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 DHEA is a steroid hormone secreted by the adrenal gland, shown in double-blind, placebo-controlled studies to have restorative and revitalizing effects. Unfortunately, natural DHEA levels decline dramatically with age. By age 70, your DHEA levels will likely be less than 30% of what they were at their peak in your 20s. And low blood levels have been associated with many degenerative conditions. DHEA provides: * Powerful defense against age-related problems including diminished muscle mass, memory loss, joint discomfort, fatigue and sleep disturbances. * Enhanced immune system function. * Nutrients essential for building and maintaining tissue. Directions: Adults, as a dietary supplement, take one to two tablets daily, preferably one tablet at breakfast (and one 8 hours later if taking two), or as recommended by your health care professional Warning: Consult with your physician first if you are female of child bearing age, pregnant, lactating, taking medication, or under a doctor's care. Keep away from children. This product is for adults only. Generally persons under age 30 should not use it Micron 5 DHEA is a trademark of McPherson Laboratories, Inc. It offers unsurpassed quality with the following special features: 1. Micronized to 5 Microns - for better absorption and less side effects. 2. Minimum of at least 99.0% purity by HPLC. 3. Celloluse gum coated to protect DHEA from being damaged by stomach acids. 4. Slow release formulation to reduce body stress. 5. US FDA Registered manufacturing facility for the manufacture of drugs and medical devices. 6. Made to meet pharmaceutical specifications - not the lower food supplement specifications. 7. Excellent for use in clinical research. 8. Unsurpassed bioavailability. Micron 5 DHEA was used in clinical studies on human subjects by leading DHEA researchers. We offer a celloluse gum coated, slow release DHEA product produced using the highest quality Micron 5 DHEA source material and produced to meet pharmaceutical standards at a facility registered with the US FDA for the manufacture of drugs and medical devices. We know that you are looking for the highest quality DHEA product, and we are confident that our product will fill your need. Micron Size: Our Micron 5 DHEA is the smallest micron size DHEA commercially available in the market. Micronized dhea offered by our competitors normally have a particle size in the range of 15 to 20 microns. By calculation, our Micron 5 DHEA has about 9 times the surface area, and about 27 times the number of DHEA particles per unit weight, when compared with a 15 micron dhea. Our smaller micron size would make our DHEA product much more bioavailable and effective. Purity: We use only pharmaceutical grade DHEA having a purity of at least 99.0% by HPLC. The purity of our current batch of DHEA source material is reported to be 101.2% HPLC by an independant testing laboratory (Vanguard Scientific). They also remarked that our DHEA source material is the purest DHEA that they have ever tested, and told us that most of the DHEA tested by them produce results of between 94% and 96% by HPLC. Celloluse Gum Coated: Our DHEA crystals are first coated with a celloluse gum powder before the mixture is mixed with the rest of the excipients to form the DHEA slow release tablet. When ingested, the celloluse gum powder forms a gummy layer, protecting the DHEA crystals from being damaged by the stomach acids. Later, the gummy layer is worn away slowly by the rubbing action of the intestines, exposing the DHEA crystals for absorbsion and use by the body. Slow Release Formulation: Our DHEA tablets are specially formulated for slow release action, whereas most DHEA preparations offered by our competitors are not. We believe that slow release action is essential for any hormone supplement because it more closely mimicks the body’s production of that hormone, and is needed to reduce stresses to the body caused by ingestion of that hormone supplement. Also, the body does not produce hormones in batches, so why do we take a non-slow release hormone supplement? US FDA Registered Manufacturing Facility: Our DHEA tablets are produced and packaged at a facility registered with the US FDA for the manufacture of drugs and medical devices, and are produced to meet pharmaceutical standards. Our competitors offer DHEA manufactured to meet only the lower food supplement standard, and could potentially offer products that are sub potency and super potency. If you are planning to offer DHEA as a prescription item, or for a scientific study, you can appreciate the need for accuracy and consistancy of product dosage. Otherwise results and accuracy of the treatment