260

ORIGINAL ARTICLES

Epidemiology and Neurobiology of Female Sexual Dysfunction

Anita H. Clayton, MD
Department of Psychiatry & Neurobehavioral Sciences, University of Virginia, Charlottesville, VA, USA

DOI: 10.1111/j.1743-6109.2007.00609.x

ABSTRACT

Introduction. Although several conceptual frameworks for female sexual dysfunction (FSD) have been advanced,
there still is considerable disagreement over what constitutes a normal vs. abnormal response. Sexual dysfunction is
a disturbance in sexual functioning involving one or multiple phases of the sexual response cycle or pain associated
with sexual activity, while a sexual disorder includes both dysfunction and marked distress.
Aim. Review the literature regarding the epidemiology and neurobiology of FSD.
Methods. Review of the literature.
Results. While a wide range of epidemiologic studies has been published, it is still difficult to determine the scope
of FSD and sexual disorders in the general population. It is becoming clear that good sexual health is associated with
good physical and mental health as well as compatible relationships with one’s sexual partner. Central nervous system
(CNS) control of the sexual response is a relatively new area of scientific exploration.
Conclusions. We are improving our understanding of the contributions of the CNS neuroendocrine and neurotrans-
mitter systems that modulate sexual behavior. Clayton AH. Epidemiology and neurobiology of female sexual
dysfunction. J Sex Med 2007;4(suppl 4):260–268.
Key Words. Female Sexual Dysfunction; Epidemiology; Neurobiology

Introduction genital vasocongestion such as photoplethysmog-

raphy [4]. In addition, sexual satisfaction is not

T he definition and correlates of female sexual

response and female sexual dysfunction
(FSD) continue to evolve. Although several con-
ceptual frameworks for FSD have been advanced,
there still is considerable disagreement over what
constitutes a normal vs. abnormal response [1,2]. A
better perspective might be that some women have
higher desire than their partner, some have similar
levels of desire, and some women have lower
desire [3]. The first group clearly has desire that is
sustained through the arousal phase. The latter
may experience responsive desire with stimulation,
which overlaps with cognitive/central arousal; thus
for some women, desire and arousal may not be
distinct entities. Genital sexual arousal as self-
reported by women appears to be more consis-
tently reproducible as a measurement tool than
so-called “objective” feedback measurements of
coherently linked to orgasm. The net result is that
the definitions of both “normal” and “abnormal”
sexual function are highly contextualized within an
individual patient’s life experiences.
Definitions
Sexual dysfunction is a disturbance in sexual func-
tioning involving one or multiple phases of the
sexual response cycle or pain associated with sexual
activity [5]. A sexual disorder is sexual dysfunction
that meets the Diagnostic and Statistical Manual
of Mental Disorders, 4th Edition (DSM-IV) crite-
ria for sexual disorders, and includes both dys-
function and marked distress. Without distress,
dysfunction does not require evaluation or treat-
ment. Some reports include sexual complaints
which are the expression of discontent or pain.

