Life Extension Magazine®

Active couple supplementing with DHEA at danger from congress ban

Congress Seeks to Ban DHEA

A bill in Congress would outlaw DHEA by re-classifying it as an “anabolic steroid drug.” Life Extension reveals why DHEA is not a steroid drug and how depriving Americans of DHEA’s anti-aging benefits would be a windfall for drug companies.

Scientifically reviewed by Dr. Gary Gonzalez, MD, in August 2023. Written by: William Faloon.

A bill has been introduced in Congress that would classify DHEA as an “anabolic steroid drug” and thus make it illegal for Americans to obtain.

DHEA, however, is not an anabolic steroid drug. It is a natural hormone that declines as people mature past the age of 30.

Low DHEA levels have been related with degenerative conditions associated with aging.1-28 A large volume of published scientific studies reveals that supplemental DHEA can provide unique health benefits.29-62

For more than a decade, DHEA has been sold as a dietary supplement. The availability of DHEA supplements has enabled many aging Americans to avoid the risks associated with declining DHEA levels. It is in the financial interests of pharmaceutical companies to have DHEA banned so that aging people will have to rely instead on expensive prescription drugs.

If Congress is persuaded by drug lobbyists to outlaw DHEA supplements, more Americans will become vulnerable to declining DHEA levels, resulting in an economic bonanza for pharmaceutical companies.

In this report, we expose shocking facts behind this new attack on DHEA so that citizens will be armed with the information they need to dissuade Congress from prohibiting this lifesaving hormone.

On March 5, 2007, legislation was introduced that would add dehydroepiandrosterone, or DHEA, to the list of anabolic steroids that are classified as controlled substances under the Anabolic Steroid Control Act.63

DHEA, a natural hormone, does not function like muscle-building anabolic steroid drugs. In fact, no scientific studies indicate that DHEA increases muscle mass in young men with already-adequate DHEA levels.

To frighten the public into thinking that DHEA poses a danger, a blatantly false press release is now circulating in Congress. Here is an excerpt from this press release:“Like all steroids, DHEA has a number of potential long-term physical and psychological effects, including heart disease, cancer, stroke, liver damage, severe acne, baldness, dramatic mood swings, and aggression.” 64

As you will read next, these allegations are totally inconsistent with the scientific literature. Even more disturbing is that a basis for this new attack on DHEA comes from those who have a huge financial interest in turning DHEA into an expensive prescription drug.

DHEA Protects Against Heart Disease—It Does Not Cause It!

Drugs to prevent and treat heart disease generate more profit for pharmaceutical companies than any other class of medication. The use of DHEA as a dietary supplement has been increasing as new studies reveal that DHEA might reduce heart attack risk.7-10,12,26,27,65-69 Pharmaceutical companies thus face huge economic losses if too many Americans use low-cost DHEA supplements and reduce their reliance on expensive cardiac drugs.

To give you an idea of the magnitude of loss faced by drug companies, a study published in October 2006 showed that higher DHEA levels resulted in improved ejection fractions (a measurement of the heart’s pumping capacity) and lower levels of a blood marker that indicates serious congestive heart failure.26

This same study analyzed the relationship of DHEA, free testosterone, and insulin-like growth factor-1 (IGF-1) to mortality in men suffering from chronic heart failure. The chart below reveals the startling results when these three hormones were correlated with three-year survival:

Hormone Status Three-Year Survival
High levels of
DHEA, testosterone,
and IGF-1
Deficiency in one
hormone (DHEA,
, or IGF-1)
Deficiency in two
hormones (DHEA,
, or IGF-1)
Deficiency in all
three hormones (DHEA,
, and IGF-1)

The doctors who conducted this study concluded that a deficiency in any of these hormones is “an independent marker of poor prognosis.”

Based on this one study alone, pharmaceutical companies stand to earn billions of dollars of additional profits from cardiac drugs if Congress bans DHEA supplements.

Pharmaceutical lobbying has already curtailed Americans’ access to inexpensive ways to boost testosterone and IGF-1, though certain nutrients have been shown to boost IGF-1 and testosterone in some studies.53,68,70

Cardiac Dangers Associated with Low DHEA

Epidemiological studies show that low levels of DHEA in men correlate with a higher risk of cardiovascular disease. The Massachusetts Male Aging Study followed 1,700 men between the ages of 40 and 70 for nine years. The authors found that men in the lowest quartile of serum DHEA at baseline were 60% more likely to develop ischemic heart disease, suggesting a valuable role for DHEA in averting the nation’s leading cause of death.9

Additionally, higher DHEA levels seem to positively affect endothelial cell signaling, which could have important implications for avoiding heart disease. In a subset of men from the Baltimore Longitudinal Study of Aging, levels of hormones (including DHEA) were measured and correlated with arterial stiffness (using ultrasound imaging of the carotid arteries). Men with higher levels of testosterone and DHEA had less stiffness of the arteries, indicating a decreased risk of cardiovascular events such as heart attacks.65

A similar link between low serum DHEA levels and greater risk for carotid artery disease was demonstrated last year in a study of young women with polycystic ovary syndrome, a condition associated with an increased risk of cardiovascular disease and metabolic syndrome.71

Sen. Hatch to Oppose DHEA Ban

Sen. Orrin Hatch (R-UT), who was instrumental in the passage of the 1994 Dietary Supplement and Health Education Act (DSHEA) and remains one of Congress’ staunchest advocates of health freedom, told Life Extension that he opposes S. 762 and other efforts to re-classify DHEA as an anabolic steroid.

According to Hatch, the proposed legislation “specifically overturns the exemption we made for DHEA.” The senator notes that DHEA was exempted from the list of banned anabolic steroids under DSHEA because “there is no evidence that DHEA has posed any health problem.”

“In fact, [DHEA] is being used safely by many Americans who recognize its potential,” says Sen. Hatch. “I’ll be working to make certain the Senate does not pass this unwise bill.”

A study in animals in 2006 shed further light on how DHEA promotes cardiovascular health.66 Researchers fed young and old female mice a daily DHEA supplement. After 60 days of treatment, the investigators measured the stiffness of the test animals’ left ventricle, the heart’s major pumping chamber. The DHEA-supplemented older mice had decreased left ventricular stiffness compared to the non-supplemented older animals.

The scientists concluded that DHEA supplementation is capable of reversing the left ventricular stiffness that accompanies aging, thus promoting youthful structure and function in the heart’s tissues.

Another animal study simulated the depressed cardiovascular function (shock) that follows major trauma.72 In response to administration of a DHEA metabolite, the depression of cardiovascular function and organ blood flow induced by shock was reversed. The dangerous inflammatory cytokine interleukin-6 (IL-6), which had been elevated in the state of simulated shock, was also reduced by this DHEA metabolite. The investigators concluded that treatment with this metabolite could be valuable in restoring cardiovascular function and correcting abnormal cytokine levels.

Furthermore, investigators determined that DHEA injected directly into the coronary arteries of pigs produced acute dilation of the blood vessels, with associated increases in coronary blood flow.67

DHEA Protects Against Atherogenic Risk Factors

A number of studies indicate that DHEA helps protect aging adults against atherosclerosis and its life-threatening consequences, such as coronary artery dis-ease.7-10,26,27,31,32,65,68,69,73-75 Several mechanisms of action may account for these benefits.

