Which Hormone Can Cause Decreased Sexual Desire When Present in Either Low or High Levels?
J Turk Ger Gynecol Assoc. 2022 Dec; 18(4): 210–218.
Role of hormones in hypoactive sexual desire disorder and current treatment
Ahmed AlAwlaqi
1 Department of Obstetrics and Gynaecology, University of Saarland, Homburg, Deutschland
Houda Amor
1 Section of Obstetrics and Gynaecology, University of Saarland, Homburg, Germany
Mohamed E. Hammadeh
1 Department of Obstetrics and Gynaecology, Academy of Saarland, Homburg, Germany
Received 2022 Jun 16; Accepted 2022 Oct 12.
Abstruse
Over the decades, female person sexual dysfunction (FSD) has grown to be an increasingly potential problem that complicates the quality of life amid women. In the current review, FSD refers to recurrent and persistent problems with sexual orgasm, desire, or response. One of the most common subtypes of FSD that has evoked increased research interest in the scientific customs is hyposexuality. Today, there is a consensus that hyposexuality is a multifactorial condition that manifests with reduced sexual want resulting in meaning interpersonal distress. The objective of the electric current review was to examine how hormonal contour triggers propagate hypoactive sexual desire disorder (HSDD), and to highlight effective treatment interventions that can exist used to manage the condition. The current review describes HSDD as a sexual dysfunction characterized by the absenteeism or lack of sexual want and fantasies for sexual activities. The review argues that even if the role of sexual hormones is essential in modulating HSDD through therapeutic interventions, an effective comprehension of the biologic mechanisms underlying HSDD is necessary. There is a consensus in the literature that HSDD still poses significant challenges due to the lack of properly formulated treatment regimens and absence of clear clinical guidelines. That is, a amend intervention consisting of both psycho-relational and biologic aspects is compulsory if tailored management and accurate diagnosis of HSDD in clinical practice are to be realised. The review concludes that, to date, a reliable clinical intervention to manage hyposexuality is still absent and more interventions, in terms of condom and efficacy, are required. Thus, boosted investigation is required to document precise hormonal or not-hormonal pharmacotherapeutic agents for individualised intendance among patients with HSDD.
Keywords: Hyposexuality, hormone, women, menopause, hypoactive
INTRODUCTION
The problem of low sexual desire affects women of all ages, which contributes to potential negative outcomes including reduced well-being and quality of life (1,2). Over the years, low sexual desire has been widely regarded as role of broader female sexual dysfunction (FSD) weather condition (iii), of which HSDD is more than prevalent (4,5). According to the American Psychiatric Association'southward Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), HSDD is defined as a persistent absenteeism of sexual craving for sexual activities (6). However, the International Nomenclature of Illness by the World Health Organization (7) and the DSM-IV tool (6) take reached a consensus that the definition of HSDD must include several aspects of authentic diagnosis. These include the presence of interpersonal difficulties and/or personal distress, in add-on to the lack of sexual desires or fantasies for sexual practice-related activities (6,7). A similar claim has also been supported by the American Foundation for Urologic Illness, on the basis that both sexually-related private distress and low sexual desire should exist observed for a person to exist positively diagnosed equally having HSDD (vii,eight).
Often, when cases of depression sexual desire are reported, the most mutual diagnosis is assumed to be generalised acquired HSDD. HSDD is mostly not reliant on a specific state of affairs, and oft develops at a time when the want for sex is assumed to be ordinary (viii). As such, the presence of HSDD may manifest every bit a comorbidity in addition to a dysfunctional sexual experience, fifty-fifty if no exclusive connexion can be made with the physiologic effects of a therapeutic agent or medical conditions (9). Recently, the International Consultation on Sexual Medicine (10) recommended the need to redefine HSDD because of the diverse heterogeneity amidst women and their sexual responses. Equally such, co-ordinate to Sand and Fisher (eleven), a new definition for HSDD is set to be taken into consideration in the upcoming DSM-5.
Today, the aetiology of HSDD has not been holistically agreed upon, although scholars and researchers agree that the status is multifactorial (12). To elaborate, HSDD has been elucidated to be triggered by factors such as psychiatric issues (12), behavioural components (13), and neuroendocrine changes (fourteen,15). Previous studies largely centred on agreement how biologic and behavioural aspects contribute to HSDD, with a primary focus on assessment tools; the apply of hormonal assays and validated behavioural questionnaires (12). Irrespective of their use, nonetheless, these methods have non completely helped in resolving the puzzle and yielding satisfactory elaboration for the development and cause of FSD weather condition, and specifically HSDD.
The next section discusses how ageing factors, such as menopause, are associated with HSDD. 2d, the correlation between hormonal profile and HSDD will be detailed, taking into account medical factors that tin consequence in a hormonal imbalance. Third, the psychological and psychosocial factors and their effect on HSDD are also outlined. Fourth, the current handling plans for HSDD are discussed before offer concluding remarks on the current review issue.
AGEING FACTORS, MENOPAUSE, AND HSDD
Despite the current consensus in the literature that FSD can manifest at whatsoever age in a adult female's life, researchers such equally Sarrel (16) documented that during menopause, up to twoscore% of women experience reduced sexual libido. Moreover, this merits has been supported past a survey (17) undertaken on 31,581 women aged 18 years and above in the Us of America. The report found that the higher prevalence of HSDD was in women above the age of 45 years, and distress was reported to exist a major business among younger women (12.3%) compared with older women (7.4%) aged ≥65 years.
Although sexuality is essential to both young and older women, lack of a satisfying sexual life negatively impacts on the overall quality of life (18). The trend is particularly reflected among female groups that experience an unexpected rapid reject in hormone levels every bit a effect of chemical menopause or fifty-fifty post-surgical events. Figure i shows hormone production as a function of age, both before and after menopause (19). As evident, between the age of 20 and forty years, there is an increment in the product of sex hormones, before a gradual decline is experienced during menopause and post-menopause years of 45 years and in a higher place.
