27/12/2019 A New Look at Coconut Oil - The Weston A.

Price Foundation

The Weston A. Price Foundation

A New Look at Coconut Oil

JANUARY 1, 2000 BY MARY ENIG, PHD (HTTPS://WWW.WESTONAPRICE.ORG/AUTHOR/MENIG/)

Health and Nutritional Bene ts from Coconut

Oil: An Important Functional Food for the 21st
Century
Presented at the AVOC Lauric Oils Symposium, Ho Chi Min City, Vietnam, 25 April 1996

Abstract
Coconut oil has a unique role in the diet as an important physiologically functional food.
The health and nutritional bene ts that can be derived from consuming coconut oil have
been recognized in many parts of the world for centuries. Although the advantage of
regular consumption of coconut oil has been underappreciated by the consumer and
producer alike for the recent two or three decades, its unique bene ts should be
compelling for the health minded consumer of today. A review of the diet/heart disease
literature relevant to coconut oil clearly indicates that coconut oil is at worst neutral with
respect to atherogenicity of fats and oils and, in fact, is likely to be a bene cial oil for
prevention and treatment of some heart disease. Additionally, coconut oil provides a
source of antimicrobial lipid for individuals with compromised immune systems and is a
nonpromoting fat with respect to chemical carcinogenesis.

I. Introduction
Mr. Chairman and members of the ASEAN Vegetable Oils Club, I would like to thank you for
inviting me to participate in this Lauric Oils Symposium. I am pleased to have the
opportunity to review with you some information that I hope will help redress some of the
anti-tropical oils rhetoric that has been so troublesome to your industry.

I will be covering two important areas in my presentation. In the rst part, I would like to
review the history of the major health challenge facing coconut oil today. This challenge is

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based on a supposed negative role played by saturated fat in heart disease. I hope to
dispel any acceptance of this notion with the information I will present to you today. I will
show you how both animal studies and human studies have exonerated coconut oil of
causing the problem.

In the second part of my talk I will suggest some new directions where important positive
health bene ts are seen for coconut oil. These bene ts stem from coconut oil’s use as a
food with major antimicrobial and anticancer bene ts. I will present to you some of the
rationale for this e ect and some of the supporting literature.

The health and nutritional bene ts derived from coconut oil are unique and compelling.
Although the baker and food processor have recognized the functional advantages of
coconut oil in their industries, over most competing oils, for many years, I believe these
bene ts are underappreciated today by both the producer and the consumer. It is time to
educate and reeducate all t hose who harbor this misinformation.

Historically, coconuts and their extracted oil have served man as important foods for
thousands of years. The use of coconut oil as a shortening was advertised in the United
States in popular cookbooks at the end of the 19th century. Both the health-promoting
attributes of coconut oil and those functional properties useful to the homemaker were
recognized 100 years ago. These same attributes, in addition to some newly discovered
ones, should be of great interest to both the producing countries as well as the consuming
countries.

II. Origins of the Diet/Heart Hypothesis

Although popular literature of epidemiological studies usually attribute an increased risk
of coronary heart disease (CHD) to elevated levels of serum cholesterol, which in turn are
thought to derive from a dietary intake of saturated fats and cholesterol. But, saturated
fats may be considered a major culprit for CHD only if the links between serum cholesterol
and CHD, and between saturated fat and serum cholesterol are each rmly established.
Decades of large-scale tests and conclusions therefrom have purported to establish the
rst link. In fact, this relationship has reached the level of dogma. Through the years
metabolic ward and animal studies have claimed that dietary saturated fats increase
serum cholesterol levels, thereby supposedly establishing the second link. But the
scienti c basis for these relationships has now been challenged as resulting from large-
scale misinterpretation and misrepresentation of the data. (Enig 1991, Mann 1991, Smith

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1991, Ravnskov 1995)

Ancel Keys is largely responsible for starting the anti-saturated fat agenda in the United
States. From 1953 to 1957 Keys made a series of statements regarding the atherogenicity
of fats. These pronouncements were:

“All fats raise serum cholesterol; Nearly half of total fat comes from
vegetable fats and oils; No di erence between animal and vegetable
fats in e ect on CHD (1953); Type of fat makes no di erence; Need to
reduce margarine and shortening (1956); All fats are comparable;
Saturated fats raise and polyunsaturated fats lower serum cholesterol;
Hydrogenated vegetable fats are the problem; Animal fats are the
problem (1957-1959).”

