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The Mayo Clinic cites DHEA as a treatment for a remarkable range of conditions, including adrenal insufficiency, depression, obesity, lupus, Alzheimer’s disease, cardiovascular disease, cervical cancer, chronic fatigue syndrome, critical illness, Crohn’s disease, HIV/AIDS, menopausal disorders, infertility, myotonic dystrophy, psoriasis, rheumatoid arthritis, schizophrenia, septicemia, sexual dysfunction, and skin aging, among others. 


DHEA is able to provide such a wide variety of benefits because it is important for the maintenance of almost all the body’s hormones. Hormones are chemicals which act as signals between cells. They pass on instructions which initiate important biological reactions. Proper hormone regulation is vital to optimal performance.

By regulating hormone production and providing material support for low hormone levels, DHEA helps the body take care of itself and maintain normal functioning.

 

(See ingredient listing.)

DHEA (dehydroepiandrosterone) is a hormone secreted by the adrenal glands.  It is used by the body to make testosterone, estrogen, and other hormones.  After the age of 30, however, DHEA levels begin to decrease.  Low DHEA levels have also been found in anorexics, people with kidney disease, type II diabetics, AIDS patients, the adrenal insufficient, vegetarians, and the critically ill.
 
DHEA also has important biological functions itself. Recent experimental and human studies show that DHEA is involved in a large variety of natural processes, including immune function, brain function, bone metabolism, blood lipid metabolism, energy metabolism, the regulation of normal blood sugar and insulin levels, and the maintenance of lean body mass.

DHEA Plus also contains Pregnenolone:

 

Pregnenolone is reported to improve energy levels, vision, memory, clarity of thinking, well-being, and libido. 

Dr. Eugene Roberts, Ph.D., states that pregnenolone “appears to be the most potent memory enhancer yet reported in animals.”  Pregnenolone is often referred to as the “grandparent” of steroid hormones in mammals. Pregnenolone is made from cholesterol in the adrenal glands and to a lesser extent in the brain, liver, skin, testes and ovaries. Once synthesized, pregnenolone is converted to DHEA or to progesterone. Progesterone is used to make cortisol, aldosterone, androstenedione, estrogen, and testosterone.

Pregnenolone may also be secreted directly into the blood, where it performs many actions of its own. Recent studies show that pregnenolone is important for the function of brain, nervous tissue, liver, pancreas, reproductive tissues, pituitary and skin.  Pregnenolone is found in higher concentrations in the central nervous system compared to the peripheral tissues, a factor which may reflect its importance in brain function.

As with DHEA, pregnenolone production declines with age. It is estimated that pregnenolone production is about 60% less at age 75 than at age 35.  Pregnenolone levels may also decline under various conditions of stress, such as acute and chronic infections and trauma.  Supplementation of DHEA and pregnenolone together may assist the body’s natural balance of these hormones and subsequent metabolism.More info.

 

 

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FROM THE MAYO CLINIC'S REPORT ON DHEA

Background:

DHEA (Dehydroepiandrosterone) is an endogenous hormone (made in the human body), and secreted by the adrenal gland. DHEA serves as precursor to male and female sex hormones (androgens and estrogens). DHEA levels in the body begin to decrease after age 30, and are reported to be low in some people with anorexia, end-stage kidney disease, type 2 diabetes (non-insulin dependent diabetes), AIDS, adrenal insufficiency, and in the critically ill. DHEA levels may also be depleted by a number of drugs, including insulin, corticosteroids, opiates, and danazol.

There is sufficient evidence supporting the use of DHEA in the treatment of adrenal insufficiency, depression, induction of labor, and systemic lupus erythematosus.
No studies on the long-term effects of DHEA have been conducted. DHEA can cause higher than normal levels of androgens and estrogens in the body, and theoretically may increase the risk of prostate, breast, ovarian, and other hormone-sensitive cancers. Therefore, it is not recommended for regular use without supervision by a licensed health professional.