J Sex Med 2007;4(suppl 4):260–268 © 2007 International Society for Sexual Medicine
Epidemiology and Neurobiology of FSD
The American Psychiatric Association’s defini-
tions for FSD and Hypoactive Sexual Desire
Disorder (HSDD) focus on persistent or recurrent
deficiencies or absence of sexual fantasies and
desire for sexual activity [6]. The disturbance must
cause a marked distress or interpersonal difficulty,
and cannot be better accounted for by another
primary psychiatric disorder, substance abuse, or a
general medical condition. The American Foun-
dation of Urological Disease 2000 update on FSD
included definitions for desire/interest disorder,
subjective sexual arousal disorder, genital arousal
disorder, and combined disorders [7]. These
include the following definitions, all of which
depend on either persistence or recurrence of
symptoms in order to establish a diagnosis:
• Hypoactive Sexual Desire Disorder (HSDD):
Deficiency (or absence) of sexual fantasies/
thoughts, and/or desire for or receptivity to
sexual activity, which causes personal distress.
• Sexual Aversion Disorder: Phobic aversion to
and avoidance of sexual contact with a sexual
partner, which causes personal distress.
• Sexual Arousal Disorder: Inability to attain or
maintain sufficient sexual excitement, causing
personal distress, which may be expressed as a
lack of subjective excitement, or genital (lubri-
cation/swelling) or other somatic responses.
• Orgasmic Disorder: Difficulty, delay in, or
absence of attaining orgasm following sufficient
sexual stimulation and arousal, which causes
personal distress.
• Sexual Pain Disorders: Dyspareunia is defined as
genital pain associated with sexual intercourse.
Vaginismus is currently defined as the involun-
tary spasm of the musculature of the outer third
of the vagina that interferes with vaginal pen-
etration, which causes personal distress. Nonco-
ital sexual pain disorder is defined as genital pain
induced by noncoital sexual stimulation.
Although there are strong psychological and
physical components to the definitions of various
disorders, it should be noted that neither exits in a
vacuum. In one study of college students, individu-
als with lower levels of sexual desire showed
reduced physiologic responses to appetitive
sexual stimuli as well as a higher startle response
threshold [8].
Epidemiology of FSD
The literature is now replete with studies that
attempt to quantify the extent of FSD within given
261
populations. Unfortunately, many of these studies
use nonstandard or discarded definitions of sexual
dysfunction, and results across studies have not
been consistently reproducible. Even among
major surveys with solid methodology, contradic-
tory findings appear across demographic variables
such as race, education, and socioeconomic status.
In the United States, the 1999 National Health
and Social Life Survey of 1,749 women aged 18 to
59 years provided one of the first clear glimpses at
the scope of the problem of sexual dysfunction [9].
In this survey, 43% of women claimed a sexual
dysfunction, compared with 31% of men. Interest-
ingly, women of different racial groups had dif-
fering patterns of sexual dysfunction, with black
women complaining of low sexual desire and
reporting less pleasure than white women, who
reported higher rates of sexual pain. Hispanic
women in this survey reported fewer sexual prob-
lems overall than either black or white respondents.
Another finding of the National Health and
Social Life Survey was that women with higher
educational attainment were less likely overall to
complain of sexual dysfunction than those with less
education. Among women, this difference was
especially pronounced between women with less
than a high school education compared to women
with a college degree.
These U.S. results correspond to those
reported from a British community survey of
sexual functioning among 436 women aged 35–59
who had sexual partners [10]. One-third of these
women had operationally defined sexual dysfunc-
tion, including reduced sexual interest, vaginal
dryness, infrequency of orgasm, and dyspareunia.
The risk of sexual dysfunction increased with age,
but was unrelated to socioeconomic class. In this
survey, there was no link between sexual dysfunc-
tion and gynecologic conditions, except that
women with sexual dysfunction were more likely
to report an episode of stress incontinence at least
once a week. There was no association between
sexual dysfunction and menopause in this sample.
Sexual dysfunction is widely recognized as
increasing with age. In the Reproductive Risk
Factors for Incontinence Study at Kaiser (RRISK),
2,109 women aged 40–69 years were randomly
selected from a database of long-term Kaiser
Permanente members [11]. Data were collected by
self-reported questionnaires and in-person inter-
views. The mean age of the study population was
55.9 (⫾8) years and nearly three-fourths of the
women were sexually active. The population was
also racially diverse, with less than half of the
J Sex Med 2007;4(suppl 4):260–268
262
participants identifying themselves as white (48%),
with approximately equal distribution of the
remainder describing themselves as black (18%),
Hispanic (17%), or Asian (16%).
Among this population of women who
described themselves as generally healthy, 33%
reported a problem in one or more domains
associated with sexual dysfunction. Satisfaction
with sexual activity was associated with African-
American race, lower body mass index (BMI),
and higher mental health score (all P < 0.05).
More sexual dysfunction was associated with
having a college degree or greater, poor health,
being in a significant relationship, and a low
mental health score (all P < 0.05). Some of these
results are in conflict with the earlier National
Health and Social Life Survey, particularly the
relationship between education level and sexual
dysfunction. In this survey, higher educational
levels were associated both with increased sexual
activity and increased risk of sexual dysfunction.
Few epidemiological surveys have estimated the
rates of sexual disorders in the general population
secondary to the need to assess both sexual dys-
function and associated distress. Recently, the
Prevalence and Correlates of Female Sexual Dis-
orders and Determinants of Treatment Seeking
(PRESIDE) study was undertaken in 2006 by
mailing surveys to 50,000 U.S. women [12]. The
survey population was a representative sample of
U.S. women based on a variety of demographic
variables, including age, race, geographic location,
household size, household income, and marital
status. Response rate was high, with 31,581 returns.
The results were tabulated to establish specific
sexual disorders, with rates ranging from 9.5% for
HSDD to 4.6% for Orgasm Disorder (Table 1).
Estrogen status may also be correlated with
a diagnosis of HSDD. U.S. results from the
Table 1 Prevalence of sexual disorders from the
PRESIDE survey of 31,581 women, randomized to be a
demographically representative sample of U.S. women [12]
Hypoactive Arousal
desire disorder* disorder*
Prevalence 10.0 5.4
PRESIDE [%] (9.6–10.3) (5.1–5.7)
(95%–CI)
Age-adjusted 9.5 5.1
prevalence for
U.S.
population [%]
*Definitions based on the respective domains/items of the female version of
the Changes in Sexual Functioning Questionnaire for presence of respective
sexual dysfunction, and the Female Sexual Distress Scale for dysfunction
causing distress.
J Sex Med 2007;4(suppl 4):260–268
Clayton
Women’s International Study of Health and Sexu-
ality (WISHeS) divided women into two age
groups [13]. The younger group—aged 20 to 49
years—was stratified by whether they were pre-
menopausal or were surgically menopausal. The
older group—aged 50 to 70 years—was stratified
by whether they arrived at menopause naturally or
through surgery. Mail surveys were distributed
that included validated instruments of quality of
life and/or sexual function and distress.
In the WISHeS report, the prevalence of
HSDD ranged from 9% in naturally postmeno-
pausal women to 26% in younger surgically post-
menopausal women. The prevalence of HSDD
was significantly greater among surgically post-
menopausal women, aged 20 to 49 years, than pre-
menopausal women of similar age (Table 2).
HSDD was associated with emotional and psycho-
logical distress as well as significantly lower sexual
and partner satisfaction. HSDD was also associ-
ated with significant decrements in general health
status, including aspects of mental and physical
health.
Sexual dysfunction is also commonly seen in
non-Western countries. In a survey of Moroccan
women over the age of 20, almost 30% reported a
sexual dysfunction, and 18.3% fit the definition of
HSDD [14]. Similar surveys from other countries
have come to the same conclusion—that up to
one-third of adult women suffer from a sexual dys-
function, and that the risk for sexual disorders
increases with age and diminished estrogen status.
The distribution of specific sexual disorders
within populations reporting sexual dysfunction
was analyzed in an analysis of 11 epidemiologic
studies representing more than 25,000 subjects
[15]. The authors found that among women
reporting sexual difficulties, 64% reported desire
difficulties, 31% experienced arousal difficulty, and
35% reported orgasm difficulty (Figure 1). Among
women reporting sexual dysfunction, about one-
third noted that the duration of the difficulty was
at least 6 months.
Orgasm Sexual dysfunction is not commonly associated
disorder* with treatment-seeking behavior among women.
4.7 This is compounded by the fact that clinicians
(4.4–4.9) rarely inquire about the sexual health of their
patients. In the U.S. National Health and Social
4.6
Life Survey, 20% of women who reported a sexual
dysfunction stated that they had sought medical
attention for that problem [9]. In the British com-
munity survey, only 4% of women reporting
sexual difficulties stated that they would like to
receive help for their condition [10]. Among the
Epidemiology and Neurobiology of FSD 263

