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Final Word On Soy!

Thanks for sharing......Kuso gives me gas.:laugh:
 
Soybean Consumption & Disease Incidence
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.
Abou-Issa H., Koolemans, Beynen, A, Meredith TA, Webb TE Anti tumor synergism between non-toxic dietary combinations of isotretinoin and glucarate Eur J Cancer 28A:784-788, 1992.

Cancer facts and figures--1992. American Cancer Society. Atlanta, GA, 1992.

Carroll, KK. Reveiw of clinical studies on cholesterol lowering response to soy protein. JADA 91:820-827, 1991.

Designer Foods III Proceedings, May 24, 1994, page 118-136.

Gaddi, A., et al. Dietary treatemnt for familial hypercholesterolemia--differential effects of dietary soy protein according to the apolipoprotein E phenotypes. Am J Clin Nutr 53:1191-1196, 1991.

Haenszel, W., et al. Stomach cancer among Japanese in Hawaii. JNCI 49:969-988, 1972.

Hodges, RE et al. Dietary carbohydrates and low cholesterol diets: effects on serum lipids of man. Am J Clin Nutr 20:198, 1967.

Hu J, et al. Diet and cancer of the colon and rectum: a case-control study in China. Inter J Epidemiol 20:362-367, 1991.

Ito, A. Is miso diet effective for radiatin injuries? MisoSci and Tech 39:71-84, 1991.

Ito, A. et al. Effects of soy products in reducing risk of spontaneous and neutron-induced liver tumors in mice. Int J. Oncol 2:773-776, 1993.

Japan Times, September 27, 1988.

Kanazawa, T. et al. Anti-atherogenicity of soybean protein. Ann NY Acad Sci 676:202-214, 1993

Kito, M., et al. Changes in plasma lipids in young healthy volunteers by adding an extruder cooked soy protein to conventional meals. Biosci Biotech Biochem 57:354-355, 1993.

Koo, LC. Dietary habits and lung cancer risk among Chinese females in Hong Kong who never smoked. Nutr Cancer 11:155-172, 1988.

Koury, SD et al. Soybean proteins for human diets? J Am Diabet Assoc. 52:480-484, 1968.

Lee HP et al. Dietary effects on breast cancer risk in Singapore. Lancet 337:1197-1200, 1991.

Meinertz, H. et al. Effects of soy protein and casein in low cholesterol diets on plasma lipoproteins in normolipidemic subjects. Atherosclerosis 72:63-70, 1988.

Meinertz, H. et al. Soy protein and casein in cholesterol enriched diets: effects on plasma lipoproteins in normolipidemic subjects. Am J Clin Nutr 50:786-793, 1989.

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

Nagai, M., et al. Relationship of diet to the incidence of esophageal and stomach cancer in Japan. Nutr Cancer 3:257-268, 1982.

Nutracon `95; Nutriceuticals, Dietary Supplements Functional Foods, July 11-13, Las Vegas Hilton, Las Vegas NV

Pool C. A case-control study of diet and colon cancer. Dissertation. Harvard School of Public Health. Boston, 1989.

Potter, SM et al. Depression of plasma cholesterol in men by consumption of baked products containing soy protein. Am J Clin Nutr 1993.

Proceedings from the Rutgers University Designer Foods III: Phytochemicals in Garlic, Soy and Licorice, Research Update and Implications May 23, 1994, WA DC.

Severson, RK, et al. A prospective study of demographics, diet and prostate cancer among men of Japanese ancestry in Hawaii. Cancer Res 49:1857-1860, 1989.

Sirtori, CR, et al. Soybean-protein diet in the treatment of type-II hyperlipoproteinaemia. Lancet 5:275-277, 1977.

Swanson CA, et al. Dietary determinants of lung-cancer risk: resuts from a case-control study in Yunnan province, China. Int J. Cancer 50:876-880, 1992.

Van Raaij, JMA, et al. Effects of casein versus soy protein diets on serum cholesterol and lipoproteins in young healthy volunteers. Am J Clin Nutr 34:1261-1265.

Watanabe, Y., et al. A case-control study of cancer of the rectum and the colon. Nippon Shokakibyo Gakkai Zasshi 81:185-193, 1984.

Yingman, Y., et al. A study of the etiological factors in gastric cancer in Fuzhou city. Chinese J Epidemiol 7:48-50, 1986.