Uses for DHEA based on scientific evidence:

Adrenal insufficiency
Several studies suggest that DHEA may improve well-being, quality of life, exercise capacity, sex drive, and hormone levels in people with insufficient adrenal function (Addison's disease). These studies have been small, and better research is needed to provide more definitive answers. Restoring DHEA levels to young adult values in those with partial androgen deficiency seems to benefit the age-related decline in physiological functions but however promising, placebo controlled trials are required to confirm these preliminary results. Adrenal insufficiency is a serious medical condition and should be treated under the supervision of a qualified health care professional.

Depression
The majority of clinical trials investigating the effect of DHEA on depression scores support its use for this purpose under the guidance of a specialist. Further research is needed to confirm these results.

Obesity
The majority of clinical trials investigating the effect of DHEA on weight or fat loss support its use for this purpose. Further research is needed to confirm these results.

Systemic lupus erythematosus
The majority of clinical trials investigating the effect of DHEA for systemic lupus erythematosus, support its use as an adjunct treatment. Further well-designed trials are needed to confirm these results.

Alzheimer's disease
Initial research reports that DHEA does not significantly improve cognitive performance or change symptom severity in patients with Alzheimer's disease, but some disagree. Additional study is warranted in this area.

Bone density
The ability of DHEA to increase bone density is under investigation. Effects are not clear at this time.

Cardiovascular disease
Initial studies report possible benefits of DHEA supplementation in patients with cholesterol plaques ("hardening") in their arteries. There is conflicting scientific evidence regarding the use of DHEA supplements in patients with heart failure or diminished ejection fraction. Other therapies are more proven in this area, and patients with heart failure or other types of heart disease should discuss treatment options with a cardiologist.

Cervical cancer
Initial research reports that the use of intravaginal DHEA may be safe, and may promote regression of low-grade cervical lesions. However, further study is necessary in this area before a firm conclusion can be drawn. Patients should not substitute the use of DHEA for more established therapies, and should discuss management options and follow-up with a primary healthcare professional or gynecologist.

Chronic fatigue syndrome
The scientific evidence remains unclear regarding the effects of DHEA supplementation in patients with chronic fatigue syndrome. Better research is necessary before a clear conclusion can be drawn.

Cocaine withdrawal
Preliminary study shows that DHEA is not beneficial in treating cocaine dependence,but further study is needed before a firm conclusion can be drawn.

Critical illness
Unclear scientific evidence exists surrounding the safety or effectiveness of DHEA supplementation in critically ill patients. At this time, it is recommended that severe illness in the intensive care unit be treated with more proven therapies.

Crohn's disease
Initial research reports that DHEA supplements are safe for short-term use in patients with Crohn's disease. Preliminary research suggests possible beneficial effects, although further research is necessary before a clear conclusion can be drawn.

HIV/AIDS
Although some studies suggest that DHEA supplementation may be beneficial in patents with HIV, results from different studies do not agree with each other. Most research in this area is not well designed or reported. There is currently not enough scientific evidence to recommend DHEA for this condition, and other therapies are more proven in this area.

Menopausal disorders
Many different aspects of menopause have been studied using DHEA as a treatment. When DHEA is applied topically (on the skin) as a cream, it may improve vaginal pain and discomfort associated with menopause. However, it is not clear whether DHEA cream has any benefits in treating osteoporosis after menopause. Early evidence suggests that DHEA may not be an effective treatment for hot flashes or emotional disturbances such as fatigue, irritability, anxiety, depression, insomnia, difficulties with concentration, memory, or decreased sex drive (which may occur near the time of menopause). However, some study results disagree.

Induction of labor
Preliminary evidence, suggests that DHEA may help to induce labor. Further research is needed and people who are pregnant should not self-treat.

Infertility
There are low quality studies that suggest DHEA supplementation may be beneficial in women with ovulation disorders. However, results of research in this area are conflicting, and safety is not established. There is currently not enough scientific evidence to form a clear conclusion about the use of DHEA for this condition.

Myotonic dystrophy
There is conflicting scientific evidence regarding the use of DHEA supplements for myotonic dystrophy. Better research is necessary before a clear conclusion can be drawn.

