. Follow-on times from differing pheromone
receptor proteins, either dissolved in the lymph or on the chemosensory cell surface,
are compared in accessory olfactory bulbs and differences plotted to the brain into a
chaotic pattern (reception points as the new origin). It is the reproducible chaotic
pattern which the brain recognizes as a scent.

Olfactory sensations are turned into information at the glomeruli of the

olfactory bulb, where the timing of the first, extracellular Bowman’s secretion soluble
protein conformational charge release on odorant contact, and subsequent dendrite
surface sensations are sorted out. These differences are all projected in parallel
simultaneously to the brain. Unknown chromatographic forces impart identifying
delays for chemicals moving through the Bowman's secretion and these are detected
by simple comparison in the bulb. Intensity of the signal, imparted by the odorant's

183
affinity to the OBP, is a less identifiable portion. These signals map into a chaotic
pattern recognizable to the brain as a fragrance.

If pheromone reception during lacrimation maintains a chromatographic

component, as seems indicated, then perhaps the peculiarities of the sinuses serve as
well. Sinuses have no known function and no reasonable explanation for them has
ever been found.11 The sinuses form a column of retorts opening off of the canalis
semilunaris or semilunar hiatus. Ostia (or openings) of almost all of the sinuses
connect with the semilunar hiatus. Recall, the lack of sinuses might well be
responsible for the babyish features, noted by Lorenz45 and others,77 of enlarged
forehead, small face, and chubby cheeks. The gradual development of more and
more sinuses during childhood may be correlated to sensing one's relationship and
status within a community.

OTHER HUMAN PHEROMONE RECOGNITION SYSTEMS?

This chapter has introduced one model of pheromone reception. Mattes 78

contends there is increasing evidence supporting an oral chemosensory detection
system for free fatty acids with multiple transduction mechanisms.

Other pheromone reception mechanisms should be expected, as backups or in

parallel. For instance, some research suggests that the long-chain triglycerides, a
major component of human sebum capable carrying information, are not digested but
hydrolysed taken whole into the lymph. Micelles transport hydrolized triglycerides
from gut to lymph to ovary and beyond while shorter chain cousins are relegated to
digestion in the liver.79 Thus an entirely different system exists by which probable
human lipid pheromones may have direct, unmodulated access to the reproductive
system and beyond.

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EXOCRINOLOGY

1Eibl-Eibesfeldt, Irenäus (1970a). Ethology the Biology of Behavior, translated by Erich

KlinghammeR New York: Holt, Rinehart and Winston 530 p.
2 Nicholson, B. 1983; A semiochemical addiction model for human bonding. Paper presented to the

Animal Behavior Society and the International Society for Human Ethology, Lewisburg, PA.
3 Nicholson B., Pheromones cause disease: pheromone/odourant transduction. Med Hypotheses. 2001

Sep;57(3):361-377.
4Frey WH. the II. Crying the mystery of tears. Minneapolis, Minnesota: Winston Press, Inc.
1985;174.
5Feksi A, et al. 'Maternity Blues' and hormone levels in saliva. J Affective Disord. 1984;6(3-4):
351-355.
6 Fullard RJ, Tucker DL. Changes in human tear protein levels with progressively increasing

stimulus. Investigative Ophthalmology & Visual Science. 1991;32(8):2290-301.

7 Morris, Desmond 1972; Intimate Behavior New York: Random House.
8Wyart C, Webster WW, Chen JH, Wilson SR, McClary A, Khan RM, Sobel N. Smelling a single
component of male sweat alters levels of cortisol in women. J Neurosci. 2007 Feb 7;27(6):1261-1265.
9 Sack, RA, K.O. Tan and A. Tan 1992; Diurnal tear cycle: evidence for a nocturnal inflammatory

constitutive tear fluid. Investigative Ophthalmology & Visual Science 33(3):626-640.

10 Montagna, William; Parakkal, Paul F. The structure and function of skin 3rd edition. New York:

Academic Press 1974.

11
Hafez, E.S.E. 1976; Parameters of sexual maturity in man. pp. 105-122 In: Volume 3 Sexual
Maturity: Physiological and clinical Parameters E.S.E. Hafez and JJ Peluso editors. Ann Arbor,
Michigan: Ann Arbor Science Publishers Inc. 283p.
12Drettner B. The paranasal sinuses. In: The nose: upper airway physiology and the atmospheric
environment. Proctor A.editor. Amsterdam: Elsevier Biomedical Press. 1982;145-62.
13Monti-Bloch, L., and B.I. Grosser 1991; Effect of putative pheromones on the electrical
activity of the human vomeronasal organ and olfactory epithelium. The Journal of Steroid
Biochemistry and Molecular Biology. (Proceedings of the International Symposium on Recent
Advances in Mammalian Pheromone Research.) 39(4B):573-582.
14Finck HT. Romantic Love and Personal Beauty; Their Development, Causal Relations, Historic
and Natural Peculiarities. London: MacMillan. (1891).
15 Frey WH the II, Hoffman-Ahern C, Jason RA, Lykken DT, Tuason VB. 1983; Crying Behavior in
the Human Adult. Integrative Psychiatry September-October:94-98.
16Frey WH. the II, Desota-Johnson D, Hoffman C, McCall JT. Effect of stimulus on the chemical
composition of human tears. American Journal of Opthalmology 1981;92:559-567.
17Mii, S., K. Nakamura, K. Takeo and S. Kurimoto 1992; Analysis of human tear proteins by two-
dimensional electrophoresis. Electrophoresis 13(6):379-382.
185
18 Fullard RJ, Tucker DL. Changes in human tear protein levels with progressively increasing
stimulus. Investigative Ophthalmology & Visual Science. 1991;32(8):2290-301.
19Bjerrum K, Halken P, Prause JU. The normal human tear glycoprotein profile detected with lectin
probes. Experimental Eye Research 1991;53(4):431-5.
20Pitt, B. 1978; Introduction. In Mental Illness in Pregnancy and the Puerperium. Sandler, M. editor.
Oxford: Oxford University Press.
21 Yalom ID, Lunde DT, Moos RH, Hamburg DA. “Postpartum blues” syndrome. A description and
related variables. Arch Gen Psychiatry. 1968 Jan;18(1):16-27.
22Coppen A, Stein G, Wood K. Postnatal depression and tryptophan metabolism. In: Sandler, M.
editor. Mental illness in pregnancy and the puerperium. Oxford: Oxford University Press, 1978.
23 Agache, P., D. Blanc, C. Barrand, and R Laurent R 1980; Sebum levels during the first year of
life. British Journal of Dermatology. 103:643-649.
24 Klaus, M.H., and JH. Kennell 1982; Parent-Infant Bonding. St. Louis: The C.V. Mosby Company.
25 Benfield, D. Gary, Susan A. Leib, and Jeanette Reuter 1976; Grief response of parents after referral
of the critically ill newborn to a regional centeR New England Journal of Medicine, 294(18):975.
26Lewis E, Page A. Failure to mourn at stillbirth: an overlooked catastrophe. Br J Med Psychol.
1978 Sep;51(3):237-241.
27 Brazelton TB, Tronick E, Adamson L, Als H, Wise S. Early mother-infant reciprocity. Ciba Found

Symp. 1975;(33):137-154.
28 Darwin Charles The Expression of the Emotions in Man and Animals. London: Murray. 1872;162
29Seeley, T., T. Talbot, P.R Abramson, L.B. Perry, A.B. Rothblatt, and D.M. Seeley 1980;
Thermographic measurement of sexual arousal: a methodological note. Archives of Sexual Behavior
9(2):77-86.
30Cunliffe WJ, Burton JL, Shuster S. The effect of local temperature variations on the sebum
excretion rate. British Journal of Dermatology 1970;83:650-4.
31Lorenz, T.H., D.T. Graham, and S. Wolf (1953). The relation of life stress and emotions to human
sebum secretion and to the mechanism of acne vulgaris. Journal of Laboratory and Clinical
Medicine 41:11.
32 Terkel J, Rosenblatt JS. Maternal behavior induced by maternal blood plasma injected into virgin
rats. J Comp Physiol Psychol. 1968 Jun;65(3):479-482.
33Mennella, Julie A, and Howard Moltz 1989; Pheromonal emission by pregnant rats
protects against infanticide by nulliparous conspecifics. Physiology and Behavior 46:591-595.
34Foli KJ. 2010; Depression in adoptive parents: a model of understanding through grounded theory.
West J Nurs Res. 2010 Apr;32(3):379-400.
35Wilson, Edward O. 1975; Sociobiology The New Synthesis. Cambridge, Mass.: Belknap
Press of Harvard University Press. 697p.

186
EXOCRINOLOGY
36 Nicholson, Ross (2008). Hillary’s Angel Tampa, FL: Nicholson Science, 2008.
37 Wilson Edward O. Biology and the social sciences. Daedalus. 1977 Fall;106(4):127-140.
38 Breslau N. Daily cigarette consumption in early adulthood: age of smoking initiation and duration
of smoking. Drug Alcohol Depend. 1993 Oct;33(3):287-291.
39 Ney PG. The intravaginal absorption of male generated hormones and their possible effect on

female behaviour. Med Hypotheses. 1986 Jun;20(2):221-231.

40 Gallup GG Jr, Burch RL, Platek SM. Does semen have antidepressant properties? Arch Sex Behav.

2002 Jun;31(3):289-93.
41
Basson R, Brotto LA, Petkau AJ, Labrie F. Role of androgens in women's sexual dysfunction.
Menopause. 2010 Sep-Oct;17(5):962-971.
42Lester, B., 1984; A biosocial model of infant crying. In: Lewis P. Lipsitt and Carolyn K. Rovee-
Collier editors. Advances in Infancy Research. Norwood, N.J: ABLEX Publishing.
43Kalogerakis, M.G. (1963). The role of olfaction in sexual development. Psychosomatic Medicine
25:420-432.
44 Clarke AM, Clarke ADB. Early Experience: Myth and Evidence. New York: Free Press, 1976.
45Montagu, Ashley (1959). Natural selection and the origin and evolution of weeping in man.
Science 130:1572-1573.f
46 Lipe, Hillary P. 1980; The function of weeping in the adult. Nursing Forum. 19(1):26-44.
47Arita H. Emotional tears are induced by activation of medial prefrontal cortex. Nippon Yakurigaku
Zasshi. 2007 Feb; 129(2):99-103.
48 Staples LG, McGregor IS, Apfelbach R, Hunt GE. Cat odor, but not trimethylthiazoline (fox odor),
activates accessory olfactory and defense-related brain regions in rats. Neuroscience. 2008 Feb 19;151
(4):937-47.
49Savic I, Lindström P. PET and MRI show differences in cerebral asymmetry and functional
connectivity between homo- and heterosexual subjects. Proc Natl Acad Sci U S A. 2008 Jul 8;105(27):
9403-9408.
50Gulyás B, Kéri S, O'Sullivan BT, Decety J, Roland PE. The putative pheromone androstadienone
activates cortical fields in the human brain related to social cognition. Neurochem Int. 2004 Jun;44(8):
595-600.
51Lorenz, Konrad (1963). On Agression. Translated by Marjorie Kerr Wilson (1966). New York:
Bantam Books Inc. 306 p.
52Jouventin, Pierr 1982; Visual and Vocal Signals in Penguins, their Evolution and Adaptive
Characteristics. West Berlin: Verlag Paul Parey.
53Sturkie, P.D. 1976; Kidneys, extrarenal salt excretion,and urine. pp. 275-279 Chapter 14 Avian
Physiology third edition P.D. Sturkie editor. New York: Springer-Verlag.

187
54Sevenster, P., (1977) Displacement activities. In: Grzimek's Encyclopedia of Ethology. (Ed. by
B. Grzimek). Van Nostrand Reinhold Company, New York.
55Lucas, A.M. 1980; Lipoid secretion of the body epidermis in avian skin. In: The Skin of
Vertebrates. Spearman RI.C. and P.A. Riley . editors. New York: Academic Press.
56Hopson, Janet L. 1979; Scent Signals, the Silent Language of Sex. New York: William Morrow
and Company, Inc.
57 Thiessen, Delbert D. 1988; Body temperature and grooming in the Mongolian gerbil. Annals of
the New York Academy of Sciences. 525:27-39.
58Barrera R, A. Jimenez, R Lopez, M.C. Mane, JF. Rodriguez and JM. Molleda Evaluation of total
protein content in tears of dogs by polyacrylamide gel disk electrophoresis. American Journal of
Veterinary Research 1992;53(4):454-456
59Moulton, David G. 1977; Minimum odorant concentrations detectable by the dog and their
implications for olfactory receptor sensitivity. pp. 455-464. In: Chemical Signals in Vertebrates
Müller-Schwarze, Dietland and Maxwell M. Mozell editors. New York: Plenum Press 610 p.
60Tumlinson, James H., W. Joe Lewis, and Louise E.M. Vet (1993). How parasitic wasps find their
hosts. Scientific American 266(3):100-106.
61Wysocki, Charles J Chuck 1989; Vomeronasal chemoreception: its role in reproductive fitness and
physiology. pp. 545-566. In: Neural Control of Reproductive Function: proceedings of the Fifth
Galveston Neuroscience Symposium held in Galveston, Texas, May 10-13, 1988. New York: Liss.
62Garcia-Velasco J, Mondragon M. The incidence of the vomeronasal organ in 1000 human subjects
and its possible clinical significance. The Journal of Steroid Biochemistry and Molecular Biology.
(Proceedings of the International Symposium on Recent Advances in Mammalian Pheromone
Research.) 1991;39(4B):561-563.
63Moran, David T., Bruce W. Jafek and J Carter Rowley III 1991; The vomeronasal (Jacobson's)
organ in man: Ultrasructure and frequency of occurrence. The Journal of Steroid Biochemistry and
Molecular Biology. (Proceedings of the International Symposium on Recent Advances in Mammalian
Pheromone Research.) 39(4B):545-552.
64 Hornung, David E., Donald A. Leopold, Steven L. Youngentob, Paul R Sheehe, George M. Gagne,
F. Deaver Thomas, and Maxwell M. Mozell 1987; Airflow patterns in a human nasal model. Archives
of Otolaryngology 113:169-172.
65 Holmes, Thomas H., et al. (1950). The Nose; an experimental study of reactions within the nose
in human subjects during varying life experiences with a foreward by Warfield T. Lonscope.
Springfield, Ill: Thomas.
66Mozell M Mozell (1977). Processing of Olfactory Stimuli at Peripheral Levels. pp 465-482. In:
Chemical Signals in Vertebrates Müller-Schwarze, Dietland and Maxwell M. Mozell editors. New
York: Plenum Press 610 p.
67Murlis, J 1986; The structure of odour plumes. Chapter 3, pp. 27-38 In: Mechanisms of Insect
Olfaction. Payne, T.L., Martin C. Birch, and C.E.J Kennedy editors. Oxford: Clarendon Press, 364 p.

188
EXOCRINOLOGY
68Kennedy, J H. 1984; Analytical Chemistry Principles. San Diego, California: Harcourt Brace
Javanovich, Publishers. p. 3. (753 pages).
69Hornung DE, Mozell MM. Factors influencing the differential sorption of odorant molecules across
the olfactory mucosa. J Gen Phsiol. 1977 Mar;69(3):343-361.
70 Pevsner, J, P.M. Hwang, P.b. Sklar, V.J Clark and Soloman H. Snyder 1988; Odorant-binding

protein and its mRNA are localized to lateral nasal gland implying a carrier function. Procedings of
the National Academy of Sciences 85:2383-2387.
71Lorenz, T.H., D.T. Graham, and S. Wolf (1953). The relation of life stress and emotions to human
sebum secretion and to the mechanism of acne vulgaris. Journal of Laboratory and Clinical Medicine
41:11.
72Burton, J.L., M. Cartilidge, and Sam Shuster (1973b). Variations in sebum excretion during the
menstrual cycle. Acta Dermato. Vener (Stockholm) 53:81.
73 Mozell Maxwell M. (1992). Personal communication.
74 Sobel N, Prabhakaran V, Desmond JE, Glover GH, Goode RL, Sullivan EV Gabrieli JD. Sniffing and

smelling: separate subsystems in the human olfactory cortex. Nature 1998 Mar 19;392(6673):282-6.

75 Youngentob SL, Mozell MM, Sheehe PR, Hornung DE. A quantitative analysis of sniffing strategies
in rats performing odour detection tasks. Physiol Behav 1987;41(1):59-69.
76McNair, Harold M. and Ernest J Bonelli (1969). Basic Gas Chromatography. Lithographed by
Consolidated Printers, Berkeley, California. Varian Instrument.
77Eibl-Eibesfeldt, Irena us 1975; Ethology: The Biology of Behavior, second edition. New York:
Holt, Rinehart and Winston.
78Mattes RD. Oral detection of short-, medium-, and long-chain free fatty acids in humans. Chem
Senses. 2009 Feb;34(2):145-50. Epub 2008 Dec 16.
79 Clément J. Digestion and absorption of dietary triglycerides. J Physiol (Paris). 1976;72(2):

137-170.

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Chapter 7: Human Pheromone Transduction

The human upper respiratory system is simply covered with pheromone
receptors. We have more pheromone receptor cells than any other species, as might
be expected from the beast that carries more pheromone-emitting glands than any
other species. The pheromone sensory microvillar cells, histologists call them brush
border cells, line most of the human upper-respiratory system. Every physician
remembers memorizing their odd appearance because that is the key to differentiating
upper from lower respiratory mucosa under the microscope.

In vertebrates generally, most such cells with short, non-motile cilia and their
secretory companions can be found in a specialized pair of vomeronasal organs
(VNO) located in the animal’s nasal passages. Sometimes the VNO is called
Jacobsen’s organ. Vomeronasal organs generally work with the many sebaceous
scent glands on an animal’s tail. Wagging or dragging tails lay down the animal’s
own scent and the VNO detects the scent laid previously to keep the animal on course
to utilize its territorial resources optimally. It is much like mowing a lawn because
you detect where you have been and stay close. All one need do is maintain a
constant concentration at the VNO.1

Of course, the microvillar cells of the VNO recognize territory edges, too,
(often scent marked with the egregiously mis-named ‘displacement activity’), and
perhaps recognize mates and potential mates. Humans have tiny VNOs if we have
them at all, since we have no tails. In humans, the microvillar cells escaped the tiny
organ and can be found ectopically all over the place in the upper respiratory system,
in Peyer’s patches in the digestive system, and elsewhere whenever chemosensory
work is needed, like the pituitary. There will be more about them later.

This chapter presents an electrical model of chemoreception, or chemosensory

transduction. (Three more models appear as sketches in the next chapter:
extracellular chemoreception and pheromone emission in some synaptic and
hormonal transmissions, myelin/neural function in propagating excitatory post-
synaptic potential differences (EPSPs), and ionic particle ATP-ase pumps being
membrane-bound proteins functioning as linear accelerators pumping charged
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particles against concentration gradients. These long proteins have the potential to
carry information or even power as plasma conduits in much the same way as metal
wires conduct electricity in 2010.)

CHEMORECEPTION AND TRANSDUCTION

The author’s electrical reception model posits a mucous-based extracellular

mechanism for most chemosensory transduction. The mechanism functions much
like a common gas chromatography detector, the flame ionization detector, with
considerable improvements in the biology to greatly diminish identification time.

Chemoreception builds upon ordinary biochemistry. Our cells distinguish

stereochemical subtleties easily, like unusual chain lengths, odds and even aliphatic
chains, unusual unsaturation positions, and functional groups. We have learned
already that these features distinguish pheromones.

For instance, consider enantiomers. The chemical representation for a pair of

enantiomers shows two non-superimposable mirror images. Think of a pair of
gloves, with a left (L) and a right hand (D for dextro-rotary). Enantiomeric gloves
exhibit identical physicochemical characteristics, so chemists have had a devil of a
time telling them apart down through the years. (Pasteur is famous for being the first
to succeed. He noticed tiny crystals had two distinct shapes, so he sat down under the
microscope and manually separated them with tweezers!) Blue algae, E. coli,
paramecia, hydra, lions, tigers and bears have no difficulty at all differentiating
enantiomers. We know insects recognize enantiomeric pheromones.2 Obviously,
living things found out billions of years ago how to recognize enantiomers. Cells
accept D-sugars while discarding L-sugars; similarly, only L-amino acids make it into
proteins.3,4,5 Where does such subtle recognition take place? It takes place within the
solution of the cytosol or protoplasm of the cell. If recognizing chemicals outside the
cell, look first in an exterior mucus for dissolved globular protein receptors. We will
see in a bit, how physiologists have been seeing just such receptors for many years,

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without understanding. Thus our suggestion how pheromone/odorant transduction
works has to be able to detect such things.

Physical logic suggests the model, too. Given that neural transmission
outpaces odor transmission through air, an efficient chemo-detector would appear as
near the exterior of the organism's body as other constraints allow. From economic
analysis we might expect all olfactory tissues on the exterior of the organism. This
was once the case, as indicated by ontogeny's recapitulation of phylogeny and
comparative physiology. Microbes appear to smell only at their cellular membrane.
Many modern multicellular organisms maintain exterior chemoreceptors. Witness
those in the dermis of frogs or on the feet of houseflies, seastars, spiders and
butterflies. Humans, too, maintain exposed chemoreceptor cells, such as those in the
eyes which sense irritation to redden the eyes and stimulate irritant-induced tears.
Although interior vertebrate olfactory tissues lie in permanent darkness, they maintain
ancestral camouflage patterns.

Additionally, non-motile olfactory "cilia" exhibit a strange microtubular

pattern in cross section. The pattern is of two tubulin tubes encircled by nine other
pairs.6 This demonstrates still another link with an early exterior surface function;
this time, motility. The extremely long "cilia" of mammalian olfactory
chemoreceptor neurons and the short ones of microvillar cells never move. They
float motionless within the Bowman's secretion of the olfactory mucosa yet they
resemble real cilia that can move. Cilia first evolved on the outside surface to move
the cell itself. There cilia must have gained the chemoreception and mechano-
reception capabilities evidenced by modern microbes. Incidentally, the cilia only
enhance chemoreception. Just as many unicellular creatures can smell without cilia,
so can receptor neurons function without the reception enhancement cilia provide.

With premiums for both sensitivity and speed, concentration of odorant

chemicals at the sensor might also make sense. Liquid sorbs and concentrates
airborne odorants.7 This explains why receptor tissues have moist surfaces to meet
smells.7 However, because liquid slows odorant movement relative to the gaseous
state, detectors would be expected to lie as close to the surface of the liquid film as
other constraints allow. Having receptors on the surface where the odourant or
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pheromone molecules are caught, instead of being buried behind a mucous
obstruction, makes intrinsic sense.

Cilia reach out from the microvillar cell into the liquid film, but usually not all
the way to the odor laden surface, thus propagation of signal across the liquid film at
this depth must be at least as quick as neural propagation or the neuron’s dendrites
would simply evolve closer. Odorants need ride no glacial ferry to dendritic
chemoreceptors when an electrical representation of the odorant may serve. If that
were the case and odorant chemicals were carried on the backs of much larger
molecules, the trouble and expense of maintaining partially depolarized dendrites
would be dispensable. Partially depolarized membranes are very near EPSP neural
pulse generation, so they’re easy to trigger electrically.

Dissolved proteinaceous receptors lie within the moist film covering olfactory
tissues, and the dissolved receptors transmit to underlying dendrites by affecting the
ion concentration and conductivity of the liquid film. Dendrites sense or produce an
EPSP (excitatory post synaptic response) based upon voltage: potential difference.
(Potential difference defines voltage, a bit of physics my colleagues forgot.) Thus
dendrites can easily electrically sense odorant reception in the overlying sensory
lymph film or receive increased electrical stimulation as free ion concentration
increases. Free ion concentration increases changing the potential difference, i.e. the
voltage changes, and the dendrite reception fires the axon. That may seem pretty
simple, but sensory physiologists have had a devil of a time trying to understand that
simplicity. They still think huge chemicals like proteins have minds and personalities
so that they can recognize a pheromone, grab it, and transport it over large distances
to leave it touching the cilia’s surface chemoreceptors. Never mind that chemicals
can’t move against a concentration gradient sans propulsion.

DISSOLVED RECEPTOR PROTEINS ARE EXTRACELLULAR

In preparation for odorant reception, unbound dissolved protein receptors lie

in the receptor lymph, slowly sequestering ions from the surrounding film of mucous.

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In higher animals, the receptor lymph film is pumped full of strange ions of one sort
or another. Once ions are captured by the sensory proteins (still called pheromone
binding proteins or odorant binding proteins in the literature), reception can proceed.

Concentrated by the surface of mucous covering the non-moving "ciliated"

olfactory nerve endings, the stimulator odor chemical binds loosely to the dissolved
ion-holding proteins. Binding differs from permanent bonding. Binding seems more
like a key in a lock while bonding would be like welding.

In 1998, when this author submitted his breakthrough article on pheromone

transduction8 such dissolved receptor protein and pheromone binding had already
been observed by several investigators 9,10,11 without anyone noticing any
conformational change in the protein, much less one that would release sequestered
cations to alter the voltage and create an EPSP. Eventually, the conformational
change of the pheromone binding protein and pheromone complex as hypothesized
by this author was observed12 although this author’s lone prediction had gone
unnoticed. It is frustrating that with the book open before them, colleagues cannot
abandon the ferry protein phlogiston, a concept clearly impossible. Do they have a
Charon fixation? There is no need to ferry the pheromone to the dendrite for
reception. The pheromone changes the conformation of the pheromone binding
protein right there at the surface and that change in shape causes release of charged
particles that locally change the potential difference and that is enough. So basically,
pheromone hits the PBP, the PBP changes shape, releasing both pheromone molecule
for continued duty and the numerous sequestered ions, changing potential difference,
setting off the dendrite electrically.

The dissolved proteins’ source appears to be cells at the base of the

sensillum13 or perhaps the dendritic membrane itself.14 On binding to the pheromone,
in a sudden conformational change, the receptor protein releases its previously
sequestered ions and repels the pheromone away again. Think of a lock opening
when the key is turned. Such conformational changes have also been observed 15 and
within the context of neurotransmitter reception. 16

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 Similarly, small soluble proteins, such as calmodulin, bind to cations in
solution.3 Anti-calmodulin drugs might be expected to counter pheromone binding
proteins binding calcium. In fact, the "alpha factor pheromone" looks and behaves
like a pheromone binding protein. Anti-calmodulin drugs, trifluoperazine and
chlorpromazine, counter its expected effects in yeasts,17 exactly as would be
expected.

Do odorant-protein complexes release any ions when the change in shape

takes place (conformation change)? Lymph ionic concentration changes have been
observed upon odorant stimulation.18 More details will follow.

TRANSDUCTION

The released ions themselves may be of sufficient charge and density to alter
the potential difference across the nearby partially depolarized sensory dendrite.
From their surfaces dendrites have a limit of about 5 or 10 microns into the
surrounding medium for ionic changes to optimally effect excitation.19 Olfactory
dendrites are never too far away from the chemoreceptive action.

Ion releases from a discharging pheromone binding protein (or PBP) may also
encourage further ion releases from other PBPs in a chain reaction. A voltage
sensitivity for ion sequestering proteins could help account for easier depolarization
with prior sub-threshold excitement. In addition ion release would improve solution
conductivity, varying resistance in the receptor circuit and allowing a graded flow of
current, as has been observed.20 Due to their hyperpolarization, the unusually
electrosensitive dendrites of chemosensory mucosae can perceive and conduct
currents in the low picoamp range, 21 three orders of magnitude less than other
dendrites. If not for electrical reception, why else would that be the case?

It is thought that chaotic patterns recognized by the brain as scents or

pheromonal signals result from the processing of the resulting neural inputs. 22
Inhibitory circuits in peripheral processor centers meet incoming sequential snapshots
from olfactory dendrites stimulated by ion releases from odorant-stimulated receptor
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EXOCRINOLOGY
proteins. Higher centers detect changes (the ordinate becomes the new abscissa),
with differences transmitted as recognizable chaotic patterns.

Pattern recognition may be enabled by shared capacitance switching among

proximal inter-oligodendritic axons as proposed in the author’s model of saltatory
conduction.

MODEL IN GREATER DETAIL:

The author apologizes for inserting so much detail in this monograph designed
for practicing and training physicians. This is testimony to the language barrier that
exists among those who should have already been able to follow this line of reasoning
from the author’s previously published articles. The unfortunate practice of using
graduate students to write one’s papers makes contacts with authors another exercise
in futility, since the people who really know what is going on--the young people who
have just finished the coursework--rarely communicate for the group. Of course, it
never hurts to brush up, even for general readers.

Trans-specific similarities in behavior during pheromone receptivity were

examined in the preceding chapter. Microeconomic theory predicts that reception of
chemical signals should be essentially similar at the molecular level as well. We
might expect chemoreception to vary from species to species something on a par with
photo-reception (sight) or audition (hearing) systems.

Finding so many chemical resemblances among pheromone molecules (see

Chapter 3) suggests that molecular mechanisms of pheromone reception should be
comparable, too. Vogt and his colleagues10 have found corresponding pheromone
binding protein (PBP) matches among several insect species detecting closely related
aliphatic pheromones. Thus both pheromones and pheromone receptor proteins
(PBPs) share similarities. For olfactory and somatic chemo-recognition the proposed
receptor proteins are drawing from an entire class of so-called "carrier proteins" and
antibodies. Vought and colleagues’10 narrower classification of pheromone binding
proteins vary with known interspecific and intra-specific (dimorphic) variations of
197
pheromone chemistry recognition. Clones of some pheromone-binding proteins
became available in 199223,24 as did an odorant binding protein.25,14 Sexual
chemosensory dimorphism has been grossly observed in humans where the immune
response of males and females are not identical.26 Of course more recently,
dimorphic pheromone recognition27 has been broadly recognized as the physiological
basis for sexual orientation, as this author first proposed in 1983.28 This author’s
paper caused a sensation and outbursts of laughter--this from primatologists who had
sat silent and stone-faced during films on primate copulation. While he read his paper
alone, ridiculed with catcalls as he spoke, his paper was plagiarized in print in the
‘joke journal’ “The Journal of Irreproducible Results.” He who laughs last, laughs
best.

THE PROCESS OF INSECT CHEMORECOGNITION

Entomologists and insect physiologists maintain a lead on their vertebrate

chemosensory transduction colleagues. Part of that is because insects rarely complain
much and criminals addicted to canine and feline semiochemicals see fit not to
vandalize entomology laboratories. Thus the results from insect studies guide this
science and color its presentation here.

Olfaction and pheromone recognition take place on the antennae protruding

from the heads of most insects. Attached to the antennae surface in regular order are
tiny sensory hairs. Afferent axons travel through the antenna back to the head to
report any sensations.

The sensory hairs are hollow, cuticular structures, each about 300 micrometers
long and 6 micrometers in diameter,29 with an inner lumen volume of about 10 to the
minus twelfth liter30,31 This lumen contains the sensory dendrites, whose somatic cell
bodies are buried among the epithelial cells at the base of the hair. A proteinaceous
fluid, the sensory hair lymph, bathes these dendrites (see De Kramer and Hemberger
[1987]32)33.

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The electrical model actually follows much of the old mechanical model34,35,36
closely. A pheromone molecule enters the sensory hair lymph,33 a liquid holding our
dissolved receptor proteins (pbps) that surrounds the receptor dendrite. Concentrated
the pheromone attaches to dissolved Pheromone Binding Proteins (or PBP's)
sequentially, until inactivated by sensory esterase.32 The pheromone stays in the
lymph and rarely goes anywhere near the sensory dendrite32,13 because it does not
need to physically go anywhere. Electricity does the work.

BIOCHEMISTRY OF PHEROMONE RECEPTION

This model predicts that emotional tears hold human pheromone receptor
protein for episodic chemoreception. Like insect lymph PBP, lipid carrier-type
proteins lie dissolved in the liquid Bowman's secretion covering the olfactory
mucosa37 and in emotional tears.38 Their functions in tears and olfactory mucosal
films are unknown. The higher proteinaceous component of emotional lacrimation
brings tear protein concentrations37 to levels comparable to that of various Bowman's
secretions39 and some insect sensory lymphs32 and perhaps vomeronasal mucosal
secretions. In addition to five tear-specific proteins, an unusual high molecular
weight protein, greater than 200 kD, resides in human tears.40 (A kiloDalton (kD)
equals 1000 Daltons. One Dalton is about the size of a hydrogen atom.) They may
be pheromone binding receptor proteins.

The proteinaceous secretion covering the pheromone sensing vomeronasal

organ differs from the Bowman's secretion of the olfactory mucosa. A 70 kDa
glycoprotein vomeromodulin is abundant in the lateral nasal glands and is also
present in the posterior septal and vomeronasal glands. It is highly concentrated in
the mucus of the vomeronasal organ of Jacobson but is not detectable in the mucus of
the main olfactory neuroepithelium. 41 This species specific "vomeromodulin" will be
a pheromone receptor protein within this model, functioning as previously described.

199
 Pheromone binding proteins (or PBPs) are proposed to be pheromone receptor
proteins in solution. Some PBPs are known to interact with aliphatic pheromones32
while still others are specific to steroid pheromones. 42

DIFFERENCES FROM CURRENT MODELS

Good evidence for G-protein mediated pheromone receptors on cell surfaces

abounds (e.g. Boekhoff, I. et al.,43). However excellent counter evidence against a
transduction role for G-proteins exists, at least for insects:

Female sex pheromones applied to freshly isolated, living antennae [one antenna, two
antennae-BN] of male Antheraea polyphemus and Bombyx mori [a big silk moth and the silk mothBN]
led to an increase of cGMP. A 1:1 mixture of 2 pheromone components of Antheraea polyphemus
blown for 10 sec. in physiological concentrations over their antennal branches raised cGMP levels
about 1.34fold (+/ 0.08 SEM, n = 23) from a basal level of 3.0 +/ 0.6 (SEM, n = 20) pmol/mg protein.
Similarly, bombykol [the pheromone for the silk moth, Bombyx mori, identified back in 1959-BN]
elicited a 1.29fold (+/ 0.13 SEM, n = 23) cGMP increase in antennae of male Bombyx mori from a
basal level of 2.7 +/ 0.5 (SEM, n = 24) pmol/mg protein. No cross-sensitivity was found with respect to
pheromones from either species [In line with their not responding to each others pheromones under the
EAG. -BN]. In antennae of female silk moths, the cGMP response was missing upon stimulation with
their own respective pheromones according to the known lack of pheromone receptor cells in the
female. cAMP levels in the male antennae of 14.2 +/ 2.9 (SEM, n = 4) pmol/mg protein in A.
polyphemus and 15.0 +/ 3.0 (SEM, n = 5) pmol/mg protein in B. mori were not affected by pheromone
stimulation. Within 160 sec, the extent of cGMP increase in B. mori was independent of the duration of
pheromone exposure. The levels of cGMP in pheromone-stimulated antennae of both species remained
elevated for at least 10 min., i.e., much longer than the duration of the receptor potential measured in
single-cell recordings (Ziegelberger, G., et al., 1990). 44

The G-protein pathway may have something to do with the metabolism of

receptor cells,45 but reaction-time and persistence outlive transmitted results of the
stimulus.