P value*
0.351
0.125
0.067
Table 2 Proportions of women classified as having low sexual desire and Hypoactive Sexual Desire Disorder by age and postmenopausal status in the Women’s

Surgically postmenopausal

62/197 (33)

27/197 (14)
27/62 (44)
(n = 197)
n/N (%)

Figure 1 Proportion of women with any sexual difficulty

who report each type of difficulty [15]. (䊊) Data from a
Naturally postmenopausal

single study. The area of each circle is proportional to the

sample size of the study. (䊉) Weighted average of all study
results for each type of sexual difficulty noted.
Age 50–70 years

71/252 (29)
23/71 (33)
23/252 (9)

Moroccan women surveyed, only 17% of women

(n = 252)
n/N (%)

reporting a sexual dysfunction had consulted a cli-

nician about their difficulty [14]. In a survey of
patients in four U.S. general medical practices, a
prevalence of sexual dysfunction was found in 41%
P value*

of women who responded [16]. However, while

0.028
0.025
0.002

50% of those with self-reported sexual dysfunction

stated they would like to receive medical treatment
for their condition, only 10% had received such
§Profile of Female Sexual Function Index desire domain <40 and Personal Distress Scale score <60 (HSDD).

care.
Surgically menopausal

Nonspecialist health care providers do not gen-

erally place a great deal of importance on sexual
health. Clinicians may underestimate the preva-
‡Percentage of low-desire women who were distressed. Personal Distress Scale score <60.

lence of sexual dysfunctions, and especially among

32/89 (36)
23/32 (72)
23/89 (26)
n/N (%)
(n = 89)

female patients, may be unaware of treatment

options that might prompt a referral to a sexual
health specialist. Nonspecialists also do not receive
adequate education regarding sexual disorders,
International Study of Health and Sexuality study [13]

and may be uncomfortable about making such

Premenopausal (n = 414)

Profile of Female Sexual Function Index desire domain score <40.

