Erectile Dysfunction and Comorbid

Diseases, Androgen Deficiency, and

Diminished Libido in Men
Shari R. Fine, DO

Erectile dysfunction affects an estimated one in ten men in the United States.
According to one study, the prevalence of impotence at all degrees is approximately 52% in men aged 40 to 70 years. This prevalence rate might be underestimated, given patients reluctance to discuss the issue with their physicians. Erectile dysfunction is often accompanied by comorbid conditions
because of overlapping risk factors. It is important that physicians be aware of
the frequency of this coexistence so that they may monitor all potential health
concerns and treat patients optimally.

rectile dysfunction (ED) is the persistent inability to achieve and maintain an erection sufficient for satisfactory sexual activity. It is estimated that
ED affects one in ten men in the United
States.1 According to the Massachusetts
Male Aging Study (MMAS),2 the prevalence of impotence at all degrees is
approximately 52% in men aged 40 to 70
years. This prevalence might be underestimated, given patients reluctance to
discuss the issue with their physicians.3
The current American Association
of Clinical Endocrinologists (AACE)
Guidelines4 for the workup of sexual
dysfunction suggests that if possible, the
patient and partner should be evaluated
together. This evaluation may reveal

Dr Fine is an assistant clinical professor in the

Department of Family Medicine at the University
of Medicine and Dentistry of New JerseySchool of
Osteopathic Medicine in Stratford, NJ.
This article was developed from a lecture presented by Dr Fine at an American College of Osteopathic Family Physicians symposium sponsored by
Bayer Pharmaceutical Corporation at the 108th
Annual AOA Convention and Scientific Seminar on
October 15, 2003, in New Orleans, La.
Correspondence to Shari R. Fine, DO, FACOFP,
25 McWilliams Pl, Jersey City, NJ 07302-1609.
E-mail: [email protected]

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underlying relationship and adjustment

issues, as well as difficulties in communication. Sexual history should focus on
the degree of ED, its frequency, and the
duration of the problem. Longstanding
ED may involve performance anxiety
and require psychological therapy as well
as medical treatment. Medical history
should evaluate common risk factors for
ED, as well as concomitant medications.
A history of emotional or psychological
problems (or both), or a history of previous surgical procedures should also be
noted.
In addition to the usual physical
examination parameters, anatomic abnormalities should be assessed, as well as
sensory adequacy of the nerves serving
the penis. Abnormalities that are suggestive of hormonal dysfunction should
be worked up as needed. Diagnostic tests
can help identify possible comorbidities.
Hormonal assays may include thyroid
function, if indicated, and measurement
of testosterone concentration; testosterone
concentrations should be assessed in the
morning. Vascular assessment may
include penile Doppler ultrasound examination to assess blood flow to the corpus
cavernosum.4,5

Before initiating specific treatment

modalities for ED, the physician should
first eliminate hypogonadism, other hormonal factors, and decreased libido as
primary causes. The AACE sexual dysfunction workup strategy should help
identify these causes. Patients should
receive treatment for any previously
untreated comorbidities detected during
workup. In addition to the direct impact
on patient health and risk for complications and other comorbidities, such treatment may increase the effectiveness of
ED-specific modes of therapy.
Erectile dysfunction is often accompanied by comorbid conditions because
of overlapping risk factors.6 It is important that physicians be aware of the frequency of this coexistence so that they
may monitor all potential health concerns and treat patients optimally.
Obstacles to discovering ED are
substantial, including reticence or embarrassment on the part of patient, physician, or both. An understanding of the
etiology of ED may lead to an early
rather than a delayed diagnosis of ED.
The use of simple, straightforward
screening questions can pave the way
to a more comprehensive workup. Diagnosis of ED can help uncover previously
undiagnosed comorbidities, and vice
versa. The association of ED with a
number of common disorders suggests
an important role for reciprocal diagnosis.
Regular screening for disorders frequently observed in aging men can open
the conversation to a discussion of ED.
Conversely, including a screening process for ED during a routine physical
examination may help point to previously undetected comorbidities. For
example, Burchardt et al7,8 found that
hypertensive patients with ED had a significantly higher prevalence of cardiovascular complications (P
.05) than
those without ED.
Patients with diagnosed conditions
that are frequently comorbid with ED
provide an outstanding opportunity to
facilitate discussions of sexual health.
Patients with established cardiovascular
disease, hypertension, dyslipidemia or
hyperlipidemia, diabetes mellitus,

