DHEA (dehydroepiandrosterone)

Taken by persons over the age of 40, Pro-Cell 40 supplements the dietary intake of DHEA, and may counteract the decline of the body's production of DHEA as a result of the natural aging process. It has been hypothesized by experts that DHEA taken in capsule or tablet form is not readily absorbed and that a substantial amount is excreted. This liquid formulation should be more readily absorbed thus allowing more of the DHEA taken to enter into the system. It is therefore recommended to strictly adhere to the recommended dosage. Trials have clearly shown that the body depleted of DHEA with aging and that DHEA depletion directly relates to imune system dysfunction as well as other age-related dysfunctions. DHEA and DHEAS blood serum level tests are readily available should you wish to have one. A nutritionist or practitioner can recommend where to secure proper testing.

It is recommended that you consult a physician or a nutritionist before taking this, or any, dietary supplement.

Suggested Dosage: 4 to 20 mg's (1 - 5 drops) daily. If taking more than 1 drop per day, divide dosage and take 1/2 in the a.m. and 1/2 in the p.m.

Directions for use: Divide the dosage you wish to take by four to determine the number of drops of Pro_Cill 40 to be taken.

Example: If you wish to take 12mg's, 12 divided by 4 equals 3 drops of Pro-Cell 40.

Pro-Cell 40 is best taken sublingually (under the tongue).

Pro-Cell 40 may be mixed with any liquid, but is best taken in tomato juice or other heavy fruit or vegetable juice. If taken with water, Pro-Cell 40 separates quickly as evidenced by the water becoming very cloudy and milky. Other liquids may also become cloudy with the addition of Pro-Cell 40. this is normal and should be expected.

Pro-Cell 40 may also be taken with 1/2 ounce of 60 to 100 proof alcohol. When taken with alcohol, the separation usually will not occur.

When taken with any liquid other than alcohol, Pro-Cell 40 may separate into a powder and stick to the glass. If this occurs, simply add more liquid, mix, and drink rapidly. Replace cap immediately, do not leave top off bottle for more than 15 seconds at a time.

Contents: 2200 mg's DHEA in alcohol and water. One drop equals 4 mg's. Total volume of contents, 14 ml.

Storage: Store bottle in original tube container at room temperature. Do Not Refridgerate.

This product evaporates rapidly and may leave a powder residue around the cap opening. This is normal and may b wiped off with a clean damp cloth. When using, replace cap immediately. If top is left off for more than 15 minutes, discard the entire product.

Warnings: This product contains alcohol and should not be taken by anyone having a medical condition which limits the intake of alcohol. Some foods and dietary supplements can cause adverse side effects such as, but not limited to, rashes, pain, headaches, etc. If adverse effects should occur, discontinue use. Should accidental overdose occur with this, or any other dietary supplement, contact you physician or the nearest poison control centre immediately. Keep this and all dietary supplements out of the reach of children.

Proper DHEA blood levels are necessary to maintain optimum health and to increase longevity. A rapidly increasing amount of scientific evidence suggests that DHEA blood levels can indicate future development of degenerative diseases such as cancer, memory disorders, cardiovascular disease, diabetes, osteoporosis, imune system dysfunction (MS, ALS, LUPIS) and aging. DHEA levels are also low in persons who are obese and those who have muscle atrophy. Low levels of DHEA are present in female frigidity and male impotence. DHEA levels reduce with age: the older you become, the less DHEA you have. When one reaches the age of 70 to 80 his/her DHEA levels are but 10 - 20% of the levels at age 28.

Dr. Alan R. Gaby (M.D.) is author of the book: "Preventing and Reversing Osteoporosis" (Prima Publishing). Dr. Gaby outlines DHEA benefits in treating degenerative diseases in chapter 16 of his book. The chapter title is: "DHEA: The Hormone that `DOES IT ALL'." Any practitioner that is treating patients with osteoporosis should study Dr. Gaby's book and apply his protocols to those patients. One doctor, using Dr. Gaby's treatment, reported a 24% increase in bone mass in a patient with severe osteoporosis in 12 months of treatment.

Degenerative disease status are the principal indicators of aging and DHEA appears to be the best biomarker of aging and longevity.

Studies (Loria, 1988, et al) indicate DHEA protects against viral and bacterial infections including enterovirus and other herpes infections.

Most major adrenocortical hormones induce immune suppression. DHEA has, on the other hand, prevented death in at least two different types of viruses and a fatal streptococcus infection. It appears that DHEA increases T-cell, B-cell and macrophages by interfering with glucocorticoid immuno-suppression (Loria, 1988).