Previous models classified pheromone-associated proteins dissolved in the

receptor lymphs, tears, and Bowman's secretions as "carrier proteins.”46 Supposedly
pheromonal lipids attach to proteins for transport through the aqueous film barrier to
the receptor dendrite. On the dendrite, it has been thought, surface membrane-bound
protein binds to pheromone which opens a hole in the membrane. The tiny hole, or
channel, allows ions inside to depolarize the dendrite. Similar chemically signaled
channels have been demonstrated for virtually all cells with reliable patch-clamp
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techniques.47 However, experimental difficulties have prevented identification of
protein-bound, odorant-stimulated channels in olfactory dendrites under the sensory
lymph film. The entire complement of membranous proteins for olfactory cilia have
been separated and are being sequenced. 48 This model accommodates dendritic
receptors for chromatographic diffusion timing of odorants through the film.

Poor evidence for such a carrier function for PBP does exists.42 A portion of
lipid pheromone adhering to glass can be coaxed off by adding some protein to the
brew. 13 This is much like using "enzymes" in laundry detergent. Solubility does
improve, but only at unrealistically high concentrations. The same lab saw an
impoverished pheromone reception signal set in a dendrite surrounded and wetted by
a protein-less pheromone/ionic blend. That seems to be indisputable evidence for at
least some dendritic surface receptors. But does it? Proteins of this class can turn
over in the receptor lymph at a rate of 2 X 104 proteins/second/sensillum.9 Indeed,
mRNA specific to ciliary membrane encodes a secretory protein with significant
homology to odorant binding protein (OPB). It shows significant homology to the
VEG protein, thought to be involved in taste transduction. The cloned membrane
protein is a member of the lipophilic molecule carrier protein family.14 If the
membrane does not secrete receptor proteins, some sorption of PBP to those rough
dendritic surfaces seems probable.

Finally, without any PBP, an excessive 10,000 pheromone molecules were

needed at the dendritic surface to fire the neuron. Recall that 99.96% of the
pheromone becomes attached to PBP. With PBP concentration at physiological
levels, calculation shows that under the mechanical scenario, 25 million pheromone
molecules would be needed in the lymph to fire dendritic receptors. Boding ill for the
‘ferry’ idea of old, only one or a few molecules of pheromone stimulates a
transduction event.32 Oops!

Getchell and Getchell, 49 dispute the practical necessity of carrier proteins.

They note the improbability of gaining any speed by attaching most tiny odorants to
large slow-moving proteins. Calculating diffusion coefficients through mucous they
show that carry time would exceed the speed of chemoreception by several orders of

201
magnitude. An exposed receptor dendrite fires sooner than a carrier protein can cross
the five to ten microns from the mucous surface to the dendrite wall.

The long time periods ranging from 5.4 to 16 seconds, required for OBP to transport odorants
from the mucous surface to receptor sites on the proximal cilia are, in general, not consistent with the
onset latencies of odorant-evoked excitatory discharges (Getchell, 1986) or membrane currents
(Firestein and Weblin, 1989) recorded from olfactory receptor neurons (Getchell, T.V. and M.I.
Getchell, 1990b).48

If the proteins hypothesized here to be receptor proteins are carrier proteins as

is accepted thinking, then they do a terrible transportation job. Not only do they
move too slowly to cover the required distances as indicated above, but 99.96% of
pheromone molecules stay in and among the dissolved proteins of the receptor lymph
and never reach the dendrite surface. 13

Van den Berg and Ziegelberger13 note yet another failure of the mechanical
hypothesis. "Ferried pheromones" remain in the lymph several minutes after the
electrical signal ceases.50 These difficulties along with a clearly inefficient
mechanism, pose insurmountable problems for the mechanical model, yet still it holds
on, inertia from the nineteen seventies.

The present new hypothesis satisfies all of these difficulties, although as Max
Planck so elegantly put it, we must wait for all the old men to expire. If pheromone
receptor proteins change conformation to release cations (or anions in some cases) on
binding to pheromone and sequester more only upon disassociation, then strongly
bound pheromone/protein pairs would not contribute to further stimulation. This
accounts for the signal latency and the intact pheromone presence observations.13

Thinking of this idea took up the author’s first 20 minutes study of the subject
of chemoreception (and the difficulty his colleagues have with it baffles him even
today). Half a dozen tests jumped to mind that would support or settle the issue. A
literature search indicated that every one of those tests had been done, often
elaborately, with results as predicted usually to the surprise of investigators.
Outsiders find it easier to notice the obvious.51

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The 99.96% of pheromone perpetually "in transit" can be explained better by
the new model. Since the "carrier proteins" are actually "receptor proteins" under this
new electrical model, 99.96% represents an efficiency, not a deficiency.

Meanwhile, a carrier role for fetching pheromones through mucous can also
be discounted by the kinetics associated with pheromone and pheromone binding
protein.

[T]here is a temporally weak association between individual binding protein and pheromone
molecules. Even at 109 M pheromone, a 10,000 fold excess of PBP was required to reduce the
availability of pheromone to another protein species, the SE [sensory esterase which digests
pheromone for removalBN] (Vogt, R.G. 1987).32

If the pheromone rider won't stay on the PBP horse, the rider is not being carried.

The preceding observation by Vogt32 explains the signal amplification

observed by one or a few molecules setting off a reception event from a much larger
structure, the sensory dendrite. A pheromone molecule binds to many PBPs in quick
succession.32 Because ion release is so much faster than sequestration, depolarization
(or hyperpolarization depending on the charge of the ions sequestered) could proceed
from the rapid buildup of de-sequestered ion concentration changing the relative
potential difference across the nearby dendritic membrane.

Getchell21 noticed "false positives" leading sensory dendrite firing responses

to some odorants. Such would be consistent with the new electrical method of initial
excitation. Where positives do not lead, increased lymph conductance by released
ions could let current outrun a buried "false" response.

The false positive phenomenon was described as a small-amplitude initial

positive voltage transient.21 Such small positive voltage transients would be the
residues of actual binding protein ion releases, rather than the much larger responses
of neural origin.

Getchell's calculation,48 observed sensory latencies, and known physical

location of pheromone suspended in lymph support the new model. Because
pheromone triggers cation release in the lymph that bathes and surrounds the
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dendrite, stimulus and receptors join in plenty of time. Having receptors effectively
at the receptor surface and immediately beneath it, instead of being buried behind an
aqueous mucous barrier when most pheromones for most species are hydrophobic,
does make intrinsic sense. Otherwise would not faster-moving hydrophilic
pheromones dominate the semiochemical lexicon eliminating the ‘need’ for carrier
proteins in the first place?

The puzzle of concentration dependent onset latency is explained by the

present model. The electro-olfactograph, or EOG, is similar in concept to the electro-
antennagraph previously described in chapter 3 of this book. The EOG is
characterized by a concentration dependent onset latency.21 This model explains
varying slack time nicely. Contained within the mucous or sensory lymph we find
binding proteins such as OBP, PBP, or antibodies. In the mucous/sensory lymph,
bound binding proteins release ions on contact with odorant. With more odorant
sorbed into the mucous, more binding proteins are bound at the beginning, therefore
the firing thresholds of nearby dendrites are attained sooner. Hence a concentration
dependent variation in onset latency becomes observable. There is no way to explain
concentration-dependent variation in onset latency in the old model.

Another riddle is the definable threshold observable in EOGs for different

odorants or pheromones.21 The threshold is that of the odorant concentration, not the
electrical threshold of the dendrite--that stays constant. This model predicts that such
odor concentration thresholds should vary widely for different odorant species. Such
is the case.52 Variability would follow binding affinity, mainly, but other
chromatographic variables include miscibility with the mucous, diffusion rate through
the mucous, ion-odorant binding affinity (polarity), and others. Since the old model
holds that the pheromone binding protein or odorant binding protein does all the
swimming (across the receptor lymph to release the odorant or pheromone at the
dendrite), variability due to chromatographic and intrinsic chemical variables would
play no or almost no role.

The preceding discussion utilizes the concept of concentration. Actually,

olfactory tissues measure, not concentration, but something closely related. The
information transferred to the brain is that of mass flow rate (dm/dt), unaffected by
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molar concentration (dn/dv) (see Mozell, et al., 198453 and Kurtz, D.B. and M.M.
Mozell, 198551). Some chromatographic detectors detect mass flow rate. The mass
flow rate detecting flame ionization detector (or FID) responds to ionization released
by burning a passing sample and is unaffected by concentration fluctuations just like
the case in olfaction. It should not be surprising that peripheral olfactory systems
respond to mass flow rate if they rely on similar ionic triggers as hypothesized.

Holding total moles constant and varying carrier gas volume with proportional
increases in stimulation time, researchers showed constant stimulation.51 When total
moles are held constant, mass is held constant, too. Proportionality constants are
required in both cases (olfaction and gas chromatography) to account for odorant-
specific chromatographic variables. The corresponding gc measure then, is mass flow
rate, which also does not depend upon carrier gas volume either. 54

IONIC CONCENTRATION

Extra-cellular depolarisation by released ions is the mechanism of ordinary pain

sensation on cell trauma. Escaping cell contents (K+ ions) change potential difference
at exposed pain receptors.55 (24) In odourant or pheromone reception, the ions are
released outside the cell by desequestering receptor proteins on binding to odorant
aligning polar molecules and setting up the depolarising oscillation.

In ion substitution experiments, one ion substitutes for a naturally occurring

lymph ion concentration. In vitro and in vivo these hold Na+ and K+ ions primarily
responsible for negative voltage transients recorded from the olfactory mucosa.
Oddly enough, olfaction is tetrodotoxin (TTX) insensitive, and relatively unaffected
by local anesthetics at concentrations high enough to block action potentials in the
olfactory nerve!21 The author proposed that an evaginated ion permeability of the
ciliary dendrites could explain this phenomenon in insect sensilla in his article on
transduction a decade ago. The logic went that on the antenna’s dendrites the
negatively charged "exterior" of Na+ channels would be interior, hence unavailable to
TTX (and TTX-insensitive). Local anesthetics block normal membrane receptor
dendrite stimulation not signal propagation. Apparently the ion-bloated binding

205
proteins "bursting" on odorant contact in the mucous could stimulate even a receptor-
less dendrite. The poor old pbp ferry model just throws up its hands in abject failure,
again. Recently, some membrane structures have been identified to be reversed from
what is considered normal.56 Well, what do you know? Another correct prediction
ignored.

Electrical transients can only be recorded from epithelial regions of the nasal
chamber containing olfactory mucosa.21 Only such mucosal areas harbor Bowman's
glands, secreting the dissolved odorant binding proteins amid unusual cation
concentrations.

Transients of the olfactory mucosa cannot be evoked by antidromic (against

flow) electrical stimulation of the olfactory nerve.21 Olfactory nerves, plain C-fibers,
lack the myelin associated with one-way-only axons. Some dendritic cilia of the
olfactory mucous may have evaginated excitability as the following photo suggest.
An odd constriction between the dendrite and the soma, called the ciliary root,31 may
be the membrane twisting inside-out. However, Russian researchers57 propose a
shunt circuit to account for this phenomenon.

PHASE ANGLE

Most of the new crop of researchers accept previous researchers’ work

uncritically. Where theretofore unheard of phenomena are detected, it is merely
ignored as irrelevant. Getchell21 cites one of these, another puzzle explicable by the
tired old odorant-ferrying model.

Gesteland and his colleagues studied differential impedance changes by continuously passing
a sinusoidal current [2050 cycles (cps)] to the olfactory mucosa through an injection electrode. When
odorants were delivered to the olfactory mucosa, the negative-driving process was associated with a
change in the phase angle that tentatively was identified with an inhibitory process.21

The phase angle indicates the direction of a vector sum of capacitive reactance
and inductive reactance, with resistance. A purely resistive alternating current circuit
has a phase angle of 0o. Only physical changes in resistance or capacitance* during
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the course of the cycle could explain these data. Binding and releasing ions in the
aqueous mucous would change its resistance and deliver the responses found. Indeed,
changes in lymph resistance on odorant stimulation have been shown in insects54

*or inductance Physiologically, there is nothing in the peripheral olfactory sensory system resembling
a solenoid, so perhaps inductance can be ignored as it has been.

Others have shown that changes in potassium cation concentration in the

sensory lymph follow pheromonal stimulation of the receptor.

"A high potassium content of about 200 mM has been measured in isolated receptor lymph
(Kaissling and Thorson, 1980) and also in situ by Xray micro-analysis of ultrathin cryosections
(Steinbrecht and Zierold, 1982, 1985, 1987). The later method allows the quantitative analysis of
electrolyte elements at the resolution of the electron microscope, and preliminary data indicate that
changes in the electrolyte concentrations due to stimulation of the receptors can be monitored
(Kaissling and Thorson, 1980; Steinbrecht and Zierold, 1985; R.A. Steinbrecht and K. Zierold,
unpublished results)" (Steinbrecht, R.A., 1987). (BN emphasis)

Does this observation cinch the question? More evidence supports pheromone
binding protein to be a receptor protein. De Kramer and Hemberger31 demonstrated
protein sequestration and de-sequestration of cations to equilibrium with test
electrodes definitively and elegantly. (Please refer to the graph of R1 vs. recording
time, in figure below.)

207
Figure 3 from DeKramer and Hemberger, 1987.31

"If the saline solution in the recording electrode has a conductivity which is lower or higher
than the resistivity of the receptor lymph, the rate with which [the lymph resistance] R1 changes is a
measure for the exchange rate between recording electrode and receptor lymph. In recordings of R1 it
is very striking that the first exchange of receptor lymph takes much more time than subsequent ones;
some reticular mesh apparently buffers the ion activity ..." (De Kramer and Hemberger, 1987).31

That "reticular mesh" buffering ion activity in the insect receptor lymph is here
proposed to be the pheromone binding proteins sequestering and de-sequestering
cations to accommodate changes in cationic concentration. This experiment also
neatly shows the proteins voltage sensitivity as well. Of course, holding cations,
preventing their movement sets up tiny electric fields, which maintains a capacitive
reactance.

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Is potassium the ion bound up in the lymph? DeKramer and Hemberger31
reviewed the composition of the sensory lymph filling insect sensilla. They drew
attention to the difference between total and free K+ (potassium cation)
concentrations citing Kaissling and Thorson (1980). That lab had used Xray and
flame photometric spectroscopy to confirm concentrations of 200 mM K+ (free and
bound) while the K+ activity was only 145 mM. A high potassium concentration in
sensillum lymph was later confirmed by Steinbrecht (1992). Potassium pumps
into the receptor lymph would be required for the model and these, too, have been
observed:

Another important feature of the auxiliary cells [at the base of the sensory hair lumenBN] is
their apparent resemblance to the cells of ion-transporting epithelia (Fig. 14), e.g., in insect midgut and
salivary glands (Harvey, 1980). Their elaborately folded apical membranes are thought to be the site
of an electrogenic cation pump, which mainly pumps potassium into the receptor lymph and thereby
creates a trans-epithelial voltage. ... In Bombyx mori the trans-epithelial voltage amounts to 33 mV
(Thurm and Wessel, 1979), but its influence on receptor function is still uncertain" (Steinbrecht, R.A.,
1987).

Once pumped into the lymph, K+ (potassium) ions must be contained.

Holding the evaginated ion concentration requires an electrically insulated container
and the hollow sensory hair is one.

Tight-junctional complexes join the epithelial cells and neuronal cell bodies, establishing a
high resistance barrier between the sensory hair lymph and the hemolymph (see De Kramer and
Hemberger [1987]) (Vogt, 1987).32

A strong electrical resistance exists between sensory hair lymph of the sensory hair
(or sensillum) and the hemolymph, or insect "blood."

"Beside their ontogenetic function, the auxiliary cells connect the receptor cells to the
epidermis so that the epithelial organization is maintained. Septate junctions seal the intercellular
clefts between all cells so that the trans-epithelial resistance is high. In pheromone-sensitive sensilla of
moths, but not in mechanoreceptors of crickets and flies, septate junctions are also observed where the
axon originates and the thecogen cell borders the glia cell around the axon (Keil and Steinbrecht, 1983,
1987; Steinbrecht and Gnatzy, 1984). A very close contact between the tormogen cell and the cuticle
of the hair base is the morphological correlate of a high electrical resistance between neighboring
sensilla (Keil, 1984c)" (Steinbrecht, R.A., 1987).

209
 Next, a sink for K+ ions (or a source of Na+) separate from the sensory hair
lymph and accessible to the interior of the dendrite might be required. Might this be
the work of the "specialized junction of hitherto unknown function" between
thecogen cell and receptor cell identified by Steinbrecht in 1980 (cited in Steinbrecht,
R.A., 1987)? Such an open hole could do the job. Indeed, Kuppers, Josef and Ulrich
Thurm (1979) observed an inward equilibrium continuous current of K+ ions
flowing like a bucking voltage (see figure from Basic Gas Chromatography) and a
second loop of current.

A second loop of current circuit is controlled by adequate stimulation of the sensory cell
(Thurm, 1974). The actively generated current flows back in this circuit [Actually, the continuous
bucking current is the reverse flow. It helps account for the high electro-sensitivity of these dendrites-
BN], entering the receptor cell via its stimulus-increased apical conductance, leaving the cell via its
baso-lateral membrane regions, and returning into the tormogen cell via its basolateral membrane.
. . . This second current loop in some sensilla increases receptor sensitivity (Erler and Thurm,
1978; Thurm and Gödde, in prep.). [Actually, the bucking current increases the sensitivity, just like in
GC detector circuitry-BN]

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EXOCRINOLOGY

“It is helpful to think of the electrode gap as a variable resistor R1 whose

resistance value is determined by the number of charged particles within the gap.
With carrier gas flowing a constant concentration of charged particles (due to carrier
gas impurities, liquid phase bleeding, etc.) will be present in the gap, thus causing a
constant current, I, to flow. This constant current is called the “background current”.
It is desirable to minimize the background current so small changes in current can be
more easily measured (it is easier to measure a fixed change in a small quantity than
the same change in a larger quantity). The background current is reduced to zero by
opposing it with a “bucking voltage”. Thus, under “no signal” conditions (carrier gas
flow), no net current flows, and the recorder traces a straight baseline. When a
sample component passes through the electrode gap, molecules of the component are
ionized. This increases the number of charged particles and decreases the value of
R1. This decrease permits current to flow which produces a signal which is registered
as a peak on the recorder.”

211
 The extreme sensitivity of the dendrite to polarization by very slight currents
in the picoamp range is analogous to the homeostasis of the background current
against the bucking voltage in the flame ionization detector of gas chromatography.
The few ions released or exposed by the conformational change of the pheromone
receptor proteins in the ‘gap’ are sufficient to set off the chain reaction among the
calmodulin proteins inside the dendrite electrically. In some insects with evaginated
membranes and ‘pumped’ receptor lymph, ionic concentration just beneath the
threshold of conductivity until PBP conformational change allows the passage of an
electric ‘spark‘ explains the electrical characteristics of antennae.

There are certainly plenty of voltage gated sodium channels in olfactory

neuron dendrites 58,59 and voltage sensitive calmodulin is stuffed into dendrites of
pheromone receptor dendrites to amplify depolarization. 60

Not all chemosensory antennae work as insect antennae do. The electrical model of
chemosensory transduction accommodates these, too.

b) Terrestrial Crustacea and Spiders. Measurements on representatives of Crustacea and

spiders revealed electrical properties of their sensilla clearly different from those found in insects. At
tarsal and antennal chemo and mechanoreceptive sensilla of the isopod Armadillidium (woodlouse) a
trans-epidermal voltage in the range of +15 to +35 mV exists. This voltage is not acutely O2-
dependent; no voltage change at all occurs during 6 minutes of anoxia. The TEP [trans epithelial
potential] at sites far from sensilla is only a few mV positive. The nature as well as the location of the
epidermal voltage source at these sensilla remain unknown at present. ... (Thurm, U. and G. Wessel,
1979).61

Apparently, woodlice have PBP (pheromone binding protein), but lack the (O2
sensitive) potassium pumping. PBP would gather ion from the relatively low K+
concentration of the hemolymph, resulting in relatively long latency periods when
compared to insects. Perhaps inferior chemo-sensing ability limit these organisms to
their more sedentary life strategies?

Unlike the mechanical case, for the electrical model, a simultaneous excitation
of the entire dendrite would take place on chemo-stimulation. If a mechanical
dendrite receptor depolarizes the neuron, the point of excitement would be detected
by examining firing latencies.

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Figure 1. Simultaneous recordings from the sidewall (near the hair base; lower trace) and the tip
(upper trace) of a pheromone-receptive hair of Antheraea polyphemus. The recording was made upon
stimulation with E6, Z11-16:Ac at 0℃. Note that the spike recorded from the base does not lead the
spike recorded from the tip. That means there is no starting point, that all reception on the dendrite is
simultaneous. Only electricity moves this fast.

The electrical model's simultaneous excitation can be seen above. Perhaps the
dendrite is stimulated by release of ions from a non-point source, i.e. the receptor
lymph surrounding the dendritic membrane? Indeed, if ions were released into the
receptor lymph cavity sufficient to fire the neuron, no dendritic membrane receptor
would be absolutely necessary for chemoreception. The old mechanical sensed
chemical is carried to the receptor modelers must hypothesize a special case "fast
neuron" phlogiston to account for these data.

Because more than one dendrite can dwell with the same sensillum, and
because dendrite specific reception is seen, 62,63 the author expected ionic barriers in
the sensory lymph receptacle. Such ion barriers were located, 64 and they can account
213
for much differential dendritic receptivity. In other cases, different PBPs one for each
pheromone sensed in the sensillum,10 might fire sequentially, with the second PBP2
being voltage dependent upon previous PBP1 de-sequestration/conductance. This is
life, so there will be great variability, but all variations on the same theme.

The threshold for impulse initiation to depolarizing current pulses for

olfactory dendrites is in the pico-amp (pA) range. "These are very low current
densities for impulse initiation".21 Yet the currents generated by these nerves are no
different from those of most other nerves and occur in the milliamp range. The
electrical model of chemoreception transduction accommodates the extreme
sensitivity to electric shock shown in ciliary olfactory dendrites. Super-sensitivity
allows detection of small changes in local ion concentrations in the sensory mucous.
Local ion concentration changes, as hypothesized, have been observed.54,18 Q.E.D.

Van den Berg and Ziegelberger's data13 prove that the few receptors they
propose to be on dendritic membranes cannot alone account for chemoreception.
They found that a 180 nMolar concentration of pheromone in ringer solution (or
about 10,000 pheromone molecules) was necessary to initiate a response vs. zero for
ringer. With pheromone binding 99.96% to carrier protein, then 25 million in the
lymph would be equivalent. Pheromone uptake efficiency means an exposure to
about a billion pheromone molecules would be needed to get a response from
dendritebound receptors alone. However, only a few molecules set the receptor off.

Getchell's calculation (1988), observed sensory latencies, and known physical

location of pheromone suspended in lymph support the new model. Because
pheromone triggers cation release in the lymph, stimulus and receptors join in plenty
of time. Having receptors at the receptor surface, instead of being buried behind a
mucous barrier, makes intrinsic sense.

CONFORMATIONAL CHANGES IN RECEPTOR PROTEINS

What about predictions of the new model? For instance receptor proteins are
proposed to have a conformational change to release or expose ions to effect a change
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in potential difference, voltage, across the pheromone receptive dendritic membrane.
Does pheromone binding (receptor?) protein have two conformations in vivo? Yes it
does.

In the early sixties, Maxwell M. Mozell65 first noticed an odd phenomenon in

fresh Bowman's secretion both in vivo and in vitro. He noted a change in the
viscosity of the secretion with odorant stimulation. It was this remarkable
observation that stimulated submission of this model for publication in 1998.

You can see the binding proteins changing their conformations! At X60
magnification, the mucus surface changes its reflectance.66 This is straightforward
evidence for conformational change. Mozell's viscosity changes in chemo-stimulated
mucous64 were visible to the unaided eye.

These characteristics might be expected upon conformational changes of some

odorant binding protein. In fact different conformations have even been
distinguished using electrophoretic techniques:

In acryl-amid gels under nonreducing conditions, the binding protein appears as a double
band (Kaissling et al., 1985; Klein, 1987; 32); the two populations might reflect two different
functional states. They might differ in their disulfide bridges, since the binding protein contains six
conserved cysteins, where more than one stable tertiary structure seems possible (Gyrgyi et al., 1988;
Raming et al., 1989; Raming et al., 1990). It is conceivable that the binding [...] induces a
conformational change [...] of the involved pheromone binding protein (van den Berg, M.J., and G.
Ziegelberger, 1991). 13

Such conformation changes, which have finally been admitted,67 amaze the scientific
establishment, those adherents of the old mechanical chemical ferrying to dendrite
receptor model. It is too bad that they did not notice the author’s article.8

Another characteristic of the new model is a changing electrical conductance

on odorant stimulation. Does resistance change in the sensory lymph (Bowman's
secretion, tears?) Apparently so. A Russian team found a changing electrical
resistance in insect sensilla upon odorant stimulation,54 essentially similar to the R1
of the Flame Ionization Detector of the gas chromatography, leaving a logical
consequence of the release of sequestered ions upon binding of receptor proteins.

215
 The electrical ability to affect depolarization of a membrane is distance
dependent. Sufficient potential differences to depolarize must be within about 5 to 10
microns of the dendritic membrane.19 These measures typify the width of sensory
lymph cavities within the sensillum, or sensory hair.31

DIMORPHIC RECEPTOR PROTEIN AND GLANDULAR

MORPHOLOGY

If pheromone binding proteins (PBPs) and odorant binding proteins (OBPs)

really are pheromone receptor proteins and odorant receptor proteins as hypothesized,
respectively, then PBPs must bind only to one pheromone, while OBPs must bind to
many odorants. PBPs must differ in their receptor area enough to account for that
specificity while OBPs should remain very similar. Both PBP and OBP would have
to explain their ability to sequester cations such as maintaining a negative charge.
All three conditions are met.

Odorant binding protein subfamilies associate with distinct classes of

olfactory receptor neurons in insects.10 Vogt's group10 compared fourteen OBPs and
PBPs from six species. They found PBPs to be highly variable in their sequences
when compared among species. In addition, sex specific PBPs were found in species
with sexually dimorphic pheromone discrimination. OBPs were found in both sexes
in general odor discrimination sensilla. The highly negative charge of PBPs found
was consistent with the pheromone ion sequestration and release function here
proposed. Discovery of highly positively charged PBPs, for sequestration of anions,
might plausibly be expected as well.

What information have we concerning the human case? A sexual dimorphism

in human vomeronasal organ response has been recorded for identical putative
pheromone stimulants.68 Sexual dimorphisms have been detected in adult human
tears69 and in gross immune function.70 There were significant differences in the
amounts of LF [lactoferrin] and two kinds of STPs [of five specific tear proteins] in
the different sexes. The amounts of these proteins were larger in females.66
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EXOCRINOLOGY
Dimorphic pheromone receptor proteins have been discovered in human tears and in
pheromone emitting glands.71 Some relationship must exist here. Differences in
reception reflect in differences in pheromone secretion. Sexual dimorphisms have
been detected in dermal sebaceous secretion,72 and axillary secretions.73,74

217
Is it logical that nature would emplace an aqueous barrier to a hydrophobic

pheromone requiring a larger carrier protein to slowly traverse? Kinetic studies

suggest this is impossible.

No such to and fro P-PBP traffic has ever been observed, despite numerous attempts

and approaches.

The association between pheromone and pbp is too short by orders of magnitude to

allow any transport.

Simultaneous excitement of tip and base by EAG prevent entertaining this point-

source step.

(The use of bovine serum albumin (BSA) as a control for PBP is invalid because

BSA is itself a chemosensory protein, changing conformation on contact just like

PBP.)

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EXOCRINOLOGY
Given the availability of electric communication within the body elsewhere (e.g. pain

reception on cell trauma releasing K+ ions) would not the observed voltage changes

resulting upon PBP conformational change be more easily accommodated as part of

the dendritic excitement process? After all, the sensory lymph is only as wide as the

limits of electrical excitement of a dendrite, any dendrite. Also, why else would the

dendritic membrane be maintained in a constant state of hyperpolarization if not as a

bucking voltage? Why would that membrane be so electrically sensitive, responding

to electric currents in the picoamp range? The phenomenon of "false positives"

correlates well to individual PBP conformational changes at the surface of the sensory

lymph.

If this is not a simple electrical excitation, why is the system so insulated from the

hemolymph? Why so electrically insulated from other identical systems adjacent?

Why does the lymph conductance change on odorant stimulation? The change in

potassium cation concentration observed on pheromone stimulation defines voltage

change. By calculation, the change is [K+] is enough to stimulate electrically.

219
High social standing among one's colleagues should not be sufficient to drive a

fraudulent scientific inertia, a driven mass hysteria. Thousands of scientists with

limited resources are being allocated to a solved conundrum, depriving society of

their valuable services.

1 Nicholson, B. 1985; An economic model of phermone transmission in avians. Paper presented to

the Animal Behavior Society annual meeting, Raleigh, N.C.

2Tumlinson, James H., and P.E.A. Teal 1987; Pheromone Biosynthesis and its regulation. pp 3-26.
Chapter 1. In: Pheromone Biochemistry. Prestwich, Glenn D., and Gary J Blomquist editors.
Orlando: Academic Press, Inc. 565 p.
3Stryer, Lubert 1988; Biochemistry, Third Edition. New York: W.H. Freeman and Company.
1089p.
4 Lehninger, Albert L. 1982; Principles of Biochemistry. New York: Worth Publishers, Inc. 1011p.
5 Champe PC, Harvey RA. Lippincott's Illustrated Reviews: Biochemistry. Philadelphia:

JB.Lippincott Company 441p. 1987.

6 Burkitt H George, Young Barbara, Heath John W, Wheater Paul R Wheater’s functional histology: a
text and colour atlas. New York: Churchill Livingstone, 1993.
7 Hornung DE, Mozell MM. Factors influencing the differential sorption of odourant molecules across
the olfactory mucosa. J Gen Physiol 1977;69(3):343-61.
8 Nicholson B. Pheromones cause disease: pheromone/odourant transduction. Med Hypotheses.

2001 Sep;57(3):361-377.
9Vogt, RG, A.C. Kohne, JT. Dubnau and G.D. Prestwich 1989; Expression of pheromone binding
proteins during antennal development in they gypsy moth Lymantria dispar Journal of Neuroscience.
9(9):3332
10Vogt, RG, G.D. Prestwich and M.R Lerner 1991; Odorant-binding-protein subfamilies associate
with distinct classes of olfactory receptor neurons in insects. Journal of Neurobiology. 22(1):74-84.
11 Bocskei Z, Groom CR, Flower DR, Wright CE, Phillips SE, Cavaggioni A, et al. Pheromone binding
to two rodent urinary proteins revealed by X-ray crystallography. Nature 1992;360(6400):186-188.

220
EXOCRINOLOGY
12Damberger Fred, Nikonova Larisa, Horst Reto, Peng Guihong, Leal Walter Soares, and Kurt
Wüthrich. NMR characterization of a pH-dependent equilibrium between two folded solution
conformations of the pheromone-binding protein from Bombyx mori. Protein Science (2000),
9:1038-1041.
13 Steinbrecht, Rudolf Alexander 1992; Experimental morphology of insect olfaction: tracer
studies, X-ray microanalysis, autoradiography, and immunocytochemistry with silkmoth antennae.
Microscopy Research & Technique 22(4):336-350.
14Dear TN, Campbell K, Rabbitts TH. Molecular cloning of putative odorant-binding and odorant-
metabolizing proteins. Biochemistry 1991;30(43):10376-82.
15 Van den Berg MJ & Ziegelberger G (1991) On the function of the pheromone binding protein in the
olfactory hairs of Antheraea polyphemus. J Insect Physiol 37: 79-85.
16Kanner, Baruch I. (1993). Structure and function of Sodium-coupled neurotransmitter transporters.
pp. 243-250, Chapter 19 IN: Molecular Biology and Function of Carrier Proteins Society of General
Physiologists Series, Vol 48, 46th Annual Symposium (Reuss, Luis, J M. Russell, JR, and Michael L.
Jennings, eds) New York: Rockefeller University Press 324 pages.
17Ruiz, T., and L. Rodriguez 1986; Effect of anticalmodulin drugs on the action of yeast alpha factor
pheromone. Archives of Microbiology 145(1):104-106.
18Steinbrecht, Rudolf Alexander 1987; Functional morphology of pheromone-sensitive sensilla. pp
353-384. In: Pheromone Biochemistry. Prestwich, Glenn D., and Gary J Blomquist, (eds) Orlando:
Academic Press, Inc. 565 p.
19 Ranck, James B., JR 1987; Brain stimulation, electrical, in mammals, principles and consequences

P. 170-171. In Encyclopedia of Neuroscience. George Adelman ed. Boston: Birkhauser.

20 Krapitskii, S.V., and F.G. Gribakin 1992; Electroantennogram of the American cockroach: effect
of oxygen and an electrical model. Journal of Comparative Physiology-A, Sensory, Neural, &
Behavioral Physiology 170(5):651-663.
21 Getchell TV. Functional properties of vertebrate olfactory receptor neurones. Physiol Rev 1986;66

(3):772-818.
22 Freeman WJ. The physiology of perception. Scientific American 1991 Feb;264(2):78-85.
23Raming K, Krieger J, Breer H. Molecular cloning of an insect pheromone-binding protein. Febs Lett
1989;256(1-2):215-8.
24Krieger J, Raming K, Prestwich GD, Frith D, Stabel S, Breer H. Expression of a pheromone-binding
protein in insect cells using a baculovirus vector. Eur J Biochem 1992;203(1-2):161-6.
25Dal, Monte M., I. Andreini, R. Revoltella, P. Pelosi. Purification and characterisation of two
odourant-binding proteins from nasal tissue of rabbit and pig. Comp Biochem Physiol [B] 1991;99(2):
445-51.
26Grossman CJ, Roselle GA, Mendenhall CL. Sex steroid regulation of autoimmunity. J Steroid
Biochemistry & Molecular Biology 1991;40(4-6):649-59.

