Androstenedione

Optimal result: 3.93 – 13.53 µg/g creatinine

DHEA(S), as well as its down-stream metabolites, androstenedione and testosterone, is more commonly found to be elevated in women with insulin resistance and polycystic ovarian syndrome (PCOS). These individuals usually have higher levels of insulin and LH (LH/FSH ratio is usually > 2.5 in 75% of women with PCOS), which stimulates high adrenal synthesis of DHEA(S), and high ovarian synthesis of testosterone.

In premenopausal women about half of the androstenedione is derived from the ovaries and the other half from the adrenals. At menopause, most of the androstenedione derives from DHEA(S) produced by the adrenal glands. DHEA is synthesized in the adrenal glands and is rapidly sulfated to DHEA-sulfate (DHEAS) to extend its half-life in blood. Androstenedione, the down-stream metabolite of DHEA, is further converted into testosterone and Epi-testosterone in near equal amounts in most individuals, or into estrone. More conversion to the estrogen, estrone, occurs in individuals with higher amounts of adipose (fat) tissue.

Low levels of these androgen precursors are associated with self-reported symptoms of low androgens. DHEA is commonly used as a supplement to raise testosterone levels in women. If low androgen symptoms persist, consider supplemental DHEA to raise testosterone levels, particularly if testosterone, or its down-stream and more potent metabolite DHT, are within mid range or lower.

DHEA and androstenedione are made almost exclusively by the adrenal gland (although a smaller amount is made in the ovaries). These hormones appear in urine as DHEA-S (DHEA-Sulfate), androsterone and etiocholanolone.

Androstenedione is an endogenous androgen steroid hormone and intermediate in the biosynthesis of estrone and of testosterone from dehydroepiandrosterone (DHEA). It is closely related to androstenediol. Androstenedione has been found to possess some estrogenic activity, similarly to other DHEA metabolites. However, in contrast to androstenediol, its affinity for the estrogen receptors is very low.

DHEA is not androgenic per se, in that it does not bind to cellular androgen receptors like testosterone and DHT, but it is a precursor for androstenedione, which then converts to testosterone.

Androstenedione
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