Low or absent sexual desire is the most common sexual dysfunction in women, and its prevalence peaks during midlife. Its etiology is complex and may include biologic, psychologic, and social elements. Major risk factors for its development include poor health status, depression, certain medications, dissatisfaction with partner relationship, and history of physical abuse, sexual abuse, or both. Diagnosis is based on criteria set by the Diagnostic and Statistical Manual of Mental Disorders (5th Edition) and requires that a woman experience personal distress. Clinical evaluation should include medical history, sexual history, and, sometimes, a physical examination. Laboratory data are of limited value, except when warranted by history or physical examination. Treatment options include nonpharmacologic interventions such as education, office-based counseling, and psychotherapy. Although there are no U.S. Food and Drug Administration (FDA)–approved treatments for low desire, pharmacologic agents have been used off-label for this purpose. Bupropion is an antidepressant that has been shown to improve desire in some women with and without depression. Systemic estrogen therapy is not recommended in the absence of vasomotor symptoms and is not directly associated with desire. However, vaginal estrogen is useful in patients presenting with concomitant vaginal atrophy and dyspareunia. Ospemifene is a selective estrogen receptor modulator that can be used as an alternative to vaginal estrogen. Exogenous testosterone has demonstrated efficacy in treating loss of desire in postmenopausal women. However, patients should be counseled that it is not FDA-approved for this purpose and there are limited published long-term safety data. Several agents for the treatment of low desire are currently in development. Gynecologists are in a unique position to address concerns about sexual desire in women.
Low or absent sexual desire is the most common sexual dysfunction among women.Supplemental Digital Content is Available in the Text.
Case Western Reserve University School of Medicine, Cleveland, Ohio; and the University of Texas MD Anderson Cancer Center and Baylor College of Medicine, Houston, Texas.
Corresponding author: Sheryl A. Kingsberg, PhD, Case Western Reserve University, Mailstop 5034, 11100 Euclid Avenue, Cleveland, OH 44106; e-mail: firstname.lastname@example.org.
Continuing medical education for this article is available at http://links.lww.com/AOG/A594.
Financial Disclosure Dr. Kingsberg is a paid consultant for the following pharmaceutical companies: Apricus, Emotional Brain, Teva, Pfizer, Shionogi, Trimel, Sprout, NovoNordisk, Palatin, and Metagenics. The other author did not report any potential conflicts of interest.