All types of androgens decrease with age. Fifty percent of circulating testosterone comes from ovarian and adrenal production, and this amounts to about 300 micro grams daily. The remaining 50% comes from the conversion of androgenic precursors derived from the adrenal gland and ovary. The target organs for this action is the skin, liver and adipose tissue

In the post menopausal woman, the contribution of the ovaries to the testosterone pool increases significantly from 25% to 50%. The question arises: How do testosterone levels decrease, if the ovary steps up its contribution in the post menopause? The production of testosterone prohormone DHEA and DHEAS by the adrenal gland decreases to the extent where the increased production by the ovaries cannot correct the deficit, resulting in a net decline in testosterone levels. Therefore, in surgical menopause, there is a dramatic and permanent decrease in testosterone levels.

Sex Hormone Binding Globulin ( SHBG ) binds onto testosterone more strongly than to estrogens. Only 1 to 2% of testosterone is free and physiologically active. The bound fraction includes 66% tightly bound to SHBG and 33% weakly bound to albumin.

This whole topic is bedevilled by the difficulty in measuring testosterone, especially in females. A further complicating factor is that weakly bound testosterone can easily dissociate from albumin at tissue level. Therefore serum levels may not accurately define dynamics at a cellular level.

Before we ascribe HSDD to be purely hormonal in aetiology, we have to exclude other causes; and they include psychosocial issues, psychological disorders, mental conditions and pharmacological agents. This involves taking a detailed history and allowing the patient time to express herself to practioners with a non judgemental attitude towards sexual issues.

The role of estrogens must not be forgotten. The alleviations of hot flushes, ensuring better sleep patterns and thus less fatigue, and its role in the treatment and prevention of vaginal atrophy may be enough to reverse a negative sexual cascade.

Androgens heighten response to psychosexual stimulation. They also cause external genitalia to become more sensitive leading to more consistent sexual gratification. Overall, it induces a greater sense of well being.


Testosterone therapy for women is a complex and ongoing debate. The European Union approved the use of TTP ( intrinsa ) in 2007. Personally, I feel that testosterone therapy can be safely used  after excluding` other causes of HSDD and informing patients that it is still off label therapy in South Africa. Owing to the unavailability of TTP in South Africa, I use testosterone implants. I start off with a dose of 25 milligrams. In the literature there are recommendations for a 50 milligram dose; but I have found an adequate response with the smaller dose in the majority of patients, and presumably less chance of side effects. The dose is repeated at 6 months if there has been a definite response. There is no point continuing androgen therapy in the absence of a change in HSDD. In patients who exhibit tachyphalaxis to implant therapy, I measure the free testosterone index, and only repeat the dose if the level is in the lower quartile of the normal range.

Testosterone therapy is usually given to patients after ensuring that they are well estrogenised. However, the recent ADORE study ( Climacteric2010:121 – 131 ) confirmed the efficacy of TTP in treating HSDD in naturally menopausal women with or without concomitant hormone therapy use. Thus, testosterone therapy may have a place even in patients in whom estrogens therapy is contraindicated.