Soy and Thyroid Function....

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    Soy and Thyroid Function....






    Researchers have identified that the isoflavones act as potent anti-thyroid agents, and are capable of suppressing thyroid function, and causing or worsening hypothyroidism. Soy is a phytoestrogen, and therefore acts in the body much like a hormone, so it's no surprise that it interacts with the delicate balance of the thyroid's hormonal systems. High consumption of soy products are also proven to cause goiter, (Anti-thyroid isoflavones from soybean: isolation, characterization, and mechanisms of action, Divi RL; Chang HC; Doerge DR, National Center for Toxicological Research, Jefferson, AR 72079, USA, Biochem Pharmacol, 1997 Nov, 54:10, 1087-96)

    : Biochem Pharmacol 1997 Nov 15;54(10):1087-96 Related Articles, Cited in PMC, Books, LinkOut


    Anti-thyroid isoflavones from soybean: isolation, characterization, and mechanisms of action.



    Divi RL, Chang HC, Doerge DR.

    National Center for Toxicological Research, Jefferson, AR 72079, USA.

    The soybean has been implicated in diet-induced goiter by many studies. The extensive consumption of soy products in infant formulas and in vegetarian diets makes it essential to define the goitrogenic potential. In this report, it was observed that an acidic methanolic extract of soybeans contains compounds that inhibit thyroid peroxidase- (TPO) catalyzed reactions essential to thyroid hormone synthesis. Analysis of the soybean extract using HPLC, UV-VIS spectrophotometry, and LC-MS led to identification of the isoflavones genistein and daidzein as major components by direct comparison with authentic standard reference isoflavones. HPLC fractionation and enzymatic assay of the soybean extract showed that the components responsible for inhibition of TPO-catalyzed reactions coeluted with daidzein and genistein. In the presence of iodide ion, genistein and daidzein blocked TPO-catalyzed tyrosine iodination by acting as alternate substrates, yielding mono-, di-, and triiodoisoflavones. Genistein also inhibited thyroxine synthesis using iodinated casein or human goiter thyroglobulin as substrates for the coupling reaction. Incubation of either isoflavone with TPO in the presence of H2O2 caused irreversible inactivation of the enzyme; however, the presence of iodide ion in the incubations completely abolished the inactivation. The IC50 values for inhibition of TPO-catalyzed reactions by genistein and daidzein were ca. 1-10 microM, concentrations that approach the total isoflavone levels (ca. 1 microM) previously measured in plasma from humans consuming soy products. Because inhibition of thyroid hormone synthesis can induce goiter and thyroid neoplasia in rodents, delineation of anti-thyroid mechanisms for soy isoflavones may be important for extrapolating goitrogenic hazards identified in chronic rodent bioassays to humans consuming soy products.

    PMID: 9464451 [PubMed - indexed for MEDLINE]

    One UK study of premenopausal women gave 60 grams of soy protein per day for one month. This was found to disrupt the menstrual cycle, with the effects of the isoflavones continuing for a full three months after stopping the soy in the diet. Isoflavones are also known to modify fertility and change sex hormone status. Isoflavones have been shown to have serious health effects -- including infertility, thyroid disease or liver disease -- on a number of mammals.
    How Much Soy is Safe?

    According to the Soy Online Service, for infants, any soy is too much. For adults, just 30 mg of soy isoflavones per day is the amount found to have a negative impact on thyroid function. This amount of soy isoflavones is found in just 5-8 ounces of soy milk, or 1.5 ounces of miso.
    tbc

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    http://abcnews.go.com/onair/2020/202...r_feature.html


    Scientists Protest Soy Approval
    In Unusual Letter, FDA Experts Lay Out Concerns



    Researchers Daniel Doerge and Daniel Sheehan, two of the Food and Drug Administration’s experts on soy, signed a letter of protest, which points to studies that show a link between soy and health problems in certain animals. The two say they tried in vain to stop the FDA approval of soy because it could be misinterpreted as a broader general endorsement beyond benefits for the heart. The text of the letter follows.


    DEPARTMENT OF HEALTH
    and HUMAN SERVICES
    Public Health Service
    Food and Drug Administration
    National Center For Toxicological Research
    Jefferson, Ark. 72079-9502

    Daniel M. Sheehan, Ph.D.
    Director, Estrogen Base Program
    Division of Genetic and Reproductive Toxicology
    and
    Daniel R. Doerge, Ph.D.
    Division of Biochemical Toxicology

    February 18, 1999

    Dockets Management Branch (HFA-305)
    Food and Drug Administration
    Rockville, MD 20852

    To whom it may concern,

    We are writing in reference to Docket # 98P-0683; “Food Labeling: Health Claims; Soy Protein and Coronary Heart Disease.” We oppose this health claim because there is abundant evidence that some of the isoflavones found in soy, including genistein and equol, a metabolize of daidzen, demonstrate toxicity in estrogen sensitive tissues and in the thyroid. This is true for a number of species, including humans. Additionally, the adverse effects in humans occur in several tissues and, apparently, by several distinct mechanisms.
    Genistein is clearly estrogenic; it possesses the chemical structural features necessary for estrogenic activity (; Sheehan and Medlock, 1995; Tong, et al, 1997; Miksicek, 1998) and induces estrogenic responses in developing and adult animals and in adult humans.
    In rodents, equol is estrogenic and acts as an estrogenic endocrine disruptor during development (Medlock, et al, 1995a,b). Faber and Hughes (1993) showed alterations in LH regulation following developmental treatment with genistein. Thus, during pregnancy in humans, isoflavones per se could be a risk factor for abnormal brain and reproductive tract development. Furthermore, pregnant Rhesus monkeys fed genistein had serum estradiol levels 50- 100 percent higher than the controls in three different areas of the maternal circulation (Harrison, et al, 1998). Given that the Rhesus monkey is the best experimental model for humans, and that a women’s own estrogens are a very significant risk factor for breast cancer, it is unreasonable to approve the health claim until complete safety studies of soy protein are conducted. Of equally grave concern is the finding that the fetuses of genistein fed monkeys had a 70 percent higher serum estradiol level than did the controls (Harrison, et al, 1998). Development is recognized as the most sensitive life stage for estrogen toxicity because of the indisputable evidence of a very wide variety of frank malformations and serious functional deficits in experimental animals and humans. In the human population, DES exposure stands as a prime example of adverse estrogenic effects during development. About 50 percent of the female offspring and a smaller fraction of male offspring displayed one or more malformations in the reproductive tract, as well as a lower prevalence (about 1 in a thousand) of malignancies. In adults, genistein could be a risk factor for a number of estrogen-associated diseases.
    Even without the evidence of elevated serum estradiol levels in Rhesus fetuses, potency and dose differences between DES and the soy isoflavones do not provide any assurance that the soy protein isoflavones per se will be without adverse effects. First, calculations, based on the literature, show that doses of soy protein isoflavones used in clinical trials which demonstrated estrogenic effects were as potent as low but active doses of DES in Rhesus monkeys (Sheehan, unpublished data). Second, we have recently shown that estradiol shows no threshold in an extremely large dose-response experiment (Sheehan, et al, 1999), and we subsequently have found 31 dose-response curves for hormone-mimicking chemicals that also fail to show a threshold (Sheehan, 1998a). Our conclusions are that no dose is without risk; the extent of risk is simply a function of dose. These two features support and extend the conclusion that it is inappropriate to allow health claims for soy protein isolate.
    Additionally, isoflavones are inhibitors of the thyroid peroxidase which makes T3 and T4. Inhibition can be expected to generate thyroid abnormalities, including goiter and autoimmune thyroiditis. There exists a significant body of animal data that demonstrates goitrogenic and even carcinogenic effects of soy products (cf., Kimura et al., 1976). Moreover, there are significant reports of goitrogenic effects from soy consumption in human infants (cf., Van Wyk et al., 1959; Hydovitz, 1960; Shepard et al., 1960; Pinchers et al., 1965; Chorazy et al., 1995) and adults (McCarrison, 1933; Ishizuki, et al., 1991). Recently, we have identified genistein and daidzein as the goitrogenic isoflavonoid components of soy and defined the mechanisms for inhibition of thyroid peroxidase (TPO)-catalyzed thyroid hormone synthesis in vitro (Divi et al., 1997; Divi et al., 1996). The observed suicide inactivation of TPO by isoflavones, through covalent binding to TPO, raises the possibility of neoantigen formation and because anti-TPO is the principal autoantibody present in auto immune thyroid disease. This hypothetical mechanism is consistent with the reports of Fort et al. (1986, 1990) of a doubling of risk for autoimmune thyroiditis in children who had received soy formulas as infants compared to infants receiving other forms of milk.
    The serum levels of isoflavones in infants receiving soy formula that are about five times higher than in women receiving soy supplements who show menstrual cycle disturbances, including an increased estradiol level in the follicular phase (Setchell, et al, 1997). Assuming a dose-dependent risk, it is unreasonable to assert that the infant findings are irrelevant to adults who may consume smaller amounts of isoflavones. Additionally, while there is an unambiguous biological effect on menstrual cycle length (Cassidy, et al, 1994), it is unclear whether the soy effects are beneficial or adverse. Furthermore, we need to be concerned about transplacental passage of isoflavones as the DES case has shown us that estrogens can pass the placenta. No such studies have been conducted with genistein in humans or primates. As all estrogens which have been studied carefully in human populations are two-edged swords in humans (Sheehan and Medlock, 1995; Sheehan, 1997), with both beneficial and adverse effects resulting from the administration of the same estrogen, it is likely that the same characteristic is shared by the isoflavones. The animal data is also consistent with adverse effects in humans.
    Finally, initial data fi-om a robust (7,000 men) long-term (30+ years) prospective epidemiological study in Hawaii showed that Alzheimer’s disease prevalence in Hawaiian men was similar to European-ancestry Americans and to Japanese (White, et al, 1996a). In contrast, vascular dementia prevalence is similar in Hawaii and Japan and both are higher than in European-ancestry Americans. This suggests that common ancestry or environmental factors in Japan and Hawaii are responsible for the higher prevalence of vascular dementia in these locations. Subsequently, this same group showed a significant dose-dependent risk (up to 2.4 fold) for development of vascular dementia and brain atrophy from consumption of tofu, a soy product rich in isoflavones (White, et al, 1996b). This finding is consistent with the environmental causation suggested from the earlier analysis, and provides evidence that soy (tofu) phytoestrogens causes vascular dementia. Given that estrogens are important for maintenance of brain function in women; that the male brain contains aromatase, the enzyme that converts testosterone to estradiol; and that isoflavones inhibit this enzymatic activity (Irvine, 1998), there is a mechanistic basis for the human findings. Given the great difficulty in discerning the relationship between exposures and long latency adverse effects in the human population (Sheehan, 1998b), and the potential mechanistic explanation for the epidemiological findings, this is an important study. It is one of the more robust, well-designed prospective epidemiological studies generally available. We rarely have such power in human studies, as well as a potential mechanism, and thus the results should be interpreted in this context.

