Editor's Note: Despite the mountain of conclusive research available to the public on the benefits of soy consumption--most specifically, the protein fraction, there continues to be disinformation about "anti-nutritional factors," and the "body's needs for animal proteins." To dispense these favorite arguments of the meat lobby and their apologists, in 1996 we asked Dr. Suzanne Paxton, one of the world's most respected phytopharmacologists, to write a synopsis of available findings on the nutritional benefits of soy protein, incorporating the most recent data. We proudly present her paper below. (Concluded: August, 1996; updated: March, 1998).

by Dr. Suzanne J. Paxton (R.Ph.), B.S. Biochemistry, B.S. Pharmacy, R.Ph., Pharm. D.; President, Preventive Nutrition Consultants, Inc., Seattle WA
Copyright 1996, PNC, Inc.  Preventive Nutrition Consultants, Inc., a Maryland Corporation, has served food supplement and food ingredient manufacturers since 1991 as a source of scientific information, consultation and clinical research design for the development of food supplements, pharmafoods, nutraceuticals and designer foods, as well as informing the public of the healthful phytochemical constituents of whole foods through publications, lectures and media interface. Please e-mail any comments to directly to Dr. Paxton.

Following is a commentary and review of the important medicinal effects of soy, or soy phytopharmacology. "Phyto" refers to plant and "pharmacology" refers to medicinal effects of the non-nutrient and some nutrient components of soy.

This brief expose is endeavored to address the need for understanding of the topic of the medicinal effects of the naturally-occuring biochemical constituents of soybeans for both the health-concerned layperson and the medical and scientific professional. To that end, Soy Protein: Your Key to Better Health is written in several text types, bold to leave you with quick summary points to better help you formulate the importance of soy to your diet, regular text for a more in-depth explanation for those interested in greater detail. All 218 references are in italics.

Hippocrates said, "Let your food be your medicine; let your medicine be your food."

Soy is no exception in possessing an array of important phytochemicals which current studies are revealing to have highly significant health benefits beyond simply being a source of protein in our diets. Soy exhibits high levels of significantly unique phytochemicals to merit its inclusion against all other protein sources as an imperative towards cancer and cardiovascular disease prevention which together comprise over 70% of all deaths.

In Vitro, clinical, animal, human and retrospective epidemiological human studies indicate that the frequent and high intake of fresh vegetables and fruits and grains is associated with lower cancer and heart disease incidences and that high plasma levels of ascorbate, alpha-tocopherol, beta carotene, vitamin A and certain phytochemicals are inversely related to cancer incidence. The phytochemicals that are believed to be cancer preventives generally possess one or more common biological properties-- induction of phase I or II xenobiotic detoxification enzymes, modulation of phase I and other enzyme activities, antioxidant activity, electrophile scavenging activity (i.e. they are nucleophiles), inhibition of nitrosation and, modulation of oncogene or protooncogene expression or function, DNA blocking and anti-tumor promotion activities.

But there is a lot of confusion, promoted not by scientific fact but rather competing market interests, brought upon the public as to the plusses and minuses of consuming soy - in fact, vegetable-sourced proteins in general. Proof of attribution of health benefits is sometimes direct or inferable. But in the majority of cases, soy's, and certain other phytochemicals, are scientifically interpretable as responsible factors for diminished disease rates. It is the contention of this author that, concurrent with overall markedly enhanced consumption of fruits and vegetables, soy and other vegetable protein sources are an imperative for inclusion as all or part of the evolving American dietary measures to meet protein requirements. A diet which acknowledges our susceptibility to disease states, that we are biologically "meant to" consume higher variety and quantities of WHOLE fruits and vegetables and grains in order to experience optimum human health. Not only are there great health benefits of inclusion of soy, but ALSO from the reduced health complications of meat protein sources and potentially the reduced health complications of hormone replacement therapies, antihypercholesterolemic therapies, and without hardly needing to mention-- therapies to treat advanced atherosclerosis, or worse cancer.

Emphasize variety in every dietary aspect; fruits, vegetables, grains, and protein sources in order to cover the widest nutrient and phytochemical spectrum.

Make no mistake about it, the biological health impact of these phytochemicals has not gone unnoticed by pharmaceutical interests. They seek to isolate actives, and since these food-derived chemicals are non-patentable they will produce patentable synthetic variations (Ipriflavone, a synthetic version of genistein, for example) specifically designed and even enhanced to address the disease preventive and curative capacities of the naturally-occurring versions. This is fine for a specific cancer or disease treatment or preventive. But overall, for the general public, the possible fault with this is twofold: First, it is economically and ethically misguided to not simply inform the American public, and in an aggressive manner, about the urgency and expediency of their making even simple dietary alterations based upon scientific facts rather than to try to sell them a pill or a capsule. Secondly: Again, the concept of grouped synergy comes into play, wherein NO SINGLE SYNTHETIC OR DERIVED CHEMICAL ENTITY CAN MATCH A WHOLE FOOD.

It will never duplicate the chronic baseline consumption of hundreds of phytochemicals of import to human health. Case in point, beta carotene, which is among SIX HUNDRED carotenoids in foods; it is an important contributor to health, but not the only one. Standing alone, it's health impact is minimized, whereas it is amply documented as tremendoulsly chemopreventive, as one of many carotenoids from a food source, and like soy phytochemicals it may require synergy with other constituents to produce the best effects on health. So...

... Eat your soy as a whole food, not a derivative.

Secondly, Americans eat too much meat protein, and protein in general, this adversely affects our cancer (excess protein is tumor-promoting) and heart disease rates (saturated fats and cholesterol in meats), and can contribute to other diseases, especially osteoporosis.

Third, other populations who consume less meat protein and include more soy protein are generally healthier in terms of certain lower disease rates and "diseases of affluence", i.e. cancer--breast and prostate especially, heart disease, diabetes, osteoporosis, and menopausal symptoms, to name a few. Soy's unique phytochemical, genistein, especially is important for both men and women. Based upon epidemiological data, men can look to lower risks for prostate cancer and younger women to lower risks for breast cancer and other estrogen-dependent cancers.

And the message to post-menopausal women who are considering hormone replacement therapy: Data pointing to the health risks of augmenting with conjugated estrogens and medroxyprogesterone, the expense of such, and the availability of soy products and scientific backing making consumption of soy an easy, potential alternative to alleviating symptoms pharmacologically-- a step which unlike and as opposed to taking estrogen and progesterone will decrease your incidence of cancer based upon the retrospective epidemiologic studies--ALL of this indicates that should you desire a healthful alternative to estrogen /progesterone therapy for postmenopausal symptoms (not replacement for oophorectomized women), consuming soy with 40-50 mg isoflavone content per day may obviate the need for exogenous hormone drug therapy. Check with your doctor first, of course, but soy consumption within a varied diet and with vitamin and calcium supplementation, barring allergy to soy, may be worth a trial before starting hormone therapies.

