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Volume : 3 | Issue : 4 | April 2014 ISSN - 2250-1991
187 | PARIPEX - INDIAN JOURNAL OF RESEARCH
Research Paper
Alcohol Dependence and Sexual Dysfunction : a
clinical review
Medical Science
Austin Fernandes
Senio Resident Doctor, Department of Psychiatry, Lokmanya Tilak
Municipal Medical College, Mumbai
* Avinash De Sousa
Research Associate, Department of Psychiatry, Lokmanya Tilak
Municipal Medical College, Mumbai, * Corresponding Author
KEYWORDS
alcohol dependence, sexual dysfunction, erectile dysfunction, premature ejaculation, testoster-
one, gonadal hormones.
ABSTRACT
The present paper summarizes sexual dysfunction in alcohol dependence and reviews the literature investigating the
relationship between alcohol and human sexuality. Specifically, the authors attempt to reconcile the apparent contradictions
found in the effects of alcohol on male and female sexual responding. The review concludes (a) that alcohol disinhibits
psychological sexual arousal and suppresses physiological responding, the former effect being stronger at lower doses of
alcohol and the latter effect at higher doses; (b) that although suppression is strictly pharmacological in nature, disinhibition
appears to be both pharmacological (the result of cognitive impairment) and psychological (the result of socially learned
expectancies); and (c) that expectancies and cognitive impairment can disinhibit separately or jointly. Various sexual
dysfunctions related to alcohol have been explained and elaborated.
INTRODUCTION
Nearly all the psychoactive drugs used have an effect on sex-
ual functioning and particularly erectile function. The adverse
effects of psychoactive drugs exhibit either through central
inhibitory neuroendocrine mechanisms and/or local neurovas-
cular actions, or they have an impact on the hormonal milieu.
Ethanol causes increase in inhibitory activity of GABA-A (gam-
ma-amino butyric acid) receptor and decreases the excitatory
activity of glutamate receptor in CNS. It suppresses the sex
axis and results in hypogonadism. Nicotine has a vasoconstrict-
ing effect on the penile vasculature. It also increases oxidative
stress and results in endothelial dysfunction. Morphine deriva-
tives are illegal, highly addictive and a central nervous system
depressant. They inhibit the release of luteinizing hormone
from the pituitary and also cause redirection of blood away
from the genitals. Amphetamine a potent and highly addictive
psychostimulant is known to enhance the release and block
the reuptake of dopamine and norepinephrine. MDMA which
is a ring-substituted derivative of amphetamine enhances the
release of serotonin, norepinephrine and dopamine. Cocaine is
a central nervous system and peripheral nervous system stimu-
lant with anesthetic and vasoconstricting action and is known
for inhibiting the reuptake of neurotransmitters.1
SEXUAL DYSFUNCTION DUE TO ALCOHOL
Chronic and persistent use of alcohol can cause sexual dys-
function, resulting in marked distress and interpersonal diffi-
culty which in turn, can worsen the alcohol abuse. Sexual dys-
function in the alcoholic may be due to the depressant effect
of alcohol itself, alcohol-related disease or due to a multitude
of psychological forces related to the alcohol use2.
There are a various exploratory theoretical concepts regarding
the relationship between alcohol abuse and sexual dysfunc-
tion. Biological concepts stress neurological damages or
endocrinological abnormalities3,4 , whereas psychological
concepts detail the importance of partnership conflicts
and other psychological mechanisms which generally main-
tain sexual dysfunction5. There are only a few reports con-
cerning therapeutic intervention with sexually dysfunctional
alcohol dependents.6,7
Sexual disorders approximately ranging from 8% to 58%
have frequently been reported in men who are chronic al-
coholics.8 Lemere and Smith reported that 8% of 17,000
patients treated for alcoholism had impotence.9 The re-
ported prevalence of lack of sexual desire ranges from
31% to 58% of subjects using alcohol long-term.10,11
Whalley reported that 54% of hospitalized alcoholic men
and 24% of healthy controls had erectile impotence.12
Jensen reported that 63% of married alcoholic men and
10% of controls had sexual dysfunctions, especially lack of
sexual desire.11
Bijil Simon Arackal and Vivek Benegal found that of 100 male
inpatients admitted for the treatment of alcoholism, 72 suf-
fered from sexual dysfunction and 36 out of 96 (37.5%) sub-
jects had premature ejaculation. The next most frequent sex-
ual dysfunction reported by 36 out of 100 subjects was low
sexual desire. Erectile dysfunction was reported by 33.3% of
the subjects with difficulty in achieving erection in 19 subjects
(19.79%) and difficulty in maintaining erection in 13 subjects
(13.54%). Fourteen subjects (14.58%) had a lack of pleasure
at the time of ejaculation (anorgasmia) and 10 (10.41%) had
inhibited or delayed ejaculation. People with tobacco use were
no more likely to have more sexual dysfunction than those
without tobacco use13.