221
27Bekaert KM, Tuyttens FA, Duchateau L, De Brabander HF, Aluwé M, Millet S, Vandendriessche F,
Vanhaecke L. The sensitivity of Flemish citizens to androstenone: influence of gender, age, location
and smoking habits. Meat Sci. 2011 Jul;88(3):548-52. Epub 2011 Feb 18.
28Nicholson B. A semiochemical addiction model for human bonding. Paper presented to the Animal
Behaviour Society and the International Society for Human Ethology biannual meeting, Bucknell
University Lewisburg, PA. June 12, 1983.
29Boeckh J, Kaissling KE, Schneider D. Sensillen und Bau der Antennengeissel von Telea
polyphemus (Vergleiche mit weiteren Saturniden: Antheraea, Platysamia, und Philosamia). Zool J
Anat 1960;78:559-84.
30Vogt, RG, L.M. Riddiford, and G.P. Prestwich 1985; Kinetic properties of a sex pheromone-
degrading enzyme: The sensillar esterase of Antheraea polyphemus. Proc. Natl. Acad. Sci U.S.A.
82:8827-8831.
31Keil, Thomas A. (1984a). Reconstruction and morphometry of silkmoth olfactory hairs: A
comparative study of sensilla trichodea on the antennae of male Antheraea polyphemus and Antheraea
pernyi (Insecta, Lepidoptera). Zoomorphology 104:147-156.
32DeKramer JJ, Hemberger J. The Neurobiology of pheromone reception. In: Prestwich GD,
Blomquist GJ, editors. Pheromone biochemistry. Orlando: Academic Press 1987;433-72.
33Vogt, R G. 1987; The Molecular Basis of Pheromone Reception: Its Influence on Behavior pp.
385-431 In: Pheromone Biochemistry Prestwich, Glenn D. and Gary J Blomquist, editors. Orlando:
Academic Press, Inc. 565 p.
34Kaissling, K.-E. 1974; Sensory transduction in insect olfactory receptors. In: Biochemistry of
Sensory Functions. Jaenicke, L. editor., pp. 243-273. Springer-Verlag, New York.
35Dickens JC, Callahan FE, Wergin WP, Murphy CA, Vogt RG. Intergeneric distribution and
immunolocalization of a putative odourant-binding protein in true bugs (Hemiptera, Heteroptera). J Exp
Biol 1998 Jan;201(Pt1):33-41.
36 Vogt RG, Riddiford LM. Pheromone binding and inactivation by moth antennae. Nature

1981;293:161-3.
37Pevsner J, Sklar PB, Snyder SH. Odorant-binding protein: localization to nasal glands and
secretions. Proc Natl Acad Sci U S A. 1986 Jul;83(13):4942-4946.
38Frey WH the II, Desota-Johnson D, Hoffman C, McCall JT. Effect of stimulus on the chemical
composition of human tears. Am J Opthalmol 1981;92:559-67.
39 Pevsner J, Hwang PM, Sklar PB, Clark VJ, Snyder SH. Odourant-binding protein and its mRNA are
localised to lateral nasal gland implying a carrier function. Proc Nat Acad Sci 1988;85:2383-7.
40Kuizenga A, van Haeringen NJ, Kijlstra A. Identification of lectin binding proteins in human tears.
Investigative Ophthalmol Vis Sci 1991;32(13):3277-84.
41 Khew-Goodall Y, Grillo M, Getchell ML, Danho W, Getchell TV, Margolis FL. Vomeromodulin, a
putative pheromone transporter: cloning, characterisation, and cellular localisation of a novel
glycoprotein of lateral nasal gland. Faseb J 1991;5(14):2976-82.

222
EXOCRINOLOGY
42Booth WD, von Glos KI. Pheromaxein, the pheromonal steroid-binding protein, is a major protein
synthesised in porcine submaxillary salivary glands. J Endocrinol 1991;128(2):205-12.
43 Boekhoff I, Strotmann J, Raming K, Tareilus E, Breer H. Odourant-sensitive phospholipase C in
insect antennae. Cellular Signaling 1990;2(1):49-56.
44Ziegelberger G, van den Berg MJ, KaisslingK-E, Klumpp S, Schultz JE. Cyclic GMP levels and
guanylate cyclase activity in pheromone-sensitive antennae of the silkmoths Antheraea polyphemus and
Bombyx mori. J Neurosci 1990;10(4):1217-25.
45 Ronnett GV, Snyder SH. Molecular messengers of olfaction. Trends Neurosci 1992;15(12):50813.
46Singer AG. A chemistry of mammalian pheromones. -32. Proceedings of the International
Symposium on Recent Advances in Mammalian Pheromone Research. J Steroid Biochem Mol Biol
1991;39(4B):627.
47 Kandel ER., Schwartze JH. Principles of Neural Science. New York: Elsevier. 1985:21-2.
48 Ronnett GV, Snyder SH. Molecular messengers of olfaction. Trends Neurosci 1992;15(12):50813.
49Getchell Thomas V and Marilyn L Getchell Regulatory factors in the vertebrate olfactory mucosa.
Chemical Senses 1990;15:223-231.
50 Kasang G, Proff L, Nichols M. Enzymatic conversion and degradation of sex pheromones in antennae
of the male silk worm Antheraea polyphemus. Z Naturforsch 1988;43c:275-284.
51Kuhn, Thomas (1970). The Structure of Scientific Revolutions. Chicago: University of Chicago
Press.
52 Kurtz DB, Mozell MM. Olfactory stimulation variables. which model best predicts the olfactory nerve
response? J Gen Physiol 1985;86(3):329-52.
53 Mozell Maxwell M, Sheehe PR, Swieck Jr SW, Darts DB, Hornung DE. A parametric study of the
stimulation variables affecting the magnitude of the olfactory nerve response. J Gen Physiol 1984;83(2):
233-67.
54McNair HM, Bonelli EJ. Basic Gas Chromatography. Lithographed by Consolidated Printers,
Berkeley, California. Varian Instrument. 1969.
55Guyton AC. Textbook of Medical Physiology Eighth Edition. Philadelphia: WB Saunders Company.
1991.
56L. Stowers, D. Logan LUSH Shapes Up for a Starring Role in Olfaction Cell, 2008 Jun 27;133(7):
1137-1139.
57 Krapitskii, S.V., and F.G. Gribakin 1992; Electroantennogram of the American cockroach: effect
of oxygen and an electrical model. Journal of Comparative Physiology-A, Sensory, Neural, &
Behavioral Physiology 170(5):651-663.
58 Dubin AE, Dionne VE.Action potentials and chemosensitive conductances in the dendrites of
olfactory neurons suggest new features for odor transduction. J Gen Physiol. 1994 February 1;103(2):
181-201.

223
59 Choi JS, Hudmon A, Waxman SG, Dib-Hajj SD. Calmodulin regulates current density and
frequency-dependent inhibition of sodium channel Nav1.8 in DRG neurons. J Neurophysiol. 2006 Jul;
96(1):97-108. Epub 2006 Apr 5.
60Zhainazarov AB, Doolin RE, Ache BW. Sodium-gated cation channel implicated in the activation of
lobster olfactory receptor neurons. J Neurophysiol. 1998 Mar;79(3):1349-1359.
61 Thurm, U., and G. Wessel 1979; Metabolism-dependent trans-epithelial potential differences at

epidermal receptors of Arthropods. I. Comparative data. Journal of Comparative Physiology

134:119-130.
62 O'Connell, RJ 1985; Responses to pheromone blends in insect olfactory receptor neurons. Journal

of Comparative Physiology. 156:747-761.

63O'Connell, RJ, JT. Beauchamp, and A.J Grant 1986; Insect olfactory receptor responses to
components of pheromone blends. Journal of Chemical Ecology. 12:451-467.
64Keil, Thomas A, and R Alexander Steinbrecht 1987; Diffusion barriers in silkmoth sensory
epithelia: Application of lanthanum tracer to olfactory sensilla of Antheraea polyphemus and Bombyx
mori. Tissue & Cell 19:119-134.
65 Mozell Maxwell M. 1992. Personal communication
66 Joshi H, Getchell ML, Zielinski B, Getchell TV. Spectrophotometric determination of cation

concentrations in olfactory mucus. Neurosci Lett. 1987 Dec 4;82(3):321-326.

67 Laughlin JD, Ha TS, Jones DN, Smith DP. Activation of pheromone-sensitive neurons is mediated

by conformational activation of pheromone-binding protein. Cell. 2008 Jun 27;133(7):1255-65.

68 Monti-Bloch, L., and B.I. Grosser 1991; Effect of putative pheromones on the electrical activity of
the human vomeronasal organ and olfactory epithelium. The Journal of Steroid Biochemistry and
Molecular Biology. (Proceedings of the International Symposium on Recent Advances in Mammalian
Pheromone Research.) 39(4B):573-582.

69 Mii S, Nakamura K, Takeo K, Kurimoto S. Analysis of human tear proteins by two-dimensional

electrophoresis. Electrophoresis 1992;13(6):379-382.
70 Grossman CJ, Roselle GA, Mendenhall CL. Sex steroid regulation of autoimmunity. J Steroid

Biochemistry & Molecular Biology 1991;40(4-6):649-659.

71 Spielman AI, Zeng XN, Leyden JJ, Preti G. Proteinaceous precursors of human axillary odor:
isolation of two novel odor-binding proteins. Experientia. 1995 Jan 15;51(1):40-47.
72Montagna, William, and Paul F. Parakkal 1974; The Structure and Function of Skin. New York:
Academic Press. 433 p.
73Preti, George, Winnifred Berg Cutler, Celso Ramon Garcia, George R Huggins, and Henry J
Lawley 1986; Human axillary secretions influence women's menstrual cycles: the role of donor
extract of females. Hormones and Behavior 20:474-482.
74 Cutler WB, Preti G, Krieger A, Huggins GR, Garcia CR, Lawley HJ. Human axillary secretions
influence women's menstrual cycles: the role of donor extract from men. Hormones and Behavior
1986;20:463-73.
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Chapter 8: Pheromone Control of Crime and

Drug Addiction
There is a natural distribution of criminal behavior on a continuum with filial
behavior that runs from the most malicious industrial killers to the dutiful, devoted,
respectful, affectionate and loving child at home asleep, apparently due to differential
parental solicitude. But why?

Given estimates of life spans for long ago, being orphaned has been more
common in the past, enough to affect life strategy choice on an instinctive level. On
the streets of ancient Babylon, the life of a child without parents would have been
precarious indeed. Only by stealing, robbing, selling oneself, literally doing anything
to survive, would street urchins live to reach reproductive age and have children of
their own.

How would an innocent child be persuaded by nature to adopt this highly

adaptive criminal behavior? The behavior would depend upon the absence of the
parents because filial behavior, following the wishes of one’s parents, would be more
advantageous and appropriate in the presence of parents looking out for you.
Absence of the mother and/or father, especially during critical periods, has been
associated with the appearance of juvenile delinquency to the criminal justice system
and other adolescent risk-taking. Upper respiratory changes, particularly sinus
development in infancy and childhood as discussed in chapters 2, 6, & 7 differentiate
such critical periods.

How would one positively recognize the presence of their parents and adult
relatives? (Positively because recognizing crocodiles as one’s parents has dangerous
implications for survival.) The answer, Q.E.D. is that parental pheromones stimulate
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filial behavior and that the absence of detection of parental pheromones stimulates
delinquency and other risky antics. Yes, this is easy to test. Yes, the author has tested
it dozens of times and providing parental, in particular paternal, pheromones to
criminals cures the criminal with a single large 150 mg dose for his or her lifetime.
Double-blind, cross-over, replicated clinical trials of healthy adult male facial skin
surface lipid pheromone taken by mouth have yet to receive official support. It is
hoped that this book’s publication will remedy that difficulty.

Criminal behavior is natural and useful for the advancement of humanity for
another reason beyond mere survival. A willingness to engage in what is generally
considered to be criminal behavior is important because much behavior, truth-seeking
in particular, has been mis-classified as detrimental to society and therefore criminal.
Scientific investigations and religious worship have shared official and popular
condemnation and punishment as antisocial. Human ethology’s need for blinds from
which to study all human behavior might serve as example. Indeed, the information
of this tome has been suspected of criminality with the author’s home being rifled by
searching officials in the performance of their duty, not once, but on several
occasions. One takes one’s life in one’s hands to persevere for truth, and you can just
forget about your reputation, too. Fear is a constant companion, but so is Pasteur, and
with his great example, the prospect of redemption and success. Indeed, until this
author’s research obtains wide public acceptance, his life and livelihood remain
precarious.

Established empirically from many open trial anecdotes, paternal pheromone

sufficiency allows long term maintenance of non-criminal behavior by criminals.
Criminal behaviors: murder, theft, neglect and abuse of elders or children, sexual
perversions of rape, homosexuality, bestiality, wild stunts, and drug addictions for
heroine & crack cocaine, all of these appear to involve pheromone recognition, as all
respond to 150 mg p.o. of healthy adult male facial skin surface lipid kissing
pheromone in a single dose. Again, this is merely the author’s contention based upon
his many anecdotes from 1987 to 2011.

Proof of the born again experience received from the pheromone tardily
awaits appropriate clinical trials, however, much can be gleaned from the literature as
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it now stands, plus there is no choice but to review the literature. First and foremost,
the non-conscious pheromone recognition pathways of the human brain1, 2 correspond
to areas of the brain that differ from normal when associated with criminal behavior,
with sexual perversion, 3 and with drug addiction. Animals and human beings share
pheromone sensing hardware. 45 6 7 8 9 Many articles have demonstrated that
pheromone recognition pathways in human beings involve the prefrontal cortex,
insula, amygdala, hippocampus, hypothalamus & anterior cingulate areas of the
human brain.

Noting that lower I.Q., shorter attention spans, and antisocial behavior typify
criminals, Carpenter and Nevin (2009) 10 suggest that environmental exposures known
to lower IQ and shorten attention spans among children might be considered
environmental causes of violence. As such, the causes Carpenter & Nevin discuss
have clear effects on pheromone perception and olfaction.

Better resolution of medical imaging technologies has led to better structure

identification, allowing better observation of the alignment with rarely studied
pheromone pathways. Of course, heat, air pollution (particularly high ozone
concentrations) and low wind speeds have also been associated with violent human
behavior.11 Think about this.

The author published an article in the British Journal of Dermatology in

November of 1984,12 following from a paper he presented at the International Society
for Human Ethology in June of the previous year13 in which he theorized that skin
surface pheromones would hold the key to understanding mate-mate and parental
love, criminal behavior, sexual orientation and sexual perversion. This chapter will
attempt to explain in lay terms how such a then preposterous idea could take root and
become a proscription for world-wide social change.

Microeconomic theory predicts the social and personal profitability of all

behavior, including criminal behavior. The first stumbling block was the
microeconomic axiom of perfect information, that all buyers and sellers in a market
know everything instantly. Well, in geologic time, that was true, given the human
appetite for speech. Then the human light speed communication networks were an

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evolution beyond an underlying pre-existing biological information sharing system
which must exist, too. It was hypothesized that as communicable viruses transmit
genetic biological information to all receptive beasts as fast as the fastest ship that
sails, basically all disease and vectors of disease were information sharing and
population culling devices that worked optimally.

This sounds just like Dr. Pangloss, but equations don’t lie. The next difficulty
is the economic man axiom of microeconomics. Surely human and animal and for
that matter plant and microbial appetites were optimized as well, as they had to be.
Unlimited wants was a straight up line, but the closest thing would be a climbing
logarithmic asymptote. Such functions were observable in nature as unrestrained
growth of bacterial colonies provided unlimited nutrients and space for growth and
waste disposal. And given the second law of thermodynamics, the increasing
complexity of life was only organized to drive perfect dispersal of everything. Life
itself evolves toward ever more perfect air pollution! So we could detect higher
forms of life on other planets by looking for dust clouds expanding from them at near
the speed of light.

Yes, this sounds more and more panglossian. However, in a world of perfect
information (all know all always) populated by economic men with unlimited wants
and with the free-rider problem solved (a gene is a gene is a gene), no uneconomic
behavior could exist ever. Yet in every direction, human beings wasted time on
apparently unprofitable pursuits. The epiphany came in physics class: equations
don’t lie. A primer of population biology 14 confirmed my thesis. Thus the discovery
of the underlying evolutionary worth of each human motion was discoverable by
dissection and socratic examination. I decided to begin with instinctive behaviors
such as kissing and crying.

Kissing, crying, and emotion in general had a significant literature, most of it

highly speculative and unsystematic. From ethological observation and participation,
it dawned that kissing’s biological worth must be as a transfer mechanism. Kissing
must be picking something up, so I looked on the skin where people kissed people
and found sebum. Next comparisons to similar behavior of other species beginning
with the physiology of the mistakenly mis-labeled ‘grooming’ and ‘allogrooming’
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behaviors in apes, ungulates, avians, insects … All of the ‘allogrooming’,
‘allopreening’, and ‘displacement activity’ being observed by primatologists,
ornithologists, ethologists, and entomologists was being misunderstood. All those
behaviors had to be pheromone transferring or depositing devices, too.

Furthermore, the glands under the claws, beaks, antennae, snouts, and kissing
human lips would be optimized to function at their highest levels in breeding seasons.
The microeconomic theory insisted that even the circulation to the glands would be
optimized, down to the cellular level, even down to the nuclear and genetic level:
epigenetics! So for instance, it was no surprise to discover that sea birds lacked fire
detection olfactory apparatus,15 since oceans and sea beaches don’t burn.

About one hundred and fifty milligrams of healthy adult human male facial
skin surface lipid is sufficient to alleviate criminal behavior, juvenile delinquency,
and drug addiction. Between 150 and 250 milligrams will have the effect of ending
perverse sexual behavior. Injections of pheromone receptor proteins and/or
epigenetic therapy may be needed for the very worst monsters in our prisons. Testing
will tell.

The paternal facial skin surface lipids cure for juvenile delinquency came
from empirical investigations. To the present, one hundred and two open anecdotal
trials of paternal skin surface lipid kissing pheromone on chewing gum vehicle have
resulted in complete remissions of all symptoms of delinquency, all symptoms of
criminal inclination, all symptoms of runaway behavior, all symptoms of borderline
personality disorder, all symptoms of homosexual perversion (in twelve female
lesbians and gay men), and all symptoms in one case of a perversion so problematic
to the physician with the disorder that this researcher could not be informed of its true
nature.

In 1987, a family member’s difficulties resulted in the first cure of borderline

personality disorder with criminal behavior in a fourteen year old relative.
Incarcerated and physically restrained, the family member chewed the gum and
instantly felt relief from ‘the monkey’ on his back. Removing the monkey would
become a familiar metaphor as it would be used by dozens of pheromone recipients in

229
the years to come. Further doses led to graduation from law school at the top of his
class and many promotions--a pattern of ambition repeatedly seen later.

The next family member in trouble was thwarted trying to complete his
medical degree. After complaining of ‘mitral valve prolapse’ and displaying
symptoms of agoraphobia, the pheromone gum was provided, again in desperation.
Immediate relief of symptoms began the anecdote, ending with achievement of a
tenured faculty position at an accredited medical school.

The author began solicitations to attempt double-blind clinical trials at state

and local levels in four states: New York under Cuomo, Texas under Richards,
Georgia under Miller, and Florida under Bush. Having had past associations with all
four, the author believed that obtaining cooperation from them would be easy. “I
provided Cuomo with the ‘wearing of the green’ broccoli bit famous at the 1992
Democratic convention. I was the first person outside Ann Richard’s family to
suggest that she run for governor and together with Bill Clinton the three of us had
come up with the Dead-beat Dad laws for her. I proposed the HOPE Scholarship
Program to Miller when his aide for student & university affairs, and I had been a
family friend of the Bushes, proposing back in Texas that Johnny come to Florida in
the first place. I was far wrong.” All four failed even to grant a meeting on the
subject of a cure for criminal behavior. Moreover, the doors were slammed shut by
their prison systems as well.

Bill Clinton and I had been brothers in service in Texas during the McGovern
campaign. That only infuriated the US Bureau of Prisons who dismissed my
Institutional Review Board submission out of hand. And even though this author had
personally saved the life and career of George W. Bush for his family the year before
his Clinton experience,1 that pushed the Bureau of Prisons to an uninhibited frenzy,
and my submission for a trial of the pheromone was again refused with zeal, this time
with prejudice by the bureaucracy of Bush administration. Perhaps other medically
trained people can read this monograph and recommend trials with better result?
Steal your nerve, ladies and gentlemen. Humanity does love its prisons. Getting rid
of them will be no easy task.

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The hypothesis to be tested is: Does healthy adult male facial skin surface
lipid kissing pheromone alleviate symptoms of criminal behavior and juvenile
delinquency? The method is to watch behavior records of experimental vs. control
groups and see a statistically significant decline in the experimental group receiving
pheromone gum over the control group; then with the experimental pheromone gum
supplied to the control group, to see that group recover normal behavior as well.

The materials and methods would be to select from volunteers two similar
groups from the same population of incarcerated criminals. (Some believe that sick
people lack the capacity to volunteer. The author disagrees suggesting that clinical
trials within a prison population in order to treat the malady from which the prisoners
suffer would not be exploitation. Indeed, helping prisoners recover from criminal,
perverse, and drug-addicted inclinations should be the main mission of any prison
system.) Using intermediary technicians unaware of the identity of each dose or
control, indistinguishable doses of pheromone-laced chewing gum and canola-oil
laced chewing gum would be provided to experimental and control populations,
respectively. Once a predetermined period of behavioral observation has passed, the
control population would be provided the pheromone-laced chewing gum and their
behavior assessed by observation. A statistically significant difference between un-
dosed and pheromone-dosed prisoners should be seen and pheromone-dosed
prisoners should have statistically significant decreases in recidivism. Similar
protocols in combination with epigenetic therapy, direct injection of pheromone
receptor proteins, or tear transfers (like Clockwork Orange) should also be tried.
Doing nothing is negligence.

Pheromone collection must be made from volunteer pheromone donor males

of good reputation of about ‘father age’ to the prisoner pheromone recipient. This is
the type of donation that has achieved success in previous open trials. Maternal skin
surface lipids in similar large unnatural dosage seem to stimulate homosexual
perversion as observed anecdotally in one case. However, given the ease with which
homosexuality can be cured with the paternal pheromone (eight successful open
trials), further investigations using female-donated facial skin surface pheromones
may be allowed to go forward, provided there is no sexually perverted motive by
researchers.
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PERIGRINATION

Leaving the old life and circumstances behind has been seen consistently in
those criminals, delinquents, and runaways who chewed the paternal pheromone gum.
There is little wonder why.

The very real and immediate prospect of pheromonal rehabilitation of

criminals will demand close review and careful ethological experimentation. What is
the natural history of criminal behavior? In other words, what benefit does the
existence of crime hold for mankind? Given the difficulty and expense of controlled
experiments on our fellow human beings, we will utilize animal experimentation,
famous volunteers, and exocrionological case reporting to hone the methology. 150
mg of a man’s face grease p.o. is just an approximation. Given the multiple devices
controlling human bonding, duplication of the paternal pheromone deficiency
mechanism to produce criminal behavior seems likely. Observers of criminals16 and
criminal-type pheromone deficiencies will vary across the board.

PHEROMONES SUBSTITUTION ILLNESS: DRUG ADDICTION

Addiction played a main theme in the author’s initial reports.17,18 However,

the discovery that healthy adult human male facial skin surface lipids in a single sub-
gram dose could actually resolve heroine addiction and then crack cocaine addiction
in heavy users in the field permanently, came as pleasant surprises. It makes sense
that it would be so, at least now it does. The instantaneous, complete remission of all
symptoms surprisingly without withdrawal effects, followed by adoption of healthy,
reproductive, and socially appropriate lifestyles, exceeded all expectations and is
beyond the ken of colleagues who would rather see their patients suffer than to
perform the experiment ready and waiting in the appendix to this book.

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Love-deficient, presumably pheromone deficient, people commit all the
crimes of passion, do they not? Certainly drug addicts commit regular criminal acts
in support of their addiction. The protocol in the appendix has been used to treat
dozens of criminals and delinquents, all successfully. 150 - 250 mg of healthy adult
male (over 30 years of age) facial skin surface lipid taken by mouth on a chewing
gum vehicle completely eliminates all symptoms of drug addiction instantly,
apparently at the first ten milligram exposure.

Sadly, despite several attempts, human pheromones have had little effect upon
alcoholism. Experimental exposures to ethanol had no effect on reproductive fertility
or behavior, including response to pheromones, of intact experimental animals.19 In
humans, alcohol promotes dopamine release in the brain’s nucleus accumbens, with a
preferential effect in the ventral striatum.20 The ventral striatum is unexcited in
pheromone studies,21, but it does receive tertiary projections from the olfactory and
vomeronasal amygdalae.22 Willed ceasing of alcohol consumption cures symptoms
of alcoholism. Perhaps alcohol consumption could be stopped by replacement with
heroine addiction or crack cocaine, which are more amenable to pheromone
intervention?

BORDERLINE PERSONALITY DISORDER

Pheromones are processed in the medial amygdalae and the memory-

associated hippocampi, but not the parahippocampal gyri, nor the uncuses. All four
areas are associated with abnormalities in BPD. It is asserted with fMRI evidence
that dorsolateral prefrontal cortex and the hippocampuses sustain symptoms of
borderline personality disorder.23 Lesions of the hippocampus or prefrontal cortex
change behavior stimulated by chemoreceptions in cats.24 The medial prefrontal
cortex is a projection area for the pheromone-sensing accessory olfactory bulb25
again, in cats. In humans, under fMRI the anterior part of the inferior lateral
prefrontal cortex is directly activated by the human pheromone, androstadienone.26
That is close enough for association.

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 A derivative of Omega-3 fatty acids (fish oils), which have some human
pheromonal stereochemistry, seems to improve BPD ever so slightly.27 Recall that
human sebum taken up in kissing works synergistically and species specifically just
like these variously helpful free fatty acids, so this slight dietary effect suggests a
much more potent effect from the pheromone.

Borderline sufferers share behavioral similarities to juvenile delinquents who

have responded famously in open trials of healthy adult male facial skin surface
lipids, so the prognosis for full and rapid recovery with paternal pheromone treatment
is excellent.

1Zhou W, Chen D Encoding human sexual chemosensory cues in the orbitofrontal and fusiform
cortices. J. Neurosci. 2008 Dec 31; 28(53): 14416-11421.
2Treyer V, Koch H, Briner HR, Jones NS, Buck A, Simmen DB Male subjects who could not
perceive the pheromone 5a-androst-16-en-3-one, produced similar orbito-frontal changes on PET
compared with perceptible phenylethyl alcohol (rose). Rhinology. 2006 Dec; 44(4):278-282.

3Savic I, Berglund H, Lindström P. Brain response to putative pheromones in homosexual men. Proc
Natl Acad Sci U S A. 2005 May 17;102(20):7356-7361. Epub 2005 May 9.
4Moncho-Bogani J, Martinez-Garcia F, Novejarque A, Lanuza E. Attraction to sexual pheromones
and associated odorants in female mice involves activation of the reward system and basolateral
amygdala. Eur J Neurosci. 2005 Apr;21(8):2186-2198.
5Sobel N, Prabhakaran V, Hartley CA, Desmond JE, Glover GH, Sullivan EV, Gabrieli JD. Blind
smell: brain activation induced by an undetected air-borne chemical. Brain. 1999 Feb;122 (Pt 2):
209-217.

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6Tirindelli R, Dibattista M, Pifferi S, Menini A. From pheromones to behavior. Physiol Rev. 2009
Jul; 89(3):921-956.
7Touhara K, Vosshall LB. Sensing odorants and pheromones with chemosensory receptors. Annu Rev
Physiol. 2009; 71:307-332.
8Zufall F, Leinders-Zufall T. Mammalian pheromone sensing. Curr Opin Neurobiol. 2007 Aug;17(4)
483-489. Epub 2007 Aug 20.
9Tizzano M, Sbarbati A. Hormone fatty acid modifications: gram negative bacteria and vertebrates
demonstrate common structure and function. Med Hypotheses. 2006; 67(3):513-516. Epub 2006 Apr
27.
10Carpenter DO, Nevin R. Environmental causes of violence. Physiol Behav. 2009 Sept 14; [epub
ahead of print].
11 Rotton J, Frey J. Air pollution, weather, and violent crimes: concomitant time-series analysis of
archival data. J Pers Soc Psychol. 1985 Nov;49(5):1207-1220.
12
Nicholson B. Does kissing aid human bonding by semiochemical addiction? 1984 Br J Dermatol.
Nov; 111(5):623-627.
13Nicholson B. Love and kisses: a semiochemical addiction model for human bonding. 1983. Paper
presented to the International Society for Human Ethology and Animal Behaviour Society biannual
international meeting at Bucknell University, Bucknell PA.
14 Wilson EO, Bossert WH (1971). A Primer of Population Biology Stamford: Sinauer Associates.
15 Tinbergen N The Herring Gull’s World 1989 Gilford, CT: Globe Pequot Press.
16Clinton H. It Takes a Village: And Other Lessons Children Teach Us. (1996) New York: Simon &
Schuster.
17Nicholson, B. 1983; A semiochemical addiction model for human bonding. Paper presented to the
Animal Behavior Society and the International Society for Human Ethology, Lewisburg, PA.
18Nicholson, B. 1984; Does kissing aid human bonding by semiochemical addiction? British
Journal of Dermatology 111(5):623-627.
19Fadem BH. Effects of postnatal exposure to alcohol on reproductive physiology and sexually
dimorphic behavior in a marsupial, the gray short-tailed opossum (Monodelphis domestica). Alcohol
Clin Exp Res. 1993 Aug;17(4):870-876.
20Boileau I, Assaad JM, Pihl RO, Benkelfat C, Leyton M, Diksic M, Tremblay RE, Dagher A.
Alcohol promotes dopamine release in the human nucleus accumbens. Synapse. 2003 Sep 15;49(4):
226-231.
21 Martínez-Hernández J, Lanuza E, Martínez-García F. Selective dopaminergic lesions of the ventral
tegmental area impair preference for sucrose but not for male sexual pheromones in female mice. Eur
J Neurosci. 2006 Aug;24(3):885-893.
22Martinez-Marcos A. On the organization of olfactory and vomeronasal cortices. Prog Neurobiol.
2009 Jan 12;87(1):21-30. Epub 2008 Sep 25.

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23Sala M, Caverzasi E, Lazzaretti M, Morandotti N, De Vidovich G, Marraffini E, Gambini F, Isola M,
De Bona M, Rambaldelli G, d'Allio G, Barale F, Zappoli F, Brambilla P. Dorsolateral prefrontal cortex
and hippocampus sustain impulsivity and aggressiveness in borderline personality disorder. J Affect
Disord. 2011 Jan 4; [Epub ahead of print]
24Nonneman AJ, Kolb BE. Lesions of hippocampus or prefrontal cortex alter species-typical
behaviors in the cat. Behav Biol. 1974 Sep;12(1):41-54.
25 Staples LG, McGregor IS, Apfelbach R, Hunt GE. Cat odor, but not trimethylthiazoline (fox odor),
activates accessory olfactory and defense-related brain regions in rats. Neuroscience. 2008 Feb 19;151
(4):937-947. Epub 2007 Dec 4.
26Gulyás B, Kéri S, O'Sullivan BT, Decety J, Roland PE. The putative pheromone androstadienone
activates cortical fields in the human brain related to social cognition. Neurochem Int. 2004 Jun;44(8):
595-600.
27Zanarini M C, Frankenburg F R. Omega-3 Fatty acid treatment of women with borderline
personality disorder: a double-blind, placebo-controlled pilot study. Am J Psychiatry. 2003;160(1):
167–169.

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237
Chapter 9: Pheromone Control of Sexual Desire

Syndromes

HOMOSEXUALITY

Addictions to other pheromones suggest etiologies for homosexuality,

pedophilia, habits of torture (sadism and masichism), the rapist’s addiction to female
alarm pheromone, foot & hand fetishes for those pheromones, nymphomania and
satiriasis.

Homosexuality differs from crime and drug addiction in that maternal

affection pheromone reception is adequate or compensating in the presence of
paternal pheromone deficiency. Vitamin deficiencies occur naturally, too, and can be
just as easily treated. Homosexuals obtain pleasures of the flesh to no reproductive
benefit and this has been accorded respect, properly so. The recovery of heterosexual
ideation and behavior by life-long homosexuals was, indeed, an unintended side-
effect of the paternal skin surface lipid pheromone gum. However, none of the twelve
former homosexuals expressed any interest in returning to the homosexual lifestyle,
preferring heterosexuality to homosexuality with definite certainty. Again, though, all
were taken aback by the transition and all would have rejected taking the pheromone
gum if they had truly believed that it would effect the change they experienced.
Homosexuals should therefore be excluded from trials or provided cooling off periods
before being taken into trials to give them an appetite for reproduction.

Homosexuals found themselves at sea and uncertain once their perversion was
discarded. Jessica Simpson, a movie star/singer who had appropriated the pheromone
gum from a trial participant, was able to marry only to leave her spouse after a few
years for a series of dancers and football players. Another movie star, Leelee
Sobieski, who took part in the open pheromone trials moved through several
relationships and is now engaged and expecting her first child. Kunis, Portman, Page,
Hilton, Lohan, Charlie Sheen and others are responding to therapy even now.

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Hollywood knows a good thing. Actors are willing Guinea pigs and their behavior is
easy to observe from a great distance.

According to Sokolov, 1 on grip surfaces of the hands, feet, and prehensile tails
of mammals, eccrine (perspiration) glands tend to predominate. The eccrine glands
produce the watery film that works with the serrations we call fingerprints to improve
traction and grip. Eccrine perspiration helps to move sebum and other skin gland
secretions over our skins. It may contribute to pheromone transmission and secretion.
Perspiration, as in intercourse, exaggerates and changes the distribution of sebum and
apocrine secretions. At the same time, recognizable chemical differences in hand and
foot secretions must be the physiological basis for compulsive hand and foot fetishes.

DISEASES OF ERSATS HUMAN PHEROMONES: LATAH

Latah is a shock-like condition in which the affected individual, a woman [or

a male homosexual-BN], mimics the movements and sounds of those nearby against
her [/his] will.2 Latah is characterized by an exaggerated motor startle response, often
with associated involuntary vocalizations, echolalia, echopraxia, and forced
obedience. Exaggerated startle to touch and often to frightening words (similar to
BOO!) gets worse or deeper with repeated stimuli. Latah sufferers are quickly
enticed to the Latah syndrome by relatives worried upon observing symptoms of
depression and/or exaggerated grieving after the passing of a husband. The intense
teasing replaces depression with Latah, but life-expectancy does improve, plus the
entire family is entertained! Latah patients should see full and complete recovery
upon oral administration of the healthy adult male facial skin surface lipid pheromone
as described in the appendix to this volume. Latah should resolve once the
pheromone deficiency is alleviated.

Recall how cholesterol esters are found more commonly in childhood and
neonatal sebums, differentiating them from adult-typical compositions?3 Higher
concentrations of linoleate are seen in child sebum, too.4 These, and other childhood-
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typical chemical species, should be investigated as candidates for a human child-
aversion or child recognition pheromone. A human child-aversion pheromone
explains the Kibbutz aversion data and find a place in semiochemical medical
practice for treatment of sexual child abuse resulting from pheromone receptor
protein deficiency in tears or blood.

Pheromonal aversion can involve nausea, probably involving the Peyer’s

patches full of microvillar cells in the alimentary tract. Disgust sensitivity predicts
intuitive disapproval of sexually perverted people,5 so pheromone aversion being the
cause of homophobia seems reasonable. Feelings of disgust can be encouraged or
overcome with training. Pica, eating dirt, is too common. Japanese people consume
raw fish. French people eat snails. Koreans quite happily dine on dogs. Some
Africans consume living grubs. Americans eat fast food. Taste is a malleable thing.

PHEROMONE DEFICIENCY ILLNESSES: DIVORCE

Perhaps divorce can be eradicated by the medical profession. Women now get
divorces and elect to leave their loving husbands (and vice versa) about half the time.
Occupations that keep the family away from heavy air pollution, such as those of
fishermen and park or forrest rangers, maintain pair bonds most reliably. Recently air
pollution has been associated with depression, anxiety, and learning disabilities.6 It
should please rejected husbands to know that the divorcing wife likely has hypoactive
sexual desire syndrome, and her promiscuous antics following separation are not
entirely her own decision. Divorced wives felt isolated from their husbands, as if he
were a stranger. This is a product of desperation, born of sexual frustration from
which husbands rarely suffer. Since pheromone reception (and pheromone
deficiency) are non-conscious, there is no conscious fault and no blame should be
laid.