JAOA Supplement 1 Vol 104 No 1 January 2004 S9

Checklist

Established cardiovascular disease

Atherosclerosis
Hypertension
Dyslipidemia
Hyperlipidemia,
Diabetes mellitus
Depression
Lower urinary tract symptoms
Status postprostatectomy for
prostate cancer

Figure 1. Comorbid conditions and risk factors associated with erectile dysfunction.

depression, or lower urinary tract symptoms should be evaluated for the presence of ED at every checkup.
A recent survey of male patients visiting a university-based urology clinic
showed that the average number of ED
risk factors was 2.1; however, of the 83%
of patients who reported having a primary care physician, only 23% had been
screened for ED.9,10
The Massachusetts Male Aging
Study2 also has provided perhaps the
best early description of the association
of various degrees of ED with a wide
range of comorbidities (Figure 1). Depression, established heart disease, hypertension, diabetes, and low levels of highdensity lipoprotein cholesterol were all
associated with substantial increases in
risk for ED.
The risk of ED associated with
depression is particularly striking, with
90% of severely depressed patients
having moderate to complete ED; this
statistic helps to spotlight the substantial psychological component of ED. Considerable overlap exists in these populations, and many men have two or more
of these risk factors. It is not atypical to
evaluate a patient with early-onset diabetes and uncover hypertension and
early-onset coronary artery disease, as
well.2
High rates of ED are observed in a
variety of patient populations with one or
more comorbidities. Of the comorbidities associated with high ED risk, three
have been most intensively studied in
clinical trials of phosphodiesterase-5

Figure 2. Prevalence of erectile dysfunction (ED) among men 40 to 70 years old according to
risk factor. HDL-C indicates high-density lipoprotein cholesterol. (Source: Feldman HA, Goldstein I, Hatzichristou DG, Krane RJ, McKinlay JB. Impotence and its medical and psychosocial
correlates: results of the Massachusetts Male Aging Study. J Urol. 1994;151:54-61.)

(PDE-5) inhibitors: patients with cardiovascular disease, patients with diabetes

mellitus, and patients who have undergone prostatectomy for treatment of
prostate cancer. In addition to posing
increased risk for the development of
ED, these comorbidities may increase the
severity of ED and represent additional
treatment challenges in comparison with
those encountered in the general population.

Cardiovascular Disease,
Risk Factors, and
Erectile Dysfunction
Cardiovascular disease is associated with
far higher rates of ED, and far higher rates
of severe ED, than those observed in the
general population. Data from the Massachusetts Male Aging Study2 confirmed
that heart disease in nonsmokers is associated with a greater than twofold elevation in the risk for complete ED, and

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nearly a twofold elevation in the risk for

moderate to complete ED when compared with the general population.
Patients with heart disease who smoke
face even worse odds: the risk of complete ED is more than fivefold, and that of
moderate to complete ED more than
twofold the comparable rates observed
in the general population. The presence of
hypertension doubles the risk for complete ED.
The diagnosis of ED is based on a
comprehensive sexual history, medical
history, physical examination, and diagnostic tests appropriate to the specific
condition of the patient. The initial decision to treat is based on the underlying
etiology of the patients ED and on
assessment of cardiovascular risk. Cardiovascular risk assessment should be
based on the risk of sexual activity per
se. The use of oral PDE-5 inhibitors,
based on clinical trials and postmarFine Erectile Dysfunction and Comorbid Diseases

keting experience, does not add to cardiovascular risk.

