The Female Sexual Dysfunctions and the Hypoactive Sexual Desire Disorder (HSDD)
Semir A. S. Al Samarrai
In recent years, our interest and understanding of female sexual health, function and dysfunction have grown tremendously. Female sexuality and sexual dysfunctions are more complex than male sexual dysfunctions. The common dysfunctions are:
- Sexual interest/ desire disorder
- Sexual aversion disorder
- Subjective sexual arousal disorder
- Genital sexual arousal disorder
- Continued genital and subjective arousal disorder
- Persistent sexual arousal disorder
- Woman’s orgasm disorder
- Female Infertility
The prevalence ranges of desire disorders (16%-75%), orgasmic disorders, (16%-48%) arousal disorders (12%-64%) and pain disorders (7%-58%) respectively. Anxiety, depression and marital difficulties often co-exist with female sexual dysfunctions (FSDs), either as cause or effect.
Hormone deficiencies, diabetes mellitus, cardiovascular and neurological disease, depression, medication and drug use, surgery (e.g. hysterectomy, oophorectomy), gynecological and other cancers, radiation, and stress and relationship difficulties, and some common causes of FSDs.
Many women are reluctant/ shy about discussing their sexual problems and the sexual physician must take the initiative, infertility, pregnancy loss, oophorectomy, the menopause, and mini prescription, medication especially hormonal and psychotropic, can increase the risk of FSDs.
Sexual dysfunction refers to the problem happened during the sexual response cycle.
Psychological factors have been considered to be the primary cause in FSD, while in man it’s mostly a pathophysiological problem.
The American Psychiatric Association, Diagnostic, and statistical Manual of MENTAL Disorder (DSM-IV) classifies the sexual response cycle in 4 related but neurophysiologically discrete phases.
- Appetite Desire or libido
- Arousal or excitement
- Orgasm or Climax
- Refractory or resolution
Currently, researchers are considering whether a fifth phase, namely Satisfaction, would help to further define a normal sexual function.
Historically, sexual dysfunctions have been considered psychiatric disorders.
When Masters and Johnson published Human Sexual Inadequacy in 1970 (1), they separated diagnostic criteria into premature ejaculation, ejaculatory incompetence, impotence, orgasmic dysfunction, vaginismus, and dyspareunia. Desire disorders were not a diagnostic category. However, in 1970 Harold Lief and Helen Singer Keyplan (2, 3) focused on desire as distinct phase of the sexual response. It was defined as persistent inhibition of sexual desire. In the DSM-111
Revised (4) the term “inhibitioned Sexual Desire” was replaced by the “hypoactive sexual desire disorder (HSDD)
The current incarnation of the DSM (DSM Fourth Edition, Text Revision (DSM-IV-TR) defines HSDD as:
Persistent or recurrent deficiency (or absence) of sexual fantasies/thoughts, and/ or desire for or receptivity to sexual activity which causes personal distress.
A consensus group recently suggested that the definition be further refined to include lack of responsive desire and that lack of interest is beyond normative lessening with life cycle and relationship duration.
There is minimal evidence concerning the extent of normative lessening of desire with life cycle and relationship duration (5).
Factors that contribute to desire (6)
Sexual desire can be described as composite experience consisting of different elements:
Drive (biological component)
Motivation (Cognitive Component)
Responsiveness to sexual stimuli (response component)
Drive can be considered as an internal force (appetite, energy) that pushes an individual to do something. It is usually viewed as an instinct, with inborn patterns of reaction. This part of desire has been studied extensively in animal models, and the role of steroid hormone actions in hypothalamus and limbic structures of the brain has been elucidated (7, 8). In humans the drive component would be best represented by spontaneous desire.
Motivation for sexual activity is more complex. Psychophysiological phenomenon and is much more linked to cognitive processes which are typically characterized by the concept of incentive or reward. Motivation for sexual activity may reflect a desire for sexual pleasure, intimacy, pleasing the partner, feeling desired, emotional or narcissistic satisfaction, or motives not related directly to sexual desire or behavior (e.g. financial gain) (9).
Responsiveness to sexual stimuli refers to the ability of sexual stimuli to include sexual desire, arousal, sexual behavior, and sexual pleasure in an individual. It has been useful heuristically to divide both animal and human sexual activities into so –called “appetitive” and “ consummatory” phases that roughly characterize behaviors animal engage in prior to, or during, copulation, respectively .Appetitive human sexual behaviors include solicitations, flirtations, fantasy prior to sexual interactions, and the work or strategies employed to negotiate a successful sexual interaction.