As can be seen, his ndings were inconsistent.

What was the role of the edible oil industry in promoting the
diet/heart hypothesis?

It is important to realize that at that time (1960s) the edible oil industry in the United States
seized the opportunity to promote its polyunsaturates. The industry did this by developing
a health issue focusing on Key’s anti-saturated fat bias. With the help of the edible oil
industry lobbying in the United States, federal government dietary goals and guidelines
were adopted incorporating this mistaken idea that consumption of saturated fat was
causing heart disease. This anti-saturated fat issue became the agenda of government and
private agencies in the US and to an extent in other parts of the world. This is the agenda
that has had such a devastating e ect on the coconut industry for the past decade.
Throughout the 1960s, the 1970s, the 1980s, and the 1990s, the anti-saturated fat rhetoric
increased in intensity.

What are some of the contradictions to the hypothesis blaming

saturated fat?

Recently, an editorial by Harvard’s Walter Willett, M.D. in the American Journal of Public

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Health (1990) acknowledged that even though

“the focus of dietary recommendations is usually a reduction of

saturated fat intake, no relation between saturated fat intake and risk
of CHD was observed in the most informative prospective study to
date.”

Another editorial, this time by Framingham’s William P. Castelli in the Archives of Internal
Medicine (1992), declared for the record that

“…in Framingham, Mass, the more saturated fat one ate, the more
cholesterol one ate, the more calories one ate, the lower the person’s
serum cholesterol… the opposite of what the equations provided by
Hegsted at al (1965) and Keys et al (1957) would predict…”

Castelli further admitted that

“…In Framingham, for example, we found that the people who ate the
most cholesterol, ate the most saturated fat, ate the most calories,
weighed the least, and were the most physically active.”

III. Coconut Oil and the Diet/Heart Hypothesis

For the past several decades you have heard about animal and human studies feeding
coconut oil that purportedly showed increased indices for cardiovascular risk. Blackburn et
al (1988) have reviewed the published literature of coconut oil’s e ect on serum
cholesterol and atherogenesis and have concluded that when ...[coconut oil is] fed

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physiologically with other fats or adequately supplemented with linoleic acid, coconut oil is
a neutral fat in terms of atherogenicity. After reviewing this same literature, Kurup and
Rajmohan (1995) conducted a study on 64 volunteers and found …no statistically
signi cant alteration in the serum total cholesterol, HDL cholesterol, LDL cholesterol, HDL
cholesterol/total cholesterol ratio and LDL cholesterol/HDL cholesterol ratio of
triglycerides from the baseline values… A bene cial e ect of adding the coconut kernel to
the diet was noted by these researchers.

How did coconut oil get such a negative reputation?

The question then is, how did coconut oil get such a negative reputation? The answer quite
simply is, initially, the signi cance of those changes that occurred during animal feeding
studies were misunderstood. The wrong interpretation was then repeated until ultimately
the misinformation and disinformation took on a life of its own.

The problems for coconut oil started four decades ago when researchers fed animals
hydrogenated coconut oil that was purposefully altered to make it completely devoid of
any essential fatty acids. The hydrogenated coconut oil was selected instead of
hydrogenated cottonseed, corn or soybean oil because it was a soft enough fat for
blending into diets due to the presence of the lower melting medium chain saturated fatty
acids. The same functionality could not be obtained from the cottonseed, corn or soybean
oils if they were made totally saturated, since all their fatty acids were long chain and high
melting and could not be easily blended nor were they as readily digestible.

The animals fed the hydrogenated coconut oil (as the only fat source) naturally became
essential fatty acid de cient; their serum cholesterol levels increased. Diets that cause an
essential fatty acid de ciency always produce an increase in serum cholesterol levels as
well as an increase in the atherosclerotic indices. The same e ect has also been seen when
other essential fatty acid de cient, highly hydrogenated oils such as cottonseed, soybean,
or corn oils have been fed; so it is clearly a function of the hydrogenated product, either
because the oil is essential fatty acid (EFA) de cient or because of trans fatty acids (TFA).

