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DHEA Restoration Therapy

DHEA: Background and Biology

The human body derives DHEA from cholesterol via two enzymatic reactions. First, cholesterol is converted into pregnenolone, which is sometimes referred to as “the master hormone” due to its role as a precursor to the hormonal cascade that eventually gives rise to the primary sex hormones testosterone and estrogen. Next, pregnenolone is converted into DHEA (Traish 2011; Samaras 2013; Savineau 2013).

The primary location for DHEA production is the outer layer of the adrenal glands, called the adrenal cortex; some other tissues such as the testes in men and ovaries in premenopausal women also produce DHEA, but to a much lesser extent. Production of DHEA peaks in the 2nd to 3rd decade of life. Thereafter, levels decline steadily with age (Traish 2011; Samaras 2013).

Up to the early 2000s, much of the research on DHEA focused on its role as a precursor to androgens and estrogens. However, more recent investigations revealed several biological actions mediated directly by DHEA. Studies have shown that specialized receptors on cellular membranes in the blood vessel lining (endothelium), heart, kidney, and liver interact directly with DHEA (Samaras 2013; Traish 2011). For example, one significant androgen- and estrogen-independent action of DHEA is the activation of an enzyme in blood vessels called endothelial nitric oxide synthase (eNOS), which produces the potent vasodilator nitric oxide (NO) that is important for healthy vascular function (Samaras 2013; Traish 2011; Liu 2002; Liu 2004; Simoncini 2003).