Psoriasis
Overall study results suggest that DHEA likely offers no benefit to individuals with psoriasis but some disagree. Well-designed clinical trials are required before recommendations can be made.

Rheumatoid arthritis
Preliminary evidence, from a case series, suggests that DHEA likely offers no benefit to individuals with rheumatoid arthritis. Well-designed clinical trials, with appropriate endpoints are required before recommendations can be made.

Schizophrenia
Initial research reports benefits of DHEA supplementation in the management of negative, depressive, and anxiety symptoms of schizophrenia. Some of the side effects from prescription drugs used for schizophrenia may also be relieved. Further study is needed to confirm these results before a firm conclusion can be drawn.

Septicemia (serious bacterial infections in the blood)
Unclear scientific evidence exists surrounding the safety or effectiveness of DHEA supplementation in septic patients. At this time, more proven therapies are recommended.

Sexual function / libido / erectile dysfunction
The results of studies vary on the use of DHEA in erectile dysfunction and sexual function, in both men and women. Better research is necessary before a clear conclusion can be drawn.

Sjogren's syndrome
DHEA showed no evidence of efficacy in Sjogren's syndrome in preliminary study. Without evidence for efficacy, patients with Sjogren's syndrome should avoid using unregulated DHEA supplements, since long-term adverse consequences of exposure to this hormone are unknown.

Skin aging
Preliminary study suggests the possibility of using DHEA topically as an anti-skin aging agent. Further research is needed to confirm these results.

Fibromyalgia (postmenopause)
DHEA does not seem to improve quality of life, pain, fatigue, cognitive function, mood, or functional impairment in fibromyalgia.

NOTES FROM DR ANDREW WEIL IN HIS BOOK, “HEALTHY AGING,” RANDOM HOUSE, JANUARY 2007…..

The hormone DHEA made in the adrenal gland has shown “promise in reversing some of the changes in body composition that accompany aging. It increases bone density and skin thickness and tone, and also decreases abdominal fat in elderly men and women. Abdominal fat is more of a health risk than fat elsewhere in the body because it is associated with metabolic syndrome and increased risk of heart attack and stroke. DHRA can decrease some of the abdominal fat.” It can “improve erectile dysfunction in men and increase the libido in both men and women.” Take 25-50 mg a day. It may take up to six months to see all the benefits. For women who take DHEA, stop taking if changes occur—such as acne or deepening of the voice.

RESEARCH CITATIONS:

The neurosteroid pregnenolone sulfate infused into the medial septum nucleus increases hippocampal acetylcholine and spatial memory in rats.
Author:                       Darnaudery, M : Pallares, M : Piazza, P V : Le Moal, M : Mayo, W
Citation:         Brain-Res. 2002 Oct 4; 951(2): 237-42
Abstract:        The effects of an infusion of the neurosteroid pregnenolone sulfate into the medial septum on acetylcholine release in the hippocampus and on spatial memory were evaluated in two experiments. Results show that pregnenolone sulfate enhanced acetylcholine release by more than 50% of baseline and improved recognition memory of a familiar environment. Therefore, our results suggest that the septo-hippocampal pathway could be involved in the promnesic properties of this neurosteroid.

22R-Hydroxycholesterol protects neuronal cells from beta-amyloid-induced cytotoxicity by binding to beta-amyloid peptide.
Author:                       Yao, Z X : Brown, R C : Teper, G : Greeson, J : Papadopoulos, V
Citation:         J-Neurochem. 2002 Dec; 83(5): 1110-9
Abstract:        22R-hydroxycholesterol, a steroid intermediate in the pathway of pregnenolone formation from cholesterol, was found at lower levels in Alzheimer's disease (AD) hippocampus and frontal cortex tissue specimens compared to age-matched controls. beta-Amyloid (Abeta) peptide has been shown to be neurotoxic and its presence in brain has been linked to AD pathology. 22R-hydroxycholesterol was found to protect, in a dose-dependent manner, against Abeta-induced rat sympathetic nerve pheochromocytoma (PC12) and differentiated human Ntera2/D1 teratocarcinoma (NT2N) neuron cell death. Other steroids tested were either inactive or acted on rodent neurons only.