What about the studies where animals were fed with

unprocessed coconut oil?

Hostmark et al (1980) compared the e ects of diets containing 10% coconut fat and 10%

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sun ower oil on lipoprotein distribution in male Wistar rats. Coconut oil feeding produced
signi cantly lower levels (p=<0.05) of pre-beta lipoproteins (VLDL) and signi cantly higher
(p=<0.01) alpha-lipoproteins (HDL) relative to sun ower oil feeding.

Awad (1981) compared the e ects of diets containing 14% coconut oil, 14% sa ower oil or
a 5% “control” (mostly soybean) oil on accumulation of cholesterol in tissues in male Wistar
rats. The synthetic diets had 2% added corn oil with a total fat of 16% Total tissue
cholesterol accumulation for animals on the sa ower diet was six times greater than for
animals fed the coconut oil, and twice that of the animals fed the control oil.

A conclusion that can be drawn from some of this animal research is that feeding
hydrogenated coconut oil devoid of essential fatty acids (EFA) in a diet otherwise devoid of
EFA leads to EFA de ciency and potentiates the formation of atherosclerosis markers. It is
of note that animals fed regular coconut oil have less cholesterol deposited in their livers
and other parts of their bodies.

What about the studies where coconut oil is part of the normal
diet of human beings?

Kaunitz and Dayrit (1992) have reviewed some of the epidemiological and experimental
data regarding coconut-eating groups and noted that the available population studies
show that dietary coconut oil does not lead to high serum cholesterol nor to high coronary
heart disease mortality or morbidity. They noted that in 1989 Mendis et al reported
undesirable lipid changes when young adult Sri Lankan males were changed from their
normal diets by the substitution of corn oil for their customary coconut oil. Although the
total serum cholesterol decreased 18.7% from 179.6 to 146.0 mg/dl and the LDL
cholesterol decreased 23.8% from 131.6 to 100.3 mg/dl, the HDL cholesterol decreased
41.4% from 43.4 to 25.4 mg/dl (putting the HDL values below the acceptable lower limit)
and the LDL/HDL ratio increased 30% from 3.0 to 3.9. These latter two changes would be
considered quite undesirable. As noted above, Kurup and Rajmohan (1995) studied the
addition of coconut oil alone to previously mixed fat diets and report no signi cant
di erence.

Previously, Prior et al (1981) had shown that islanders with high intake of coconut oil
showed no evidence of the high saturated fat intake having a harmful e ect in these
populations. When these groups migrated to New Zealand however, and lowered their
intake of coconut oil, their total cholesterol and LDL cholesterol increased, and their HDL

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cholesterol decreased.

What about the studies where coconut oil was deliberately fed
to human beings?

Some of the studies reported thirty and more years ago should have cleared coconut oil of
any implication in the development of coronary heart disease (CHD).

For example, when Frantz and Carey (1961) fed an additional 810 kcal/day fat supplement
for a whole month to males with high normal serum cholesterol levels, there was no
signi cant di erence from the original levels even though the fat supplement was
hydrogenated coconut oil.

Halden and Lieb (1961) also showed similar results in a group of hyperchole-sterolemics
when coconut oil was included in their diets. Original serum cholesterol levels were
reported as 170 to 370 mg/dl. Straight coconut oil produced a range from 170 to 270
mg/dl. Coconut oil combined with 5% sun ower oil and 5% olive oil produced a range of
140 to 240 mg/dl.

Earlier, Hashim and colleagues (1959) had shown quite clearly that feeding a fat
supplement to hypercholesterolemics, where half of the supplement (21% of energy) was
coconut oil (and the other half was sa ower oil), resulted in signi cant reductions in total
serum cholesterol. The reductions averaged -29% and ranged from -6.8 to -41.2%.

And even earlier, Ahrens and colleagues (1957) had shown that adding coconut oil to the
diet of hypercholesterolemics lowers serum cholesterol from, e.g., 450 mg/dl to 367 mg/dl.
This is hardly a cholesterol-raising e ect.