Percentages are based on women for whom data were available.

diagnoses [17,18]. Clinicians who receive specific

communication skills training and those who are
*Based on logistic regression model, after adjusting for age.
Age 20–49 years

comfortable addressing patients’ psychosocial con-

cerns are more likely to ask sexual health questions
96/414 (24)

56/414 (14)
56/96 (59)

[19].
n/N (%)

Confounding Factors: Comorbid Conditions

Sexual functioning and the perception of “good
Low sexual desire§ (a · b)

health” seem to go hand-in-hand. Loss of interest

Low sexual desire (a)

in sexual activity may accompany or be exacerbated

†

by chronic medical conditions that make sexual

Distressed‡ (b)

activity more physically taxing. In addition, iatro-

genic causation of sexual dysfunction is common.
For example, more women with diabetes
mellitus than control subjects reported sexual
†

J Sex Med 2007;4(suppl 4):260–268

264
dysfunction (27% vs. 15%, respectively) in this
case-control survey [20]. One hundred twenty
women attending a diabetes clinic were matched
with 180 healthy women attending an outpatient
gynecology clinic. However, no association was
found between sexual dysfunction and age, BMI,
duration of diabetes, HbA1c, use of medication,
menopausal status, or complications of diabetes.
Women with more diabetes complications,
however, reported significantly more sexual dys-
functions. Both diabetic women and controls
reporting sexual dysfunction described a lower
overall quality of their marital relationship and
more depressive symptoms than their respective
counterparts without sexual problems.
Also in diabetic women, sexual function and
sexual distress vary according to the phase of the
menstrual cycle, with decreased sexual function
and increased sexual distress compared with
control subjects during the luteal, but not the
follicular, phase of the menstrual cycle [21]. Fifty
premenopausal women with diabetes were com-
pared with 47 healthy controls via semistructured
medical interviews and self-administered ques-
tionnaires on sexual function, depression, and
sexual distress. Blood samples were also drawn to
measure indicators of diabetes, as well as to obtain
an endocrine profile during the subjects’ follicular
or luteal phase of their menstrual cycle.
The authors found that during the follicular
phase, women with diabetes had lower hormone
levels including estrogenic basal tone, delta4-
androstenedione and dihydroepandrosterone
sulfate production, and free-triiodothyronine (T3)
and free-thyroxine (T4) levels compared with
control subjects. During the luteal phase, total tes-
tosterone levels were higher in patients with dia-
betes than control subjects, while 17beta-estradiol
and progesterone levels were lower in patients
with diabetes than in the controls. These findings
may have implications related to the clinical
assessment of sexual function in premenopausal
women with diabetes.
Overactive bladder (OAB) is another common
condition that is associated with a high risk of
sexual dysfunction. In one study, 52% of women
involved in an open-label clinical trial of a therapy
for OAB reported reduced interest in sex at study
entry [22]. Patients in this study received a trans-
dermal formulation of oxybutinin for their OAB,
reporting increased interest in sex, improvement
in their sex lives, and improvements in their rela-
tionship with their partner. (P < 0.0001 from base-
line for all comparisons) at study end point.
J Sex Med 2007;4(suppl 4):260–268
Clayton
Major depressive disorder has long been associ-
ated with a reduced interest in sex [6,23]. This is
most likely due to the general anhedonia associated
with depression. Up to 80% of patients report
reduced libido as a symptom of their depression.
However, depressed patients do not generally ap-
pear to be distressed by their lack of interest in
sex.
It is also common knowledge that certain drugs
used for the treatment of depression can be associ-
ated with sexual dysfunction [24]. In a cross-
sectional observational study conducted in more
than 1,100 primary care clinics in the United States,
more than 6,200 adult patients receiving antide-
pressant monotherapy were surveyed for the pres-
ence of sexual dysfunction. Clinicians enrolled
their first five consecutive patients appearing in
their practice for any reason to avoid selection bias;
the study did not attempt to balance the patients on
the basis of antidepressant therapy; however, the
enrolled population did not differ from national
prescribing practices. In this population, the overall
prevalence of sexual dysfunction was 37%. Effects
are medication-specific, with the selective seroto-
nin reuptake inhibitors (SSRIs) and venlafaxine SR
having greater negative effects on sexual function-
ing than agents such as bupropion. These results
were consistent across both the entire study popu-
lation as well as within a subgroup of patients whose
sexual dysfunction could not be attributed to causes
other than their antidepressant regimen. This
report also found that the participating primary
care clinicians consistently underestimated the
prevalence of sexual dysfunction in their patients
taking antidepressants. Prior to receiving the
results of this study, physicians estimated that 20%
of their patients taking antidepressants would dem-
onstrate a sexual dysfunction; the reported percent-
age was almost twice that.
Drug-induced sexual dysfunction is also
attributed to a variety of agents used to treat
hypertension, schizophrenia, and certain cancers,
particularly treatments for hormone-sensitive
tumors [25]. The mechanism of action behind
iatrogenic sexual dysfunction varies by drug class.
Antihypertensive agents are proposed to cause
central adrenergic inhibition and block adrenergic
receptors, among other effects. Antipsychotics are
dopamine blockers, have anticholinergic effects,
may increase prolactin levels, and produce sedative
effects. The impact of oral contraceptives on sexual
functioning is controversial, although the prepon-
derance of the evidence suggests that only a minor-
ity of women will experience negative effects [26].
Epidemiology and Neurobiology of FSD 265