On the contrary, other scholars argue that based on longitudinal findings, human relationship problems and other non-biologic factors tin strongly bear upon on the overall sexual experience of women other than menopausal changes alone (20). For example, research from the Massachusetts Women's Health Survey reported that the onset of menopause contributes to reduced sexual want. Nonetheless, anxiety, low, and other human relationship changes including conflict in the family unit, the condition of the relationship, sexual part, and wellness of a partner can contribute to substantial FSD (21). The common assumption is that menopause contributes to reduced sexual desire as a result of depression production of hormones from the ovaries, resulting in loss of oestrogen and reduction in testosterone. The next subsections elaborate on the relationship between low testosterone and oestrogen levels on HSDD.
LOW TESTOSTERONE AND HSDD
Scholars take reported that low product of testosterone plays a central part in HSDD. One of the primal reasons in support of this claim is that testosterone initiates sexual activities and proliferates sexual desire and behaviour. In improver, testosterone is essential in modulating clitoral and vaginal physiology to facilitate genital lubrication, sensation, and engorgement (22). Therefore, a lack of testosterone has been reported to contribute to low libido and to reduced sexual pleasure and receptivity (23). Also, depression levels of testosterone have been correlated with lack of sexual motivation, fatigue, distress, and overall reduce the sense of well-being (24). Effigy two shows that there is a pregnant pass up in the production of testosterone 4 years before menopause, during menopause, and 2 years into menopause.
It is not unusual for women in their pre-menopausal years with functional ovulatory cycles to study HSDD. One of the main causes of such reduced sexual expression can be attributed to low levels of testosterone, which first to reduce in the mid-30s amongst women and continue to reduce at a abiding rate of about 50% of their highest levels by the time they reach menopause. A contempo study on women's sexuality and wellness found that young women who had undergone surgical procedures reported high levels of HSDD resulting from the effects of bilateral oophorectomy where both ovaries are removed. Such procedures take been noted to contribute to about 50% reduction in the levels of testosterone (25). Hence, at that place seems to be a close relationship betwixt the product of testosterone and reduced sexual want, with more effects felt among older women in their postal service-menopause years and women who have undergone oophorectomy compared with younger ladies and those in their premenopausal years (26).
Figure 3 further shows that with increasing age, the levels of testosterone reduce and by the fourth dimension a woman reaches menopause, the levels of testosterone are almost a quarter of what they were in their early 20s. Co-ordinate to Simon et al. (26), such a severe reduction in testosterone levels makes women gain weight, experience depressed and tired, and completely blocks virtually of their sex activity bulldoze.
Low OESTROGEN LEVELS AND HSDD
Besides depression testosterone levels, low sex drive among women can also be affected past reduced levels of oestrogen during postmenopausal years. Low levels of oestrogen results in vulvovaginal dryness and cloudburst in add-on to initiating changes of genital function through reduced sensory perception and decreased clitoral claret period (27). As such, it becomes apparent that lack of oestrogen is associated with vaginal discomfort due to dryness and genital insensitivity, making it difficult for an individual to actively respond to sexual expression and cues, considering a reduced impact on desire (28). Researchers have recommended the use of oestrogen therapies to treat dyspareunia and vaginal dryness resulting from vulvovaginal atrophy (28). However, oestrogen-based therapies accept been questioned equally to whether they contribute to the effect after precise apply in managing depression sexual desire, in the event that low sexual events results from issues such as loss of genital pleasure, sensation, or as a outcome of pain (29). Figure 4 shows the variation in oestrogen product during years of fertility, perimenopause, menopause, and post-menopause.
Every bit evident from Figure iv, in that location is a loftier variation in oestrogen production during menopause, and these fluctuations levels contribute to decreased sex libido amidst women. Besides, both peri- and mail service-menopausal individuals can feel HSDD due to low levels or deficiency in oestrogen hormone production (30,31). Laumann et al. (32) argued that menopause results when the levels of circulating oestrogen reduce, and this reduction leads to vaginal dryness, painful intercourse (dyspareunia), and inability to lubricate. In this case, oral oestrogen therapy is often recommended as a replacement to relieve mood changes, hot flashes, and alleviate irregular sleep patterns and improve the quality of life among women (33,34,35).
All the same, a study past Laumann et al. (36) on sexual dysfunction amidst American women reported that even if oestrogen replacement could help in treating the symptoms linked to menopause, it would potentially have negative impacts on the levels of testosterone and further lead to HSDD. One of the reasons for this is that oral oestrogen can increment the levels of circulating sexual practice hormone-binding globulin (SHBG) among menopausal women (37,38,39). O elaborate, SHBG has been reported as a poly peptide that can bind testosterone and as a outcome, lead to lowering of free testosterone levels in the blood (forty). Therefore, if the levels of SHBG are high, the level of free testosterone in plasma will be lower. In improver, Simon et al. (26) reported that oral oestrogen reduced both luteinizing hormone (LH) and follicle-stimulating hormone, thereby lowering total testosterone levels and reducing ovarian synthesis (26,31). Warnock et al. (xiv) likewise noted that birth control pills could lower the levels of testosterone as a result of the exogenous oestrogen plant in birth command pills, which can further reduce LH and hinder ovulation (41,42). As such, the ovarian release of oestrogen is suppressed, and as a result, sexual libido is besides affected. However, the levels of SHBG can exist reduced using testosterone replacement therapy, which works by raising the levels of free testosterone and potentially decreasing potential signs and symptoms of HSDD (43,44). The adjacent department elaborates on how hormonal influence affects FSD and contributes to HSDD in women.
