Dehydroepiandrosterone (DHEA), also known as 3-beta-hydroxyandrost-5-en-17-one, dehydroisoandrosterone, and trans-dehydroandrosterone, is a naturally occurring intermediate formed in the course of synthesis of various steroids from cholesterol. DHEA is the most abundant steroid hormone in humans and is produced mainly by the adrenal cortex as an inactive sulfate ester (DHEA-S). Both DHEA and DHEA-S are bound by serum albumin, globulins, and steroidal sex hormone binding globulin. Only a small fraction of orally administered DHEA appears in the blood at any given time as DHEA; most undergoes conversion to DHEA-S by sulfotransferases in the liver and extrahepatic tissues. DHEA is a sulfate ester, dehydroepiandrosterone sulfate (DHEA-S) and DHEA are inconvertible. DHEA is initially converted to DHEA-S, which is considered the storage form of DHEA. DHEA-S is converted back to DHEA by peripheral tissues containing DHEA sulfatases, including lymphocytes and macrophages. DHEA is subsequently metabolized to androstenedione as well as the potent androgens, testosterone and dihydrotestosterone, and the estrogens, estrone and estradiol. DHEA production also occurs in the testes, ovaries, and brain. DHEA and DHEA-S levels are higher in men, and naturally decline with age in both sexes. DHEA exhibits wide diurnal variations in endogenous production, while DHEA-S levels show little variation during the day. Changes in plasma DHEA occur in parallel to those of ACTH and cortisol, with an early morning maximum, declining levels through the daytime, and minimal secretory activity in the early part of the night.
DHEA (dehydroepiandrosterone) is thought to serve as a precursor for other steroids, leading to androgen and estrogenic steroids. DHEA has been implicated as an important factor in many conditions, including aging, cardiovascular disease, AIDS, obesity, Alzheimer's disease, breast cancer and memory function. DHEA has been proposed for use in treating many medical conditions, such as systemic lupus erythematosus, Addison's disease, reduced libido, obesity, osteoporosis. Chronic treatment with DHEA in the diet has been shown to increase longevity in rodents by retarding the development of specific diseases associated with particular strains or mutants. Thus, ameliorative biological effects have been established relating to obesity, tumor development, aging, and immune function. The steroid DHEA appears to have many of the beneficial effects of caloric restriction without actually decreasing the amount of food eaten. Dehydroepiandrosterone (DHEA) serves as the primary precursor in the biosynthesis of both androgens and estrogens. DHEA has been reported to play a mitigating role in obesity, diabetes, carcinogenesis, autoinmmunity, neurological loss of memory, and the negative effects of GCS on IL-2 production by murine T cells. A natual metabolite of DHEA is 7-keto dehydroepiandosterone (7-keto DHEA). 7-keto DHEA is not only a potent metabolite of DHEA but, unlike DHEA, cannot be converted to active androgens and estogens. Scientific research on 7-keto DHEA demonstrates that it has therapeutic applications in immune modulation, immune enhancement through T-cell upregulation, memory enhancement, and weight loss and management by means of its theromagenic-enhancing action. Human serum DHEA concentrations have been shown to decline rapidly after the age of 30 in most people, suggesting that supplementation with DHEA may have beneficial effects for many people.
It has been reported that DHEA may be useful in the treatment of osteoporosis/osteopenia. But the administration of DHEA to humans to prevent bone loss or increase bone density is not a recognized treatment for osteoporosis/osteopenia by the medical industry. DHEA and DHEAS levels normally peak in the second or third decade of life. Low endogenous levels of the natural DHEA correlate with increased risk of developing some forms of cancer, such as premenopausal breast cancer in women and bladder cancer in both sexes. Low levels of DHEA and DHEAS are associated with a variety of disease conditions, including Alzheimer's Disease and cardiovascular disease. However, high levels of DHEA (such as those caused by administration of DHEA or DHEAS) can cause cardiovascular disease due to depletion of cardiac ubiquinone. DHEA can be administered by various routes and is orally active. Direct admninistration of DHEA, DHEAS and their derivatives can lead to serious side effects. Acne, hair loss, hirsutism and deepening of the voice have been reported with use of DHEA in women. In men, excess DHEA may stimulate the growth of prostatic cancer. Direct administration of pharmacological amounts of DHEA and/or DHEAS may cause a hormonal imbalance, which may in turn cause the side effects associated with DHEA and DHEAS administration. |
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