regiment or study would be questionable. DHEA May Boost Mental, Sexual Health NEW YORK, Sep 29 (Reuters Health) -- For women who have underactive adrenal glands, treatment with the hormone dehydroepiandrosterone (DHEA) can improve their psychological well-being and sexual satisfaction, German researchers report. Normally, levels of DHEA in the body peak when a person is 20 to 30 years old, and then begin to decline gradually. However, in people with underactive adrenal glands, levels of the hormone are low, even in their youth. The precise function of the hormone is unclear, according to a team of researchers led by Dr. Wiebke Arlt, of the Medical University Hospital in Wuerzburg, Germany. Several studies have suggested, however, that elderly people who take DHEA supplements experience a number of benefits, including improved well-being, bone density and muscle strength. Arlt and colleagues set out to see if treatment with DHEA would help women with underactive adrenal glands, since the condition increases the risk of depression, anxiety and sexual problems. In the study, Arlt's team randomly assigned 24 such women to receive 50 milligrams of DHEA each day or an inactive placebo pill for 4 months. After one month of not taking either DHEA or placebo, the women switched treatments for another 4 months, according to the report in the September 30th issue of The New England Journal of Medicine. Based on questionnaires completed by the women, the investigators report that DHEA replacement improved a number of signs of psychological well-being, including depression, anxiety, hostility, and obsessive-compulsive behavior. However, these improvements only showed up after 4 months of treatment. DHEA also appeared to have a positive effect on the women's sexuality, according to the authors. While on the treatment, women reported having more frequent sexual thoughts and fantasies, greater interest in sex, as well as more sexual satisfaction, Arlt and colleagues note. Some of the improvement was gradual, however. The side effects of treatment were minor for the most part, with several women reporting greasy skin, acne and increased body hair while taking DHEA. One woman did begin to lose her hair, but the hair loss stopped when she started taking DHEA only on every other day. "We found that dehydroepiandrosterone-replacement therapy resulted in a significant improvement in well-being and sexuality in women with adrenal insufficiency," Arlt and colleagues write. Based on the findings, they recommend that DHEA should be added to the regimen of other hormones that women with the condition already take. They also write that similar research should be conducted in men to see if they will benefit from DHEA replacement as well. The findings "mark a new phase of replacement therapy for patients with adrenal insufficiency," Dr. Wolfgang Oelkers, of Klinikum Benjamin Franklin in Berlin, writes in an accompanying editorial. Oelkers agrees that a daily dose of DHEA should be considered for people with underactive adrenal glands, although he notes that they should be monitored to make sure they do not develop breast or prostate cancer. The New England Journal of Medicine 1999;341:1013-1020, 1073-1074. SALT LAKE CITY, Jan. 21 /PRNewswire/ via Individual Inc. -- Pharmadigm, Inc. today announced the publication of results from a preclinical study demonstrating that dehydroepiandrosterone (DHEA) preserves blood vessel function in tissues subjected to a six-hour interruption in blood flow (ischemia) followed by the re-flow of blood into the ischemic tissue (reperfusion). The maintenance of blood vessel function is critical to preventing permanent tissue damage caused by the inflammatory reactions initiated by reperfusion and other events such as burns. The results of the study were published in the January issue of The Journal of Trauma DHEA Possible Treatment for Impotence NEW YORK, Mar 24 (Reuters Health) -- The hormone dehydroepiandrosterone (DHEA) may be a promising alternative treatment of erectile dysfunction, according to Austrian researchers. Dr. Werner J. Reiter and colleagues at the University of Vienna, Austria, randomly assigned 40 patients with erectile dysfunction to take (an inactive) placebo or 50 milligrams of DHEA daily for 6 months. Each of the patients had normal levels of testosterone and other hormones. Those taking DHEA had "an impressive improvement in maintaining the erection after 16 weeks" of therapy, the researchers report in the March issue of Urology. DHEA treatment had no effect on prostate-specific antigen or any of the hormones monitored, and no adverse effects associated with the treatment were reported. The authors conclude that "oral DHEA treatment may be of benefit in the therapy of erectile dysfunction," but the mechanisms underlying this benefit are not yet understood. Although the study population was small, Reiter's team believes that the "data show a biologically obvious trend that justifies further extended studies." SOURCE: Urology 1999;53:590-595. DHEA treatment for Osteoporosis Effect of 12-Month Dehydroepiandrosterone Replacement Therapy on Bone, Vagina, and Endometrium in Postmenopausal Women Author(s): Labrie F, Diamond P, Cusan L, Gomez J-L, Bélanger A, Candas B Source: J Clin Endocrinol Metab. 