The cure for divorce, just one annecdote currently, is to alleviate the paternal
pheromone deficiency of the divorcing wife or husband with 150-250 mg of healthy
adult male facial skin surface lipid p.o. Follow-up to treat hypoactive sexual desire
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EXOCRINOLOGY
syndrome (if the father-emitted pheromone proves ineffective in bringing back sexual
behavior rewards) with ten to twenty milligrams of human (husband) genital and peri-
genital sebaceous and pubic scent gland secretions p.o.--or have the husband permit
vigorous fellatio prior to consensual intercourse to improve libido. Forcing the wife
to intercourse is illegal in civilized jurisdictions and counter-productive, since anger
is prophylactic to pheromone reception. Anger in either sex engorges erectile tissue
in the nasal passages to close off chemoreceptive middle and upper meati, recall.

In the case of husband and wife, the pheromones of addiction are individually
specific. The husband loves only his wife and the wife loves only her husband in
mate mate bonding, assured by their unique chemical signatures. If any divorce
persists after this book’s publication, perhaps divorce courts will one day order
professional pheromone collection and delivery to ex-spouses as part of divorce
settlements to short circuit all of the drama and criminality of sexual passion.

Treating either husband or wife with pheromones can disturb the marriage.
Any intervention should be limited and any treatments provided should be at least
token shared by both to avoid jealousy or suspicion. A 1 milligram ‘taste’ should be
supplied to the spouse to allow them to identify and begrudgingly tolerate ‘the
intruder’ as beneficial experimental exocrinology. Otherwise an osculation
quarantine should be imposed temporarily. A small amount of wine after pheromone
oral administration may reduce jealousy as well.

1 Sokolov, Vladimir Evgen'evich 1982; Mammal Skin. Berkeley: University of California Press.
695 pages, p 21.
241
2Bartelsman M, Eckhardt PP. Mental illness in the former Dutch Indies--four psychiatric syndromes:
amok, latah, koro and neurasthenia. Ned Tijdschr Geneeskd. 2007 Dec 22;151(51):2845-2851.
3 Stewart, Mary Ellen, and Donald T. Downing 1991; Unusual cholesterol esters in the sebum of

young children. Journal of Investigative Dermatology 95(5):603-606.

4 Stewart, Mary Ellen 1992; Sebaceous Stewart, gland lipids. Seminars in Dermatology Jun; 11(2):
100-105.
5Inbar Y, Pizarro DA, Knobe J, Bloom P. 2009; Disgust sensitivity predicts intuitive disapproval of
gays. Emotion. 2009 Jun;9(3):435-9.
6Fonken LK, Xu X, Weil ZM, Chen G, Sun Q, Rajagopalan S, Nelson RJ. Air pollution impairs
cognition, provokes depressive-like behaviors and alters hippocampal cytokine expression and
morphology. Mol Psychiatry. 2011 Jul 5;. [Epub ahead of print]

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Chapter 10: Pheromone Reception & Disease

! Throughout the course of medical history, distinct syndromes of unknown

etiology eventually find causation from a single root. Although many different things
seem to cause the same disease, when worked out, many different things never cause
anything. One disease, one cause. Thus malaria is caused by plasmodia vectored by
several different mosquitos. (It is misnamed, instead of “bad” swamp “air” disease, it
should be plasmodiasis.) From this long history of ever one disease: one cause, it is
intensely irritating that so many psychologists and their sympathizers among the
medical profession today adamantly and incomprehensibly attribute multiple causes
for virtually every idiopathic syndrome. Such incompetence is an embarrassment to
medicine and to science.
Our model provides an economic single justification for pheromonal sociopathy
and disease. The moderation of pathological intensity from nuisance to mortal
consequences enhances the model and explains experimental sociopathological
findings.
Now, encouraging partial case reports give us hope to control autoimmune,
other heretofore idiopathic ills, and cancer. With biochemical tracing of neurological
pathways in the brain, the ‘surprising’ abundance of human chemosensory pathways
allows the present chapter’s investigation. (If we cannot follow pheromones
themselves, we can at least follow the neurological pathways of neurons that respond
to pheromones. Happily, these pathways have been traced with good resolution.) For
pheromones to control these ills, the nerves that respond to pheromones must be
found in disease associated neuroendocrine tissues thought to control these ills. And
where pheromones fail, as in alcoholism, there must be a dearth of such pheromonal
central nervous system innervation involved in alcoholic reward centers of the brain.
This was proved to be true.

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 Humans die appropriate to population needs to maintain the hobbled
population equilibrium that got humanity this far. That is also what economics
demands if you take things to the Panglossian extreme as we have. Without the
feedback devices (pheromones) killing humans to maintain our numbers to available
resources, now it will be up to us. Human individual demise selection in an epidemic
is accomplished via human pheromones. This is just like pheromones regulating
population fertility of bacteria in an enclosed vial. Criminal behavior, susceptibility
to addictive drugs, perversion, autoimmune disease, and cancer: all can kill, prevent
or limit reproduction, or enfeeble offspring and all are essentially pheromonal.
Indeed, the evolution of autoimmune illness and sociopathy in humans and
domesticated animals may have resulted from human care-giving.

Physicians must utilize objective criteria to monitor patient welfare or well-

being. Evidence-based patient management requires that the physical exam cover
behavioral and cognitive pheromone challenges and responses systematically.
Human pheromones, the most potent of any drug class by orders of magnitude, must
be utilized to attempt to threat these diseases. Some inadvertent successes and fruits
of economic calculation augur well for near term success.

Olfaction nerve CNS pathways run with pheromone recognition pathways

some of the time as these afferent nerves coarse toward and through the brain. The
parallel arrangement allows communication between inputs which may include gates
or shoves/encouragements of capacitance via dendritic capacitance ‘analog
switching’. Please see Chapter 11. Future examination of the semiochemical
recognition areas of the brain may bring notice to these areas being damaged more
than their olfactory running mates in autoimmune disease. They might even compare
them to normal ones and find a soluble pheromone receptor protein/pheromone
etiology.

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EXOCRINOLOGY
Some sort of poisoning via the retrograde neural transport system from
olfactory mucosa to the CNS was suggested as the cause of Alzheimer's disease years
ago.1,2 The olfactory tract's neural transport system could accommodate pheromone
receptor-proteins as well as pheromones and anti-pheromones and these possibilities
must be explored systematically.

The invariable finding of severe and even maximal involvement of the olfactory regions in
Alzheimer’s disease is in striking contrast to the minimal pathology in the visual and sensorimotor
areas of the neocortex and cannot be without significance. In the olfactory system, the sites that are
affected—the anterior olfactory nucleus, the uncus, and the medial group of amygdaloid nuclei—all
receive fibres directly from the olfactory bulb. These observations at least raise the possibility that the
olfactory pathway is the site of initial involvement of the disease.
[A] large majority of patients with Parkinsonism has olfactory dysfunction, as measured by
tests of odor identification and detection. This disorder seems to be (1) stable over time, (2) present
relatively early in the disease process, (3) general in nature, (4) independent of motor and cognitive
aspects of the disease, and (5) indistinguishable, at present, from the olfactory disorder observed in
Alzheimer’s disease. 3

People with Parkinson's, and other neurological disorders secrete sebaceous

secretion copiously.4 A sebaceous, kiss-transferred, addictive pheromone5 would thus
provide an increased incentive for patient maintenance by the family and predicts
more family accommodation for them.

Fruit flies see a lone pheromone receptor protein homologue in their

hemolymph in response to viral infection, with receptor proteins themselves strongly
expressed during metamorphosis, suggesting that they participate as chemosensory
molecules in tissue remodeling.6 Thus improves the case that pheromone receptor
proteins must surely be active during embyological development of the human being,
and susceptible to pheromonal influence to account for the currently unknown
etiologies of birth defects and still-birth.

Indeed, resistance or immunity of pathogenic bacteria to antibiotics is

pheromone based,7 as is pathogenicity.8 Evolving from bacteria, we should be able to
respond in kind, would you not think so? After all, individual cells of the body have
not lost the sense of smell, so necessary to life as colonial bacteria. Indeed, assembly
into an organism should require greater cellular chemosensory acuity, and greater
specialization.

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ANGER or AGGRESSION PHEROMONE IN AUTOIMMUNE

DISEASE:

Anger pheromones 9,10 may logically be suspected of both neurotoxic and

autoimmune pathogenicity. Incurring wrath might indicate diminished usefulness for
group survival and may be directly poisonous by pheromone. A righteous wrath, as
when the victim agrees with the emitter/perpetrator and tears-up at the rebuke
(enhancing receptivity), might be more poisonous still. Because superior and middle
meati of both nasal passages close off by anger-stimulated erectile tissue
engorgement,11 therefore anger must itself be prophylactic against auto-reception.
Thus, self-righteous anger is also tonic against the unjust wrath of others. The hardy
survival of angry and mean patients on the wards is well known to every physician
and illustrative.

The evolution of this device becomes warranted when one considers the
following. A hunter-gathering group rid of slackers would be expected to outperform
those groups lacking an efficient mechanism to dispose of their unprofitable hangers-
on. In the absence of effective predators, healthy group members inconvenient to the
group could suffer timely demise semiochemically via any number of means,
depending upon population needs. 12 Violent criminal behavior would be conspecific
predation under this model and was examined elsewhere in the previous chapter.
(Similarly, the presence of ‘pet-food’ isles in grocery stores is solid evidence for
semiochemical parasitism.)

Candidates for anger pheromones, antipheromones, and pheromone-binding

proteins might be found in human saliva. Anger pheromones appear in rodent
saliva.13,5 Watching angry medical school professors screaming with rage, they do
seem to spit tiny hate packets of saliva, sometimes it lands on their beards or even
their eyebrows. (No wonder judges and priests sit up high and wear robes with all the
self-righteous sputtering?) If one must communicate with an angry fellow human
being, doing so by telephone or other electronic means may be the safer strategy.
Howard Hughes thought so.

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EXOCRINOLOGY
Perhaps some anger pheromones may be found among the chemically reactive
conjugated dienes of the human male scalp, 14 since "blowing one's top" may indicate
increased emissions from scalp scent glands. Given the susceptibility of sebaceous
secretions to heat,15 "hot heads" may be semiochemically dangerous to health.
Systematic testing of various chemical species against psychogenic lachrymal fluid in
the presence of sensitive electrodes and under UV examination for conformational
change would be a logical place to begin.

AUTOIMMUNE NEURODEGENERATIVE DISEASES:

ALZHEIMER’S DISEASE

Alzheimer’s disease affects the olfactory nerve with a rhyno-central

progression suggesting initial insult via the olfactory nerve.16

Aberrant expression of 14-3-3 proteins is associated with both Alzheimer’s

and Parkinson’s diseases. The insect homolog is found widely, but includes antenna
and pheromone glandular locations, suggesting pheromone receptor protein function,
along with its association with Heat Shock Protein 60 (Hsp60) 17 Hsp10 is also a
partner with Hsp60 to provide the two conformations needed for functionality as
dissolved pheromone receptor proteins (PBPs or Pheromone Binding Proteins in
other discussions in this book). Hsp10 interacts with “deoxyribonucleic acid
checkpoint inactivation, termination of M-phase, messenger ribonucleic acid export,
import of nuclear proteins, nucleocytoplasmic transport, and pheromone signaling
pathways.” “Recent data suggest that Hsp10 may be not only a component of the
folding machine but also an active player of the cell signaling network, influencing
cell cycle, nucleo-cytoplasmic transport, and metabolism, with putative roles in the
lack of cell differentiation and in the inhibition of apoptosis.”18

Idiopathic inflammation is thought to be the cellular basis for Alzheimer’s

disease. Inflammation is essentially an alarm pheromone response of the body’s
individual cells and soldier cells called by those individual cells by scent emissions,
just like ants and termites.
247
 NSAIDs affect alarm pheromone reception responses of the body. So does a
mist of aspirin calm bees as well as smoke?

AGE RELATED MACULAR DEGENERATION

Since a diet high in omega-3 fatty acids such as those from fish oil improves macular
degeneration outcomes in women, 19 it seems reasonable to expect that the human
pheromone that these two chemicals resemble might prevent this unfortunate
outcome. Testing will tell.

SUBORDINATE PHEROMONE in SUDDEN INFANT DEATH

SYNDROME (SIDS), BLIGHTED OVUM, BIRTH DEFECTS,

ANOREXIA NERVOSA, BULIMIA NERVOSA, OBESITY, and

INFERTILITY

Prolonged stress warps reproduction to adjust population fertility to stressful

circumstances, reducing gametogenesis & libido, elevating still-birth rates, and
inflicting poor prenatal and maternal care of children. Pheromones emitted during
stress may provide positive evidence to stimulate those difficulties, but lack of
pheromone reception can accomplish the same ends. Conflicting inputs suggest that
pheromones can work in opposition to blunt or counteract each other, similar to the
way hormones can be seen to work in opposition. Of course, that has been the
observation from anecdotes so far. Economically, pheromones must be involved with
all reproductive behavior/libido, from behavioral fertility, gametogenesis, conception,
gestation, growth and development to maturity and old age. The delivery of stress
information to the individual human being cannot be entirely hormonal, and once the
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pheromone has been received, an acknowledgement signal pheromone may be
needed. Poor wound healing, enhanced disease rates, shortened lifespans, female
acyclicity, high infant mortality and cardiovascular disease depend upon stress, too,
and provide opportunities to utilize oppositional pheromones (like ‘kissing’
pheromones) to relieve them. It is likely that the pheromone responsible for Anorexia
Nervosa is the axillary stress pheromone responsible for most of the effects of stress
on reproduction and on populations generally.

Why? Pheromones limit species fertility to available resources.20, 21

Pheromones are why Malthus was all wrong. Subordinate pheromones are typical of
stressed, grouped fertile females and emitted by puberty-delayed adolescents22 and
human anorexia nervosa sufferers and their poisonous dyads.23 On the same
continuum as delaying puberty are behavioral infertility, obesity, physical infertility,
blighted ovum, spontaneous abortion, birth defects, sudden infant death syndrome,
physical child abuse, sexual child abuse, juvenile delinquency, running away, criminal
behavior, homosexuality, sadomasochism, homosexuality, fetishes and other sexual
perversions. All diminish effective population fertility and are, or must surely be,
controlled by human pheromones. Liberal administration of healthy adult (over 30
for methylation) male facial skin surface lipids p.o. in doses around 150-250 mg
should diminish the burden considerably.

Pheromones kill fetuses and cause their resorption in laboratory animals,24, 25

yet before this author’s landmark paper in 2001, the possibility had never been raised
that pheromones could explain the nearly identical phenomenon in human beings.
(Given the ubiquity and credence for such laboratory animal testing as medical
research to be applied to medical treatment of human beings, this thinking deficiency
is difficult to explain.) Unexplained spontaneous abortion and blighted ovum must
have pheromonal cause in humans.

Subordinate female-emitted pheromone is even more suspect in sudden infant

death syndrome (SIDS) and an axillary semiochemical phero-pathogen appears most
likely. 26 Coleman-Phox Odouli and Li found that the use of a fan during sleep
reduced the risk of sudden infant death syndrome,27 suggesting an airborne pathogen.
Airborne pheromones travel in plumes of sufficient concentration to be
249
recognizable.28 Surely then, pheromone plumes are being disrupted by the fans used
to cause the observed protection from SIDS, preventing or decreasing the reception of
poisonous human pheromone. The effect was more pronounced if the nose was less
well exposed and with higher temperature (higher axillary emissions from the
poisoner). The protection diminished with the use of a pacifier, which increases nasal
breathing past chemoreceptive mucosae. Everything fits.

SIDS is common in infants only after they attain six weeks of age, and the
protection during the neonatal period baffles other thoughtless investigators.29 In a
striking early observation, Darwin noted psychogenic lachrymation only after the first
six weeks of age. 30 This is the neonatal protected period, and recognizing that tears
function in pheromone reception, then an exocrinological SIDS etiology is
demonstrated. Subordinate maternal axillary emissions due to stress and low
hierarchical status (relieved somewhat by increased status) are the most likely culprits
for sudden infant death syndrome, and covering the mother's axillae with petroleum
jelly whilst she is in an apneaic infant's breathed atmosphere must be taken as a
prudent and easy precaution.

As precaution against stillbirth and blighted ovum, withholding other male

‘kissing’ pheromones from pregnant, lactating, or potentially pregnant females is a
reasonable precaution to avoid any human Bruce effect killing of fetuses. Wives with
husbands might also be omitted to save the ladies semiochemical discomfort from
jealousy.

The anger pheromone alluded to above is also a candidate with either parent
the potential source. In which case, admonishing parents to never dispense anger
pheromone over helpless infants may suffice to diminish our population’s burden of
SIDS and failure to thrive victims. Needless to say, pheromone-barrier shower caps
may replace wigs and high rostrums in courts of law, if courts and laws are even
necessary once pheromones are under control.

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EPILEPSY

Right temporal lobe epileptics complicated by depression have hippocampal

atrophy that cannot be explained by epilepsy alone. 31 Similarly petite mal epilepsy
has been treated effectively with the paternal pheromone in just one case. Alarm
pheromones cause convulsions in rats treated with the tri-cyclic anti-depressant,
imipramine.32 Epileptogenic tissues of the central nervous system are all pheromone
reception pathways and association areas.

AUTISM

An autistic child pays little attention to parents, or anyone. He conserves his

energy. Autism must be pheromonal. Genetically identical twins can express autism
in a single sibling. Families in which one monozygotic twin is diagnosed with autism
spectrum disorder, the second twin is unlikely to receive the same diagnosis after
elapse of twelve months.33 This suggests economic titration.

Experimental pheromone deficits give mice symptoms of autism.34 In

humans, autism causes significant reductions in grey matter volume of medial
temporal, fusiform, and cerebellar regions.35 Cerebellar atrophy must be
consequential damage, since the cerebellum is unassociated with either pheromone
reception or olfaction. However, the right orbitofrontal cortex, right fusiform cortex,
and right hypothalamus respond to airborne natural human sexual sweat. 36 Young
children with autism spectrum disorders show more olfactory sensitivities than
children with other developmental delays. 37 The olfactory and pheromone
recognition pathways (both chemoreceptive, after all) run parallel for much of their
runs, recall. Pheromone recognition and reward systems for socialization can account
for all symptoms of autism.

Recall that twelve cases of sexual perversion have been remedied with human
adult male facial skin surface lipid by mouth, demonstrating that pheromone
reception is, itself, subject to pheromonal regulation. These observations suggest a

251
poisonous pheromone reception as the cause of autism. Early onset (after the six
week pre-lacrimation hiatus) suggests a parental source.

Predictions, anyone? Of course some central CNS damage must be

pheromonally inflicted, but there are simpler explanations for symptoms. The autistic
child would have chemically strange emotional tears, perhaps with fewer pheromone
receptor proteins, or with inactivated/poisoned pheromone receptor proteins, or even
aberrant lachrymal ionic concentrations.

Autism, like physical child abuse, may be semiochemically treatable.

Parental facial skin surface lipids provided to the autistic child by mouth should
provide full recovery when treated early to avoid the consequential cell death
cascade. Differential parental solicitude in identical twins would thus account for
differential pheromone reception histories predisposing for the illness. Measuring
that may prove more difficult than just trying various doses of parental love
pheromones for those already autistic. Perhaps in concert with intravenous epigenetic
therapy for resistant cases, maternal and/or paternal facial or other (areolar?)
protective skin lipids can be therapeutic?

The possibility of helpful omega-3 fatty acid treatment in autism38 is

suggestive that human skin surface lipid pheromone may have important therapeutic
effects. Omega-3 fatty acids are, after all, only poor substitutes for the
stereochemically similar human skin surface lipids.

POST TRAUMATIC STRESS DISORDER RESOLVED BY

PHEROMONES

PTSD patients display smaller amygdalae and reduced anterior cingulate gray
matter density on MRI scans of the brain.39 Reductions have also been found
hippocampus and rostral anterior cingulate cortex in PTSD. 40 Thus, PTSD is
impaired extinction of fear. 41 So why would we need biological cowards? Now that
question can be answered.
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The two amygdalae are pheromone association areas of the brain. You see,
animals need to back off the established territories of their conspecifics to avoid chaos
in divisions of resources for feeding and breeding, they need innately respect the
property of others and without law and order, they need to be biologically afraid.
This is why Konrad Lorenz’s trespassing rats climb trees in fear of smaller rats who
had previously and quite carefully marked their territory.

Omega-3 fatty acids may provide relief from PTSD. 42 Fish oil seems to be a
poor substitute for kisses. The similar human kissing pheromone mixture, synergistic
and species-specific, must be even more beneficial against PTSD.

The treatment for PTSD is located at the end of this volume. That protocol
essentially increases one’s hierarchical status, biologically increasing the rank of the
patient. Post Traumatic Stress Disorder now becomes a trivial affliction, easily
remedied, with serial administrations of 150 to 250 mg of healthy over 30 year old
adult male facial skin surface lipid by mouth on a chewing gum vehicle. The MRI
should note improvements and guide titration of the dose, first observing then
allowing for regeneration time. Over doses of the facial skin surface lipid would
reward cowardly privates with artificially enhanced self-confidence of major
generals, and thus these should be avoided. Officers in the field can stimulate resolve
and increase morale by providing soldiers with the paternal facial pheromone, as well
as the pheromones of loved ones left behind.

Ancient war fighters leave no reports of PTSD in returning veterans.

Pheromones are why. We scrub our soldiers clean to protect them from disease but
that destroys the microflora that give them band loyalty. The same microflora are
transferred by handshaking and backslapping. In addition, our soldiers suffer from
pheromone deficiencies that cause difficulties during their service as well as upon
their return.

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ALARM PHEROMONE IN INFECTIOUS DISEASE

SUSCEPTIBILITY AND CANCER

At this author's suggestion, alarm pheromones were tested to demonstrate their

ability to affect immunity, suppressing cell-mediated immunity and enhancing
humoral in laboratory mice.43 Alarm and anxiety in human beings diminish disease
resistance44 and predisposes to cancer. 45 Pheromones of alarm in humans diminish
resistance to the cancer cells that are thought to arise spontaneously, giving rise to
cancers. As the author has had no interest in oncology and only the slightest training
in medical school, this area will be left to others. The first place to begin will be to
observe for beneficial effects of skin surface and other pheromones in cancer patients
of all types and stages, then onto anti-stress pheromone manipulations. Stressful
pheromone emitters in waiting rooms on cancer wards likely increase cancer risk.

AUTOIMMUNE DISEASE: DIABETES

Type I Diabetes (known as juvenile onset or insulin dependent diabetes

mellitus) should respond well to oral administration of adult male facial skin surface
lipids of about 150-250 mg doses as needed. This human male facial skin surface
lipid pheromone therapy has never been tried, but given its innocuousness (the
equivalent of kissing Daddy a lot), it should be. The author predicts that progression
of the disease will be halted, perhaps with full and immediate recovery. Full recovery
even after the loss of all beta pancreatic cells may be had with pheromone therapy
alone, but almost certainly with epigenetic therapy.

Why does the author have such high hopes for curing this illness? After all,
nothing else has ever worked.

The disease provides human population ecological benefit in a reliably regular

syndrome: it kills people quickly. Expedient jettison of underperforming troupe
members would be a hallmark of Type I Diabetes. Secondly, diabetes is described as

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an acceleration of aging, and pheromones can affect the insulin signaling pathway to
enhance experimental longevity.46, 47

In small open trials, the healthy adult male facial skin surface lipid pheromone
seems to reliably halt the progression of Alzheimer’s disease, an autoimmune disease.
The eating disorders have characteristics of autoimmune disease, too, and they have
autoimmune characteristics. The prospect for pheromone and epigenetic therapies
gives hope for all autoimmune disease sufferers everywhere.

Given that modernity has seen dramatic increases in the prevalence of Type
II, while Type I is no more prevalent than in olden times, air pollution is unlikely to
be involved in the etiology for Type I but it might be for Type II. That would put
Type II and Alzheimer’s disease in the same category of increasing prevalence.

The seasonal onset of Type I in winter and early spring suggest closer
proximity to the pathological pheromone emitter from cold huddling. Critical periods
of susceptibility between ages 5-7 and 11-13 suggest sinus development specific to
those ages increases risk of developing Diabetes Type I. Thus a larger, heavier,
specifically targeted chemical would first insult a person to diabetes, perhaps a toxic
pheromone receptor protein. The episodes of pheromone reception (tears in the
patient) and emission (anger/disappointment in the pheromone poison source person)
associated with onset episodes are also indicative.

The Human Lucocyte Antigen (HLA) can be discerned via pheromonal human
chemosensory analysis,48 while HLA antigens, particularly DR3 and DR4, have
strong association with Type I Diabetes. Pheromone receptor protein (murine major
urinary protein-1) abundance in the liver is affected by the insulin-sensitizing drug
rosiglitazone,49 which is highly suggestive, while the same pheromone receptor
protein regulates glucose and lipid metabolism,1, 4 both of which are disjointed in
diabetes.

Diabetes diminishes olfaction and may even cause complete anosmia, while
insulin can improve olfaction in mice. 50 Diabetic and non-diabetics have different
protein sets in their olfactory bulbs. 51

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 The sex ratio of 3:1 females to males preponderance likely puts Type II into
the volatile pheromone group (along with most autoimmune diseases), since sex
ratios of pheromone induced puberty delay (AN) are similarly skewed male.

The resolution of diabetes gravitas with delivery suggests that feto-receptor

proteins also clearing the system with delivery, may be involved, too.

Moreover, a biochemical process for the cause of diabetes has recently

presented itself. The reader will remember that medium and especially long chain
free fatty acids of unusual chain length, unsaturation position, methylation, etc. are
proposed to be human pheromones (see Chapter 3). Free fatty acid receptors,
GPR120 and GPR40 whose endogenous ligands are medium- and long-chain free
fatty acids, are thought to play an important physiological role in insulin release. 52 If
these puppies are pheromone receptors (which they certainly are), then their
stimulation with the pheromone of the human face should benefit normal release of
insulin, opposing Diabetes Type I and II, curing or at least halting the progression of
diabetes.

AUTOIMMUNE DISEASE: JURJANI’S OR GRAVES DISEASE

The sex ratio of 5-10:1 females to males preponderance likely puts Graves
disease into the volatile pheromone group (along with most autoimmune diseases),
since sex ratios of pheromone induced puberty delay (anorexia nervosa) are similarly
skewed male. Frequent adolescent onset also is suggestive for the same reason.
Waxing and waning of symptoms suggests pheromone etiology, too.

Excessive lacrimation is a symptom of Graves‘ ophthalmopathy, and given

that pheromones have been discovered in emotional tears recently at this author’s
suggestion53, lacrimation in excess may signal the pheromone receptivity necessary to
overcome the illness.

The improvement of some clinical symptoms with beta-blocker therapy has

suggested disruption of adrenergic pathways between the locus ceruleus and the

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frontal lobe.54 Both brain structures maintain pheromonal neural pathways.55 56 57
Thus pheromone therapy alone or combined with epigenetic chemotherapy should be
curative.

AUTOIMMUNE DISEASE: LUPUS

Inflammation is a pheromone-mediated response, generally. Systemic lupus

erythematosus (SLE) waxes and wanes as a pheromone-mediated condition might.
This suggests episodic activity. Lupus’ association with stress suggests the sebaceous
anti-stress pheromones should diminish attacks.

Lupus responds to NSAIDs, which are anti-pheromonal. Response to

NSAIDs is a red flag for pheromone-mediated ills. The body’s defenses like
inflammation, can be stimulated by alarm pheromones. 58 Non steroidal anti-
inflammatory drugs block the breakdown of long chain free fatty acids.

Lupus also responds to anti-malarials. Quinine, which, like aspirin, derives

from tree bark and serves as anti-herbivory allomones. (Quinine and indeed, the
caffein in tea and coffee, are both insect repellants/antifeedants and the same fruit fly
taste receptors for them also detect the male-avoidance cuticular pheromone. 59)
Qinidine is a diastereometic stereoisomer of quinine (roughly same chemicals, same
bonds, but “different handedness”). Quinine helps lupus, quinidine can cause a form
of lupus, both are telling.

Quinidine, procainamide, hydralazine, isoniazid, and phenytoin may cause

appearance of anti-nuclear antibodies that signal for lupus in the blood and reversible,
drug-induced lupus symptoms. Qinidine and procainamide are both local anesthetics
that diminish cardiac arrhythmias. Qinidine is, as mentioned, the diastereomer of the
anti-malarial quinine and found with it in the cinchona tree bark. Like many
pheromones that depend upon stereochemical shapes, the effects of qinidine and
quinine differ dramatically in their medicinal effects on humans. Procainamide helps
some arrhythmia patients that fail to respond to quinidine, and marked variation in
bioavailability of an active metabolite seems to be genetically (or perhaps
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epigenetically) dependent. Procainamide is a derivative of procaine anesthetic which
renders animals temporarily anosmic, unable to smell.

Hydralazine lowers blood pressure, another likely pheromone-mediated illness

since blood pressure responds to stress. Hydralazine also seems to improve murine
multiple sclerosis,60 another likely pheromone-mediated illness (in humans).
(Interestingly, CNS myelin--white matter, degraded in MS, is promoted by maternal
pheromone of the lactating rat. 61)

Isoniazid is, of course, the anti-TB antibiotic that will turn the urine orange.
Anti-biotics as a class are allomones or artificial allomones. Isoniazid also has anti-
depressant activity and is among the most common causes of drug-induced seizures in
the US.62

Phenytoin is the Dilantin used to diminish epileptic seizures. Epileptic

seizures seem to respond to human pheromone anecdotally. Phynytoin, like
procainamide and quinidine, acts as a cardiac anti-arrhythmia drug.

Abnormal protein levels in the urine associated with lupus indicate kidney
involvement. The kidneys in many species emit protein binding proteins as
pheromones in exactly the same way as lupus affected kidneys. A lipocalin (a protein
family that includes pheromone receptor proteins) is a biomarker for lupus
nephritis.63, 64

Brain deficits in severe SLE can be localized to the cerebellum’s atrophy. The
cerebellum in humans: fine motor skills. The cerebellum’s neuron generation is
affected by pheromones in goldfish.65

Being first to suggest that SLE is a human pheromone response means that all
these secondary associations are the only ones available. Hopefully, epigenetic and
pheromone therapy will alleviate this illness or at least ameliorate its course. Once
the pheromonal poison responsible for systemic lupus erythematosus is discovered,
semiochemical aseptic techniques and interventions may prove to be of therapeutic
benefit.

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EXOCRINOLOGY

AUTOIMMUNE DISEASE: ARTHRITIS

Pheromones must control the incidence of juvenile rheumatoid arthritis.

HLA-B27 histocompatibility antigen is associated with risk of evolving
spondyloarthropathy in older boys with pauciarticular JRA. HLA-B27 heavy-chain
homodimer formation can be induced by dendritic cell activation.66 Dendrites, the
reader will recall, are the nerve cell ‘roots’ that respond to pheromone receptor
protein activation as explained in Chapters 6 &7 of this volume. So, pheromone hits
pheromone receptor protein, which activates the dendritic cell, which induces HLA-
B27 to poison the joints in arthritis some way we do not yet understand.

Weaker HLA associations exist for other subtypes (HLA-DR5, HLA-DR8,

HLA-DR4). Of course the HLA Human Leucocyte Antigen or Major
Histocompatibility Complex is just a dense set of genes on chromosome #6. The
MHC (the name of this homologous area for all animals except humans) controls
immunity and chemorecognition, which includes pheromone recognition. Of course,
pheromone recognition is, essentially, the immune system’s ability to detect self from
non-self. MHC class I (not olfaction located in the class III area) generated proteins
respond to pheromones to block pregnancy in the mouse.67 And the MHC class I
genes influence the amounts of testosterone-mediated pheromones.68 The skin
surface lipid human pheromone (see appendix) may halt the progression of
rheumatoid arthritis.

Flooding pheromone reception pathways with ‘good father’ pheromones via

the protocol in the appendix should alleviate arthritis and return early onset patients
to good health. Concomitant epigenetic therapy with DNA hypomethylation drug 5-
azacytidine or equivalent may be needed to ‘reset’ cell nuclei for the influence of the
new pheromone, particularly when remodeling of tissues to normal is promoted.
Alternatively, epigenetic therapy may not be required, since DNA hypomethylation
has been observed in rheumatoid arthritis synovial fibroblasts 69 implicating a
pheromonal or pheromone deficient causative hypomethylation. We should try the
pheromone alone first, and then go from there.
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AUTOIMMUNE DISEASES: DEPRESSION

General anesthetics like halothane, enflurane, and ether inhibit GABA,

gamma-aminobutyric acid, catabolism in the brain. That leaves more GABA, for
more neural inhibition, for more anesthesia to avoid the pain and memory of surgery,
maybe. Basically, general anesthetics are just harmless solvents that loosen up the
oligodendritic (connected) and Schwann cell (unconnected) capacitors that run up and
down most nerve axons, increasing the dielectric in the gaps between capacitance
holding conductive ‘foil’ and keeping signals from accomplishing saltatory
conduction. See Chapter 11.

Metabotropic gamma-aminobutyric acid(B) (GABAB) receptors for the major

inhibitory transmitter GABA, together with metabotropic glutamate (mGLuRs)
receptors, the extracellular calcium-sensing receptors (CaSRs), some V2R70
pheromone receptors and T1R taste receptors, belong to the family of 3 G-protein-
coupled receptors (GPCRs). GABAB receptors are known to control neuronal
excitability and modulate synaptic neurotransmission, playing an important role in
many physiological activities. These receptors are widely expressed and distributed in
the nervous system and have been implicated in a variety of neurodegenerative and
pathophysiological disorders including epilepsy, spasticity, chronic pain, depression,
schizophrenia and drug addiction. 71 Drug addiction’s cure will soon be a fait accompli
and its cure should eventually drag the others into the light as well.

To form a functional receptor entity, GABAB receptors must exist as a

heterodimer consisting of GABAB1 and GABAB2 receptor subtypes with two 7-
transmembrane proteins, and these subunits arise from distinct genes. The GABAB1
subunit binds the endogenous ligand within its extracellular N-terminus, whilst the
GABAB2 subunit is not only essential for the correct trafficking of the GABAB1
subunit to the cell surface, but is also responsible for the interaction of the receptor
with its cognate G-protein.10

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Sound familiar? The GABAB1 subunit seems to be a pheromone receptor
protein and probably does absolutely no ferrying or ‘trafficking’ of any kind. The
reason it is responsible for the interaction of the receptor is because it is changing
conformation (the reason for the sulfide bridges, etc.) to release or display ions to
alter nearby dendritic potential difference: voltage. Voltage, depolarization from
chemical ion presence just outside the dendrite is perceived centrally via EPSP.

Post-partum depression is induced usually on the third day after birth just
before fourth day neonatal emissions onto kissable skin surfaces of sebaceous
pheromone. PPD stimulates lacrimation with bond-enhancing pheromone receptor
proteins in it. (See chapters 6 & 7.) The cure for this post-partum depression might
be to transfer sebaceous secretions of the forehead and face of the neonate or infant
during the first year of life into the mouth of the post-partum depression patient. That
is what the pheromone receptivity is there for, after all, to bond the mother to the
infant. The extreme receptivity of post-partum depression may be compensating for
some other difficulty in the pheromone recognition system as it is seen less in
experienced mothers, so this is probably not autoimmune in nature at all, except
perhaps in the general sense.

