Circulating Androgen Levels and Self-Reported Sexual Function in Women
Circulating Androgen Levels and Self-Reported Sexual Function in Women
Abstract & Commentary
By Sarah L. Berga, MD, James Robert McCord Professor and Chair, Department of Gynecology and Obstetrics, Emory University, School of Medicine, Atlanta.
Dr. Berga is a consultant for Pfizer, Organon, and Women First, Inc., and is involved in research for Berlex and Health Decisions, Inc.
Synopsis: Neither total nor free testosterone levels were predictive of low female sexual function and the majority of women with low dehydroepiandrosterone-sulfate (DHEA-S) levels did not report low sexual function.
Source: Davis SR, et al. Circulating androgen levels and self-reported sexual function in women. JAMA. 2005;294: 91-96.
The aim of this study was to explore the hypothesis that androgen levels gated sexual function in women. To diminish the biases inherent in the study of women seeking medical attention, Davis and colleagues surveyed a community population. Women were recruited by the random selection method using an electoral roll database for Victoria, Australia. Women between the ages of 18 to 75 years who were free of potentially confounding conditions were included. A total of 18,021 women were identified but only 1021 were included in the analysis. Premenopausal women had blood samples taken after cycle day 8 to avoid the early nadir in androgens of the early follicular phase. Total testosterone, free testosterone, dehydroepiandrosterone-sulfate, androstenedione, and SHBG were measured. Sexual functioning was assessed using a validated psychometric questionnaire, the Profile of Female Sexual Function, which consists of 7 domains: desire, arousal, orgasm, pleasure, sexual concerns, responsiveness, and self image. There is no total score. A detailed and sophisticated analysis using receiver operator characteristic (ROC) curves was performed. The ROC curves showed no association between total or free testosterone and any index of sexual function. Androstenedione levels were weakly correlated with arousal and pleasure in women older than age 45 and with responsiveness in women younger than age 45. The strongest associations were found between DHEA-S levels and sexual functioning, particularly in women over age 45 years, but the majority of women with low sexual functioning did not have low DHEA-S levels.
Commentary
There has been considerable controversy over the contribution of circulating androgen levels, particularly testosterone, to female sexual functioning. While it is clear that psychosocial factors influence sexual drive and sexual behavior, there has been considerable enthusiasm for the notion that testosterone is the main determinant of libido and sexual responsivity in women. This notion is largely predicated on the assumption that the determinants of sexual functioning are similar in men and women. Unfortunately, the relationship between circulating androgens and sexual functioning does not appear to be as straightforward in women as it appears to be in men. The current study results do not exclude a role for hormones, or androgens in particular, as contributors to sexual functioning in women, but neither do they demonstrate a robust dose-response curve between endogenous androgens and any aspect of reported sexual function in women.
What should the clinician think or do? Even if the relationship between circulating androgens and sexual functioning in women is ambiguous, there are still some simple clinical concepts that underpin diagnostic clarity. A critical question to ask anyone who reports the new onset of low libido is whether the loss is global or specific to the current partner. The aim of this question is to differentiate between biological versus dyadic issues as a cause of sexual dysfunction. A person who has an isolated loss of libido toward their partner is most likely dealing with dyadic issues. Individuals who report that they have always had low libido, regardless of partner, are unlikely to have a hormonal or dyadic cause, but they may have a psychosocial antecedent such as stress, depression, childhood abuse or neglect, or gender identity issues as the cause. A hormonal etiology is more likely if there has been a change in sexual functioning in association with an abrupt or identifiable change in hormones, such as that which may accompany oophorectomy. Aging per se seems to alter sexual functioning, although it has been difficult to concretely characterize the impact of age on sexuality because of the wide population variability. Davis et al point out that these data do not definitively exclude a role for exogenous androgen replacement in the treatment of female sexual dysfunction. Old assumptions die hard. Clearly, there is more to androgen action than circulating androgen levels, be they endogenous or exogenous. Recent studies have pointed to a role for oxytocin in gating both attachment and sexual functioning and a role for pheromones as determinants of attraction. On the other hand, stress hormones, depression, and many antidepressants suppress libido and sexual responsivity. The biology of sexuality is more complicated than one would suppose. Given its critical nature, it should not be too surprising to find redundancy in the biological mediators of sexual function. The flip side of redundancy, however, may be that no one agent can pack a punch.
The aim of this study was to explore the hypothesis that androgen levels gated sexual function in women. To diminish the biases inherent in the study of women seeking medical attention, Davis and colleagues surveyed a community population.Subscribe Now for Access
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