HORMONAL INFLUENCE AND ANDROGEN DEFICIENCY
In women, androgens are C19 steroids generated from cholesterol, where the main sources of release are from the adrenal glands, peripheral tissues, and the ovaries. Effigy v shows steroidogenesis of androgens in women. Androgens are released from peripheral tissues such every bit cutaneous, muscle, and adipose tissues. Figure 1 shows that testosterone (T) represents the final production in the androgen pathway and it results from the conversion of androstenedione (A) nowadays in plasma. One-half of the androgens come from the ovaries, 25% of the androgens are produced in the adrenal glands, and the other 25% comes from the conversion of androstenedione in peripheral tissues. In addition, the principal precursor of both androstenedione and testosterone androgens is dehydroepiandrosterone (DHEA), half of which is produced in the adrenal glands and 20% is generated from the ovaries; 30% is derived from dehydroepiandrosterone sulphate (DHEAS) that circulates in the blood. During mail-menopause, DHEA, which is the main source of androgens, experiences an up to threescore% decline resulting in hypoandrogenism, which can affect the normal sexual response in women (45).
As noted from the ageing factors associated with FSD, women can experience the effcets before and after menopause every bit a result of androgen hormone deficiency (46). Long earlier menopause, and specifically from the 2nd half of the pre-menopausal years when a woman is aged between 30 and 50 years, the development of androgen hormones reduces from the ideal rate observed during puberty and up to the late 20s or early 30s (47,48). All the same, from the mid-30s, the normal activities of the ovaries reduce, and the process of ovulation becomes irregular.
As shown in Effigy 6, in irregular ovulation cycles, there is less progesterone release, and in cycles where at that place is no ovulation, there is no release of progesterone (49). As such, as the levels of progesterone beginning to fall, the menstrual bicycle becomes shorter and the lack of progesterone results in a hormonal imbalance where there is oestrogen authority. The oestrogen dominance is shown in Figure 3, in relation to progesterone levels that are lower than normal among pre-menopausal women (49). Some of the symptoms linked to increased production of oestrogen at this age include depressive mood and anxiety. As an private transitions into menopause (perimenopausal age), the irregular release of androgen hormones go longer, and women may have reduced sexual desire for prolonged months because they receive irregular menstrual cycles (50,51,52). At the age of fifty years, most women experience a meaning reduction in the amounts of androgen, while the values for testosterone and oestrogen reach their minimum levels (53,54,55).
The process is characterised by the loss of androgen hormones with the situation reported to be worse in persons with hypopituitarism, bilateral oophorectomy, and Addison's disease. Withal, the natural development of menopause can also result in reduced production of androgens (56,57). In near cases, androgen deficiency is difficult to place, and about women correlate their reduced sexual desires with lifestyle issues or psychological distress as opposed to biologic changes in their bodies (58). Some of the experiences can outcome in an inexplicable lack of energy, tiredness, low self-motivation, disturbed sleep, a complete lack of sexual desire, and low self-esteem or poor general well-beingness (59,lx). Low levels of androgens in women and reduced sexual want can be diagnosed by examining levels of SHBG and testosterone because initial findings reported from women that have undergone surgery are equally elaborated below.
OOPHORECTOMY, HYSTERECTOMY, AND HSDD
Fifty-fifty if the changes in hormone contour amongst young women who have undergone hysterectomy and oophorectomy might non entirely affect sexual expression, the increased prevalence of HSDD in young women compared with pre- and post-menopausal women is a strong indicator for the bear upon of hormonal levels on sexual desire (61,62,63). The historic period-associated reduction in androgen hormones parallels the age-linked increase in HSDD among women, mainly in those who take reached natural levels of menopause with depression sexual desire compared with pre-menopause women, further indicating the central role that hormones play in HSDD (64,65). As discussed before, low levels of oestrogen are largely associated with dyspareunia and vulvovaginal mucosa changes, a move that can contribute to reduced sexual want among affected women (46,47).
In past studies, women who take undergone oophorectomy have shown to take associated low levels of sexual want and increased distress or poor overall well-being. One study found lower levels of androgen hormones in good for you pre-menopausal women who reported having low sexual desire compared with women without a like trouble (66). The marked decline in depression levels of testosterone later on surgery has been linked to low sexual want (67,68), because most studies have focused on rubber, efficacy, and testosterone-route therapy to treat reduced sexual desire. Women who undergo bilateral oophorectomy experience a decline in testosterone between 40% and 50% from pre-surgical levels, and reduced libido between thirty% and l% (69,70). In addition to surgical procedures, a number of medical factors can also affect hormonal levels in women and contribute towards HSDD as discussed in the next section.
MEDICAL FACTORS LINKED TO HSDD
A number of studies have also found a positive human relationship between hypersexuality and medical factors. Some researchers reported that some treatments and medical atmospheric condition could negatively affect sexual desire among women. Tabular array ane summarises some diseases that have possible negative impacts on sexual libido. Medical interventions and diseases can change the physiology of sexual response both peripherally and centrally (71,72). Moreover, the presence of sexual disorders, including loss of sensitivity and pain, can trigger negative responses that can make such women lose interest in sexual expression (73).
Table 1
Likewise the chronic conditions that contribute to HSDD, Table two lists some common medicines reported to cause reduced sexual urge among women. For example, drugs that give healing benefits for diseases may negatively touch on on sexual response amid women (77). In almost gynaecologic atmospheric condition, oral contraceptives are often used together in pregnancy prevention. For years, the combination and blazon of progestin and oestrogen have closely been reported in dealing with beneficial gynaecologic diseases and pregnancy prevention (78,79). Withal, nevertheless the existing literature findings, the impact that these drugs have on women's sexual changes however remain controversial (80).