Depressed people shed slightly more emotional tears than people not suffering
from depression and there is a sexual dimorphism of tears and of depression with
female preponderance. Perhaps depression is just a state of extreme pheromone
receptivity that feeds back on itself, perhaps due to pheromone poisoning by some
‘hot head.’ Oral administration of 150 to 250 mg of healthy adult male facial skin
surface lipid taken by mouth on chewing gum vehicle should alleviate the condition
instantaneously with or more probably without coordinated epigenetic therapy.

Fluoxetine, an antidepressant in humans, disrupts reproductive behavior in

goldfish72 and rats.73 Exposure to female pheromones during pregnancy causes
postpartum anxiety in mice.74 All are suggestive even if you have to think about it a
little.

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AUTOIMMUNE DISEASE: ANKYLOSING SPONDYLITIS

Ankylosing spondylitis is strongly associated with the major

histocompatibility complex (MHC) class I antigen HLA-B27. Multiple diverse
infections and allergies were seen in these patients.75 HLA-B27 is observed on
dendrites after their stimulation.33 Recall that pheromones interact with pheromone
receptor proteins released from dendrites into intercellular spaces to stimulate
dendrites in the model of chemosensory transduction explained in Chapter 7 of this
tome.

Here is a good time to point out that this broad spectrum psychopatholytic and
anti-autoimmune human pheromone is so obviously innocuous (people never despair
of kissing, do they?) and so readily available everywhere (male researchers need
literally look no further than the ends of their own noses), that clinical trials of the
pheromone should be brought rapidly against every disease, illness, or condition.
Physicians remember how many years they tolerated bacterial stomach ulcers while
literally holding the tools to defeat it in our idle hands. A sample protocol is
appended with clear instructions to patients, physicians, pheromone donors, and
technicians to begin clinical trials to test the benefit of healthy adult male facial skin
surface lipid p.o. instantly.

AUTOIMMUNE DISEASES: ASTHMA

Vasopressin exerts a local anti-inflammatory effect on the lung through the

V2R in a murine model of sepsis.76 It would make sense that pheromone receptors
(V2R) of the lung would be involved in asthmatic attacks. Lung inflammation may
be influenced by perception of pathogenic pheromones (kairomones to us) emitted by
pneumonia’s various septic causes as well as detrimental human pheromones setting
them off. V2R and V1R pheromone receptors may be among the huge contingent of

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microvillar pheromone sensory cells that cover so much of the human upper
respiratory system.

Among the first allergens in animal dander to be categorized is a lipocalin,77

an obvious pheromone reception protein in this book’s model of pheromone
reception. Dander is generally pheromonal to the species from which it comes, it
erupts from the skin and has species-specific value.

In addition to pheromone-laden dander, pollens being gametes emit

pheromones and even allomones,78 yes, as do mold spores (more gametes), house
dust (mites),79 and feather pillows (the reader will remember the uropygial sebaceous
glands of waterfowl from Chapter 3 on pheromone chemistry) are also common
allergens. Various low molecular weight chemicals can cause occupational asthma80
among these are isocyanates which have pheromonal effects in a number of
species,81,82 aldehydes which are also commonly pheromonal, 83,84 as are anhydrides85
colophony,86 sulfates, 87 amines, 88,89 acrylates,90 dyes are used to trace pheromones and
pheromone reception pathways,91 and, of course, metallic salts especially odd
metallic salts, take key roles in pheromone reception. Oh my! Everything that
triggers asthma is or is potentially of a pheromonal nature. Perhaps that is because
asthma is itself, a disease of pheromonal etiology or perhaps it is mere coincidence.
Testing can find out.

As asthma waxes and wanes, and since many, nearly half of juveniles ‘grow
out’ of it reaching adulthood, asthma should respond favorably to oral administration
of 150-250 mg of human adult male facial skin surface lipid on a chewing gum
vehicle. Please see appendix for protocol, collection method, and so on.

263
DISEASES OF ERSATS HUMAN PHEROMONES: CRIME AND

OBSESSIVE COMPULSIVE DISORDER

Criminal behavior and obsessive compulsive behavior can be attenuated by

brain surgery, commonly called lobotomy, to the human pheromone reception,
association, and processing pathways. The surgery was developed empirically from
beneficial CNS injuries with outcomes training the surgeon and guiding the knife (or
icepick) to the orbitofrontal area of the brain through the ocular orbit by lifting up the
eyelid.

Criminal behavior and OCD share dysfunction of the prefrontal-striatal-

thalamic circuit. The orbitofrontal area unconsciously processes
pheromones92,93,94,95,96 with the majority of reports in humans. Orbitofrontal lesions
may produce abnormal social conduct. 97

The amygdala processes pheromones, too, another area for lobotomizing

surgeons bent on curing violent compulsive psychopaths. Gray matter density in the
left superior temporal lobe and the left orbitofrontal cortex diminishes in suicidal
schizophrenics.98 The two amygdalae and the orbitofrontal cortex limbic network
underpin the neurobiological basis of psychopathy (attempted murder, multiple rape
kidnappings).99,100 Schizophrenic psychopaths have blunted amygdala responses to
fearful faces. 101 Interestingly, left amygdala volume diminishes and right amygdala
volume increases with severe early institutional deprivation.102 These disturbances of
pheromone processing will abate with paternal facial skin surface pheromone therapy
and MRI scanning can provide documentary evidence of cure.

Human pheromone deficiency of both the parents typifies criminal behavior

(stealing property, gambling, robbing, burglary, truancy, delinquency). Recall a
sufficiency or excess of maternal facial skin surface lipid coupled with a deficiency of
paternal facial skin surface lipid seems to result in homosexuality. Criminal gang
loyalty might result from paternal deficiency and/or maternal deficiency temporarily
sated by gang comfort pheromones and the paternal pheromone deficiency
amelioration of criminal thrills.
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Criminal behavior declines in high winds,103 plausibly because high winds
dissipate autoemissions or victim emissions during crimes which attenuate the
paternal pheromone deficiency. Criminal behavior increases with ground-level ozone
concentration104 perhaps also because ozone irritates chemoreceptive mucosae and
because ozone attacks pheromones via ozonolysis.

Scattered anecdotal reports from newspapers suggest that serial appetitive

rapists may prefer unintoxicated victims. Such rapists can attack elderly women who
can still produce alarm pheromone. Since rapists frequently fail to inseminate
victims, pheromonal emissions from the victim may be the addictive pheromone at
play. Appetites for torture and rape may evolve from pubertal sexual horseplay and
scary movie dates. An addiction to alarm pheromone may plausibly be the device
behind human brutality and sexual assault for sexual predators, rapists, and torturers.
If so, identifiable human pheromone receptor proteins may divulge the propensity
preemptively.

Juvenile OCD patients share disfunction of the prefrontal-striatal-thalamic

circuit with involvement of other basal ganglia structures (putamen globus pallidus)
and the thalamus in contrast to adults which report mainly involvement of the caudate
nucleus and orbitofrontal cortex. 105 This ripening of pheromone deficiency responses
may reflect changing bonding pheromone preferences of ontogeny, perhaps. The
transition suggests useful clinical observations during experimental administration of
paternal facial skin surface lipid human pheromone. One might expect a return to the
juvenile phase of brain activity during recovery.

Another group using different methodology found consistent activation in

cortical and subcortical regions of the orbitofrontal and anterior cingulate loops. The
left dorsal frontoparietal network, including the dorsolateral prefrontal cortex and
precuneus, and the left superior temporal gyrus were likely OCD activated.

The orbitofrontal area unconsciously processes pheromones 106,107,108,109,110

with the majority of reports in humans. The lateral prefrontal cortex and the superior
temporal cortex are both activated by the airborne pheromone androstadienone in
humans.111 Recall that pheromone and olfactory pathways run parallel part of the

265
way into the CNS. It should come as no surprise that there is impairment of olfactory
identification in obsessive-compulsive disorder.112,113

OCD and depression can benefit from electroshock therapy. Perhaps the
mechanism renews pheromone receptor proteins much the way blood bubbles in an
electric field. OK, this seems strange. You see, hemoglobin loses its load of carbon
dioxide and 2,3 bisphosphoglycerate in the right ventricle by the QRS transient
electric field’s tugging at unlike charges. Understand that when water or any polar
liquid is subjected to electric fields, as in the heart, all the dipoles align--then the
released dipoles swing out of alignment and then back again into alignment. This is
how the T-Wave, J-Wave, and U-wave show up on an EKG. All the swinging and
tugging gets the ions and partial dipoles separated, hemoglobin turns somewhat buff
colored immediately before being pumped into the lung for oxygenation and adoption
of the familiar red conformation. 2,3 BPG’s higher affinity for hemoglobin now
goest to work to deliver oxygen from the blood to the tissues.

Something of the same sort probably takes place in the brain under
electroshock therapy. The pheromone receptor proteins throughout the pheromone
reception system and the brain are ‘cleaned’ of charged sticky sludge and become
ready to receive normal social pheromonal receptions again, roughly. It is cool to
watch this on a microscope slide with the naked eye, blood turns yellow and
effervesces in a small electric field. Shock-caused conformational changes of
olfactory receptor proteins change surface reflectance, and alter their twist under UV
irradiation. This should not prove difficult to more formally observe.

OCD has been linked to abnormalities with the neurotransmitter serotonin.

Animal pheromone reception is modulated by serotonin.114 Indeed, animal
pathological grooming disorders respond to serotonin enhancing drugs.115 Please
recall animals groom and allogroom for sebaceous pheromones.

OCD patients will respond favorably to treatment with healthy adult male
facial skin surface lipids taken by mouth, as should patients with trichotillomania,
body dysmorphic disorder, olfactory reference syndrome, compulsive skin picking,

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compulsive wound picking, and onychophagia. Please see the appendix at the end of
the book.

DISEASES OF ERSATS HUMAN PHEROMONES: PHOBIAS

Phobias replace pheromone with terror. One unreportable case of severe

agoraphobia complicated by mitral valve prolapse has been cured by the author.
These fears will mostly succumb to the paternal/parental protocol of the appendix.

DISEASES OF ERSATS HUMAN PHEROMONES: GILES DE LA

TOURETTE’S SYNDROME

Tourette’s syndrome is similar to Latah, criminal behavior, obsessive

compulsive disorder and compulsive gambling in that an appetite builds for the tic
behavior. The syndrome is relieved by rest and exaggerated by stress. Tourette’s
waxes and wanes, tics come and go, and up to 50% of patients show marked
improvement after a good rest and progressively during the teenage years. Tics kept
past 15 years tend to remain chronically.

The author suggested the use of mecamylamine,116 the most central acting
nicotinic anti-hypertensive drug, in place of raw nicotine being used to treat severe
Tourettes at a local college, because of the devastating peripheral side effects that the
nicotine being used had on the children. Of course, the equivalent of having
Tourettes patients smoke cigarettes was not truly therapeutic, and the trials failed.117
Human pheromone therapy for one Tourette’s syndrome patient improved his
condition and seems to make up for the author’s earlier transgression. Tourette’s
syndrome patients may benefit from paternal facial skin surface lipids alone, however
267
optimal therapy may include maternal facial skin surface lipids as well. The logic for
paternal (and perhaps maternal) facial skin surface therapy is that stress exaggerates
the condition. Axillary stress/alarm/fear pheromones may work in opposition to
pheromone reception of facial skin surface lipids. Pheromones working in opposition
can overcome previously pheromone-stimulated behavior in mice.118 Paternal facial
skin surface lipid pheromone from an over 30 year old male donor, should overcome
and cure Tourettes’ syndrome, perhaps even resolving tics in adults if the pheromone
is provided in concert with epigenetic therapy and/or artificial pheromone receptivity
enhancement by psychogenic lacrimation (watching sad movies).

DISEASES OF ERSATS HUMAN PHEROMONES: GAMBLING

Gambling addiction, is very similar to divorce, delinquency, and running

away, as a criminal behavior. The act of gambling obtains hormonal stimulation
rewards and probably autoemission and autoreception of pheromones from risky
behavior, just like other criminal and delinquent behavior. Gambling addiction, like
them, should be amenable to oral administration of healthy human adult male facial
skin surface lipid ‘kissing daddy pheromone’ 150 mg or more in one single dose. See
appendix.

AUTOIMMUNE DISEASES: ALS

Amyotrophic lateral sclerosis progresses at various rates, probably dependent

upon semiochemical exposures which vary from individual to individual. Happy
people last longer. Uncontrollable periods of laughing or crying seen in many ALS
patients suggest pheromone receptivity is being stimulated to contest against the
disease, just as uncontrolled crying of the 3rd day blues contests against bonding
failure in new mothers. This indicates that the disease should be treatable with human
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pheromone to provide a miracle cure for the disease. Thus after oral administration of
healthy adult male facial skin surface lipid 150-250 mg, the progression of ALS
should stop, followed by complete remission of the disease, the disappearance of all
symptoms and complete and rapid asymptomatic recovery.

Schwann cells can depend upon pheromones for normal development in

laboratory animals, thus autoimmune diseases that affect myelination may be simple
pheromone deficiencies. Given their life-threatening nature, they are more likely to
be caused by unfortunate sympathetic reception of poisonous human pheromones.
The nearly even sex ratio likely dismisses axillary contribution, but this is only an
informed guess.

GABA is diminished in the CSF with increased noradrenalin in both blood

and CSF (it passes the bbb, blood-brain large molecule barrier).

Flexible pheromone commerce needs feedback. There are curious physical

skin changes119 in ALS and weird immunity from bedsores, even at the terminal
stage.120 A similar weird immunity to respiratory illness is seen in Anorexia Nervosa
patients.121 ALS patients are more likely to have high densities of Interleukin-6 (IL-6)
in the epidermis. IL-6 family proteins act as pheromone receptor proteins. 122
Increased amyloid beta protein has been found in the skin of patients with ALS. 123
Increased expression of insulin-like growth factor I has been found in ALS.124
Insulin-like growth factors respond to pheromones125 and are probably pheromone
receptor proteins. ALS patients have impaired glucose tolerance.126

Eccrine perspiration was elevated (hyperhydrosis) early in ALS, while

perspiration declined by 40% over a six month interval.127 This suggests an
attempted biological self-remediation of poisonous pheromone reception.

AUTOIMMUNE DISEASE DUE TO BIRTH DEFECTS:

269
 There is one report of mandibuloacral dysplasia improvement after chewing
the pheromone chewing gum. Premature aging progeriod disorders may respond to
paternal facial skin surface lipid pheromone treatment, too.

One of the problem genetic loci known for MAD is for the zinc
metalloproteinase (ZMPSTE24),128 which may cause MAD by affecting prelamin A
processing.129 ZMPSTE24 was originally discovered in yeast as an enzyme required
for maturation or processing of the mating pheromone a-factor.130 These diseases are
plainly genetic, but the author has strangely benefitted one case with 150-250 mg
healthy over-30 adult male facial skin surface lipid provided per os and he is at a loss
as to why. Perhaps this is an epigenetic effect?

CYSTIC FIBROSIS:

Cystic fibrosis and other inheritance-based genetic abnormalities may benefit

from pheromone treatment as a palliative, but hope for a cure is unforeseen. (Of
course, we thought the same thing about drug addiction.) With epigenetic therapy,
there may be hope of some relief in some patients.

On a brighter note, the author noticed that the cystic fibrosis protein defect in
transmembrane ion transporter molecules effected loss of magnetic containment to
disable transport. Ion transporter proteins generally contain particle confinement
fields that allow ions to pass membranes without waters of hydration. (Artificially
adjoining these will potentially provide biological ‘plasma conduits’ consisting of
long proteins that need no external magnetic containment field, no vacuum pumping,
and no metal conductors.) My point here is to propose a novel radiological treatment
for easing symptoms of cystic fibrosis. Opening those microscopic containment
fields to the passage of ions may be attempted with exogenous magnetic fields.
Electromagnets (and motors if necessary) are relatively inexpensive. Since magnetic
fields are imperceptible, applying various electromagnetic stimulation to the most
affected areas during rest periods should allow increased longevity and improved
quality of life in cystic fibrosis patients.
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You see, CFTR, the cystic fibrosis transmembrane conductance regulator, has
significant amino acid homology and length conservation with alpha-factor
pheromone export systems proteins, hemolysin B, the MHC-linked peptide
transporter, HAM1. 131 The CFTR lacks a pairing of juxtaposed magnetic (Hückel’s
rule) amino acids right at the bottom of the tube that lets ions pass through without
waters of hydration. The tube is so tiny that even water is excluded, so no vacuum
pumping is needed and maintaining the magnetic fields requires no refrigeration,
obviously, since it works at body temperature. Anyway, the highly suspicious
homology (except for the magnetic defect that actually causes cystic fibrosis by
preventing transmembrane transport of chloride ion) suggests a pheromonal
association, so there actually is hope of a significant improvement with pheromone
therapy. If this works, it is a gift from God. If it does not work, then it is an amazing
coincidence.

PHEROMONAL ECLAMPSIA, PHEROMONAL PRE-ECLAMPSIA

AND PHEROMONAL PREMATURE LABOR

The control of phenotype from among a database of choices (oocytes and

presented spermatozoa) is influenced by pheromones. More human fetuses are lost
than delivered because choices are being made with pheromonal information having
significant, even fatal influence.

Fetal growth is compromised in animal models with high cortisol availability

and cortisol can be stimulated by 11beta-HSD2.132 The author believes that 11beta-
HSD2 may be a human placental pheromone or receptor, for a number of reasons.
First, 11beta-HSD2 shares the trouble caused by a pollutant with pheromone
‘transport’ proteins,133 suggesting it may have chemosensory receptor function.
Second, cortisol can be stimulated in women by human pheromone from the male
axilla.134

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 Cortisol is the stress hormone, increasing blood pressure, increasing blood
sugar, and reducing immune responses. Pre-eclampsia and eclampsia (pre-eclampsia
with seizures) are associated with diabetes mellitus of pregnancy, a risk factor. Thus
the male may emit the airborne pheromone which causes the pregnant woman to
secrete cortisol, which stimulates some aspects of pre-eclampsia: hypertension of
pregnancy, gestational edema, and diabetes mellitus of pregnancy. Since only 5% of
pregnant women suffer from pre-eclampsia and a tiny percentage of them reach
eclampsia, and since pregnancy is strongly associated with males, some other device
must be involved. That device may be a simple pheromone deficiency, perhaps a
deficiency of healthy adult male facial or other skin surface lipid? Reduced pre-
eclampsia is associated with increased fellatio and ingestion of semen.135 Koelman,
Coumans, Nijman, Doxiadis, Dekker, and Claas suggested that soluble HLA found in
semen transferred paternal immunity. Their findings suggest that soluble HLA may
be a pheromone receptor protein that conveys pheromone recognition.
Epidemiological studies attribute the cause of preeclampsia to genetic effects of the
mother, both mother and father, a couple effect, and unmeasured factors such as the
effect of the length of the sexual relationship and even a ‘dangerous’ father effect.136
All suggest pheromonal etiology and pheromone treatment.

Cortisol levels are higher in constitutional delay of puberty in girls.137

Male airborne pheromone increases cortisol levels in women, but males
generally stimulate acceleration of puberty! Honestly, the likelihood of
elucidating every pheromone response from browsing the medical and
scientific literature is not very high. Pheromone effects on human physiology
and disease are, happily, easy to test.

This author discovered that Chronic Fatigue Syndrome and obesity-

related spacial perception changes responded to the application of thick gobs of
petroleum jelly under the arms. The jelly prevented the auto-emitted axillary
pheromones from reaching the nose. Similar axillary petroleum jelly therapy
might control hypertension, diabetes, Alzheimer’s disease, anorexia nervosa,
and bulimia nervosa. Alternatively, anti-septic bathing may also be beneficial
for these pathological conditions, as it destroys the skin surface microflora that
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is thought responsible for processing axillary apocrine emissions into human
pheromones. This is just an idea, but it might just work.

Recently, skin surface microflora have been examined across and within
species of amphibians utilizing genetic sequencing techniques.138 This group
recognized stable communities of microflora that differed from place to place,
even anatomically, just as this author found with his own nose many years ago.

PHEROMONAL CAUSATION OF PSYCHIATRIC DISORDERS:

The development of the tics of Tourette's syndrome, the obsessions of OCD,

the binge eating behaviors of bulimia, and the self-starvation of anorexia share
‘abnormal development of [pheromonal-BN] frontostriatal circuits.’ 139 Epilepsy,
spasticity, chronic pain, depression, schizophrenia, and drug addiction should respond
favorably to human adult male facial skin surface lipids taken by mouth. Drug
addiction has been treated with complete success in three cases so far (2011) and
epilepsy, one. Epileptic lesions and surgical interventions affect the pheromone
reception and processing pathways in the brain. Meanwhile, alarm pheromones have
contributed to clonic epileptic convulsions in rats. 140

Schizophrenics and other psychiatric patients suffer from mild alterations in

immune functions and their illnesses have autoimmune features. Autoimmune
sufferers succumb to more than their fair share of psychiatric disorders, too,
frequently with olfactory impairment. A large cluster of olfactory receptor genes has
been mapped in proximity to the HLA/MHC locus on chromosome 6. The HLA/
MHC and linked olfactory receptor genes on chromosome 6 are clustered in
haplotypes and are highly polymorphic.141

Impulsive dysfunctional schizophrenics maintain lower orbitofrontal and

hippocampal volumes. Orbitofrontal cortex is dysmorphic in criminals while both are
pheromone processing and memory areas.

273
 Schizophrenia does not plague us until after puberty. It is similar to Multiple
Sclerosis (MS), Anorexia Nervosa (AN), and Bulimia Nervosa in this regard. Might
peri-pubertal onset point to development of secondary sex characteristics as playing
some role? And dwelling with one’s family reduces schizophrenic symptoms and
increases symptom-free episodes. Family therapy is effective in treating
schizophrenics while friend therapy fails. What differs? Kissing differentiates the
two. That certainly suggests that susceptibility to schizophrenia follows from some
family pheromone deficiency. It might be the father’s emissions, or the mothers, or
even baby’s, but it would be less likely to be pheromone emissions from sibling
children because their levels are low, and we don’t kiss our siblings that much
anyway.

Sad to say, exaggerated emission of a short-chain lipid, trans 3-methyl-2-

hexenoic acid normally found in human perspiration and produced by specialized
skin surface and axillary scent gland microflora, is closely associated with
schizophrenia. Indeed, the odor is characteristic142 although that is disputed. For
some inexplicable reason, no one has ever observed if schizophrenia improves when
the 3-methyl-2-hexenoic acid is prevented from reaching the nose. Bathing
schizophrenics in a bathtub of water with a quarter cup of ordinary household bleach
and a quarter cup of vinegar should reset the microflora by antisepsis. Healthy
microflora could then be transferred to the aseptic skin.

Incidentally, (E)-3-methyl-2-hexenoic acid is reputed to be a pheromone for

Anopheles gambiae. which carries malaria.

Given the improved grades seen in delinquents and runaways after being
supplied with the paternal facial skin surface lipid pheromone, given schizophrenia’s
frequent onset after some life disturbance (as with diabetes I), schizophrenics should
benefit from oral paternal pheromone therapy. Why not try it? Masculine facial
sebum may be robust enough. Receptivity could be enhanced by examining
Bowman’s secretion and inoculating with pheromone receptor proteins, transferring
pheromonal microflora, or by merely providing some stimulus to psychogenic
lacrimation (such as letting pheromone recipients view the Hollywood film, All Mine
To Give), a good cry.
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1Ferreyra-Moyano H, Barragan E. The olfactory system and Alzheimer's disease. Int J Neurosci 1989
Dec;49(3-4):157-9.
2Kurtz P, Schuurman T, Prinz H. Loss of smell leads to dementia in mice: is Alzheimer's disease a
degenerative disorder of the olfactory system? J Protein Chem. 1989 Jun;8(3):448-451.
3 Doty RL, Snow JB. Age-related alterations in olfactory structure and function. In: Margolis FL,

Getchell TV, editors. Molecular Neurobiology of the Olfactory System. New York: Plenum Press.
1988:355-374.
4 Pochi PE, Strauss JS, Mescon H. Sebum production and fractional 17-ketosteroid excretion in

Parkinsonism. J. Invest. Dermatol 1962;38:45.

5 Nicholson B. Does kissing aid human bonding by semiochemical addiction? Br J Dermatol 1984

Nov;111(5):623-627.
6Sabatier L, Jouanguy E, Dostert C, Zachary D, Dimarcq JL, Bulet P, Imler JL. Pherokine-2 and
pherokine-3. Eur J Biochem. 2003 Aug;270(16):3398-407.
7Brurberg MB, Nes IF, Eijsink VG. Brurberg MB, Nes IF, Eijsink VG. Pheromone-induced
production of antimicrobial peptides in Lactobacillus Mol Microbiol. 1997 Oct;26(2):347-60.
8 Schlievert PM, Gahr PJ, Assimacopoulos AP, Dinges MM, Stoehr JA, Harmala JW, Hirt H, Dunny

GM. Aggregation and binding substances enhance pathogenicity in rabbit models of Enterococcus
faecalis endocarditis. Infect Immun. 1998 Jan;66(1):218-223.
9 Sandnabba N. Differences between aggressive and non-aggressive mice in odour signals and marking

behaviour. In: Chemical Signals in Vertebrates. MacDonald DW, Müller-Schwarze D, Natynczuky SE,
editors. Oxford: Oxford University Press. 1990:125-38.
10Chamero P, Marton TF, Logan DW, Flanagan K, Cruz JR, Saghatelian A, Cravatt BF, Stowers L.
Identification of protein pheromones that promote aggressive behaviour. Nature. 2007 Dec 6;450
(7171):899-902.
11Holmes, Thomas H., et al. (1950). The Nose; an experimental study of reactions within the nose in
human subjects during varying life experiences with a foreword by Warfield T. Lonscope.
Springfield, Ill: Thomas.

275
12Wynne-Edwards VC. Animal Dispersion in Relation to Social Behaviour. Edinburgh: Oliver and
Boyd. 1962.
13Albone ES. Mammalian Semiochemistry The Investigation of Chemical Signals Between Mammals.
Chichester, England: J Wiley & Sons Limited, 1984.
14Weitkamp AW, Smiljanic A, Rothman S. The free fatty acids of human hair fat. J Am Chem Soc 1947
Aug;69:1936-9.
15106. Cunliffe WJ, Burton JL, Shuster S. The effect of local temperature variations on the sebum
excretion rate. Br J Dermatol 1970;83:650-654.
16Hardy JA, Mann DM, Wester P, Winblad B. An integrative hypothesis concerning the pathogenesis
and progression of Alzheimer's disease. Neurobiol Aging. 1986 Nov-Dec;7(6):489-502.
17 Tabunoki H, Shimada T, Banno Y, Sato R, Kajiwara H, Mita K, Satoh J. Identification of Bombyx

mori 14-3-3 orthologs and the interactor Hsp60. Neurosci Res. 2008 Jul;61(3):271-80. Epub 2008 Apr
3.
18 Czarnecka AM, Campanella C, Zummo G, Cappello F. Heat shock protein 10 and signal
transduction: a "capsula eburnea" of carcinogenesis? Cell Stress Chaperones. 2006 Winter;11(4):
287-94
19 Christen WG, Schaumberg DA, Glynn RJ, Buring JE. Dietary {omega}-3 Fatty Acid and Fish
Intake and Incident Age-Related Macular Degeneration in Women. Arch Ophthalmol. 2011 Mar
14; [Epub ahead of print]
20Nicholson B. A semiochemical addiction model for human bonding. Paper presented to the Animal
Behaviour Society and the International Society for Human Ethology, Bucknell University Lewisburg,
PA. June 12, 1983.
21 Drickamer LC, Mikesic DG. Urinary chemosignals, reproduction, and population for house mice

(Mus domesticus) living in field enclosures. J Chem Ecol 1990;16(10):2955-2968.

22Drickamer LC. Puberty-influencing chemosignals in house mice: ecological and evolutionary
considerations. In: Duvall D, Müller-Schwarze D, Silverstein RM, editors. Chemical Signals in
Vertebrates 4. New York: Plenum Press 1986:441-456.
23 Nicholson B Pheromones cause disease: the exocrinology of anorexia nervosa Med Hypotheses

2000; 54(3): 438-443.

24 Bruce HM. An exteroceptive block to pregnancy in the mouse. Nature 1959;184:105.
25Keverne EB, Rosser AE. The evolutionary significance of the olfactory block to pregnancy. In:
Chemical Signals in Vertebrates 4. Duvall D, Müller-Schwarze D, Silverstein RM, editors. New York:
Plenum Press. 1986:433-439.
26 Nicholson B. Human pheromones in the pathogenesis of autoimmune and behavioural illness. Paper
presented, informally, to the International Society of Chemical Ecology, University of Hull, England,
July 17, 1987.
27Coleman-Phox K, Odouli R, Li DK. Use of a fan during sleep and the risk of sudden infant death
syndrome. Arch Pediatr Adolesc Med. 2008 Oct;162(10):963-968.

276
EXOCRINOLOGY
28 Willis MA, Avondet JL, Finnell AS. Effects of altering flow and odor information on plume
tracking behavior in walking cockroaches, Periplaneta americana (L.). J Exp Biol. 2008 Jul;211(Pt
14):2317-2326.
29Valdes-Dapena MA. Sudden infant death syndrome: a review of the medical literature 1974-1979.
Pediatrics 1980;66(4):597-614.
30 Darwin, Charles. The Expression of the Emotions in Man and Animals. London: Murray. 1872:162.
31Shamim S, Hasler G, Liew C, Sato S, Theodore WH. Temporal lobe epilepsy, depression, and
hippocampal volume. Epilepsia. 2009 May;50(5):1067-1071. Epub 2008 Nov 19.
32Abel EL, Bilitzke PJ, Cotton DB. Alarm substance induces convulsions in imipramine-treated rats.
Pharmacol Biochem Behav. 1992 Mar;41(3):599-601.
33Rosenberg RE, Law JK, Yenokyan G, McGready J, Kaufmann WE, Law PA. Characteristics and
concordance of autism spectrum disorders among 277 twin pairs. Arch Pediatr Adolesc Med. 2009
Oct;163(10):907-914.
34Nicot A, Otto T, Brabet P, Dicicco-Bloom EM. Altered social behavior in pituitary adenylate
cyclase-activating polypeptide type I receptor-deficient mice. J Neurosci. 2004 Oct 6;24(40):
8786-8795.
35Toal F, Daly EM, Page L, Deeley Q, Hallahan B, Bloemen O, Cutter WJ, Brammer MJ, Curran S,
Robertson D, Murphy C, Murphy KC, Murphy DG. Clinical and anatomical heterogeneity in autistic
spectrum disorder: a structural MRI study. Psychol Med. 2009 Nov 6;. [Epub ahead of print]
36Zhou W, Chen D. Encoding human sexual chemosensory cues in the orbitofrontal and fusiform
cortices. J Neurosci. 2008 Dec 31;28(53):14416-14421.
37 Wiggins LD, Robins DL, Bakeman R, Adamson LB. Brief report: sensory abnormalities as
distinguishing symptoms of autism spectrum disorders in young children. J Autism Dev Disord. 2009
Jul;39(7):1087-1091. Epub 2009 Mar 13.
38Meiri G, Bichovsky Y, Belmaker RH. Omega 3 fatty acid treatment in autism. J Child Adolesc
Psychopharmacol. 2009 Aug;19(4):449-51.
39Rogers MA, Yamasue H, Abe O, Yamada H, Ohtani T, Iwanami A, Aoki S, Kato N, Kasai K.
Smaller amygdala volume and reduced anterior cingulate gray matter density associated with history of
post-traumatic stress disorder. Psychiatry Res. 2009 Dec 30;174(3):210-216. Epub 2009 Nov 13.
40 Felmingham K, Williams LM, Whitford TJ, Falconer E, Kemp AH, Peduto A, Bryant RA. Duration
of posttraumatic stress disorder predicts hippocampal grey matter loss. Neuroreport. 2009 Oct 28;20
(16):1402-1406.
41 Milad MR, Pitman RK, Ellis CB, Gold AL, Shin LM, Lasko NB, Zeidan MA, Handwerger K, Orr
SP, Rauch SL. Neurobiological basis of failure to recall extinction memory in posttraumatic stress
disorder. Biol Psychiatry. 2009 Dec 15;66(12):1075-1082. Epub 2009 Sep 12.
42Matsuoka, Yutaka. Clearance of fear memory from the hippocampus through neurogenesis by
omega-3 fatty acids: A novel preventive strategy for posttraumatic stress disorder?
BioPsychoSocial Medicine 2011, 5:3

277
43Cocke R, Thiessen D. Alarm chemosignals suppress the immune system. In: Chemical Signals in
Vertebrates V. MacDonald DW, Müller-Schwarze D, Natynczuky SE, editors. Oxford: Oxford
University Press. 1990:125-138.
44Salo M. Effects of anaesthesia and surgery on the immune response. In: Trauman, Stress, and
Immunity in Anaesthesia and Surgery. New York: Butterworth Scientific. 1982:211-53.
45Fan RL, Zheng SH, Wu ZS. [Study on the relationship between lung cancer at preclinical stage and
psycho-social factor. A case-control study]. Chung Hua Lin Hsing Ping Hsueh Tsa Chih 1997 Oct;18(5):
289-92.

46 Ogg S, Paradis S, Gottlieb S, Patterson GI, Lee L, Tissenbaum HA, Ruvkun G. The Fork head
transcription factor DAF-16 transduces insulin-like metabolic and longevity signals in C. elegans.
Nature. 1997 Oct 30;389(6654):994-999.
47Hahm JH, Kim S, Paik YK. Endogenous cGMP regulates adult longevity via the insulin signaling
pathway in Caenorhabditis elegans. Aging Cell. 2009 Aug;8(4):473-483. Epub 2009 May 31.
48 Pause BM, Krauel K, Schrader C, Sojka B, Westphal E, Müller-Ruchholtz W, Ferstl R. The human
brain is a detector of chemosensorily transmitted HLA-class I-similarity in same- and opposite-sex
relations. Proc Biol Sci. 2006 Feb 22;273(1585):471-478.
49 Hui X, Zhu W, Wang Y, Lam KS, Zhang J, Wu D, Kraegen EW, Li Y, Xu A. Major urinary protein-1
increases energy expenditure and improves glucose intolerance through enhancing mitochondrial
function in skeletal muscle of diabetic mice. J Biol Chem. 2009 May 22;284(21):14050-7. Epub 2009
Mar 31.
50
Marks DR, Tucker K, Cavallin MA, Mast TG, Fadool DA. Awake intranasal insulin delivery
modifies protein complexes and alters memory, anxiety, and olfactory behaviors. J Neurosci. 2009
May 20;29(20):6734-6751.
51 Dennis JC, Coleman ES, Swyers SE, Moody SW, Wright JC, Judd R, Zhong Q, Morrison EE.
Changes in mitotic rate and GFAP expression in the primary olfactory axis of streptozotocin-induced
diabetic rats. J Neurocytol. 2005 Mar;34(1-2):3-10.
52 Hara T, Hirasawa A, Sun Q, Sadakane K, Itsubo C, Iga T, Adachi T, Koshimizu TA, Hashimoto T,

Asakawa Y, Tsujimoto G. Novel selective ligands for free fatty acid receptors GPR120 and GPR40.
Naunyn Schmiedebergs Arch Pharmacol. 2009 Sep;380(3):247-55. Epub 2009 May 27.
53 Gelstein S, Yeshurun Y, Rozenkrantz L, Shushan S, Frumin I, Roth Y, Sobel N. Human tears contain
a chemosignal. Science. 2011 Jan 14;331(6014):226-30. Epub 2011 Jan 6.
54Ljunggren JG (August 1983). "[Who was the man behind the syndrome: Ismail al-Jurjani, Testa,
Flajina, Parry, Graves or Basedow? Use the term hyperthyreosis instead]". Lakartidningen 80 (32–33):
2902. PMID 6355710.
55Winberg J, Porter RH. Olfaction and human neonatal behaviour: clinical implications. Acta
Paediatr. 1998 Jan;87(1):6-10.
56Batterton MN, Robarts D, Woodley SK, Baum MJ. Comparison of odor and mating-induced
glomerular activation in the main olfactory bulb of estrous female ferrets. Neurosci Lett. 2006 Jun
12;400(3):224-9. Epub 2006 Mar 10.