Episodic erectile failure in alcoholic men is fairly routine, found
to be significantly higher in men consuming more than three
standard units of alcohol (12 g ethanol) daily and in subjects
smoking more than 10 cigarettes/day.14 Van Thiel and Lester83
reported that 61% of alcohol dependent patents had sexual
dysfunction, the most common being erectile dysfunction fol-
lowed by reduced sexual desire. Erectile dysfunction and re-
duced sexual desire were frequently seen to be coexisting. 15,
16 Vijayasenan,17 found that of 97 male inpatients admitted for
the treatment of alcoholism, 71% suffered from sexual dys-
function for a period of more than 12 months prior to admis-
sion to a hospital. The disturbances noted were diminished
sexual desire (58%), ejaculatory incompetence (22%), erectile
impotence (16%) and premature ejaculation (4%). Virtually all
aspects of the human sexual response are affected by alcohol
especially sexual desire and erection.18
Schiavi et al.19 failed to find any difference in sexual dysfunc-
tion in alcoholics abstinent for 2-3 months in comparison with
a nonalcoholic control group, speculating that alcohol-induced
Volume : 3 | Issue : 4 | April 2014 ISSN - 2250-1991
188 | PARIPEX - INDIAN JOURNAL OF RESEARCH
sexual dysfunction was reversible with abstinence.
Alcoholic men have reported impotence and diminished heter-
osexual desire and activity. Objective behavioural studies have
been completed on the effects of alcohol on sexual arousal
in response to an erotic or control film. It has been consist-
ently observed that alcohol attenuates sexual responsivity, as
defined by measures of penile tumescence, in healthy young
men. Reports of sexual arousal and estimates of penile erec-
tion were positively correlated with penile tumescence in
men.20, 21
Despite evidence to the contrary, subjects often continued
to believe that alcohol enhanced their sexual function. These
data illustrate the difficulty in reconciling objective and subjec-
tive information about sexual behaviour. Rubin and Henson22
have concluded that an individual whose threshold for penile
erection and/or ejaculation has been raised by the ingestion of
alcohol may consider this depressant effect to be an enhance-
ment of sexual abilities because it increases the time available
for sexual stimulation of his partner which could well increase
the probability of her being brought to orgasm.
Effects of alcohol on sexual function by amount of alcohol
Small doses of alcohol can cause: Release of inhibition in-
creased aggression, increased desire, increased arousal, control
of premature ejaculation, decreased penile tumescence
Moderate doses of alcohol can cause: longer foreplay, in-
creased time to erection, difficulty in maintaining erection, un-
certain orgasm, decreased penile tumescence.
Large doses of alcohol can cause: Impotence both erectile and
ejaculatory, thoughtlessness, unpleasant ejaculation, aggres-
siveness.
Chronic alcoholism may lead to loss of libido, loss of sexual
satisfaction, erectile impotence, decreased testosterone, infer-
tility, breast development, decreased body hair, shriveled testi-
cles 23
ALCOHOL AND ERECTILE DYSFUNCTION
In textbooks,24, 25 review articles26, 27 or clinical teachings alco-
hol is since long considered to be responsible for ED. It was a
long-held empirical observation that acute alcohol intoxication
increases sexual desire but inhibits sexual performance. The
scientific explanation is that alcohol is a central nervous sys-
tem depressant, but it also leads to disinhibition and increases
sexual desire.24 Epidemiological studies have shown numerous
risk factors for ED, such as age, variables related to diabetes,
depression, hypertension and smoking. With more evidence
gathered, the risk of alcohol consumption in ED seemed more
equivocal. ED has also been said to be the harbinger of car-
diovascular events. Endothelial dysfunction has been hypoth-
esized to result from cardiovascular risk factors such as hy-
pertension or diabetes, which in turn leads to ED, myocardial
infarction and stroke.28
There are various possible mechanisms by which alcohol may
cause erectile dysfunction. Erectile dysfunctions have more
than one cause. Central nervous system effects tend to be
more pronounced when levels are rising than when falling.