A mice study (Ben-Nathan, 1991) using animals with viral encephalitis indicated DHEA reduces viremia and mortality.

Rats inoculated with the virulent West Nile Virus nad then stressed by cold water immersion had a 67% mortality rate. DHEA treated rats in the study had a mortality rate of but 34% (a 50% reduction of death rate).

Numerous studies have shown that DHEA reduces the replication of the AIDS (HIV-1) virus. Low blood levels of DHEA are present with increased progression of HIV to full blown AIDS (Jacobson 1991). When mice are given a lethal dose of lipopolysaccharide, and endotoxin, they have a mortality rate of 95%. Mortality is reduced from 95% to 24% with a of DHEA. Lipopolysaccharide administration results in high levels of tumor necrosis. DHEA significantly blocks this necrosis. T-Cell have a specific DHEA receptor. DHEA may regulate interleukin-2 production to improve immune function (Meikle, 1992). Drug-induced T-cell, B-cell, and antibody production suppression in rats are reversed after DHEA administration (Rasmussen, 1991).

In a study using NZB mice, a model for the development of autoimmune diseases such as lupus erythematosus, autoantibodies are restrained by DHEA treatment (Lucas 1988). This suggests that DHEA therapy may be of great benefit in all autoimmune related conditions.

Diabetics suffer a higher incidence of cardiovascular diseas than people with normal carbohydrate metabolism. Recent studies suggest that one cause of increased cardiovascular disease in diabetics may be reduced levels of DHEA caused by high levels of insulin. DHEA's multiple anti-atherogenic effects are thus thwarted when levels are abnormally low in diabetics. Since aging and obesity are both characterized by hyperinsulinemic insulin resistance (Nestler, 1992), it's quite possible that the dramatically increased incidence of mature-onset diabetes and weight gain in older adults may be caused, in part, by the precipitous decline in DHEA levels with advancing age.

"Energy wastage" is thought to be one of the ways that DHEA reduces body weight. In a study with rats, DHEA seemed to exert part of its anti-obesity and anti-diabetic effects through increased hepatic glucose oxidation and reduced gluconeogenesis (McIntosh, 1991). Obesity and diabetes are characterized by high levels of insulin.

In both insulin resistant mutant mice and in normal aging mice, DHEA increases sensitivity to insulin, thereby potentiating the effects of this important hormone (Coleman, 1984). Rats genetically predisposed to diabetes do not develop the disease when given DHEA, nor do they suffer damage to "islet cells" which produce insulin in the pancreas when given DHEA (Gordon, 1987). Some clinicians have reported that DHEA treatment reduces the need for insulin in humans.

One of the most striking effects of DHEA is its ability to induce weight loss in laboratory animals, even when these animals are given as much food as they want. This remarkable finding by Dr. Arthur Schwartz of Temple University Medical School in the 1980's produced tremendous interest in the possibility of using DHEA as a weight loss therapy in humans. Recent research has begun to show how DHEA exerts its extraordinary weight loss effects.

A recent study in diabetes prone rats indicates that one of DHEA's weight reducing mechanisms may operate through the increase of serotonin levels in the hypothalamus region of the brain, thereby increasing the release of cholecystokinin (CCK), the satiation hormone. CCK reduces one's desire in the hypothalamus, which was associated with increased CCK activity, reduced food intake, and lower body fat.

DHEA also is believed to produce its anti-obesity effects by its anti-glucocorticoid activity (Wright, 1992). In this study, DHEA blocked the activity of the glucocorticoid-induced enzymes, tyrosine aminotransferase and ornithine decarboxylase, in genetically obese rats leading to substantial weight loss in these animals.

Among the other mechanisms proposed to explain DHEA's ability to induce weight loss and fat reduction are its effects on lipogenesis, substrate cycling, peroxisome proliferation, mitochondrial respiration, protein sythesis, and thyroid hormone function. Beyond its inhibition of fat synthesis and depostition, DHEA operates via mechanisms which help to EXPEND energy rather than store it for future use (Berhanier, 1993). DHEA can prevent obesity inmice genetically predisposed to obesity. When given DHEA, the body weights of genetically obese mice reached that of lean mice independent of any alteration in food intake (Yen, 1977). Even middle aged, genetically obese mice are thin after being given DHEA (Cleary, 1986). Rats whose obesity had been induced by high calorie diet, lost weight rapidly when treated with DHEA. DHEA also produced lipid and insulin lowering effects (Mohan, 1990).