The effect of 22R-hydroxycholesterol was found to be stereospecific because its enantiomer 22S-hydroxycholesterol failed to protect the neurons from Abeta-induced cell death. Moreover, the effect of 22R-hydroxycholesterol was specific for Abeta-induced cell death because it did not protect against glutamate-induced neurotoxicity. The neuroprotective effect of 22R-hydroxycholesterol was seen when using Abeta1-42 but not the Abeta25-35 peptide. To investigate the mechanism of action of 22R-hydroxycholesterol we examined the direct binding of this steroid to Abeta using a novel cholesterol-protein binding blot assay. Using this method the direct specific binding, under native conditions, of 22R-hydroxycholesterol to Abeta1-42 and Abeta17-40, but not Abeta25-35, was observed.

These data suggest that 22R-hydroxycholesterol binds to Abeta and the formed 22R-hydroxycholesterol/Abeta complex is not toxic to rodent and human neurons. We propose that 22R-hydroxycholesterol offers a new means of neuroprotection against Abeta toxicity by inactivating the peptide.

Expression of steroidogenic acute regulatory protein in cultured Schwann cells and its regulation by cAMP.
Author:                       Benmessahel, Y : Guennoun, R : Cadepond, F : Baulieu, E E : Schumacher, M : Groyer, G
Citation:         Ann-N-Y-Acad-Sci. 2002 Nov; 973: 83-7
Abstract:        In steroidogenic cells the steroidogenic acute regulatory (StAR) protein plays a key role in the transport of cholesterol to the inner mitochondrial membrane, where the first step of steroidogenesis, the conversion of cholesterol to pregnenolone, takes place. cAMP is a known positive regulator of StAR gene expression and steroid biosynthesis in steroidogenic cells. As some steroids, such as progesterone, can also be synthesized de novo in the central and peripheral nervous systems and display neuroprotective and neurotrophic effects, we decided to verify the effect of cAMP on StAR gene expression in cultured Schwann cells. We observed that (1) in the presence of serum, forskolin, an agent known to elevate intracellular cAMP, induced both a morphological change and proliferation of cultured Schwann cells; (2) StAR mRNA and protein were expressed in Schwann cells; (3) unexpectedly, forskolin and 8 Br-cAMP, a cell-permeant analogue of cAMP, extinguishcd StAR gene expression; and (4) this response was similar in the presence or absence of serum.

Evidence for the biosynthesis of DHEA from cholesterol by first-trimester human placental tissue: source of androgens.
Author:                       Loganath, A : Peh, K L : Wong, P C
Citation:         Horm-Metab-Res. 2002 Mar; 34(3): 116-20
Abstract:        With a view to establishing whether first-trimester human placentas possess the ability to synthesize DHEA from cholesterol, homogenates of this tissue obtained from two groups of women undergoing elective termination of normally progressing pregnancy between 10 - 12 weeks gestation (n = 5, age 23 - 29 years and n = 5, age 21 - 27 years) were incubated separately with [26-(14)C]cholesterol for the generation of [14C]isocaproic acid + pregnenolone and [7n-3H]pregnenolone for the biosynthesis of [3H]DHEA. Controls consisted of homogenates heated in a boiling water bath for 10 min. Using the reverse-isotope dilution analysis, desmolase efficiency expressed as mean specific activity of [14C]isocaproic acid varied from 282 to 725 dpm/mmol, while that of 17 alpha-hydroxylase and steroid C-17,20-lyase, catalyzed conversion of [7n-3H]pregnenolone to [3H]DHEA varied from 3498 to 26 258 dpm/mmol. The corresponding efficiencies of enzymicconversion varied between 5.8 x 10( -2) and 1.5 x 10( -1) % for [14C]isocaproic acid, but between 5.5 x 10( -2) and 4.1 x 10( -1) % for [3H]DHEA. No such metabolite was evident in the controls of heat-denatured homogenates. These are the first study results to demonstrate that early placentas are capable of converting cholesterol to pregnenolone to DHEA, contrary to the widely held concept of DHEA production by fetal and maternal adrenal glands. This finding has important physiological implications and could provide a new dimension to the concept of fetoplacental steroidogenesis.