    Does the Asian experience provide us with reassurance that isoflavones are safe? A review of several examples lead to the conclusion “Given the parallels with herbal medicines with respect to attitudes, monitoring deficiencies, and the general difficulty of detecting toxicities with long Iatencies, I am unconvinced that the long history of apparent safe use of soy products can provide confidence that they are indeed without risk.” (Sheehan, 1998b).

    It should also be noted that the claim on p. 62978 that soy protein foods are GRAS is in conflict with the recent return by CFSAN to Archer Daniels Midland of a petition for GRAS status for soy protein because of deficiencies in reporting adverse effects in the petition. Thus GRAS status has not been granted. Linda Kahl can provide you with details. It would seem appropriate for FDA to speak with a single voice regarding soy protein isolate.
    Taken together, the findings presented here are self-consistent and demonstrate that genistein and other isoflavones can have adverse effects in a variety of species, including humans. Animal studies are the front line in evaluating toxicity, as they predict, with good accuracy, adverse effects in humans. For the isoflavones, we additionally have evidence of two types of adverse effects in humans, despite the very few studies that have addressed this subject. While isoflavones may have beneficial effects at some ages or circumstances, this cannot be assumed to be true at all ages. Isoflavones are like other estrogens in that they are two-edged swords, conferring both benefits and risk (Sheehan and Medlock, 1995; Sheehan, 1997). The health labeling of soy protein isolate for foods needs to considered just as would the addition of any estrogen or goitrogen to foods, which are bad ideas.
    Estrogenic and goitrogenic drugs are regulated by FDA, and are taken under a physician’s care. Patients are informed of risks, and are monitored by their physicians for evidence of toxicity. There are no similar safeguards in place for foods, so the public will be put at potential risk from soy isoflavones in soy protein isolate without adequate warning and information.
    Finally, NCTR is currently conducting a long-term multigeneration study of genistein administered in feed to rats. The analysis of the dose range-finding studies are near-complete or complete now. As preliminary data, which is still confidential, maybe relevant to your decision, I suggest you contact Dr. Barry Delclos at the address on the letterhead, or email him.

    Sincerely,
    Daniel M. Sheehan
    Daniel R. Doerge

    Enclosures
    cc: Dr. Bernard Schwetz, Director, NCTR
    Dr. Barry Delclos

    REFERENCES
    Cassidy, A, Bingham, S, and Setchell, KDR. Biological effects of soy protein rich in isoflavones on the menstrual cycle of premenopausal women. Am. J. Clin. Nutr. 60, 333- 340, 1994.

    Chorazy, P.A., Himelhoch, S., Hopwood, N, J., Greger, N. G., and Postellon, D.C. Persistent hypothyroidism in an infant receiving a soy formula: Case report and review of the literature. Pediatrics 148-150, 1995.

    Divi, R. L., Chang, H. C., and Doerge, D.R. Identification, characterization and mechanisms of anti-thyroid activity of isoflavones from soybean. Biochem. Pharrnacol. 54, 1087-1096, 1997.

    Divi, R.L. and Doerge, D.R. Inhibition of thyroid peroxidase by dietary flavonoids. Chem. Res. Toxicol. 9, 16-23, 1996.

    Levy, JR, Faber, FA,Ayyash, L, and Hughes, CL. The effect of prenatal exposure to phytoestrogen genistein on sexual differentiation in rats. Proc. Sot. Exp. Biol. Med. 208, 60-66, 1995.

    Fort, P., Lanes, R., Dahlem, S., Reeker, B., Weyman-Daum, M., Pugliese, M., and Lifshitz, F. Breast feeding and insulin-dependent diabetes mellitus in children. J. Am. Coil. Nutr. 5,439-441, 1986.

    Fort, P, Moses, N., Fasano, M, Goldberg, T, and Lifshitz, F. Breast and soy-formula feedings in early infancy and the prevalence of autoimmune thyroid disease in children. J. Am. Coil. Nutr. 9, 164-167, 1990.

    Harrison, R. M.. Phillippi, P. P., and Henson, M.C. Effects of genistein on estradiol production in pregnant Rhesus monkeys (A4acaca Mulatta). Am. J. Primatology 45, 183, 1998.

    Hydovitz, JD, Occurrence of goiter in an infant on a soy diet. New Eng. J. Med. 262, 351-353, 1960.

    Irvine, CHG, Fitzpatrick, MG, and Alexander, SL. Phytoestrogens in soy-based infant foods: Concentrations, daily intake, and possible biological effects. Proc. Sot. Exp. Biol. Med. 217,247-253, 1998.

    Ishizuki, Y., Hirooka, Y., Murata, Y., and Togasho, K. The effects on the thyroid gland of soybeans administered experimentally to healthy subjects. Nippon Naibunpi gakkai Zasshi 67,622-629, 1991.

    Kimura, S, Suwa, J, Ito, B and Sate, H. Development of malignant goiter by defatted soybean with iodine-free diet in rats. Gann 67, 763-765, 1976.

    McCarrison, R. The goitrogenic action of soybean and groundnut. Indian J. Med. Res. 21, 179-181, 1933.

    Medlock, K. L., Branham, W. S., Sheehan, D.M. The effects of phytoestrogens on neonatal rat uterine growth and development. Proc. Sot. Exp. Biol. Med. 208:307-313, 1995.

    Medlock, K.L., Branham, W. S., Sheehan, D.M. Effects of coumestrol and equol on the developing reproductive tract of the rat. Proc. Sot. Exp. Biol. Med., 208:67-1, 1995. Miksicek, RJ. Estrogenic flavonoids: Structural requirements for biological activity. Proc. Sot. Exp. Biol. Med. 208,44-50, 1995.

    Pinchers, A, MacGillivray, MH, Crawford, JD, and Freeman, AG. Thyroid refractoriness in an athyreotic cretin fed soybean formula, New Eng. J. Med., 265, 83-87, 1965.

    Setchell, KDR, Zimmer-Nechemias, L, Cai, J, and Heubi, JE. Exposure of infants to phyto-estrogens from soy-based infant formula. Lancet, 350,23-27, 1997.

    Sheehan, D.M. Literature analysis of no-threshold dose-response curves for endocrine disrupters. Teratology, 57,219, 1998a.

    Sheehan, D.M. Herbal medicines and phytoestrogens: risklbenefit considerations. Proc. Sot. Exp. Biol. Med., 217,379-385, 1998b.

    Sheehan, D.M. Isoflavone content of breast milk and soy formulas: Benefits and risks. Clin. Chem., 43:850, 1997.