Risk Factors
Risk factors for cardiovascular disease
are also associated with increased risk
for ED. A low high-density lipoprotein
cholesterol level increases the risk of both
complete and moderate to complete ED
(Figure 2).2 The presence of hypertension
is associated with a significant increase in
the risk of the development of ED.
In a survey of male outpatients at
the Hypertension Center of Columbia
University using the International Index
of Erectile Function (IIEF), Burchardt and
colleagues11 found that 71 (68.3%) of the
104 respondents (mean age, 62 years)
had some degree of ED. Of the 71 hypertensive patients with ED, 47 (66%) had
complete ED, 16 (23%) had moderate
ED, and 8 (11%) had mild ED. These data
strongly suggest that hypertension is correlated not only with the presence of ED,
but also with increased severity of ED.
A great deal of work during the past
two decades has illustrated the critical
role dysfunction of the vascular endothelium plays in linking disease states with
outcomes. Conditions that lead to oxidative stress, such as hypertension, tobacco
use, diabetes, and others, may be the
common denominator in producing
endothelial dysfunction. This dysfunction in turn leads to atherosclerosis,
which may be a causative factor in many
cases of ED.12
The assessment of cardiovascular
risk should focus on the risk of sexual
activity itself. Sexual activity can trigger
myocardial infarction (MI), but in a study
of patients who had a nonfatal MI, only
about 1% were associated with sexual
activity during the preceding 2 hours.13
Even for patients with a 10% annual risk
of MI, sexual activity causes only a transient increase in risk from 10 in 1 million
per hour to 20 in 1 million per hour. The
estimated energy used for sexual intercourse is approximately equivalent to
that of climbing one flight of stairs and
less than that of golf or dancing.13

Treatment
Cardiovascular risk is an important consideration in prescribing phosphodiesterase type 5 (PDE-5) inhibitors for ED
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because of the frequent association

between ED and cardiovascular disease
and cardiovascular risk factors.
The cardiovascular safety profile of
PDE-5 inhibitors, demonstrated both in
clinical trials and postmarketing evaluations, strongly suggests that risk assessment should be based on the inherent
risk of sexual activity and that PDE-5
inhibitors do not increase that risk.14
However, PDE-5 inhibitors should never
be prescribed for, or used by, patients
taking nitrates. A synergistic interaction
between nitrates and PDE-5 inhibitors
may lead to dangerous hypotension.15
In general, the patient with ED comorbid
with cardiovascular disease will benefit
from the current strategies for cardiovascular risk assessment and risk management.
Safety data from a range of clinical
trials indicate that PDE-5 inhibitors do
not add incremental risk to existing risk
based on preexisting cardiovascular
status.

Diabetes Mellitus and

Erectile Dysfunction
Diabetes mellitus is a profound comorbidity for ED. Diabetes may contribute to
ED in several ways. Diabetic neuropathy
may compromise neural pathways
important in the erectile response. Occlusive diabetic vasculopathy may limit
blood flow into the corpus cavernosum.
Impairment of nitric oxidedependent
smooth muscle relaxation may also prevent adequate blood flow to support
erectile function.16 Endothelial dysfunction is believed to be the common
denominator in diabetic vasculopathy,
associated with pathologic effects in both
small and large vessels. These effects may
be the primary link between diabetes
and ED.

Prevalence
The prevalence of ED among men with
diabetes is higher than that among nondiabetic men at all ages.2,17 The risk of
diabetes-associated ED is correlated with
increasing age, duration of diabetes, and
development of diabetic neuropathy and
microangiopathy. The dramatic increase
in diabetes-associated ED with increased
age may account for a substantial fraction of the age-dependent increase in

prevalence observed in the overall population.

The Massachusetts Male Aging
Study2 showed that the prevalence of
ED is high among diabetic men, and the
proportion of diabetic men with moderate to complete ED is higher than the
proportion in the general population.
The odds ratio is a measure of the comparative likelihood of the development of
a given condition between two different
populations. The Cologne Male Survey,
a study of 8000 men in Germany by
Braun and colleagues,17 evaluated the
impact of various factors on the risk of
ED. The study showed that the odds ratio
for the development of ED in diabetic
men versus nondiabetic men was 3.95;
that is, the presence of diabetes increased
the likelihood of the development of ED
by nearly fourfold.2,17