1997; 82:3498-3505. Abstract: The effect of 12-month dehydroepiandrosterone (DHEA) replacement therapy has been evaluated in 14 60- to 70-yr-old women who received daily applications of a 10% DHEA cream. Vaginal epithelium maturation was stimulated by DHEA administration in 8 of 10 women who had a maturation value of zero at the onset of therapy, whereas a stimulatory effect was also seen in all three women who had an intermediate vaginal maturation index before therapy. The estrogenic effect of DHEA observed in the vagina was not observed in the endometrium, which remained atrophic in all women. Most interesting, the bone mineral density significantly increased at the hip from 0.744 ± 0.021 to 0.759 ± 0.025 g/cm2 after 12 months of treatment (P <0.05). These changes in bone mineral density were associated with a significant 20.0% decrease (P < 0.01) in plasma bone alkaline phosphatase and a 28% decrease in the urinary ydroxyproline/creatinine ratio. A 2.1-fold increase over the control value (P < 0.01) in plasma osteocalcin was concomitantly observed. The present data describe for the first time a series of medically important beneficial effects of DHEA therapy in postmenopausal women through transformation of the precursor steroid DHEA into androgens and/or estrogens in specific peripheral intracrine tissues without significant adverse effects. The stimulatory effect on the vaginal epithelium in the absence of stimulation of the endometrium is of particular interest because it eliminates the need for progestin replacement therapy. On the other hand, the stimulatory effect on bone mineral density accompanied by an increase in serum osteocalcin, a marker of bone formation, suggests stimulation of bone formation by the androgenic action of DHEA, a finding of particular interest for both the prevention and treatment of osteoporosis. DHEA treatment as it related to HGH DHEA is produced by the adrenal glands. It begins to drop when we are thirty years old and declines linearly until we die. DHEA plays a important role in lowering our cholesterol, keeping our hearts healthy, minimizing fat deposition, preventing the development of diabetes, arthritis, and senility. We use DHEA as an essential part of our treatment program and monitors DHEA sulfate levels to assure optimal blood DHEA levels. DHEA Lowers blood cholesterol Improves Heart Health Slows onset or progression of diabetes Favorably impacts arthritis Reverses declining mental acuity Effects of replacement dose of dehydroepiandrosterone in men and women of advancing age Aging in humans is accompanied by a progressive decline in the secretion of the adrenal androgens dehydroepiandrosterone (DHEA) and DHEA sulfate (DS), paralleling that of the GH-insulin-like growth factor-I (GH-IGF-I) axis. Although the functional relationship of the decline of the GH-IGF-I system and catabolism is recognized, the biological role of DHEA in human aging remains undefined. To test the hypothesis that the decline in DHEA may contribute to the shift from anabolism to catabolism associated with aging, we studied the effect of a replacement dose of DHEA in 13 men and 17 women, 40-70 yr of age. A randomized placebo-controlled cross-over trial of nightly oral DHEA administration (50 mg) of 6-month duration was conducted. During each treatment period, concentrations of androgens, lipids, apolipoproteins, IGF-I, IGF-binding protein-1 (IGFBP-1), IGFBP-3, insulin sensitivity, percent body fat, libido, and sense of well-being were measured. A subgroup of men (n = 8) and women (n = 5) underwent 24-h sampling at 20-min intervals for GH determinations. DHEA and DS serum levels were restored to those found in young adults within 2 weeks of DHEA replacement and were sustained throughout the 3 months of the study. A 2-fold increase in serum levels of androgens (androstenedione, testosterone, and dihydrotestosterone) was observed in women, with only a small rise in androstenedione in men. There was no change in circulating levels of sex hormone-binding globulin, estrone, or estradiol in either gender. High density lipoprotein levels declined slightly in women, with no other lipid changes