In a controlled trial, 24 older men orally ingested 50 mg of DHEA or a placebo at bedtime for two months. The researchers then measured arterial dilation and blood flow. While the placebo-treated subjects had no changes in any of the parameters measured, the DHEA-treated men experienced increased levels of a substance that helps blood vessels to dilate, as well as decreasing levels of a marker for blood clotting. They also had lower levels of artery-clogging low-density lipoprotein (LDL) after treatment than did the controls. Based on the beneficial effects of short-term DHEA treatment, the researchers concluded that long-term DHEA supplementation may prevent atherosclerotic changes caused by falling levels of vessel-dilating biochemicals.68

Of the many tactics that can be deployed to increase one’s life span, supplementing with DHEA seems particularly beneficial, as new findings imply that higher levels of DHEA are associated with a longer life span.4

Scientists recently examined data on nearly 1,000 older Taiwanese adults to determine the relationship between DHEA levels and three-year mortality risk.

At the study’s end three years later, the data analysis revealed that participants with lower DHEA levels had a 64% greater risk of death than did individuals with higher DHEA levels. The study authors concluded that lower levels of DHEA have a notable effect in increasing mortality risk, and that optimal DHEA levels may help to promote longevity.4

The press release attacking DHEA that is now circulating in Congress states that DHEA use is associated with heart disease. This is a blatantly false allegation, as can be clearly seen by examining published scientific studies showing that DHEA most likely protects against heart disease.7-9, 26,27,65-69

Higher DHEA Levels Tied to Lower Mortality Risk

Of the many tactics that can be deployed to increase one’s life span, supplementing with DHEA seems particularly beneficial, as new findings imply that higher levels of DHEA are associated with a longer life span.4

Scientists recently examined data on nearly 1,000 older Taiwanese adults to determine the relationship between DHEA levels and three-year mortality risk.

At the study’s end three years later, the data analysis revealed that participants with lower DHEA levels had a 64% greater risk of death than did individuals with higher DHEA levels. The study authors concluded that lower levels of DHEA have a notable effect in increasing mortality risk, and that optimal DHEA levels may help to promote longevity.4

The press release attacking DHEA that is now circulating in Congress states that DHEA use is associated with heart disease. This is a blatantly false allegation, as can be clearly seen by examining published scientific studies showing that DHEA most likely protects against heart disease.7-9, 26,27,65-69

DHEA Protects the Brain—It Does Not Cause Stroke!

DHEA is especially abundant in the human brain. Many earlier stud-ies reported a protective effect of DHEA against the deterioration of mental function with aging.21,51,56-58,76-81 Those stricken with Alzheimer’s and other neurodegenerative diseases, for instance, have lower levels of DHEA.79,80 A recent Canadian study found that rats implanted with a high dose of DHEA showed significantly less hippocampal damage after stroke was induced (88% injured neurons in the placebo group compared to only 60% in those given DHEA).81

It has been demonstrated that DHEA markedly inhibits the inflammatory cytokines tumor necrosis factor-alpha (TNF-alpha) and IL-6 in glial cells.82 The ability to lower the levels of these inflammatory mediators may be an important part of the neuroprotective mechanism of DHEA.

In addition, DHEA has been shown to protect against the toxicity of the amyloid-beta protein and excess glutamate.76 Treatment with glutamate produced a copious increase in the neuronal glucocorticoid receptor. Treatment with DHEA reversed this increase, demonstrating the anti-glucocorticoid action of DHEA.

A study conducted in Cambridge, England, compared DHEA and cortisol levels in clinically depressed patients (categorized as “major depressives”) with a matched group of patients in remission from depression and healthy controls.21 Both morning and evening levels of DHEA were lowest in depressed patients. Depressed patients showed low DHEA relative to high cortisol levels (similar to the ratio shift seen in aging). The authors point out that DHEA not only protects against harmful effects of excess cortisol, but also may have mood-improving properties and that this may have “significant implications” for the treatment of depression.52,83-92

DHEA’s ability to protect the hippocampus and enhance its activity is important in regard to Alzheimer’s disease. Studies have generally found increased cortisol and lower DHEA in Alzheimer’s disease patients.80 Excess cortisol damages the hippocampus and potentiates amyloid-beta toxicity.80 DHEA is believed to be able to antagonize the destructive effects of excess cortisol.83,93,94

The authors of a recent study have concluded that dementia is correlated with low DHEA more so than with high cortisol.80 Another study also showed that while normal aging results in decreased DHEA levels, victims of dementia have even lower levels of DHEA than do the healthy elderly.95

DHEA is protective against a wide range of neurological disorders.21,51,52,56-58,76-78,80,81,96-98 DHEA has never been shown to increase stroke risk, as the bogus press release circulating in Congress alleges.

Congress Seeks To Ban DHEA: What You Need to Know
  • A bill recently introduced in Congress would classify the popular supplement dehydroepiandroesterone (DHEA) as an anabolic steroid drug. If the proposed bill becomes law, DHEA would be regulated as a controlled substance and would no longer be readily available as a nutritional supplement.
  • DHEA is not an anabolic steroid drug, but rather a natural hormone that is essential for good health. Since DHEA levels in the human body decline after the age of 30, many people rely on DHEA supplements to combat diseases associated with aging.
    A wealth of research demonstrates that optimal DHEA levels can help protect against heart disease, cognitive decline, and premature death.
  • Those seeking to ban DHEA claim
    that it causes many adverse effects in the body, including mood swings and liver toxicity. However, no substantial scientific evidence exists to support these claims; in fact, in the more than 10 years that DHEA has been available as a dietary supplement, there have been no reports of serious adverse health effects related to DHEA.
  • If DHEA becomes a controlled substance, Americans will have lost a valuable weapon for averting the diseases of aging. To preserve your freedom to use DHEA and other dietary supplements, contact your Senators and Representative and urge them to vote against Senate bill S.762 and House bill H.R.1249.

Animal Study Data Misused to Discredit DHEA’s Well-Established Safety Profile

One way scientists evaluate for toxicity is to have animals consume large amounts of a compound and then carefully assess them for organ damage. However, different animal models need to be used in different situations—a “one-size-fits-all” approach makes for bad science.

One such example is the use of animal models to assess for liver toxicity with compounds that are peroxisome proliferators. Peroxisome proliferators are potent rat carcinogens in the liver. However, this experimental model is not valid to assess human liver toxicity for these types of compounds.

There are significant species differences in response to peroxisome proliferators. Rats and mice are very sensitive to the toxic effects of these compounds, but peroxisome proliferators do not produce toxicity in species like guinea pigs, monkeys, and humans at dose levels that produce a dramatic toxic response in rodents.99

Scientists have published research papers indicating that peroxisome proliferators do not pose a liver toxicity risk to human beings. One researcher noted, “it is reasonable to conclude that the encountered levels of exposure to these non-genotoxic agents (peroxisome proliferators) do not present a hepatocarcinogenic hazard to humans.”100

Since DHEA is a peroxisome proliferator, it comes as no surprise that liver damage ocurred when scientists administered huge doses of a well-known carcinogen, N-nitrosomorpholine, and huge doses of DHEA in the diets of lab rats, roughly the human equivalent of 6774 mg of DHEA daily! Contrast this enormous amount of DHEA with the typical 15-75 mg per day of DHEA used by healthy aging humans.101

Valid animal models that have been used to assess the liver toxicity risk of DHEA in humans have found no evidence of liver injury or toxicity. For example, a study showed that rats and mice given large amounts of DHEA in the diet displayed increased liver enzyme levels associated with lipid accumulation in rodent liver, but no such increase was shown in guinea pigs.102 Another study showed evidence of increased liver enzyme levels when DHEA was administered to mice at a human-equivalent dose of about 1700 mg per day of DHEA. However, in guinea pigs, a valid animal species for comparison to humans in this context, there was no evidence of toxicity at a human-equivalent dose of over 4500 mg per day of DHEA.103

Even ignoring the fact that rats and mice are invalid models to assess for liver toxicity risk in humans with supplements like DHEA, and ignoring the fact that appropriate animal models for extrapolation to humans do not show any evidence of liver injury risk with DHEA, the rat-mouse DHEA studies on liver toxicity use enormous amounts of DHEA—doses equivalent to 130 times the average 50 mg of DHEA per day used by healthy adults.