Treatment
In assessing the results of placebo-controlled trials among diabetic men, all three
PDE-5 inhibitors demonstrated significant improvement versus placebo.18-20
After 12 weeks of treatment with sildenafil, diabetic patients with ED responding
to Sexual Encounter Profile (SEP) questions 2 and 3 (Q2, Q3) reported significant improvements over placebo in
achieving and maintaining erections.
However, in this study, efficacy in patients
with severe ED was not discerned.18 In a
study of vardenafil hydrochloride in men
with diabetes, a subset analysis demonstrated significant improvement in erectile
function versus placebo in men with
severe ED at baseline (IIEF erectile function domain score
11).19 Improvement
was assessed in this study using the stringent SEP Q3. Likewise, after 3 months of
treatment with tadalafil, patients with diabetes who had moderate ED recorded
clinically significant improvements in the
ability to achieve and maintain erections
compared with patients receiving
placebo.20 Vardenafil also demonstrated
sustained improvement in erectile function for 6 months.19

Androgen Deficiency and

Erectile Dysfunction
Prevalence
Currently available evidence indicates
that ED and androgen deficiency are two

JAOA Supplement 1 Vol 104 No 1 January 2004 S11

independently distributed disorders with

some degree of overlap. A clear correlation does not appear to exist between
erectile function and testosterone concentration. Buvat and Lemaire21 evaluated serum testosterone concentrations in
1022 men with ED. Only 10% (107) were
found to have a low testosterone concentration (
300 ng/dL) on initial assay;
of these, 40% had a testosterone concentration in the normal range on a repeated
assay.21
Korenman and colleagues22 studied
testosterone concentrations in young
(aged 20 to 44 years) potent men, potent
men older than 50 years, and impotent
men older than 50 years to assess the
relationship, if any, between impotence
and testosterone concentration. Testosterone concentrations in impotent and
potent older men were comparable; both
groups had significantly lower levels
than younger potent men. The fraction of
bioavailable testosterone was significantly (P
.001) higher in younger men
than in older men (both impotent and
potent older men had similar levels of
bioavailable testosterone). Forty-eight
percent of older potent men and 39% of
impotent older men were hypogonadal,
defined as having a mean bioavailable
testosterone concentration of less than
2.3 nmol/L, which was 2.5 SD below the
mean level in younger potent men.
Korenman and colleagues22 concluded
that no clear correlation existed between
testosterone or bioavailable testosterone
levels and erectile function, and that secondary hypogonadism and impotence
are common, but independently distributed, conditions in aging men.

Diagnosis
The definition of androgen deficiency is
not clear-cut; the AACE recommends
using a combination of history, physical
examination, and laboratory evaluations.23 Clinical problems that may be
associated with decreased testosterone
concentrations in older men include
sexual dysfunction, muscle wasting and
weakness, increased ratio of fat to lean
body mass, osteopenia, increased fractures in the central skeleton (hip and
vertebrae), decreased body hair,
decreased hematopoiesis, and memory
loss.24 There exists no unambiguous def-

inition for low testosterone concentration; testosterone levels fluctuate on a

diurnal basis and may vary significantly
hour to hour.
Normal testosterone concentrations are defined differently depending
on the reference source:
 The Merck Manual lists a range of
294 ng/dL to 833 ng/dL25;
 the prescribing information for testosterone gel lists a range of 298 ng/dL to
1043 ng/dL26; and
 the AACE guidelines for treating
hypogonadism suggest a range of
280 ng/dL to 800 ng/dL.23
The initial laboratory criterion for
diagnosis of hypogonadism is the total
testosterone concentration; the AACE
suggests that the free testosterone or the
sex hormone-binding globulin level may
be useful in cases in which clinical findings and laboratory values are difficult to
reconcile.23
The AACE23 recommends that prior
to initiating testosterone replacement, a
complete physical examination and laboratory workup should be conducted,
focusing on the identification of possible
prostate or breast cancer. This examination should include a digital rectal examination, prostate-specific antigen (PSA)
test, and careful evaluation of the breast.
Absolute contraindications to testosterone replacement therapy are prostate
cancer and breast cancer.