And in what forms? Data appears to indicate tofu, soy flour, soy milk and isolated soy protein products as most efficacious in terms of disease prevention, even as only part of a non-vegetarian diet. Vary your plant protein sources, minimize your animal protein sources. Take a multivitamin with calcium if your diet warrants it. Low fat soy milk and tofu have fewer isoflavones. You need to get 40-50 g of soy protein a day for best cancer and cardiovascular prevention benefits, about 1 or 2 1/2 cup cooked servings. Tofu or soy milk has about 7 grams of protein per serving. Try to get 3-four ounce servings of tofu or 3 cups of soy milk; or whole soy WITH the fat is best.

Seattle Times, Moly Martin Pacific Magazine: Messina "On Fitness: Savoring Soy--From little beans many benefits grow", January 28, 1996

Potential synergy with isoflavones and other estrogenic phytosterols may prove important as opposed to one single molecular entity such as genistein.

Soy's isoflavone genistein, again, is a natural analog to the drug tamoxifen, which is also, oddly, an estrogen with antiestrogen activity. Thus, both soy and tamoxifen seem to block estrogen's ability to stimulate malignant (tumor promoting) changes in breast tissue, while promoting beneficial effects on the skeleton and cardiovascular system. Other soy compounds may also halt the growth of cancerous cells even though they do not have any estrogen receptors to block, meaning soy may fight cancer in at least two or more separate ways. Thus, soy may help prevent cancer in both pre and post menopausal women, independently of estrogen supplies. Isoflavones also have been shown to destroy certain cancer gene enzymes that can propagate and transform a normal cell into a cancer cell, cause cancer cell differentiation (reverting it back to normal states), and inhibit blood vessel growth to larger tumors.

Isoflavones are a type of estrogen, though 500-1,000 fold weaker than human estrogen. Called an "estrogenomimetic", since it mimics estrogen, soy isoflavones "clog up" estrogen receptor sites on cells of say the breast tissue, blocking potent estrogen from linking up, affecting cell turnover rates, which also increase the rate of DNA reproduction and thus the possibilities for mutations or errors, which can lead to malignant transformations, or cancer. Soy isoflavones diminish the possibilities of mutations leading to cancer in estrogen-responsive tissues by slowing cell turnover rates. But at the same time these molecules occupy estrogen receptor sites on the cell, isoflavones produce mild estrogenic effects, enough to, ongoing studies show, potentially calm the symptoms of menopause.

Too much of the hormones you make naturally can increase your risk of cancer; soy helps diminish the risk.

Breast cancer rates are linked in with a woman's reproductive history. The longer the body is bathed with estrogens, the higher is a woman's risk of developing cancer. The earlier a woman starts menstruating and the later she stops, the higher is her risk for cancer, especially breast cancer. If a woman has had few or no pregnancies and long reproductive years, she has a higher risk of getting breast cancer. Women are less at risk for developing breast cancer, however, if they have an early menopause or if they have their ovaries removed surgically so that menopause is induced, however other complications from hormone replacement therapies for oophorectimized (removal of the ovaries) women will usually outweigh the benefits of lowered breast cancer risk.

The older a woman is when she first becomes pregnant, the higher is her risk of developing breast cancer. A woman who delivers her first child after the age of 35 has a threefold higher risk of developing breast cancer than a woman who bears her first child before the age of 18. Women who never become pregnant and women who never menstruate have a three or four times higher risk of developing cancer, especially breast cancer. In addition, if a woman had an abortion in the first trimester of her first pregnancy, whether it was spontaneous or induced, she is 2.5 times more likely to develop breast cancer.

Women with "lumpy breast disorders" fibrocystic disease --of which some conditions can be inconsequential--others can predispose to breast cancer-- is affected by caffeine, hormonal changes, reduction in fat intake. A USC study showed exercise in females reduced estrogen levels leading to irregular menses but also reduced breast cancer incidence. Soy intake can increase an average menstrual cycle by 2.5 days, which means a lower concentration of estrogen exposure of breast tissue over time.

Since soybeans are full of plant estrogens and estrogen promotes breast cancer, how do soybeans prevent breast cancer? It's a paradox; soybeans seem to mimic the body's estrogen without having its detrimental effects.

There are three clinical studies ongoing to officialize the linkup between soy's beneficial effects on menopause; Bowman Gray School of Medicine at Wake Forest University, Winston-Salem, NC, by Greg Burke, M.D. who heads a study of 240 women over age 45 with night sweats or hot flashes. The women take 8 oz of soy beverage per day with 1 mg, 34 mg or 50 mg isoflavones, tracking hot flashes, night sweats, and menopausal symptoms such as anxiety or mood swings. Two other studies at Tufts headed by Dr. Gorbach involve 60 women subjects with hot flashes followed for 3 months, they will eat either two specially designed almond-or chocolate flavored soy breakfast bars that contain 20 mg isoflavones each, totaling 40 mg per day, or two placebo bars without. In another study on soy and flax, by Mark Wahlqvist at Monash University in Victoria, Australia, show estrogenic activity from soy protein (i.e. soybeans, TVP, tofu, milk and tempeh, not soy sauce or oil) and flax lignans in 25 postmenopausal women via vaginal smears showing cell maturation accelerated, an indicator of estrogenic activity. According to Dr. Gorbach, preliminary data for soy to address symptoms of menopause looks promising.

Though studies have not reached ultimate completion, there is still great logic in implementing a trial of soy instead of hormone replacement therapy, because...

There are risks associated with Hormone Replacement Therapy (HRT) for postmenopausal women. Formerly called Estrogen Replacement Therapy, ERT, but progesterone routinely is added as a therapeutic component.

à A review of exogenous (not produced by the body) hormones and their relationship to cancers will help elucidate the logic of the potential for soy as a hormone replacement alternative.

Too much of the hormones we are exposed to from the `outside' can increase our risk of cancer; soy helps to diminish this risk.