noted for either gender. Insulin sensitivity and percent body fat were unaltered. Although mean 24-h GH and IGFBP-3 levels were unchanged, serum IGF-I levels increased significantly, and IGFBP-1 decreased significantly for both genders, suggesting an increased bioavailability of IGF-I to target tissues. This was associated with a remarkable increase in perceived physical and psychological well-being for both men (67%) and women (84%) and no change in libido. In conclusion, restoring DHEA and DS to young adult levels in men and women of advancing age induced an increase in the bioavailability of IGF-I, as reflected by an increase in IGF-I and a decrease in IGFBP-1 levels. These observations together with improvement of physical and psychological well-being in both genders and the absence of side-effects constitute the first demonstration of novel effects of DHEA replacement in age-advanced men and women. Morales AJ, Nolan JJ, Nelson JC, Yen SS. Effects of replacement dose of dehydroepiandrosterone in men and women of advancing age. J Clin Endocrinol Metab 1994;78:1360-1367. DHEA by Ward Dean, M.D., and Steven Wm. Fowkes 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 refunctions, but the specific biological role of DHEA itself is not so well understood. 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. 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." 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. Of the 5000 women followed in the study, 27 developed cancer. Most of the 27 had abnormally low levels of DHEA. If low DHEA levels contributed to breast cancer, might the opposite be true? Many years later, Dr. Arthur Schwartz of Temple University found that supplemental DHEA significantly protected cell cultures from the toxicity of carcinogens. Cell cultures usually respond to powerful carcinogens with mutations (changes in DNA), transformations (changes in cell appearance), and a high rate of cell death. But when Schwartz added DHEA along with the carcinogen, all three of these effects were significantly diminished. Subsequent studies [Schwartz, 1979] identified powerful protective effects of supplemented DHEA for breast-cancer-prone mice. The results of the experiment was clear after 8 months. The control animals were "getting cancer left and right" while the DHEA animals had no tumors. In two later studies with different strains of mice, Schwartz found 75% and 100% reductions in tumor incidence at 8 months of age and 50% and 75% reductions at 15 months of age [Schwartz, 1981; 1984]. DHEA has demonstrated protective effects for cancers of the skin, lungs, bowel, breast and liver. According to William Regelson, "Whenever [DHEA] has been tested in a model of carcinogenesis and tumor induction, DHEA has preventative effects." Although DHEA is now beginning to be tested in human cancer, it is still to early to know whether the successes achieved in animals will be realized in humans. The Anti-Obesity Factor At about the same time that Schwartz was investigating the anti-cancer properties of DHEA, Dr. Terrence T. Yen was studying the effect of DHEA on genetically obese mice. Although the DHEA-treated mice ate normally, they remained thin -- and they lived longer than control mice. This "leanness" effect was also conspicuously noted by Dr. Schwartz. In another experiment, Dr. M. P. Cleary found that even middle-aged obese rats lost weight when fed DHEA-supplemented food. Diabetes, a typical complication of obesity, was also dramatically decreased. DHEA and Glucose Metabolism 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. DHEA and Appetite 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. DHEA and Aging 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. Enhancing Brain Function DHEA may also be intimately involved in protecting brain neurons from senility-associated degenerative conditions, like Alzheimer's disease. Not only do neuronal degenerative conditions occur most frequently when DHEA levels are lowest, but brain tissue contains many times more DHEA than is found in the bloodstream. One of the scientists at the forefront of this field of research is Dr. Eugene Roberts who found that very low concentrations of DHEA were found to "increase the number of neurons, their ability to establish contacts, and their differentiation" in cell cultures. He also found that DHEA also enhanced long-term memory in mice undergoing avoidance training. It may play a similar role in human brain function. Drs. Roberts and Fitten report initial research on "Serum steroid levels in two old men with Alzheimer's disease before, during and after oral administration of DHEA" in the book The Biologic Role of Dehydroepiandrosterone. Roberts' and Fitten's