Ethanol (ethyl alcohol) impairs a spinal reflex which causes
both decreased sensation and decreased innervation for erec-
tion, but it has also been shown to decrease serum testoster-
one levels23.
The phenomenon of erectile dysfunction is caused by the
stimulating and then destructive effect of alcohol on the neu-
rologic reflex arc subserving erection. This arc theoretically in-
cludes29:
1) The cerebral cortex, from which sexual thoughts arise,
2) the anterior portion of the temporal lobe, which determines
intensity of libido,
3) perhaps the hypothalamus,
4) the spinal cord reflex centers for erection, and
5) the peripheral nerves that convey sensory and vasomotor
impulses to and from the genital organs.
Sung Chul Kam30 sought to investigate the effects of ethyl
alcohol on corporal tissue tonicity, as well as the intracellu-
lar calcium concentration ([Ca2+]) and potassium [K] channel
activity of corporal smooth muscle. Ethyl alcohol induced a
sustained increase in [Ca2+] in a dose-dependent manner, Ex-
tracellular application of ethyl alcohol significantly increased
whole-cell K+ currents in a concentration-dependent manner.
Ethyl alcohol caused a dose-dependent increase in cavernosal
tension by alterations to [Ca2+]. Although ethyl alcohol did not
affect KCa channels directly, it increased the channel activi-
ty by increasing [Ca2+]. The increased corpus cavernosal tone
caused by ethyl alcohol might be one of the mechanisms of
ED after heavy drinking
LANDMARK STUDIES ON ERECTILE DYSFUNCTION DUE TO
ALCOHOL
The Health Professionals Follow-up Study (HPFS)31, 32 provided
much evidence on the influence of lifestyle factors on the de-
velopment of ED.
The HPFS cross-sectional study31 involved 31 742 men aged
53–90 and was probably the largest cross-sectional study on
ED to date. The multivariate-adjusted Relative Risk (RR) for ED
was decreased with moderate levels of alcohol consumption.
The RRs were 1.0 (0.9–1.2), 0.9 (0.8–1.0), 0.8 (0.7–1.0) and
1.0 (0.8–1.2) for 0.1–4.9, 5.0–14.9, 15–29.9, ≥ 30.0g/day of
alcohol consumption respectively , after adjustments for co-
morbidity, medication, smoking status, physical activity, televi-
sion watching, body mass index (BMI) and other factors.
The HPFS prospective cohort study32 demonstrated the inde-
pendent effects of physical activity (RR 0.7, 95% CI, 0.7–0.8),
obesity (multivariate RR 1.9, 95% CI, 1.6–2.2) and smoking
(RR 1.5, 95% CI, 1.3–1.7) on the development of ED. Around
51529 health professional men were recruited at baseline, af-
ter inclusion of those who were healthy at baseline and exclu-
sion of those lost to follow-up, 22 086 men were computed
in the analysis. No significant difference in risk of developing
ED was found in all categories of alcohol consumption: multi-
variate adjusted RR 1.0 (0.9–1.1), 1.0 (0.9–1.1), 1.0 (0.9–1.1)
and 1.1 (1.0–1.2), for 0.1–4.9, 5.0–14.9, 15–29.9, ≥ 30.0 g/
day of alcohol consumption respectively. Statistical adjust-
ments were made for age, marital status, smoking, alcohol
and BMI
The Massachusetts Male Aging Study (MMAS)33 involved a
baseline cohort of 1709 men, but the analysis was restricted
to only 513 men without ED at baseline. The adjusted inci-
dence for ED was 16% (95% CI, 12–22), 16% (11–23) and
15% (8–24) in those with <1 drink/day, 1–3 drinks/day and
≥4 drinks/day of alcohol consumption respectively. This inci-
dence figure was adjusted for age, active and passive smok-
ing, overweight, hypertension, physical activity, cholesterol,
fat intake, testosterone, depression and antihypertensive
medication intake. It is also found that the OR (adjusted for
the same variables) for ED was 0.95 (95% CI, 0.54–1.67) and
0.87 (0.41–1.86) in those with 1–3 drinks/day and ≥4 drinks/
day of alcohol consumption respectively, using <1 drink/day as
reference, although the result was not statistically significant.
O’Farrell et al. found that alcoholic men had over three times
the prevalence of serious ED (i.e., at least 25% of the time) of
demographically similar nonalcoholic men.34. Another study
by Snyder and Karacan measured nocturnal penile tumescence
in a sample of 26 alcoholic men going through detoxification.
