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DHEA is produced in the adrenal glands and can become either testosterone or estrogen.  For this reason, stimulation of production of this hormone can be affective for women in Menopause.  Its role as a precursor hormone is less understood and the source of much current scientific work.  It is difficult for searchers 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. Still, supplementing 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.

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DHEA and Cancer

Early reports from England [Bulbrook, 1962, 1971] suggested that DHEA was abnormally low in women who developed breast cancer, even as much as nine years prior to the onset or diagnosis of the disease. Dr. Arthur Schwartz of Temple University found that supplemental DHEA significantly protected cell cultures from the toxicity of carcinogens.

While the mechanics are still not completely understood, numerous studies exist attesting to a correlation of DHEA and this type of anti-cancerous property.  Some suspect it is the effect of DHEA on immune antioxidants.  DHEA is known to improve lipid antioxidant functioning when Vitamin E levels are low.

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DHEA & the Immune System

DHEA has been reported to counteract the thymic involution [shrinking of the thymus gland] and immuno-suppression caused by corticosteroids. This affects the ability of immune surveillance and antigen presentation.  Studies suggest these cells may be a site of DHEA. 

In test-tube studies, DHEA is not shown to have any direct anti-viral activity.  It is therefore believed that it is the interaction of DHEA with other amino acids, proteins, and hormones that affects this response in living organisms.

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DHEA and Aging

In animal studies, DHEA has shown to extend rodent lifespans up to 50%. The animals not only lives longer, they looked younger. The graying, course-haired controls could easily be distinguished from the sleek, black-haired, DHEA-treated animals.  Similar findings are seen human studies. 

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DHEA and Glucose Metabolism

Investigators have shown that DHEA inhibits glucose-6-phosphate dehydrogenase (G6PDH), an enzyme that breaks down glucose. G6PDH is shown to turn glucose into fat by changing anabolic activity into catabolic energy metabolism.

DHEA also enlarges the liver and improves its catalase activity resulting in improvement of the antioxidant enzymes and proliferation of the peroxisomes (cellular organelles which help to eliminate toxins) produced in this organ.  

Glucose Metabolism affects appetite and weight gain.  Since G6PDH is inhibited the body’s ability to synthesize fat from carbohydrates means that sources of fat become more important. This has a direct impact on appetite. In studies done to assess DHEA benefits in animals, it was found that those treated with improved DHEA levels consistently weighed less than control animals, even when their appetites dictated a food increase.  In other words, increases in appetite, when indulged, did not negate the anti-obesity property of DHEA.

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Enhancing Brain Function

DHEA is even more concentrated in the brain than in the bloodstream. Many neurologically degenerative patients such as those with Alzheimer's Disease show very low DHEA levels in the brian. Early research in this field by Dr. Eugene Roberts found that DHEA added in small concentrations to cell cultures were found to “increase the number of neurons, their ability to establish contacts, and their differentiation”. He also found that DHEA also enhanced long-term memory in mice undergoing avoidance training. It is suggested that a similar function exists in the human brain.

References

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Bulbrook RD, Hayward JL and Spicer CC. Abnormal excretion of urinary steroids by women with early breast cancer. Lancet 2: 1238-40, 1962.

Bulbrook RD, Hayward JL and Spicer CC. Relation between urinary androgen and corticoid excretion and subsequent breast cancer. Lancet 2: 395-98, 1971.

Chen TT, et al. Prevention of obesity in Avy/a mice by dehydroepiandrosterone. Lipids 12: 409-13, 1977.

Cleary MP and Fisk JF. Anti-obesity effect of two different levels of dehydroepiandrosterone in lean and obese middle-aged female Zucker rats. International Journal of Obesity 10(3): 193-204, 1986.

Coleman DL, Leiter EH and Applezweig N. Therapeutic effects of dehydroepiandrosterone metabolites in diabetes mutant mice (C57BL/KsJ-db/db). Endocrinology 115: 239-43, 1984.

Coleman DL, Leiter EH and Schweizer RW. Therapeutic effects of dehydroepiandrosterone (DHEA) in diabetic mice. Diabetes 31: 830-33, 1982.

Coleman DL, Schweizer RW and Leiter EH. Effect of genetic background on the therapeutic effects of dehydroepiandrosterone (DHEA) in diabetes-obesity mutants and in aged normal mice. Diabetes 33: 26-32, 1984.

de Peretti E and Forest MG. Pattern of plasma dehydroepiandrosterone sulfate levels in humans from birth to adulthood: Evidence for testicular production. J Clin Endocrinol Metab 47: 572-77, 1978.

Kahn, Carol. Beyond the Double Helix: DNA and the Quest for Longevity, Times Books, 1985, page 143. A thorough and highly readable “inside” account of DHEA research.

Loria RM, Regelson W and Padgett DA. Immune response facilitation and resistance to virus and bacterial infections with dehydroepiandrosterone (DHEA). In: The Biologic Role of Dehydroepiandrosterone (DHEA), Mohammed Kalimi and William Regelson [Eds], page 107-130, Walter de Gruyter, New York, 1990. ISBN 3-11-012243-X.

Loria RM and Padgett DA. Androstenediol regulates systemic resistance against lethal Infections in mice. Annals of NY Academy of Sciences 685: 293-95, 1993.

Nyce JW, Magee PN, Hard GC and Schwartz AG. Inhibition of 1,2-dimethylhydrazine-induced colon tumorigenesis in Balb/c mice by dehydroepiandrosterone. Carcinogenesis 5: 57-62, 1984.

Orentreich N, Brind JL, Rizer RL and Vogelman JH. Age changes and sex differences in serum dehydroepiandrosterone sulfate concentrations throughout adulthood. J Clin Endocrinol Metab 59: 551-55, 1984.

Pashko LL and Schwartz AG. Effect of food restriction, dehydroepiandrosterone, or obesity on the binding of 3H-7,12-dimethylbenz(alpha)anthracene to mouse skin DNA. J Gerontology 38: 8-12, 1983.

Schwartz AG. Inhibition of spontaneous breast cancer formation in female C3H(Avy/a) mice by long-term treatment with dehydroepiandrosterone. Cancer Research 39: 1129-32, 1979.

Schwartz AG, Hard GC, Pashko LL, Abou-Gharbia M and Swern D. Dehydroepiandrosterone: An antiobesity and anti-carcinogenic agent. Nutrition and Cancer 3: 46-53, 1981.

Schwartz AG, Nyce JW and Tannen RH. Inhibition of tumorigenesis and autoimmune development in mice by dehydroepiandrosterone. Mod Aging Res 6: 177-84, 1984.

Schwartz AG, Fairman DK and Pashko LL. The Biological Significance of Dehydroepiandrosterone. In: The Biologic Role of Dehydroepiandrosterone (DHEA), Mohammed Kalimi and William Regelson [Eds], Walter de Gruyter, New York, 1990.

Yen TT, Allan JA, Pearson DV, Acton JM and Greenberg MM. Prevention of obesity in Avy/a mice by dehydroepiandrosterone. Lipids 12: 409-13, 1977.