    Sheehan, D.M. and Medlock, K.L. Current issues regarding phytoestrogens. Polyphenols Actualities, 13:22-24, 1995.

    Sheehan, D. M., Willingham, E., Gaylor, D., Bergeron, J. M., and Crews, D. No threshold dose for oestradiol-induced sex reversal of turtle embryos: How little is too much? Environmental Health Perspectives, February, 1999 issue, in press.

    Shepard, TH, Pyne, GE, Kirschvink, JF, and McLean, CM. Soybean goiter. New Eng. J. Med. 262, 1099-1103, 1960.

    Tong, W, Perkins, R, Xing, L, Welsh, WJ, and Sheehan, DM. QSAR models for binding of estrogenic compounds to estrogen receptor alpha and beta subtypes. Endo. 138, 4022- 4025, 1997. Van Wyk, JJ, Arnold, MB, Wynn, J, and Pepper, F. The effects of a soybean product on thyroid function in humans, Pediatrics 24,752-760, 1959.

    White, L, Petrovitch, H, Ross, GW, and Masaki. Association of mid-life consumption of tofu with late life cognitive impairment and dementia: The Honolulu-Asia Aging Study. The Neurobiol. of Aging, 17 (suppl 4), S 121, 1996a.

    White, L, Petrovich, H, Ross, GW, Masaki, KH, Abbot, RD, Teng, EL, Rodriguez, BL, Blanchette, PL, Havlik, RJ, Wergowske, G, Chiu, D, Foley, DJ, Murdaugh, C, and Curb, JD. Prevalence of dementia in older Japanese-American men in Hawaii, JAMA 276, 955-960, 1996b.

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    Studies showing the general adverse effests of Soybeans: 1971-2001-1971 ( from the Weston A. Price Foundation)


    Wallace, GM. Studies on the Processing and Properties of Soymilk. J Sci Food Agri 1971 Oct;22:526-535. In order to neutralize the protease inhibitors (enzymes that inhibit the digestion of protein) in soy, it must be heated to very high temperatures under pressure and for considerable time. This process unfortunately denatures the overall protein content of soy, rendering it largely ineffective.

    1974
    Joseph, JR. Biological and Physiological Factors in Soybeans. JOACS, 1974 Jan;51:161A-170A. In feeding experiments, use of soy protein isolate (SPI) increased requirements for vitamins E, K, D and B12 and created deficiency symptoms of calcium, magnesium, manganese, molybdenum, copper, iron and zinc.

    1975
    Nutrition during Pregnancy and Lactation. California Department of Health, 1975. Soy is listed as a minor source of protein in Japanese and Chinese diets. Major sources of protein listed were meat including organ meats, poultry, fish and eggs.

    1976
    Searle CE, ed, Chemical Carcinogens, ACS Monograph 173, American Chemical Society, Washington, DC, 1976. Asians throughout the world have high rates of thyroid cancer.

    1977
    Chang KC, ed, Food in Chinese Culture: Anthropological and Historical Perspectives, New Haven, 1977. This survey found that soy foods accounted for only 1.5 percent of calories in the Chinese diet, compared with 65 percent of calories from pork.

    ?1978
    FDA ref 72/104, Report FDABF GRAS - 258. In 1972, the Nixon administration directed a reexamination of substances believed to be GRAS in the light of any scientific information then available. This reexamination included casein protein which became codified as GRAS in 1978. In 1974, the FDA obtained a literature review of soy protein because, as soy protein had not been used in food until 1959 and was not even in common use in the early 1970s, it was not eligible to have its GRAS status grandfathered under the provisions of the Food, Drug and Cosmetic Act.

    1979
    Evaluation of the Health Aspects of Soy Protein Isolates as Food Ingredients. Prepared for FDA by Life Sciences Research Office, Federation of American Societies for Experimental Biology, 9650 Rockville Pike, Bethesda, MD 20014, Contract No, FDA 223-75-2004, 1979. In this document, the FDA expresses concern about nitrites and lysinoalanine in processed soy. Even at low levels of consumption—averaging one-third of a gram per day at the time—the presence of these carcinogens was considered too great a threat to public health to allow GRAS status. Soy protein did have approval for use as a binder in cardboard boxes and this approval was allowed to continue because researchers considered that migration of nitrites from the box into the food contents would be too small to constitute a cancer risk. FDA officials called for safety specifications and monitoring procedures before granting of GRAS status for food. These were never performed. To this day, use of soy protein is codified as GRAS only for limited industrial use as a cardboard binder.

    1979
    Torum, B. Nutritional Quality of Soybean Protein Isolates: Studies in Children of Preschool Age. Soy Protein and Human Nutrition, Harold L Wilcke and others, eds, Academic Press, New York, 1979. A group of Central American children suffering from malnutrition was first stabilized and brought into better health by feeding them native foods, including meat and dairy products. Then for a two-week period these traditional foods were replaced by a drink made of soy protein isolate and sugar. All nitrogen taken in and all nitrogen excreted were measured. The researchers found that the children retained nitrogen and that their growth was “adequate,” so the experiment was declared a success. However, the researchers noted that the children vomited “occasionally,” usually after finishing a meal; over half suffered from periods of moderate diarrhea; some had upper respiratory infections; and others suffered from rash and fever. It should be noted that the researchers did not dare to use soy products to help children recover from malnutrition, and were obliged to supplement the soy-sugar mixture with nutrients largely absent in soy products, notably vitamins A, D, B12, iron, iodine and zinc.

    1981
    Casey CE and others . Availability of zinc: loading tests with human milk, cow’s milk, and infant formulas. Pediatrics 1981;68(3):394-6. Female subjects consumed 25 mg of zinc with milk or formula, the amount of which was calculated to provide 5 gm of protein, after an eight-hour fast. Blood samples were taken prior to (base line) and at 30-minute intervals for three hours after consumption of zinc. The plasma response with human milk was significantly greater than with cow’s milk and all the formulas. The response with cow’s milk and a cow’s milk-based formula was one third that with human milk; responses with a soy-based and two casein hydrolysate-based formulas were even lower.

    1981
    Lebenthal E and others. The development of pancreatic function in premature infants after milk-based and soy-based formulas. Pediatr Res 1981 Sep;15(9):1240-1244. Soy formula fed to premature babies caused in increase in digestive enzymes compared to milk-fed babies, indicating low digestibility of soy formula.

    1982
    Murphy PA. Phytoestrogen Content of Processed Soybean Foods. Food Technology. 1982:50-54. One hundred grams of soy protein, the maximum suggested cholesterol-lowering dose in the FDA-sanctioned health claim, can contain almost 600 mg of isoflavones.

    1983
    Wenk GL and Stemmer KL. Suboptimal dietary zinc intake increases aluminum accumulation into the rat brain. Brain Res 1983;288:393-395. Zinc deficiency will cause more aluminum to be absorbed into the body in general, and into the brain in particular. Aluminum will be absorbed by competing for binding sites on a zinc-containing ligand. Fluoride and phytates in soy formula will induce zinc deficiency.

    1983
    Poley JR and Klein AW. Scanning electron microscopy of soy protein-induced damage of small bowel mucosa in infants. J Pediatr Gastroenterol Nutr 1983 May;2(2):271-87. Soy feeding caused damage to small bowel mucosa in 2 infants. The damage was similar to that of celiac disease and consistent with a lectin-induced toxicity.

    1983
    Tait S and others. The availability of minerals in food, with particular reference to iron. Journal of Research in Society and Health, April 1983;103(2):74-77. When precipitated soy products like tofu are consumed with meat, the mineral blocking effects of the phytates are reduced. The Japanese traditionally eat a small amount of tofu or miso as part of a mineral-rich fish broth, followed by a serving of meat or fish.

    1983
    Ross RK. Effect of in-utero exposure to diethylstilbesterol on age at onset of puberty and on post-pubertal hormone levels in boys,” Canadian Medical Association Journal 1983, May 15;128(10):1197-8. Male children exposed during gestation to diethylstilbesterol (DES), a synthetic estrogen that has effects on animals similar to those of phytoestrogens from soy, had testes smaller than normal on maturation.

    1984
    Ologhobo AD and others. Distribution of phosphorus and phytate in some Nigerian varieties of legumes and some effects of processing. Journal of Food Science. January/February 1984;49(1):199-201. The phytic acid in soy is highly resistant to normal phytate-reducing techniques, such as soaking or long, slow cooking.

    1994
    Hawkins NM and others. Potential aluminium toxicity in infants fed special infant formula. J Pediatr Gastroenterol Nutr 1994;19(4):377-81 (1994). Researchers found aluminum concentrations of 534 micrograms/L in soy formula, as compared to 9.2 micrograms/L in breast milk. The authors concluded that infants may be at risk from aluminium toxicity when consuming formula containing more than 300 micrograms/L.