Etiology and Pathogenesis
A.) Biomedical Factors: Disease and Drug Use:
1.) Hyper-and Hypothyroidism: One study showed an increase in lubrication problems and problems with orgasm in hypothyroidal women compared with an age-matched control group, with an increase in depressive symptoms No significant difference in desire ( 10)
2.) Urinary incontinence: Prevalence rates from 0.6% to 64% are reported (11). The women have significantly more incidence of low desire, arousal difficulties and pain (12).
3.) Diabetes : There seems to be a considerable difference in the prevalence of sexual dysfunction in patients with type 1 diabetes (18%) relative to patients with type 2 diabetes (42%). The predominant symptoms are largely arousal based including arousal dysfunction and decreased lubrication in women. Low desire seems more related to depression and relationship status in female diabetic patients than related to the disease per se (13-18).
4.)Coronary Artery Disease: Higher incidence of sexual arousal disorder but not HSDD in moment (19).
5.)Hypertension: The impact of hypertension or treatment of hypertension in women is not clear one cross-sectional study found decreased desire compared with the control group (20,21)
6.)Arthritis: This disease may lead to a dramatic decrease in mobility and to chronic pain and thus impair sexual function (22)
7.) Spinal Cord Injuries, Multiple Sclerosis (MS), Neuromascular Disorders: There is a direct impact of these disease states on the neuromuscular and neurovascular elements of the sexual response. The effect on desire is in general indirect and mediated by arousal disorders and pain (23, 24).
8.)Parkinson’s Disease, Dementia: It is known that hypothalamic sexual centers are connected to control nervous neurotransmitter pathways and may be therefore influenced by disturbances of dopaminergic, serotoninergic, adrenergic, and gamma-aminobutyric acid (GABA) ergic action. The changes can result in decreased desire but also in increased desire and hypersexual behavior (e.g., as occurs in patients with decreased frontal lobe function in dementia) (25-27).
9.)Schizophrenia: Sexual dysfunction is estimated to affect 30-80% of patients with schizophrenia and is a major cause of poor quality of life (28).
10.)Pituitary Tumors and Hyperprolactenemia: The main mechanism is supposedly the inhibitory impact of elevated prolactin on the dopaminergic system (29). Dopamine acts as a prolactin inhibitory factor, and decreased dopaminergic function in general may lead to HSDD and hypoprolactenemia.
11.)Cancer: Malignant diseases especially in the urogenital region may have various negative consequences for the female patient’s sexual function and thereby affect indirectly or directly desire. The disease itself and the subsequent surgery and radiation can lead to destruction of sexual organs, as occurs in vulvar, vaginal, uterine, and ovarian cancers. These are often accompanied by disfigurement of the body that impacts negatively on sexual self-image. Advanced disease is frequently accompanied by additional stressors like urine and stool incontinence,anuspraeter,etc.(30-38).
Major Depression is the most important clinical condition having an impact on desire. This disorder or group has a complex pathogenesis and certainly is not defined and determined by purely neurotransmitter dysregulation. It is now generally accepted that there is a neurobiological component which is characterized by altered functions especially of noradrenergic and serotoninergic systems. (39-41)
12.) Anxiety: The role of anxiety disorders in the pathogenisi of low desire is controversial. In sexually healthy woman anxiety-inducing techniques have been found to significantly increase psycho physiological sexual arousal. This may be via increased sympathetic nervous system activity. Subjective sexual arousal, however, has been shown to be increased, decreased, or unaffected by anxiety (42- 44). Due to the close link between desire and arousal some of these findings maybe of clinical importance for women with Hypoactive Sexual Desire Disorder. (HSDD)
Both prescription and over-the-counter medication have the capability to alter arousal, desire, and orgasm. The mechanisms can be divided into central nervous, peripheral nervous, neurovascular and neuromotor, endrocrine, and local. Any medication that alters blood flow (e.g. antihypertensive) affects the central nervous system (CNS) (e.g.psychotrophics) or dries the skin or mucous membranes (e.g. antihistamines) may disrupt normal sexual function (45, 46). One of the major clases of medications that impact sexuality is the selective serotonin reuptake inhibitors (SSRIs), frequently used to treat depression in both pre-and primenopausal woman. The risk/benefit ratio with use of these agents is based on individual need and response. When depression is severe, SSRIs may allow an increase activity by treating the underlying process. However, in many patients SSRIs are diminish or eliminate the ability to achieve orgasm, and severely diminish sexual arousal and desire (47, 48). The mechanism for this inhibitionmay be though decreased dopamine transmission (leading to increase prolactin levels), or by stimulation postsynaptic serotonin receptors that blunt sexual arousal and desire. Stimulation of 5-HTIb, 5HT2 and SHT3 receptors appears to inhibit sexual desire (13, 47,48).