278
EXOCRINOLOGY
57Pause BM, Lübke K, Laudien JH, Ferstl R. Intensified neuronal investment in the processing of
chemosensory anxiety signals in non-socially anxious and socially anxious individuals. PLoS One.
2010 Apr 23;5(4):e10342.
58Arakawa H, Arakawa K, Blandino P Jr, Deak T. The role of neuroinflammation in the release of
aversive odor cues from footshock-stressed rats: Implications for the neural mechanism of alarm
pheromone. Psychoneuroendocrinology. 2011 May;36(4):557-568.
59 Lacaille F, Everaerts C, Ferveur JF. Feminization and alteration of Drosophila taste neurons induce
reciprocal effects on male avoidance behavior. Behav Genet. 2009 Sep;39(5):554-563.
60Leung G, Sun W, Zheng L, Brookes S, Tully M, Shi R. Anti-acrolein treatment improves behavioral
outcome and alleviates myelin damage in experimental autoimmune encephalomyelitis mouse.
Neuroscience. 2011 Jan 26;173:150-5. Epub 2010 Nov 26.
61Schumacher SK, Moltz H. Prolonged responsiveness to the maternal pheromone in the
postweanling rat. Physiol Behav. 1985 Mar;34(3):471-473.
62 Minns AB, Ghafouri N, Clark RF. Isoniazid-induced status epilepticus in a pediatric patient after
inadequate pyridoxine therapy. Pediatr Emerg Care. 2010 May;26(5):380-381.
63Rubinstein T, Pitashny M, Levine B, Schwartz N, Schwartzman J, Weinstein E, Pego-Reigosa JM,
Lu TY, Isenberg D, Rahman A, Putterman C. Urinary neutrophil gelatinase-associated lipocalin as a
novel biomarker for disease activity in lupus nephritis. Rheumatology (Oxford). 2010 May;49(5):
960-971. Epub 2010 Feb 9.
64Brunner HI, Mueller M, Rutherford C, Passo MH, Witte D, Grom A, Mishra J, Devarajan P. Urinary
neutrophil gelatinase-associated lipocalin as a biomarker of nephritis in childhood-onset systemic
lupus erythematosus. Arthritis Rheum. 2006 Aug;54(8):2577-2584.
65Chung-Davidson YW, Rees CB, Bryan MB, Li W. Neurogenic and neuroendocrine effects of
goldfish pheromones. J Neurosci. 2008 Dec 31;28(53):14492-14499.
66 Santos SG, Lynch S, Campbell EC, Antoniou AN, Powis SJ. Induction of HLA-B27 heavy chain
homodimer formation after activation in dendritic cells. Arthritis Res Ther. 2008;10
(4):R100. Epub 2008 Aug 29.
67Thompson RN, McMillon R, Napier A, Wekesa KS. Pregnancy block by MHC class I peptides is
mediated via the production of inositol 1,4,5-trisphosphate in the mouse vomeronasal organ. J Exp
Biol. 2007 Apr;210(Pt 8):1406-1412.
68Novotny MV, Soini HA, Koyama S, Wiesler D, Bruce KE, Penn DJ. Chemical identification of
MHC-influenced volatile compounds in mouse urine. I: Quantitative Proportions of Major
Chemosignals. J Chem Ecol. 2007 Feb;33(2):417-34. Epub 2006 Dec 27.
69 Karouzakis E, Gay RE, Michel BA, Gay S, Neidhart M. DNA hypomethylation in rheumatoid
arthritis synovial fibroblasts. Arthritis Rheum. 2009 Nov 30;60(12):3613-3622. [Epub ahead of print]
70Ryba NJ, Tirindelli R. A new multigene family of putative pheromone receptors. Neuron. 1997
Aug;19(2):371-379.
71Ong J, Kerr DI. Clinical potential of GABAB receptor modulators. CNS Drug Rev. 2005 Autumn;
11(3):317-34.

279
72Mennigen JA, Lado WE, Zamora JM, Duarte-Guterman P, Langlois VS, Metcalfe CD, Chang JP,
Moon TW, Trudeau VL. Waterborne fluoxetine disrupts the reproductive axis in sexually mature male
goldfish, Carassius auratus. Aquat Toxicol. 2010 Nov 15;100(4):354-64. Epub 2010 Sep 22.
73 Bataineh HN, Daradka T. Effects of long-term use of fluoxetine on fertility parameters in adult male
rats. Neuro Endocrinol Lett. 2007 Jun;28(3):321-325.
74Larsen CM, Grattan DR. Exposure to female pheromones during pregnancy causes postpartum
anxiety in mice. Vitam Horm. 2010;83:137-49.
75 Zochling J, Bohl-Bühler MH, Baraliakos X, Feldtkeller E, Braun J. The high prevalence of
infections and allergic symptoms in patients with ankylosing spondylitis is associated with clinical
symptoms. Clin Rheumatol. 2006 Sep;25(5):648-658. Epub 2005 Dec 23.
76Boyd JH, Holmes CL, Wang Y, Roberts H, Walley KR. Vasopressin decreases sepsis-induced
pulmonary inflammation through the V2R. Resuscitation. 2008 Nov;79(2):325-31.
77 Mäntyjärvi R, Parkkinen S, Rytkönen M, Pentikäinen J, Pelkonen J, Rautiainen J, Zeiler T, Virtanen
T. Complementary DNA cloning of the predominant allergen of bovine dander: a new member in the
lipocalin family. J Allergy Clin Immunol. 1996 Jun;97(6):1297-1303.
78Brodmann J, Twele R, Francke W, Yi-bo L, Xi-qiang S, Ayasse M. Orchid mimics honey bee alarm
pheromone in order to attract hornets for pollination. Curr Biol. 2009 Aug 25;19(16):
1368-1372. Epub 2009 Aug 6.
79Shimizu N, Miwa K, Noge K, Yakumaru R, Mori N, Kuwahara Y. Stereochemistry of female-
specific normonoterpenes, sex pheromone candidates from the acarid mite, Tyreophagus sp.
(Astigmata: Acaridae). Biosci Biotechnol Biochem. 2009 Oct;73(10):2332-4. Epub 2009 Oct 7.
80Di Stefano F, Verna N, Di Giampaolo L, Schiavone C, Di Gioacchino G, Balatsinou L, Burge PS,
Boscolo P, Di Gioacchino M. Occupational asthma due to low molecular weight agents. Int J
Immunopathol Pharmacol. 2004 May-Aug;17(2 Suppl):77-82.
81 Tótha M, Csonka E, Bakcsa F, Benedek P, Szarukán I, Gomboc S, Toshova T, Subchev M, Ujváry I.
Species spectrum of flea beetles (Phyllotreta spp., Coleoptera, Chrysomelidae) attracted to allyl
isothiocyanate-baited traps. Z Naturforsch C. 2007 Sep-Oct;62(9-10):772-778.
82Tóth M, Csonka E, Bartelt RJ, Cossé AA, Zilkowski BW, Muto SE, Mori K. Pheromonal activity of
compounds identified from male Phyllotreta cruciferae: field tests of racemic mixtures, pure
enantiomers, and combinations with allyl isothiocyanate. J Chem Ecol. 2005 Nov;31(11):
2705-20. Epub 2005 Oct 25.
83 Krückert K, Flachsbarth B, Schulz S, Hentschel U, Weldon PJ. Ethyl-branched aldehydes, ketones,
and diketones from caimans (Caiman and Paleosuchus; Crocodylia, Reptilia). J Nat Prod. 2006 Jun;69
(6):863-870.
84Wood WF. Volatile components in metatarsal glands of sika deer, Cervus nippon. J Chem Ecol.
2003 Dec;29(12):2729-2733.
85Villet RH. Involvement of amino and sulphydryl groups in olfactory transduction in silk moths.
Nature. 1974 Apr 19;248(450):707-709.

280
EXOCRINOLOGY
86Trapp S, Croteau R. Defensive resin biosynthesis in conifers. Annu Rev Plant Physiol Plant Mol
Biol. 2001 Jun;52:689-724.
87Bhatt JP, Sajwan MS. Ovarian steroid sulphate functions as priming pheromone in male Barilius
bendelisis (Ham.). J Biosci. 2001 Jun;26(2):253-263.
88 Liberles SD. Trace amine-associated receptors are olfactory receptors in vertebrates. Ann N Y Acad

Sci. 2009 Jul;1170:168-172.

89Jarriault D, Barrozo RB, de Carvalho Pinto CJ, Greiner B, Dufour MC, Masante-Roca I,
Gramsbergen JB, Anton S, Gadenne C. Age-dependent plasticity of sex pheromone response in the
moth, Agrotis ipsilon: combined effects of octopamine and juvenile hormone. Horm Behav. 2009 Jun;
56(1):185-91. Epub 2009 May 3.
90Schildnecht H, Winkler H, Maschwitz U. On arthropod defense substances. XXXI. Comparative
chemical studies of substances contained in the pygidial defense bullae of carabids. Z Naturforsch B.
1968 May;23(5):637-644.
91 AiH, Kanzaki R. Modular organization of the silkmoth antennal lobe macroglomerular complex
revealed by voltage-sensitive dye imaging. J Exp Biol. 2004 Feb;207(Pt 4):633-644.
92Zhou W, Chen D. Encoding human sexual chemosensory cues in the orbitofrontal and fusiform
cortices. J Neurosci. 2008 Dec 31;28(53):14416-14421.
93Treyer V, Koch H, Briner HR, Jones NS, Buck A, Simmen DB. Male subjects who could not
perceive the pheromone 5a-androst-16-en-3-one, produced similar orbitofrontal changes on PET
compared with perceptible phenylethyl alcohol (rose). Rhinology. 2006 Dec;44(4):278-282.
94 Gelez H, Fabre-Nys C. Neural pathways involved in the endocrine response of anestrous ewes to
the male or its odor. Neuroscience. 2006 Jul 7;140(3):791-800. Epub 2006 May 2.
95Savic I, Berglund H, Lindström P. Brain response to putative pheromones in homosexual men.
Proc Natl Acad Sci U S A. 2005 May 17;102(20):7356-61. Epub 2005 May 9.
96Moncho-Bogani J, Martinez-Garcia F, Novejarque A, Lanuza E. Attraction to sexual pheromones
and associated odorants in female mice involves activation of the reward system and basolateral
amygdala. Eur J Neurosci. 2005 Apr;21(8):2186-2198.
97Jurado MA, Junqué C. Criminal behavior after orbitofrontal lesion. Actas Esp Psiquiatr. 2000 Sep-
Oct;28(5):337-341.
98Aguilar EJ, García-Martí G, Martí-Bonmatí L, Lull JJ, Moratal D, Escartí MJ, Robles M, González
JC, Guillamón MI, Sanjuán J. Left orbitofrontal and superior temporal gyrus structural changes
associated to suicidal behavior in patients with schizophrenia. Prog Neuropsychopharmacol Biol
Psychiatry. 2008 Oct 1;32(7):1673-1676. Epub 2008 Jul 11.
99Craig MC, Catani M, Deeley Q, Latham R, Daly E, Kanaan R, Picchioni M, McGuire PK, Fahy T,
Murphy DG. Altered connections on the road to psychopathy. Mol Psychiatry. 2009 Oct;14(10):
946-953, 907. Epub 2009 Jun 9.
100 Shamay-Tsoory SG, Harari H, Aharon-Peretz J, Levkovitz Y. The role of the orbitofrontal cortex in
affective theory of mind deficits in criminal offenders with psychopathic tendencies. Cortex. 2009
May 18; [Epub ahead of print]

281
101Dolan MC, Fullam RS. Psychopathy and functional magnetic resonance imaging blood
oxygenation level-dependent responses to emotional faces in violent patients with schizophrenia. Biol
Psychiatry. 2009 Sep 15;66(6):570-577. Epub 2009 May 15.
102Mehta MA, Golembo NI, Nosarti C, Colvert E, Mota A, Williams SC, Rutter M, Sonuga-Barke EJ.
Amygdala, hippocampal and corpus callosum size following severe early institutional deprivation: the
English and Romanian Adoptees study pilot. J Child Psychol Psychiatry. 2009 Aug;50(8):
943-951. Epub 2009 Apr 17.
103Rotton J, Frey J. Air pollution, weather, and violent crimes: concomitant time-series analysis of
archival data. J Pers Soc Psychol. 1985 Nov;49(5):1207-1220.
104Rotton J, Frey J. Air pollution, weather, and violent crimes: concomitant time-series analysis of
archival data. J Pers Soc Psychol. 1985 Nov;49(5):1207-1220.
105 Huyser C, Veltman DJ, de Haan E, Boer F. Paediatric obsessive-compulsive disorder, a

neurodevelopmental disorder? Evidence from neuroimaging. Neurosci Biobehav Rev. 2009 Jun;33(6):
818-30. Epub 2009 Jan 21.
106 Zhou W, Chen D. Encoding human sexual chemosensory cues in the orbitofrontal and fusiform

cortices. J Neurosci. 2008 Dec 31;28(53):14416-14421.

107 Treyer V, Koch H, Briner HR, Jones NS, Buck A, Simmen DB. Male subjects who could not

perceive the pheromone 5a-androst-16-en-3-one, produced similar orbitofrontal changes on PET

compared with perceptible phenylethyl alcohol (rose). Rhinology. 2006 Dec;44(4):278-282.
108 Gelez H, Fabre-Nys C. Neural pathways involved in the endocrine response of anestrous ewes to

the male or its odor. Neuroscience. 2006 Jul 7;140(3):791-800. Epub 2006 May 2.
109Savic I, Berglund H, Lindström P. Brain response to putative pheromones in homosexual men.
Proc Natl Acad Sci U S A. 2005 May 17;102(20):7356-61. Epub 2005 May 9.
110Moncho-Bogani J, Martinez-Garcia F, Novejarque A, Lanuza E. Attraction to sexual pheromones
and associated odorants in female mice involves activation of the reward system and basolateral
amygdala. Eur J Neurosci. 2005 Apr;21(8):2186-2198.
111 Gulyás B, Kéri S, O'Sullivan BT, Decety J, Roland PE. The putative pheromone androstadienone
activates cortical fields in the human brain related to social cognition. Neurochem Int. 2004 Jun;44(8):
595-600.
112 Barnett R, Maruff P, Purcell R, Wainwright K, Kyrios M, Brewer W, Pantelis C. Impairment of
olfactory identification in obsessive-compulsive disorder. Psychol Med. 1999 Sep;29(5):1227-1233.
113 Hermesh H, Zohar J, Weizman A, Voet H, Gross-Isseroff R. Orbitofrontal cortex dysfunction in

obsessive-compulsive disorder? II. Olfactory quality discrimination in obsessive-compulsive disorder.

Eur Neuropsychopharmacol. 1999 Sep;9(5):415-420.
114 Roelofs WL. Chemistry of sex attraction. Proc Natl Acad Sci U S A. 1995 Jan 3;92(1):44-49.
115Feusner JD, Hembacher E, Phillips KA. The mouse who couldn't stop washing: pathologic
grooming in animals and humans. CNS Spectr. 2009 Sep;14(9):503-513.

282
EXOCRINOLOGY
116Sanberg PR, Shytle RD, Silver AA. Treatment of Tourette's syndrome with mecamylamine.
Lancet. 1998 Aug 29;352(9129):705-706.
117 Silver AA, Shytle RD, Sheehan KH, Sheehan DV, Ramos A, Sanberg PR. Multicenter, double-
blind, placebo-controlled study of mecamylamine monotherapy for Tourette's disorder. J Am Acad
Child Adolesc Psychiatry. 2001 Sep;40(9):1103-1110.
118 Drickamer LC. Acceleration and delay of sexual maturation in female house mice (Mus

domesticus) by urinary chemosignals: mixing urine sources in unequal proportions. Journal of

Comparative Psychology 1988;102(3):215-21.
119
Ono S, Hu J, Shimizu N, Imai T, Nakagawa H. Increased interleukin-6 of skin and serum in
amyotrophic lateral sclerosis. J Neurol Sci. 2001 Jun 15;187(1-2):27-34.
120 Ono S. Skin changes in amyotrophic lateral sclerosis. Brain Nerve. 2007 Oct;59(10):1099-1107.
121 Mustafa A, Ward A, Treasure J, Peakman M. T lymphocyte subpopulations in anorexia nervosa and
refeeding. Clin Immunol Immunopathol. 1997 Mar;82(3):282-289.
122 Rollmann SM, Houck LD, Feldhoff RC. Proteinaceous pheromone affecting female receptivity in a
terrestrial salamander. Science. 1999 Sep 17;285(5435):1907-1909.
123 Tamaoka A, Matsuno S, Ono S, Shimizu N, Shoji S. Increased amyloid beta protein in the skin of
patients with amyotrophic lateral sclerosis. J Neurol. 2000 Aug;247(8):633-635.
124 Ono S, Hu J, Imai T, Shimizu N, Tsumura M, Nakagawa H. Increased expression of insulin-like
growth factor I in skin in amyotrophic lateral sclerosis. J Neurol Neurosurg Psychiatry. 2000 Aug;69
(2):199-2003.
125 Li W, Kennedy SG, Ruvkun G. daf-28 encodes a C. elegans insulin superfamily member that is
regulated by environmental cues and acts in the DAF-2 signaling pathway. Genes Dev. 2003 Apr 1;17
(7):844-58. Epub 2003 Mar 21.
126Pradat PF, Bruneteau G, Gordon PH, Dupuis L, Bonnefont-Rousselot D, Simon D, Salachas F,
Corcia P, Frochot V, Lacorte JM, Jardel C, Coussieu C, Forestier NL, Lacomblez L, Loeffler JP,
Meininger V. Impaired glucose tolerance in patients with amyotrophic lateral sclerosis. Amyotroph
Lateral Scler. 2009 Mar 20;. [Epub ahead of print].
127Beck M, Giess R, Magnus T, Puls I, Reiners K, Toyka KV, Naumann M. Progressive sudomotor
dysfunction in amyotrophic lateral sclerosis. J Neurol Neurosurg Psychiatry. 2002 Jul;73(1):68-70.
128Agarwal AK, Zhou XJ, Hall RK, Nicholls K, Bankier A, Van Esch H, Fryns JP, Garg A. Focal
segmental glomerulosclerosis in patients with mandibuloacral dysplasia owing to ZMPSTE24
deficiency. J Investig Med. 2006 May;54(4):208-213.
129
Agarwal AK, Fryns JP, Auchus RJ, Garg A. Zinc metalloproteinase, ZMPSTE24, is mutated in
mandibuloacral dysplasia. Hum Mol Genet. 2003 Aug 15;12(16):1995-2001.
130Barrowman J, Michaelis S. ZMPSTE24, an integral membrane zinc metalloprotease with a
connection to progeroid disorders. Biol Chem. 2009 Aug;390(8):761-773.

283
131Manavalan P, Smith AE, McPherson JM. Sequence and structural homology among membrane-
associated domains of CFTR and certain transporter proteins. J Protein Chem. 1993 Jun;12(3):
279-290.
132Aufdenblatten M, Baumann M, Raio L, Dick B, Frey BM, Schneider H, Surbek D, Hocher B,
Mohaupt MG. Prematurity is related to high placental cortisol in preeclampsia. Pediatr Res. 2009
Feb;65(2):198-202.
133Wong JS, Gill SS. Gene expression changes induced in mouse liver by di(2-ethylhexyl) phthalate.
Toxicol Appl Pharmacol. 2002 Dec 15;185(3):180-196.
134 Wyart C, Webster WW, Chen JH, Wilson SR, McClary A, Khan RM, Sobel N. Smelling a single

component of male sweat alters levels of cortisol in women. J Neurosci. 2007 Feb 7;27(6):1261-1265.
135 Koelman CA, Coumans AB, Nijman HW, Doxiadis II, Dekker GA, Claas FH. Correlation between

oral sex and a low incidence of preeclampsia: a role for soluble HLA in seminal fluid? J Reprod
Immunol. 2000 Mar;46(2):155-166.

136
Dekker G, Robillard PY, Roberts C. The etiology of preeclampsia: the role of the father. J Reprod
Immunol. 2011 Apr 27; [Epub ahead of print]
137Błogowska A, Rzepka-Górska I, Krzyzanowska-Swiniarska B. Is neuropeptide Y responsible for
constitutional delay of puberty in girls? A preliminary report. Gynecol Endocrinol. 2004 Jul;19(1):
22-25.
138McKenzie VJ, Bowers RM, Fierer N, Knight R, Lauber CL. Co-habiting amphibian species harbor
unique skin bacterial communities in wild populations. ISME J. 2011 Sep 29. doi: 10.1038/ismej.
2011.129. [Epub ahead of print]
139 Marsh R, Maia TV, Peterson BS. Functional disturbances within frontostriatal circuits across
multiple childhood psychopathologies. Am J Psychiatry. 2009 Jun;166(6):664-674. Epub 2009 May
15.
140Abel EL, Bilitzke PJ, Cotton DB. Alarm substance induces convulsions in imipramine-treated rats.
Pharmacol Biochem Behav. 1992 Mar;41(3):599-601.
141 Ortega-Hernandez OD, Kivity S, Shoenfeld Y. Olfaction, psychiatric disorders and autoimmunity:

is there a common genetic association? Autoimmunity. 2009 Jan;42(1):80-88.

142Brewer WJ, Wood SJ, Pantelis C, Berger GE, Copolov DL, McGorry PD. Olfactory sensitivity
through the course of psychosis: Relationships to olfactory identification, symptomatology and the
schizophrenia odor. Psychiatry Res. 2007 Jan 15;149(1-3):97-104. Epub 2006 Dec 5.

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Chapter 11: Atherosclerosis

When the author was fiddling around in his laboratory (investigating the
effects of low cardiac voltage electric pulses on human blood), atherosclerotic
plaques formed. Wow! Such plaques had to be electroplated onto vessel walls! The
idea explained too much not to be true. It accounted for the plaque build-up in areas
of blood turbulence, spared small diameter blood vessels, spared veinous vessels,
even atherosclerotic deposits appearing on synthetic vascular prostheses explanted
from humans. The atherosclerogenic effects of diabetic blood sugar levels, the
nicotine of cigarette smoking, and body habitus all gained a unified explanation in the
equation describing electrodeposition. Reviewing the literature, the phenomenon had
already been observed and proposed as a model, even though the mechanism by
which the plaques formed went unrecognized, amazingly.

Atherosclerotic plaques electrodeposite when blood is used as electrolyte

between cathode and anode, and accounts for the resemblance of the
electrostimulation model of atherosclerosis1,2,3 to clinical findings. The kicker was
that electroplating explained both the mixed tightly spaced crystalline deposits typical
of atherosclerotic plaques (which could never be explained by any other mechanism
physical or biological) and the blister formations seen in brittle plaques (another
previously inexplicable phenomenon), plus it explained the influence of oxygen
radicals on thromboembolic risk.

This is a book about human pheromones, right? Atherosclerosis as

electrodeposition initiated by human pheromone accounts for all the beneficial effects
of dietary fishoil, trans fatty acids and saturated fats, as well as their synergy and
species specificity. Moreover, plant allomones like aspirin, cinnamon, quinidine, and
dozens of others have similar beneficial cardiac effects that must be based, at least in
285
part, upon their natural anti-herbivory semiochemical function. (Indeed, common
antibiotics are naturally allomones, it is often how they were discovered in the first
place.) Other hypotheses4 on the etiology of atherosclerosis were primitive by
comparison, unable to account for every single risk factor for the disease as this one
does.

Artificial atherosclerotic plaques can be formed by low voltage

electrodeposition both in animal models and as nodal accumulations from blood in
pulsitile, low voltage electric fields: that much we knew. The oddities of
atherosclerosis are explained mathematically as elements of electrodeposition, i.e.
variables in the electroplater’s equation with just a few perfectly legitimate
mathematical substitutions. Atherosclerotic plaques are essentially crystaline with
many different crystals (with vastly different temperatures of crystalization) in
juxtaposition that form at constant human body temperature: only electrodeposition
can account for these phenomena. The phenomenon of electrodeposition
mathematically explains the perverse effect of body habitus: why short thick people
are so much more susceptible to atherosclerosis than tall skinny ones. The new
explanation also takes care of why only conductive innervated arteries are affected
leaving non-conductive, non-innervated veins and cut and resected arteries
completely free of any plaques whatsoever. Electrodeposition provides the reason
for allograft immunity as being due to the broken electrical ciruit. Electrodeposition
explains why electrogenic organ proximity is associated with atherosclerosis (heart,
gut, brain, & kidneys). Electroplater experience also shows why heavier deposits of
plaque are observed under blood turbulence. That same turbulence, produced by
shaking articles being plated in the electrolyte bath, is used in the electroplating
process to speed deposition! Blood turbulence effects on atherosclerosis had baffled
feable minds for generations. Electrodeposits are easily effected on plastics and
atherosclerotic plaques have been recorded on artificial plastic vessel prostheses.

Explaining how plaques form on the interiors of blood vessels is a triumph of

modern medicine, but the why remained open for a nanosecond. Electrodeposition
stimulated centrally by a human pheromone trigger explains human behavior
associated with atherosclerosis, and why central lesions on pheromone reception
pathways can stimulate systemic atherosclerosis in animals. High status increases the
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size of some glands, while stress increases alarm pheromone emissions. (The why
behind goosepimples and throwing ones hands in the air in panic.) Species-specific
beneficial effects of fish oils, health effects of emotion and the anti-sudden infant
syndrome (SIDS) effect of fans in nurseries were also elucidated in the same context.
That was a summary, so pay close attention to the science part, following.

LOW VOLTAGE ELECTRODEPOSITION OF ATHERSCLEROTIC

PLAQUE

The first four phases of atherosclerotic plaque accumulation are mainly by

lipid accumulation. 5 When the author passed a small current controlled by a
metronome intermittently through whole human blood, electrodeposited
atherosclerotic-like plaques formed on the aluminum anode. The experimentally
electrodeposited plaque was identical in adherence, thickness, color, consistency, and
texture to atherosclerotic plaques observable in human anatomical dissection. The
characteristic creepy crackling sound on manipulation was also identical. Early
plaque adherence to large arteries also forms patterns closely resembling unfinished
electrodeposition of metals on substrates.

Review of the literature showed that low voltage, intermittent pulsatile DC

electrodeposition was applied in an animal model of atherosclerosis. Betz and
1-3
associates discovered atheroma and plaque formation between two gold electrodes
electrically stimulating rabbit carotid arteries in vivo. Their model was an accurate
representation of all stages of plaque development. An atheroma appeared beneath
the anode only with cholesterol diet and subendothelial fibromuscular proliferates
without,2 and deposits even varied with electric field strength,3 but the notion of
electrochemical deposition eluded them. Their finding of gold particles in the arterial
wall2 demonstrated electro-deposition as the operative process, but they missed it
entirely. The anodal accumulation should also have shed light on the mechanism, but

287
no. They left it a mystery. What is worse, all the learned colleagues reading the
article over the years failed to think of electrodeposition, too. Just where did they
believe that the gold in their deposits of plaque had come? It had to have come from
their own gold electrode.

The literature also revealed a small indirect relationship between hematocrit

and atherosclerosis 6 or none at all. 7 The equation for electrodeposition in ohmic
materials8 with hematocrit in denominator explains this phenomenon and others.

weight of electro deposit = (I * t * A)/(z * F)

or by substitution

where I = V/R, from basic physics

and R = Δ * L/a, again from basic physics

and Δ , the resistivity of blood, which depends on the hematocrit as

Δ = 53.2 * e0.022H Function per Geddes and Sadler, 1973.9

Thus:
 
Atherosclerotic plaque mass = f  ___VtAa___________ 
 
 53.2 e0.022H LzF 
 
V = voltage in volts
I = current in amps
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t = time in seconds
A = atomic weight of species deposited
z = valence of species deposited
F = Faraday's constant of 96,500 coulombs (amp-sec.)
H = blood hematocrit
L = length of conductor (basically aorta length, explaining body habitus effects)
a = cross sectional area of conductor > 6 mm (complex function), (again, primarily the aorta
here.) Aortas are wider in wide people and thinner in skinny people.

Is that cool or what!

Another powerful prediction made by the model is that factors affecting the
cross-sectional area and length of the aorta would affect atherosclerosis, predicting
that obesity and short stature would carry additional risk. Obese people of short
stature do carry increased risk of atherosclerosis and heart disease!10, 11

Concentration of the electrolyte, agitation, temperature, addition agents and

the nature of the electrolyte also contribute to electrodeposition. Addition agents
employed in metallurgical electrodeposition include sugars, camphor, coal-tar
derivatives, colloidal gelatin, agar, glue, rubber or casein. Organic agents such as
sugar, coal tars, and casein improve adhesion but do not increase deposits per se. 8
Agitation also speeds electrodeposition8 but oddly, like concentration & temperature,
does not appear in theoretical calculations. Both are species-specific near-constants
anyway.

Not all atherosclerotic plaque accumulation is electrodeposition. Cholesterol

dissolves preferentially in lipid bilayers, for instance, and would accumulate where
lipid tails accumulate. But even cholesterol forms liquid crystals in the plaques! 11, 12
Nothing but electrodeposition can explain that.

Why small diameter arteries and capillaries remain clear of atherosclerotic

plaques has been a baffling problem,13 after all, if atherosclerosis resulted from some
blood born factor, presumably that factor was also present in arterioles, capillaries,
and veins, right? Electrodeposition in atherosclerosis explains why small diameter
arteries remain plaque-free. Diameters of 6 mm and smaller are avoided by

289
electroplaters as impractical. 8 No other model even comes close to explaining this
characteristic of atherosclerosis. Now it is no longer a mystery.

Another unusual characteristic of atherosclerotic plaques is that they tend to

form in areas of high blood turbulence. Areas of high turbulence within the arterial
system are unusually prone to plaque buildup.14 Again, this phenomenon is explained
by principles of electrodeposition. Although omitted from their basic equation, it is a
truism among electroplaters that the greater the agitation, the greater the
electrodeposition!8 Platers use special agitation jigs routinely.

Mantovani et al14 found lipid deposits in synthetic vascular prostheses

explanted from humans.15 Electrodeposits onto porous plastic tubing explains their
finding. Lipid uptake in synthetic vascular prostheses depended on the duration of
implantation of the prosthesis and on the sex of the patient.15 Lipid uptake also
depended upon the internal diameter of the prosthesis.15 Electrodeposition is a
function of time, and diameter of the tube8 since resistance varies with diameter and
current inversely with resistance. Along with hematocrit, 15 arterial diameters and
lengths depend upon age and sex. Without controlling for these anatomical
differences, men accumulate plaque faster than women do.16

The appearance of crystals in atherosclerotic plaques as amorphous and

crystalline phases has puzzled observers.17 Electrodeposition explains amorphous
and crystalline layers of variably sized crystals that are closely matched!18
Cholesterol and calcium are closely associated in crystal agglomerates within
atherosclerotic lesions.19 Again, mixed crystal deposition is typical of alloy
electroplating of alloyed metals,19 too! Organic and inorganic constituents of
atherosclerotic lesions accumulating together, as observed by Lee et al.,18 are
consistent with electrodeposition. Fine crystal grains form near the substrate with
much coarser grains at greater distances from the substrate in electrodeposition,19
following the same pattern as observed in early atherosclerotic plaques! Crystallinity
varies as a physical property 20 and virtually all chemical species capable of
crystallizing from blood are represented in atherosclerotic plaques,18 even cholesterol
as a liquid crystal.21 Over-voltage deposition results in larger unstable crystals being
electrodeposited.19 Depending upon voltage, electrodeposits can form different
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structures: amorphous layers (blisters), pyramids, spirals, whiskers and dendrites. In
electrodeposition, increasing ion concentration, higher temperature, and increasing
turbulence result in increased crystal size, while organic agents (such as sugar and
coal tars), increasing current density, and polarization result in finer grain deposits
(smaller crystal size).19

Autografted arteries occlude less frequently after bypass surgery.14 Autografts

are not as electrically active as the original coronary arteries they replace, due to
surgical denervation and scar tissue’s electrical discontinuity. Mammary arteries
similarly situated to occlusive arteries, seldom harbor atherosclerotic lesions,14 but the
mammary arteries are not within the heart’s electro-stimulation circuit. Scar tissue is
much less conductive than healthy coronary pathways as observable on EKG. Do
you see? Another conundrum falls.

Electrodeposition explains the accumulation of plaques within arteries

supplying electrogenic organs. The heart and mesentery are highly electrogenic.
Like the heart, the brain and kidney both possess their own electrical pacemakers. 22

As when an artery is autografted, in internally irradiated arteries restenoses

form less frequently.23 Radiation scars. Radiation scarring compromises the
electrical conductivity of the artery or innervation.

Atherosclerotic plaques are also discontinuous and focal.14 Discontinuous

deposits may suggest electrodeposition due to focal anodal charge.
Electrodepositions persist after removal of an electrical stimulus, so atherosclerotic
electrodeposition may be episodic. Normal lab values and the current of the anodal
QRS complex of the AV node can be inserted into the above equation and would be
sufficient to deposit atherosclerotic plaque mass. Try it!

An inward rectifier current is present in arterial smooth muscle cells 24 while

veins lack it. There is evidence that steady direct currents are generated in living
bone by metabolic activity.25

Yet another unusual characteristic of atherosclerosis is the unusual propensity

of diabetics to develop hardening of the arteries.26 Sugar is among the organic agents
291
used by electroplaters found empirically to improve electro-deposit consistency and
adherence to substrates but does not increase mass of deposition per se.8

Tar and nicotine may enhance atherosclerosis in tobacco users. Coal tars, like
sugar, are used to enhance adhesion in the electroplating process.8 Cigarette tar may
behave similarly in the blood.

A class of nicotinic sites consists of chemoreceptors on sensory nerve endings

-- especially certain chemo-sensitive nerve endings in the coronary arteries, the
carotid and aortic bodies.27 These are among the commonest sites of atherosclerotic
plaque electrodeposition! Pharmacological activation of these sites by nicotine from
inhaled tobacco smoke would depolarize them, slightly enhancing anodal
electrodeposition of anionic lipids from the blood. This explains why tobacco
smokers are more susceptible to atherosclerosis along with other factors such as wall
permiability to electronegative species.28

Reactive oxygen species have been implicated in the pathogenesis of

atherosclerosis and hypertension, in part by promoting vascular smooth muscle cell
growth.29 Oxidation as utilized in fuel cells, generates DC currents. Bioelectric
sources are mathematically capable of electrodepositing the heaviest atherosclerotic
plaques. Small voltages between electrodes around the carotid artery produce
vascular smooth muscle growth1 with electrodeposition functioning.