Hormones in the environment and in our food: Regarding diethylstilbestrol, or DES, for example, there was shown a higher risk of vaginal and cervical adenocarcinomas and dysplasia in women who were exposed to the drug as fetuses. Sons of DES exposed mothers have reproductive and urinary tract abnormalities, including undescended testes, which may lead to cancer of the testes if uncorrected. In Italy from 1977-1979 there was an epidemic of breast enlargement in children caused by DES in meat. There are still hormones of unknown origin often used in meats. As for oral contraceptives: The great majority of studies show an increased risk of developing breast cancer in those who use oral contraceptives. Comprehensive reviews of all previous epidemiological studies that have been reported confirm that oral contraceptives are a risk factor for breast cancer, cardiovascular disease and liver and cervical cancers. Progesterone contraception and that combined with estrogen for HRT which supposedly reduces endometrial cancer rates and bleeding, is linked with increased breast, cervical and uterine and ovarian cancer in women. There are risks associated with hormone replacement therapies to address menopausal symptoms which imply an increase in the rate of hormone-related cancers; there are reduced risks of hormone-related cancers associated with soy consumption to accomplish the same benefits in menopause.

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Soy can help many. More on Hormone Replacement Therapies: The Life expectancy in women today is 86, average menopausal age is 51.5 years, one-sixth of the US population is postmenopausal women. The number of women age 65 and over will double by the year 2000, and about 75% of all American females it is predicted will endure menopausal symptomatologies, particularly hot flashes. Estrogens are used to prevent osteoporosis and minimize the effects of menopausal symptoms, like hot flashes, vulvovaginal dryness, urinary frequency, urgency, incontinence, dyspareunia (difficult or painful intercourse), and skin and hair changes associated with inadequate estrogen and relative androgen excess. With employment of estrogens, there is also an increase in the development of endometrial cancer, so that progesterones are added in to diminish this risk, however, this in effect increases the risk of several other cancers.

Colditz, et al. 1990. Prospective study of Estrogen Replacement Therapy and Risk of Breast Cancer in Postmenopausal Women. JAMA 264(20):2648-53.

Henderson, et al. 1982. Endogenous hormones as major factor in human cancer. Cancer Research 42:3232-3239.

Kirk, M.E. 1979. Tumorigenic aspects. Int J. Gyn OBS 16: 473-478

Schwarz, barry, 1981. Does Estrogen Cause Adenocarcinoma of the Endometrium. Len Ob Gyn 24:790-795.

Our environment contains many powerful carcinogens, in our air, water, food, and the electromagnetic fields around us. Lag time between tumor initiation events and promotion towards frank malignancy causes attribution uncertainties. We must clean our environment, but do we must do as much as we can dietarily and otherwise to maintain our health status.

Soy intake is extensively documented to have retrospective epidemiologal links to disease prevention.

Data on Soy Consumption and Cancer, Heart Disease and Menopausal Syndrome Prevention: In Countries around the World, especially in the East, soy consumption is strongly linked with cancer rate reduction, especially, breast, colo-rectal, stomach, lung and prostate, significantly reducted heart disease rates, and especially reduction of menopausal symptomatologies such that the need for hormone replacement therapies might be precluded:

The greater share of US soy is grown for animal livestock feed, much of the balance is shipped to Japan for human consumption. The US breast cancer rate is four-fold that of Japan, five-fold that of China, and TEN-fold that of Korea--one in nine American women will get breast cancer, the US prostate cancer rates are comparatively five-fold, thirty-fold and six-fold, respectively--one in eleven American men will get prostate cancer. And, interestingly, Japanese and American men experience the same rate of histologic prostate cancer, yet American men suffer five times the clinical rate. Soy inclusion into Eastern diets does not wholly verify attribution as these diets are lower in fat, animal product and higher in fruit, vegetable and fiber than US diets. And yet, retrospective epidemiologic links reflect that frequent consumption of whole soyfoods reduces cancer, heart disease and menopausal symptomatology rates as evidenced by the following examples:

• A 1,500 subject Chinese lung cancer incidence study linked inversely proportional soy consumption with lung cancer incidence; the highest intake showing up to a 50% reduction.
• Eight thousand Japanese-American males consuming tofu once per week were three times as likely to get prostate cancer as those who ate it daily.
• Familial hypercholesterolemic children from Austria on 30% fat diet (Type II) plus 20% soy protein achieved a 37% reduction in LDL without much effect on HDL cholesterol.
• In a China study soy consuming subjects experienced one third the rectal cancer rates of light consumers.
• In a Japan study, soybean or tofu consumption of 1-2 servings a week reduced the rectal cancer risk by 80%+ and colon cancer by 40%+.
• In a Singapore study, women with the lowest, i.e. 50% breast cancer risk had consumed about two servings or 55 grams of soy per day compared with nonconsumers or rare consumers.
• In China, soy milk consumption was linked with 50% risk reduction for stomach cancer, and 40% lower for regular soy consumption.
• In Hong Kong daily consumption allowed for a 50% reduction in lung cancer incidence compared to much lower consumptions.
• In the US tofu consumption was linked with 50% reduction in colon cancer rates.
• Japanese Hawaiians consuming tofu experienced a third lower risk of stomach cancer than non-consumers.
• Many studies point to LDL cholesterol reduction by a minimum of 15% or more via inclusion of soy protein in the diet, especially in conjunction with a low cholesterol diet.
• Mildly hypercholesterolemic men from the University of Illinois achieved significant blood LDL cholesterol reduction from a 50 g protein intake from soy milk versus casein or milk protein.
• Soymilk has been shown to inhibit the oxidisability of LDL cholesterol in humans.
• Miso soup was implicated as preventing Nagasaki radiation damage in human patients, and in another study in a 66% risk reduction for stomach cancer.
• Italian familial hypercholesterolemic children on a concurrent low fat/soy protein (20 g per day) diet reduced LDL cholesterol by 26%
• Japanese men adding 20 g soy protein without other changes to the diet experienced lowered cholesterol levels.
• Soy also blocks formation of nitrosamines, the worlds most dreaded carcinogen, leading to liver cancer. Soy substances did the job better than ascorbate, which is put into cured meats which contain nitrates and nitrites, explicitly to inhibit nitrosamines.

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As a result of a NCI June 27, 1990 Symposium on the Anticancer Effects of Soybeans, the participants agreed that soy played a strong role in preventing cancer and identified five individual anticarcinogens in soybeans, after which time NIC allocated $3 million for research on the anticancer effects of soybeans. Soy phytochemicals address a Soy phytochemicals address a wide range of conditions.

Following is a listing detailing the phytochemical components of greatest interest as well as their mechanisms of action and efficacy study results.