You W-C, et al. Diet and high risk of stomach cancer in Shandong, China. Cancer Res 48:3518-3523, 1988.

Block, G.: Fruits, vegetables, and cancer prevention: a reviewof the epidemiological evidence Nutriton and Cancer 1992; 18:1-29.

Caragay, A.B.: Cancer preventive foods and ingredients. Food Technology 1992; 46:65-68.

Messina, M.: The roleof soyproducts in reducing risk of cancer. J NCI 1991; 83(8): 541-46.

Steinmetz, K.A.: Vegetales, fruit and cancer. I. Epidemilogy. Cancer Causes Contol 1991; 2(50:325-57. and II: Mechanisms. 2(6):427-42.

Barnes, S.: Soybeans inhibit mammary tumors in modelsof breast cancer. Progress in Clin and Biological Research, 1990; 347:239-53.

Howe, G.E.: Dietary factors and risk of breast cancer. J NCI 1990 82(7):561-69.

Adlecreutz, H.: Diet and breast cancer. Acta Oncologica 1992; 31(2): 175-81.
 
Soy As An Antiestrogen
A review of endogenous (made within the body) hormones and their relationship to cancers will help elucidate the potential for soy as an antiestrogen.
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.
 
FOCUS on Hormone-Related Conditions: Menopause and Cancer...
There's no word for "hot flash" in the Japanese language. Why the difference in rates of hormone related and other cancers (in both men and women) and vastly lower rates of menopausal symptoms between the US and Asian countries? The link points to soy consumption: For over 2,000 years the Asian diet has included foods made from the soybean; the typical Asian woman consumes 30-50 mg isoflavones from her soyfoods, often up to 100 mg per day without side effects or known toxicities. Soybean isoflavones are phytoestrogens, natural compounds which manipulate estrogen as well as directly inhibiting the growth of cancer cells, theoretically reducing the risk of breast cancer in women of all ages. Genistein, the most potent isoflavone, is similar to tamoxifen, given to certain women to help prevent breast cancer and its spread. More: Phytoestrogens given to animals in the form of a high soy diet were protected against carcinogen-induced cancers. Rats fed soy had 40-65% fewer breast cancers. Also, genistein alone protected against breast tumors. Studies are ongoing to determine if soy milk diminishes the biological risk for breast cancer in women as predicted via epidemiological retrospective studies from Singapore where women halved their risk via double the normal soy intake. Dr. Herman Adlercreutz at the University of Helsinki found that Japanese near Kyoto with the highest urine concentrations of isoflavonoids were protected against breast and prostate cancer. Typically the women ate three ounces of soy products a day, including tofu, miso, fermented soy and boiled soybeans.
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.
 
What Is "IN" Soy?
Chemopreventive Activity of Soy Phytochemicals
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.



Isoflavones
Isoflavones in soy are a unique and critical component for inclusion into the diets of everyone. Isoflavones can help prevent breast cancer and other estrogen responsive cancers, and may have potential as a low dose (40 - 50 mg per day) substitute for hormone replacement therapy in postmenopausal women by forestalling complications of menopause in women such as vulvovaginal dryness and hot flashes while simultaneously reducing the risks for heart disease via cholesterol reduction.
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.

Adlercreutz, H. Dietary phyto-estrogens and the menopause in Japan. Lancet 339:1233, 1992.

Adlercreutz, H., et al. Excretion of the lignans enterolactone and enterodiol and of equol in omnivorous and vegetarian women and in women with breast cancer. Lancet 2:1295-1299, 1982.

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

Akiyama, T. et al. Use and specificity of genistein as inhibitor of protein-kinases. Meth Enzymol 201:362-370, 1991.

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.

Axelson, M., et al. Soya--a dietary source of the nonsteroidal oestrogen equol in man and animals. J Elndocrinol 102:49-56, 1984.

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.

Biggers, JD, et al. Oestrogenic activity of subterranean clover. Biochem J. 58:278-282, 1954.

Bowen, R. et al. Antipromotional effect of the soybean isoflavone genistein. Proc Am Assoc Cacner Res 34:555 (Abstr 3310), 1993.

Braden AWH et al. The oestrogenic activity and metabolism of certain isoflavones in sheep. Aust J Agric Res 18:335-348, 1967.

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.