    1985
    Rackis JJ and others. The USDA trypsin inhibitor study. I. Background, objectives and procedural details. Qualification of Plant Foods in Human Nutrition, 1985;35. Diets of soy protein isolate high in trypsin inhibitors caused depressed growth and enlargement and pathological conditions of the pancreas, including cancer, and enlarged thryoid glands in rats. Analyses for this study showed that trypsin inhibitor content of soy protein isolate can vary as much as fivefold. Even low-level-trypsin-inhibitor SPI feeding resulted in reduced weight gain compared to controls. Soy protein isolate and textured vegetable protein made from soy protein isolate are used extensively in school lunch programs, imitation foods, commercial baked goods, diet beverages, meal replacements and fast food products. They are heavily promoted in Third World countries and form the basis of many food giveaway programs.

    1986
    McGraw MD and others. Aluminum content in milk formulae and intravenous fluids used in infants. Lancet I:157 (1986). Carefully collected human breast milk contained 5 to 20 micrograms aluminum per liter; concentrations were 10 to 20 fold greater in most cow’s milk-based formulas and 100-fold greater in soy-based formulas.

    1986
    Fort P and others. Breast feeding and insulin-dependent diabetes mellitus in children. J Am Coll Nutr 1986;5(5):439-441. Twice as many soy-fed children developed diabetes as those in a control group that was breast fed or received milk-based formula. It was based on this study that the American Academy of Pediatrics took a position of opposition to the use of soy infant formula. This objection was later dropped after the AAP received substantial grants from the Infant Formula Council.

    1986
    Freni-Titulaer LW and others. Am J Dis Child 1986 Dec;140(12):1263-1267.Soy infant feeding was associated with higher rates of early development in girls, including breast development and pubic hair before the age of eights, sometimes before the age of three.

    1987
    Dabeka RW and McKenzie AD. Lead, cadmium, and fluoride levels in market milk and infant formulas in Canada. J Assoc Off Anal Chem 1987;70(4):754-7 (1987). Soy based or milk-free formulas contained about 8-15 times more cadmium than milk-based formulas as well as high amounts of fluoride.

    1987
    Katz SH. Food and Biocultural Evolution: A Model for the Investigation of Modern Nutritional Problems. Nutritional Anthropology, Alan R. Liss Inc., 1987, p 50. During the Chou Dynasty (1134 - 246 BC) the soybean was designated one of the five sacred grains, along with barley, wheat, millet and rice. However, the pictograph for the soybean, which dates from earlier times, indicates that it was not first used as a food; for whereas the pictographs for the other four grains show the seed and stem structure of the plant, the pictograph for the soybean emphasizes the root structure. Agricultural literature of the period speaks frequently of the soybean and its use in crop rotation. Apparently the soy plant was initially used as a method of fixing nitrogen. The soybean did not serve as a food until the discovery of fermentation techniques, sometime during the Chou Dynasty. Katz speculates that the rise of liver cancer in Africa is caused by the introduction of soy foods into the African diet.

    1989
    El Tiney A. Proximate Composition and Mineral and Phytate Contents of Legumes Grown in Sudan. Journal of Food Composition and Analysis 1989;2:67-68. Soybeans are listed as having some of the highest levels of phytic acid of all legumes. Phytic acid blocks the absorption of zinc, iron, copper and magnesium.

    1989
    Sandstrom and others. Effect of protein level and protein source on zinc absorption in humans. J Nutr 1989 Jan;119(1):48-53. When precipitated soy products like tofu are consumed with meat, the mineral blocking effects of the phytates are reduced. The Japanese traditionally eat a small amount of tofu or miso as part of a mineral-rich fish broth, followed by a serving of meat or fish.

    1990
    Campbell TC. The Cornell-China-Oxford Project on Nutrition, Health and Environment. 1990; Chen J and others. Diet, Lifestyle and Mortality in China. A study of the characteristics of 65 counties. Monograph, joint publication of Oxford University Press, Cornell University Press, China People’s Medical Publishing House. 1990. This exhaustive study of Chinese diets found that legume consumption ranged from 0 to 58 grams per day, with an average of 13 gams. Assuming that two-thirds of this is from soy beans, then consumption averages about 9 grams of soy products per day. Isoflavone content would probably be about 10 mg/day.

    1990
    Fort P and others. Breast and soy-formula feedings in early infancy and the prevalence of autoimmune thyroid disease in children. J Am Coll Nutr 1990;9:164-167. This study documents the association of soy formula feeding in infancy with autoimmune thryoid problems.

    1990
    Dabeka RW and McKenzie AD. Aluminium levels in Canadian infant formulate and estimation of aluminium intakes from formulae by infants 0-3 months old. Food Addit Contam 1990;7(2):275-82. Researchers found that aluminum content in soy formula for 1-3 month old infants could result in an intake of 363 micrograms/kg/day (2088 micrograms/day) alone, not including potential contribution from other foods or water.

    1991
    Hagger C and Bachevalier J. Visual habit formation in 3-month-old monkeys (Macaca mulatta): reversal of sex difference following neonatal manipulations of androgen. Behavior and Brain Research 1991, 45:57-63. Male infants undergo a “testosterone surge” during the first few months of life, when testosterone levels may be as high as those of an adult male. During this period, the infant is programed to express male characteristics after puberty, not only in the development of his sexual organs and other masculine physical traits, but also in setting patterns in the brain characteristic of male behavior. In monkeys, deficiency of male hormones impairs the development of spatial perception (which, in humans, is normally more acute in men than in women), of learning ability and of visual discrimination tasks (such as would be required for reading.)

    1994
    Messina MJ and others. Soy Intake and Cancer Risk: A Review of the In Vitro and In Vivo Data,” Nutrition and Cancer, 1994, 212):113-131. This study fueled speculation on soy’s anticarcinogenic properties. The authors noted that in 26 animal studies, 65 percent reported protective effects from soy. At least one study was left out, in which soy feeding caused pancreatic cancer, the 1985 study by Rackis. In the human studies listed, the results were mixed. A few showed some protective effect but most showed no correlation at all between soy consumption and cancer rates. “. . the data in this review cannot be used as a basis for claiming that soy intake decreases cancer risk.” In a subsequent book, The Simple Soybean and Your Health, Messina recommends 1 cup or 230 grams of soy products per day in his “optimal” diet as a way to prevent cancer.

    1995
    Chorazy PA and others. Persistent hypothyroidism in an infant receiving a soy formula: case report and review of the literature. Pediatrics 1995 Jul;96(1 Pt 1):148-50. the study describes a case of persistent hypothyroidism in an infant who had received soy formula.

    1995
    Anderson JW and others. Meta-analysis of the Effects of Soy Protein Intake on Serum Lipids. New England Journal of Medicine, 1995 3335):276-82. The FDAs allowance of a health claim for soy protein is based largely on this meta-anaylsis, sponsored by Protein Technologies International. However, the study authors discarded eight studies for various reasons, leaving a remainder of 29. The published report suggested that individuals with cholesterol levels over 250 mg/dl would experience a “significant” reduction of 7 to 20 percent in levels of serum cholesterol if they substituted soy protein for animal protein. Cholesterol reduction was insignificant for individuals whose cholesterol was lower than 250 mg/dl. In other words, for most of the population, the substitution of meat with soy will not bring blood cholesterol levels down.

    1996
    Harras A, ed. Cancer Rates and Risks, 4th Edition, 1996, National Institutes of Health, National Cancer Institute. This report shows that the Japanese, and Asians in general, have lower rates of breast and prostate cancer but much higher rates of other types of cancer, particularly cancer of the esophagus, stomach, pancreas and liver.

    1996
    Fukutake M and others. Quantification of genistein and genistin in soybeans and soybean products. Food Chem Toxicol 1996;34:457-461. Average isoflavone consumption in Japan was found to be about 10 mg per day.

    1997
    IEH assessment on Phytoestrogens in the Human Diet, Final Report to the Ministry of Agriculture, Fisheries and Food, UK, November 1997. This exhaustive report on phytoestrogens, prepared by the British government, failed to find much evidence of benefit and warned against potential adverse effects.

    1997
    Herman-Giddens ME and others. Secondary Sexual Characteristics and Menses in Young Girls Seen in Office Practice: A Study from the Pediatric Research in Office Settings Network. Pediatrics, 1997 Apr;994):505-512. Investigators found that one percent of all girls now show signs of puberty, such as breast development or pubic hair, before the age of three; by age eight, 14.7 percent of white girls and almost 50 percent of African-American girls had one or both of these characteristics. The widespread use of soy-based formula, beginning in the 1970s, is a likely explanation for the increase in early maturation in girls.

