DHEA supplements are becoming increasingly popular with bodybuilders as a way to maximize their gains. DHEA, or dehydroepiandrosterone, is an adrenal hormone that occurs naturally in the body and is believed to help improve muscle strength, reduce fatigue, boost testosterone levels, increase muscle mass, and reduce fat. In this article, we'll explore the benefits of taking a DHEA supplement for bodybuilding and how to get the most out of it.
Dehydroepiandrosterone (pronounced dee-hi-dro-epp-ee-ann-dro-stehr-own), or DHEA as it is more often called, is a steroid hormone produced in the adrenal gland. It is the most abundant steroid in the bloodstream and is present at even higher levels in brain tissue. DHEA levels are known to fall precipitously with age, falling 90% from age 20 to age 90. DHEA is known to be a precursor to the numerous steroid sex hormones (including estrogen and testosterone) which serve well-known functions, but the specific biological role of DHEA itself is not so well understood. It is difficult for researchers to separate the effects of DHEA from those of the primary sex steroids into which it is metabolized. The apparent lack of any direct hormone action for DHEA has prompted the suggestion that it may serve the role of a "buffering hormone" which would alter the state-dependency of other steroid hormones. Although the specific mechanisms of action for DHEA are only partially understood, supplemental DHEA has been shown to have anti-aging, anti-obesity and anti-cancer influences. In addition, it is known to stabilize nerve-cell growth and is being tested in Alzheimer's patients. Our understanding of the specific mechanisms of DHEA in metabolism has recently been advanced by the publication of The Biologic Role of Dehydroepiandrosterone (DHEA), edited by Mohammed Kalimi and William Regelson [1990]. This book presents 24 chapters from scientists around the world who are conducting DHEA research. The breadth of the work is impressive. As Drs. Regelson, Kalimi and Loria stated in their introductory remarks, "DHEA modulates diabetes, obesity, carcinogenesis, tumor growth, neurite outgrowth, virus and bacterial infection, stress, pregnancy, hypertension, collagen and skin integrity, fatigue, depression, memory and immune responses." With this wide range of potential clinical uses, it is amazing that more books about DHEA have not been written. The introductory chapter, by the editors and Roger Loria, briefly reviews DHEA's biochemistry, endocrinology, and potential clinical uses. They contend that it is perhaps the most significant endocrine biomarker known, and further postulate that all of its effects may be explained by its action as a precursor hormone which provides "a host of steroid progeny with which to maintain the broad balance of host response related to species and individual survival."
Investigators have shown that DHEA inhibits glucose-6-phosphate dehydrogenase (G6PDH), an enzyme that breaks down glucose. There are two glucose-metabolizing pathways in the body, the catabolic, energy-yielding pathway and the anabolic, biosynthetic pathway. G6PDH happens to be the first enzyme in the biosynthetic pathway, the one which results in the synthesis of fatty acids and ribose (the sugar used in making deoxyribonucleic acid, or DNA). In simple language, G6PDH turns glucose into fat. DHEA's inhibition of G6PDH may redirect glucose from anabolic fat-production into catabolic energy metabolism, thus creating a leaner metabolism. This function of DHEA is well reviewed by Arthur Schwartz and colleagues in their chapter on "The Biological Significance of Dehydroepiandrosterone" in The Biologic Role of Dehydroepiandrosterone. They assert that DHEA-mediated reductions in ribose-5-phosphate activity may be centrally responsible for the anti-tumor promoting, anti-tumor initiating, and possibly the anti-atherogenic properties of DHEA. They also note that DHEA 1) produces hepatomegaly (liver enlargement), 2) stimulates liver catalase activity (a protective antioxidant enzyme), and 3) causes proliferation of peroxisomes (cellular organelles which specialize in oxidative processing and the decomposition of hydrogen peroxide). The absence of such influences with synthetic analogs of DHEA (like 16-alpha-fluoro-5-androsten-17-one) prompts Schwartz and colleagues to recommend that such analogs be considered for clinical applications in humans. Toxicity factors still need to be assessed.
In different experiments, DHEA supplementation has resulted in increased, decreased and unchanged food consumption. Dr. Schwartz found that it is the level of dietary fat influences food consumption. DHEA-treated rats on a high-fat diet ate less food than control rats while those on a low-fat diet ate more. Since DHEA inhibits G6PDH activity and suppresses the body's ability to synthesize fat from carbohydrate, dietary sources of fat become more important. This can affect changes in appetite. But despite possible increases in food intake, DHEA-treated animals consistently weighed less than control animals. In other words, increases in appetite, when indulged, did not negate the anti-obesity property of DHEA.
The body's production of DHEA drops from about 30 mg at age 20 to less than 6 mg per day at age 80. According to Dr. William Regelson of the Medical College of Virginia, DHEA is "one of the best biochemical bio-markers for chronologic age." In some people, DHEA levels decline 95% during their lifetime -- the largest decline of an important biochemical yet documented. In animal studies, DHEA extends rodent lifespans up to 50%. The animals not only lived longer, they looked younger. The graying, course-haired controls could easily be distinguished from the sleek, black-haired, DHEA-treated animals. DHEA levels are directly related to mortality (the probability of dying) in humans. In a 12-year study of over 240 men aged 50 to 79 years, researchers found that DHEA levels were inversely correlated with mortality, both from heart disease and from all causes. This finding suggests that DHEA level measurements can become a standard diagnostic predictor of disease, mortality and lifespan. Furthermore, if animal results hold true, supplemental DHEA may prevent disease, reduce mortality, and extend lifespan in humans.
DHEA may be unique among hormones for it's lack of specificity for hormone receptor sites. Just as vitamin E has never been shown to have a specific metabolic role (it is only proven essential as a general antioxidant), DHEA may serve an equally general purpose. "DHEA is the first example of a buffer action for hormones that I know of," states William Regelson. "It is a broad-acting hormone that only demonstrates itself under a specific set of circumstances. In that way, it is like a buffer against sudden changes in acidity or alkalinity. That is why when you get older, you're much more vulnerable to the effects of stress. As DHEA declines with age, you are losing the buffer against the stress-related hormones. It is the buffer action that [helps prevent] us from aging." The decrease of DHEA with age may result in gradual decline of a system for suppressing enzyme systems responsible for creating the building blocks of new cells, like lipids, nucleic acids (RNA and DNA) and sex steroids. The resulting rise in enzymatic activity in advanced age may be responsible for the proliferative events (cancer) and degenerative disease that become more frequent in advanced age. In this respect, DHEA might be best considered to be an anti-hormone, which might "de-excite" steroid-sensitive receptors that would otherwise lead to enhanced metabolic activity.
Exact dosages for humans have not been clearly determined. Daily dosages vary from 5 to 10 mg to as much as 2000 mg, with 5, 10, 25 and 250 mg being the range for typical tablet and capsule sizes. DHEA is usually split into 2-4 daily doses, especially at the higher dosage levels. We recommend that dosage be adjusted to bring blood DHEA and DHEA-S measurements towards young-adult levels. These blood tests can be ordered by your physician (don't forget to get your first test before you start taking DHEA).
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