Among biological correlates, decreased gonadal release of steroid hormones (e.g. androgens and/or estrogens) induced by either hypogonadal status, or through negative hormonal feedback. (e.g. in the case of individuals highly sensitive to oral contraceptives or taking anabolic androgens) is often accompanied by a noticeable decrease in sexual desire (49).
a.) Estrogens: Increases in self-reported sexual desire are highest in women during ovulation (50), when estradiol level peak. Increased estrogen action increases Vaginal Blood Flow (VBF) while a decreased concentration diminishes (VBF). The mechanism by which this occurs is related to estrogen stimulation of the release of vasoactive substances such as nitric oxid by endothelial cells, which induces vasodilatation.
b.) Progestin: In rats and other animals, progestins like progesterone facilitate solicitations and lordosis (51). However, progesterone treatment without estrogen to hypogonadal pre or post-menopausal women does not facilitate easier of desire (44).
c.) Androgen: Testosterone interacts with androgen receptors with highest concentrations in the substantia nigra/ventral tegmental area, the hypothalamus, and the preoptic area. Testosterone is also the primary precursor for estradiol biosynthesis in the brain, indeed, the testosterone concentration in the brain is 7 to 10 times higher than the estrogen with the highest ratio of
testosterone v.s. estradiol in the preoptic area. This distribution corresponds with the highest activity of the enzyme aromatase, which is responsible for converting androgens into estrogen. (52, 53). Thus, the free circulating concentration of estrogen and testosterone in plasma does not necessarily correlate with what is occurring in the brain. The effects of testosterone are difficult to distinguish from those of estradiol, and combined replacement therapy using both steroid generally results in a better enhancement of sexual desire than either steroid alone (54)
Sexual desire, arousability, and frequency of sexual intercourse have been correlated with the midmenstrual cycle increase in testosterone concentration, but as mentioned above, there is also an estrogen peak at midcycle. Some crossectional studies have shown a correlation between free testosterone and desire, whereas others could not find such a correlation (53,54). It is important to realize that the amount of biologically active testosterone depends not only on the aromatase activity but also on the concentration of steroid hormone binding globulins (SHBGs) in free circulation.
The menopausal transition has been associated with a decline in desire and subjective arousal among women. HSDD as the most frequently reported sexual problem in women, ranging from 15% to 25% in premenopausal women to 40-50% in postmenopausal women (55). Well-designed longitudinal studies have shown an increase in sexual dysfunction with aging with a major negative impact on desire and a correlation with decline in estrogen (56,57). It must be noted however that the decline in circulating estrogens is correlated with an increase in dyspareunia and lubricantion difficulties. Those could lead secondarily to diminished desire or avoidance sexual activity.
The postpartum period is associated with high sustained levels of prolactin and estradiol that may induce inhibitory feedback on brain mechanisms that excite sexual desire. Accordingly, reports indicate that a woman’s interest in sexual activity changes after childbirth. A substantial proportion of women (range 47% to 57%) interviewed at 3 months postpartum noted a decreased interest in sexual activity. However decreased desire during this period could also be attributed to fatigue. Pain, and concern over injury. An additional contributing factor in the postpartum period is the hypoestrogenism induced by lactational amenorrhea, which may lead to atrophy and dryness of the vaginal mucosa thus making intercourse painful and contributing to reactive lowered desire. Despite any changes
in desire, more than 80% of women resume sexual activity by 6 weeks postpartum (58).