Also reduced is LDL oxidation which can lead to atherosclerosis, and blood thinning helping to prevent heart attacks and stroke. Additionally, isoflavones may prevent or slow prostate cancer growth in men significantly. Isoflavones help prevent DNA damage leading to mutations by acting as antioxidants, block blood vessel growth to tumors (antiantiogenesis factors), cause certain tumor cells to revert to their `differentiated' or noncancerous state, and inhibit tumor cells by inhibiting their products.

Soybeans are quite uniquely rich in phytoestrogens called isoflavones resemble estrogens greatly in structure acting as strong competetive estrogen receptor weak agonists--estrogenomimetics. In vying for receptors yet eliciting little signal potency in high estrogen females, they act as antiestrogens and in fact mute administered estrogens in test subjects. Isoflavones are orally absorbed, achieve good blood levels and genistein is excreted renally as equol in the urine of most people.

In one study women's menstrual cycles were increased by 2.5 days per cycle, additionally the gonadal-pituitary axis was affected with decreased LHRH levels as well; thus overall long term soy intake reduces replication thus, the mutation rate of mammary tissue.

Isoflavones increase hepatic P450 isozymes and prostglandin synthase and reduce Benzo[a]pyrene metabolism. Tamoxifen utilized in estrogen receptor positive mammary tumor patients or high-risk breast cancer patients as an estrogen blocker enigmatically also shows proestrogenic effects likely attributable to a dual isomeric version of the drug molecules whereas genistein, daidzen and other isoflavones are strongly estrogen receptor competitive weak agonists. Tamoxifen is being utilized as an antiestrogen in a 16,000 woman breast cancer chemoprevention study by the NCI.

Retrospective epidemiologic attribution links isoflavones to a reduced breast cancer risk with vegetarian and Asian groups commensurate with high isoflavone renal product excretion. Animal cancer soy inclusion dietary studies show at least a 50% reduction in breast and prostate tumors compared to isoflavone absent soy controls. Over 200 scientific papers published on genistein detail in vitro cancer cell inhibition for mammary, colon, prostate, lung, skin and leukemia cancer cell lines.

Animal in vivo data show that genistein directly inhibits skin and precolon tumors. Genistein is a good antioxidant, an extremely potent tyrosine kinase inhibitor; tyrosine kinase concentration in breast epithelium being a good indicator as to malignancy-- and other oncogene protein product inhibitor--the theory being that if you can inhibit the activity of this enzyme along with others overproduced you can stop a normal cell from being transformed into a cancer cell.

When DNA damage has accumulated beyond repair and an inheritable irreversible mutation (such as a deletion of a tumor-suppression gene) has occurred, usually oncogenes become activated. When this happens, oncogene protein products, usually enzymes like tyrosine kinase get over-expressed. If these isoflavones get into the breast compartment and keep this oncogene product in check, it may partially explain lower incidences of breast cancer as seen in Oriental women who consume up to 100 mg of isoflavones daily as opposed to Western families.

Genistein causes direct tumor cell differentiation (of de-differentiated cells) and acts as an antiangiogenesis factor slowing tumor growth, though at higher levels than required to initially prevent cancer cell growth. Additionally, genistein affects atherosclerosis thus heart disease in its antithrombin effects, inhibitory activity of smooth muscle cell proliferation hence plaque formation and antioxidant qualities preventing oxidation of LDL. By adding isoflavones to the diet, cholesterol levels can drop by as much as 35%. A recent study showed that genistein inhibited human prostate cancer cell lines and may possibly delay onset of clinical prostate cancer by 10-15 years. Genistin is the beta-glucoside conjugate of genistein; genistein and soybean flour with genistin reserves and normal genistein levels were both shown to induce P450 xenobiotic metabolizing isozymes, likely though genistein which is highest in fermented soy is better assimilated, genistein in lower levels in nonfermented still shows activity, and higher quantities of the less pungent nonfermented products can be consumed, which do exhibit the chemopreventive effects.

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Adlercreutz, H., et al. Lignan and phytoestrogen excretion in Japanese consuming traditional diet. Scand J Clin Invest 48:190, 1988.

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Akiyama, T. et al., Genistein, a specific inhibitor of tyrosine-specific protein kinase. J Biol Chem 262-5592-5595, 1987.

Asahi, M. et al. Thrombin-induced human platelet aggregation is inhibited by protein tyrosine kinase inhibitors. ST 638 and genistein. FEBS 309:10-14, 1992.

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Barnes, S., et al. Soybeans inhibit mammary tumor growth in models of breast cancer. In Mutagens and carcinogens in the diet MW Pariza, ed. pp239-253, Wiley-Liss, NY 1990.

Bickoff EM, et al. Relative potencies of several estrogen-like compounds found in forages. Agric Food Chem 10:410-412, 1962.

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Carter, MW, et al. Estimation of estrogenic activity of genistein obtained from soybean meal. Proc Soc Exp Biol Med 84:506-507, 1953.

Cassidy, A, et al. Biological effects of plant estrogens in premenopausal women. Fed Am Soc Exp Biol 7 (abstr): A866, 1993.

Cheng, E. et al. Burroughs W. Estrogenic activity of some isoflavone derivatives. Science 120:575-576, 1954.

Cheng, E., et al. Burroughs W. Estrogenic activity of isoflavone derivatives extracted and prepared from soybean oil meal. Science 118:164-165, 1953.

Esaki, H., et al. Antioxidative Activity of Fermented Soybean Products. Food Phytochemicals For Cancer Prevention/ Fruits and Vegetables: Edited by Huang, Osawa, Ho and Robert Rosen, ACS Symposium Series 546; copyrigh 1994, American Chemical Society Press.

Farmakalidis, E. et al. Oestrogenic potency of genistein and daidzin in mice. Fd Chem Tox 23:741-745, 1985.

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Folman, Y, et al. Effect of norethisterone acetate, dimethylstilbesterol, genistein and coumesterolon uptake of [3H]oestradiol by uterus, vagina and skeletal muscle of immature mice. J Endocrinol 44:213-218, 1969.

Folman, Y. et al. The interactin in the immature mouse of ptentoestrogens with coumestrol, genistein and other utero-vaginotrophic compounds of low potency. J. Endocrinol 34:215-225, 1966.

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Kitts, DD, et al. Uterine weight changes and 3H-uridine uptake in rats treated with phytoestrogens. Can J Animal Sci 60:531-534, 1980.

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Messina, MJ, et al. Soybean intake and cancer risk: a review of the in vitro and in vivo data. Nutr Cancer. Manuscript

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Noteboom, WE et al. Estrogenic efffect of genistein and coumestrol diacetate. J Endocrinol 73:736-743, 1963.