They found that alcoholic men were more likely to have fewer,
slower, and less rigid nocturnal erections than a nonalcoholic
comparison group.35
PREMATURE EJACULATION DUE TO ALCOHOL USE
Studies have quoted the presence of premature ejaculation
in alcoholics. Secondary premature ejaculation is sometimes
Volume : 3 | Issue : 4 | April 2014 ISSN - 2250-1991
189 | PARIPEX - INDIAN JOURNAL OF RESEARCH
found in association with alcohol-related peripheral neuropa-
thy36.
In a study by C. Basile Fasolo et al among lifestyle habits
(smoking, alcohol, and physical activity), only alcohol drinking
had a relation in this study with an increased risk of Premature
Ejaculation.37
Mandell et al. interviewed 44 male volunteers consecutively
admitted to outpatient treatment in a county alcoholism pro-
gram. Fifty-three per cent of the subjects were still drinking
minimally or in moderation at the time of the interview. Quan-
tity, frequency, and duration of drinking, from onset of regular
drinking to present, were related to sexual dysfunctions. Dur-
ing heavy drinking. 59% of patients experienced erection dys-
function, 48% reported ejaculation incompetence, and 84.4%
had experienced at least one kind of sexual dysfunction38.
STUDY QUOTING NO DIFFERENCE IN SEXUAL DYSFUNC-
TION DUE TO ALCOHOL
Gumus et al39 conducted a study on forty-five chronically alco-
holic men and a control group of thirty healthy non-alcoholic
volunteers. Each of the men in the study and control group
were interviewed on the basis of a sexual dysfunction ques-
tionnaire by an urologist. Blood samples were collected for
evaluation of hormone levels. The sexual desire and erection
scores of alcoholic men were not statistically different from
those of the control group. Fourteen out of the 45 alcohol-
ic men complained of loss of erection during sexual activity
however it was not statistically significant. No significant dif-
ference in hormone levels between groups was found except
for Follicle Stimulating Hormone (FSH). He concluded that in
the absence of hepatic and gonadal failure in chronically alco-
holic men, there is no significant difference in serum hormonal
levels, sexual dysfunction form, and sexual functions between
alcoholics and normal healthy non-alcoholic men.
EFFECTS OF ALCOHOL ON PITUITARY AND GONADAL
HORMONES
Shakespeare40 was among the first to comment on alcohol-in-
duced changes in pituitary-gonadal function.
Macduff: What three things does drink especially provoke?
Porter: Marry, sir, nose painting, sleep and urine. Lechery, sir,
it provokes and unprovokes. It provokes the desire but takes
away the performance.
Although extensive studies on the effects of alcohol on pitu-
itary secretions of vasopressin and ethanol-induced diuresis
have been done41, the relations between the effects of alcohol
on pituitary-gonadal hormones and sexual function have only
recently been elucidated.
The activity of the hypothalamic–pituitary–adrenal (HPA) axis42
and the hypothalamo–pituitary–gonadal (HPG) axis19 is affect-
ed by alcohol. Though the underlying mechanisms have not
been completely identified, animal and laboratory studies indi-
cate that alcohol suppresses the activity of the HPG axis by in-
hibiting the secretion of hypothalamic-gonadotropin-releasing
hormone (GnRH) and/or pituitary luteinizing hormone (LH)43,44
RELATIONSHIP OF ALCOHOL INDUCED LIVER DISEASE
AND; PITUITARY AND GONADAL FUNCTIONS
In 1926 clinical reports of gynecomastia and testicular atrophy
in alcoholics with cirrhosis of the liver began to appear in the
medical literature45. Many reports of similar phenomena were
later published and several investigators explored the relations
between alcohol-induced liver disease and derangements in
steroid homeostasis.46 Testicular atrophy and gynecomastia de-
veloping in alcoholic men with liver disease as a consequence
of a specific disorder involving estrogen metabolism have not
been established.47 It is doubtful whether cirrhosis itself is a
primary factor in feminization of male alcoholics. Summerskill
and his co-workers48 have reported a higher incidence of gy-
necomastia in men with alcohol related cirrhosis than in men
with cirrhosis unrelated to alcohol. Galvao-Teles and his associ-
ates also obtained similar findings.48
Van Thiel and his associates49 conducted detailed studies of 40
men with alcohol-related hepatic disease, and reported that,
primary gonadal failure as well as hypothalamic-pituitary sup-
pression are demonstrable in men with alcoholic liver disease.