Androgen Deficiency in Specific Clinical Conditions like Post-Ovarectomy Hypopituitarism, Adrenal Insufficiency: Longitudinal measurements among women after bilateral oophorectomy have shown an approximate 50% reduction in testosterone and a 40-50% reduction in androstenedione levels. In these women there is a correlation between testosterone and HSDD in so far as the decline in testosterone correlates to desire (59)
Oral Contraceptives: Combined oral contraceptives containing ethinylestradiol increase SHBG titers and this decrease available testosterone. This could contribute to a lack of desire and reduce subjective arousability (60). Due to the fact that oral contraceptives are linked to a myriad psychological and biological actions, some of which may have a positive impact on sexuality (e.g. reduce anxiety about unwanted pregnancy, diminish dysmenorrheal, attenuate acnc, etc), it is very difficult to discern the clinical effect of the decrease of free testosterone in users of some oral contraception (61,62), and clinical studies have been inconclusive: some reporting decreased desire, some no change in desire, and others increased sexual desire.
B.) IDIVIDUAL PSYCHOLOGICAL FACTORS:
A large number of psychological factors can lead to low sexual desire:
1.) Negative Early Environment:
The quality of attachment to parents and caregivers seem to foster sexual comfort and identity. Dysfunctional early relationships with caregivers can have a large psychological impact on later sexual function and ability to form long-lasting relationships
2.) Sexual Abuse and Emotional Neglect in Childhood:
Several studies have shown variable long term effects on a female adult’s sexuality after childhood abuse or neglect. One of the sequelae is low desire and sexual aversion disorder. Low sexual desire is the sexual concern most commonly reported by women survivors of sexual abuse (63- 67).
3.) Traumatic Experince During Puberty:
Research among adolescents has shown that negative first sexual experiences and especially humiliation and harassment may have harmful long-term consequences for the internal sexual script which determines positive and negative attributions to one’s sexual life (68).
4.) Perceived Distress: Studies have shown that psychosocial stress in general may reduce the motivation to become sexually active. Apart from cognitive processes there may be an incremental effect of a stress-induced cortisol secretion (69) that leads to decrease desire secondary to the impact or fear of
the stressful event. It must be remembered, however, that some stressors can act to enhance sexual arousal and desire in women. Cases of perceived distress that impact negatively on sexual desire may be due to unavoidable stressors of high impact or that are chronic rather than acute in nature.
5.) Performance Anxiety (Concerns) and Anxious Apprehension: The model of performance anxiety was largely derived from male patients with erectile dysfunction. For woman sexual performance concerns have a different focus because the signs of sexual arousal are less publicly evident. For women there is a large arrary of sexual concerns (Worries about pleasing her partner, fear of partner rejection, fear of pregnancy and sexually transmitted infections (STIs), unease related to the ability to reach orgasm, etc. (67). As with some types of perceived distress, such fears can focus an individual’s attention on ways to avoid sexual activity.
Distraction has been shown to be detrimental to female sexual function, especially subjective arousal and desire linked with sexual arousal (70, 71). However, the ability to be distracted from sex-related cues decreases in women during ovulation, but not during a late luteal period, suggesting that attention to sexual incentives is stronger when cycling estradiol levels are highest. Thus, the ability of distraction to impact negatively in sexual desire may vary across the menstrual cycle in women.
7.) Expectation (Anticipation) of a Negative Experience:
Low self-esteem combined with anticipation of negative outcome may diminish the receptivity for erotic and sexual cues and lead to inhibition and avoidance of a possible sexual interaction. Individuals that experience this may well withdraw from many types of social interaction (72).
8.) Body Image Self-Consciousness:
Self-Consciousness concerns of individual’s body image have a generally negative impact on female sexual function, above and beyond actual body size or general body image dissatisfaction (73, 74
9.) Relationship Factors:
Although research into the relationship factors that may contribute to HSDD or sexual arousal disorder (SAD) is scant, clinical experience and correlational studies show a close link between relationship and sexual satisfaction. However there is not a strict interdependence (both domains can operate independently meaning that couples with a good quality of their relationship may have severe sexual problems and couples with marital difficulties may function sexually in positive way. Another difficulty in the clinical evaluation of relationship factors is the question of cause and effect. What came first? Did sexual dissatisfaction lead to relationship problems or did couple
maladjustment lead to sexual dysfunction? Additionally, in some couples one problem maybe unconsciously used to “resolve” or “disguise” another problem which is experienced as even more threatening than the sexual dysfunction itself (75).