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Petersen, Greg, et al. The Prostate, Volume 22, 1993, 335-345.

Pratt, DE et al. Source of antioxidant activity of soybeans and soy products. J. Food Sci 44:1720-1722, 1979.

Saiaslani, F.S., et al. Genistein and Soybean Flour Induce P45 in Streptomyces griseus. Biochem Biophys Res Commun. 1986, 141, 405-410.

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Shutt, DA, et al. Steroid and phytoestrogen binding to sheep uterine receptors in vitro. Je Endocrinol 52:299-310, 1972.

Shutt, DA. Interaction of genistein with oestradiol in the reproductive tract of the ovarietomized mouse. J Endocrinol 37:231-232, 1967.

Sit K-H, et al. Effects of genistein on ATP induced DNA synthesis and intracellular alkalinization in Chang liver cells. Japan J Pharmacol 57:1109-1111, 1991.

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Tang, BY, et al. Effect of equol on oestrogen receptors and on synthesis of DNA and protein in the immature rat uterus. J Endocrinol 85:291-297, 1980.

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Watanabe, T. et al. Induction of in vitro differentiation of mouse erythroleukemia cells by genistein, an inhibitor of protein kinases. Cancwer Res 51:764-768, 1991.

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Welshons, WV, et al. A sensitive bioassay for detection of dietary estrogens in animal feeds. J Vet Diagn Invest 2:268-273, 1990.

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Wong E, et al. The oestrogenic activity of red clover isoflavones and some of their degradation products. J Endocrinol 24:341-348, 1962.

Saponins have a potential role as cancer preventive agents acting as antioxidants, antimutagens and even antiretrovirals in vitro HIV studies and anti-DNA virals in Epstein-Barr virus inhibition studies. In one study, saponins were shown to directly inhibit colon cancer. Possible attribution as a colon cancer preventive based on retrospective epidemiologic studies of vegetarians and Asian populations places saponins intake as a possible important chemopreventive measure. Saponins can stimulate immunity, directly slay certain cancer cells, slow the growth of cancerous cervical and skin cells, and can even reverse the proliferation of cancerous colon cells. The Japanese eat five times these cancer fighters than Americans; Westernized vegetarians eat about 345 mg saponins per day. Saponins are steroid glycosides with detergent properties, sometimes used as foaming agents in foods and cosmetics, they very often have low LD50's and often potent medicinal effects. Soy saponins resemble cholesterol in structure and are thought to lower cholesterol by enhancing excretion or blocking absorption of cholesterol.

Calvert, GD, et al. A trial of the effects of soya-bean flour and soya-bean saponins on plasma lipids, faecal bile acids and neutral sterols in hypercholesterolaemic men. Br J Nutr 45:277-281, 1981.

Elias, R, et al. Antimutagenic activity of some saponins isolated from Calendula officianalis L, C. arvenis L. and Hedera helix L. Mutagenesis 5:327-331, 1990.

George et al: Food Cosmet. Toxicol, 3, 81, 1965.

Liener, IE. Factors affecting the nutritional quality of soya products. J Am Oil Chem Soc 58:406-415, 1981.

Nakashima H, et al. Inhibitory effect of glycosides like saponin from soybean on the infectivity of HIV in vitro. AIDS 3:655-658, 1989.

Oakenfull, D. Saponins in Food--a review. Food Chem 6:19-40, 1981.

Ohominami, H., et al. Effect of soyasaponin on lipid metabolism. Proc Symp Wakan-Yaku 14:157-162, 1981.

Ridout CL, et al. UK mean daily intakes of saponins, intestine permabilizing factors in legumes. Food Sci Nutr 42F-111-116, 1988.

Tanizam, H. et al. Inhibitory effect of soyasaponins on the increase of lipid peroxide by adriamycin (ADR) in mice. Proc Symp Wakan-Yaku 15:119-123, 1982.

Tokuda, H., et al. Inhibitory effects of 12-O-tetrdecanoylphorbol-13-acetate and teleocidin B induced Epstein-Barr virus by saponin and its related compounds. Cancer Lett 40:309-317, 1988.

Phytosterols are plant steroidal-like compounds similar to cholesterol in appearance. Sitosterol for example differs by only an ethyl group on C-24 from the animal version of the cholesterol molecule--the soy stigmasterols are used as precursors for steroid drug syntheses. The soy sterols, are not physiologically active, are not highly absorbed and precipitate bile acids thus reducing enterohepatic recycling of colon tumor-promoting biliary components which may result in oxidative damage to crypt cells and micronuclei accumulation. One type of phytosterol in the lab reduced colon tumor incidence by 50 percent, and was effective against skin cancer; retrospective epidemiologic studies possibly implicate phytosterols with the low incidence of colon cancer in Japanese, vegetarians, and Seventh Day Adventists, though again attribution is difficult in that these populations generally consume more plant foods. Our western diet yields 80 mg of phytosterols per day; the Japanese consume about 400 mg per day.

Deschner, EE et al. The kinetics of the protective effect of Beta-sitosterol against MNU-induced colonic neoplasia. J Cancer Res Clin Oncol 103:49-52, 1982.

Hirai K. et al. Cholesterol, phytosterol and polyunsaturated fatty acid levels in 1982 and 1957 Japanese diets. J Nutr Sci Vitaminol 32:363-372, 1986.

Janezic, S, et al. Role of dietary phytosterol in colon carcinogenesis. Abstr Proc 34th Annu Mtg Can Fed Biol Soc., Kingston, Ontario, 1991.

Raicht RF, et al. Protective effect of plant sterols against chemically induced colon tumors in rats. Cancer Res 40:4-3-405, 1980.

Weihrauch, JL et al. Sterol content of foods of plant origin. JADA 73:399-47. Hill, MJ. Bile acids and colorectal cancer: hypothesis. Eur J. Cancer Prev 1 (Suppl 2):69-73, 1991

Yasukawa, K., et al. Sterol and triterpene derivatives from plants inhibit the effects of tumor promoter and sitosterol and betulinic acid inhibit tumor formatin in mouse skin two-stage carcinogenesis. Oncology 48:72-76, 1991.

Soy bran or hulls, high in phytates have been vilified as antinutrient factors for binding calcium, magnesium, zinc and iron in the intestines and preventing absorption. Not surprisingly, researchers attempt to remove it via processing and genetic engineering of the bean.

