Increasing women’s sexual desire

How to increasing women’s sexual desire

How to increasing women’s sexual desire

Ovarian steroids (estradiol, testosterone, and progesterone) modulate sexual desire, or libido, in women. The gradual and age-related cessation of ovarian function associated with natural menopause decreases levels of ovarian steroids, accompanied by diminished sexual desire in a significant portion of postmenopausal women. Similarly, women who undergo bilateral oophorectomy (surgical menopause) routinely report a postoperative decline in sexual desire after experiencing an abrupt and pronounced drop in circulating levels of ovarian steroids. This menopause related decrease in sexual desire can be extreme and even debilitating; the Women’s International Study of Health and Sexuality (WISheS) found that roughly 9-percent of naturally and up to 26-percent of surgically postmenopausal women suffer from a persistent and distressing lack of sexual desire. Steroid hormones do not create sexual desire, but women’s sexual desire is clearly subject to hormonal influence. The identity of the ovarian steroid(s) critical for the modulation of women’s sexual desire, however, remains a topic of debate.

Both estradiol and testosterone have been implicated as the steroid that critically modulates sexual desire in women; although, estradiol seems at first glance to be the more likely candidate for this role. In all other mammalian species that have been studied, estradiol is critical for the expression of species typical female sexual behavior female rodents, ungulates, and carnivores all cease mating following ovariectomy, and female mating behavior can be reinstated by exogenous estradiol, without an accompanying androgen. The hormonal modulation of female sexual motivation has been particularly well studied in rhesus monkeys, which share many aspects of reproductive biology in common with women, including an approximately 28 day menstrual cycle with nearly identical patterns of hormonal fluctuation. Female rhesus monkey sexual motivation varies across the menstrual cycle, and female sexual behavior correlates with estradiol but not testosterone. Female rhesus monkey sexual motivation decreases following ovariectomy, and treatment with exogenous estradiol increases sexual motivation in ovariectomized females. If women’s sexual desire was under androgenic rather than estrogenic modulation, it would discriminate humans as unique amongst mammals. Nonetheless, testosterone is currently, and frequently, prescribed off-label for the treatment of low libido in postmenopausal women, and the idea of testosterone as a possible cure all for female sexual dysfunction remains common and popular.

estrogen-only therapies that produced periovulatory levels of circulating estradiol increased sexual desire in postmenopausal women. Estradiol presumably impacts female sexual functioning by acting on the central nervous system to increase sexual desire; however, these central effects are likely moderated by peripheral effects of estradiol acting directly on the genitals. Estradiol acts on the walls of the vagina to increase lubrication. Dyspareunia (painful intercourse) related to genitourinary atrophy is commonly associated with sexual dysfunction in postmenopausal women, and decreasing dyspareunia by increasing vaginal lubrication could conceivably indirectly increase women’s sexual desire by making sexual intercourse more pleasurable.

Ten out of twelve studies found that supraphysiological testosterone enhanced the effectiveness of an estrogen therapy at increasing sexual desire in postmenopausal women. The reason for this improved effectiveness of an estrogen in combination with supraphysiological testosterone remains unknown, but may reflect testosterone’s aromatization to estradiol, and/or the dynamic relationship between estradiol, testosterone, and sex hormone binding globulin.

There is little support for the notion that testosterone is the critical libidinal hormone for women. The likelihood that an androgen only clinical treatment will meaningfully increase women’s sexual desire is minimal, and the focus of pharmaceutical companies on the development of androgen therapies for the treatment of female sexual desire disorders is likely misplaced. Given that elevated estradiol levels within physiological range increase women’s sexual desire without concurrent androgen therapy, the use of supraphysiological testosterone to treat low sexual desire in women may be inappropriate. Future studies should focus on establishing the threshold level of estradiol required to reliably produce a meaningful increase in sexual desire in post-menopausal women, and examining the comparative effectiveness of different estradiol treatment regimens. Whether safety concerns about exposure to elevated estradiol can be addressed via novel steroid formulations or treatment regimens should also needs to be investigated.

Read More:

Flibanserin and Female hypoactive sexual desire disorder

Reference:
Increasing women’s sexual desire: The comparative effectiveness of estrogens and androgens, Hormones and Behavior by Cappelletti, Maurand, Wallen, Kim

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