10.) Partner’s Sexual Dysfunction:
A considerable number of studies have shown that sexual dysfunction of male partner especially erectile dysfunction and premature ejaculation has negative impact on the female partner’s desire (76). Treatment of the male partner can lead to an amelioration of the female partner’s lack of desire (77)
11.) Duration of the relationship and Routine:
Some Community surveys have shown that the duration of relationship is inversely correlated to sexual desire and arousal distress was, however, not assessed, so this does not necessarily reflect HSDD (78)
12.) Global Dissatisfaction with the Relationship:
Compared with women without HSDD, women with HSDD report poorer dyadic adjustment, greater dissatisfaction with conflict resolution in their relationship, and less attraction to and emotional closeness with their partners. Furthermore, those
women found that relationship factors were major contributors to their sexual problems (79,80).
13.) Communication Deficits:
Difficulties in the ability to express needs, wishes, and fears between partners are often an immediate and direct factor which impacts negatively on a woman’s desire to engage in sexual activity. Men seem to have more inhibition in term of communicating about emotional and sexual issues (81-84) than women.
1.) Masters WH, Johnson VE. Human sexual inadequacy. Boston, MA: Little Brown; 1970.
2.) Lief HI. Inhibited sexual desire. Med Aspects Hum Sex 1977; 7:94-5.
3.) Kaplan HS. Hypoactive sexual desire disorder. J Sex Marital Ther 1977; 3:3-9
4.) American Psychiatric Association. Diagnostic and statistical manuel of mental disorders. 3rd Edition. Washington, DC: Americxan Psychiatric Press; 1987
5.) Basson R, Leiblum S, Brotto L, Derogatis L, Fourcroy J, Fugl-Meyer K, Graziottin A, Heiman JR, Laan E, Meston C, Schover L, VAN Lankveld J, Wejimar Schultz W. Definitions of women’s sexual dysfunction reconsidered: Advocating expansion and revision. J Pshosom Obstet Gynaecol 2003;24:221-9
6.) Levine S. Sexuality in mid-life. New York: Plenum; 1988
7.) Pfaff DW. Drive: Neurobiological and molecular mechanisms of motivation. Cambridge, MA:MIT Press; 1999
8.) Pfaus JG Pathways of sexual desire.J Sex Med 2009;6:1506-33
9.) Basson R. Using a different model for female sexual response to address women’s problematic low sexual desire. J Sex Marital Ther 2001;27:395-403
10.) Salonia A, Lanzi R, Nappi RE, Gatti E, Moltoni G, Rigatti P, Lanzi R. Sexual dysfunction in dysthyroidal women. Int J Impot Res 2002; 14(suppl 4):52-8
11.) Salonia A, Zanni G, Nappi RE, Briganti A, Deho F, Fabbri F, Colombo R, Guazzoni G, Di Giolamo V, Rigatti P, Montorsi urinary tract symptoms and urinary incontinence: Results of a cross-sectional study. Eur Urol 2004; 45:642-8
12.) Shaw C. A systemic review of the literature on the prevalence and the prevalence of urinary leakage during sexual activity. Eurol 2002; 42::432-40
13.) Enzlin P, Mathieu C, Vanderschueren D, Demyttenaere K. Diabetes and female sexuality: A review of 25 year’s research. Diabet Med 1998;15:809-15
14.) Schreiner-Engel P, Schiavi RC, Vietorisz D, Smith H. The differential impact of diabetes type on female sexuality. JPsychosom Res 1987;31::23-33
15.) Erol B, Tefekli A, Ozbery I, Salman F, Dincag N, Kadioglu A, Tellaloglu S. Sexual dysfunction in type II diabetic females: A comparative study. J Sex Marital Ther 2002;28(suppl 1): 55-62
16.) Schiel R. Muller UA. Prevalence of sexual disorders in a selection-free diabetic population (JEVIN). Diabetes Res Clin Pract 1999;44:115-21
17.) Enzlin P. Mathieu C, Van Den Bruel A, Bostels J, Vanderschueren D, Demyttenaere K. Sexual dysfunction in women with type 1 diabetes. Diabetes Care 2002;25:672-7
18.) Enzlin P, Mathieu C, Van Den Bruel A, Vanderschueren D, Demyttenaere K. Prevalence and predictors of sexual dysfunction in patients with type 1 diabetes. Diabetes Care 2003;26:409-14
19.) Salonia A, Briganti A, Montorsi P. Sexual dysfunction in women with coronary artery disease. Int J Impot Res 2002; 14 (suppl 4):80-92.