Bierenbaum et al (1967) followed 100 young men with documented myocardial infarction
for 5 years on diets with fat restricted to 28% of energy. There was no signi cant di erence
between the two di erent fat mixtures (50/50 corn and sa ower oils or 50/50 coconut and
peanut oils), which were fed as half of the total fat allowance; both diets reduced serum

cholesterol. This study clearly showed that 7% of energy as coconut oil was as bene cial to
the 50 men who consumed it as for the 50 men who consumed 7% of energy as other oils
such as corn oil or sa ower. Both groups fared better than the untreated controls.

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More recently, Sundram et al (1994) fed whole foods diets to healthy normo-
cholesterolemic males, where approximately 30% of energy was fat. Lauric acid (C12:0)
and myristic acid (C14:0) from coconut oil supplied approximately 5% of energy. Relative to
the baseline measurements of the subjects prior to the experimental diet, this lauric and
myristic acid-rich diet showed an increase in total serum cholesterol from 166.7 to 170.0
mg/dl (+1.9%), a decrease in low density lipoprotein cholesterol (LDL-C) from 105.2 to
104.4 mg/dl (-0.1%), an increase in high density lipoprotein cholesterol (HDL-C) from 42.9
to 45.6 mg/dl (+6.3%). There was a 2.4% decrease in the LDL-C/HDL-C ratio from 2.45 to
2.39. These ndings indicate a favorable alteration in serum lipoprotein balance was
achieved when coconut oil was included in a whole food diet at 5% of energy.

Tholstrup et al (1994) report similar results with whole foods diets high in lauric and
myristic acids from palm kernel oil. The HDL cholesterol levels increased signi cantly from
baseline values (37.5 to 46.0 mg/dl, P<0.01) and the LDL-C/HDL-C ratios decreased from
3.08 to 2.69. The increase in total cholesterol was from 154.7 (baseline) to 170.9 mg/dl on
the experimental diet.

Ng et al (1991) fed 75% of the fat ration as coconut oil (24% of energy) to 83 adult
normocholesterolemics (61 males and 22 females). Relative to baseline values, the highest
values on the experimental diet for total cholesterol was increased 17% (169.6 to 198.4
mg/dl), HDL cholesterol was increased 21.4% (44.3 to 53.8 mg/dl), and the LDL-C/HDL-C
ratio was decreased 3.6% (2.51 to 2.42).

When unprocessed coconut oil is added to an otherwise normal diet, there is frequently no
change in the serum cholesterol although some studies have shown a decrease in total
cholesterol. For example, when Ginsberg et al provided an “Average American” diet with 2-
3 times more myristic acid (C14:0), 4.5 times more lauric acid (C12:0), and 1.2 times more
palmitic and stearic acid (C16:0 and C18:0) than their “Mono[unsaturated]” diet and the
National Cholesterol Education Program “Step 1” diet, there was no increase in serum
cholesterol, and in fact, serum cholesterol levels for this diet group fell approximately 3%
from 177.1 mg% to 171.8 mg% during the 22 week feeding trial.

It appears from many of the research reports that the e ect coconut oil has on serum
cholesterol is the opposite in individuals with low serum cholesterol values and those with
high serum values. We see that there may be a raising of serum total cholesterol, LDL
cholesterol and especially HDL cholesterol in individuals with low serum cholesterol. On

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the other hand there is lowering of total cholesterol and LDL cholesterol in
hypercholesterolemics as noted above.

Studies that supposedly showed a hypercholesterolemic e ect of coconut oil feeding, in

fact, usually only showed that coconut oil was not as e ective at lowering the serum
cholesterol as was the more unsaturated fat being compared. This appears to be in part
because coconut oil does not drive cholesterol into the tissues as does the more
polyunsaturated fats. The chemical analysis of the atheroma shows that the fatty acids
from the cholesterol esters are 74% unsaturated (41% is polyunsaturated) and only 24%
are saturated. None of the saturated fatty acids were reported to be lauric acid or myristic
acid (Felton et al 1994).

Should coconut oil be used to prevent coronary heart disease?