THE PHEROMONE ETIOLOGY OF ATHEROSCLEROSIS

Free fatty acids are carried in the blood by albumin and other carrier
proteins.30 Carrier proteins have been implicated as pheromone receptor proteins in
pheromone transduction.31 CD36 is a scavenger receptor important for lipoprotein
binding and uptake of cholesterol and lipids in vertebrates. In humans, loss of CD36
is linked to a wide range of disorders including insulin resistance, dyslipidemia, and
atherosclerosis.32 CD36 should be a pheromone receptor protein.33,34 Albumin
changes conformation35 on binding to pheromone,36,37 releasing ionic species 38 that

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alter the potential difference of nearby dendritic membranes to transduce
chemoreception.31

Heat shock proteins are a group of twenty-five highly conserved proteins up

or down regulated in response to stress that show extensive homology at the DNA and
protein level among bacterial and mammalian species. Stress releases alarm
pheromone in many species, including man. The heat shock proteins play an active
role in the development of autoimmune diseases in animals, and have been implicated
in human autoimmune diseases (i.e. rheumatoid arthritis, multiple sclerosis). An
induced immune response against heat shock protein 65 (HSP-65) results in
atherosclerotic lesions in normocholesterolemic rabbits 39,40,41 while HSP 60 antibody
is associated with atherosclerosis.42 Acquired thermotolerance of cells is unrelated to
the rapid synthesis of the characteristic spectrum of heat shock proteins. 43 HSP 90,
HSP 70 HSP 65, and HSP 28 all stain one way in normal-appearing regions of aorta,
but develop a heterogeneous pattern in the presence of atherosclerosis. 44 Given that
heat shock proteins are emitted under circumstances of alarm, they may serve as
extracellular pheromone receptor proteins. Changes of conformation upon
pheromone recognition could account for Johnson et al.’s41 inhomogeneity (but so
might simple precipitation). Heat shock proteins are necessary for pheromone
reception in yeast and other species 45,46,47 to account for its electrical effect upon
pheromone exposure33-35 albumin must release charged particles like pheromone
binding proteins.31 Release of free fatty acids on pheromone reception would allow
their accumulation out of solution as fatty streaks by electrolytic attraction to artery
walls.

Pheromones probably are responsible for most epigenetic effects observed in

atherosclerosis. Pheromones immediately release behavioral and physiological
changes, but they also alter behavior and physiology throughout ontogeny and even to
follow-on generations. Permanet changes in behavior and physiology suggest
epigenetic changes on DNA imprinted by pheromones. Phylogenic earliness is
evidenced by the pheromone release of epigenetic changes (fruiting bodies) in
colonial fungi.48 Pheromones do change the quartenary structure of DNA (e.g. the
pheromone stimulated localization of genes to the nuclear periphery), leading to an
abacus-like cellular memory effect.49 Pathological epigenetic changes induced by
293
pheromones should be discoverable and should be reversible with epigentic and
pheromone therapy.

Dissatisfaction with one’s social circumstances is associated with

susceptibility to atherosclerosis and sudden cardiac death. 50 Lin et al. 51 associated
population density with atherosclerosis experimentally in female mice. Increasing
population density leads to increased puberty delay pheromone emissions 52 which in
this population53 is the likely cause of increased atherosclerosis. Given that
pheromones affect the immune system,54 and murine pheromone chemistry is already
fathomed,55 testing the pheromone hypothesis will be straightforward.

The sebaceous kissing pheromone of human beings56 has a large triglyceride

component with uniquely diverse stereochemistry 57 typical of pheromones of most
other species. A diversity of chain lengths can be found in the walls of atherosclerotic
plaque covered arteries,58 the unusual variety of chain lengths, simultaneous
appearance of odd and even chain lengths53 indicate that these lipids may be similar
to unique sebaceous lipids and or even sebaceous in origin (taken into the body by
kissing).51 Although Claire et al.53 failed to specify unsaturation position, it is
plausibly the same unique diversity of fatty acids, esters and triglycerides associated
with skin surface sebaceous film.52 The utility of these inhomogeneous components in
atherosclerotic lesioned aorta is suggested by the effects of similar lipids. Unusual
lipids in large, dietary quantities especially the omega-3 long chain fatty acids have a
protective effect against atherosclerosis 59,60,61 among many other physiological and
behavioral effects.62 All such effects have been observed or would be expected of
human pheromones. For instance, Dietary supplementation with either
eicosapentaenoic63 or docosahexaenoic64 acids decreases natural killer cell activity.
The same phenomenon is seen for murine stress pheromones in much smaller doses.65
Similarly, a diet high in fruits and raw vegetables alters gene function to improve
heart disease outcomes. 66 Ecological perception determining health & disease
includes perception of diet as well as social perception via pheromones.

Men’s regularly kissing a female spouse is anecdotally associated with an

increased life span by five years.67 Presumably frequency of kissing is inversely
proportional to social dissatisfaction. Atherosclerosis being the most frequent cause
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EXOCRINOLOGY
of death, the possible longevity benefit suggests that the kissing transfer of human
sebum, containing a diverse mixture of human typical free fatty acids, triglycerides,
esters and cholesterol esters, may produce some part of this benefit.

The lipids exchanged in kisses are hundreds of oddly substituted and straight
chain, saturated and mono-enoic, cis free fatty acids and triglycerides and their esters,
alcohols and metabolites. Unlike dietary lipids, these unique skin surface lipids vary
widely in both odd and even chain length from 7 carbons to 28 in a chain.52 While
kissing does not provide dietary quantities of these unusual lipids, dietary quantities
are necessary for pheromonal effect only from near-pheromonal species68 such as the
aforementioned n-3 (omega 3) long chain fish oils.

Omega-3 fatty acids may provide relief from PTSD, 69 benefit infant growth
and development, reduce rheumatoid arthritis pain and reduce overall and
cardiovascular mortality, myocardial infarction, and sudden cardiac death.70 Fish oil
seems to be only a partial substitute for kisses. The similar human kissing pheromone
mixture, synergistic and species-specific, must be even more beneficial against PTSD,
heart disease, and infant mortality.

Synergy has been observed in these and other beneficial health effects of
unusual dietary cis-monoenoic free fatty acids. 71 Synergy of action is another
characteristic typical of pheromones,72 and all are cis shaped in humans.

Pheromones are the most potent of all medicines often effective at the ultra-
trace level. 73 500 fold smaller quantities of pheromonal sebaceous skin lipids have
been found to elicit comparable activity when unsaturation position is displaced one
carbon on the chain.62

The beneficial health effects of some dietary fatty acids are species specific.63
Pheromones are species specific within ecological niches.65 Rats74 and mice75 have
pheromonal lipids in their furs somewhat similar to human sebum, and may help to
account for their unfortunate habitat choice in proximity to us.

Various trans-fatty acids have beneficial effects for particular species in large
dietary quantities.76 These may resemble species-specific pheromonal lipids
295
transferred in maternal and sexual contacts & via allogrooming, or they may have
anti-pheromonal effects.

Some dietary trans-mono- and polyenoic lipids increase coronary artery

disease while others, do not.77 Constitutional isomers of human-specific pheromonal
sebaleic acid were found in both groups. Sebaleic acid, the free fatty acid C18:2) 5,8
and found only on human skin surfaces is exclusively human.52 Sebaleic acid may be
potently beneficial in the treatment of autoimmune illnesses, if presented with
synergistic human sebaceous lipids in appropriate quantities. Anecdotal evidence in
my laboratory suggests that this same healthy adult male facial skin surface lipid
taken p.o. can be a broad-spectrum sociopatholytic with 150 mg in a single dose
curing criminal behavior, sexual perversions, and non-alcoholic drug addiction.

Because hostile social environments and low social support are associated
with increased carotid atherosclerosis 78 anger or aggression pheromones79 become
prime suspects. There has been no human anger pheromone yet identified, but
masculine testosterone diminishes upon exposure to female tears.80 Polyene lipids,
even conjugated trienoics, are found in the hair fat of men81 and would be candidates
for "hot-headed" emission. Indeed trienoic free fatty acids, perhaps the C18:3) 6,8,9
triene of human male hair lipid,75 are seen in atherosclerotic aorta walls as both free
fatty acid and triglyceride while absent from healthy aortic tissues.53 Its presence as
an irritant to vascular innervation might contribute to atherosclerosis
electrodeposition.

Because anger causes erection of nasal tumescence tissues to block the

chemosensory superior and middle meati,82 anger is prophylactic against
autoreception and alloreception of air-born human pheromones. So which patient
survives best on the wards, the weepy one or the angry one? Angry, aggressive
patients survive because they avoid pheromonal insults that lacrimating patients
receive. Such insults include air-born pheromones that probably cause sudden infant
death syndrome (SIDS), since electric fans have been associated with improved
prognosis83 and electric fans dissipate the pheromone plumes holding clinically
relevant concentrations of pheromones. Calm wind conditions are required for
pheromone communication in many species. Windy days see reduced crime, while
296
EXOCRINOLOGY
calm winds encourage criminal behavior in humans,84,85 another likely insult escaped
by angry patients.

So why do some people get plaque accumulation when others with the same
risk factors do not? A strike of substrate or special cleaning procedures may be
needed to improve cohesion and initiate deposition on metals, glass, and plastic.
8,86,87,88 Presumably, something akin takes place intravascularly. Pheromone

receptions are also individually unique and account for accumulated epigenetic
differentiation between identical twins.

CLINICAL IMPLICATIONS

A formula derived empirically from electroplating experience explains the

biological mechanism of atherosclerotic electrodeposition. The formula shows how
currents of injury, advanced age, and large body size with short stature and other
factors may contribute to risk of atherosclerosis. Avoiding chronic anemia (raising
hematocrit) or anything increasing the resistivity of blood should decrease
atherosclerotic electrodeposition.

Given that the first four phases of atherosclerosis progress mainly by lipid
accumulation,5 these might be reversed by vascular insertion of pulsatile low voltage
DC electrodes for plaque electroacquisition and removal via the femoral artery.
Ultrasound might smooth such electronic stripping of plaques as it does in
electrodeposit removal.75

One beneficial and two detrimental pheromone sets are suggested in the
pathogenesis of atherosclerosis deriving from kissing, stress, and anger, respectively.
Lacrimation increases with stress and may indicate pheromone receptivity32 instead of
a specific pheromone set. Human pheromones have not yet been tested in the
pathology or treatment of atherosclerosis. If pathological autoimmune and cancerous
epigenetic changes are indeed induced by pathogenic human pheromones, then

297
human pheromone remedies from among the human skin surface lipids or other
semiochemical (naturally derived non-steroidal anti-inflamatory drugs, statins, taxol,
and quinine are all allomones) interventions may prove beneficial or perhaps even
curative.

Epigenetic pheromone therapy may be promising. For instance, low dose

decitabine combined with healthy adult male facial skin surface secretion (paternal
kiss) pheromone and perhaps non-steroidal anti-inflamatory drugs for their
pheromone prophillaxis, may prove particularly useful in the treatment of
atherosclerosis and heart disease, as well.

1Apfel H, Friedmann B, Betz. Experimentelle arteriosklerose: Räumliche Proliferatausbildung als

Folge ortsabhängig unterschiedlicher elektrischer Feldstärke? In: Heinle H, Schulte H, Schaeffer H,
editors. Vieweg Verlag Braunschweig 1992;306-12.
2Betz E, Schlote W. Responses of vessel walls to chronically applied electrical stimuli. Basic Res
Cardiol Jan/Feb;74(1):10-20.
3 Apfel H, Friedmann B, Betz E, Meyer-Waarden K. [Distribution of the electric field in producing
arteriosclerotic changes in the vascular wall by electrostimulation]. Biomed Tech (Berl) 1990;35 Suppl
3:310-311.
4 Tegos TJ, Kalodiki E, Sabetai MM, Nicolaides AN. The genesis of atherosclerosis and risk factors: a

review. Angiology 2001 Feb;52(2):89-98.

5Schoen FJ, Cotran RS. Blood Vessels. In: Cotran RS, Kumar V, Collins T, editors. Robbins
pathologic basis of disease 6th ed. Philadelphia: WB Saunders Company; 1999. p.493-541.
6Hartley CJ, Reddy AK, Madala S, Martin-McNulty B, Vergona R, Sullivan ME, Halks-Miller M,
Taffet GE, Michael LH, Entman ML, Wang YX. Hemodynamic changes in apolipoprotein E-knockout
mice. Am J Physiol Heart Circ Physiol 2000 Nov;279(5):H2326-34.
7Jeng JS, Chung MY, Yip PK, Hwang BS, Chang YC. Extracranial carotid atherosclerosis and
vascular risk factors in different types of ischemic stroke in Taiwan. Stroke 1994 Oct;25(10):1989-93.
8Glasstone S. The Fundamentals of Electrochemistry and Electrodeposition. American
Electroplaters' Society Palisade, New Jersey: Franklin Publishing Company, Inc; 1943.
9Geddes LA, Sadler C. The specific resistance of blood at body temperature. Medical and Biological
Engineering 1973 May: 336-9.
10Kortelainen ML, Sarkioja T. Coronary atherosclerosis associated with body structure and obesity in
599 women aged between 15 and 50 years. Int J Obes Relat Metab Disord 1999 Aug;23(8):838-44.
298
EXOCRINOLOGY
11Scolari F, Tardanico R, Zani R, Pola A, Viola BF, Movilli E, Maiorca R. Cholesterol crystal
embolism: A recognizable cause of renal disease. Am J Kidney Dis 2000 Dec;36(6):1089-109.
12Hata Y, Insull W Jr. Significance of cholesterol esters as liquid crystal in human atherosclerosis.
Jpn Circ J 1973 Mar;37(3):269-75.

13 Libby P. Atherosclerosis. In: Fauci AS, Martin JB, Braunwald E, Kasper DL, Isselbacher KJ,

Hauser SL, et al., editors. Harrison's principles of internal medicine. 14th ed. New York: McGraw-Hill
Health Professions; 1998. p.1345-1352.
14Mantovani D, Vermette P, Guidoin R, Laroche G. Lipid uptake in synthetic vascular prostheses
explanted from humans. Biomaterials 1999 Jun;20(11):1023-32.
15 Hillman RS. Anemia. In: Fauci AS, Braunwald E, Isselbacher KJ, Wilson JD, Martin JB, Kasper

DL, et al., editors. Harrison's principles of internal medicine. 14th ed. New York: McGraw-Hill
Health Professions Division; 1998. p. 334-339.
16 Di Tullio MR, Sacco RL, Savoia MT, Sciacca RR, Homma S. Gender differences in the risk of
ischemic stroke associated with aortic atheromas. Stroke 2000 Nov;31(11):26237.
17Lee YS, Chen HC, Lai SM. High resolution electron microscopic investigation of atomic structural
images in human atherosclerotic plaque. Proc Natl Sci Counc Repub China B 1992 Oct; 16(4):
169-176.
18
Paunovic M, Schlesinger M. Fundamentals of Electrochemical deposition. Wiley-Interscience John
Wiley & sons, Inc. New York; 1998.
19Hirsch D, Azoury R, Sarig S, Kruth HS. Colocalization of cholesterol and hydroxyapatite in human
atherosclerotic lesions. Calcif Tissue Int 1993 Feb;52(2):94-8.

20 Morrison RT, Boyd RN. Organic chemistry. 5th ed. Boston: Allyn and Bacon, Inc.;1987.
21 Juhasz J. [Embolism caused by cholesterol crystal] Orv Hetil 1961 Sep 10;102:1729-34.

22 With enzymatic processes yielding opposite polarity of proximal & distal convoluted tubule lumens
(Brenner BM, Mackenzie HS, 1998 Harrison’s) and medullary salt bridges, kidney structure combines
elements of both fuel cell and battery. The juxtaposition of proximal and distal convoluted tubules and
the potential difference of their lumens demonstrates catagorically that the kidney electrically scrubs
blood of charged particles for waste removal much as similar devices remove polluting charged
particles from industrial pollution.
23Waksman R, Robinson KA, Crocker IR, Gravanis MB, Cipolla GD, Seung KB, et al. Intracoronary
radiation decreases the second phase of intimal hyperplasia in a repeat balloon angioplasty model of
restenosis. Int J Radiat Oncol Biol Phys 1997 Sep 1;39(2):475-80.
24Quayle JM, McCarron JG, Brayden JE, Nelson MT. Inward rectifier K+ currents in smooth muscle
cells from rat resistance-sized cerebral arteries. Am J Physiol 1993 Nov;265(5 Pt 1):C1363-70.
25 Otter MW, McLeod KJ, Rubin CT. Effects of electromagnetic fields in experimental fracture repair.

Clin Orthop 1998 Oct;(355 Suppl):S90-104.

299
26Alexander CM, Landsman PB, Teutsch SM. Diabetes mellitus, impaired fasting glucose,
atherosclerotic risk factors, and prevalence of coronary heart disease. Am J Cardiol 2000 Nov 1;86(9):
897-902.
27Pappano AJ. Wantanabe AM. Cholinoceptor-activating & cholinesterase-inhibiting drugs. In:
Katzung BG, editor. Basic & clinical pharmacology. Norwalk, Connecticut: Appleton & Lange
Division of Prentice Hall; 1992. p. 88-102.
28Allen DR, Browse NL, Rutt DL, Butler L, Fletcher C. The effect of cigarette smoke, nicotine, and
carbon monoxide on the permeability of the arterial wall. J Vasc Surg 1988 Jan;7(1):139-52.

29 Liao DF, Jin ZG, Baas AS, Daum G, Gygi SP, Aebersold R, Berk BC. Purification and
identification of secreted oxidative stress-induced factors from vascular smooth muscle cells. J Biol
Chem 2000 Jan 7;275(1):189-96.
30Malloy MJ, Kane JP. Agents used in hyperlipidemia. In: Katzung BG, editor. Basic & clinical
pharmacology. 6th ed. Norwalk, CT: Apple & Lange; 1995. p. 522-35.
31 Nicholson B. Pheromones cause disease: pheromone/odourant transduction. Med Hypotheses 2001

57(3):361-377.

32Jin X, Ha TS, Smith DP. SNMP is a signaling component required for pheromone sensitivity in
Drosophila. Proc Natl Acad Sci U S A. 2008 Aug 5;105(31):10996-11001. Epub 2008 Jul 24.
33 Rogers ME, Sun M, Lerner MR, Vogt RG. Snmp-1, a novel membrane protein of olfactory neurons
of the silk moth Antheraea polyphemus with homology to the CD36 family of membrane proteins. J
Biol Chem. 1997 Jun 6;272(23):14792-14799.
34Martin C, Chevrot M, Poirier H, Passilly-Degrace P, Niot I, Besnard P. CD36 as a lipid sensor.
Physiol Behav. 2011 Feb 24; [Epub ahead of print]

35 Barnes C, Lewis TJ. Shear-wave detection of structural effects in aqueous solutions of bovine
serum albumin and hemoglobin. J Acoust Soc Am 1991 Sep;90(3):1287-1297.

36 Vogt RG. The molecular basis of pheromone reception: its influence on behaviour. In: Prestwich

GD, Blomquist GJ, editors. Pheromone biochemistry. Orlando: Academic Press. 1987:385-431.

37 Van den Berg MJ, Ziegelberger G. On the function of the pheromone-binding protein in the
olfactory hairs of Antheraea polyphemus. J Insect Physiol 1991;37:79-85.

38 Vogt RG, Prestwich GD, Lerner MR. Odourant-binding-protein subfamilies associate with distinct
classes of olfactory receptor neurones in insects. J Neurobiol 1991;22(1):74-84.

39Gruber R, Lederer S, Bechtel U, Lob S, Riethmuller G, Feucht HE. Increased antibody titers against
mycobacterial heat-shock protein 65 in patients with vasculitis and arteriosclerosis. Int Arch Allergy
Immunol 1996 May;110(1):95-98.

40 Afek A, George J, Gilburd B, Rauova L, Goldberg I, Kopolovic J, Harats D, Shoenfeld

Y.Immunization of low-density lipoprotein receptor deficient (LDL-RD) mice with heat shock protein
65 (HSP-65) promotes early atherosclerosis. J Autoimmun 2000 Mar;14(2):115-121.

300
EXOCRINOLOGY
41Mukherjee M, De Benedictis C, Jewitt D, Kakkar VV. Association of antibodies to heat-shock
protein-65 with percutaneous transluminal coronary angioplasty and subsequent restenosis. Thromb
Haemost 1996 Feb;75(2):258-260.
42Zhu J, Quyyumi AA, Rott D, Csako G, Wu H, Halcox J, Epstein SE. Antibodies to human heat-
shock protein 60 are associated with the presence and severity of coronary artery disease: evidence for
an autoimmune component of atherogenesis. Circulation 2001 Feb 27;103(8):1071-1075.
43Barnes CA, Johnston GC, Singer RA. Thermotolerance is independent of induction of the full
spectrum of heat shock proteins and of cell cycle blockage in the yeast Saccharomyces cerevisiae.J
Bacteriol 1990 Aug;172(8):4352-4358.
44Johnson AD, Berberian PA, Tytell M, Bond MG.Atherosclerosis alters the localization of HSP70 in
human and macaque aortas. Exp Mol Pathol 1993 Jun;58(3):155-68.
45Louvion JF, Abbas-Terki T, Picard D. Hsp90 is required for pheromone signaling in yeast. Mol Biol
Cell 1998 Nov;9(11):3071-3083.
46Louvion JF, Warth R, Picard D. Two eukaryote-specific regions of Hsp82 are dispensable for its
viability and signal transduction functions in yeast. Proc Natl Acad Sci U S A 1996 Nov 26;93(24):
13937-42.
47Savarit F, Sureau G, Cobb M, Ferveur JF. Genetic elimination of known pheromones reveals the
fundamental chemical bases of mating and isolation in Drosophila. Proc Natl Acad Sci U S A 1999
Aug 3;96(16):9015-20.
48Mayrhofer S, Jan M. Weber JM, Pöggeler S. Pheromones and Pheromone Receptors Are Required
for Proper Sexual Development in the Homothallic Ascomycete Sordaria macrospora. Genetics, 2006
March; 172:1521-1533.
49 Brickner DG, Cajigas I, Fondufe-Mittendorf Y, Ahmed S, Lee P-C, Widom J, Brickner JH. H2A.Z-
mediated localization of genes at the nuclear periphery confers epigenetic memory of previous
transcriptional state. PLoS Biol, 2007 April;5(4):e81.
50Krishnan KR. Depression as a contributing factor in cerebrovascular disease. Am Heart J 2000
Oct;140(4 Suppl):70-76.

51Lin AH, Castle CK, Melchior GW, Marotti KR. The effect of population density on the
development of experimental atherosclerosis in female mice. Atherosclerosis 1995 May;115(1):85-88.
52 Drickamer LC. Puberty-influencing chemosignals in house mice: ecological and evolutionary
considerations. In: Duvall D, Müller-Schwarze D, Silverstein RM, editors. Chemical signals in
vertebrates 4. New York: Plenum Press; 1986. p.441-456.
53Drickamer LC, Mikesic DG. Urinary chemosignals, reproduction, and population for house mice
(Mus domesticus) living in field enclosures. J Chem Ecol 1990;16(10):2955-2968.

54Cocke R, Thiessen D. Alarm chemosignals suppress the immune system. In: MacDonald DW,
MüllerSchwarze D, Natynczuky SE, editors. Chemical signals in vertebrates 5. Oxford: Oxford
University Press, 1990:125-138.

301
55Novotny M, Jemiolo B, Harvey S. Chemistry of rodent pheromones: molecular insights into
chemical signaling in mammals. In: Macdonald DW, Müller-Schwarze D, Natynczuk SE, editors.
Chemical signals in vertebrates 5. Oxford: Oxford University Press; 1990. p.1-23.
56Nicholson B. Does kissing aid human bonding by semiochemical addiction? [Comment] Brit J
Dermatol 1984 Nov;111:623-627.
57Nicolaides N. Skin lipids: their biochemical uniqueness, unlike internal organs, the skin
biosynthesizes and excretes unusual fat soluble substances. Science 1974 Oct 4;186:19-26.
58 Claire M, Jacotot B, Robert L. Characterization of lipids associated with macromolecules of the
intercellular matrix of human aorta. Connect Tissue Res 1976;4(2):61-71.

59 Yamada T, Strong JP, Ishii T, Ueno T, Koyama M, Wagayama H, Shimizu A, Sakai T, Malcom GT,
Guzman MA Atherosclerosis and omega-3 fatty acids in the populations of a fishing village and a
farming village in Japan. Atherosclerosis 2000 Dec;153(2):469-481.
60
Angerer P, von Schacky C. n-3 polyunsaturated fatty acids and the cardiovascular system. Curr
Opin Lipidol 2000 Feb;11(1):57-63.
61Das UN. Beneficial effect(s) of n-3 fatty acids in cardiovascular diseases: but, why and how?
Prostaglandins Leukot Essent Fatty Acids 2000 Dec;63(6):351-362.
62Connor WE. Importance of n-3 fatty acids in health and disease. Am J Clin Nutr 2000 Jan;71(1
Suppl):171S-175S.
63 Thies F, Nebe-von-Caron G, Powell JR, Yaqoob P, Newsholme EA, Calder PC. Dietary
supplementation with eicosapentaenoic acid, but not with other long-chain n-3 or n-6 polyunsaturated
fatty acids, decreases natural killer cell activity in healthy subjects aged >55 y. Am J Clin Nutr 2001
Mar;73(3):539-48.
64 Kelley DS, Taylor PC, Nelson GJ, Schmidt PC, Ferretti A, Erickson KL, Yu R, Chandra RK,
Mackey BE. Docosahexaenoic acid ingestion inhibits natural killer cell activity and production of
inflammatory mediators in young healthy men. Lipids 1999 Apr;34(4):317-324.
65 Cocke R, Thiessen D, Nicholson B. Alarm chemosignals suppress the immune system. In:
MacDonald DW, Müller-Schwarze D, Natynczuk SE, editors. Chemical signals in vertebrates 5.
Oxford: Oxford University Press; 1990. p.125-131.

66 Ron Do, Changchun Xie, Xiaohe Zhang, Satu Mannisto, Kennet Harald, Shofiqul Islam, Swneke D.
Bailey, Sumathy Rangarajan, Matthew J. McQueen, Rafael Diaz, Liu Lisheng, Xingyu Wang, Kaisa
Silander, Leena Peltonen, Salim Yusuf, Veikko Salomaa, James C. Engert, and Sonia S. Anand The
Effect of Chromosome 9p21 Variants on Cardiovascular Disease May Be Modified by Dietary Intake:
Evidence from a Case/Control and a Prospective Study PLoS Med 9(10): e1001106. doi:10.1371/
journal.pmed.1001106
67 Coleman V. The story of medicine. London: R. Hale;1985. P 1.

68Silverstein RM. Chemistry of insect communication. In: Lewis T, editor. Insect communication.
London: Academic Press; 1984. p. 105-21.

302
EXOCRINOLOGY
69Matsuoka, Yutaka. Clearance of fear memory from the hippocampus through neurogenesis by
omega-3 fatty acids: A novel preventive strategy for posttraumatic stress disorder?
BioPsychoSocial Medicine 2011, 5:3
70Oh R. Practical applications of fish oil (Omega-3 fatty acids) in primary care. J Am Board Fam
Pract. 2005 Jan-Feb;18(1):28-36.

71Pakala R, Radcliffe JD, Benedict CR. Serotonin-induced endothelial cell proliferation is blocked by
omega-3 fatty acids. Prostaglandins Leukot Essent Fatty Acids 1999 Feb;60(2):115-123.

72 Silverstein RM, JO. Rodin, and D.L. Wood Sex attractants in frass produced by male Ips confusus

in ponderosa pine. Science 1966;154:509-510.

73 Wilson EO. Pheromones. Scientific American 1963;208:100-106.

74 Nicolaides N, Ansari MNA. Fatty acids of unusual double-bond positions and chain lengths found
in rat skin surface lipids. Lipids 1968;3(5):403-410.
75Wilkinson DI, Karasek MA. Skin lipids of a normal and a mutant (asebic) mouse strain. J Invest
Dermatol 1966;47(5):449-455.
76
Kritchevsky D. Antimutagenic and some other effects of conjugated linoleic acid. Br J Nutr. 2000
May;83(5):459-465.
77 Hodgson JM, Wahlqvist ML, Boxall JA, Balazs ND. Platelet trans fatty acids in relation to
angiographically assessed coronary artery disease. Atherosclerosis. 1996 Feb;120(1-2):147-154.
78 Knox SS, Adelman A, Ellison RC, Arnett DK, Siegmund K, Weidner G, Province MA. Hostility,
social support, and carotid artery atherosclerosis in the National Heart, Lung, and Blood Institute
Family Heart Study. Am J Cardiol 2000 Nov 15;86(10):1086-1089.
79 Sandnabba K. Differences between aggressive and non-aggressive mice in odour signals and
marking behaviour. In: MacDonald DW, Müller-Schwarze D, Natynczuk SE, editors. Chemical
signals in vertebrates 5. Oxford: Oxford University Press; 1990. p.459-464.

80Shani Gelstein, Yaara Yeshurun, Liron Rozenkrantz, Sagit Shushan, Idan Frumin, Yehudah Roth,
and Noam Sobel Human Tears Contain a Chemosignal. Science 1198331Published online 6 January
2011 [DOI:10.1126/science.1198331]
81Weitkamp AW, Smiljanic AM, Rothman S. The free fatty acids of human hair fat. J Am Chem Soc
1947;69:1936-1939.
82 Holmes TH, et al. The Nose; an experimental study of reactions within the nose in human subjects

during varying life experiences with a forward by Warfield T. Lonscope. Springfield, Ill: Thomas;
1950.
83Coleman-Phox K, Odouli R, and Li D. Use of a fan during sleep and the risk of sudden infant death
syndrome. Arch Pediatr Adolesc Med. 2008;162(10):963-968.
84 Rotton J, Frey J. Air pollution, weather, and violent crimes: concomitant time-series analysis of
archival data. J Pers Soc Psychol. 1985 Nov;49(5):1207-1220.

303
85 Indeed in open, anecdotal trials, my laboratory has effected cures of criminal behavior, addiction,
and sexual perversion with a home remedy of healthy adult male facial skin surface lipid pheromone
delivered p.o. in a single 150mg dose on chewing gum vehicle. We now have a double-blind, cross-
over trial under way.
86 Val'syunene YI, Rachinskas VS. Electrodeposition of magnetic coatings on glass. In: Slutzkin D.

editor. Electrodeposition of metals; proceedings of the 10th Lithuanian conference of electrochemists,

Dec. 12-13 1968. Jerusalem: Israel Program for Scientific Translations; Springfield, Va.: U.S. Dept. of
Commerce, Clearinghouse for Federal Scientific and Technical Information; 1970.
87 Kochergin SM, Vyaseleva GY. Electrodeposition of metals in ultrasonic fields. New York:
Consultant's Bureau; 1966.

88 Saubestre EB, Typical processing and operating sequences b. plastics. In: Graham AK, editor.
Electroplating Engineering Handbook. 3rd ed. New York: Van Nostrand Reinhold Company; 1971. p.
212-213.

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EXOCRINOLOGY

Chapter 12: The Function of Myelin

The Schwann/oligodendritic cells/axon device propagates transients

electrically, utilizing serial discharges of electric and magnetic fields. With current at
the node of Ranvier, a triphasic signal results, inductive and capacitative discharges
leading and lagging, respectively.

The peculiar structure of myelinated axons persuades us both the error of

previous models and the correctness of this one. The Schwann cell wraps numerous
times around the axon. Unnecessary for insulation function, wraps thinned to an
extreme constrain cell maintenance unnecessarily. A simple fat cell would do a better
insulating job than a Schwann cell.

Electrically conductive "dense lines" found in Schwanns serve no insulative

purpose, but must be present to induce an opposite charge for this proposed
capacitative function. Maintaining that conductivity comes at an economic cost, as
well. The dense line conductivity exceeds that of normal somatic cytoplasm.
Specialized rigid proteins for the purpose also obstruct cell maintenance.

As expected by economic theory, Schwann cell membranes are both the best
and the thinnest dielectrics available to the body. Both characteristics enhance
capacitive properties as all cell membranes except the outer one intervene between
planes hypothesized to bear opposite charges.

Unwound, each Schwann cell shows an enormous surface area. Again this is
unnecessary for insulation. However, capacitors improve directly with increased
surface area. If Schwann cells function as capacitors, their enormous surface areas
perform an important service.
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 All Schwann cells along a particular peripheral nervous system nerve unwind
to equal surface areas irrespective of the body tissue traversed by that nerve. Yet,
different tissues possess differing insulating properties. Accordingly, maintaining
uniform insulating cells allocates resources sub-optimally.

Capacitors in series add capacitance as inverses yielding one capacitance

smaller than any. Given that capacitance is expensive and logarithmically more
expensive as surface area and capacitance increases, and given identical biological
material constrains, circuits of capacitors in series are most economical when every
capacitor is of equal capacitance.

From basic physics, equilibrium would oppose unequal contributions. At the

same time, equal capacitances for sequentially discharging capacitors optimizes
functionally as well as economically. Serial discharges of capacitances propagating
signals like falling dominos would require equal capacitances, much like dominos
require equal potential energies. Equal surface areas in similarly constructed
capacitors yield equal capacitances.

Summation of capacitance in series.

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Electrical diagram of capacitors in series.

Distributed energy storage in the magnetic fields of inductors formed by

lapping Schwann wraps and enhanced by the axon core (like a solenoid) might be
expected, too. The reactances, inductive and capacitative, would reach equilibrium at
equal values. Current across a node of Ranvier would then reflect local capacitance
and inductance in a biphasic pulse with inductance leading, capacitance following.
Such bi-modality is seen and (hypothesized as erroneously) attributed to respective
membrane permeabilities of Na+ and K+.

Capacitance of a parallel plate condenser, the area of whose plates is A and the

distance between them d, is given as

C = (KA)/(4(pi)d)

where K is the dielectric constant of the medium.

307
Capacitors in cross section. The one at lower left looks much like a Schwann cell or
an oligodendrite wrapping an axon.

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EXOCRINOLOGY

309
Schwann cells all exactly the same size, but only on the same axon.

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Oligodendrocytes can connect more than thirty axons this way, shifting charge among
each wrapping inside the blood-brain barrier inside the central nervous system--the
brain and spinal cord. Schwann cells are for peripheral nerves.

Saltatory neural conduction would be Schwann cells along axons acting

sequentially as capacitors discharging one after another as the tide of slightly
increased charge advances. Nodes of Ranvier excite in sequence. Inter nodal ion
pumping would provide efficiently distributed energy sources.

CNS oligodendrites would perform similarly. However, oligodendrites,

wrapping many different axons, would share capacitances among parallel axons, to
switch and alter neural transmissions in associations. Oligodendrites would then be
the transistor of the central nervous system. The "white matter" making up about
40% or so of the brain’s mass, would assume intelligent functionality rather than
unintelligent and witless insulation. The gradual accumulation of oldigodendrites in
human adolescence now makes better sense.
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 Synesthetes, people who associate colors with letters for instance, mix
perceptions localized to adjacent areas of the brain. If oligodendrites of the white
matter are shared capacitance switches, now we know how: parasitic capacitance.