Ferguson, DJP, et al. Morphological evaluation of cell turnover in relation to the menstrual cycle in the "resting" human breast. Br J Cancer 44:177-181, 1981.

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.

Fotsis, T. et al. Genistein, a dietary derived inhibitor of in vitro antiogenesis. Proc Natl Acad Sci USA 90:2690-2694, 1993.

Golder, MP et al. Plasma hormones in patients with advanced breast cancer treated with tamoxifen. Eur J cancer 12:719-723, 1976.

Jackson, RL et al. Antioxidants: A biological defense mechanism for the prevention of atherosclerosis. Medicinal Res Rev 13:161-182, 1993.

Jordon, VC, et al. Endocrine effects of adjuvant chemotherapy and long term tamoxifen administration of node-positive patients with breast cancer. Cancer Res 47:624-630, 1987.

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

Konda, K., et al. Induction of in vitro differentiation of mouse embryonoal carcinoma (F9) cells lby inhibitors of topoisomerases. Cancer Res 51:5398-5404, 1991.

Marshall, E. Search for a killer: focus shifts from fat to hormones. Science 259:818-821, 1993.

Martin, PM, et al. Phytoestrogen interaction with estrogen receptors in human breast cancer cells. J Endocrinol 103:1860-1867, 1978.

Mayr U., et al. Validation of two in vitro test systems for estrogenic activites with zearlenone, phytoestrogens and cereal extracts. Toxicology 74:135-149, 1992.

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

Miller, WR. Endocrine treatment for breast cancer. Biological rationale and current progress. J Steroid Biochem 47:474-480, 1990.

Millington, AJ, et al. Bioassay of annual pasture legumes. The oestrogenic activity of nine strains of Trifolium subterranean L. Aust J. Agric Res 15:527, 1964.

Morley, FHW, et al. Proc NW Soc Anim Prod 28:11-17, 1968

Naim, M, et al. Soybean isoflavones, characterization determination and antifungal activity. J Ag Food Chem 22:806-810, 1974.

Natalie Angier. New York Times Science Times p. B5. April 13, 1993.

Newsome FE, et al. Action of phyto-estrogens coumestrol and genistein on cystosolic and nuclear oestradiol 17B receptors in immature rat uterus. Animal Reprod Sci 3:233-245, 1980.

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

Ogawara, H., et al. A specific inhibitor for tyrosine protein kinase from pseudomonas. J. Antibiot 39:606-608, 1986

Paterson AHG, et al. Can tamoxifen prevent breast cancer? Can Med Assoc J 148:141-144, 1993.

Perel, E, Lindner, HR. Dissociation of uterotrophic action from implanatin inducing activity in two non-steroidal oestrogens (coumestrol and genistein). J. Reprod Fert 21:171-175, 1970.

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.

Setchell ,KDR, et al. Nonsteroidal estrogens of dietary origin: possible roles in hormone-dependent disease. Am J. Clin Nutr 40:569-578, 1984.

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.

Somjen, D, et al. Specificities in the synthesis of cytoplasmic estrogen-induced uterine protein. Mol Cell Endocrinol 4:353-358, 1976.

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.

Treloar, AE, et al. Variation of the human menstural cycle through reproductive life. Int J Fertil 12:77-126, 1970.

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.

Welshons WV, et al. Stimulation of breast cancer cells in vitro by the environmental estrogen enterolactone and phytoestroegn equol. Breast Cancer Res Treatment 10:169-175, 1987.

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

Willis, KJ et al. Recurrent breast cancer terated with the anti-estrogen tamoxifen: correlation between hormonal changes and clinical course. br Med J 1:425-428, 1977.

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



Saponins
 
Saponins
Saponins may prevent cancer by protecting DNA from damage, are antiviral in in vitro studies, and directly inhibits colon cancer. Saponins may be cardioprotective via their ability to lower cholesterol.

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
Phytosterols may help prevent heart disease and certain cancers, especially colon cancer by inhibiting cell division and proliferation:
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.
 
Excellent research and posting Kuso :thumb:

Primarily the reasons why we were very "Pro-soy" until maybe 3 or 4 years ago.....(please note the age of most of the references)


A lot of the research focusing on foods and fermented soy products...not concentrates and isolates. (With the contention always that feremnted soy products have always been beneficial)

When certain isoflavones began to become prevelant in the Women's Health field (esp for hot flashes and hormonal balancing), questions began to arise concerning estrogen linked cancers.....it was found the "Red Clover" had more beneficial properties than soy, w/o the soy's constituents exerting a stronger estrogenic effect than prevously thought, soy is now being avoided at all cost by women w/breast cancer (stats are heading to 1 in 3 will contract breast cancer during their life) esp estrogen related BC.