There is another aspect to the coronary heart disease picture. This is related to the
initiation of the atheromas that are reported to be blocking arteries. Recent research is
suggestive that there is a causative role for the herpes virus and cytomegalovirus in the
initial formation of atherosclerotic plaques and the recloging of arteries after angioplasty.
(New York Times 1991) What is so interesting is that the herpes virus and cytomegalovirus
are both inhibited by the antimicrobial lipid monolaurin; but monolaurin is not formed in
the body unless there is a source of lauric acid in the diet. Thus, ironically enough, one
could consider the recommendations to avoid coconut and other lauric oils as contributing
to the increased incidence of coronary heart disease.

Perhaps more important than any e ect of coconut oil on serum cholesterol is the
additional e ect of coconut oil on the disease ghting capability of the animal or person
consuming the coconut oil.

IV. Coconut Oil and Cancer

Lim-Sylianco (1987) has reviewed 50 years of literature showing anticarcinogenic e ects
from dietary coconut oil. These animal studies show quite clearly the nonpromotional
e ect of feeding coconut oil.

In a study by Reddy et al (1984) straight coconut oil was more inhibitory than MCT oil to
induction of colon tumors by azoxymethane. Chemically induced adenocarcinomas
di ered 10-fold between corn oil (32%) and coconut oil (3%) in the colon. Both olive oil and
coconut oil developed the low levels (3%) of the adenocarcinomas in the colon, but in the

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small intestine animals fed coconut oil did not develop any tumors while 7% of animals fed
olive oil did.

Studies by Cohen et al (1986) showed that the nonpromotional e ects of coconut oil were
also seen in chemically induced breast cancer. In this model, the slight elevation of serum
cholesterol in the animals fed coconut oil was protective as the animals fed the more
polyunsaturated oil had reduced serum cholesterol and more tumors. The authors noted
that “…an overall inverse trend was observed between total serum lipids and tumor
incidence for the 4 [high fat] groups.”

This is an area that needs to be pursued.

V. Coconut Oil Antimicrobial Bene ts

I would now like to review for you some of the rationale for the use of coconut oil as a food
that will serve as the raw material to provide potentially useful levels of antimicrobial
activity in the individual.

The lauric acid in coconut oil is used by the body to make the same disease- ghting fatty
acid derivative monolaurin that babies make from the lauric acid they get from their
mothers= milk. The monoglyceride monolaurin is the substance that keeps infants from
getting viral or bacterial or protozoal infections. Until just recently, this important bene t
has been largely overlooked by the medical and nutrition community.

Recognition of the antimicrobial activity of the monoglyceride of lauric acid (monolaurin)

has been reported since 1966. The seminal work can be credited to Jon Kabara. This early
research was directed at the virucidal e ects because of possible problems related to food
preservation. Some of the early work by Hierholzer and Kabara (1982) that showed
virucidal e ects of monolaurin on enveloped RNA and DNA viruses was done in
conjunction with the Center for Disease Control of the US Public Health Service with
selected prototypes or recognized representative strains of enveloped human viruses. The
envelope of these viruses is a lipid membrane.

Kabara (1978) and others have reported that certain fatty acids (e.g., medium-chain
saturates) and their derivatives (e.g., monoglycerides) can have adverse e ects on various
microorganisms: those microorganisms that are inactivated include bacteria, yeast, fungi,
and enveloped viruses.

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The medium-chain saturated fatty acids and their derivatives act by disrupting the lipid
membranes of the organisms (Isaacs and Thormar 1991) (Isaacs et al 1992). In particular,
enveloped viruses are inactivated in both human and bovine milk by added fatty acids
(FAs) and monoglycerides (MGs) (Isaacs et al 1991) as well as by endogenous FAs and MGs
(Isaacs et al 1986, 1990, 1991, 1992; Thormar et al 1987).

All three monoesters of lauric acid are shown to be active antimicrobials, i.e., alpha-,
alpha’-, and beta-MG. Additionally, it is reported that the antimicrobial e ects of the FAs
and MGs are additive and total concentration is critical for inactivating viruses (Isaacs and
Thormar 1990).

