Conclusions

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Androgens consist of 19 carbon steroids that are synthesized in endocrine tissues from cholesterol as substrate or via conversion from other androgens or precursor steroids in the periphery, including liver, gonads, and adrenal. The commonly studied androgens and androgen metabolites in the human include DHEA and its metabolite DHEAS, A4, and testosterone and its 5a-reduced metabolite, the potent androgen DHT. Circulating levels of androgens are similar in male and female children prior to adrenarche.

During adrenarche, plasma levels of DHEA and DHEAS achieve adult levels at an earlier stage of development than do those of testosterone. Although they are usually temporally linked, the onsets of adrenal and gonadal maturation are not functionally interdependent. In adult women, the adrenals and ovaries contribute variably to the circulating levels of androgens, although in general A4 is derived in roughly equal amounts from the ovary and the adrenal, whereas testosterone is derived approximately 25% from the adrenal, 25% from the ovary, and 50% from the peripheral conversion of A4. DHT is produced in peripheral tissues from testosterone and circulates at levels of about one-third to one-half that of testosterone. DHEA and DHEAS are almost exclusively of adrenal origin. DHEA is secreted in a pulsatile manner and demonstrates a diurnal rhythm that is similar to that of cortisol in young women.

In pregnancy, circulating levels of testosterone, A4, and DHT are all increased relative to those in nonpregnant women, although circulating levels of DHEAS at term are 50% or less than those in nonpregnant women. Interestingly, the maternal concentrations of DHEAS, A4, and testosterone have recently been shown to decrease with increasing maternal age in women in late gestation. The serum levels of testosterone and A4 are fairly stable for about 3 years prior to menopause, with a tendency to decline progressively thereafter. Alternatively, the age-associated declines in DHEA and DHEAS, consistent with the fact that these steroids are primarily of adrenal origin, are more related to age per se than to abrupt changes in ovarian function during the perimenopausal period. The steroidogenic defect that occurs in aging appears to be localized primarily to the zona reticularis of the adrenal. Although the role of the ovary in androgen production in postmenopausal women has been the topic of many studies, it still remains ill-defined. Finally, estrogen treatment of postmenopausal women has not been shown to have consistent effects on the androgenic milieu of women.

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