20.) Okeahialam BM, Obekahialam BM, Obeka NC. Sexual dysfunction in female hypertensives. J Natl Med Assoc 2006; 98:638-40
21.) Burchardt M, Burchardt T, Anastasiadis AG, Kiss AJ, Baer L, Pawar RV, de la Taille A, Shabsigh A, Ghafar MA, Shabsigh R. Sexual dysfunction is common and overlooked in female patients with hypertension. J Sex Marital Ther 2002;28:17-26
22.) Panus RS, Mihailescu GD, Gomisiewiez MT, Sutaria SH, Wallace DJ. Sex and arthritis. Bull Rheum Dis 2000;49:14.
23.) Sipski ML, Alexander CJ. Sexual activities, response and satisfaction in women pre-and post spinal cord injury. Arch Phys Med Rehabil 1993;74:1025-9
24.) Hennessy A, Robertson NP, Swinger R, Compston DA. Urinary fecal and sexual dysfunction in patients with multiple sclerosis. J Neurol 1999; 246:1027-32
25.) Yu M, Roane DM, Miner CR, Fleming M, Rogers JD. Dimensions of sexual dysfunction in Parkinson disease. Am J Geriatr Psychiatry 2004;12:221-6
26.) Dunn KM, Croft PR, Hackett GI. Association of sexual problems with social, psychological, and physical problems in men and in women: A cross sectional population survey. J Epidemiol Community Health 1999;53:144-8.
27.) Hawton K, Gath D, Day A. Sexual Function in a community sample of middle-aged women with partners: Effect of age, marital, socioeconomic, psychiatric, gynecological and menopausal factors. Arch Sex Behav 1994;23:375-95.
28.) Baggaley M. Sexual dysfunction in schizophrenia: Focus on recent evidence. Hum Psychopharmacol 2008;201-9.
29.) Hulter B, Lundberg PO. Sexual function in women with hypothalamo-pituitary disorders. Arch Sex Behav 1994; 23:171-83
30.) Juraskova I, Butow P, Robertson R, Sharpe L, Mcleod C. Hacker N. Post treatment sexual adjustment following cervical and endometrial cancer: A qualitative insight. Psychoocology 2003;12:267-79.
31.) Bloom JL, Stewart SL, Chang S, Banks PJ. Then and now: Quality of life of young cancer survivors. Psychoocology 2004;13:147-60
32.) Graziottin A. Castoldi E. Sexuality and breast cancer. A review. In Studd J, ed. The management of the menopause. The millennium review. New York: Parthenon;2000:211-20
33.) Sheppard C, Whitely R. Psychosexual problems after gynaecological cancer. J Br Menopause Soc 2006;12:24-7.
34.) Kornblith AB, Ligibel J. Psychosocial and sexual functioning of survivors of breast cancer. Semen Oncol 2003;30:799-813.
35.) Jensen PT, Groenvold M, Klee MC, Thranov I, Petersen MA, Machin D. Early stage cervical carcinoma, radical hysterectomy and sexual function. A longitudinal study. Cancer 2004;100:97-106 .
36.) Butler-Manuel SA, Buttery LD, A’Hern RP, Polak JM, Barton DP. Pelvic nerve plexus trauma at radical hysterectomy and simple hysterectomy and sexual function. The nerve content of the uterine supporting ligaments. Cancer 2000; 89:834-21.
37.) Cundiff GW, Fenner D. Evaluation and treatment of women with rectocele: Focus on associated defecatory and sexual dysfunction. Obstet Gynecolm2004;104:1403-21.
38.) Fokdal L, Hoyer M, Meldgaard P, von der Masse H. Long-term bladder, colorectal, and sexual functions after radical radiotherapy for urinary bladder cancer. Radiother Oncol 2004; 72:139-45.
39.) Kennedy SH, Dickens SE, Eisfeld BS, Bagby RM. Sexual dysfunction before antidepressant therapy in major depression. J Affect Disord 1999; 56:201-8.