Table ii
Furthermore, there is increased connection between the oral contraceptive prescription in some women with vulvar vestibular pain. In patients with depression, serotonin-norepinephrine reuptake inhibitors (SNRI) and selective serotonin reuptake inhibitors (SSRI) medications are ordinarily prescribed antidepressants, although they usually result in agin events, including arousal difficulties, absent orgasm, delayed orgasm, and decreased want. However, there continue to be few issue studies evaluating the most effective agents in the direction of FSD (80). The adjacent section discusses some treatment approaches in the management of hormone-induced HSDD among women.
TESTOSTERONE TREATMENT AND Want
Poor awareness of FSD and the complex bug linked to HSDD evolution have largely reduced the formulation and research of therapeutic interventions for persons with depression sexual desire (81). Several studies have been undertaken to assess the impact that sex hormones (androgens) have in HSDD management amongst afflicted women in menopause (82,83). Nevertheless, a proper agreement of the pathophysiology and physiology has triggered positive research progress in both pre- and post-menopausal female populations. The research process has also been encouraged by the demand to have appropriate exclusion and inclusion criteria for FSD in clinical inquiry using meliorate belittling tools to examine main outcome measures suitable in medication interventions (84,85,86).
In nearly cases, hormone therapy (using oestrogen alone) equally indicated in oestrogen-progestin therapy (OPT) is widely used among menopausal women that have an intact uterus. Thus, the utilize of EPT is express to women who report early symptoms (mainly hot flashes) as the first line of defense throughout the menopausal transition phase (lxxx). Local and systemic employ of oestrogen lonely (OT) or with EPT has been reported every bit being an effective intervention in suppressing symptoms of vulvovaginal atrophy. The intervention has been reported to better the sexual life of affected populations as a effect of better lubrication (82,86). However, despite the reduction in dyspareunia, some women with FSD accept been reported to be unresponsive because the OPT/OT does not have a consistent effect on the increase in sexual activity or desire, mainly amongst women grouped under surgical menopause (87,88).
Greenblatt et al. (89) conducted a randomised clinical trial and found that low sexual desire responded highly effectively to androgen therapies (AT). The authors also pointed out that low sexual desire responded even better to a combination of OT/AT, equally opposed to using OT solitary in ovariectomised women. Since this research, several studies have likewise demonstrated that androgens take an important role to play in terms of improving arousal and suppressing the negative impacts of FSD among women who have attained menopause. However, about studies have been based on supra-physiologic doses of hormone administration with testosterone (ninety).
Some Cochrane reviews have recently explored the risks and benefits of therapy, in addition to OPT+ OPT alone for both pre-menopausal and mail service-menopausal women where researchers included 35 studies with near 4800 participants. Virtually of the trials, which had several therapy regimens (including subcutaneous implants, intramuscular injections, gels or transdermal patches, and oral tablets), recruited but post-menopausal women–both surgically and naturally menopausal–with low sexual desires. The medium intervention period was vi months and ranged from one and half months to 24 months. A pooled approximation from the examined clinical trials indicated that by calculation therapy to hormone therapy, the women'south sexual response improved and led to improved satisfaction in sexual incidents among post-menopausal women. These beneficial effects were reported and measured for coital frequency, desire, responsiveness, and sexual practice (91,92).
Withal, some adverse effects were also reported, including increased cases of acne and excess hair growth and reduced levels of high-density lipoprotein. When this intervention was discontinued, the effect was similar for both groups. Amidst the perimenopausal women, however, there was insufficient evidence nearly the efficacy of this treatment or for additional outcomes that were explored, including body composition, cognition, menopausal symptoms, fatigue, and well-being. Another study examined the effect of transdermal T patch in postal service-menopausal women with HSDD. The randomised, double-blind, and placebo-controlled inquiry was evaluated over a 24-week period with over 1200 participants who were surgically menopausal with HSDD and received affiliated oestrogen therapy (93,94,95).
The baseline research reported that women had three episodes of increased sexual desire during the first 4 weeks when the 300 μg T patch was used compared with a single satisfying event among the placebo grouping. Withal, a 450 μg T patch had no benefits compared with a non-intervention placebo group, indicating the absence of dose-response from additional T patch intervention (94). Besides increased sexual activity, there were besides improvements in domains of sexual functions amongst women who received T patches and those from the placebo group including pleasure, orgasm, distress, sexual self-image, responsiveness, concerns, and desire. As a result, there was an increment in sexual episodes with the utilize of the therapy compared with placebo (95). As such, the use of hormone therapy shows pregnant improvement of sexual response and suppression of HSDD among women with the status.
In conclusion FSD, grouped either as HSDD, has been shown to be a highly prevalent sexual condition, which has negative outcomes on the women's well-beingness and sexual life. Despite this, HSDD remains a common underdiagnosed status by physicians, and it also has few treatment regimens. Nevertheless, a number of factors accept recently converged to create a suitable shift toward greater awareness and attending. For case, increased focus on hypoactive sexuality as a topic in menopause research has increased interest in the field of female person fertility and further changed the previous focus on the topic. The shift has also resulted from a change in societal perception virtually women'due south privilege to a healthy sexual lifestyle, fifty-fifty if most post-menopausal women yet possess the perception that sexuality is a taboo subject.
Today, the increased search for constructive pharmacologic agents to manage various biologic causes of HSDD is a principal indicator of the strong forces that are currently initiating more than attending on the topic among physicians and researchers. Most studies have now weighed in past including FSD as a illness area that deserves unique and separate research focus. In add-on, a number of pharmacologic agents have been designed to target HSDD and are in various stages of clinical trials. However, the field withal continues to face some hurdles including a lack of data, defoliation over medications and management, and the discomfort associated with addressing the field of study of sexuality. Therefore, the value of the electric current review will be enhanced by addressing the current barriers to the topic and committing more than resource to agreement the role that hormones play in HSDD.