Treatment
Considerations of relative contraindications to testosterone replacement therapy
should be based on the patients specific
status. A prolactin-secreting tumor
should be ruled out if the testosterone
concentration is low and the luteinizing
hormone level is low. Testosterone
replacement will not be successful if an
untreated prolactinoma is present. Both
sleep apnea and polycythemia can be
exacerbated by testosterone supplementation.
The patients age should also be considered in light of the increased incidence
of prostate cancer after age 60 years.
Testosterone replacement reduces sperm
counts and fertility; therefore, it should
not be used in men wishing to sustain
fertility. Any existing symptomatic prostatism should be carefully evaluated

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and treated prior to testosterone supplementation.23

Administration options for testosterone supplementation include:

an injection of 200 mg every 2 weeks,
or 300 mg every 3 weeks (this regimen
should restore the serum level of testosterone to mid-normal after 1 week);

scrotal transdermal patch, one patch
every morning (this option should restore
the serum level of testosterone to midnormal after 4 hours);

nonscrotal transdermal patch, one
patch every evening (this option should
restore the serum level to mid-normal
after 8 to 12 hours);

testosterone gel, 5 g, 7.5 g, or 10 g
every morning (this modality should
restore the serum level of testosterone to
mid-normal range after 4 hours).24
Absolute contraindications to any
form of testosterone supplementation
include suspected or confirmed prostate
or breast cancer and desired fertility.23
The AACE recommends frequent, regular follow-up in men receiving testosterone replacement therapy. For the first
year of therapy, follow-up examinations
and laboratory values should be scheduled every 3 to 4 months, and every 6 to
12 months thereafter for the first
18 months. Follow-up assessments
should include:

confirmation of normal-range serum
testosterone concentrations;

digital rectal examination;

PSA test;

breast examination for breast cancer or
gynecomastia;

hematocrit testing (the AACE recommends hematocrit testing every 6
months for the first 18 months of therapy;
if the hematocrit is stable, testing should
be done annually thereafter23); and

assessment of sleep apnea, which may
manifest as obviously disordered sleep or
as daytime fatigue. (A more detailed
sleep study may be indicated if sleep
apnea is a possibility.)
Testosterone replacement therapy
should be discontinued in patients with
an abnormal finding on digital rectal
examination, elevated or increasing PSA
level, symptomatic prostatism (which
should be evaluated and treated before
reinitiating therapy), hematocrit greater
than 0.50 (may decrease or discontinue
Fine Erectile Dysfunction and Comorbid Diseases

Erection (arousal)

Erectile Dysfunction

Priapism

Erectile deformity

Diminished libido

Excessive libido

Libido (desire)

Ejaculation/orgasm

Premature, delayed
or retrograde
ejaculation

Anorgasmia

Anejaculation

Satisfaction/resolution

Figure 3. Male sexual response cycle and associated disorders.

testosterone replacement therapy), or

sleep apnea.23
In a review of a small, limited selection of studies of testosterone therapy in
men with various forms of sexual dysfunction, Tenover27 found that men with
low libido had general improvement in
libido with testosterone therapy, but ED
was only occasionally improved by
testosterone therapy.
The possibility that the physicians
ability to detect prostate cancer may be
different for hypogonadal than for eugonadal men suggests that patients should
be screened for prostate cancer before
testosterone replacement therapy. The
treatment decision should be based on
the elimination of absolute contraindications (prostate cancer, breast cancer,
and desired fertility); and on consideration of relative contraindications (sleep
apnea, polycythemia, age relative to
prostate cancer risk). Prolactinoma
should be ruled out.

Follow-up
Follow-up of men receiving testosterone
replacement therapy should be scheduled every 3 to 4 months for the first year
of therapy, then every 6 to 12 months
thereafter. Follow-up should include digital rectal examination, PSA test, breast
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evaluation, hematocrit, serum lipid levels,

and assessment of possible sleep apnea.
Testosterone therapy should be discontinued in patients who have abnormal
findings on digital rectal examination,
elevated or increasing PSA level, symptomatic prostatism, hematocrit greater
than 0.50, or sleep problems. Under no
circumstances should oral androgen
preparations be used for testosterone
supplementation.