Phytates are present in many other plant sources, for example in wheat hulls at quite high rates. In NORMAL diets in which soy is being consumed with a calcium supplement added into the diet, or dietary calcium sources emphasized, or as a partial replacement for meat OR in combination with other plant protein sources, and where soy is not the sole dependent source for amino acids, such loss can be looked on as minimal. And actually the fact is that diets LOWER in overall protein have an associated lower risk of osteoporosis; apparently the types of amino acids comprising the bulk of the protein intake dictate the risk factors for osteoporosis to some degree; in the case of soy which is low in sulfur-containing amino acids, stronger bones are maintained because there is less calcium excretion as the sulfate salt. Whereas an equivalent weight protein from milk, meat or casein equates to much higher calcium losses, which are also proportionate with higher meat protein intakes due to insoluble calcium phosphate fecal losses.

Additionally, it has been speculated and proven that because phytates which are the storage form for plant phosphorus bind excess iron which promotes free radical DNA damage in the colon it can reduce this local oxidative damage. Phytates are associated with plant fiber which also reduces the incidence of colon cancer, and phytates directly reduce serum cholesterol and triglycerides, a partial risk factor for athersclerosis.

Phytates prevent absorption of excess iron in its most oxidative ionized form. Excess iron at the level of the colon, and systemically, can lead to an enhanced oxidative environment which is implicated in heart disease, diabetes, arthritis and, of course, cancer. Additionally, phytates enhance NK cells, and can directly control many types of cancer cell growth.

Anand, CR, et al. Effect of protein intake on calcium balance of young men given 500 mg calcium daily. J Nutr 104:695-700, 1974.

Basat, A, et al. Oxidative stress. Biochemistry and human diseases. Pharm Weekbl (Sci) 11:199-206, 1989.

Baten, A., et al. Inositol-phosphate-induced enhancement of NK cell activity correlates with tumor suppression. Carcinogenesis 10:1595-1598, 1989.

Beardk JL Are we at risk for heart disease because of normal iron status? Nutr rev 51:112-115, 1993.

Breslau, NA, et al. Relationship of animal protein-rich diet to kidney stone formation and calcium metabolism. J Clin Endocrinol metabol 66:140-146, 1988.

Draper HH, et al. Antioxidants and cancer. J Agric Food Chem 32:433-435, 1984.

Erdman, JW, et al. Soy products and the human diet. Am J. Clin Nutr 49:725-737, 1989

Fleckenstein-Grun, et al. Calcium--a neglected key factor in arteriosclerosis. The pathogenic role of arterial calcium overload and its prevention by calcium antagonists. Annals Med 23:589-599, 1991.

Gey, KF, et al. Plasma levels of antioxidant vitamisn in relation to ischemic heart disease and cancer. Am J Clin Nutr 45: 1368-1377.

Graf E, et al. Phytic acid. J Biol Chem 262:11647-11650, 1987.

Graf, E, et al. Dietary suppression of colonic cancer. Cancer 56:717-718, 1985.

Graf, E. et al. Antioxidant functions of phytic acid. Free Rad Biol Med 8:61-69, 1990. Nelson, RL. Dietary iron and colorectal cancer risk. Free Rad Biol Med 12:161-168, 1992.

Hann H-WL, et al. Iron enhances tumor growth. Cancer 68:2407-2410, 1991.

Harland, BF et al. Phytate in foods. Wld Rev Nutr Diet 32:235-259, 1987.

Heaney, RP, et al. Soybean phytate content: effect on calcium absroption. Am J. Clin Nutr 53:745-747, 1991.

Heaney, RP. The role of nutrition in prevention and management of osteoporosis. Clin Obst and Gynecol 50:833-850, 1997.

Jarivall, RJ et al. Lowering of serum cholesterol and triglycerides and modulation of divalent ctions by dietary phytate. J Appl Nutr 42:18-28, 1990.

Kalu, DN et al. Modulation of age-related hyperparathyroidism and senile bone loss in Fischer rats by soy protein and food restriction. Endocrinol 122:1847-1854, 1988.

Lauffer RB. Iron balance, St Martin's Press. NY 1991.

Linkswiler, HM, et al. Protein-induced hypercalciuria. Fed Proc 40:2429-2433, 1981.

Lotspeich, WD. Renal tubular reabsorption of inorganic sulfate in the normal dog. Am J Physiol 151:311-318, 1974.

Maga, JA., Phytate: its chemistry, occurrence, food interactions, nutritional significance, and methods of analysis. J Agric Food Chem 20:1-9, 1982.

Margen, S, et al. Studies in calcium metabolism. I. The calciuretic effect of dietary protein AJCN 27:584-589, 1974.

McClellan, WS, et al. Prolonged meat diets with a study of the metabolism of nitrogen, calcium, and phosphorus. J Biol Chem 87:669-680, 1930.

Nelson, RL et al. The effect of iron on experimental colorectal carcnogenesis. Anticancer Res 9:1477-1482, 1989.

Nielson, BK, et al. effect of phytate on colonic epithelial cell proliferation. Cancer Lett 37:317-325, 1987.

Schuette, SA, et al. Studies on the mechanisms of protein-induced hypercalciuria in oder men and women. J Nutr 110:305-315, 1980.

Seely S. Is Calcium excess in Western diet a major cause of arterial disease? Int J Cardiol 33:191-198, 1991.

Shamsudden AM et al. Inosital hexaphosphate inhibits large intestinal cancer in F344 rats 5 months after induction by azoxymethane. Carcinogenesis 10:625-626, 1989.

Shamsudden, A.M., et al. Suppression of large intestinal cancer in F344 rats by inositol hexaphosphate. Carcinogenesis 9:577-580, 1988.

Shamsudden, AM, et al. Inositol and inositol hexaphosphate suppress cell proliferation and tumor formation in CD-1 mice. Carcinogenesis 10:1461-1463, 1989.

Shamsuddin, AM. Phytate and Colon Cancer Risk. Am J Clin Nutr 55:478-485, 1992.

Siegers CP, et al. Dietary iron enhances the tumor rate in dimethylhydrazine induced colon carcinogenesis in mice. Cancer Lett 41:251-256, 1988.

Thompson, LU, et al. Phytic acid and minerals: effect on early markers of risk for mamamry and colon carcinogenesis. Carcinogenesis 12:2041-20451, 1991.

Ullah, A., et al. Dose dependent inhibition of large intestinal cancer by inositol hexaphosphate in F344 rates. Carcinogenesis 11:2219-2222, 1990. Jariwalla, RJ, et al. Effects of dietary phytic acid (phytate) on the incidence and growth rate of tumors promoted in Fischer rats by a magnesium supplement. Nutr Res 8:813-827, 1989.