Other medical conditions associated with sexual

dysfunction include neurologic diseases such as
multiple sclerosis, and spinal cord injury; athero-
sclerosis and other cardiac diseases; gynecologic
conditions such as endometriosis, fibroids, infec-
tions, and prolapse, as well as obstetrical condi-
tions related to previous operative delivery, tears,
or episiotomy [27].

Neurobiology of Sexual Response and

Sexual Dysfunction
The fact that central nervous system (CNS)-acting
medications may have a profound effect on sexual
functioning raises important considerations about
the neurobiology of sexual response and sexual
dysfunction.
Although there are still large gaps in our under-
standing of CNS control of female sexual function,
it appears that the female genital response ema-
nates from several areas, including the brain stem, Figure 2 Central effects of neurotransmitters and hor-
hypothalamic structures (such as the medial pre- mones on sexual functioning (adapted from Munarriz et al.
optic area, ventromedial nucleus, and para- [28]). The symbols indicate a positive effect (+); negative
effect (-); and unknown effect (?). (Adapted from Clayton
ventricular nucleus), and forebrain structures,
[28])
including the amygdala [28]. Sexual response is
primarily mediated by spinal cord reflex responses
ine release in the medial preoptic area under basal
affecting genital and nongenital anatomic areas.
conditions and with sexual stimulation. Hormonal
The pudendal nerve provides the primary afferent
priming of ovariectomized female rats increases
reflex, while the efferent reflex is coordinated
extracellular levels of dopamine in the medial
through somatic activity, including pelvic floor
muscle contraction mediated through the bulb-
ocavernosus reflex emanating from sacral cord
segments, as well as, autonomic nerve stimulation
of the vaginal and clitoral cavernosa.
We are also improving our understanding of
the contributions of the neuroanatomical, neu-
roendocrine, and neurochemical systems that
modulate sexual behavior [29]. Sex steroids and
neurotransmitters play a role in both CNS effects
and peripheral response in the genitalia (Figures 2
and 3).
In the CNS, the neurotransmitter dopamine
appears to modulate sexual desire. In addition,
dopamine, along with norepinephrine, increases
the sense of sexual excitement and the desire to
continue sexual activity [30]. Increasing levels of
serotonin (e.g., reuptake inhibition as with the
SSRIs) can diminish the effects of both dopamine
and norepinephrine [31].
Estrogen and testosterone function may, at least
in part, be modulated by the effects of serotonin Figure 3 Peripheral effects of neurotransmitters and hor-
mones on sexual functioning (adapted from Munarriz et al.
activity in the hypothalamus and associated limbic [28]). The symbols indicate a positive effect (+); negative
structures [30]. In both male and female rats, the effect (-); and unknown effect (?). (Adapted from Clayton
presence of testosterone is permissive for dopam- [28])