Diminished Libido in Men

and Erectile Dysfunction
Erectile dysfunction, androgen deficiency, and decreased libido appear to
be independently distributed, but overlap
to some extent. Androgen deficiency or
decreased libido or both may play a
causative role in some cases of ED, but
many or most cases of ED appear to be
primarily vasculogenic. Decreased libido
may be the result of androgen deficiency,
but it also may be psychogenic.
Although the term libido is frequently used to simply denote sexual
desire, the Oxford English Dictionary definition hints at the true complexity of the
term.28 Libido involves spontaneous
sexual thoughts and fantasies, as well as
attentiveness to external sexual stimuli
that may be visual, auditory, or tactile.

Prevalence
The true incidence or prevalence rates
of low sexual desire disorders are elusive and difficult to assess. Laumann and
colleagues29 analyzed data from the
National Health and Social Life survey,
a 1992 study of sexual behavior in a
sample of 1749 women and 1410 men
(aged 18 to 59 years) selected to be demographically representative of the US population. Laumann and his colleagues estimated the prevalence of low-desire
disorders to be about 5% in men and
22% in women.29 Panser and colleagues,30
in a survey of 2215 men (aged 40 to 79
years) using a self-administered questionnaire, found a clear increase with age
for all sexual dysfunctions. Of men aged
70 to 79, 25.9% reported absent sexual
drive, versus 0.6% of men aged 40 to 49
years (P
.001).
Segraves and Segraves31 studied the
frequency of hypoactive sexual desire
disorder (HSDD) among a group of 906
men and women recruited for a multisite
pharmaceutical study based on a complaint of sexual dysfunction. In this
highly selected population, 89% of the
women and 30% of the men had a primary diagnosis of HSDD. Among the
women with a primary HSDD diagnosis,
41% had at least one other sexual dis-

JAOA Supplement 1 Vol 104 No 1 January 2004 S13

order; among the men with a primary

HSDD diagnosis, 47% also reported
some degree of ED. Other secondary
disorders included inhibited ejaculation.31

has reduced sexual desire, the physician

may consider organic causes such as
hormonal deficiencies, or psychogenic
causes such as stress or partnership
issues.32

Risk Factors and

Sexual Response

Evaluation

Low libido is associated with a number

of risk factors. It may develop as a secondary condition because of other disorders, including:

androgen deficiency;

use of certain medications, including
selective serotonin-reuptake inhibitors
and antiandrogens;

other sexual disorders such as ED due
to fear of humiliation;

psychiatric or psychological problems
such as depression; and

systemic illnesses such as arthritis.4
The male cycle of sexual response
(Figure 3) can be divided into four phases:

libido (desire), consisting of fantasies
and thoughts about sexual activity and
the desire to have sexual activity;

erection (arousal), involving a subjective sense of sexual pleasure accompanied by physiologic changes, ie, penile
tumescence and erection;

ejaculation/orgasm, comprising a
peaking in sexual pleasure, a sensation of
ejaculatory inevitability, and ejaculation
of semen; and

satisfaction/resolution, consisting of
a sense of muscular relaxation and general well-being.
Sexual dysfunction is characterized
by a disturbance in the processes that
make up the cycle of sexual response,
including:

diminished or excessive libido;

ED, priapism, or erectile deformity;

premature, delayed, or retrograde
ejaculation;

anorgasmia; or

anejaculation.
Sexual dysfunction also includes
pain associated with sexual intercourse,
caused by conditions such as fibrous
cavernitis (Peyronies disease) or chronic
pelvic pain syndrome. Although this
model is not entirely evidence-based, it
may be helpful to physicians seeking to
diagnose various conditions that may
occur at different points in the cycle of
sexual response. For example, if a patient

As with other sexual disorders, workup

of suspected low libido should begin
with a detailed sexual and medical history involving the couple. The sexual history may reveal other underlying problems to which low libido is secondary,
such as relationship issues or organic ED.
The medical history and evaluation
(using appropriate diagnostic tests) can
help rule out systemic illness, depression
or other psychological problems, alcohol
or drug abuse, medication side effects,
and androgen deficiency. Self-administered questionnaires such as the Sexual
Desire Inventory developed by Spector
and colleagues33 may also be useful.4
Disorders of libido can be an important contributor to and cause of sexual
dysfunction. Libido disorders are frequently difficult to diagnose, are often
overlooked, and not adequately treated.
Libido disorders may be secondary to
other sexual dysfunction, and they can
affect the response to therapy for ED.
Because low sexual desire may not be
pathologic, self-reported distress is an
essential component of the diagnosis.
Androgen deficiency can reduce libido
and is reversible on treatment; this cause
should be excluded at the outset of any
workup of libido problems.