40.) Frolich P, Meston C. Sexual functioning and self-reported depressive symptoms among college women. J Sex Res 2002; 39:321-5.
41.) Bartlik B, Kocsis JH, Legree R, Villaluz J, Kosoy A, Gelenberg AJ. Sexual dysfunction secondary to depressive disorders. J Gend Specific Med 1999; 2:52-60.
42.) Meston CM, Heiman JR. Ephredine-activated physiological sexual arousal in women. Arch Gen Psychiatry 1998; 55:652-6.
43.) Trudel G, Landry L, Larose YC. Low sexual desire: the role of anxiety, depression and marital adjustment. Sex Marital Ther 1997;12:95-9.
44.) Barlow DH. Causes of sexual dysfunction: The role of anxiety, and cognitive interference. J Consult Clin Psychol 1986; 54:140-8.
45.) Segraves RT, Balon R. Sexual pharmacology. Fast facts. New York and London:WW Norton;2003.
46.) Krebs M, Leopold K,Hinzpeter A, Schafer M. Current schizophrenia drugs: Efficacy and side effects. Expert Opin Pharmacother 2006; 7:1005-16.
47.) Gregorian RS, Golden KA, Bahce A, Goodman C, Kwong WJ, Khan ZM. Antidepressant medications. Curr Womens Health Rep 200 r45
48.) Clayton AH, Female sexual dysfunction related to depression and antidepressant medications. Curr Womens Health Rep 2002;2:182-7.
49.) Davis SR, Guay AT, Shifren JL, Mazer NS. Endocrine aspects of female dysfunction. J Sex Med 2004;1:82-6
50.) Stanislaw H, Rice FJ. Correlation between sexual desire menstrual cycle characteristics. Arch Sex Behav 1988;17:499-508.
51.) Giraldi A, Marson L, Nappi R, Pfaus J, Traish AM, Vardi Y, Goldstein I. Physiology of female sexual function: Animal models J Sex Med 2004;1:237-53.
52.) Vermuelen A, Verdonck L. Plasma androgen levels during the menstrual cycle. Am J Obster Gynecol 1976;125:491-4.
53.) Davis SR, Davison SL, Donath S, Bell RJ. Circulating androgen levels and self reported sexual function in women. JAMA 200; 294:91-6.
54.) Sherwin BB, Gelfand MM, Brender W. Androgen enhances sexual motivation in females: A prospective, crossoves study of sex steroid administration in the surgical menopause. Psychosom Med 1985;47:339-51.
55.) Dennerstein L, Lehert P, Burger M. The relative effects of hormones and relationship factors on sexual function of women through the natural menopausal transition. Maturitas 1997; 26:83-92.
56.) Dennerstein L, Lehert P, Burger M. The relative effects of hormones and relationship factors on sexual function of women through the natural menopausal transition. Fertile steril 2005; 84:174-80.
57.) Dennerstein L, Guthrie JR, Hayes RD, DeRogatis LR, Lehert P. Sexual function, dysfunction, and sexual distress in a prospective, population-based sample of mid-aged Australlian-born women. J Sex Med 2008; 5:2291-9.
58.) Bitzer J, Alder J. Sexuality during pregnancy and the postpartum period. J Sex Educ Ther 2000;25:49-58.
59.) Barbosa-Vargas E, Pfaus JG, Woodside B. Sexual behavior in lactating rats: Role of estrogen-induced progesterone receptos. Horm Behav 200;56:246-53.
60.) Miller KK, Biller BM, Beauregard C, Lipman JG, Jones J, Schoenfeld D, Sherman JC, Swearingen B, Loefffler J, Klibanski A. Effects of testosterone replacement in androgen-deficient women with hypopituitarism: A randomized, double-blind, placebo-controlled study. J Clin Endocrinol Metab2006;91:1683-92.
61.) Warnock JK, Clayton A, Croft H, Segraves R, Biggs FC. Comparison of androgens in women with hypoactive sexual desire disorder: Those on Combined Oral Contraceptives (COCs) vs. those not on COCs. J Sex Med 2006; 3:878-82.
62.) Bancroft J, Hammond G, Graham C. Do oral contraceptives produce irreversible effects on women’s sexuality? J Sex Med 2006; 3:567-72.