    1998
    Nagata C and others. Decreased serum total cholesterol concentration is associated with high intake of soy products in Japanese men and women. J Nutr 1998 Feb;128(2):209-13. This study included a survey of soy consumption among Japanese men and women. Consumption of soy products was about 54 grams per day for women and 64 grams per day for men. The total amount of soy protein from these products was 7-8 grams providing about 25 mg isoflavones.

    1998
    Irvine CH and others. Phytoestrogens in soy-based infant foods: concentrations, daily intake and possible biological effects. Proc Soc Exp Biol Med 1998 Mar;217(3):247-53. Researchers found that soy formulas provide infants with a daily dose rate of 3 mg/kg body weight total isoflavones, “which is maintained at a fairly constant level between 0-4 months of age. . . . This rate of isoflavone intake is much greater than that shown in adult humans to alter reproductive hormones.”

    1998
    Yaffe K and others. Serum estrogen levels, cognitive performance, and risk of cognitive decline in older community women. J Am Geriatr Soc 1998 Jul;46(7):918-20. Women in the higher estrone quartiles had lower performance on two cognitive tests.

    1998
    Irvine CH and others. Daily intake and urinary excretion of genistein and daidzein by infants fed soy- or dairy-based infant formulas. Am J Clin Nutr 1998 Dec;68(6 Suppl):1462S-1465S. Researchers found that “young infants are able to digest, absorb, and excrete genistein and daidzein from soy-based formulas as efficiently as do adults consuming soy products.

    1999
    Eklund G and Oskarsson A. Exposure of cadmium from infant formulas and weaning foods. Food Addit Contam 16(12):509-19 (1999). Cadmium was 6 times higher in soy formulas than cow’s milk formulas.

    1999
    Olguin MC and others. Intestinal alterations and reduction of growth in prepuberal rats fed with soybean [Article in Spanish]. Medicina (B Aires) 1999;59:747-752. Rats fed soy-based chow had reduced growth and an increase in gastrointestinal problems compared to controls.

    1999
    Nilhausen K and Meinertz H. Lipoprotein(a) and dietary proteins: casein lowers lipoprotein(a) concentrations as compared with soy protein. Am J Clin Nutr 1999;69:419-25. Many studies have shown that soy consumption can lower serum cholesterol levels. These studies have led to claims that soy can prevent heart disease. However, the theory that high cholesterol levels cause heart disease is becoming more and more untenable. Cholesterol levels are not a good marker for proneness to heart disease. However Lipoprotein(a) or Lp(a), does serve as a good marker for heart disease. This study indicates that soy raises Lp(a), meaning that it is likely to contribute to heart disease.

    1999
    Food Labeling: Health Claims: Soy Protein and Coronary Heart Disease, Food and Drug Administration 21 CFR Part 101 (Docket No. 98P-0683). This US government document allows a health claim for foods containing 6.25 grams of soy protein per serving. The original petition, submitted by Protein Technologies International (a division of Dupont), requested a health claim for isoflavones, the estrogen-like compounds found plentifully in soybeans, based on assertions that “only soy protein that has been processed in a manner in which isoflavones are retained will result in cholesterol-lowering.” In 1998, the FDA made the unprecedented move of rewriting PTI’s petition, removing any reference to the phytoestrogens and substituting a claim for soy protein, a move that was in direct contradiction to the agency’s regulations. The FDA is authorized to make rulings only on substances presented by petition. The abrupt change in direction was no doubt due to the fact that a number of researchers, including scientists employed by the US government, submitted documents indicating that isoflavones are toxic. The regulations stipulate that 25 grams of soy protein per day, as part of a diet low in saturated fat and cholesterol, may reduce the risk of heart disease. Twenty-five grams soy protein can contain from 24-125 mg isoflavones, depending on processing methods. Many letters were written in protest, expressing concerns about mineral blocking effects, enzyme inhibitors, goitrogenicity, endocrine disruption, reproductive problems and increased allergic reactions from consumption of soy products.

    1999
    Sheehan DM and Doerge DR, Letter to Dockets Management Branch (HFA-305) February 18, 1999. A strong letter of protest from two government researchers at the National Center for Toxicological Research urging that soy protein carry a warning label rather than a health claim.

    1999
    Ginsburg J and Prelevic GM. Is there a proven place for phytoestrogens in the menopause?” Climacteric, 1999;2:75-78. Quantification of discomfort from hot flashes is extremely subjective and most studies show that control subjects report reduction in discomfort in amounts equal to subjects given soy.

    1999
    White L. Association of High Midlife Tofu Consumption with Accelerated Brain Aging. Plenary Session #8: Cognitive Function, The Third International Soy Symposium, Program, November 1999, page 26. An ongoing study of Japanese Americans living in Hawaii found a significant statistical relationship between two or more servings of tofu per week and “accelerated brain aging.” Those participants who consumed tofu in mid life had lower cognitive function in late life and a greater incidence of Alzheimer’s and dementia.

    2000
    Clarkson TB. Soy phytoestrogens: what will be their role in postmenopausal hormone replacement therapy? Menopause 2000 Mar-Apr;7(2):71-5. Soy did not prevent bone loss when measured at autopsy in female monkeys who had had their reproductive organs removed.

    2000
    Vincent A and Fitzpatrick LA. Soy isoflavones: are they useful in menopause? Mayo Clin Proc 2000;75:1174-84. “Current data are insufficient to draw definitive conclusions regarding the use of isoflavones as an alternative to estrogen for hormone replacement in postmenopausal women.”

    2000
    North K and Golding J. A maternal vegetarian diet in pregnancy is associated with hypospadias. The ALSPAC Study Team. Avon Longitudinal Study of Pregnancy and Childhood. BJU Int 2000 Jan;85(1):107-113. Vegetarian women are more likely consume more soy than the general population. Incidence of hypospadias was twice as great in vegetarian mothers than in nonvegetarian mothers. Hypospadias is a birth defect due to interrupted development of the penis.

    2000
    Nakamura Y and others. Determination of the levels of isoflavonoids in soybeans and soy-derived foods and estimation of isoflavonoids in the Japanese daily intake. J AOAC Int 2000;83:635-650. This survey found that average isoflavone consumption in Japan is about 28 mg per day.

    2000
    Bee G. Dietary Conjugated Linoleic Acids Alter Adipose Tissue and Milk Lipids of Pregnant and Lactating Sows. J Nutr 2000;130:2292-2298. Dietary mixtures for pigs, which are carefully formulated to promote reproduction and growth, allow approximately 1 percent of the ration as soy in a diet based on grains and supplements. (Pigs have a digestive system similar to humans.) The Central Soya Company, Inc. website gives a range of 2.5 percent to 17.5 percent soy in the diet of pigs, citing a number of anti-nutritional components that “have been documented to cause gastrointestinal disturbance, intestinal damage, increased disease susceptibility and reduced performance in pigs.”

    2000
    Vegetarian diet in pregnancy linked to birth defect. British Journal of Urology International, 2000 Jan;85:107-113. Mothers who ate a vegetarian diet during pregnancy had a fivefold greater risk of delivering a boy with hypospadias, a birth defect of the penis. The authors of the study suggested that the cause was greater exposure to phytoestrogens in soy foods popular with vegetarians.

    2001
    Strom BL and others. Exposure to soy-based formula in infancy and endocrinological and reproductive outcomes in young adulthood. JAMA 2001 Nov 21;286(19):2402-3. Although reported in the media as a vindication of soy infant formula, the study actually found that soy-fed infants had more reproductive problems and more asthma as adults.

    2001
    Massey LK and others. Oxalate content of soybean seeds (Glycine max: Leguminosae), soyfoods, and other edible legumes. J Agric Food Chem 2001 Sep;49(9):4262-6. Soy foods were found to be high in oxalates and likely to contribute to kidney stones.

    2001
    Khalil DA and others. Soy protein supplementation increases serum insulin-like growth factor-I in young and old men but does not affect markers of bone metabolism. J Nutr 2002 Sep;132(9):2605-8. Men consuming soy protein had higher levels of insulin-like growth factor-I (IGF-I) than those consuming milk protein. According to many other studies (but not stated in the report), high levels of IFG-I are also found in rBGH milk and have been implicated in causing hormonal cancers.


    --------------------------------------------------------------------------------

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    Mostly good....

    The Soy-Thyroid Connection
    by Linda Knittel

    Now that soy has finally established itself in the diet of mainstream America, and good-tasting soy spreads, burgers and sandwich slices have replaced bland slabs of tofu in the minds of consumers, this wonder food is beginning to get some bad press. It seems a handful of studies are claiming to have linked soy consumption to serious health conditions such as hypothyroidism. However, before you rush back to eating hot dogs and drinking cow's milk, be sure you have all the facts; for while soy may raise health concerns for certain individuals, for most it is an all-natural way to help prevent cancer, hormonal symptoms, osteoporosis and heart disease.