J Sex Med 2007;4(suppl 4):260–268

266
preoptic area, and dopamine may activate addi-
tional CNS steroid receptors. Estrogen, however,
appears to play only an indirect role in the sexual
response cycle [31].
Other hormones also are involved in CNS
modulation of sexual behavior. These include oxy-
tocin, which may enhance sexual receptivity
and is associated with perineal contractions and
increased systolic blood pressure at the time of
orgasm [32,33]. On the down-regulation side, the
pituitary hormone prolactin negatively influences
the sexual excitement phase, and is inversely
related to dopamine function [31].
In the periphery, sex hormones are important
mediators of genital structure and function [29,34].
They also influence stasis with one another; for
example, increased levels of estrogen result in rising
levels of sex hormone-binding globulin, which then
leads to the reduction of free testosterone. Nitric
oxide (NO) and vasoactive intestinal peptide are
implicated in engorgement of clitoral tissue follow-
ing sexual stimulation; however, adequate levels of
estrogen and free testosterone are needed in order
for NO to stimulate vasocongestion. Peripheral
serotonin has negative effects on vasocongestion,
NO function, and sensation.
Melanocortins are a newly described group of
small protein hormones that appear to have both
CNS and peripheral effects on sexual function
[35]. Five melanocortin receptors have been iden-
tified, associated with complex pathways related to
skin pigmentation, weight, and sexual response.
Melanocortin signaling activates adenylate cyclase,
leading to increased levels of cyclic adenosine
monophosphate, which is responsible for driving
various physiologic functions. Each of the five
melanocortin receptors has a different binding
affinity for the various melanocortin peptides. The
melanocortin-4 receptor (MC4R), implicated in
the control of food intake and energy expenditure,
also modulates erectile function and sexual behav-
ior [36]. In animal and human models, MC4R
agonists are directly erectogenic, and also provoke
an increase in sexual behaviors, which will be
reviewed in this supplement by Pfaus et al. Of
interest is the potential interrelationship between
appetite and sexual response that may be mediated
by MC4R. There are several examples where
satiety and sexual function may be modulated by
the same neurotransmitter, including the role of
the satiety hormone leptin on reproductive func-
tion [37–39]. This leads to the theory that energy
homeostasis and reproductive function are broadly
linked.
J Sex Med 2007;4(suppl 4):260–268
Clayton
Assessment of Patients with FSD
Our understanding of the biological and neurobio-
logical correlates of sexual response is improving.
Identifying and assessing women with sexual com-
plaints is still a relatively labor-intensive process.
However, that does not mean that patients with
sexual dysfunctions must necessarily undergo
extensive physical examinations in order to be
properly diagnosed and treated. A physical exami-
nation may not be required, or helpful in reaching
a diagnosis of HSDD, for example, where no
physical abnormalities account for the lack of
sexual desire. However, physical exams are useful
in ruling out other, treatable causes of sexual dys-
function and may also be appropriate as part of
good general medical care.
Diagnosis of female sexual disorders ideally
begins with a biopsychosocial assessment, where
two partners are interviewed together and then
individually [2]. The assessment should investigate
any predisposing factors, such as past sexual
trauma; current precipitating or perpetuating
factors, including interpersonal relationships; and
any past or present medical/surgical conditions,
including pharmacologic treatments, which might
affect sexual functioning.
Physical examination should be conducted in
women who complain of dyspareunia, or who have
a history of pelvic trauma or other medical or
psychiatric conditions. Differential diagnosis of
dyspareunia requires an evaluation of both the
location of pain as well as factors that may suggest
a confounding issue (e.g., pain only with a specific
partner, etc.) [40]. In women with suspected
HSDD, differential diagnosis may suggest exami-
nations of genital neurologic status and vaginal
structure and muscle tone in order to rule out
other treatable conditions [41].
Conclusions