The properties that determine the anti-infective action of lipids are related to their
structure; e.g., monoglycerides, free fatty acids. The monoglycerides are active,
diglycerides and triglycerides are inactive. Of the saturated fatty acids, lauric acid has
greater antiviral activity than either caprylic acid (C-10) or myristic acid (C-14).

The action attributed to monolaurin is that of solubilizing the lipids and phospholipids in
the envelope of the virus causing the disintegration of the virus envelope. In e ect, it is
reported that the fatty acids and monoglycerides produce their killing/inactivating e ect by
lysing the (lipid bilayer) plasma membrane. However, there is evidence from recent studies
that one antimicrobial e ect is related to its interference with signal transduction (Projan
et al 1994).

Some of the viruses inactivated by these lipids, in addition to HIV, are the measles virus,
herpes simplex virus-1 (HSV-1), vesicular stomatitis virus (VSV), visna virus, and
cytomegalovirus (CMV). Many of the pathogenic organisms reported to be inactivated by
these antimicrobial lipids are those known to be responsible for opportunistic infections in
HIV-positive individuals. For example, concurrent infection with cytomegalovirus is
recognized as a serious complication for HIV+ individuals (Macallan et al 1993). Thus, it
would appear to be important to investigate the practical aspects and the potential bene t

of an adjunct nutritional support regimen for HIV-infected individuals, which will utilize
those dietary fats that are sources of known anti-viral, anti-microbial, and anti-protozoal
monoglycerides and fatty acids such as monolaurin and its precursor lauric acid.

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No one in the mainstream nutrition community seems to have recognized the added
potential of antimicrobial lipids in the treatment of HIV-infected or AIDS patients. These
antimicrobial fatty acids and their derivatives are essentially non-toxic to man; they are
produced in vivo by humans when they ingest those commonly available foods that
contain adequate levels of medium-chain fatty acids such as lauric acid. According to the
published research, lauric acid is one of the best “inactivating” fatty acids, and its
monoglyceride is even more e ective than the fatty acid alone (Kabara 1978, Sands et al
1978, Fletcher et al 1985, Kabara 1985).

The lipid coated (envelop) viruses are dependent on host lipids for their lipid constituents.
The variability of fatty acids in the foods of individuals accounts for the variability of fatty
acids in the virus envelop and also explains the variability of glycoprotein expression.

Loss of lauric acid from the American diet

Increasingly, over the past 40 years, the American diet has undergone major changes.
Many of these changes involve changes of fats and oils. There has been an increasing
supply of the partially hydrogenated trans-containing vegetable oils and a decreasing
amount of the lauric acid-containing oils. As a result, there has been an increased
consumption of trans fatty acids and linoleic acid and a decrease in the consumption of
lauric acid. This type of change in diet has an e ect on the fatty acids the body has
available for metabolic activities.

VI. Lauric Acid in Foods

The coconut producing countries

Whole coconut as well as extracted coconut oil has been a mainstay in the food supply in
many countries in parts of Asia and the Paci c Rim throughout the centuries. Recently
though, there has been some replacement of coconut oil by other seed oils. This is
unfortunate since the bene ts gained from consuming an adequate amount of coconut oil
are being lost.

Based on the per capita intake of coconut oil in 1985 as reported by Kaunitz (1992), the per
capita daily intake of lauric acid can be approximated. For those major producing countries
such as the Philippines, Indonesia, and Sri Lanka, and consuming countries such as
Singapore, the daily intakes of lauric acid were approximately 7.3 grams (Philippines), 4.9

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g p y pp y g pp
grams (Sri Lanka), 4.7 grams (Indonesia), and 2.8 grams (Singapore). In India, intake of
lauric acid from coconut oil in the coconut growing areas (e.g., Kerala) range from about 12
to 20 grams per day (Eraly 1995), whereas the average for the rest of the country is less
than half a gram. An average high of approximately 68 grams of lauric acid is calculated
from the coconut oil intake previously reported by Prior et al (1981) for the Tokelau
Islands. Other coconut producing countries may also have intakes of lauric acid in the
same range.