Footnotes
Ethics Committee Approval: Department of Obstetrics and Gynaecology; University of Saarland; 66421 Homburg/Saar, Frg.
Peer-review: Externally peer-reviewed.
Contributed by
Author Contributions: Concept - A.A., H.A., M.Eastward.H.; Design - A.A., H.A., M.Due east.H.; Supervision - A.A., H.A., M.Due east.H.; Materials - A.A., H.A., M.E.H.; Writer - A.A., H.A., Yard.East.H.
Disharmonize of Involvement: No conflict of interest was declared by the authors.
Financial Disclosure: The authors declared that this study has received no fiscal support.
References
one. Aslan E, Fynes Yard. Female sexual dysfunction. Int Urogynecol J Pelvic Floor Dysfunct. 2008;19:293–305. [PubMed] [Google Scholar]
ii. Laumann EO, Paik A, Rosen RC. Sexual dysfunction in the United States: prevalence and predictors. JAMA. 1999;281:537–44. [PubMed] [Google Scholar]
3. Basson R, Wierman ME, van Lankveld J, Brotto L. Summary of the recommendations of sexual dysfunction in women. J Sex Med. 2010;7:314–26. [PubMed] [Google Scholar]
4. Bitzer J, Brandenburg U. Psychotherapeutic interventions for female person sexual dysfunction. Maturitas. 2009;63:160–iii. [PubMed] [Google Scholar]
5. Hayes RD, Dennerstein L, Bennett CM, Fairley CK. What is the "true" prevalence of female sexual dysfunctions and does the way we assess these weather condition have an impact? J Sex Med. 2008;5:777–87. [PubMed] [Google Scholar]
half-dozen. American Psychiatric Association. Diagnostic criteria from DSM-IV-TR. Washington, DC. American Psychiatric Association. 2000 [Google Scholar]
7. Basson R, Berman J, Burnett A, Derogatis L, Ferguson D, Fourcroy J, et al. Report on the International Consensus Development Conference on female sexual dysfunction: definition and nomenclature. J Urol. 2000;163:888–93. [PubMed] [Google Scholar]
8. Basson R, Leiblum S, Brotto 50, Derogatis L, Fourcroy J, Fugl-Meyer Grand, et al. Revised definitions of women's sexual dysfunction. J Sex Med. 2004;1:40–viii. [PubMed] [Google Scholar]
9. Basson R, Wierman ME, van Lankveld J, Brotto L. Summary of the recommendations on sexual dysfunctions in women. J Sex Med. 2010;7:314–26. [PubMed] [Google Scholar]
10. Brotto L, Bitzer J, Laan E, Leiblum Southward, Luria Grand. Women's sexual desire and arousal disorder. J Sex Med. 2010;vii:586–614. [PubMed] [Google Scholar]
11. Sand M, Fisher WA. Women'south endorsement of models of female sexual response: the nurses' sexuality written report. J Sex Med. 2007;4:708–xix. [PubMed] [Google Scholar]
12. Simon JA. Depression sexual want is it all in her head? Pathophysiology, diagnosis, and treatment of hypoactive sexual want disorder. Postgrad Med. 2010;122:128–36. [PubMed] [Google Scholar]
thirteen. Leiblum SR, Koochaki PE, Rodenberg CA, Barton IP, Rosen RC. Hypoactive sexual desire disorder in postmenopausal women: The states. results from the women'southward international report of health and sexuality (WISHeS) Menopause. 2006;13:46–56. [PubMed] [Google Scholar]
14. 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. [PubMed] [Google Scholar]
xv. Abdallah RT, Simon JA. Testosterone therapy in women: its role in the management of hypoactive sexual want disorder. Int J Impot Res. 2007;xix:458–63. [PubMed] [Google Scholar]
16. Sarrel PM. Sexuality and menopause. Obstet Gynecol. 1990;75(4 Suppl):26–30. [PubMed] [Google Scholar]
17. Shifren JL, Monz BU, Russo PA, Segreti A, Johannes B. Sexual problems and distress in The states women: prevalence and correlates. Obstet Gynecol. 2008;112:970–eight. [PubMed] [Google Scholar]
18. Bradford A, Meston CM. Senior sexual health: the effects of aging on sexuality. In: VandeCreek 50, Peterson FL, Bley JW, editors. Innovation in Clinical Practice: Focus on Sexual Health. Sarasota, FL. Professional Resource Press. 2007:34–45. [Google Scholar]
19. Dennerstein Fifty, Dudley E, Burger H. Are changes in sexual functioning during midlife due to aging or menopause? Fertil Steril. 2001;76:456–60. [PubMed] [Google Scholar]
20. Hayes R, Dennerstein L. The affect of crumbling on sexual office and sexual office and dysfunction in women: a review of population based studies. J Sex Med. 2005;ii:317–30. [PubMed] [Google Scholar]
21. Avis NE, Stellato R, Crawford S, Joannes C, Longcope C. Is there an clan between menopause status and sexual functioning? . Menopause. 2000;7:297–309. [PubMed] [Google Scholar]
22. Nappi RE, Detaddei S, Ferdeghini F, Brundu B, Sommacal A, Polatti F. Role of testosterone in feminine sexuality. J Endocrinol Invest. 2003;26(3 Suppl):97–101. [PubMed] [Google Scholar]
23. Davis SR, Tran J. Testosterone influences libido and well-being in women. Trends Endocrinol Metab. 2001;12:33–seven. [PubMed] [Google Scholar]
24. Simon JA. Estrogen replacement therapy: Effects on the endogenous androgen milieu. Fertil Steril. 2002;77(Suppl 4):77–82. [PubMed] [Google Scholar]