It is ludicrous to suggest that DHEA be banned on the basis of invalid animal models that use human-equivalent doses of DHEA that are more than 100 times greater than those used by healthy adults. An important study in JAMA in 2006 showed signs of liver damage in patients who consumed 4 grams daily of Tylenol® (acetaminophen) for two weeks.104 This means that taking two Extra Strength Tylenol® caplets, four times daily, can generate evidence of liver damage. Yet the misleading press release being circulated in Congress suggests that DHEA should be outlawed because it causes “liver damage.” This is an egregious distortion of the facts—especially when there are no reported human cases of liver damage caused by DHEA in the scientific literature.

DHEA Can Cause Acne in Women— When the Dose Is Too High

Women tend to require less DHEA than men. When a woman takes too much DHEA, acne can result, but this dissipates when the DHEA dose is lowered.

We at Life Extension have never heard of “severe acne” being caused by DHEA, as the biased press release being circulated in Congress asserts. If the worst that can happen to women is temporary acne in response to excessive intake of DHEA, this would appear to be a small price to pay in relation to the multiple health benefits DHEA has been shown to confer.

The potential acne effect of DHEA on women has been long known, and women usually stay at moderate 15-50 mg/day DHEA doses and avoid acne altogether.

DHEA Does Not Cause Hair Loss

We could find no reports that DHEA causes hair loss. While one could propose a theoretical basis that somehow orally ingested DHEA would increase dihydrotestosterone (DHT) enough to promote hair loss, there is no evidence to show that this has ever actually happened.

If DHEA were to increase dihydrotestosterone, the solution would be to take a 5-alpha reductase inhibitor (like low-dose Proscar®) or possibly saw palmetto extract to block this effect.

DHEA Does Not Cause “Wild Mood Swings and Aggressiveness”

DHEA’s role as an antidepressant has been rigorously examined for years. During these many trials, researchers routinely found that when taken daily, DHEA supplements effectively reduced depressive episodes and enhanced mood. In fact, according to one major study in the UK, as many as 67% of men and 82% of women reported a noticeable decrease in their depressive symptoms while taking as little as 25 mg per day of DHEA.65 In addition, women suffering from adrenal insufficiency have reported an improved sense of well-being and an associated increase in both sexual interest and sexual satisfaction while taking DHEA.50

Sexual function is closely linked with emotional health and well-being, and scientists now know that DHEA levels are strongly associated with healthy sexual function. Two recent studies found that sexual function105 and overall self-reported health and functional status106 were better among women with relatively high levels of DHEA. Even low-dose DHEA supplementation may be effective in providing these benefits. For example, in a group of women with systemic lupus erythematosus, daily doses of DHEA as low as 20-30 mg improved health-related quality of life and sexual interest and activity compared to placebo.61 Other researchers have reported notable improvements in libido and mood in women who supplemented with DHEA.107,108

Even more promising are studies suggesting that, in addition to its positive impact on depression and sexual function, DHEA may help to manage symptoms of schizophrenia. Based on their preliminary findings demonstrating DHEA’s efficacy in reducing symptoms of schizophrenia,84 researchers further noted improvement in illness severity and anxiety in a group of schizophrenic patients who received DHEA in addition to their anti-psychotic medications.97 The study authors attributed this specific anxiety-reducing effect to DHEA’s influence on the brain’s GABA receptors, which are central to regulating mood.97

To characterize DHEA as causing “wild mood swings and aggressiveness,” as was done in the press release circulating in Congress, is the exact opposite of the beneficial psychological effects that DHEA exerts on the body.

DHEA and Cancer

No human study in which DHEA was administered as a supplement or drug has ever shown that it causes cancer. Petri dish and live animal studies show that DHEA may protect against certain cancers.41-46,109-145 Human studies that measure DHEA blood levels and correlate them to future cancer risk are contradictory and not representative of the DHEA protocols used by health-conscious people today.

Why Laypeople Confuse DHEA with Synthetic Steroid Drugs

DHEA is produced mainly in the adrenal glands and serves as a natural precursor and balancer to many hormones in the body. While DHEA is defined as a “steroidal hormone,” that does not equate to an “anabolic steroid drug.”

By way of example, the bioactive form of vitamin D in the blood (calcitriol) is a “steroid hormone,” but no one is yet suggesting that vitamin D be banned. In fact, both vitamin D and DHEA are synthesized from cholesterol, the most common sterol found in the body.

DHEA exerts very weak androgenic (testosterone-like) and estrogenic (estrogen-like) activity, and can be converted into metabolites, depending on the body’s need and hormone balance.146 Under normal conditions, the conversion of DHEA to testosterone is tightly controlled by the body. DHEA has been consistently shown to not influence testosterone levels in young men.147-149

If DHEA did function as an anabolic androgenic steroid, then aging men would not be seeking prescription testosterone drugs to reverse certain symptoms of aging.

Since medical science defines DHEA as a “steroidal hormone,” some lawmakers in Congress now think it should be classified as a “controlled substance” and removed from the marketplace. This is quite an allegation when one considers that DHEA has been freely sold in the United States for over 10 years, with no reports of serious adverse events.

The problem is that members of Congress are not scientists, and they are unable to differentiate between natural steroidal substances in the body (such as cholesterol, vitamin D, and DHEA) and the synthetic anabolic steroid drugs that are abused by some bodybuilders.

What Is an “Anabolic Steroid Drug”?

According to the United States government’s own Medline Medical Dictionary, an anabolic steroid is defined as:

“Any of a group of usually synthetic hormones that are derivatives of testosterone, are used medically especially to promote tissue growth, and are sometimes abused by athletes to increase the size and strength of their muscles and improve endurance.” (Medline-March 12, 2007)150

Based on the government’s own definition of “anabolic steroid,” DHEA does not fit into this category. Controlled clinical trials indicate that its use in young adults does not result in performance-related gains, and it is not associated with the myriad side effects that accompany anabolic steroid abuse.147-149,151-153 DHEA is sold as a natural (not synthetic) hormone and is not a derivative of testosterone.154

Anabolic steroid drug abuse is purported to result in cardiovascular conditions such as hypertension, atherosclerosis, and blood clotting, liver conditions such as jaundice and hepatic carcinoma, tendon damage, reduced fertility and breast enlargement (in males), and adverse psychological and behavioral effects. DHEA does not exert these effects.155,156

Moreover, surveys of weightlifters and other athletes conducted by Harvard University researchers show that DHEA is rarely used to increase muscle size or strength or to improve endurance.157 Therefore, the notion that DHEA is in any way comparable to controlled anabolic steroid drugs is scientifically unfounded and legally invalid.