Female sexual dysfunction is common, but, unfor-
tunately, is not currently a focus of general medical
care. Sexual dysfunction in women increases with
age and declining estrogen status. Sexual activity is
seen as a sign of youth and vitality. Therefore, one
might expect that its importance will increase in
our aging society, and that more and more women
will not blithely consider the lack of a pleasurable
sex life to be a natural part of growing old.
FSD and sexual disorders are multifactorial
in nature; thus greater understanding of the com-
plex interrelationship between hormonal, neuro-
biological, and psychosocial systems is needed in
Epidemiology and Neurobiology of FSD
order to appropriately identify and manage
patients for whom reduced sexual interest and
functioning is a personal concern.
Corresponding Author: Anita H. Clayton, MD,
Department of Psychiatry & Neurobehavioral Sciences,
University of Virginia, Northridge Building, Suite 210,
2955 Ivy Road, Charlottesville, VA 22903, USA. Tel:
(434) 243-4646; Fax: (434) 243-4743; E-mail: ahc8v@
virginia.edu
Conflict of Interest: None declared.
Statement of Authorship
Category 1
(a) Conception and Design
Anita H. Clayton
(b) Acquisition of Data
Anita H. Clayton
(c) Analysis and Interpretation of Data
Anita H. Clayton
Category 2
(a) Drafting the Article
Anita H. Clayton
(b) Revising It for Intellectual Content
Anita H. Clayton
Category 3
(a) Final Approval of the Completed Article
Anita H. Clayton
References
1 Masters WH, Johnson VE. Human sexual response.
Boston: Little, Brown & Co; 1966.
2 Basson R, Brotto LA, Laan E, Redmond G, Utian
WH. Assessment and management of women’s
sexual dysfunctions: Problematic desire and arousal.
J Sex Med 2005;2:291–300.
3 Sand M, Fisher WA. Women’s endorsement of
models of female sexual response: The nurses’ sexu-
ality study. J Sex Med 2007;4:708–19.
4 Rellini A, Meston C. The sensitivity of event logs,
self-administered questionnaires and photoplethys-
mography to detect treatment-induced changes in
Female Sexual Arousal Disorder (FSAD) diagnosis.
J Sex Med 2006;3:283–91.
5 Clayton AH, Harsh V. Hypoactive sexual desire
disorder in women. Directions in psychiatry
2006;26:227–33.
6 American Psychiatric Association. Diagnostic and
statistical manual of mental disorders. 4th edition
(DSM-IV). Washington, DC: The American Psy-
chiatric Association; 1994.
7 Basson R, Berman J, Burnett A, Derogatis L, Fer-
guson D, Fourcroy J, Goldstein I, Graziottin A,
267
Heiman J, Laan E, Leiblum S, Padma-Nathan H,
Rosen R, Segraves K, Segraves RT, Shabsigh R,
Sipski M, Wagner G, Whipple B. Report of the
international consensus development conference on
female sexual dysfunction: Definitions and classifi-
cations. J Urol 2000;163:888–93.
8 Giargiari TD, Mahaffey AL, Craighead WE,
Hutchison KE. Appetitive responses to sexual
stimuli are attenuated in individuals with low levels
of sexual desire. Arch Sex Behav 2005;34:547–56.
9 Lauman EO, Paik A, Rosen RC. Sexual dysfunction
in the United States: Prevalence and predictors.
JAMA 1999;281:537–44.
10 Osborn M, Hawton K, Gath D. Sexual dysfunction
among middle-aged women in the community. BMJ
1998;296:959–62.
11 Addis IB, Van den Eeden SK, Wassel-Fyr CL, Vit-
tinghoff E, Brown JS, Thom DH; for the Repro-
ductive Risk Factors for Incontinence Study at
Kaiser (RRISK) Study Group. Sexual activity and
function in middle-aged and older women. Obstet
Gynecol 2006;107:755–64.
12 Clayton AH, Shifren JL, McKinlay J, Monz B,
Russo P, Segreti A, Johannes CB. Hypoactive sexual
desire disorder: Prevalence and differential diagno-
sis. Program and Abstracts of the 1st World Con-
gress for Sexual Health and 18th Congress of the
World Association for Sexual Health. April 15–19,
2007, Sidney, Australia. Abstract S25–2.
13 Leiblum SR, Koochaki PE, Rodenberg CA, Barton
IP, Rosen RC. Hypoactive sexual desire disorder
in postmenopausal women: US results from the
Women’s International Study of Health and
Sexuality (WISHeS). Menopause 2006;13:46–56.
14 Kadri N, McHichi Alami KH, McHakra Tahiri S.
Sexual dysfunction in women: Population-based
epidemiological study. Arch Womens Ment Health
2002;5:59–63.
15 Hayes RD, Bennett CM, Fairley CK, Dennerstein
L. What can prevalence studies tell us about female
sexual difficulty and dysfunction? J Sex Med 2006;
3:589–95.
16 Dunn KA, Croft PR, Hackett GI. Sexual problems:
A study of the prevalence and the need for health
care in the general population. Fam Pract 1998;
15:519–24.
17 Wimberly YH, Hogben M, Moore-Ruffin J, Moore
SE, Fry-Johnson Y. Sexual history-taking among
primary care physicians. J Natl Med Assoc 2006;
98:1924–9.
18 Bachmann G. Female sexuality and sexual dysfunc-
tion: Are we stuck on the learning curve? J Sex Med
2006;3:639–45.
19 Tsimtsiou Z, Hatzimouratidis K, Nakopoulou E,
Kyrana E, Salpigidis G, Hatzichristou D. Predictors
of physicians’ involvement in addressing sexual
health issues. J Sex Med 2006;3:583–8.
20 Enzlin P, Mathieu C, Van den Bruel A, Bosteels
J, Vanderschueren D, Demyttenaere K. Sexual
J Sex Med 2007;4(suppl 4):260–268
268
dysfunction in women with type 1 diabetes. Diabe-
tes Care 2002;25:672–77.
21 Salonia A, Lanzi R, Scavini M, Pontillo M, Gatti E,
Petrella G, Licata G, Nappi RE, Bosi E, Briganti A,
Rigatti P, Montorsi F. Sexual function and
endocrine profile in fertile women with type 1 dia-
betes. Diabetes Care 2006;29:312–6.
22 Sand PK, Goldberg RP, Dmochowski RR,
McIlwain M, Dahl NV. The impact of the overac-
tive bladder syndrome on sexual function: A pre-
liminary report from the Multicenter Assessment of
Transdermal Therapy in Overactive Bladder with
Oxybutynin trial. Am J Obstet Gynecol 2006;
195:1730–5.
23 Casper RC, Redmond DE Jr, Katz MM, Schaffer
CB, Davis JM, Koslow SH. Somatic symptoms in
primary affective disorder. Presence and relation-
ship to the classification of depression. Arch Gen
Psychiatry 1985;42:1098–104.
24 Clayton AH, Pradko JF, Croft HA, Montano B,
Leadbetter RA, Bolden-Watson C, Bass KI,
Donahue RMJ, Jamerson BD, Metz A. Prevalence
of sexual dysfunction among newer antidepressants.
J Clin Psychiatry 2002;63:357–66.
25 Smith PJ, Talbert RL. Sexual dysfunction with anti-
hypertensive and antipsychotic agents. Clin Pharm
1986;5:373–84.
26 Schaffir J. Hormonal contraception and sexual
desire: A critical review. J Sex Marital Ther
2006;32:305–14.
27 Pauls RN, Kleeman SD, Karram MM. Female
sexual dysfunction: Principles of diagnosis and
therapy. Obstet Gynecol Surv 2005;60:196–205.
28 Munarriz R, Kim NN, Goldstein I, Traish AM.
Biology of female sexual function. Urol Clin North
Am 2002;29:685–93.
29 Clayton AH. Sexual function and dysfunction in
women. Psychiatr Clin North Am 2003;263:673–82.
30 Hull EM, Lorrain DS, Du J, Matuszewich L,
Lumley LA, Putnam SK, Moses J. Hormone-
neurotransmitter interactions in the control of
sexual behavior. Behav Brain Res 1999;105:105–16.
J Sex Med 2007;4(suppl 4):260–268
Clayton
31 Halaris A. Neurochemical aspects of the sexual
response cycle. CNS Spectrums 2003;8:211–6.
32 Cushing BS, Carter CS. Prior exposure to oxytocin
mimics the effects of social contact and facilitates
sexual behavior in females. J Neuroendocrinol 1999;
11:765–9.
33 Melis MR, Argiolas A. Central oxytocinergic
neurotransmission: A drug target for the therapy of
psychogenic erectile dysfunction. Curr Drug
Targets 2003;4:55–66.
34 Imbimbo C, Gentile V, Palmieri A, Longo N,
Fusco F, Granata AM, Verze P, Mirone V. Female
sexual dysfunction: An update on physiopath-
ology. J Endocrinol Invest 2003;26(3 suppl):102–4.
35 Voisey J, Carroll L, van Daal A. Melanocortins and
their receptors and antagonists. Curr Drug Targets
2003;4:586–97.
36 Van der Ploeg LH, Martin WJ, Howard AD,
Nargund RP, Austin CP, Guan X, Drisko J, Cashen
D, Sebhat I, Patchett AA, Figueroa DJ, DiLella AG,
Connolly BM, Weinberg DH, Tan CP, Palyha OC,
Pong S-S, MacNeil T, Rosenblum C, Vongs A,
Tang R, Yu H, Sailer AW, Fong TM, Huang C, Tota
MR, Chang RS, Stearns R, Tamvakopoulos C,
Christ G, Drazen DL, Spar BD, Nelson RJ, MacIn-
tyre DE. A role for the melanocortin 4 receptor in
sexual function. PNAS 2002;99:11381–6.
37 Wade GN, Lempicki RL, Panicker AK, Frisbee
RM, Blaustein JD. Leptin facilitates and inhibits
sexual behavior in female hamsters. Am J Physiol
1997;272(Pt 2):R1354–8.
38 Schneider JE, Zhou D, Blum RM. Leptin and
metabolic control of reproduction. Horm Behav
2000;37:306–26.
39 Schneider JE, Zhou D. Interactive effects of central
leptin and peripheral fuel oxidation on estrous
cyclicity. Am J Physiol 1999;277(Pt 2):R1020–4.
40 Heim LJ. Evaluation and differential diagnosis
of dyspareunia. Am Fam Physician 2001;63:1535–44.
41 Warnock JJ. Female hypoactive sexual desire disor-
der: Epidemiology, diagnosis and treatment. CNS
Drugs 2002;16:745–53.