 

PREGNENOLONE: A BRIEF GUIDE

Pregnenolone is a natural hormone that cannot be patented. Back in the 1940's, when researchers started experimenting with the use of pregnenolone, they realized that it could be helpful for people under stress and it could increase energy in those who were fatigued. However, about the same time, cortisol, another closely related hormone, was discovered. Cortisol stole the limelight. When cortisol was given to individuals with rheumatoid arthritis, there were outstanding short-term improvements.

Photographs of these remarkable recoveries were circulated and the medical community was impressed. Scientists basically put pregnenolone aside to focus on cortisol. The structure of cortisol was altered to make similar molecules such as dexamethasone and prednisone, much more powerful steroids. Dexamethasone and other similar corticosteroids could be patented, and thus a pharmaceutical company could make a lot of money.

Pregnenolone has stayed in relative obscurity since the 1940's, with only rare mentions in the medical literature. There have only been a few studies published on pregnenolone in recent years, and only a couple involve human subjects.

BENEFITS OF PREGNENOLONE
Some people find pregnenolone improves energy levels, vision, memory, clarity of thinking, wellbeing, and often sexual enjoyment or libido. Pregnenolone may be considered a good brain enhancer in those who are deficient. Studies in rodents show pregnenolone to be one of the most effective and powerful memory boosters. Pregnenolone may increase levels of acetylcholine in the hippocampus and other memory regions in the brain.  Some women report lessening of hot flashes or premenstrual symptoms. However, pregnenolone is not risk-free.

POSSIBLE PREGNENOLONE SIDE EFFECTS

Overstimulation and insomnia -- low doses could be helpful for sleep when taken in the morning.

Irritability, anger or anxiety -- low doses could actually ease a person into a relaxed feeling, while higher amounts may lead to irritability.

Acne

Headaches

Possible scalp hair loss if used daily for prolonged periods. Pregnenolone converts into DHEA, which in turn converts into testosterone and possibly on to DHT. Pregnenolone also can be converted into progesterone.

Irregularities of heart rhythm, HEART PALPITATIONS, even on as low a dose as 10 mg

Unknown effects on the thyroid gland or other organs and tissues.

Dr. Sahelian says: "I do not feel comfortable with the high dosages of DHEA and pregnenolone sold over the counter. I think a maximum of 5 mg is acceptable. Hormones are powerful substances that have significant short and long-term effects. They can be very helpful if used appropriately but can cause serious harm if misused. One of the side effects is heart palpitations or arrhythmias. Use hormones in low doses and for short periods of time. Take frequent breaks which I call hormone holidays."


REFERENCES

Barrett-Connor E, Ferrara A. Dehydroepiandrosterone, dehydroepiandrosterone sulfate, obesity, waist-hip ratio, and noninsulin-dependent diabetes in postmenopausal women: the
Rancho Bernardo Study. J Clin Endocrinol Metab 1996;81:59-64.

Barrett-Connor E, Kritz-Silverstein D, Edelstein SL. A prospective study of dehydroepiandrosterone sulfate (DHEAS) and bone mineral density in older men and women. Am J Epidemiol 1993;137:201-206.

Berdanier CD, Parente JA, Jr., McIntosh MK. Is dehydroepiandrosterone an antiobesity agent? FASEB J 1993;7:414-419.

Daynes RA, Araneo BA, Ershler WB, Maloney C, Li GZ, Ryu SY. Altered regulation of IL-6 production with normal aging. Possible linkage to the age-associated decline in dehydroepiandrosterone and its sulfated derivative. J Immunol 1993;150:5219-5230.