Let Your Voice Be Heard on Capitol Hill

There is at least one pharmaceutical company lobbyist for each member of Congress. Drug lobbyists function solely to persuade Congress to enact laws that make pharmaceutical companies more money. They have no interest in protecting the American public’s health.

If DHEA is classified as a “controlled substance,” pharmaceutical companies stand to earn enormous profits from the drugs Americans will need to treat disorders as diverse as:

  • Type II diabetes
  • Hypertension
  • Depression
  • Coronary and systemic atherosclerosis
  • Osteoporosis
  • Chronic inflammation.

Members of Congress have been victimized by a misinformation campaign designed to disparage DHEA for the purpose of having it reclassified as an “anabolic steroid drug.” Consumers must rally to overcome this deceptive attempt to deny Americans continued access to this scientifically validated supplement safely used by millions of Americans each day.

Another troublesome aspect about this charade to discredit DHEA is that it could provide a springboard for pharmaceutical companies to attack other supplements that compete against their drug sales. So whether you use DHEA or not, the hoax being perpetrated in Congress is a genuine threat to health freedom across the board.

The Senate bill that seeks to ban DHEA is S.762. The companion House bill is H.R.1249. To register your opposition to these bills, call 1-202-224-3121.

To write your Senators and Representative, use the form letter on page 35 following the scientific references for this article, or log on to to conveniently send this letter via email to your members of Congress.



1. Ravaglia G, Forti P, Maioli F, et al. The relationship of dehydroepiandrosterone sulfate (DHEAS) to endocrine-metabolic parameters and functional status in the oldest-old. Results from an Italian study on healthy free-living over-ninety-year-olds. J Clin Endocrinol Metab. 1996 Mar;81(3):1173-8.

2. Ravaglia G, Forti P, Maioli F, et al. Dehydroepiandrosterone-sulfate serum levels and common age-related diseases: results from a cross-sectional Italian study of a general elderly population. Exp Gerontol. 2002 May;37(5):701-12.

3. Celec P, Starka L. Dehydroepiandrosterone—is the fountain of youth drying out? Physiol Res. 2003;52(4):397-407.

4. Glei DA, Goldman N. Dehydroepiandrosterone sulfate (DHEAS) and risk for mortality among older Taiwanese. Ann Epidemiol. 2006 Jul;16(7):510-5.

5. Mazat L, Lafont S, Berr C, et al. Prospective measurements of dehydroepiandrosterone sulfate in a cohort of elderly subjects: relationship to gender, subjective health, smoking habits, and 10-year mortality. Proc Natl Acad Sci USA. 2001 Jul 3;98(14):8145-50.

6. Stahl F, Schnorr D, Pilz C, Dorner G. Dehydroepiandrosterone (DHEA) levels in patients with prostatic cancer, heart diseases and under surgery stress. Exp Clin Endocrinol. 1992;99(2):68-70.

7. Thijs L, Fagard R, Forette F, Nawrot T, Staessen JA. Are low dehydroepiandrosterone sulphate levels predictive for cardiovascular diseases? A review of prospective and retrospective studies. Acta Cardiol. 2003 Oct;58(5):403-10.

8. Herrington DM. Dehydroepiandrosterone and coronary atherosclerosis. Ann NY Acad Sci. 1995 Dec 29;774:271-80.

9. Feldman HA, Johannes CB, Araujo AB, et al. Low dehydroepiandrosterone and ischemic heart disease in middle-aged men: prospective results from the Massachusetts Male Aging Study. Am J Epidemiol. 2001 Jan 1;153(1):79-89.

10. Khalil A, Fortin JP, LeHoux JG, Fulop T. Age-related decrease of dehydroepiandrosterone concentrations in low density lipoproteins and its role in the susceptibility of low density lipoproteins to lipid peroxidation. J Lipid Res. 2000 Oct;41(10):1552-61.

11. Thomas N, Morris HA, Scopacasa F, Wishart JM, Need AG. Relationships between age, dehydro-epiandrosterone sulphate and plasma glucose in healthy men. Age Ageing. 1999 Mar;28(2):217-20.

12. Kapoor D, Malkin CJ, Channer KS, Jones TH. Androgens, insulin resistance and vascular disease in men. Clin Endocrinol (Oxf). 2005 Sep;63(3):239-50.

13. Haden ST, Glowacki J, Hurwitz S, Rosen C, LeBoff MS. Effects of age on serum dehydroepiandrosterone sulfate, IGF-I, and IL-6 levels in women. Calcif Tissue Int. 2000 Jun;66(6):414-8.

14. Paolisso G, Ammendola S, Rotondi M, et al. Insulin resistance and advancing age: what role for dehydroepiandrosterone sulfate? Metabolism. 1997 Nov;46(11):1281-6.

15. Kameda W, Daimon M, Oizumi T, et al. Association of decrease in serum dehydroepiandrosterone sulfate levels with the progression to type 2 diabetes in men of a Japanese population: the Funagata Study. Metabolism. 2005 May;54(5):669-76.

16. Beishuizen A, Thijs LG, Vermes I. Decreased levels of dehydroepiandrosterone sulphate in severe critical illness: a sign of exhausted adrenal reserve? Crit Care. 2002 Oct;6(5):434-8.

17. Aydin T, Karacan I, Demir SE, Sahin Z. Bone loss in males with ankylosing spondylitis: its relation to sex hormone levels. Clin Endocrinol (Oxf). 2005 Oct;63(4):467-9.

18. Osmanagaoglu MA, Okumus B, Osmanagaoglu T, Bozkaya H. The relationship between serum dehydroepiandrosterone sulfate concentration and bone mineral density, lipids, and hormone replacement therapy in premenopausal and postmenopausal women. J Womens Health (Larchmt). 2004 Nov;13(9):993-9.

19. Szathmari M, Szucs J, Feher T, Hollo I. Dehydroepiandrosterone sulphate and bone mineral density. Osteoporos Int. 1994 Mar;4(2):84-8.

20. Heinz A, Weingartner H, George D, et al. Severity of depression in abstinent alcoholics is associated with monoamine metabolites and dehydroepiandrosterone-sulfate concentrations. Psychiatry Res. 1999 Dec 20;89(2):97-106.

21. Michael A, Jenaway A, Paykel ES, Herbert J. Altered salivary dehydroepiandrosterone levels in major depression in adults. Biol Psychiatry. 2000 Nov 15;48(10):989-95.

22. Basar MM, Aydin G, Mert HC, et al. Relationship between serum sex steroids and Aging Male Symptoms score and International Index of Erectile Function. Urology. 2005 Sep;66(3):597-601.

23. Muller M, Grobbee DE, den T, I, Lamberts SW, van der Schouw YT. Endogenous sex hormones and metabolic syndrome in aging men. J Clin Endocrinol Metab. 2005 May;90(5):2618-23.

24. Genazzani AR, Inglese S, Lombardi I, et al. Long-term low-dose dehydroepiandrosterone replacement therapy in aging males with partial androgen deficiency. Aging Male. 2004 Jun;7(2):133-43.

