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Prasterone & dehydroepiandrosteron

Prasterone is a synthetic version of dehydroepiandrosterone, which is an androgen secreted by the adrenal cortex mainly. Prasterone will mimic the actions of dehydroepiandrosterone, which is a precursor of both testosterone and estradiol. Normally dehydroepiandrosterone is secreted in minute quantities with minimal androgenic activity on its own, as stated by Guyton and Hall (2006). However, when used pharmacologically, Prasterone will be peripherally converted to the more potent testosterone and dihydrotestosterone.

In turn, the converted testosterone will act around the body to increase protein formation and muscle development, increasing bone matrix, and increasing the basal metabolic rate. This is the basis for its use as an anti-aging hormone, or a performance enhancer. In accordance with the actions of testosterone as mentioned Harvey and Champe (2009), Prasterone will increase lean body mass, muscle strength and bone matrix density. The increase in bone matrix density is pharmacologically useful when a patient is on chronic glucocorticoid treatment as researched by Mease et al.

(2005). However, in prepubertal males, the excessive androgens can cause premature penile enlargement and early development of secondary sexual characteristics. In females, Prasterone can potentially cause virilization leading to acne, hirsutism, loss of scalp hair, deepening of voice, etc. Eventually, the testosterone formed from Prasterone will be metabolized to a 17-ketosteroid and excreted by the kidneys. An index of the amount of androgens can be monitored during Prasterone therapy through the levels of 17-ketosteroids in the urine.

Dean (2000) performed a study, and showed that high doses of Prasterone can cause severe psychiatric issues, and therefore should be avoided in individuals under 35, as Dehydroepiandrosterone levels are usually normal below that age and start falling after 30 years of age. Prasterone comes in tablet form commonly. However, a topical cream form and an injection are both available. In a clinical trail done by Kocis (2005), oral forms of Prasterone of 100-200mg/day were administered, and they resulted in supraphysiological levels of dehydroepiandrosterone. Citations:

1) Guyton and Hall, 2006, Medical Physiology, Elselvier, New Delhi 2) Harvey and Champe, 2009, Lippincott’s Illustrated Reviews: Pharmacology, Wolters Kluwer, New Delhi 3) Philip J Mease, Ellen M Ginzler, Oscar S Gluck, Michael Schiff, Allan Goldman, Maria Greenwald, Stanley Cohen, Rita Egan, Betty J Quarles, and Kenneth E Schwartz. Effects of prasterone on bone mineral density in women with systemic lupus erythematosus receiving chronic glucocorticoid therapy. The Journal of Rheumatology April 1, 2005 vol. 32 no. 4 616-621 4) Dean, Prasterone and Mania, The Annals of Pharmacotherapy: Vol. 34, No. 12, pp. 1419-1422

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