Sex hormones only part of the equation in modulating HSDD

Apart from the essential role that sex hormones play in modulating hypoactive sexual desire disorder (HSDD) through therapeutic interventions, a comprehensive understanding of the biologic mechanisms underlying the disorder is imperative, according to a literature review in The Journal of the Turkish-German Gynecological Association.

Conducted by Ahmed AlAwlaqi, MBBS, MSc, and colleagues in the Department of Obstetrics and Gynecology at the University of Saarland in Homburg, Germany, the review underscores the agreement in the literature that HSDD remains a significant challenge, lacking both well-conceived and formulated treatment regimens and concise clinical guidelines.

Safe and effective intervention, encompassing both psycho-relational and biologic aspects of HSDD, is still needed, including precise hormonal or non-hormonal pharmacotherapeutic agents. The authors advocate allocating more resources toward understanding the role that hormones play in HSDD and note the multiple hurdles to be addressed, such as lack of information about HSDD, confusion over medications and management, and discomfort about discussing sexuality.

Female sexual dysfunction (FSD) can occur both before and after menopause because of androgen deficiency. Androgens in women are C19 steroids generated from cholesterol and produced by the ovaries (50% of the time), adrenal glands (25%) and conversion of androstenedione in peripheral tissues (25%). Likewise, the chief precursor of both androstenedione and testosterone is dehydroepiandrosterone (DHEA), which is produced in the adrenal glands (50%), ovaries (20%) or derived from dehydroepiandrosterone sulphate (DHEAS) that circulates in the blood (30%).

The main source of androgens is DHEA, which can be depleted by as much as 60% during postmenopause. That results in hypoandrogenism, which can negatively impact the normal sexual response in women. Moreover, in irregular ovulation cycles, there is less progesterone release, resulting in a hormonal imbalance and oestrogen dominance.

As a woman transitions into menopause from perimenopause, “the irregular release of androgen hormones becomes longer, and women may have reduced sexual desire for prolonged months,” the authors wrote. By age 50, most women experience a significant reduction in androgen. Testosterone and estrogen values also reach their minimum levels at this age.

Low levels of estrogen are mostly associated with dyspareunia and changes in vulvovaginal mucosa, which can contribute to reduced sexual desire. Loss of androgen hormones reportedly is worse in women with hypopituitarism, bilateral oophorectomy and Addison’s disease. But natural menopause can also result in reduced production of androgens.

For the most part, androgen deficiency is difficult to detect and many women attribute their reduced sexual desires to lifestyle or psychological distress rather than biologic changes. Low levels of androgens in women and decreased sexual desire can be diagnosed by assessing levels of sex hormone-binding globulin (SHBG) and testosterone.

Three treatments to manage hormone-induced HSDD among women are estrogen-progestin therapy (OPT), androgen therapy (AT) and a testosterone transdermal patch.

One study found that ovariectomized women with low sexual desire responded better to a combination of OT/AT than to OT alone. But most subsequent studies concluding that androgens contribute greatly to improving arousal and suppressing FSD have been based on supra-physiologic doses of hormones.