De Pergola G, Triggiani V, Giorgino F, et al. The free testosterone to dehydroepiandrosterone sulphate molar ratio as a marker of visceral fat accumulation in premenopausal obese women. Int J Obes Relat Metab Disord 1994;18:659-664.

De Pergola G, Cospite MR, Giagulli VA, et al. Insulin-like growth factor-1 (IGF-1) and dehydroepiandrosterone sulphate in obese women. Int J Obes Relat Metab Disord 1993;17:481-483.

De Pergola G, Giagulli VA, Garruti G, et al. Low
dehydroepiandrosterone circulating levels in premenopausal obese women with very high body mass index. Metabolism 1991;40:187-190.

Hall GM, Perry LA, Spector TD. Depressed levels of dehydroepiandrosterone sulphate in postmenopausal women with rheumatoid arthritis but no relation with axial bone density. Ann Rheum Dis 1993;52:211-214.

Herranz L, Megia A, Grande C, Gonzalez-Gancedo P, Pallardo F. Dehydroepiandrosterone sulphate, body fat distribution and insulin in obese men. Int J Obes Relat Metab Disord 1995;19:57-60.

Ishihara F, Komatsu M, Yamada T, et al. Role of dehydroepiandrosterone and dehydroepiandrosterone sulfate for the maintenance of axillary hair in women. Horm Metab Res 1993;25:34-36.

Jakubowicz DJ, Beer NA, Beer RM, Nestler JE. Disparate effects of weight reduction by diet on serum dehydroepiandrosterone-sulfate levels in obese men and women. J Clin Endocrinol Metab 1995;80:3373-3376.

Leblhuber F, Neubauer C, Peichl M, et al. Age and sex differences of dehydroepiandrosterone sulfate (DHEAS) and cortisol (CRT) plasma levels in normal controls and Alzheimer's disease (AD). Psychopharmacology (Berl) 1993;111:23-26.

Legrain S, Berr C, Frenoy N, Gourlet V, Debuire B, Baulieu EE. Dehydroepiandrosterone sulfate in a long-term care aged population. Gerontology 1995;41:343-351.

Miklos S. Dehydroepiandrosterone sulphate in the diagnosis of osteoporosis. Acta Biomed Ateneo Parmense 1995;66:139-146.

Montanini V, Simoni M, Chiossi G, et al. Age-related changes in plasma dehydroepiandrosterone sulphate, cortisol, testosterone and free testosterone circadian rhythms in adult men. Horm Res 1988;29:1-6.

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.

Nestler JE, Clore JN, Blackard WG. Dehydroepiandrosterone: the "missing link" between hyperinsulinemia and atherosclerosis? FASEB J 1992;6:3073-3075.

Nordin BE, Robertson A, Seamark RF, et al. The relation between calcium absorption, serum dehydroepiandrosterone, and vertebral mineral density in postmenopausal women. J Clin Endocrinol Metab 1985;60:651-657.

Orentreich N, Brind JL, Vogelman JH, Andres R, Baldwin H. Longterm longitudinal measurements of plasma dehydroepiandrosterone sulfate in normal men. J Clin Endocrinol Metab 1992;75:1002-1004.

Smith CP, Dunger DB, Williams AJ, et al. Relationship between insulin, insulin-like growth factor I, and dehydroepiandrosterone sulfate concentrations during childhood, puberty, and adult life. J Clin Endocrinol Metab 1989;68:932-937.

Szathmari M, Szucs J, Feher T, Hollo I. Dehydroepiandrosterone sulphate and bone mineral density. Osteoporos Int 1994;4:84-88.

Taelman P, Kaufman JM, Janssens X, Vermeulen A. Persistence of increased bone resorption and possible role of dehydroepiandrosterone as a bone metabolism determinant in osteoporotic women in late postmenopause. Maturitas 1989;11:65-73.

Usiskin KS, Butterworth S, Clore JN, et al. Lack of effect of dehydroepiandrosterone in obese men. Int J Obes 1990;14:457-463.

 

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anti-aging properties of DHEA

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