Vucenik, I. et al. Antitumor activity of phytic acid (inositol hexaphosphate) in murine transplated and metastatic fibrosarcoma, a pilot study. Cancwer Lett 65:9-13, 1992.

Brandon, D, Bates, AH, Friedman, M., ELISA analysis of soybean trypsin inhibitors in processed foods. Nutritional and toxicological consequences of food processing. M. Friedman, Ed., Plenum Press, NY 1991.

Frenkel, K., et al., Chymotrypsin-specific protease inhibitors decrease H2O2 formation by activated human polymorphonuclear leukocytes. Carcnogenesis 8:1207-1212, 1987

Goodhart/Shils; Modern Nutrition in Health and Disease, Sixth Edition, pp65, 502-503, 464-466, 475, 511, 575; Lea andFebiger, Philadelphia 1980.

Kunitz, M. Crystallization as a trypsin inhibitor from soybean. Science 101:668-669, 1945

Messadi, DV etal. Inhibition of oral carcinogenesis by a protease inhibitor. JNCI 76:447-452, 1986.

Osborene TB, Mendel LB. The use of soybean as a food. J. Biol. Chem 32:369-387, 1917.

Rackis JJ Significance of soya tripsin inhibitors in nutrition. JAOCS 58:495-501, 1981.

St Clair, WH, Billings, PC, Carew, JA, Keller-McGandy, C., Newberne P., Kennedy, AR. Suppression of dimethylhydrazine-induced carcinogenesis in mice by dietary addition of the Bowman-Birk protease inhibitor. Cancer Research 50:580-586, 1990.

St Clair, WH, et al. The effects of the Bowman-Birtk protease inhibitor on c = myc expression and cell proliferation in the unirradiated and irradiated mouse colon. Cancer Lett 52: 145-152, 1990.

Takahashi, M., et al. Inhibitory effects of soybean trypsin inhibitor during initiation and promotion phases of N-nitrosobis(2-oxopropyl_amine-induced hamster pancreatic carcinogenesis. Chemically induced cell proliferation: implications for risk assessment. pp145-154, Wiley Liss, Inc., NY 1991.

Troll, W., Wiesner, R., Belman, S., Shellabarger, J. Inhibition of carcinogenesis by feeding diets containing soybeans. Proc. Am Assoc Cancer Research 20:265 (abstract 1075), 1979.

Troll, W., Wiesner, R., Shallabarger, CJ. Holtzmn, S., Stone, J.P. Soybean diet lowers breast tumor incidence in irradiated rats. Carcinogenesis 1:469-472, 1980.

Von Hofe, E., et al. Inhibition of N-nitrosomethylbenzylamine-induced esophageal neoplasms by the Bowman-Birk protease inhibitor. Carcinogenesis 12:2147-2150, 1991.

Weed HG, McGandy, RB, Kennedy, AR. Protection against dimethylhydrazeine-induced adenomatous tumors of the mouse colon by the dietary addition of an extract of soybeans containing the Bowman-Birk protease inhibitor. Carcinogenesis 6: 1239-1241, 1985.

Witschi, H., et al. Modulation of lunt tumor development in mice with the soybean-derived Bowman-Birt protease inhibitor. Carcinogenesis 10:2275-2277, 1989.

Link to our Table of Soy Phytochemical Components to see nutrient comparisons of common sources of commercially available soy protein.

Fenwick , DE, etal Saponin content of food plants and some prepared foods J. Sci Food Agric 34:186-191, 1983. Oakenful, D. Saponins in Food--a review. Food Chem6:19-40, 1981.

Graf E, Eaton JW., Antitoxin functions of phytic acid. Free Rad Biol Med 8:61-69, 1990.

Harland, BF, Oberleas D. Phytate in Foods Wld Rev Nutr Diet 32:235-259, 1987.

Messina, The Simple Soybean and Your Health, pl74, Avery Publishing Group, 1994.

Phillipy, BG, Johnston MR, Tao S-H, Fox MRS, Inositol Phosphates in Processed Foods J Food Sci 53:496-499, 1988.

Potter, JD, Topping DL, Oakenfull D. Soya, Saponins and Plasma Cholesterol. Lancet 223, January 27, 1979. DiPietro CM, Liener, IE. Soybean Protease Inhibitors in Foods. J Food Sci 54:606-617, 1989.

PreventionAugust 1996 p67; Promine D., Central Soya Col, Inc., Illinois; G.L. 750, Griffith Labs Pty. Ltd., Victoria; Maxten, C, Miles Labs Australia Pty. Ltd., Victoria

Sources: Ridout CL, Wharf SG, Price KR, Johnson LT, Fenwick GR UK mean daily intakes of saponins--intestine permeabiliziang factors in legumes. Food Sci Nutr 42F:111-116, 1988.

Take Care High Protein Beverage Powder (Nutritious Foods, Inc.)

Thompson, DB, Erdman, JW. Phytic Acid Determinatin in Soybeans J Food Sci 47:513-1982.

*MS/HPLC Analysis; Center for Advanced Food Technology, Rutgers University, August, 1996.

Newmark HL, et al. Plant phenolics as inhibitors of mutational and percarcinogenci events. Can J Physiol Pharmacol 65:461-466, 1987.

Newmark, HL, et al. A hypothesis for dietary components as blocking agents of chemical carcinogeneis: plant phenolics and pyrolle pigments. Nutr Cancer 6:58-70, 1984.

Ramakrihna MBV, et al. Determination of phenolic acids in different soybean varieties by reversed phase high performance liquid chromatography. J Fd Sci Technol 26:154-155, 1989.

Soy and all beans contain indigestible complex sugars which lower intestinal bacteria digest and metabolize, producing some degree of flatugenic gasses.

Certain soy processes can remove the lion's share of these sugars and thus any gas problems, while retaining sufficient quantities to encourage bifidobacteria growth, a beneficial bacteria in our colon's natural flora which preferentially assimilates these complex sugars, and is associated with colon cancer reduction and cholesterol reduction.

Soy contains three sugars of particular interest, stachyose, verbascose and raffinose which are preferentially metabolized by normal flora colonic bifidobaceria and other bacterium to hydrogen and carbon dioxide; bifidobacteria populations have been associated with reduced fecal carcinogens thus colon cancer (50% reduction in animal studies) and are encouraged preferentially above harmful bacteria proliferation in the presence of these nutrients. They break down soluble fiber in the colon and produce products that may help to lower blood cholesterol.

