Sexual dysfunction is common in women of all ages, but for women in menopause (both natural and surgically induced) the symptoms are elevated due to declining levels of estrogen and testosterone. Although estrogen therapy improves vaginal dryness and pain, some women prefer to use a non-estrogen option.
Sex steroids are vital for healthy tissue integrity of the labia, vagina, lower urinary tract and supporting pelvic structures. These tissues are rich in estrogen and androgen receptors. These hormones enhance blood flow to the genital tract which is necessary for general arousal and lubrication.
The fall in estrogen at menopause and the decline in androgens (mainly testosterone) as we age results in vulvovaginal atrophy (VVA) and an increase in vaginal PH. Theses changes allow the environment to be vulnerable for vaginal infections. Symptoms include vaginal dryness, irritation, itching, infection and pain with intercourse. This leads to diminished sexual desire, arousal difficulties, reduced physical and emotional satisfaction, and relationship issues.
Vaginal estrogen therapy can thicken and revascularize the vaginal tissue, lower the PH and normalize vaginal flora. Although data show that vaginal estrogen acts locally, some studies have shown blood estradiol levels increase with vaginal estrogen application. Therefore, researchers have looked for alternatives for women whom cannot or should not risk raising their level of estrogen such as women who have had estrogen receptor positive breast cancer. The adrenal hormone dehydro-epiandrosterone (DHEA) is an important precursor for the biosynthesis of estrone and testosterone.
A randomized controlled trial of the daily application of three different doses of vaginal DHEA ovules (3.25 mg, 6.5 mg, or 13 mg) was studied over 12 weeks in 218 postmenopausal women who met the entry criteria of dyspareunia (pain with intercourse). This one study resulted in a number of publications to support the effectiveness of this treatment for VVA. In these publications the investigators reported an improvement in the vaginal cells and a reduction in PH. At 12 weeks, the total Menopause Quality of Life Questionnaire (assessing sexual desire, vaginal dryness, intimacy) scores showed significant greater response for each treatment group verses placebo.
The improvements seen in this study are interesting. It is possible that the DHEA effects were due to local metabolism to estrone (stored estrogen) and testosterone which binded to the local receptors. Considering how well drugs are absorbed through the vaginal mucosa, this is reassuring. DHEA may be considered a promising treatment alternative but further studies are needed to confirm efficacy and safety. Ideally future studies should evaluate less frequent administration of the DHEA ovule because most women may not like the daily administration.
Reference: Davis, S. “DHEA for Urogenital Atrophy and Sexual Function.” The North American Menopause Society e-consult, Medscape Edition. Jan, 15, 2015.