63.) Wallwiener M, Wallwiener LM, Seeger H, Mueck AO, Zipfel S, Bitzer J, Wallwiener CW. Effects of sex hormones in oral Contraceptives on the female sexual function score: A study in German female medical students. Contraception 2010; 82:15-9.
64.) Leonard LM, Follete VM. Sexual functioning in women reporting a history of child sexual abuse: Review of the empirical literature and clinical implications. Annu Rev Sex Res 2002;13:346-87.
65.) Fergusson DM, Mullen PE. Childhood sexual abuse: An evidence based perspective. Thousand Oaks, CA: Sag; 1999.
66.) Meston CM, Heiman JR. Sexual abuse and sexual function: Examination of sexually relevant cognitive processes. J Consult Clin Psychol 2000; 68:399-406.
67.) Oberg K, Fugl-Meyer A. On sexual well-being in sexually abused Swedish women: Epidemiological aspects. Sex Relatsh Ther 2002; 17:329-41.
68.) Elmerstig E, Wijma B, Swahnberg K. Young Swedish women’s experience of pain and discomfort during sexual intercourse. Acta Obstet Gynecol Scand 2009;88:98-103.
69.) Crabston-Cuebas MA, Barlow DH. Cognitive and affective contributions to sexual arousal functioning. Annu Rev Sex Res 1990; 1:119-61.
70.) Adams AE, Haynes SN, Brayer MA, Cognitives distraction in female sexual arousal. Psychophysiology 1985;22:689-96.
71.) Dove NL, Wiederman MW. Cognitive distraction and women’s sexual functioning. J Sex Marital Ther 2000;26:67-78.
72.) Kaplan HS. Anxiety and sexual dysfunction. J Clin Psychiatry 1988; 49:21-5.
73.) Weiderman MW. Women’s body image self-conciousness during physical intimacy with the partner. J Sex Res 2000;37:60-8
74.) Faith M, Schare M. The role of body image in sexually avoidant behavior. Arch Sex Behav 1993; 22:345-56.
75.) Aubin S. Heiman JR. Sexual dysfunction from a relationship perspective. In: Harvey JH, Wenzel A, Sprecher S, eds. The handbook of sexuality in close relationships. Mahwah: Erlbaum; 2004:477-517.
76.) Dean J, Rubio-Aurioles E, mCcABE M, Eardley I, Speakman M, Buvat J, de Tejada IS, Fisher w. Integrating partners into erectile dysfunction treatment: Improving the sexual experience for the couple. Int J Clin Pract 2008; 127-33.
77.) Goldstein I, Fisher WA, Sand M, Rosen RC, Mollen M, Brock G, Karlin G, Pommerville P, Bangerter K, Bandel tj, Derogatis LR, Vardenafil Study Group, Women’s sexual function impoves when partners are administered vardenafil for erectile dysfunction: A Prospective , randomized , doubleblind , placebo-controlled trial. J. Sex Med 2005; 2:819-32.
78.) Klusmann D. Sexual motivation and the duration of partnership. Arch Sex Behav 2002; 31:275-87.
79.) Trudel G, Boulos L, Benoit M. Dyadic adjustment in couples with hypoactive sexual desire. J Sex Educ Ther 1993; 19:31-6.
80.) Banmen J, Vogel NA. Therealtionship between marital quality and interpersonal sexual communication. Fam Ther 1985; 12:45-58.
81.) Metz me, Epstein N. Assesing the role of relationship conflict in sexual dysfunction. J Sex Marital Ther 2002; 28:139-64.
82.) Purnine DM, Carey MP. Interpersonal Communication and sexual adjustment: The roles of understanding and agreement. J Consult Clin Psychol 1997;65:1017-25.
83.) Zimmer D. Interaction patterns and communication and sexual distressed, martially distressed, and normasl couples; Two experimental studies. J Sex Marital Ther 1983; 9:251-65.
84.) Rust J, Golombock S, Collier J. Marital problems and sexual dysfunction; how are they related? Br J Psychiatry 1988; 152:629-31.
Correspondence:Prof. Dr. SEMIR AHMED SALIM AL SAMARRAI
Professor Doctor of Medicine-Urosurgery, Andrology, and Male Infertility
Dubai Healthcare City, Dubai, United Arab Emirates.
Mailing Address: Dubai Healthcare City, Bldg. No. 64, Al Razi building, Block D,
2nd floor, Dubai, United Arab Emirates, PO box 13576