25. Khorram O, Vu L, Yen SS. Activation of immune function by dehydroepiandrosterone (DHEA) in age-advanced men. J Gerontol A Biol Sci Med Sci. 1997 Jan;52(1):M1-M7.

26. Jankowska EA, Biel B, Majda J, et al. Anabolic deficiency in men with chronic heart failure: prevalence and detrimental impact on survival. Circulation. 2006 Oct 24;114(17):1829-37.

27. Moriyama Y, Yasue H, Yoshimura M, et al. The plasma levels of dehydroepiandrosterone sulfate are decreased in patients with chronic heart failure in proportion to the severity. J Clin Endocrinol Metab. 2000 May;85(5):1834-40.

28. Sacco M, Valenti G, Corvi MP, Wu FC, Ray DW. DHEA, a selective glucocorticoid receptor antagonist: its role in immune system regulation and metabolism. J Endocrinol Invest. 2002;25(10 Suppl):81-2.

29. Roberts E. The importance of being dehydroepiandrosterone sulfate (in the blood of primates): a longer and healthier life? Biochem Pharmacol. 1999 Feb 15;57(4):329-46.

30. Williams JR. The effects of dehydroepiandrosterone on carcinogenesis, obesity, the immune system, and aging. Lipids. 2000 Mar;35(3):325-31.

31. Valenti G, Denti L, Maggio M, et al. Effect of DHEAS on skeletal muscle over the life span: the InCHIANTI study. J Gerontol A Biol Sci Med Sci. 2004 May;59(5):466-72.

32. Jesse RL, Loesser K, Eich DM, et al. Dehydroepiandrosterone inhibits human platelet aggregation in vitro and in vivo. Ann NY Acad Sci. 1995 Dec 29;774:281-90.

33. Casson PR, Andersen RN, Herrod HG, et al. Oral dehydroepiandrosterone in physiologic doses modulates immune function in postmenopausal women. Am J Obstet Gynecol. 1993 Dec;169(6):1536-9.

34. Kawano H, Yasue H, Kitagawa A, et al. Dehydroepiandrosterone supplementation improves endothelial function and insulin sensitivity in men. J Clin Endocrinol Metab. 2003 Jul;88(7):3190-5.

35. Dhatariya K, Bigelow ML, Nair KS. Effect of dehydroepiandrosterone replacement on insulin sensitivity and lipids in hypoadrenal women. Diabetes. 2005 Mar;54(3):765-9.

36. Casson PR, Faquin LC, Stentz FB, et al. Replacement of dehydroepiandrosterone enhances T-lymphocyte insulin binding in postmenopausal women. Fertil Steril. 1995 May;63(5):1027-31.

37. Sun Y, Mao M, Sun L, et al. Treatment of osteoporosis in men using dehydroepiandrosterone sulfate. Chin Med J (Engl). 2002 Mar;115(3):402-4.

38. Villareal DT, Holloszy JO, Kohrt WM. Effects of DHEA replacement on bone mineral density and body composition in elderly women and men. Clin Endocrinol (Oxf). 2000 Nov;53(5):561-8.

39. Labrie F, Diamond P, Cusan L, et al. Effect of 12-month dehydroepiandrosterone replacement therapy on bone, vagina, and endometrium in postmenopausal women. J Clin Endocrinol Metab. 1997 Oct;82(10):3498-505.

40. Adachi M, Takayanagi R. Role of androgens and DHEA in bone metabolism. Clin Calcium. 2006 Jan;16(1):61-6.

41. Aoki K, Nakajima A, Mukasa K, et al. Prevention of diabetes, hepatic injury, and colon cancer with dehydroepiandrosterone. J Steroid Biochem Mol Biol. 2003 Jun;85(2-5):469-72.

42. Prough RA, Lei XD, Xiao GH, et al. Regulation of cytochromes P450 by DHEA and its anticarcinogenic action. Ann NY Acad Sci. 1995 Dec 29;774:187-99.

43. Schwartz AG, Pashko LL. Cancer prevention with dehydroepiandrosterone and non-androgenic structural analogs. J Cell Biochem Suppl. 1995;22:210-7.

44. Inano H, Ishii-Ohba H, Suzuki K, et al. Chemoprevention by dietary dehydroepiandrosterone against promotion/progression phase of radiation-induced mammary tumorigenesis in rats. J Steroid Biochem Mol Biol. 1995 Jul;54(1-2):47-53.

45. Melvin WS, Boros LG, Muscarella P, et al. Dehydroepiandrosterone-sulfate inhibits pancreatic carcinoma cell proliferation in vitro and in vivo. Surgery. 1997 Apr;121(4):392-7.

46. Moore MA, Weber E, Thornton M, Bannasch P. Sex-dependent, tissue-specific opposing effects of dehydroepiandrosterone on initiation and modulation stages of liver and lung carcinogenesis induced by dihydroxy-di-n-propylnitrosamine in F344 rats. Carcinogenesis. 1988 Aug;9(8):1507-9.

47. Osawa E, Nakajima A, Yoshida S, et al. Chemoprevention of precursors to colon cancer by dehydroepiandrosterone (DHEA). Life Sci. 2002 Apr 19;70(22):2623-30.

48. Yang S, Fu Z, Wang F, Cao Y, Han R. Anti-mutagenicity activity of dehydroepiandrosterone. Zhonghua Zhong Liu Za Zhi. 2002 Mar;24(2):137-40.

49. Yoshida S, Honda A, Matsuzaki Y, et al. Antiproliferative action of endogenous dehydroepiandrosterone metabolites on human cancer cell lines. Steroids. 2003 Jan;68(1):73-83.

50. Arlt W, Callies F, van Vlijmen JC, et al. Dehydroepiandrosterone replacement in women with adrenal insufficiency. N Engl J Med. 1999 Sep 30;341(14):1013-20.

51. Herbert J. Neurosteroids, brain damage, and mental illness. Exp Gerontol. 1998 Nov;33(7-8):713-27.

52. Schmidt PJ, Daly RC, Bloch M, et al. Dehydroepiandrosterone monotherapy in midlife-onset major and minor depression. Arch Gen Psychiatry. 2005 Feb;62(2):154-62.

53. 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 Jun;78(6):1360-7.

54. Juhasz-Vedres G, Rozsa E, Rakos G, et al. Dehydroepiandrosterone sulfate is neuroprotective when administered either before or after injury in a focal cortical cold lesion model. Endocrinology. 2006 Feb;147(2):683-6.

55. Parsons TD, Kratz KM, Thompson E, Stanczyk FZ, Buckwalter JG. Dhea supplementation and cognition in postmenopausal women. Int J Neurosci. 2006 Feb;116(2):141-55.

56. de B, V, Vieira MC, Rocha MN, Viana GS. Cortisol and dehydroepiandosterone sulfate plasma levels and their relationship to aging, cognitive function, and dementia. Brain Cogn. 2002 Nov;50(2):316-23.

57. Magri F, Terenzi F, Ricciardi T, et al. Association between changes in adrenal secretion and cerebral morphometric correlates in normal aging and senile dementia. Dement Geriatr Cogn Disord. 2000 Mar;11(2):90-9.

58. Karishma KK, Herbert J. Dehydroepiandro-sterone (DHEA) stimulates neurogenesis in the hippocampus of the rat, promotes survival of newly formed neurons and prevents corticosterone-induced suppression. Eur J Neurosci. 2002 Aug;16(3):445-53.