data are the best we've seen regarding acute and chronic changes in numerous hormone levels following various oral doses of DHEA (see adjacent graphs). Because of the short peak duration of DHEA (heavier line in illustration), they recommend that future studies or therapeutic trials use time-release capsules or transdermal patches to provide more uniform delivery of DHEA. Levels of pregnenolone and 17-alpha-pregnenolone, the direct precursors to DHEA, were too low to be measured in the two patients illustrated, but Roberts and Fitten present data from three other Alzheimer's patients. Their data indicate that in all three patients, "control values for pregnenolone and 17-alpha-pregnenolone not only were below the means for the population controls, they were lower than the lowest values." In other words, the highest of the Alzheimer's patients was lower than the lowest of the population controls. When they were administered 400 mg of DHEA, all three experienced decreased levels of 17-alpha-pregnenolone. Pregnenolone levels increased in two patients and fell in the third. In the two patients experiencing increased pregnenolone and decreased 17-alpha-pregnenolone in response to DHEA, levels of 17-alpha-pregnenolone rebounded strongly at 24 hours. Roberts and Fitten suggest that "a prolonged inhibition of 17-alpha hydroxylation occurred as a result of continued DHEA intake." DHEA and Immune Function DHEA is known to enhance general immune response. Oral and subcutaneous DHEA has been observed to protect rodents against the lethality of RNA and DNA viruses, and lethal bacterial infections. Drs. Loria, Regelson and Padgett report in The Biologic Role of Dehydroepiandrosterone (DHEA) that a single subcutaneous dose of DHEA is considerably more effective in protecting against infection than oral dosing. Intraperitoneal [within the abdominal cavity] injections were completely ineffective. Dr. Loria and colleagues noted that subcutaneous dosing did not result in the typical weight loss observed with oral DHEA. Presumably it works by a different mechanism. DHEA has been reported to counteract the thymic involution [shrinking of the thymus gland] and immuno-suppression caused by corticosteroids. But the special role of skin tissues in the immune facilitating properties of DHEA suggest a different mechanism is involved. Cutaneous immune cells, such as Langerhans cells and keratinocytes, are believed to play a role in "immune surveillance" and "antigen presentation." These cells may be a site of DHEA's action. Subcutaneous injection of DHEA results in the "formation of a local deposit leading to a relatively prolonged exposure to the lymphoid system." DHEA skin patches might provide a similar exposure. The delay in protective effect of subcutaneous DHEA has prompted Loria and colleagues to postulate that a DHEA metabolite is involved in cutaneous immune enhancement. In a recent paper [Loria and Padgett, 1993], they advance androstenediol [5-androsten-3-beta-17-beta-diol] as the active metabolite, the production of which is predominantly localized in the skin and brain. They found that androstenediol was significantly more effective than DHEA (10,000 times more with coxsackievirus B4!). Neither DHEA nor androstenediol have any direct (in vitro) antiviral activity. The amount of viral load in heart, spleen, pancreas, liver and blood tissues was unaffected by either DHEA or androstenediol administration. The effect of these steroids appears to be strictly mediated through stimulation of lymphocytes, lymphoid organs, and immune-modulating cytokines [immune hormones]. DHEA: The Buffering Steroid? 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. Dosage 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). Conclusion Because of its generally universal function in human metabolism, DHEA is being associated with numerous human maladies. For example, DHEA has recently been found to have a highly statistically significant correlation with vertebral bone density in postmenopausal women suggesting that DHEA (and other weak androgens) may protect against osteoporosis. This, and its low toxicity, may tend to give DHEA the same panacea stigma that the antioxidants vitamin E and C suffer. References: Barrett-Connor E, Khaw KT and Yen SS. A prospective study of dehydroepiandrosterone sulfate, mortality, and cardiovascular disease. New England Journal of Medicine 315(24): 1519-24, 11 December 1986. 