    It took a while, but after recognizing that soy's once anecdotal health benefits were substantiated by hordes of sound clinical studies, the U.S. Food and Drug Administration (FDA) announced soy's addition to its list of health-promoting foods. According to the official health claim released in October 1999, adding 25 grams of soy protein a day to a low-fat diet can lower cholesterol and therefore reduce the risk of coronary heart disease.

    Besides protecting the heart, however, the main isoflavones contained in soybeans — daidzein and genistein — are responsible for helping to prevent osteoporosis, as well as relieving the hormone-induced symptoms associated with menopause such as hot flashes. Furthermore, these phytoestrogens have been shown to inhibit the growth of several forms of cancer, including breast, colon and prostate cancers. But the news is not all positive; recently soy consumption has been associated with the suppression of thyroid function.

    The thyroid gland, located near the front of the neck, is responsible for controlling metabolism via the release of hormones. Since the isoflavones in soy have the ability to act as hormones in the body, they seem capable of disrupting the functions of the endocrine system, including those associated with the thyroid. While a few studies have added some credence to this theory, there is not yet a clear understanding of the extent to which soy interferes with thyroid function.

    In a 1991 Japanese study published in the journal Nippon Naibunpi Gakkai Zasshi, researchers revealed that excessive soybean ingestion (30 grams per day for 3 months) by 14 healthy men led to suppressed thyroid function in half of them, as determined by constipation, fatigue and the growth of goiters (enlargement of the thyroid). Furthermore, a month after the study was completed, all symptoms subsided and thyroids returned to normal.

    While the outcome of this Japanese study may sound clear cut, many researchers are not alarmed by these results because they believe such a strong reaction to soy was the result of an already existing tendency towards low thyroid function, rather than it being the standard reaction for healthy individuals. "I don't discount that study but the results seem a bit strange," says Mark Messina, Ph.D., a well-respected soy researcher and author. "And if you look at recent, more controlled studies, that have spanned a longer amount of time, explain exactly what is being eaten, and determine whether subjects are iodine replete or not, you see there is nothing going on."

    This Japanese study and a few like it have raised some interesting issues in terms of soy consumption and suggest that a deeper investigation into the link between soy isoflavones and thyroid function is clearly warranted, especially in light of the fact that nearly 10 percent of the adult population suffers from subclinical hypothyroidism. However, such concerns do not negate the cancer-fighting, bone-preserving, heart-disease preventing actions that soy foods have been shown to exert in most individuals.

    "Some people who are sensitive to low thyroid might do better staying away from soy protein because it does have a thyroid-inhibiting effect, which could result in a lack of energy, weight gain and things of that sort," says Jack Challem, founder/writer of the Nutrition Reporter newsletter, and co-author of The Health Benefits of Soy (Keats, 1996). Fortunately determining if you have a healthy thyroid can be done via a simple blood test.

    "This is a readily identifiable problem," says Messina. "In fact, The American Thyroid Association recommends people have their thyroid checked every five years beginning at age of 35."

    For most of us who test normal, adding a moderate amount of soy foods to the diet is a smart move. For example, a single serving size of tofu or tempeh usually provides between 10 and 15 grams of soy protein, a number below the FDA's recommended 25 grams per day, but one that is more in line with what is consumed by Asian populations. "What it comes down to is [to] eat soy a couple of times a week," says Challem. "I wouldn't recommend that anyone build three meals a day around it."

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    Why would you bother posting this ( or these as many are reposts ) again in a new thread when this was being discussed here

    Either way, as you yourself stated yesterday,

    Dr.Pain
    Having only made a cursory run through some literature....it appears both goitertropic/genic tendencies w/these foods, are only prevelent w/iodine deficiency......



    quote:
    A number of commonly eaten foods have been shown to interfere with the use of iodine by the thyroid, thus reducing production of thyroid hormone and causing goiter. These foods, known as goitrogens, include vegetables in the Brassica family such as broccoli, cabbage, kale and mustard,17 millet,18 soybeans,19 pine nuts20 and some seed meals used in animal feeds.21 22 These foods can be safely eaten in moderate amounts by people who consume adequate iodine.23 A combination of low iodine intake and high intake of goitrogenic foods increases the likelihood of goiter.24 25

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    Now, would this be applicable to Soy Foods or Soy byproducts ?

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    It's ambiguous, some say both, others say foods are fine?

    One study w/Japanese men used fermented....

    My contentions is that the powders are the main culprit


    DP

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    Originally posted by kuso
    Why would you bother posting this ( or these as many are reposts ) again in a new thread when this was being discussed here

    Either way, as you yourself stated yesterday,
    Some of the studies are repetitive,, many aren't, but the evidence which you asked for......seems the soy involves many more mechanisms, hormones and subhormones than Brassica, and is not curable/treatable, just with iodine stimulating TSH production.

    I requested help finding more details on Brassica, my research turns up only positives!



    You asked to see the difference?

    DP

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    I don`t even no why I bother as this seems to have become something you feel you need to win, but anyway.............

    Originally posted by Dr. Pain
    Some of the studies are repetitive,, many aren't, but the evidence which you asked for......seems the soy involves many more mechanisms, hormones and subhormones than Brassica, and is not curable/treatable, just with iodine stimulating TSH production.
    Other than the first post, the others I believe are reposts so I`ve done nothing but scan them. in that scan I have seen NOTHING comparing brassica to soy, nor ANY mention of brassica at all so what was it that caused you to draw this conclusion?


    Originally posted by Dr. Pain
    I requested help finding more details on Brassica, my research turns up only positives!
    Maybe thats because you`ve spent so much time looking to discredit soy rather than search for brassica. Do you know believe that brassica has no effect whatsoever because you couldn`t find it?



    Effects of Soy Protein on Postmenopausal Women and Men with Elevated Plasma Lipids.

    J.A. Eden, R. Mackey, and A. Ekangaki; Sydney Menopause Centre, Royal Hospital for Women, Randwick, NSW, Australia.

    Previous studies established that soy protein has a cholesterol-lowering effect, but many questions remain. For example, does soy protein affect the lipid profile of men and women in a similar matter and are the isoflavones responsible for this lipid effect? Numerous concerns about soy protein have also been raised. We performed three studies to examine these questions in some detail.

    Study 1 involved 54 postmenopausal women with a total cholesterol level (TC) > 5.5 mmol/L after a 4-wk cholesterol-lowering diet. Subjects were randomly assigned to receive normal soy protein (ISP+) containing 65 mg isoflavone or soy protein with isoflavones alcohol- extracted (ISP-) for 12 wk. Subjects were reassessed 4 wk after (off phase) the end of the 12-wk treatment phase. The following were measured at intervals: TC, triglyceride (TG), HDL, LDL, luteinizing hormone (LH), follicle-stimulating hormone (FSH), sex hormone-binding globulin (SHBG), thyroid-stimulating hormone (TSH), bone markers (bALP, osteocalcin, and urinary deoxypyridinoline), as well as glucose and insulin response to a glucose load. The mean age of subjects was 57 y; mean baseline cholesterol was 7.3 mmol/L. There was no weight change over the study period. There were five dropouts, leaving 49 for analysis. The mean lipid reductions were 4.3% for TC and 6.1% for LDL. No difference was seen between ISP+ and ISP-, implying that some component other than isoflavones was responsible for the lipid-lowering effect. No effect was seen on glucose metabolism, TSH, bone markers (apart from a mild effect on urinary deoxypyridinoline), FSH, or Greene menopause scores. A mild but significant effect was seen for ISP+ on serum levels of LH, and a significant reduction was seen for SHBG in the ISP+ group. Interestingly the levels of SHBG return to normal during the off phase.

    Study 2 was an uncontrolled study of 27 men with a TC level > 5.5 after a 4-wk cholesterol-lowering diet. During the 12-wk study period, all subjects were given 28 g soy protein containing 65 mg isoflavone. Subjects were reassessed 4 wk after (off phase) the end of the 12-wk treatment phase. The following were measured: lipid profile, LH, FSH, SHBG, TSH, androgen profile. The mean age of subjects was 52 y; mean baseline TC was 6.8 mmol/L. The average increase in HDL cholesterol was 9.5%; this value returned to baseline during the off phase. There was no effect on TSH, testosterone, androstenedione, LH, and FSH. As was seen in the study with women, there was a > 10% decrease in SHBG and a nonsignificant increase in DHEA (P = 0.06).
    GOITER (colloid goiter, hypothyroid) is caused by a simple deficiency of nutrients (i.e., iodine, copper, molybdenum, the amino acid tyrosine, etc.). Nitrates are goiterogenic (stimulate goiter formation); they are found in luncheon meats, hot dogs, sausages, and a variety of prepared meat products. Another source of goiterogens is the nitrates in fertilizers, which gets into well water. If you get your water from a farm well, have it tested for nitrates because they are carcinogenic as well as goiterogenic. Cabbage, broccoli, and Brussels sprouts are also goiterogenic.
    Thermic Effect Of Food
    Roughly 10% of the calories you consume are used to process - digest, absorb, transport, metabolise and store as energy - the foods that you eat. When your body processes food, it uses energy (calories) and gives off heat. This is referred to as thermogenesis.