59. Mills SJ, Ashworth JJ, Gilliver SC, Hardman MJ, Ashcroft GS. The sex steroid precursor DHEA accelerates cutaneous wound healing via the estrogen receptors. J Invest Dermatol. 2005 Nov;125(5):1053-62.

60. Ayhan S, Markal N, Siemionow K, Araneo B, Siemionow M. Effect of subepineurial dehydroepiandrosterone treatment on healing of transected nerves repaired with the epineurial sleeve technique. Microsurgery. 2003;23(1):49-55.

61. Nordmark G, Bengtsson C, Larsson A et al. Effects of dehydroepiandrosterone supplement on health-related quality of life in glucocorticoid treated female patients with systemic lupus erythematosus. Autoimmunity. 2005 Nov;38(7):531-40.

62. Steel N. Dehydro-epiandrosterone and ageing. Age Ageing. 1999 Mar;28(2):89-91.

63. Available at: Accessed April 1, 2007.

64. Available at: Accessed April 1, 2007.

65. Hougaku H, Fleg JL, Najjar SS, et al. Relationship between androgenic hormones and arterial stiffness, based on longitudinal hormone measurements. Am J Physiol Endocrinol Metab. 2006 Feb;290(2):E234-42.

66. Alwardt CM, Yu Q, Brooks HL, et al. Comparative effects of dehydroepiandrosterone sulfate on ventricular diastolic function with young and aged female mice. Am J Physiol Regul Integr Comp Physiol. 2006 Jan;290(1):R251-6.

67. Hutchison SJ, Browne AE, Ko E, et al. Dehydroepiandrosterone sulfate induces acute vasodilation of porcine coronary arteries in vitro and in vivo. J Cardiovasc Pharmacol. 2005 Sep;46(3):325-32.

68. Martina V, Benso A, Gigliardi VR, et al. Short-term dehydroepiandrosterone treatment increases platelet cGMP production in elderly male subjects. Clin Endocrinol (Oxf). 2006 Mar;64(3):260-4.

69. Barrett-Connor E, Khaw KT, Yen SS. A prospective study of dehydroepiandrosterone sulfate, mortality, and cardiovascular disease. N Engl J Med. 1986 Dec 11;315(24):1519-24.

70. Morales AJ, Haubrich RH, Hwang JY, Asakura H, Yen SS. The effect of six months treatment with a 100 mg daily dose of dehydroepiandrosterone (DHEA) on circulating sex steroids, body composition and muscle strength in age-advanced men and women. Clin Endocrinol (Oxf). 1998 Oct;49(4):421-32.

71. Vryonidou A, Papatheodorou A, Tavridou A, et al. Association of hyperandrogenemic and metabolic phenotype with carotid intima-media thickness in young women with polycystic ovary syndrome. J Clin Endocrinol Metab. 2005 May;90(5):2740-6.

72. Shimizu T, Choudhry MA, Szalay L, et al. Salutary effects of androstenediol on cardiac function and splanchnic perfusion after trauma-hemorrhage. Am J Physiol Regul Integr Comp Physiol. 2004 Aug;287(2):R386-90.

73. Origlia C, Pescarmona G, Capizzi A, et al. Platelet cGMP inversely correlates with age in healthy subjects. J Endocrinol Invest. 2004 Feb;27(2):RC1-4.

74. Okamoto K. Relationship between dehydroepiandrosterone sulfate and serum lipid levels in Japanese men. J Epidemiol. 1996 Jun;6(2):63-7.

75. Shono N, Kumagai S, Higaki Y, Nishizumi M, Sasaki H. The relationships of testosterone, estradiol, dehydroepiandrosterone-sulfate and sex hormone-binding globulin to lipid and glucose metabolism in healthy men. J Atheroscler Thromb. 1996;3(1):45-51.

76. Cardounel A, Regelson W, Kalimi M. Dehydroepiandrosterone protects hippocampal neurons against neurotoxin-induced cell death: mechanism of action. Proc Soc Exp Biol Med. 1999 Nov;222(2):145-9.

77. Garcia-Estrada J, Luquin S, Fernandez AM, Garcia-Segura LM. Dehydroepiandrosterone, pregnenolone and sex steroids down-regulate reactive astroglia in the male rat brain after a penetrating brain injury. Int J Dev Neurosci. 1999 Apr;17(2):145-51.

78. Kalmijn S, Launer LJ, Stolk RP, et al. A prospective study on cortisol, dehydroepiandrosterone sulfate, and cognitive function in the elderly. J Clin Endocrinol Metab. 1998 Oct;83(10):3487-92.

79. Carlson LE, Sherwin BB, Chertkow HM. Relationships between dehydroepiandrosterone sulfate (DHEAS) and cortisol (CRT) plasma levels and everyday memory in Alzheimer’s disease patients compared to healthy controls. Horm Behav. 1999 Jun;35(3):254-63.

80. Murialdo G, Nobili F, Rollero A, et al. Hippocampal perfusion and pituitary-adrenal axis in Alzheimer’s disease. Neuropsychobiology. 2000;42(2):51-7.

81. Li H, Klein G, Sun P, Buchan AM. Dehydroepiandrosterone (DHEA) reduces neuronal injury in a rat model of global cerebral ischemia. Brain Res. 2001 Jan 12;888(2):263-6.

82. Kipper-Galperin M, Galilly R, Danenberg HD, Brenner T. Dehydroepiandrosterone selectively inhibits production of tumor necrosis factor alpha and interleukin-6 [correction of interlukin-6] in astrocytes. Int J Dev Neurosci. 1999 Dec;17(8):765-75.

83. Young AH, Gallagher P, Porter RJ. Elevation of the cortisol-dehydroepiandrosterone ratio in drug-free depressed patients. Am J Psychiatry. 2002 Jul;159(7):1237-9.

84. Strous RD, Maayan R, Lapidus R, et al. Dehydroepiandrosterone augmentation in the management of negative, depressive, and anxiety symptoms in schizophrenia. Arch Gen Psychiatry. 2003 Feb;60(2):133-41.

85. Young AH, Gallagher P, Porter RJ. Elevation of the cortisol-dehydroepiandrosterone ratio in drug-free depressed patients. Am J Psychiatry. 2002 Jul;159(7):1237-9.

86. Valtysdottir ST, Wide L, Hallgren R. Mental wellbeing and quality of sexual life in women with primary Sjogren’s syndrome are related to circulating dehydroepiandrosterone sulphate. Ann Rheum Dis. 2003 Sep;62(9):875-9.

87. Jozuka H, Jozuka E, Takeuchi S, Nishikaze O. Comparison of immunological and endocrinological markers associated with major depression. J Int Med Res. 2003 Jan;31(1):36-41.

88. Schmidt PJ, Murphy JH, Haq N, Danaceau MA, St CL. Basal plasma hormone levels in depressed perimenopausal women. Psychoneuroendocrinology. 2002 Nov;27(8):907-20.

89. Bloch M, Schmidt PJ, Danaceau MA, Adams LF, Rubinow DR. Dehydroepiandrosterone treatment of midlife dysthymia. Biol Psychiatry. 1999 Jun 15;45(12):1533-41.

90. Wolkowitz OM, Reus VI. Neurotransmitters, neurosteroids and neurotrophins: new models of the pathophysiology and treatment of depression. World J Biol Psychiatry. 2003 Jul;4(3):98-102.