Calloway, DH, et al. Reduction of intestinal gas-forming properties of legumes by traditional and experiemntal food processing methods. J Food Sci 36:251-255, 1971.j

Hayakawa, K, et al. Effects of soybean oligosaccharides on human faecal flora. Micro Ecol in Health and Disease 3:293-303, 1990.

Olson, A.C.: Nutrient composition of and digestive response to whole and extracted dry beans. J Ag and Food Chem; 1982; 30:26-32.

Rackis JJ. Flatulence caused by soya and its control through processing. JOACS 58:503-509, 1981.

Racks, JJ et al. Soybean factors relating to gas production by intestinal bacteria. J Food Sci 35:634-639, 1970.

Tackis, JJ, et al. Flavor and flatulence factors in soybean protein products. J Agr Food Chem 18:977-982, 1970.

Boron in soybeans where its levels are exceptionally high, may stimulate endogenous estradiol 17B in and of itself, acting like a mild estrogen replacement therapy. Blood levels with only 3 mg of added boron showed doubled the levels of the estradiol precursor testosterone. Additionally, boron is required for bone mineralization; with insufficient boron, the body cannot retain critical calcium according to Dr. Forrest H. Nielsen at the USDA Human Nutrition Research Center in North Dakota. Postmenopausal women on low-boron diets were more apt to lose calcium and magnesium, bone-strengthening minerals, but with 3 mg of boron, their calcium losses dropped by 40 percent. Vegetarians have less osteoporosis, likely due to the steroid hormone increase with boron.

Heaney, R.P.: Calciumin theprevention and treatment of osteoporosis J Int Med 1992: 231:169-180.

Nielsen, F.H.: Boron--an overlooked element of potential nutritional importance. Nutrition Today, January/February 1988: 4-7.

Lecithin contains phosphatidyl choline, a precursor to acetylcholine, the predominant parasympathetic nervous system neurotransmitter, essential for a healthy nervous system. Lecithin is a type of emulsifying fat made from degummed soy oil, with cardiovascular disease prevention data of cholesterol lowering but at quite high doses. Soy lecithin may contribute to lower gallstone incidence in vegetarians. Lung tumor s were reduced by roughly one half in one study.

Brook, JG, et al. Dietary soya lecithin decreases plasma triglyceride levels and inhibits collagen and ADP-induced platelet aggregation, Biochem Med Metab Biol 35:31-39, 1986.

Knuiman, JT, et al. Lecithin intake and serum cholesterol. Am J Clin Nutr 49:266-268, 1989.

Morrison, LM. Serum cholesterol reduction with lecithin. Geriatrics 13:12-19, 1958.

Pixley, F., et al Effect of vegetariansim on development of gall stones in women. Br Med J 291:11-12, 1985

Tompkins, RK., et al. Relationship of biliary phosphlipid and choelsterol concentrations to the occurrence and dissolution of human gallstones. Annals Surg 172:936-945, 1970.

Yun T-K. Usefulness of medium-term bioassay determining formations of pulmonary edema in NIH(GP- mice for finding anti-carcinogenic agens from natural products. J Toxicol 16 (Suppl 1): 53-62, 1991.

Soybeans also contain omega-three fatty acids, which have cardioascular (antihyperlipidemic, antithrombotic) and cancer, arthritus, diabetes (antiinflammatory) disease advantages via prostaglandin effects, i.e. encouraging PGE1 and PGE3 formation. DHA from Omega-3's are essential during pregnancy and early child development, for brain and eyesight development, and may differentiate the 8 point IQ higher status of breast fed babies over formula-fed babies. Requirements are approximately 1 gram per day; soy contains 3.2 g per 100 g green soy.

Anti, M.: Effect of omega-3 fatty acison rectal mucosal cell proliferation n subjects at risk for colon cancer. Gastroenterology 1992; 103-883-91.

Goldberg, I. Functional Foods pp366-367, Chapman and Hall, London, 1994

Horticulture and Human Health; Bruno Quebedeaux Ed.Prentice Hall Inc. NJ 1988

Karmali,l R.A.: Omega-3 fatty acids and cancer. J Int Med 1989; 225 (suppl. 1): 197-200.

Leaf, A. Cardiovascular effects of omega-3 fatty acids. NEJM 1988; 318:549-57.

Milner, M.R.: Usefulness of fish oil supplements in preventing clinical evidence of restonsis after percutaneous transluminal coronary angioplasty. Am J Cardiology, 1989; 64(5)294-99.

Newton, Ian. Prepared Foods, August 1996 pg 59.

Simoupoulos, A.P.: Omega-3 fatty acids in growth and development and in health and disease. Nutrition Today, May/June 1988:12-18.

Swern D, ed. Bailey's industrial oil and fat products. Vol. 1 4th ed. John Wiley and Sons, NY 1987. Committee on Diet and Health, Food and Nutrition Board, Commission on Life Sciences, National Research Council. Diet and health. Chap 7, National Academy Press. Wash. DC 1989.

Vitamin E is extracted from soy oil, and has a wealth of data as a lipid-soluble antioxidant involved in stalling the lipoperoxidative cascade leading to atherosclerosis, potentially involved in cancer risk reduction, especially colon cancer.

DeCosse, J.J.: Effect of wheat fiber, and vitamins C and E on rectal polyps in patients with familial adenomatous polyposis. J NCI, 1989;81(17):1290-97.

Gey, K.F.: Inverse correlation between plasma vitamin E and mortality from ischemic heart disease in cross-cultural epidemiology. American J Con Nutr 1991; 53(Suppl. 1):326S-34S.

Verlangieri, Anthony: Effects of d-a-tocopherol on experimentally induced primate atherosclerosis. J Am College of Nutr, 1992; 11(2):130-137.

Folate is also high in soybeans, which is linked with homocysteine clearance and prevention of neural tube defects; persons consuming greater quantities of leafy green vegetables had a lower lung cancer incidence; lung cancer patients' lung tissue was deficient in this B vitamin, which causes more chromosome breakage and susceptibility to tumor initiation. Part of the reason for excessive heart disease related to low xestrogen concentration in postmenopausal women is that estrogen helps clear homocysteine, a waste product from excess methionine breakdown. Folate helps fclear homocysteine, which can cause arteriolar nicking and lead to the atherogenesis lipoperoxidative cascade. Folate in excess can be tumor promoting however, it should be a nutrient taken in the form of food instead of a supplement except before and during pregnancy.

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