DHEA was given to five male, normal weight subjects at a dose of 1600 mg per day, divided into 4 doses. After 28 days, with diet and physical activity remaining normal, 4 of the 5 exhibited a mean body fat decrease of 31% with no overall weight change. This meant that their fat loss was balanced by a gain in muscle mass characteristic of youth! At the same time, their LDL levels fell by 7.5 % to confer protection against cardiovascular disease. (Nester, 1988).

Epidemiologic studies indicate that the risk of developing a wide variety of cancers id directly related to teh serum or urinary levels of DHEA or DHEA Sulfate. In laboratory studies, DHEA has prevented the occurrence of many different types spontaneous and chemically induced tumors, including chemically induced adenocarcinoma of the colon (Schulz, 1992), lung cancer (Pashko, 1984), skin cancer (Pashko, 1985), and spontaneous viral-induced breast cancer (Schwartz, 1981).

The hypothesis that DHEA inhibits fat formation through reduced activity of the enzyme G6PDH is often studied as a possible mechanism for the anti-cancer benefits of DHEA. Because of the similarity of DHEA to other sex hormones, there has been some concern that it might be implicated as a possible cause of prostate enlargements, but this has been found not to be the case (Regelson, 1988).

In hypercholesterolemic rabbits receiving heart transplants, administration of DHEA significantly retarded the progression of atherosclerosis. There was even a greater reduction in atherosclerotic rabbits who did not undergo heart transplants (Eich, 1993). In rabbits who had their arteries damaged to encourage the formation of atherosclerotic plaque, DHEA reduced plaque by almost 50% over controls in inverse proportion to the level of serum DHEA (Gordon, 1988). This finding is especially important to those who have undergone coronary-bypass surgery because grafted blood vessels are especially susceptible to new atheroscierotic formation.

Acute heart attacks are associated with low levels of DHEA and high density lipoprotein (HDL) (Ruiz Salmeron, 1992). In a study spanning nearly two decades, men's DHEA-S levels were found to be lower in patients who died of coronary heart disease than in controls (LaCroix, 1992). When DHEA-S levels were measured in 103 middle-aged males undergoing elective coronary angiography, the lowest levels of DHEA-S corresponded to the greatest arterial blockage. In 103 women studies at the same time, no association between DHEA levels and coronary disease was found, (Herrington, 1990). In yet another sudy of 32 men, aged 26-40 years, low levels of DHEA were found in men who had suffered myocardial infarction at least 3 to 4 months prior to the study (Slowinska-Srzdnicka, 1989). Atherosclerosis is a proliferative disease with both initiating and promoting factors participating in it's development. In studies with rabbits fed with a diet of 0.5% DHEA elevating their DHEA levels six-fold, a 50% reduction in atherosclerosis was observed as compared to placebo.

In studies with humans, it has been reported that the DHEA-Sulfate level is independently and inversly related to death from any cause and death from cartiovascular disease in men older than 50. In a study of 242 men between 50 and 79, a DHEA-S level below 1.4 mg/ml was associated with 1.5 fold higher death rate from any cause, a 3.3 fold higher death rate from cardiovascular disease, and a 3.2 fold higher death rate from ischemic heart disease. As suggested by the rabbit studies, the determination of baseline DHEA and DHEA-S levels in younger men, and proper administration in advancing years, could be useful in helping to avoid cardiovascular disease.

A recent study in 8 postmenopausal women concluded that DHEA may add to the benefits of estrogen therapy. The fact that DHEA protects against neoplasia, osteoporosis, and cardiac disease, suggests that DHEA should be effecive in treating the decline in function due to menopause (Buster, 1992). The use of the estrogen-receptor blocking homone melatonin is also suggested for women ongoing estrogen replacement therapy.

When the circulating levels of DHEA-S were studied in 86 patients with Alzheimer's disease and multi-infarct dementia, Alzheimer's patients had lower serum levels than controls. It was concluded that DHEA may relieve amnesia that contributes to dementia or is caused by it (Nasman, 1991). Other studies have shown that DHEA and DHEA-S levels are exceedingly low at ages when the incidence of Alzheimer's Diseases begins to increase markedly. DHEA may play a significant role in maintaining the function of neuonal cells, and DHEA supplementation may prevent neuronal loss and/or damage, thus slowing the progress of Alzheimer's disease (Bologa, 1987).

The exploration of DHEA's impact on memory and cognition is quite recent. Of primary note are the age related declines in circulating brain levels of DHEA that can be correlated with declining levels of potassium channel functions.