    Therefore, if you consume 3000 calories, 300 of them will be used for processing. Now, depending on the types of foods you eat, your calorie expenditure may either increase or decrease to some extent. This is due to the thermic effect of food, which basically means that processing different types of food requires different amounts of energy or heat production. As a whole, proteins offer the greatest thermic effect, and fats the least. Brussel sprouts and cabbage, it is claimed, are capable of evoking a goiterogenic effect (a slowing down of your metabolism) when consumed in large quantities. So in an attempt to really dial in your diet you may also want to consider the thermic effect of the food you eat.
    4. Soy contains goiterogenic compounds, which undermine the healthy functioning of the thyroid gland. As Dr. Harold Kristal points out, "Sub-clinical hypothroidism is already such a common health problem that caution is certainly warranted."

    In addition, three further points need to be made.

    One: Most of the soybeans produced in the U.S. are genetically engineered, the implications of which have not yet been fully understood.

    Two: The healthiest soy foods are the fermented ones such as tempeh and miso, which don't have any of the problems mentioned above but aren't necessarily the ones we're eating the most of.

    Three: Probably most importantly, the phytoestrogens in soy -- those very compounds so touted for their health benefits -- are actually a mixed blessing. Yes, they are weaker than "real" estrogen, and yes they bind to the estrogen receptors in your body, which partially prevent the body's own estrogen from binding to those sites and possibly causing mischief. But they can theoretically help reduce the downside of estrogen (breast cancer, for example). Doesn't it make sense to consider whether that benefit might be washed away by consuming so much of the phytoestrogens that you might as well be taking the "real" thing?

    I posed these questions to Dr. Barry Sears, who just wrote a very good book about incorporating soy into his Zone-type diet (The Soy Zone) when he was on my radio show last week. Going down the list of arguments made by Fallon and Enig, I basically said to him "Barry, you got 'lot of 'splaining to do!"

    While I can't say he put my mind at ease 100 percent, his answers definitely shed some light on the situation.

    For one thing, in the best of all possible worlds, Dr. Sears doesn't recommend that you get all of your protein from soy. A mix of soy and animal products would be ideal, and with that, I agree completely.

    For another, Dr. Sears agrees that while the health benefits of some of these soy compounds are unquestionable, it's the old American propensity for thinking "if some is good, a hundred times that is better" that is causing a lot of the problem. It's one thing to get a reasonable dose of isoflavones -- such as genistein -- from soy. It's quite another to take isolated supplements of these compounds in amounts several hundred times what is found in the food. In high amounts, isoflavones may have negative effects on other hormones (such as thyroid), and taking hundreds of times the dosage of a weaker estrogen might well be erasing the benefits of phytoestrogens in the first place.

    Finally, who knows what the cumulative effect of having this much phytoestrogen exposure in our food supply has had on sexual maturity and development in young people?

    I agree completely with Dr. Sears that soy can be part of a healthy diet, but for right now, I don't think we should eat unlimited amounts of it, and I definitely don't think we should be taking supplements of concentrated isoflavones.

    And I am pretty sure that the best soy products continue to be those that are fermented, rather than those that are highly processed.


    http://fn.cfs.purdue.edu/bot/Publica...ina_J_Nutr.pdf

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    Okay, i think all of these threads should be consolidated into one and should be called "Soy War: DP v. Kuso"
    "The greatest obstacle to knowledge is not ignorance but the illusion of knowledge." -Barry Marshall, Nobel Laureate

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    I see two people posting information for the site, both pro and con, and stating their opinions...I don't see why anyone thinks someone is trying to win?

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    I agree!

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    ZINC

    Zinc and Thyroid function.

    Zinc increases thyroid function and is usually high in hypers and low in hypos. Studies show that hypers usually have low zinc in the blood and this information seems to be the source of the very common nutritional advice that hypers need zinc. I have found that this is exactly the wrong thing to do in most cases. Some hypers are deficient in both copper and zinc, but usually even these persons should start supplementing with copper first, before zinc supplementation is begun. Generally for hyperthyroidism, copper should be supplemented first, then iron, and then zinc only if necessary. For hypothyroidism, zinc should be supplemented first (along with selenium). When nighttime rapid heart beat begins, then iron and copper should be added. One unsuspected zinc source: Some sunscreens use zinc as a physical sun block and I have these to avoid the dangerous chemicals present in most sun screens. However, I noticed that often I would get an increase in hyper symptoms after being in the sun. I now think that the zinc from the sun screen is absorbed into the body and can be a significant source of zinc, and therefore a possible cause of hyperthyroidism.


    Zinc can get depleted by high phytates, such as in soy, oats, wheat, or other grains. Rapeseed meal (canola oil is made from rapeseeds) has been shown to reduce thyroid function in experimental animals. The following study shows that zinc supplementation can reverse some of these negative effects from rapeseed.

    Title
    Beneficial effect of zinc supplementation on reproduction in rats fed rapeseed protein concentrate.
    Author
    Shah BG; Giroux A; Belonje B; Jones JD
    Source
    Nutr Metab, 23(4):275-85 1979
    Abstract
    Three groups of 33 90-day-old female Sprague-Dawley rats were fed, ad libitum, the following diets for 2 weeks before breeding. Diet 1 (D1) contained 20% protein from casein, diet 2 (D2) had the same level of protein from Tower rapeseed (Brassica napus) protein concontrate (RPC) and diet 3 (D3) was the same as D2 with a zinc supplement (70 mg/l) in the drinking water. From each group 6 animals were killed before breeding and 5-9 animals were killed at 1 and 2 weeks of gestation and post-partum. From each rat, blood, thyroids, liver and femur were collected for the determination of zinc, copper, iron, manganese, calcium and magnesium. As a measure of the reproductive performance, body weight, number of pups in the uterus or delivered live or dead, and gestations days before parturition were recorded. The pups were examined for obvious deformities and also analysed for the above mineral elements by atomic absorption spectroscopy. In group D2, levels of zinc in maternal serum, liver, femur and in the pups were significantly lower than the comparable levels in the other two groups. The zinc supplemented RPC-fed group did not show the anorexia experienced by the unsupplemented group and there was neither a significant difference between reproductive performances of groups D1 and D3 nor was there any significant difference between the zinc levels determined. It was concluded that the toxic symptoms caused by RPC feeding was attributable to zinc deficiency probably caused by the high phytate level in the RPC

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    BTW...seems tapioca is also off limits
    Bourdoux, P.; Delange, F.; Gerard, M.; Mafuta, M.; Hanson, A.;
    Ermans, A. M. (1978) Evidence that cassava ingestion increases
    thiocyanate formation: A possible etiologic factor in endemic goiter. J
    Clin Endocrinol Metab 46(4):613-621

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    some general DON`T do`s for those with Hypothyroidism

    Dietary restriction vs. vegetarianism
    Caloric restriction should be avoided as this can reduce metabolic rate up to 20% within 14 days even while exercising. Decreases in T3, fT3, and increases in rT3 have been found in a low carbohydrate, 800 Kcal per day diet. On the other hand, a vegetarian diet can increase the resting metabolic rate by 11%

    Lifestyle factors
    Smoking has harmful effects on the thyroid. A study evaluating one hundred thirty-five female hypothyroid patients and a similar number of controls relative to cigarette smoking observed a statistically significant relationship between smoking and increased levels of hypothyroidism. The authors conclude that smoking has both a goitrogenic effect and other basic thyroid dysfunction influences.

    Alcohol
    Excessive alcohol consumption may be harmful to hypothyroid patients. Low T3 and T4 levels are found in alcoholic cirrhosis patients and animals exposed to ethanol have impaired hepatic 5'-deiodiniation, meaning that their liver's ability to convert T4 to T3 is impaired.

    Caffeine, helpful in the short term
    Hypothyroidism causes an increase in three inhibitory molecules, alpha adrenergic receptors, phosphodiesterase and G1 proteins (the latter increases cellular sensitivity to adenosine and adenosine receptor binding). Phosphodiesterase inactivates cAMP. Adenosine activates an inhibitory GTP-binding protein (G1) that also decreases cAMP formation. I have always advocated avoidance of caffeine, especially in the form of coffee however, caffeine in moderate doses inhibits these potent enzymes phosphodiesterase and adenosine, which are both metabolic inhibitors. Caffeine, theophylline and theobromine are also adenosine receptor antagonists. Caffeine has a half-life of 5.2 hours. It is a central nervous system stimulant and thus for most people must be avoided before sleep. It can also exacerbate osteoporosis and fibrocystic breast disease. In large doses, tolerance develops and various other disorder may develop, ranging from arrythmia to a form of mania known as caffeineism. I recommend taking caffeine in the form of green tea, and only in a dose that does not overly stimulate the individual. When thyroid hormone levels have been normalized, the dose of caffeine can be reduced.