The US experience

In the United States today, there is very little lauric acid in most of the foods. During the
early part of the 20th Century and up until the late 1950s many people consumed heavy
cream and high fat milk. These foods could have provided approximately 3 grams of lauric
acid per day to many individuals. In addition, desiccated coconut was a popular food in
homemade cakes, pies and cookies, as well as in commercial baked goods, and 1-2
tablespoons of desiccated coconut would have supplied 1-2 grams of lauric acid. Those
foods made with the coconut oil based shortenings would have provided additional
amounts.

Until two years ago, some of the commercially sold popcorn, at least in movie theaters,
had coconut oil as the oil. This means that for those people lucky enough to consume this
type of popcorn the possible lauric acid intake was 6 grams or more in a three (3) cup
order.

Some infant formulas (but not all) have been good sources of lauric acid for infants.
However, in the past 3-4 years there has been reformulation with a loss of a portion of
coconut oil in these formulas, and a subsequent lowering of the lauric acid levels.

Only one US manufactured enteral formula contains lauric acid (e.g., Impact7); this is
normally used in hospitals for tube feeding; it is reported to be very e ective in reversing
severe weight loss in AIDS patients, but it is discontinued when the patients leave the

hospital because it is not su ciently palatable for oral use. The more widely promoted
enteral formulas (e.g., Ensure7, Nutren7) are not made with lauric oils, and, in fact, many
are made with partially hydrogenated oils.

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There are currently some candies sold in the US that are made with palm kernel oil, and a
few specialty candies made with coconut oil and desiccated coconut. These can supply
small amounts of lauric acid.

Cookies such as macaroons, if made with desiccated coconut, are good sources of lauric
acid, supplying as much as 6 grams of lauric acid per macaroon (Red Mill). However, these
cookies make up a small portion of the cookie market. Most cookies in the United States
are no longer made with coconut oil shortenings; however, there was a time when many
US cookies (e.g., Pepperidge Farm) were about 25% lauric acid.

Originally, one of the largest manufacturers of cream soups used coconut oil in the
formulations. Many popular cracker manufacturers also used coconut oil as a spray
coating. These products supplied a small amount of lauric acid on a daily basis for some
people.

How much lauric acid is needed?

It is not known exactly how much food made with lauric oils is needed in order to have a
protective level of lauric acid in the diet. Infants probably consume between 0.3 and 1
gram per kilogram of body weight if they are fed human milk or an enriched infant formula
that contains coconut oil. This amount appears to have always been protective. Adults
could probably bene t from the consumption of 10 to 20 grams of lauric acid per day.
Growing children probably need about the same amounts as adults.

VII. Recommendations
The coconut oil industry needs to make the case for lauric acid now. It should not wait for
the rapeseed industry to promote the argument for including lauric acid because of the
increased demand for laurate. In fact lauric acid may prove to be a conditionally essential
saturated fatty acid, and the research to establish this fact around the world needs to be
vigorously promoted.

Although private sectors need to ght for their commodity through the o ces of their
trade associations, the various governments of coconut producing countries need to put
pressure on WHO, FAO, and UNDP to recognizes the health importance of coconut oil and
the other coconut products. Moreover, those representatives who are going to do the

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p p g g
persuading need to believe that their message is scienti cally correct — because it is.

Among the critical foods and nutrition “buzz words” for the 21st Century is the term
“functional foods.” Clearly coconut oil ts the designation of a very important functional
food.

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About Mary Enig, PhD

Mary G. Enig, PhD, FACN, CNS, was an expert of international renown in the eld of lipid
chemistry. She headed a number of studies on the content and e ects of trans fatty
acids in America and Israel and successfully challenged government assertions that
dietary animal fat causes cancer and heart disease. Recent scienti c and media
attention on the possible adverse health e ects of trans fatty acids has brought
increased attention to her work. She was a licensed nutritionist, certi ed by the
Certi cation Board for Nutrition Specialists; a quali ed expert witness; nutrition
consultant to individuals, industry and state and federal governments; contributing
editor to a number of scienti c publications; Fellow of the American College of
Nutrition; and President of the Maryland Nutritionists Association. She authored over

60 technical papers and presentations and was the author of Know Your Fats, a primer
on the biochemistry of dietary fats as well as of Eat Fat Lose Fat (Penguin, Hudson Street
Press, 2004).

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