25. Leiblum SR, Koochaki PE, Rodenberg CA, Barton IP, Rosen RC. Hypoactive sexual desires disorder in postmenopausal women: US results from the Women's International Written report of Health and Sexuality (WISHeS) Menopause. 2016;thirteen:46–56. [PubMed] [Google Scholar]
26. Simon J, Klaiber East, Wiita B, Bowen A, Yang HM. Differential effects of estrogen-androgen and estrogen-only therapy on vasomotor symptoms, gonadotropin secretion, and endogenous androgen bioavailability in postmenopausal women. Menopause. 1999;6:138–46. [PubMed] [Google Scholar]
27. Suckling J, Lethaby A, Kennedy R. Local oestrogen for vaginal cloudburst in postmenopausal women. Cochrane Database Syst Rev. 2003;CD001500 [PubMed] [Google Scholar]
28. Avis NE, Stellato R, Crawford South, Joannes C, Longcope C. Is at that place an association betwixt menopause status and sexual functioning? Menopause. 2000;seven:297–309. [PubMed] [Google Scholar]
29. Gracia CR, Sammel MD, Freeman EW, Liu 50, Hollander L, Nelson DB. Predictors of decreased libido in women during the late reproductive years. Menopause. 2004;11:144–50. [PubMed] [Google Scholar]
30. Suckling J, Lethaby A, Kennedy R. Local oestrogen for vaginal atrophy in postmenopausal women. Cochrane Database Syst Rev. 2003;CD001500 [PubMed] [Google Scholar]
31. Casson PR, Elkind-Hirsch KE, Buster JE, Hornsby PJ, Carson SA, Snabes MC. Issue of postmenopausal estrogen replacement on circulating androgens. Obstetr Gynecol. 1997;90:995–8. [PubMed] [Google Scholar]
32. Laumann EO, Nicolosi A, Glasser DB, Paik A, Gingell C, Moreira E, et al. Sexual issues among women and men aged 40-lxxx y: Prevalence and correlates identified in the global study of sexual attitudes and behaviors. Int J Impot Res. 2005;17:39–57. [PubMed] [Google Scholar]
33. Kingsberg SA. The impact of aging on sexual role in women and their partners. Arch Sex activity Behav. 2002;31:431–7. [PubMed] [Google Scholar]
34. Kennedy SH, Dickens SE, Eisfeld BS, Bagby RM. Sexual dysfunction before antidepressant therapy in major depression. J Touch Disord. 1999;56:2001–8. [PubMed] [Google Scholar]
35. Casper RC, Redmond DE Jr, Katz MM, Schaffer CB, Davis JM, Koslow SH. Somatic symptoms in primary affective disorder. Presence and relationship to the classification of depression. Curvation Gen Psychiatry. 1985;42:1098–104. [PubMed] [Google Scholar]
36. Laumann EO, Paik A, Rosen RC. Sexual dysfunction in the United States: prevalence and predictors. JAMA. 1999;281:537–44. [PubMed] [Google Scholar]
37. Nappi RE, Wawra M, Schmitt Due south. Hypoactive sexual desire disorder in postmenopausal women. Gynecol Endocrinol. 2006;22:318–23. [PubMed] [Google Scholar]
38. Warnock JJ. Female hyperactive sexual desire disorder: Epidemiology, diagnosis, and handling. CNS Drugs. 2002;16:745–53. [PubMed] [Google Scholar]
39. Hawton K, Gath D, Twenty-four hour period A. Sexual function in a customs sample of eye-aged women with partners: furnishings of age, marital, socioeconomic, psychiatric, gynecological, and menopausal factors. Arch Sex Behav. 1994;23:375–95. [PubMed] [Google Scholar]
40. Bonierbale M, Lancon C, Tignol J. The ELIXIR study: evaluation of sexual dysfunction in 4557 depressed patients in France. Curr Med Res Opin. 2003;19:1114–24. [PubMed] [Google Scholar]
41. van Lankfeld JJ, Grotjohann Y. Psychiatric comorbidity in heterosexual couples with sexual dysfunction assessed with the composite international diagnostic interview. Arch Sex Behav. 2000;29:479–98. [PubMed] [Google Scholar]
42. Freidman S, Harrison Yard. Sexual histories, attitudes, and behavior of schizophrenic and ''normal'' women. Curvation Sexual activity Behav. 1984;13:555–67. [PubMed] [Google Scholar]
43. Kodesh A, Weizman A, Aizenberg D, Hermesh H, Gelkopf G, Zemishlany Z. Selegiline in the treatment of sexual dysfunction in schizophrenic patients maintained on neuroleptics: a pilot study. Clin Neuropharmacol. 2003;26:193–five. [PubMed] [Google Scholar]
44. Rees PM, Foeler CJ, Maas CP. Sexual dysfunction in men and women with neurological disorders. Lancet. 2007;369:512–25. [PubMed] [Google Scholar]
45. Fonseca HP, Scapinelli A, Aoki T, Aldrighi JM. Androgen deficiency in women. Rev Assoc Méd Bras. 2010;56:579–82. [PubMed] [Google Scholar]
46. Park K, Jeong GW. The role of functional MRI in neural assessment of female person sexual dysfunction. Curr Sex Wellness Rep. 2007;four:33–40. [Google Scholar]
47. Woodard TL, Diamond MP. Contribution of imaging to our understanding of sexual function and dysfunction. Adv Psychosom Med. 2008;29:150–68. [PubMed] [Google Scholar]
48. Arnow BA, Millheiser Fifty, Garrett A, Lake Polan G, Glover GH, Colina KR, et al. Women with hypoactive sexual want disorder compared to normal females: a functional magnetic resonance imaging written report. Neuroscience. 2009;158:484–502. [PubMed] [Google Scholar]
49. Quirk FH, Heiman JR, Rosen RC, Laan East, Smith MD, Boolell M. Development of a sexual role questionnaire for clinical trials of female sexual dysfunction. J Womens Health Gend Based Med. 2002;eleven:277–89. [PubMed] [Google Scholar]