91. van BF, Verkes RJ. Neurosteroids in depression: a review. Psychopharmacology (Berl). 2003 Jan;165(2):97-110.

92. Wolkowitz OM, Reus VI, Roberts E, et al. Antidepressant and cognition-enhancing effects of DHEA in major depression. Ann NY Acad Sci. 1995 Dec 29;774:337-9.

93. Meno-Tetang GM, Blum RA, Schwartz KE, Jusko WJ. Effects of oral prasterone (dehydroepiandrosterone) on single-dose pharmacokinetics of oral prednisone and cortisol suppression in normal women. J Clin Pharmacol. 2001 Nov;41(11):1195-205.

94. Valenti G. Andrenopause: an imbalance between dehydroepiandrosterone (DHEA) and cortisol secretion. J Endocrinol Invest. 2002 25(10 suppl):29- 35.

95. Genazzani AD, Lanzoni C, Genazzani AR. Might DHEA be considered a beneficial replacement therapy in the elderly? Drugs Aging. 2007;24(3):173-85.

96. Wojtal K, Trojnar MK, Czuczwar SJ. Endogenous neuroprotective factors: neurosteroids. Pharmacol Rep. 2006 May;58(3):335-40.

97. Strous RD. Dehydroepiandrosterone (DHEA) augmentation in the management of schizophrenia symptomatology. Essent Psychopharmacol. 2005;6(3):141-7.

98. Ferrari E, Casarotti D, Muzzoni B, et al. Age-related changes of the adrenal secretory pattern: possible role in pathological brain aging. Brain Res Brain Res Rev. 2001 Nov;37(1-3):294-300.

99. Lai DY. Rodent carcinogenicity of peroxisome proliferators and issues on human relevance. J Environ Sci Health C Environ Carcinog Ecotoxicol Rev. 2004 May;22(1):37-55.

100. Bentley P, Calder I, Elcombe C, Grasso P, Stringer D, Wiegand HJ.Hepatic peroxisome proliferation in rodents and its significance for humans. Food Chem Toxicol. 1993 Nov;31(11):857-907.

101. Metzger C, Bannasch P, Mayer D. Enhancement and phenotypic modulation of N-nitrosomorpholine-induced hepatocarcinogenesis by dehydroepiandrosterone. Cancer Lett. 1997 Dec 23;121(2):125-31.

102. Imai K, Kudo N, Koyam M, Shirahata A, Kawashim Y.Effects of dehydroepiandrosterone on oleic acid formation in the liver of rats, mice and guinea pigs. Jpn J Pharmacol. 2001 Aug;86(4):437-47.

103. Sakuma M, Yamada J, Suga T. Comparison of the inducing effect of dehydroepiandrosterone on hepatic peroxisome proliferation-associated enzymes in several rodent species. A short-term administration study. Biochem Pharmacol. 1992 Mar 17;43(6):1269-73.

104. Watkins PB, Kaplowitz N, Slattery JT, et al. Aminotransferase elevations in healthy adults receiving 4 grams of acetaminophen daily: a randomized controlled trial. JAMA. 2006 Jul 5;296(1):87-93.

105. Morrell MJ, Flynn KL, Done S, et al. Sexual dysfunction, sex steroid hormone abnormalities, and depression in women with epilepsy treated with antiepileptic drugs. Epilepsy Behav. 2005 May;6(3):360-5.

106. Santoro N, Torrens J, Crawford S et al. Correlates of circulating androgens in mid-life women: the study of women’s health across the nation. J Clin Endocrinol Metab. 2005 Aug;90(8):4836-45.

107. Buvat J. Androgen therapy with dehydroepiandrosterone. World J Urol. 2003 Nov;21(5):346-55.

108. Arlt W. Androgen therapy in women. Eur J Endocrinol. 2006 Jan;154(1):1-11.

109. Simile M, Pascale RM, De Miglio MR, et al. Inhibition by dehydroepiandrosterone of growth and progression of persistent liver nodules in experimental rat liver carcinogenesis. Int J Cancer. 1995 Jul 17;62(2):210-5.

110. Green JE, Shibata MA, Shibata E, et al. 2-difluoromethylornithine and dehydroepiandrosterone inhibit mammary tumor progression but not mammary or prostate tumor initiation in C3(1)/SV40 T/t-antigen transgenic mice. Cancer Res. 2001 Oct 15;61(20):7449-55.

111. Lubet RA, Gordon GB, Prough RA, et al. Modulation of methylnitrosourea-induced breast cancer in Sprague Dawley rats by dehydroepiandrosterone: dose-dependent inhibition, effects of limited exposure, effects on peroxisomal enzymes, and lack of effects on levels of Ha-Ras mutations. Cancer Res. 1998 Mar 1;58(5):921-6.

112. Perkins SN, Hursting SD, Haines DC, et al. Chemoprevention of spontaneous tumorigenesis in nullizygous p53-deficient mice by dehydroepiandrosterone and its analog 16alpha-fluoro-5-androsten-17-one. Carcinogenesis. 1997 May;18(5):989-94.

113. Ciolino H, MacDonald C, Memon O, Dankwah M, Yeh GC. Dehydroepiandrosterone inhibits the expression of carcinogen-activating enzymes in vivo. Int J Cancer. 2003 Jun 20;105(3):321-5.

114. Loria RM. Immune up-regulation and tumor apoptosis by androstene steroids. Steroids. 2002 Nov;67(12):953-66.

115. Bradlow HL, Sepkovic DW. Diet and breast cancer. Ann NY Acad Sci. 2002 Jun;963:247-67.

116. Solerte SB, Fioravanti M, Vignati G, et al. Dehydroepiandrosterone sulfate enhances natural killer cell cytotoxicity in humans via locally generated immunoreactive insulin-like growth factor I. J Clin Endocrinol Metab. 1999 Sep;84(9):3260-7.

117. Mei JJ, Hursting SD, Perkins SN, Phang JM. p53-independent inhibition of nitric oxide generation by cancer preventive interventions in ex vivo mouse peritoneal macrophages. Cancer Lett. 1998 Jul 17;129(2):191-7.

118. D’Ambrosio SM, Gibson-D’Ambrosio RE, Wani G, et al. Modulation of Ki67, p53 and RARbeta expression in normal, premalignant and malignant human oral epithelial cells by chemopreventive agents. Anticancer Res. 2001 Sep;21(5):3229-35.

119. Weber E, Moore MA, Bannasch P. Phenotypic modulation of hepatocarcinogenesis and reduction in N-nitrosomorpholine-induced hemangiosarcoma and adrenal lesion development in Sprague-Dawley rats by dehydroepiandrosterone. Carcinogenesis. 1988 Jul;9(7):1191-5.

120. Prough RA, Lei XD, Xiao GH, et al. Regulation of cytochromes P450 by DHEA and its anticarcinogenic action. Ann NY Acad Sci. 1995 Dec 29;774:187-99.

121. Schwartz AG and Pashko LL. Cancer prevention with dehydroepiandrosterone and non-androgenic structural analogs. J Cell Biochem Suppl. 1995;22:210-7.

122. Greenwald P, Kelloff GJ, Boone CW, McDonald SS. Genetic and cellular changes in colorectal cancer: proposed targets of chemopreventive agents. Cancer Epidemiol Biomarkers Prev. 1995 Oct;4(7):691-702.