Treatment
Testosterone deficiency is associated with
decreased overall sexual desire and a
reduced frequency of sexual fantasies
and spontaneous erections. On testosterone supplementation in androgendeficient men, studies have demonstrated
increased overall sexual activity, sexual
desire, sexual fantasies, and sleep-related
erections. Although testosterone supplementation in androgen-deficient men
seems to increase overall sexual desire
and activity, it has no clear-cut effect on
erectile capability.34-36
Testosterone has been shown to be
an important regulator of spontaneous
sexual thoughts and feelings, the attentiveness to erotic stimuli, and sponta-

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neous erections, but it does not appear to

affect erectile response to visual erotic
stimuli.
Erectile dysfunction, androgen deficiency, and libido are independently distributed conditions. Erectile dysfunction
does not imply androgen deficiency; less
than 10% of older men with ED are
hypogonadal. Testosterone supplementation may not improve ED. Testosterone
is not necessary for stimulus-evoked erections. Decreased libido may be related
to androgen deficiency. Thus, testosterone supplementation may increase
libido, and improved libido may increase
the response to PDE-5 inhibitors and
other treatment modalities for ED.

Comment
The prevalence of ED is rising sharply
worldwide as the result of population
growth overall and graying population trends. The presence of ED in a
patient is frequently an indicator of
comorbidities, including cardiovascular
disease, diabetes, dyslipidemia, and
depression. Despite its prevalence and
an increasing awareness among the
affected population, ED remains severely
underdiagnosed and patients undertreated for it. Erectile dysfunction can
result from psychological or organic
causes, or a mixture of both; regardless of
the underlying etiology, psychological
factors are almost always involved.
In patients with comorbid diseases
and ED, treatment should start with
lifestyle and medication modification,
followed by a combination of psychosocial counseling and oral therapy. Oral
PDE-5 inhibitors have been shown to
provide excellent efficacy in the treatment of ED in the general population
and across a range of ages and background comorbidities. Oral PDE-5
inhibitors have also been shown to
demonstrate an excellent safety and tolerability profile. Side effects are typically
transient and related to the vasodilatory
effects of the agents.18-20
Aging is associated with a gradual
decrease in bioavailable testosterone and
an increase in the prevalence of androgen
deficiency. Testosterone replacement
therapy in hypogonadal men has been
shown to increase strength, bone mass,
and lean body mass. Testosterone
Fine Erectile Dysfunction and Comorbid Diseases

replacement therapy in hypogonadal

men has also been correlated with
increased libido and improved sense of
well-being. Testosterone replacement has
no clear-cut effect on ED, although it may
improve the effectiveness of pharmacologic modes of therapy for ED. Testosterone replacement in hypogonadal men
restores prostate volume and PSA levels
to those seen in age-matched eugonadal
men. Testosterone replacement therapy
may increase hematocrit and lead to fluid
retention and sleep apnea.
Primary care physicians should
understand the importance of detecting
disorders of libido. Untreated low libido
may lead to emotional gridlock between
partners and the cessation of physical
affection. Low libido can lead to ED and
other organic and psychogenic sexual
disorders. Low libido can also influence
the effectiveness of therapeutic modalities
used to treat other sexual dysfunctions.
Finally, some cases of low libido are associated with androgen deficiency, for
which patients can be treated.

References
1. Jackson G, Bettridge J, Dean J, Hall R, Holdright
D, Holmes S, et al. A systematic approach to erectile dysfunction in the cardiovascular patient: A
consensus statement. Int J Clin Pract. 1999; 53:445451.
2. Feldman HA, Goldstein I, Hatzichristou DG, Krane
RJ, McKinlay JB. Impotence and its medical and
psychosocial correlates: results of the Massachusetts
Male Aging Study. J Urol. 1994;151:54-61.
3. Hanson-divers C, Jackson SE, Lue TF, et al. Health
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