50. Eickhoff SB, Laird AR, Grefkes C, Wang LE, Zilles 1000, Pull a fast one on PT. Coordinate-based activation likelihood interpretation meta-analysis of neuroimaging information: a random-effects approach based on empirical estimates of spatial uncertainty. Hum Brain Mapp. 2009;xxx:2907–26. [PMC free article] [PubMed] [Google Scholar]
51. Karama Due south, Lecours AR, Leroux JM, Bourgouin P, Beaudoin G, Joubert South, et al. Areas of brain activation in males and females during viewing of erotic moving picture excerpts. Hum Encephalon Mapp. 2002;sixteen:i–thirteen. [PMC costless article] [PubMed] [Google Scholar]
52. Woodard TL, Collins K, Perez K, Balon R, Tancer ME, Kruger G, et al. What kind of erotic picture clips should nosotros utilise in female sexual activity research? An exploratory written report. J Sexual activity Med. 2008;5:146–54. [PubMed] [Google Scholar]
53. Derogatis LR, Rosen R, Leiblum S, Burnett A, Heiman J. The Female person Sexual Distress Scale (FSDS): initial validation of a standardized scale for cess of sexually related personal distress in women. J Sexual practice Marital Ther. 2002;28:317–30. [PubMed] [Google Scholar]
54. Gizewski ER, Krause East, Karama Due south, Baars A, Senf W, Forsting M. In that location are differences in cerebral activation between females in distinct menstrual phases during viewing of erotic stimuli: A fMRI report. Exp Encephalon Res. 2006;174:101–8. [PubMed] [Google Scholar]
55. Castelli F, Happe F, Frith U, Frith C. Move and heed: a functional imaging report of perception and interpretation of circuitous intentional movement patterns. Neuroimage. 2000;12:314–25. [PubMed] [Google Scholar]
56. Jeong GW, Park K, Youn G, Kang HK, Kim HJ, Seo JJ, et al. Assessment of cerebrocortical regions associated with sexual arousal in premenopausal and menopausal women past using BOLD-based functional MRI. J Sex Med. 2005;2:645–51. [PubMed] [Google Scholar]
57. Kodesh A, Weizman A, Aizenberg D, Hermesh H, Gelkopf M, Zemishlany Z. Selegiline in the treatment of sexual dysfunction in schizophrenic patient maintained on neuroleptics: a pilot study. Clin Neuropharmacol. 2003;26:193–5. [PubMed] [Google Scholar]
58. Rees PM, Foeler CJ, Maas CP. Sexual function in men and women with neurological disorders. Lancet. 2007;369:512–25. [PubMed] [Google Scholar]
59. Zvadinov R, Zorzon M, Locatelli L, Stival B, Monti F, Nasuelli D, et al. Sexual dysfunction in multiple sclerosis: a MRI neurophysiological and urodynamic study. J Neurol Sci. 2003;210:73–6. [PubMed] [Google Scholar]
threescore. Knegtering H, Boks M, Blijd C, Castelein S, van den Bosch RJ, Wiersman D. A randomized open characterization comparison of the impact of olanzapine versus risperidone on sexual functioning. J Sex Marital Ther. 2006;32:315–26. [PubMed] [Google Scholar]
61. Bhasin S, Enzlin P, Coviello A, Basson R. Sexual dysfunction in men and women with endocrine disorders. Lancet. 2007;369:597–611. [PubMed] [Google Scholar]
62. Kadioglu P, Yalin Every bit, Tiryakiodlu O, Gazioglu North, Oral G, Sanli O, et al. Sexual dysfunction in women with hyperprolactinemia: a pilot study study. J Urol. 2005;174:1921–5. [PubMed] [Google Scholar]
63. Arlt W, Callies F, Van Vlijmen JC, et al. Dehydroepiandrosterone replacement in women with adrenal insufficiency. N Engl J Med. 1999;341:1013–20. [PubMed] [Google Scholar]
64. Aslan G, Köseoğlu H, Sadik O, Gimen S, Cihan A, Esen A. Sexual function in women with urinary incontinence. Int J Impot Res. 2005;17:248–51. [PubMed] [Google Scholar]
65. Fogari R, Preti P, Derosa G, Marasi G, Zoppi A, Rinaldi A, et al. Effective antihypertensive treatment with valsartan or atenolol on sex and plasma testosterone and hypertensive men. Eur J Clin Pharmacol. 2002;8:177–lxxx. [PubMed] [Google Scholar]
66. Burrows LJ, Basha One thousand, Goldstein AT. The effects of hormonal contraceptives on female sexuality: a review. J Sex Med. 2012;9:2213–23. [PubMed] [Google Scholar]
67. Pastor Z, Holla K, Chmel R. The influence of combined oral contraceptives on female sexual desire: a systematic review. Eur J Contracept Reprod Wellness Care. 2013;18:27–43. [PubMed] [Google Scholar]
68. Schaffir J. Hormonal contraception and sexual want: a critical review. J Sexual activity Marital Ther. 2006;32:305–xiv. [PubMed] [Google Scholar]
69. Pauls RN, Kleeman SD, Karram MM. Female sexual dysfunction: principles of diagnosis and therapy. Obstet Gynecol Surv. 2005;60:196–205. [PubMed] [Google Scholar]
70. Alexander GM, Sherwin BB, Bancroft J, Davidson DW. Testosterone and sexual behavior in oral contraceptive users and not-users: a prospective study. Horm Behav. 1990;24:388–402. [PubMed] [Google Scholar]
71. Bancroft J, Sartorious N. The furnishings of oral contraceptives on well-being and sexuality. Oxf Rev Reprod Biol. 1990;12:57–92. [PubMed] [Google Scholar]