Soy formula even before the GMO controversy has be proven to be estrogenic (young girls reaching puberty much sooner on soy).....and goiter tropic.....the thyroid controversy just coming to light.

We can't dismiss soys benfits as "Old research"......but we must filter in the new data and let each individual decide if soy is right for them. With the amount of hypothyroidism I see......I see a definite corelation to soy consumption, and feel prone to advise people to avoid, or carefully consider "excess" soy intake! :D


Excellent thread developing here!

DP
 
IML Gear Cream!
Small addendum...circa 1992-93...the USDA dictated the "Food Pyramind" based on studies (perhaps funded by the wrong groups, Ornish et al)....in an effort to "improve health!"

Eat this way and lower heart disease, obesity, etc....but what happened...

The Obesity rate doubled, the diabetic rate doubled, and age onset diabetics never/hardly before seen in people under the late thirties, is now common in 8 year olds.

Of course there are several factors in this, but the point being that the Pyramid was the "science of the time"....as I believe we wil come to look at some of the research on soy!

JMHO :D

DP
 
Originally posted by Dr. Pain
it was found the "Red Clover" had more beneficial properties than soy,


I`d be very interested on any studies/reasearch you may have on this, as well as on the the affects on goiter and other thyroid problems relating to soy.



Originally posted by Dr. Pain
thought, soy is now being avoided at all cost by women w/breast cancer (stats are heading to 1 in 3 will contract breast cancer during their life) esp estrogen related BC.

I believe in Oz those stats are correct for both breast, and prostate cancer. I do find the statement rather surprising though. I`ve never seen anywhere warning against soy for those with breast cancer, and as you know, Japan has the lowest levels of both cancers in the world, with one of the highest intacts of a variety of soys.

Originally posted by Dr. Pain
We can't dismiss soys benfits as "Old research"......but we must filter in the new data and let each individual decide if soy is right for them.

I couldn`t agree more, which is why I posted. it is also quite difficult to find much recent main streem research into soy at all which makes things harder.
 
Originally posted by Dr. Pain

Of course there are several factors in this, but the point being that the Pyramid was the "science of the time"....as I believe we wil come to look at some of the research on soy!

Of course, we could also find out that the research that "proved" the negative attributes of soy to have been funded by "the wrong gruops" too :D
 
We are going to have to leave the research to others...time constraints for me...

I am aware of the positve research...and the Japanese research including "Brain Shrinkage" from soy consumption (seriously)...and have no doubt that "soy foods" having been around for more than 5000 years have, beneficial properties:D
The Pain's have eaten mega soy over the years...lol

MP and I suffer from hypothyroidism (runs in her family, not mine), and MP suffers form Estrogen Dominance........we have also seen a corealtion, perhaps form the other differences in the American versus Japanese diet, where soy has contributed to both good and bad estrogens, stalled w8 loss, and it's avoidance has been the suggestion of many local Doctors/Oncologists in all Breast Cancers...not just Estrogen linked (why take risks)

Conversely, we have local Cardiogists/Urologists promoting soy, esp in men for the the reduction of Test, increases in Estrogen for treating Prostate Cancer (the wrong approach), and reduction of Cholesterol, theoretically reducing CHD..(again the wrong approach) :D

DP
 
Originally posted by kuso
Of course, we could also find out that the research that "proved" the negative attributes of soy to have been funded by "the wrong gruops" too :D

Agreed! :thumb:
 
Originally posted by Dr. Pain
stalled w8 loss, and it's avoidance has been the suggestion of many local Doctors/Oncologists in all Breast Cancers...not just Estrogen linked (why take risks)

It`s late, and my brain is fried, but why is this even an issue? Sufferers of breast cancer normally waste away anyway so I`m sure none of them would care too much about a little bit of bw left on...........I must be missing the issue here.
 
A more recent one, and one that has a lose connection to my other thread in here....