THE TRIGGER ZONE

Summation describes the strange behavior of the trigger zone of the axon
hillock. The axon hillock is that part of the axon extending from a nerve cell body to
the first Schwann cell. This axon hillock has no special structures, and looks to all
the world like a simple cell membrane. However, magical powers are attributed to it.

The axon hillock's so called "trigger zone" appears to control the phenomena
of "summation," propagation, excitation, and inhibition, all while exhibiting the
keenest electro-sensitivity of any cell area. That is quite a feat for a simple membrane.
Summation describes the trigger zone's mysterious ability to count up additions and
subtractions of electrical stimulation over a short period. When the energy inserted
into the trigger zone is high enough over a short, nerve specific period the axon fires,
or propagates an excitation (excitatory postsynaptic potential, or EPSP) down the
axon.

The trigger zone's magic summation behavior could be duplicated simply by

filling and emptying charged ions (capacitance) into the wound Schwann cell right at
the edge of the trigger zone. It becomes a circuit describable by physics instead of
bio-mumbo-jumbo. Depleting charge from the Schwann would inhibit firing.
Several circuit devices could short and restore capacitors across subsequent nodes of
Ranvier in series depending upon voltages applied. A voltage sensitive switch, on
and off, must be found within the Schwann/node interface.

No structure in trigger zones is capable of EPSP and IPSP summation. A

voltage sensitive switch shorted capacitance (and parallel resistance / inductance
representing heat and conduction losses and delayed inductor contribution) in series
could account for summation, accommodation, and habituation in an electrical model
of neural function.
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HEAT OF CAPACITORS GENERATED WITHOUT O2

Myelinated neurons put off a lot of heat. They are 50 X's hotter than
unmyelinated C-fibers of the same size. Yet oxygen consumption is 6% for white
matter vs. 94% for grey matter! Only a functioning capacitor would heat with a low
O2 consumption.

In-cord coordinated movements (decerebrate cat on a treadmill) and the need

for neural decussation follow from oligodendritic shared capacitance switching and
limited capacitance transmission. Thus oligodendrites would "connect" crossing
nerves and severing the cord below decussation would eliminate all but neural
bilateral coordination.

Schwann and especially oligodendritic capacitors are variable. How do you

vary that capacitance? Just shrink or swell the cell, the plates move closer or further
apart, affecting capacitance. Thus the same old neurotransmitter/hormone receptor
mediated channels on the cell membrane which normally affect cell turgidity, also
alter neural function. Given shared capacitance switching, a neurohormone can
switch firing programs, and alter behavior.

The mechanism for gross chemical neurological influence, hormones that

affect the nervous system, would involve influencing membrane bound Na+ ports on
the Schwann cell surface. H+ ATPase regulates turgidity in the cell by controlling
ionic concentrations. Swelling or shrinking of cells is managed thereby. The same
mechanism is proposed for neurohormones. They merely behave exactly like they
have been shown to behave. They affect the salt balance inside the Schwann cell by
binding and triggering membrane bound proteins which loosen or tighten the ion
channel. With a higher interior salt concentration, water moves into the Schwann
cell. Water moving into the Schwann cell causes "dense lines" and "thin lines" to
move apart slightly by cellular swelling. Moving apart conductive surfaces in a
capacitor (the ‘d’ in our capacitance formula) diminishes capacitance, changing neural
function.

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LINEAR ACCELERATORS IN ION TRANSPORT PROTEINS

This last model better explains the kinetics and characteristics of

transmembrane ion transmission. Physical and economic efficiencies of cation and
anion propulsion argue for use of a simple machine, the linear particle accelerator, in
transmembrane ion displacement. Particle confinement devices identical to those of
linear accelerators are found in trans-membranous alpha helixes surrounding rigidly
juxtaposed Hückel’s rule magnets. Other oddities of kinetics, structure and function
find explanations within the model as well.

Phenyl groups set up strong magnetic fields detectable by nuclear magnetic

resonance techniques.1 By Lentz's law, current flows in a direction setting up
magnetic fields to oppose movement. Thus, the circulation of electrons of two phenyl
groups (or other similar magnetic field producing molecular structure) would flow to
oppose a mutual approach, and to withhold from a mutual withdrawal. Synchronized
approaches and withdrawals of serial phenyl pairs would open and close a linear
accelerator. Such approaches and withdrawals characterize vibration. Given the
length of the Alpha protein tube with phenyl groups in regular fixed opposition, the
natural frequency for the effect can be calculated. Failure of these tiny linear
accelerators, where Hückel’s rule amino acids fail to juxtapose to form the
containment field, is behind cystic fibrosis. Illuminating these broken cystic fibrosis
channel containing tissues with magnetic fields should have an observable and
perhaps beneficial effect.

By lining up these natural linear accelerators which transport ions across

membranes and joining the parts together in longer than natural rows, we can make
room temperature superconductor plasma conduits to carry protons or perhaps
microscopic ion propulsion devices. Biologists can now be rocket scientists!

In addition to Scotty’s ion power, a compact phasor design might be produced

which requires neither vacuum nor cryo-magnetic devices. The tiny diameter of the

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tube creates a perfect vacuum without pumps. Many such tubes may be laid down in
a fascist bundle.

Those interested must size the tube in proton ATP-ase, since it appears to be
the best candidate at first inspection. Calculate or determine resonant frequencies.
Count the juxtaposed Hückel’s rule amino acid side chains (at nodes?). Determine if
frequencies match observed conformational change frequencies. You may need to
‘peg’ the chain straight to some crystal to get started.

The old model of ion membrane transport--say in the nephron--calls for

mechanical binding and releasing of cations across membranes with all sorts of
baroque biochemical nonsense. The membranes of the proximal and distal tubules of
the glomeruli require a charge gradient between proximal and distal tubules to have a
potential difference sufficient to move those charged particles out of circulation. This
means that JG cells must function electrically, in similar means. Yet another medical
school physiology mystery solved.

Such movements of charged particles under the crazy-quilt of old models all
require co-transport of waters of hydration, which, from kinetic studies, would be
impossibly slow. The new model would transport only the cation (or anion) through a
virtually frictionless mechanism.

If you were God, which would you choose? It is funny that the invention of the linear
accelerator was hailed as the first invention divorced from natural precursors (e.g. the
electric motor has a naturally flagellar precursor). Oops! Each cell in our body has
hundreds of thousands of working linear accelerators, proton ATP-ase and others.

Rapid and regular conformational movements of proximal protein picking up

and releasing, say, a couple of magnesium cations in each iteration could act as the
pumping mechanism. This heretofore unexplained movement has been observed and
recorded. The charge on two magnesium cations are close enough and large enough
to have a significant repulsive charge effect on a proton's acceleration.

The design utilizes similar principles as a linear accelerator. The design

consists of a proteinaceous alpha helix. Within the lipophilic interior of the helix,
315
tryptophan phenyl groups repeatedly oppose each other in pairs. Oppositions across
the interior of the tube are phenyl end to phenyl center, thereby bringing opposite
magnetic fields into close, but just wide enough juxtaposition. Magnetic fields on a
number of molecular structures affects their NMR spectrometry, and is an effect
utilized in their detection. A representation of the toroidal magnetic field of a phenyl
group can be seen in the figure. These form the containment field guideway for
charged particles.

Additionally, particle acceleration is currently accomplished by a rapid

conformational change in another (or another part of the) protein nearby. A pair of
large cations are picked up near the proximal end of the alpha helix's tube. The
conformational change, ATP driven, moves the two cations distally beside the tube,
accelerating a proton or other cation through the tube.

Note that waters of hydration are left behind and only the particle moves
down the tube. Of course, the tube's girth being so small and fixed, contamination
risks diminish so that no vacuum is required. The event is friction free. Particles
move where they are aimed by the opposing opposite magnetic fields (North beside
South).

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The design is sensitive to amino acid substitution into the "gun barrel" of the
helix. Any substitution that results in bending renders the accelerator nonfunctional.
However, other than linear shapes might be feasible.

The Cl channels2 (Li, M., et al., 1988) may function similarly. The lack of
tryptophan's phenyl group at the interior base of the alphahelix closes ion exchange in
cystic fibrosis. In addition, an unexplained sensitivity to electric fields has been
reported (Li, M., et al., 1988).

[L]arge depolarizations increase the likelihood that Cl channels will open for
the first time (activate) in excised patches. Once a Cl channel was activated by
depolarization, it remained activated, even at hyperpolarized voltages, .... The way in
which depolarization modifies Cl channels is unknown but a voltage of +120 mV is
about 160-180 mV away from the normal membrane voltage, creating a very strong
electric field.

Multilayer stacked accelerators may have been described in chloroplasts, with

the significance of the structures not elucidated.

We have the ability to synthesize proton ATPase, or a portion of the helix

repeatedly. A tube such as that described above of any length can be manufactured,
however some substrate would be required to maintain linearity to which side chains
might attache. A crystal, perhaps?

The author is tempted to suggest a "dilithium crystal."

A MODEL OF MUSCLE FUNCTION

Current thinking has it that muscle contraction is stimulated electrically,

fueled chemically, and carried out mechanically.3 The thing between actin and
myosine appears more likely to be a levatation process, somewhat like a maglev train.
317
Thus only an amplification would be needed rather than two (2!) energy
transductions, plus even the energy of the activating motor neuron is utilized. The
friction question becomes manageable, since levitated surfaces never touch. This
model's correctness is obvious enough so as to require no further discussion. I will
leave it to experimentalists to work out the details.

1Silverstein Robert M., Bassler, G. Clayton, and Morrill, Terrence C. Spectrometric Identification of
Organic Compounds. 4th edition. New York: John Wiley & Sons.
2 Li M, McCann JD, Liedtke CM, Nairn AC, Greengard P, Welsh MJ. Cyclic AMP-dependent protein
kinase opens chloride channels in normal but not cystic fibrosis airway epithelium. Nature. 1988 Jan
28;331(6154):358-360.
3 Stryer, Lubert 1988; Biochemistry, Third Edition. New York: W.H. Freeman and Company.
1089p.

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Chapter 13: The Future

This book, for better or worse, is the birth of the medical specialty of
exocrinology. Perhaps the most obvious change for the future by exocrinology will
be the absence of criminals. Soon, we will need no prisons, no police, no locks, no
fences, no military, and we will have no practice of medicine as we know it. It will
be like the abandonment of tuberculosis sanitariums closed by inoculations and
antibiotics.

The cure for criminal behavior will see changes reminiscent of the changes
observed with the finding of the cure for tuberculosis, too. Institutions to deal with
criminals, with sexual perversion, with drug addiction, with unwed mothers, and
many more social ills will close and society overall will become more efficient. The
pace of the change is already gaining speed. The crime rate in the author’s new home
town of Tampa keeps dropping and dropping, but pheromone therapy contributes but
a small part of the decrease. Clearing ozone from local power plants probably helps
the most. Every successful criminal pheromone therapy (all have been successful)
takes off the street another criminal to improve our statistics. Soon, the need for
hiring policemen, the need for training policemen, these will decline and people who
would have endured that occupation will become available for other work. Similarly,
cured criminals will be available to become model employees, eager to learn, eager to
excel.

Sexual perverts will diminish in danger and number as the cure for their
ailment reaches their worried parents. The “cure” for homosexuality is just too easy
and universally available (on the end of every healthy father’s nose). Given the
fatherly desire for grandchildren, the “malady” will not “fester” much longer in
children. Exocrinologists will detect insufficient pheromone receptor proteins and
319
remedy them. On the plus side (for perverted people that is), receptivity for
homosexual pheromones may be manipulable as well.

Population rebelliousness may subside, too. Jihadists will be treated with the
pheromone, doubtless decried as forced sacraments. (Of course, providing
pheromone on chewing gum to captured enemy soldiers will be Christ’s sacrament of
communion. Christ must have been the first exocrinologist. That last supper was so
very much a meal of pheromones! And that intense feeling eating what remained of
Christ’s medicine chest three days after crucifixion, so yes they felt the presence of
Jesus Christ three days after his death.) The pheromone exposure history of Moslem
people, essentially smelling the feet in front of them, has enabled the jihad
phenomenon, which would be juvenile delinquency and criminality in western
cultures that lack forced daily foot-sniffing. The holy exposures to each other’s feet
by having all face Mecca, the fast of Ramadan, these have saved Muslims from many
Christian ills, so the great prophet Mohammed also was an exocrinologist. Human
pheromones, discovered and used by Jesus, will drown feelings of jihad entirely. The
air pollution that drives the jihad phenomenon, particularly high ozone
concentrations, must also drop to effectively end this rebellion against science,
learning, and wisdom.

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Here is a NASA map 1 of fine particulate matter in the air, roughly air
pollution. The correlation with social turbulence and rebellion is suggestive.

Nosocomial and community acquired infections will respond to human

pheromone therapy. Receiving one’s family pheromones will become standard
compassionate care for our death beds. Methicillin Resistant Staphylococcus aureus,
MRSA patients with weakened immune systems and others with weakened immunity,
all should benefit from pheromone therapy immediately. Even DIC, disseminated
intravascular coagulation, should respond to conventional antibiotic therapy and 150
mg of adult male facial skin surface lipid p.o. Why? Infection is allowed by the
human semiochemical commerce as a pheromonal mechanism to shed population in
the face of limited resources. Look at the siege of Mafeking. They kept great
records, and those that suffered most were lowest in hierarchical status. Look at the
death camps of the nazis, where low status, even the simple pheromone receptivity of
lacrimation, tears, could be counted on to reduce chances for survival. Pheromones
limit populations to available supplies of food and shelter, even behind barb wire.
Human crime and autoimmune pathology provide the lacking predation. Generally
more successful species (like humans and livestock) see increased parasitism. The
mechanism of reduced immunity is just a tuning of the pheromone vs allomone
recognition system that we call the immune system.

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 Animals caring for each other evolved in colonial bacteria, and before,
because a gene is a gene is a gene. The free-rider problem of economics and the
problem of altruism are both solved when one recognizes that improving the
prospects for one’s own genes is accomplished when those same genes reside in
others, too. Indeed, with the similarity of genomes, the wonder is that greater care is
not taken to preserve each other and nature everywhere.

In our time, autoimmune disease and cancers will cease to exist, as pheromone
therapy will be curative. Autoimmune disease and cancer probably evolved to
augment natural population pruning immediately after the invention of medicine back
at the dawn of time. Just as having antibiotics for soldiers gave the Allied armies
advantages against the Axis, caring for the sick ever more effectively advanced
societies. Exocrinology will bias the balance of life furthering that human
advantage.

Our schools will become centers of brilliance and creativity when all students
are free from their spiritual demons. Imagine a high school with only dedicated
students, none ever dropping out, with all seeking excellence to the very best of their
abilities. Indeed, we may see the need to establish special Orwellian reservations to
maintain the sparks to creativity that perversion and mental illness both provide.

The author is no stranger to educational innovation. In the 1950s, educational

achievement in Georgia, the author’s home state in America, averaged only to the
fourth grade. Now two years of college training is the norm because this author
proposed the HOPE Scholarship Program for free college education of deserving
students. The program was subsequently emulated in 23 US states.

The parasitism that is pet ownership will lessen to more manageable levels.
Allomones of dogs, cats, and horses that reduce our population fertility and diminish
the semiochemical commerce will be seen as the dangers they are. With wide
availability of healthy adult human male facial skin surface lipids, animal rights
activists will recover their sanity again, perhaps enough to contribute themselves to
scientific advancement. Similarly, those scientists and physicians who engage in

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human, animal, and plant torture to assuage their bloody appetites will find peace,
happiness, and an end to their unbearable suffering.

Oddly, match-makers can use artificial pheromone exchanges to increase

chances of bonding success. The approximate ratio of acceptable to unacceptable
skin surface lipids from the opposite sex seems to be about four out of ten. The ratio
of highly desirable samples might be about one out of ten. That means that true love
is not really that far away. Mutual delight and devotion at one chance in one hundred
(the product of the probabilities of delightful matches for each spouse) suggests more
work is needed, but it also suggests that such services may be profitable.

In addition to better life matches (and thereby perhaps more blissful

marriages), divorce rates should sink to more manageable levels. This is because
divorce is treatable with human pheromone therapy.

Not all will be peace and light. This book will eventually cause great tumult
at least academically. Psychology will have to become something else since its
central dogma will be all hollowed out and gone. The idea that bad thinking causes
disease will give up the ghost, taking with it, much of the up to now reasonable
argument for political correctness. Criminology will itself become academically
criminal given the complete barn door misses of its savagely devoted adherents.
Sociology and anthropology will move over and add chemists. College students will
begin a much more arduous course of study, too, “Oh happy day!”. Having several
Ph.D.’s in different disciplines will become commonplace, just like Star Trek.

That is not to say that observers of family life will all suddenly be looking for
new jobs. We will still need surveillance of treated families, because relieving
pressure in one place will probably cause problems to bubble up in another.
Pheromone therapy will be reserved for serious cases, but the simmering difficulties
that caused that serious case may find vent elsewhere. We must be vigilant and
professional, and kind.

This book has taken controversial stands well beyond the work of some of the
greatest scientists who ever lived: Vero Copner Wynn Edwards,2 Iränus Eibl-

323
Eibesfeldt,3 Edward O. Wilson. 4 Hopefully my facile analyses will not embarrass
them too badly.

Humanity is a herd being managed by nature, optimization algorithms with

feedback loops provide a population homeostasis, we just do not know much about it.
Not to worry, if humanity fails, nature has a fall back position, and if that fails, well,
there are lots of bare rocks that are earth’s size floating about in space.

Given the awkwardness of humanity’s situation, manipulating our own

pheromones overmuch will increase our numbers out of all proportion driving our
populations to crash eventually, leaving that cinder behind. Malthus misjudged the
rate of increasing agricultural productivity. Thus blanket applications of human
paternal pheromones to high government officials, corporate CEOs or to all military
personnel to assure ethical war-making or to end all suicidal ideation will backfire.
We must reserve pheromone therapy for those of us with problems or illnesses, or else
appropriate levels of risk-taking in the society will diminish. We can’t all be
president.

Without governance, a reasonable expectation of perhaps another

millennium’s survival might be expected. Perhaps the Christian thing to do would be
for me to immediately suffer crucifixion, withhold this book from publication, and let
these advances slumber another two thousand years.

Instead let us take faith in our hands, time delivers us all to the new future
ahead and we must geoengineer it. We will adjust, overcome, and survive. No longer
will we humans lie, cheat, steal or kill like Scarlet O’Hara in Margaret Mitchell’s
Gone with the Wind. We will need greater food resources for the coming population
boom. We must build great air ships to circle our globe and stand between ocean and
desert to stir the atmosphere bringing moisture and fertility to badlands. (The umbra
cast on the ground causes a Coriolis circular flow of air around it, pulling the
moisture ashore.) The future holds shaded glaciers and cities. We will clean our
atmosphere. We will drain the sea into the low places of the earth to lower sea level
and save our coasts. Our marginal lands will bloom. We will build space ships, and
we will go out among the stars of our new destiny. Nothing will hold us back. Amen.

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1 http://www.nasa.gov/topics/earth/features/health-sapping.html
2Wynn-Edwards, V.C. (1962). Animal Dispersion in Relation to Social Behavior. Oliver & Boyd,
London.
3 Eibl-Eibesfeldt, Irenäus. (1970). Ethology the Biology of Behavior, translated by Erich

Klinghammer New York: Holt, Rinehart and Winston 530 p.

4 Wilson, Edward O. 1975; Sociobiology The New Synthesis. Cambridge, Mass.: Belknap Press of

Harvard University Press. 697p.

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Appendix: Administering and collecting healthy

adult male facial skin surface lipid

Pheromone Gum Treatment for

Addiction and Criminal Behavior
Prepared by: B. Nicholson, Senior Scientist in Charge for Nicholson Science, Tampa, Florida
Nicholson Science [email protected]

Executive Summary
Objective
Test Nicholson Science, Inc. hypothesis that criminal behavior, drug-seeking or addictive behavior, and
sexual perversions are due to deficiency of healthy human adult male facial skin surface lipid pheromone,
or ‘unconditional paternal love and affection’.
Goals
To examine the health benefits of our ‘family therapy provided on chewing gum vehicle” including but not
limited to criminal behavior as confirmed by arrest records, drug-seeking or addictive behavior as
confirmed by toxicology screen, and/or sexual perversion of homosexuality as confirmed by marriage
records. In addition, autoimmune diseases of various kinds should benefit dramatically from pheromone
therapy.
Solution
A double-blind, cross-over experimental protocol exposing seventy participants in equal proportion to
Nicholson Science home remedy of harmless chewing gum and harmless healthy human adult male facial
skin surface lipid pheromone (face grease) or canola oil placebo is proposed.
Materials and Methods
Human healthy adult male facial skin surface lipid pheromone is a common environmental substance in
constant contact with human skin and ingested by human populations by millions of kilograms on an
everyday basis (during and after affectionate behavior). No allergies to face grease have ever been reported
in the medical literature. To guard against transmission of infection, the pheromone donors in obvious good
health were provided with a physician administered history and physical examination and tested for HIV,
Hep B, and Hep C.
All participants will receive information about the experiment and their express, written consent obtained
and kept on file. However, anyone may leave the trial at any time without penalty. Thirty-five placebos and
thirty-five home remedies will be supplied to seventy physician-selected diagnosed drug addicts with
empirical evidence of addictive drug exposure, and/or criminals with verifiable records of recent arrest.
(These criteria may be narrowed or expanded by your doctor to match available patient population.)
Results will be monitored for a convenient period of time for all seventy in the trial. Then, upon completion
of the time period, the key will be broken open and those in the placebo group will be provided the
pheromone gum, and those results monitored. The key will remain in the possession of your doctor, to be
broken only in the event of emergency or when your doctor sees fit. Because chronic criminality and drug
addiction may cause brain damage, younger participants will be preferred, i.e. those most prone to
recidivism.

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Expected Results
Open, anecdotal trials of identical doses of healthy human adult male facial skin surface lipid on chewing
gum vehicle taken by mouth have resulted in behavioral improvement in 73 of 73 cases observed by non-
physician Nicholson. Full and complete recoveries, with resumption of family life, increased ambition, higher
grades, and promotion have been observed anecdotally and is expected. Pheromone-stimulated
recoveries from autoimmune diseases have also been reported, but may not be common enough to
warrant reporting. Recoveries from long term autoimmune diseases like diabetes type 1 and Alzheimer’s
disease may take years or they may not be possible if all tissue is destroyed.
Side Effects
A following effect has been observed in children and young teens. It is an unusual curiosity about the trials
and about pheromone donors. It lasts for only a few days. Jealousy can be caused artificially by the
pheromone gum, not in the proband, but in the proband’s osculation partner. Apparently, intuition is a
chemosense. Scope or Listerine mouthwash before osculation is suggested, or just quarantine by no
kissing for 6 to 8 days. Ambition increases. Grades improve. Goal setting takes place and goals are
attained in every case so far. Spontaneous recovery from autoimmune diseases (epilepsy, hypothyroidism,
Graves aut, diabetes, arthritis, Alzheimer’s disease).
• No complaints have been lodged.
• Pheromone is odorless, colorless, tasteless, and imperceptible in action after initial relief.
• Several recipients have made glowing video taped self-reports, available for viewing on DVD, ask your
doctor.
• Complete recoveries from criminal and misbehavior (petty delinquency, minor assaults, repeated running
away, juvenile burglary, recalcitrance with poor scholastic performance) n=70; drug addiction (1
methadone, 1 crack cocaine), n=2; and homosexual ideation and behavior (1 juvenile male, 7 female) n=8.
Homosexuals have not complained and none wished to revert to homosexual behavior, but three
confessed something shocking. Had they known that the pheromone would work, they would never have
consented. For that reason, consenting homosexual adults must be excluded from these trials initially.
Alcoholics (n=4) have not recovered. (Ethanol is processed in the liver and uses a different pathway from
direct-acting addictive drugs). Alcoholics must be excluded from these trials initially. Pheromone Gum
Treatment for Addiction and Criminal Behavior

Informed Consent Form

Thank-you for offering to test human paternal skin surface lipid pheromone on chewing gum. You must be
in good
general health, and able to consent on your own to participate. Homosexual people must be excluded for
technical
reasons. Alcoholics must also be excluded. You must agree not to take aspirin, addictive drugs, or
antibiotics for three
days prior to chewing the gum unless your doctor says that you must. You will also need to avoid deep
kissing your
spouse or significant other on the mouth for a week or two. You must allow us to inspect your medical and
legal
records.
We promise never to disclose your name or identifying information to anyone, ever, except government
officials who need
to know.
First of all, just because you are reading this and said you may want to participate, you are under no
obligation to do
anything. You can stop right now or at any time. You do not have to report any results to Nicholson
Science or to
anyone else, either. Your contact information can be erased and no record will be kept if you withdraw, just
tell us. After
you chew the gum, we must keep a record, however, for the government to see if they ever decide to look.
Your name
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EXOCRINOLOGY
will never be published in any medical journal or news articles that we write, ever.
Double-blind Cross-over Experiment
This is a double-blind cross-over experiment. Double-blind means the person giving you the gum will not
know if it is
placebo gum or pheromone gum. We will use the numbers engraved on the can tops to tell whether you
got the
pheromone gum or the placebo gum after distribution and the first evaluation is over. Cross-over means
that people who
don’t get the pheromone gum do get it from us later. The experiment means that we must give participants
such as
yourself, fake placebos about half the time to keep things scientific. Besides your doctor in an emergency,
nobody
locally knows which is which, pheromone gum or placebo gum. Each looks exactly alike, tastes alike, and
is packaged
alike. You will definitely get the pheromone gum we are testing, but you may get it right away, or you may
get it after a
period of time. No matter what, you will get it, so be sure we have your contact information on file where
you receive the
gum.
Free of Charge
This pheromone gum for delinquency, criminal behavior, and/or drug addiction is provided free of charge to
you for you to
chew to hopefully cure yourself of criminal behavior, runaway behavior, or addictive drug-seeking. You may
not sell it or
give it away to anyone else as that would be unethical and inappropriate.
This is an unpaid enrollment in a clinical trial being run by Nicholson Science, a natural products health care
company.
Enrollees are maintained in anonymity, but information obtained from you may be provided to government
agencies as
required by law.
Home Remedy Test
This is not an investigational new drug, this is a home remedy that is not subject to FDA oversight. It
combines ordinary
chewing gum and about 0.01% adult male facial skin surface lipid that we believe is a human pheromone.
We do not process the putative pheromone in any way, but we are careful to prevent contamination or
spoilage. That is
what the can is for. Other human pheromones are passed through the air. Even human pheromones
produced from petroleum, are completely unregulated everywhere in the world. Pheromones often have
very specific stereochemistry, and enantiomers or mirror images of pheromones have poisoned pheromone
receptors in animals, so the racemic mixtures produced from petroleum-based products might theoretically
be dangerous. FDA doesn't worry. Dozens of human pheromone flavors similar to this one are for sale on
Ebay. No adverse consequences have ever been reported anywhere to our knowledge, but there is always
a first time. Our pheromone gum is of non-racemic stereochemistry and a natural, unprocessed flavor that
you cannot see, taste or smell. Even though human pheromones are the most potent drugs ever
discovered, their power and potential have until now remained obscure. We do know that pheromone
reception presents as “intuition”, and is both cryptic and insidious. We believe that you will get better, and
may even feel better initially if you have a severe deficiency, but in a few days after chewing all the gum, you
will not notice any changes in the way you feel. In our previous experience, your chief complaint of bad
behavior will stop, but the change will not be noticeable to you. For instance, if you are in school, you will
only notice that your grades improve if you are making bad grades because of your pheromone deficiency.
Source of the Pheromone Gum Home Remedy and Placebo Gum
You are getting human paternal pheromone gum obtained from the skin of an adult male donor in excellent
health,
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without skin blemishes. All donors have been screened and cleared by physicians after physical
examination and testing
for blood born viruses. Volunteer donors are men of good character, with no criminal background, and
living in families
as fathers and uncles. They are not paid for their services.
The Placebo is also ordinary Wrigley’s chewing gum, in the same flavor. Each piece is unwrapped and
about 10
milligrams of a tasteless oil (canola oil) is applied, then re-wrapped and packaged exactly like the
Pheromone Gum, so
that no one without the key can tell which is which. Keeping the key secret is very important in scientific
experiments to
avoid unintentional errors.
Discussion
Human pheromones are passed in kissing between people. Our best guess is, when we fail to get enough
pheromone
from our families during quality time spent with parents, we contract a range of aberrant behavioral
conditions. This team
believes that each of these conditions may be amenable to pheromone treatment. We propose that the
condition
caused by surplus of maternal pheromone and deficiency of paternal pheromone is homosexual behavior.
Similarly we
think that there is a condition which is caused by deficiency of human pheromone of both maternal and
paternal
pheromone and it is juvenile delinquency and/or criminal behavior, borderline personality disorder, and
perhaps, some
forms of hysteria probably including obsessive-compulsive disorder. The more extreme deficiencies caused
by lack of
parental closeness cause violent behavior or addictive drug seeking, we think.
The root cause of the paternal pheromone deficiency is under investigation. Parental withdrawal and lack of
receptivity
toward parents in youngsters seems to be due mostly to air pollution, but we do not know for sure. Ozone
is the most
closely correlated pollutant, which makes sense because ozone irritates pheromone receptive areas of the
olfactory and
respiratory tract. Ozone also attacks pheromones chemically (ozonolysis). We believe that these super
sized natural
doses of pheromone seem to cure these detrimental effects of ozone pollution.
We expect that delinquency and criminal behavior can be stopped completely with a single 15 piece dose
of this human
pheromone. One dose (or fake placebo) is supplied on fifteen pieces of fresh, new, dry sugarless chewing
gum obtained
from a store. We use sugarless chewing gum because it keeps longer and because it maintains the
pheromone near
receptors in the nose, mouth, and upper respiratory system. (The upper respiratory system is covered with
pheromone-receptive microvillar or brush border cells.)
Previous Experience with Pheromone Gum Home Remedy
In previous open trials, just anecdotes really, illegal drug-seeking behavior has been cured twice out of two
tries by this
dosage of paternal skin surface lipid chewing gum. Both cases resulted in complete remission of all
symptoms.
Recipients ceased inappropriate sexual promiscuity and resumed normal age-appropriate sexual behavior.
We must exclude homosexual people from this trial for technical reasons. Homosexual behavior in both
young men and

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EXOCRINOLOGY
women also seems to be treatable by approximately 150 mg of the human pheromone on chewing gum
vehicle,
however relapses occur and booster doses may be necessary to sustain heterosexuality. We have had
eight successes
out of eight tries, so far. However, homosexuals are to be excluded from this trial because they have told us
that loss of
homosexual ideation and behavior is a detrimental side effect.

Side Effects Observed in Previous Open Trials

Side effects can include jealousy. It is why you need not to kiss anyone on the mouth for a few days after
you take the
pheromone gum. The jealousy that is created artificially by a tiny dose of human pheromone is real to the
jealous person,
so avoid it by not kissing anyone on the mouth. Jealousy, like anger, is a dangerous human emotion, but
since we know
the conditions that cause it, we can avoid any problems.
Another side effect is "following effect". The dosed and now former delinquent or problem child feels a
slight euphoria
and a deep sense of gratitude which passes within a few days. The euphoria’s intensity depends upon the
extent of the
pheromone deficiency. No criminal, no addict, nor any homosexual has expressed any interest in returning
to former
lifestyles, but Nicholson Science cannot change your lifestyle. You have the free will to do that yourself, as
we believe
you will discover once “the monkey is off your back.”
Ambition and improved job or school performance has been observed, too. Goals are set and achieved.
Ten people who suffered from autoimmune diseases suddenly began to recover and this surprised them
enough that
they sought medical advice on an emergency basis. Nicholson Science will not reimburse you or indemnify
you for your
health care. We wish we could.
Risks
The pheromones are odorless, colorless, tasteless, and imperceptible in action. We believe that they are
inherently safe,
but we could be wrong. So far as we know, no human being has ever kissed another human being and
gotten an
allergic reaction. We use good laboratory practices and good sanitary hygiene in collecting human
pheromone. We do
not use universal precautions (like in surgical operating rooms) in collection of pheromone because people
can have
dangerous allergies to the latex of gloves. The pheromone on the chewing gum vehicle is exposed briefly to
ultraviolet
light at antibiotic wavelengths just like many fruits and vegetables and is kept desiccated in a nobel gas
atmosphere (no
oxygen to cause spoilage) in a sealed and light proof aluminum can. The chewing gum as it came from the
store
contains USDA approved preservatives, which also deter spoilage.
There is minimal risk of infection for transmissible infectious diseases. However, it is less than the ordinary
risk of kissing
the donor on the cheek because we UV sterilize, desiccate the gum, keep it sealed in a can, and use a
preservative-protected chewing gum vehicle, Wrigley’s Rain Spearmint gum.
We believe that addictive substances are ersatz pheromones. (Indeed most addictive substances, many
NSAIDS, and

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antibiotics and are also semiochemicals that plants and microbes use to influence behavior of animals, but
processing is
generally required to recover them from natural sources.) Avoid the use of addictive substances, aspirin,
and antibiotics if
allowed by your physician during the administration period. It usually takes a few hours to chew all 15
pieces of the gum
serially. Human paternal pheromone chewing gum has been effective in every case where addicted loved
ones suffered
from criminal behavior. Every time, the addictive substance seeking was eliminated and criminality ceased.
Yours in service,
B. Nicholson, Senior Scientist in Charge.
Call long distance (1-813 830-1432) to report any problems or concerns by leaving a message.
Mechanism of action.
Methamphetamine attacks the nucleus accumbens, a pheromone reception center. By providing a small
amount of the
pheromone, 150 mg or less than half an average aspirin tablet, methamphetamine is no longer sought.

Collection of healthy adult male facial skin surface lipid

Donors must be family men of good character, heterosexual, non-perverted, over 30 years of age, in good
health, pass a physical examination, be tested free of blood born viruses, and without skin lesions or
clinical skin infections.
Donors must agree to avoid cosmetics (except morning use of pure soap), to avoid any medications, to
avoid any intoxicating beverages or substances for three days prior to the test.
Donors must be free of allergies to chewing gum.
The facial skin surface sebaceous skin surface lipid pheromone should be collected by a technician over
three sessions over no fewer than three days (each session at least twelve hours apart or until 15 to 25
pieces of pheromone gum are collected.
Using a clean dinner plate, open 5 pieces of Wrigley’s Rain Chewing gum (or equivalent), saving the
wrappers. Artificially sweetened gum is used.
Tare the weight of the fresh, dry, new gum.
Rub the gum on the face of the donor anywhere a child would kiss his/her father.
Reweigh the gum. Collect until 10 milligrams have been collected. Use both sides if necessary.
Irradiate gum with biocidal UV lamp for 30 seconds per side.
Re-wrap the gum.
Label each piece of the gum: “Doner #, date collected, HOME REMEDY Experimental use only. Not for
resale Fresh until (get date from retail package)”, and any other pertinent information at the discretion of
the local supervising IRB, Institutional Review Board for human subjects.

NICHOLSON SCIENCE PROVIDES THIS PROTOCOL TO THE GENERAL PUBLIC AS A PUBLIC

SERVICE. DONATIONS, WHICH ARE NOT TAX DEDUCTIBLE, SHOULD BE SENT VIA PAYPAL TO

[email protected]

Suggested donation is $25.00 US per person cured.

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