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Soy Protein Bodybuilding

Article care of

Soy, Estrogen and You

The amount of attention that soy has been receiving in the U.S. has been astounding considering there are no conclusive, long term studies on the effects of soy and/or soy isoflavones on humans. I would like you to note that published studies from Universities and Medical researchers differ greatly between the US and most of Europe. This is probably due to the fact that the US government has been actively promoting soy and funding research that is in favor of soy to boost the US agricultural economy.

Science and Soy

The fact of the matter is soy research is not complete and it may have as many harmful characteristics as helpful. Current soy research is best explained by Herman Adlercreutz, M.D., of the University of Helsinki, Finland: “no evidence in the literature suggesting that phytoestrogens (plant estrogens), present in such amounts in human food that they could have biological effects, stimulate already existing cancer, and there is also no evidence that such phytoestrogens could initiate cancer." (1).

Soy and Menopause

After menopause or a hysterectomy a women produces less estrogen. Soy isoflavones do look promising in stimulating estrogen receptors that are neglected because of decreased production of natural estrogen by the body. There has also been some indication that the stimulation of estrogen receptors after menopause or hysterectomy can retard the onset of osteoporosis. Quite a few studies indicate that soy may reduce the intensity and/or the frequency of “Hot flashes” in menopausal women.

Soy and Child Development

Very little research has been done indicating whether the phytoestrogens found in soy can alter endocrine development in children. So far the only documented research on prepubescent mammals has been performed on rats. The hormonal development of a fetus could also be effected by an abundance of phytoestrogens; again adequate studies on humans have not been performed to draw a concrete conclusion either way.

The following are results from some of the only studies done on the effects of phytoestrogens in mammals:

Rat pups, exposed to high doses of the plant estrogen coumestrol (found in sunflower seeds and oil and alfalfa sprouts) through their mother's milk, suffered permanent reproductive problems: female pups when grown did not ovulate, and males had altered mounting behavior and fewer ejaculations (2).

Neonatal and immature rats exposed to coumestrol experienced estrogen-related responses, such as premature estrous cycles. Coumestrol also interrupted ovarian cycles in adult female rats (3).

Newborn rats exposed to the phytoestrogen genistein (a compound found in soy products), experienced altered hormone secretions and the onset of puberty may have been delayed because female rats were exposed to the compound as fetuses (3).

Effects of soy in men

A major concern of men is the possible effects of soy on the male endocrine (hormonal) system. While there have been few studies addressing the effects of phytoestrogen in males, what conclusions have been drawn are negative. 3a, 17B- androstanediol glucuronide and androstanediol glucuronide are DHT metabolites and are essential for male secondary sex characteristics as well as the anabolism of skeletal muscle. Obviously decreases in these hormones mean less lean mass, more stored body fat, and a possible retardation of male secondary sex characteristics.

“In males, levels of 17B-estradiol and testosterone were not affected, but levels of 3a, 17B- androstanediol glucuronide (a metabolite of dihydrotestosterone) and dehydroepiandrosterone sulfate were decreased by 13% and 14%, respectively, after 2-4 weeks of daily soya ingestion.” (8)

Soy and Cancer

Soy research has indicated that it may contain cancer-preventing properties by binding to estrogen receptors there by disabling estrogen from further stimulating cancer cells much as tamoxifen citrate does. The isoflavones found in soy are antioxidants and can help decrease damage from free radicals however most antioxidants in the American diet are derived from other sources than isoflavones. The effects of soy on preexisting cancer are unclear and supplementing soy for modern cancer treatments (as suggested by a few so-called health care professionals) is not only careless it’s down right irresponsible and unprofessional.

a. Genistein (a predominant component of soy), which has only 1/1,000 the hormonal activity of estrogen, attaches to the breast cells (4) estrogen receptors and by doing so blocks the more potent female hormone from attaching. (5)

b. Recent research by Catherine Rice-Evans, Ph.D., co-director of the International Antioxidant Research Center at Guy's Hospital, London, has demonstrated that isoflavones are also powerful antioxidants. Like other antioxidants, they can reduce the long-term risk of cancer by preventing free radical damage to deoxyribonucleic acid (DNA).

c. Two recent studies conducted by a team of American and Chinese researchers found that Daidzein (a component of soy) may reduce the risk of cancer by activating immune cells. In experiments with laboratory mice, researchers found that Daidzein, but not genistein, increased the activity of lymphocytes (T cells) and macrophages (a type of white blood cell). (6)

d. Although soy isoflavones look promising in the prevention of breast and endometrial cancers, researchers and clinicians have expressed caution and are reluctant to use the substances in the treatment of active cancer. Although isoflavones may help treat some cancers, the data are inconclusive; hence the hesitation. Charles Simone, M.D., author of Breast Health (Avery, 1995), discourages his breast cancer patients from eating any soy foods because their effect on active cancers is not known. (7)

A possible explanation of why plants produce phytoestrogens

Some scientists believe that plants make phytoestrogens as a defense mechanism to stop or limit predation by plant-eating animals (9,10,11). Instead of protecting themselves with thistles or thorns or tasting bad, these plants use chemicals that affect the predatory animal's fertility.

Although using estrogen-mimicking compounds for protection may sound far-fetched, it makes sense from an evolutionary stance. Many real-life examples support the theory that plants and animals change together, or co-evolve, over time.

The explanation goes something like this: to avoid predation, plants produce compounds (phytoestrogens) that limit an herbivores reproduction. Thus, the predator's population decreases and more plants prosper.

But remember, because of genetic differences, not all species or individuals of a given species will react to the phytoestrogens in the same way. While some herbivores may show fertility problems, others may acquire resistance - like some insects are resistant to pesticides and some bacteria that can survive antibiotics. Likewise, some humans may be more susceptible to the benefits and risks of phytoestrogens than others.


1. Adlercreutz H, Mazur W. Phytoestrogens and western diseases. Annals of Medicine 1997;29:95-120.

2. Whitten, P., C. Lewis and F. Naftolin. 1993. A Phytoestrogen diet induces the premature anovulatory syndrome in lactationally exposed female rats. Biology of Reproduction 49:1117-21.

3. Barrett, J. 1996. Phytoestrogens: Friends or Foes? Environmental Health Perspectives 104:478-82.

4. Stockard, C.R. and G.N. Papanicolaou. 1917. Am. J. Anat. 22:225.

5. Allen, E. and Doisy, A.E. 1923. An ovarian hormone: preliminary report on its localization, extraction and partial p Hughes, C. 1988. Phytochemical mimicry of reproductive hormones and modulation of herbivore fertility by phytoestrogens. Environmental Health Perspectives 78:171-75.

6. Urification and actions in test animals. JAMA 81: 819.

7. Simone CB, Breast cancer: nutrition and lifestyle modification to augment oncology care. 26th Annual Nutritional Medicine Today Conference; 1997 Apr 18-20; Toronto, Ontario, Canada

8. Supported by USPHS CA56273, CA65628, CA45181, John Sealy Memorial Endowment Fund for Biomedical Research, American Institute for Cancer Research grant 95B119, and NIH NCRR GCRC grant M01 RR00073

9.Ehrlich, P. and P.H. Raven. 1964. Butterflies and plants: A study of coevolution. Evolution 18:586-608.

10.Guillette, L.J. Jr. 1995. Endocrine disrupting environmental contaminants and developmental abnormalities in embryos. Human and Ecological Risk Assessment 1(2):25-36.

11.Hughes, C. 1988. Phytochemical mimicry of reproductive hormones and modulation of herbivore fertility by phytoestrogens. Environmental Health Perspectives 78:171-75.


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