Male alcohol addicts who had little evidence of liver disease
were also observed to have gynecomastia and testicular atro-
phy.50 Van Thiel and Lester51 concluded that alcohol use itself,
without associated liver disease, might produce disorders of
gonadal steroid function. This hypothesis has been substanti-
ated in a number of recent studies in human beings and an-
imals.
Iturriaga et al52 assessed the relationship of ethanol ingestion
induced hypoandrogenism in male subjects with its relation-
ship with the degree of liver damage and alcohol abstinence.
After two different abstinence periods they measured plasma
sex hormones in 30 alcoholic patients without liver failure. It
was found that on admission total Testosterone levels were
similar to controls. Histologically, 9 patients had normal liver;
14 had moderate alterations and 7 showed marked altera-
tions. Hormonal values were not different in these 3 groups.
Around 11 days after admission, when these patients were to
be discharged it was observed that Testosterone, Estrogen and
FSH did not show significant changes but LH decreased. They
concluded that alcoholic patients without clinical signs of liver
failure have normal plasma testosterone levels, irrespective of
their histologic liver alterations.
EFFECT OF ALCOHOL ON TESTOSTERONE
Naturalistic studies show, chronic alcohol intake reduces plas-
ma testosterone levels in men.53 Interestingly, plasma testoster-
one levels decrease in dependent men after experimental ex-
posure to the sight and smell of alcohol even without alcohol
consumption54. In fact in the studies conducted by Ruusa et al
in non-cirrhotic alcoholic men, there was an increase in tes-
tosterone concentrations during withdrawal and returned to
normal limits after three weeks of abstinence55
It appears that alcohol-induced decrement in testosterone may
have several interacting biologic processes. Vitamin A metabo-
lism in the testes is inhibited by alcohol56, and this effect may
contribute to an inhibition of steroid production in the testes.
Alcohol not only accelerates the rate of testosterone degrada-
tion in the liver57 but also decreases testosterone production.58
The recent studies with healthy, nonalcoholic men have sup-
ported the hypothesis that alcohol-induced suppression of tes-
tosterone is primarily due to ethanol’s effect on the target or-
gan (the testes) rather than an ethanol-mediated effect on the
pituitary trophic hormone (luteinizing hormone). Data indicate
that ethanol inhibits testosterone biosynthesis in the testes at
the intracellular level rather than the membrane level of the
Leydig cell.59
Ethanol-induced inhibition of testosterone biosynthesis in Ley-
dig cells probably occurs because levels of nicotinamide ade-
nine dinucleotide are reduced in the testes when ethanol is
oxidized.
A factor contributing to the decreased plasma concentration
of testosterone in chronic alcoholics is the ethanol induced in-
crease in the metabolic clearance rate of testosterone, which
is due, at least in part, to the increased activity of the hepatic
5 α-reductases, microsomal enzymes responsible for their re-
versible metabolism of Δ 4-3-ketosteroids such as testoster-
one.60 This enzyme converts testosterone to dihydrotestoster-
one, which in the liver is a catabolic reaction. An additional
factor to be considered as a mechanism leading to low plasma
levels of testosterone is the ethanol induced enhancement of
adrenal cortisol secretion61, because it has been shown that
exogenously administered cortisol and dexamethasone can de-
press testicular production of testosterone62
Volume : 3 | Issue : 4 | April 2014 ISSN - 2250-1991
190 | PARIPEX - INDIAN JOURNAL OF RESEARCH
The importance of alcohol-induced derangements in testos-
terone biosynthesis and associated changes in luteinizing-hor-
mone secretory activity extends beyond the dramatic cases
of feminization in adult male alcoholics. A number of clinical
surveys have suggested that alcohol affects libidinal function
and sexual behaviour in otherwise normal men.63 Masters and
Johnson64 have reported that the second most frequent factor
associated with impotence in the men whom they examined
was “directly related to a specific incidence of acute ingestion
or to a pattern of excessive alcohol intake per se.”
The mechanisms underlying alcohol-induced sexual arousal
are not well understood although it can be understood that
a decrement in sexual performance is associated with an al-
cohol-induced decrement in testosterone levels in men. The
findings by LaFerla and his associates65 indicate a correlation
between degree of sexual arousal and increments in plasma
luteinizing-hormone levels in men. It is possible that a surge in
levels of the hormone associated with a decrement in plasma
testosterone after acute alcohol intake66 is implicated in alco-
hol-induced sexual arousal.
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