Female Sexual Dysfunction

Female sexual dysfunction is more than the inability to produce a biological response to a stimulus; it is of multifactorial etiology. There is no “little blue pill” or quick fix. To fully understand each case, it is crucial for a physician to tend to all of the factors contributing to decreased libido, which includes a biopsychosocial model of sexual function, as well as the functional domains affected1. The ovaries produce testosterone and dehydroepiandrosterone (DHEA). The adrenals also produce dehydroepiandrosterone sulfate (DHEAS). DHEA and DHEAS can both by converted to testosterone by the brain, bone, and adipose tissue1. Testosterone appears to influence a woman’s libido or desire, as shown through a significant association with low …show more content…
The study was conducted on premenopausal women between the ages of 30 and 45 with a body mass index between 18 and 35 kg/m2. The women included in the trial scored less than 42 on the Sabbatsberg Sexual Self-Rating Scale, indicating diminished sexuality, and had no evidence of clinical depression as determined by the Beck Depression Inventory. The women were assigned to groups randomly for which they would undergo a treatment with either 10 mg of placebo or testosterone 1% cream for 12 weeks applied to the inner thigh, then go through a 4 week washout period and switch to the opposite treatment for another 12 weeks. Measurements of serum testosterone concentrations were taken at the beginning and end of each 12-week period, as well as sexual self-rating scores. At the end of the study, Goldstat and colleagues found the mean serum testosterone increased significantly more with testosterone treatment than with placebo. The Sabbatsberg Sexuality Scale scores increased significantly when women were treated with testosterone, compared to a decreased in scores when treated with …show more content…
This study was conducted on women aged 31 to 56 yeas that had undergone bilateral salpingo-oophorectomy and hysterectomy before natural menopause at least a year prior to the study. All women had serum testosterone concentrations and serum free testosterone concentrations lower than the median values for normal premenopausal women. After a 4-week baseline period, the women received in random order for 12 weeks each with concurrent oral estrogen therapy, placebo, testosterone 150 μg per day, and testosterone 300 μg per day. Serum testosterone, free testosterone, and total testosterone was measured at base line, 4, 8, and 12 weeks of each treatment period. Evaluation of sexual function and mood was measured by the Brief Index of Sexual Functioning for Women at the end of the base line period and at week 12 of each treatment period. An increase in testosterone serum concentrations and free testosterone was noted with each increase in dose of testosterone when compared to placebo. A significant increase in frequency of sexual activity and pleasure was found with the 300 μg dose of testosterone dose when compared with

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