123. Melvin WS, Boros LG, Muscarella P, et al. Dehydroepiandrosterone-sulfate inhibits pancreatic carcinoma cell proliferation in vitro and in vivo. Surgery. 1997 Apr;121(4):392-7.

124. Hursting SD, Perkins SN, Haines DC, Ward JM, Phang JM. Chemoprevention of spontaneous tumorigenesis in p53-knockout mice. Cancer Res. 1995 Sep 15;55(18):3949-53.

125. Ledochowski M, Murr C, Jager M, Fuchs D. Dehydroepiandrosterone, ageing and immune activation. Exp Gerontol. 2001 Nov;36(10):1739-47.

126. Williams JR. The effects of dehydroepiandrosterone on carcinogenesis, obesity, the immune system, and aging. Lipids. 2000 Mar;35(3):325-31.

127. Kavanaugh C, Green JE. The use of genetically altered mice for breast cancer prevention studies. J Nutr. 2003 Jul;133(7 Suppl):2404S-9S.

128. Jozuka H, Jozuka E, Suzuki M, Takeuchi S, Takatsu Y. Psycho-neuro-immunological treatment of hepatocellular carcinoma with major depression—a single case report. Curr Med Res Opin. 2003;19(1):59-63.

129. Yang NC, Jeng KC, Ho WM, Hu ML. ATP depletion is an important factor in DHEA-induced growth inhibition and apoptosis in BV-2 cells. Life Sci. 2002 Mar 15;70(17):1979-88.

130. Schulz S, Klann RC, Schonfeld S, Nyce JW. Mechanisms of cell growth inhibition and cell cycle arrest in human colonic adenocarcinoma cells by dehydroepiandrosterone: role of isoprenoid biosynthesis. Cancer Res. 1992 Mar 1;52(5):1372-6.

131. Dashtaki R, Whorton AR, Murphy TM, et al. Dehydroepiandrosterone and analogs inhibit DNA binding of AP-1 and airway smooth muscle proliferation. J Pharmacol Exp Ther. 1998 May;285(2):876-83.

132. Wang TT, Hursting SD, Perkins SN, Phang JM. Effects of dehydroepiandrosterone and calorie restriction on the Bcl-2/Bax-mediated apoptotic pathway in p53-deficient mice. Cancer Lett. 1997 Jun 3;116(1):61-9.

133. Regelson W, Loria R, Kalimi M. Dehydroepiandrosterone (DHEA—the “mother steroid.” I. Immunologic action. Ann NY Acad Sci. 1994 May 31;719:553-63.

134. Perkins SN, Hursting SD, Kim K, Poetschke K, Heather L, Richie ER. Mechanisms underlying the anti-lymphoma activity of dehydroepiandrosterone: studies in murine thymocytes and murine T-cell hybridoma cells. cancer Epidem Biomark Prevent. 2002;11(10):1233s.

135. Hsu HC. Dehydroepiandrosterone (DHEA) sulfotransferase gene expression in human hepatocellular carcinoma: an age-dependent prognostic factor. Proc Am Assoc Cancer Res. 1995;36:208.

136. Osawa E, Nakajima A, Yoshida S, et al. Chemoprevention of precursors to colon cancer by dehydroepiandrosterone (DHEA). Life Sci. 2002 Apr 19;70(22):2623-30.

137. Bulbrook RD, Hayward JL, Spicer CC. Relation between urinary androgen and corticoid excretion and subsequent breast cancer. Lancet. 1971 Aug 21;2(7721):395-8.

138. Eaton NE, Reeves GK, Appleby PN, Key TJ. Endogenous sex hormones and prostate cancer: a quantitative review of prospective studies. Br J Cancer. 1999 Jun;80(7):930-4.

139. Vatten LJ, Ursin G, Ross RK, et al. Androgens in serum and the risk of prostate cancer: a nested case-control study from the Janus serum bank in Norway. Cancer Epidemiol Biomarkers Prev. 1997 Nov;6(11):967-9.

140. Stahl F, Schnorr D, Pilz C, Dorner G. Dehydroepiandrosterone (DHEA) levels in patients with prostatic cancer, heart diseases and under surgery stress. Exp Clin Endocrinol. 1992;99(2):68-70.

141. Schatzl G, Madersbacher S, Thurridl T, et al. High-grade prostate cancer is associated with low serum testosterone levels. Prostate. 2001 Apr;47(1):52-8.

142. Schatzl G, Reiter WJ, Thurridl T, et al. Endocrine patterns in patients with benign and malignant prostatic diseases. Prostate. 2000 Aug 1;44(3):219-24.

143. Huot RI, Shain SA. Differential metabolism of dehydroepiandrosterone sulfate and estrogen conjugates by normal or malignant AXC/SSh rat prostate cells and effects of these steroid conjugates on cancer cell proliferation in vitro. J Steroid Biochem. 1988 Jun;29(6):617-21.

144. McCormick DL, Rao KV. Chemoprevention of hormone-dependent prostate cancer in the Wistar-Unilever Rat. Eur Urol. 1999 May;35(5-6):464-7.

145. Ponholzer A, Plas E, Schatzl G, Jungwirth A, Madersbacher S. Association of DHEA-S and estradiol serum levels to symptoms of aging men. Aging Male. 2002 Dec;5(4):233-8.

146. Longcope C. Dehydroepiandrosterone metabolism. J Endocrinol. 1996 Sep;150 SupplS125-7.

147. Wallace MB, Lim J, Cutler A, Bucci L. Effects of dehydroepiandrosterone vs androstenedione supplementation in men. Med Sci Sports Exerc. 1999 Dec;31(12):1788-92.

148. Brown GA, Vukovich MD, Sharp RL, et al. Effect of oral DHEA on serum testosterone and adaptations to resistance training in young men. J Appl Physiol. 1999 Dec;87(6):2274-83.

149. Brown GA, Vukovich MD, Reifenrath TA, et al. Effects of anabolic precursors on serum testosterone concentrations and adaptations to resistance training in young men. Int J Sport Nutr Exerc Metab. 2000 Sep;10(3):340-59.

150. Available at: Accessed April 1, 2007.

151. Welle S, Jozefowicz R, Statt M. Failure of dehydroepiandrosterone to influence energy and protein metabolism in humans. J Clin Endocrinol Metab. 1990 Nov;71(5):1259-64.

152. Nissen SL, Sharp RL. Effect of dietary supplements on lean mass and strength gains with resistance exercise: a meta-analysis. J Appl Physiol. 2003 Feb;94(2):651-9.

153. Bahrke MS, Yesalis CE. Abuse of anabolic androgenic steroids and related substances in sport and exercise. Curr Opin Pharmacol. 2004 Dec;4(6):614-20.

154. Delbeke FT, Van EP, Van TW, Desmet N. Prohormones and sport. J Steroid Biochem Mol Biol. 2002 Dec;83(1-5):245-51.

155. Hartgens F, Kuipers H. Effects of androgenic-anabolic steroids in athletes. Sports Med. 2004;34(8):513-54.

156. Mottram DR, George AJ. Anabolic steroids. Baillieres Best Pract Res Clin Endocrinol Metab. 2000 Mar;14(1):55-69.

157. Pope HG. Current state of DHEA in the marketplace. Washington, DC: Council for Responsible Nutrition; 2003.