Even small amounts of DHEA and DHEA-S were found to lessen amnesia and enhance long-term memory in mice. In vitro studies have shown that small concentrations of DHEA can enhance neuronal and glial survival in the brain cells of a mouse. Therefore, the conclusion may be that DHEA compoiunds might help in the treatment of neurodegenerative memory disorders in man (Roberts, 1987). Memory enhancement was achieved by the addition of DHEA to the water supply of mice. There was a small range of dose benefit relationship. When too little DHEA was given, memory benefits dropped off steeply, as was the case when too much DHEA was given (Roberts, 1988). Improved memory was found in mice in one study, even when DHEA was administered after the learning experience has occurred (Flood, 1988b). DHEA-S improved memory retention in middle-aged and old mice to the high levels observed in young mice. Even very low levels of DHEA can increase the number of neurons in the brain, as well as their ability to establish contact with other neurons, and to differentiate. Supplementation with DHEA can prevent neuronal loss and/or damage (Bologa, 1987). In 61 men in nursing homes, ages 57-104, plasma DHEA-S levels were inversely related to the presence of organic brain syndrome and to the degree of dependence in performing the activities of daily living. These men had mean DHEA-S levels that were significantly lower than men of similar ages living outside the nursing home. There were 40% subnormal DHEA-S levels in the nursing home men compared to only 6% subnormal DHEA-S levels for the outside men. Plasma DHEA-S was subnormal in 80% of the nursing home men who had deteriorated to the point where they required total care (Rudman, 1990). In one study in mice, it was found that the memory-enhancing effects of DHEA occurred even when DHEA was given one hour after training! In this study, there was improved memory retention over a much wider dose range than is usual for excitatory memory enhancers, giving rise to the idea that DHEA may modulate the transcription of intermediate early genes needed for the plastic changes that occur during memory processing (Flood, 1992).

Subjects suffering from unipolar depression were given various forms of pharmacotherapy and behavioral therapy. The DHEA-S levels of 47 subjects showed a positive correlation with rating scale improvement as their depression was relieved (Tollefson, 1990).

Aging humans is characterized by reduced control over the production of cytokine interleukin-6. IL-6 is thought to play an important role in controlling abnormal cell proliferation. The loss of control over IL-6 has been shown to be preventable or even reversible with DHEA-S treatment in old mice. When treated, these mice also exhibited lower than normal levels of serum amyloid-P substance, serum lg, and tissue specific autoantibodies, compared with untreated, aged controls. Because each of these measures is aging related, these findings provide evidence that DHEA may help to slow "normal" aging. (Daynes, 1993).

The antibody response of mice to a vaccine was found to decline with age at Kentucky University's Sanders-Brown Center on Aging. Yet, DHEA significantly enhanced their splenic immune responses and the discrepancy was reversed (Gar, 1993). Other studies have shown similar immune dysfunction reversals with DHEA (Araneo, 1993). Studies have shown that DHEA can increase life spans by 50% in laboratory animals (Regelson, 1986). DHEA levels were found to be inversely related to death due to all causes in men over 50 (Barret-Conner, 1986). Mice did not age as rapidly when fed DHEA, and maintained their youthful hair color and sleekness, compared with the graying, coarsening hair of the control animals (Ragelson, 1986).

Synthetic analogs of DHEA have been developed in an effort to elimiante the potiential liabilities of DHEA, such as increased uterine weight in sexually immature female rats and of increased seminal vesicle weight in castrated male rats. These analogs do not increase liver weight or stimulate liver catalase activity in mice (Schwartz, 1988). However, considerable testingremains to be done before the analogs achieve the status of natural DHEA. Other side effects will become apparent in any analog of DHEA. Do not prescribe natural DHEA for sexually immature females or castrated males.

There is considerable evidence for the effect of DHEA on bone in humans. Decreased DHEA levels have been observed in women with decreased vertebral density and forearm mineral content. Women with Addison's Disease also have reduced forearm bone density and lower DHEA levels than age-matched postmenopausal controls. In animal studies, laboratory induced thyroid gland tumors have been prevented by dietary DHEA therapy. In humans, thyroid dysfunction is associated with DHEA and DHEA-S metabolism alterations. In contrast, women with primary hyperthyroidism have elevated DHEA-S levels.

DHEA is a naturally produced steroid hormone. Therefore, in order to produce a desired effect through administration, it is necessary to produce DHEA at purity levels as close as possible to the DHEA prduced by the various steroidogenic tissues of the human body. To be sure the highest purity level (99.9+%) is maintained one should prescribe liquid DHEA. Liquid DHEA provides maximum obtainable bio-availability and assures the proper dose is being prescribed (12 to 30 mg every day or every other day).

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