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. July 25, 1997 NEW YORK (Reuters) - While not as rapid or extreme as the menopause that women go through in their 50s, men also suffer from declining hormone levels as they age, according to a Missouri researcher. Such a decline may result in waning strength and sexual interest, and even memory problems, said Dr. John Morley, a professor of geriatrics at St. Louis University in Missouri. And treatment with male hormones, such as testosterone, may help relieve such problems in at least some men. "This is a normal part of aging in the same way that losing estrogen is a normal part of aging in women," he said. "For many years people believed that when women were menopausal, that was fine and you wouldn't do anything about it. Now I think we know that for many, but not all women, replacing estrogen makes a major difference to their health risk and how they do down the line." Dropping estrogen levels increase a woman's risk of heart disease and the bone-thinning disorder, osteoporosis. Many women now use hormone replacement therapy to replace lost estrogen, though they must also take a second hormone to combat an increased risk of cancer of the uterine lining. In a study of 56 healthy men who ranged in age from 20 to 84, Morley and colleagues looked at how hormone or growth factor levels changed with age. They found the most significant changes in bioavailable testosterone (BT, a type of testosterone not bound to other molecules), dehydroepiandrosterone sulfate (DHEAS, a testosterone precursor molecule), and the ratio of insulin-like growth factor 1 (IGF-1) to growth hormone (GH). So, is it possible to return reduced blood levels of bioavailable testosterone in older individuals to those found in young adults? According to a second study by the same researchers, men who took moderate daily doses of DHEA, a testosterone precursor available in health food stores, did have higher levels of DHEA and DHEAS in their blood - but not testosterone. Indeed, high oral doses of DHEA may actually reduce testosterone levels. "It looks like bioavailable testosterone is more useful than DHEAS," Morley said. "It looks like (DHEAS and DHEA) are not as useful to the older male as testosterone. That doesn't mean they won't have a use, that just means that if your problem is low testosterone, you should replace low testosterone - not try to give a precursor and see if you get a benefit from that." But doctors won't be handing out testosterone to every aging male that walks through their door, Morley said. The men who are most likely to benefit are those whose hormones levels are similar to that seen in younger males with hypogonadism, or underproduction of hormones from the testes. "It's very much like a woman who is having menopause and she comes in and says 'I'm having hot flashes. I can't stand it. Have you got something that will stop this?' Estrogen is the answer there," Morley said. "If a man comes in and says, 'My enthusiasm for sex is low. I'm not getting hard erections. My memory is not as good as it was. I am not thinking quite as well. I don't have the same strength,' or 'I am losing a bit of height because of osteoporosis,"' then declining testosterone might be the culprit, he said. SOURCE: Proceedings of the National Academy of Sciences (1997;94:7537-7542) Androstenediol (4-AD) is a natural occurring androgen metabolite, found in all animals (meat), and is both a direct precursor and metabolite to testosterone. It is a very obscure compound that is not widely discussed in the literature like other androgens are. In all mammals, 4AD is produced in the gonads and adrenal glands. The oral form of 4AD is metabolized in the liver to become testosterone via an enzymatic pathway. This exciting new product is Androdiol in a sublingual cyclodextrin form. A University study revealed that Cyclo-Diol delivers 260% more testosterone conversion than 100mg of oral Androdiol. When a prohormone is taken orally, it is subject to First Pass (the body breaks it down which is not good because it leaves very little active hormone life). The hormone is in and out of the system very quickly. Cyclodextrin is a molecule with a water compatible exterior and a water incompatible interior. The ANDRODIOL™ or NORANDRODIOL™ molecule is placed inside the Cyclodextrin. The water compatible exterior of the Cyclodextrin will camouflage the water incompatible molecule, the pro-hormone. Your bloodstream will allow it to enter immediately, and the pro-hormone will be released into your body. It is taken by placing in the lining of the cheek or under the tongue. It goes directly into the blood stream. It works rapidly regardless of whether you have eaten recently or not. In summary, cyclodextrin complexes taken sublingually (under the tongue) get pro-hormones into the bloodstream much better than orally taken capsules since over 90% of orally taken pro-hormones are never utilized by the body.
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