72. Bancfroft J, Sherwin BB, Alexander GM, Davidson DW, Walker A, et al. Oral contraceptives, androgens and the sexuality of young women, II. the part of androgens. Arch Sex Behav. 1991;20:121–35. [PubMed] [Google Scholar]
73. Panzer C, Wise S, Fantini One thousand, Kang D, Munarriz R, Guay A, et al. Impact of oral contraceptives on sex activity hormone-binding globulin and androgen levels: a retrospective report in women with sexual dysfunction. J Sex Med. 2006;3:104–13. [PubMed] [Google Scholar]
74. Caruso S, Agnello C, Intelisano G, Farina M, Di Mari 50, Cianci A. Sexual behavior of women taking depression-dose contraceptive containing xv microg ethinylestradiol/lx microg gestodene. Contraception. 2004;69:237–40. [PubMed] [Google Scholar]
75. Bitzer J, Tschudin S, Meier-Burgoa J, Armbruster U, Schwendke A. Effects on the quality of life of a new oral contraceptive containing thirty mcg EE and 3 mg drospirenone (Yasmin) Praxis (Bern 1994) 2003;92:1177–84. [PubMed] [Google Scholar]
76. Sanders SA, Graham CA, Bass JL, Bancroft J. A prospective study of the effects of oral contraceptives on sexuality and well-being and their human relationship to discontinuation. Contraception. 2001;64:51–8. [PubMed] [Google Scholar]
77. Davis AR, Castano PM. Oral contraceptives and libido in women. Annu Rev Sex Res. 2004;15:297–320. [PubMed] [Google Scholar]
78. Wallweiner CW, Wallweiner LM, Seeger H, Mück AO, Mück J, Wallweiner Yard. Prevalence of sexual dysfunction and bear upon of contraception in female person German medical students. J Sex Med. 2010;7:2139–48. [PubMed] [Google Scholar]
79. Bazin S, Bouchard C, Brisson J, Morin C, Meisels A, Fortier M. Vulvar vestibulitis syndrome: an exploratory instance-control report. Obstet Gynecol. 1994;83:47–50. [PubMed] [Google Scholar]
eighty. Greenstein A, Ben-Aroya Z, Fass O, Militscher I, Roslik Y, Chen J, et al. Vulvar vestibulitis syndrome and estrogen dose of oral contraceptive pills. J Sex activity Med. 2007;4:1679–83. [PubMed] [Google Scholar]
81. Davis SR, Davison SL, Donath Due south, Bell RJ. Circulating androgen levels in cocky-reported sexual function in women. JAMA. 2005;294:91–6. [PubMed] [Google Scholar]
82. Nappi RE, Polatti F. The use of estrogen therapy in women's sexual functioning (CME) J Sexual practice Med. 2009;six:603–16. [PubMed] [Google Scholar]
83. Panzer C, Guay A. Testosterone replacement therapy in naturally and surgically menopausal women. J Sex Med. 2009;68:8–eighteen. [PubMed] [Google Scholar]
84. Althof SE, Dean J, Derogatis LR, Rosen RC, Sisson M. Current perspectives on the clinical assessment and diagnosis of female person sexual dysfunction and clinical studies of potential therapies: a statement of concern. J Sex Med. 2005;ii(Suppl 3):146–53. [PubMed] [Google Scholar]
85. Nappi RE. New attitudes to sexuality in the menopause: clinical evaluation and diagnosis. Climacteric. 2007;10 (Suppl 2):105–viii. [PubMed] [Google Scholar]
86. Davis SR, Nijland EA. Pharmacological therapy for female sexual dysfunction: has progress been made? Drugs. 2008;68:259–64. [PubMed] [Google Scholar]
87. Alexander JL, Kotz K, Dennerstein L, Kutner SJ, Wallen K, Notelovitz M. The effects of postmenopausal hormone therapies on female sexual functioning: a review of double-bullheaded, randomized controlled trials. Menopause. 2004;11:749–65. [PubMed] [Google Scholar]
88. Modelska K, Cummings S. Female sexual dysfunction in postmenopausal women: systematic review of placebo-controlled trials. Am J Obstet Gynecol. 2003;188:286–93. [PubMed] [Google Scholar]
89. Greenblatt RB, Barfield Nosotros, Garner JF, Calk GL, Harrod JP Jr. Evaluation of an estrogen, androgen, estrogen-androgen combination, and a placebo in the treatment of the menopause. J Clin Endocrinol Metab. 1950;ten:1547–58. [PubMed] [Google Scholar]
90. Panzer C, Guay A. Testosterone replacement therapy in naturally and surgically menopausal women. J Sex Med. 2009;68:8–18. [PubMed] [Google Scholar]
91. Somboonporn West, Davis S, Seif MW, Bell R. Testosterone for peri-and postmenopausal women. Cochrane Database Syst Rev. 2005;CD004509 [PubMed] [Google Scholar]
92. Somboonporn Westward, Bell RJ. The benefits and risks of testosterone therapy for postmenopausal women taking HT. Cochrane Database Syst Rev. 2010 [Google Scholar]
93. Braunstein GD. Prophylactic of testosterone handling in postmenopausal women. Fertil Steril. 2007;88:one–17. [PubMed] [Google Scholar]
94. Buster JE, Kingsberg SA, Aguirre O, Brown C, Breaux JG, Buch A, et al. Testosterone patch for low sexual desire in surgically menopausal women: a randomized trial. Obstet Gynecol. 2005;105:944–52. [PubMed] [Google Scholar]
95. Simon J, Braunstein Yard, Nachtigall L, Utian W, Katz M, Miller S, et al. Testosterone patch increases sexual activeness and want in surgically menopausal women with hypoactive sexual want disorder. J Clin Endocrinol Metab. 2005;ninety:5226–33. [PubMed] [Google Scholar]
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5776161/
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