Soy protein prevents skin tumors from developing in mice, UC Berkeley researchers find
15 October 2001
By Sarah Yang, Media Relations


Berkeley - New research at the University of California, Berkeley, may add yet another boost to the healthy reputation of the humble soybean. A study published Oct. 15 in the journal Cancer Research shows that mice with the soy protein lunasin applied to their skin had significantly lower rates of skin cancer than mice without the lunasin treatment.
More than two years ago, the same UC Berkeley researchers discovered that injecting the lunasin gene into cancer cells in a culture stopped cell division. In their latest work, they tested whether the lunasin protein could prevent normal cells from becoming cancerous in both cell cultures and in mice.

In the study, varying doses of lunasin were applied to groups of mice over a period of 19 weeks. They were compared with a control group that had received no lunasin treatments. After the mice were exposed to chemical carcinogens, the group that had received the highest lunasin dose of 125 micrograms twice a week had a 70 percent lower incidence of tumors than the control group.

"In the high dose group, some mice did develop some tumors, but there were fewer tumors per mouse and there was a two-week delay in their appearance compared with the control group," said Ben O. de Lumen, nutritional sciences professor in UC Berkeley's College of Natural Resources and principal investigator of the study.

De Lumen is a member of UC Berkeley's Health Sciences Initiative, a partnership among biomedical sciences and technology programs geared towards advancing research into today's major health problems. He heads the lab where lunasin's anti-cancer properties were first discovered, and where Alfredo Galvez, lead author of the study, worked as a post-doc researcher. Other authors of the report include Na Chen, a doctoral student, and Janet Macasieb, an undergraduate student, both from the Division of Nutritional Sciences and Toxicology at UC Berkeley.

The researchers got clues on how lunasin works through tests in cell cultures. They showed that lunasin binds to deacetylated histones, a specific form of protein in a cell that helps package the long strands of DNA into tight coils. Lunasin seems to target cells before these histones undergo acetylation, a crucial step recently linked to cell proliferation and the formation of cancer.

In one of the tests, the cells from a lunasin culture showed an 80 percent lower incidence of transformation into cancer cells compared with non-lunasin cultures after exposure to carcinogens.

"The chemical changes that occur in normal cells before and during cancer formation signal lunasin," said de Lumen. "We believe lunasin is like a watchdog; it's out there sniffing. When it sees a normal cell transforming, it gets in there and attacks the cell."

Studies on the health effects of soy products have been building over the years. Epidemiological studies in Japan and China, where soy-rich diets are common, show people in those regions have significantly lower rates of certain cancers and heart disease than people in Western countries, where typical diets contain little to no soy.

In 1999, the U.S. Food and Drug Administration allowed manufacturers to use food labels stating that eating 25 grams of soy protein a day may help reduce the risk of heart disease. Foods must contain at least 6.5 grams of soy protein per serving to qualify for the label.

Much of the spotlight has focused on isoflavones, a soy phytoestrogen that acts like a weak form of the hormone estrogen, and the Bowman-Birk protease inhibitor (BBI), another soy component with potential anti-cancer properties.

Galvez, who has since co-founded a biotech company in Fairfield, Calif., said lunasin stands out among the other soy agents because of its unique mechanism of action. "It's based on chromatin modification, which now a lot of cancer researchers are investigating," he said.

Still, many promising anti-cancer agents never make it from the lab onto drugstore shelves, and research into lunasin is still in its infancy, said de Lumen. But he said this study suggests interesting directions for future studies and applications of lunasin.

"The key for developing a product into oral medicine is the bioavailability of the compound," said de Lumen. "How much of it is absorbed, and how much ends up in the tissue? For lunasin, we don't know the answer, yet. But the obvious application of this result is that we could formulate a lunasin product that could be applied to the skin. It could maybe be applied in a sunscreen."
 
Originally posted by Dr. Pain
We are going to have to leave the research to others...time constraints for me...

Well, I had a very quick look, and found this quote, so will leave it til I have some time to do some snopping, unless someone has a study NOT finaced by them?

Most of the studies on red clover have been sponsored by Novogen, a company that produces a red clover product called Promensil.
 
Kuso, soy sucks. Get over it.
 
Originally posted by Twin Peak
Kuso, soy sucks. Get over it.


Sucks for what though? Over all health or as a protein supp? As for the latter I agree completely, otherwise...show me the studies that refute all of the former ones?

(And no, I don`t mean the one article at test )
 
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