John E. Buster, MD

For many women, the 50s are a milestone decade. Typically marked by onset of menopause, these can be years for celebrating fulfillment of life's goals and expressing sexuality free from the need for contraception. For some women, however, the menopausal transition brings with it female sexual dysfunction (FSD), a continuum of psychosexual disorders centered on loss of sexual desire with interrelated problems of arousal, orgasm, and sexual pain. FSD impact is subtle but insidious. It can be minor and short term or of long duration and debilitating, leading to emotional disturbances that affect quality of life in both family relationships and the workplace.  

Despite the consequences of FSD, however, physicians rarely ask women older than age 50 if they are having issues with their sexuality, because if the answer is yes, many clinicians are uncomfortable with the dialogue that is sure to follow. This article reviews criteria for recognized categories of FSD and hallmarks for diagnosis and provides an overview of pharmacologic and nonpharmacologic treatments that help restore a patient's sexual satisfaction. 

FSD has a reputation for being intractable and difficult to treat, but informed physicians know otherwise and no longer ignore these conditions just because women do not ask about them. As shown in Table 1, several legitimate ICD-9 diagnostic codes exist for FSD.

Aging has an adverse impact on endocrinology in women aged 50 and beyond, which in turn can undermine sexual desire, alter its clinical expression, and impact diagnosis and treatment of FSD. 

Estrogen and androgen production, which both are involved with initiation and maintenance of female sexual response, decline with age.

Estradiol secretion, chaotic during perimemenopausal years, declines to very low levels after menopause. Estrogen withdrawal increases tissue fragility, vaginal and urinary infections, irritation, dryness, urogenital pain, and susceptibility to vaginal tissue trauma. Declining estrogen impairs sexual desire indirectly, in that it induces vulovaginal atrophy, leading to sexual pain and trauma during intercourse. Finally, neuroendocrine estrogen depletion adversely impacts sexual response, as expressed in mood swings, hot flushes, irritability, memory lapses, and insomnia. 

Androgens produced in vivo are secreted into the circulation from the ovary or converted from adrenal dehydroepiandrosterone sulfate (DHEA-S) within target tissues. Production from both sources declines with age.

 Testosterone secretion in both pre- and postmenopausal women derives principally from the ovaries.

  During the reproductive years, a mid-cycle rise in testosterone occurs in conjunction with the luteinizing hormone (LH) surge; this is directly linked to increased mid-cycle sexual desire in reproductive-aged women.

  In postmenopausal women, ovarian testosterone is secreted tonically in association with chronically elevated LH, but the midcycle surge is lost. 

With age, levels of dehydroepiandrosterone sulfate (DHEA-S), a pro-hormone secreted by the androgen adrenal cortex, relentlessly decline.

  DHEA-S originates almost exclusively from the zona reticularis, or innermost zone, of the adrenal cortex.

  The zona reticularis undergoes genetically determined atrophy (apopotosis) with age, leading to age-related decline in DHEA-S production.

  As a pro-hormone, DHEA-S must be converted into testosterone and dihydrotestosterone (DHT) in target tissues.

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For many women, the 50s are a milestone decade. In addition to other changes, menopause can bring about sexual dysfunction.

John E. Buster, MD

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