    Stress
    Stress in the form of high cortisol can block the conversion of T4 to T3, and in fact can promote the conversion of T4 to the inactive r-T3. Efforts must be made to get stress under control. Many modalities such as Tai Chi, Yoga, meditation, cognitive therapy, etc. can be employed to reduce the response to stress. Deep breathing is one of the simplest ways to change to a "rest and digest" metabolic state.

    Sleep
    Sleep-deprivation produces elevations of T4, fT4, T3 and rT3. The long-term implications of this are not clear but it appears that the thyroid is responding to sleep-deprivation as a stressful event.

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    and a few more

    Iodine and Tyrosine Ð the biggest factors The two most important nutrient deficiencies associated with hypothyroidism are iodine and the amino acid Tyrosine. In this country, iodine deficiency is rare as iodine is routinely added to salt and the American diet is generally high in salt. In undeveloped countries where iodine is deficient in the soil and little fish and sea vegetables are consumed, iodine is a major cause of goiter and a form of physical and mental retardation known as Cretinism. Some 800,000,000 people worldwide suffer from iodine deficiency and goiter. The RDA for iodine is 150 mcg per day for adults age 11 and above, 175 mcg per day in pregnancy and 200 mcg during lactation. Lab tests for iodine include plasma iodine (by neutron activation analysis and urinary iodine. Hair trace mineral analysis may also be used to screen for iodine deficiency. Excess iodine may cause inhibition of TRH and TSH however. The dietary intake of iodine in the United States is estimated to be over 600 . Levels in excess of that amount are not recommended.
    Tyrosine is the core of the thyroid hormone molecule. A molecule of thyroglobulin contains 134 tyrosines, although only a handful of these are actually used to synthesize T4 and T3. Deficient intake, digestion or metabolism of tyrosine may be a cause of hypothyroidism. Tyrosine is a non-essential amino acid in that it can be made from phenylalanine. However, some people have an enzyme deficiency and thus have difficulty in converting phenylalanine to tyrosine. Supplemental tyrosine may be taken in 500-1000 mg doses tid.

    Mercury and Selenium
    Mercury toxicity can block the conversion of T4 to T3. Similarly Selenium deficiency will also prevent the conversion of T4 to T3. Selenium is a chelator of mercury and can be used with dimercaptosuccinic acid to remove mercury toxicity from the body.

    Zinc
    Zinc supplementation re-established normal thyroid function in hypothyroid disabled patients treated with anti-convulsants. In a study, 9 of 13 patients with low free T3 and normal T4 had mild to moderate zinc deficiency. After oral supplementation with zinc sulfate (4-6 mg/kg body weight for 12 months), levels of serum free T3 and T3 normalized, serum rT3 decreased and TRH induced TSH reaction normalized. Since copper exerts an antagonistic role, high copper may inhibit thyroid hormone activity. A study of fourteen pre-adolescent hypothyroid patients and a similar number of controls for serum zinc levels revealed zinc levels were significantly lower in the hypothyroid children before supplementation with thyroxine. The authors suggest that there is an association with zinc deficiency and thyroid function. A study of twelve hyperthyroid and seven hypothyroid patients relative to zinc tolerance found that high levels of zinc excretion were observed in hyperthyroid cases and zinc deficiency was observed in hypothyroid patients leading the authors to conclude that zinc levels were a marker of thyroid function. Zinc and thyroid hormone levels both decline with age and may be related. Children's with Down's syndrome have many symptoms in common with hypothyroidism and are also commonly deficient in zinc, suggesting an association.

    Protein and liver disease
    Protein deficiency, starvation, cirrhosis or other liver disease can reduce the amount of transport proteins available to carry the T4 to the cell. In the case of liver disease, overall nutrition and specifically, glutathione may be helpful in promoting normal liver function.

    Krebs cycle nutrients
    At the level of cellular utillization, CoEnzyme Q10, magnesium and B vitamins may be helpful as they play roles in the Krebs cycle. B vitamins might have more direct roles as well. In animals, B12 deficiency is associated with slight reduction of type I 5'-deiodinase activity and with significant reduction in serum T3. In a study of fifty-two patients under psychiatric care for B-vitamin deficiencies, it was observed that in the female patients where there was depression and a low thyroid index, there was also a deficiency of vitamin B2.
    On the other hand, extreme doses of niacin (mean 2.6 grams daily for an average duration of 1.3 years) revealed significant decreases in serum T4, T3 and TBG with no alterations in free T4 and TSH levels. Similarly, lipoic acid taken with T4 resulted in a 57% reduction in the expected rise in T3 values in just 9 days, suggesting that lipoic acid should not be taken with exogenous T4. Vitamins C and E only improved hepatic 5' Ðdeiodinization in conditions of increased lipid peroxidation due to heavy metal toxicity.

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    Originally posted by kuso
    BTW...seems tapioca is also off limits
    Damn...I have tapioca once every ten years...and I was due!


    I'm not sure about other foods, but we have seen a few cases of zinc/cooper inbalance from soy foods over the years...( I know that iron is related, but we are seeing a lot of negative info surrounding iron, a whole other issue)

    As far as phylates, didn't one of the studies suggest cooking or fermenting changed that?


    DP

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    And foods to avoid says

    Foods to avoid
    Thiocyanate glucosides, substances found in vegetables from the cabbage (brassica) family, have an antagonistic effect on the binding of iodine in the thyroid. Persons with hypothryoidism would do well to limit consumption of raw brussel sprouts, cabbage, kale, broccoli and cauliflower. Cooking negates this effect. Soy isoflavones also appear to exert a negative effect on thyroid hormone activity. Animals fed soy protein experienced a decline in T4, free T4 and T3 while experiencing an increase in r-T3. In one study, 37 healthy adults consumed 30 grams of soybeans for 1-3 months. They experienced significantly increased TSH levels and hypometabolic symptoms suggestive of functional thyroid hormone deficiency (malaise, constipation, sleepiness). Goiters appeared in half the subjects. Symptoms disappeared after one month cessation of soy ingestion.
    Last is rather important I believe...though I must admit. I`m researching under the influence.

    malaise for DaMayor means a hazy feeling of not being well....hardly a scientific way of testing.

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    Originally posted by kuso
    some general DON`T do`s for those with Hypothyroidism
    Iodine and Tyrosine Ð the biggest factors The two most important nutrient deficiencies associated with hypothyroidism are iodine and the amino acid Tyrosine. In this country, iodine deficiency is rare as iodine is routinely added to salt and the American diet is generally high in salt. In undeveloped countries where iodine is deficient in the soil and little fish and sea vegetables are consumed, iodine is a major cause of goiter and a form of physical and mental retardation known as Cretinism. Some 800,000,000 people worldwide suffer from iodine deficiency and goiter. The RDA for iodine is 150 mcg per day for adults age 11 and above, 175 mcg per day in pregnancy and 200 mcg during lactation. Lab tests for iodine include plasma iodine (by neutron activation analysis and urinary iodine. Hair trace mineral analysis may also be used to screen for iodine deficiency. Excess iodine may cause inhibition of TRH and TSH however. The dietary intake of iodine in the United States is estimated to be over 600 . Levels in excess of that amount are not recommended.
    Tyrosine is the core of the thyroid hormone molecule. A molecule of thyroglobulin contains 134 tyrosines, although only a handful of these are actually used to synthesize T4 and T3. Deficient intake, digestion or metabolism of tyrosine may be a cause of hypothyroidism. Tyrosine is a non-essential amino acid in that it can be made from phenylalanine. However, some people have an enzyme deficiency and thus have difficulty in converting phenylalanine to tyrosine. Supplemental tyrosine may be taken in 500-1000 mg doses tid.

    Mercury and Selenium
    Mercury toxicity can block the conversion of T4 to T3. Similarly Selenium deficiency will also prevent the conversion of T4 to T3. Selenium is a chelator of mercury and can be used with dimercaptosuccinic acid to remove mercury toxicity from the body.

    Zinc
    Zinc supplementation re-established normal thyroid function in hypothyroid disabled patients treated with anti-convulsants. In a study, 9 of 13 patients with low free T3 and normal T4 had mild to moderate zinc deficiency. After oral supplementation with zinc sulfate (4-6 mg/kg body weight for 12 months), levels of serum free T3 and T3 normalized, serum rT3 decreased and TRH induced TSH reaction normalized. Since copper exerts an antagonistic role, high copper may inhibit thyroid hormone activity. A study of fourteen pre-adolescent hypothyroid patients and a similar number of controls for serum zinc levels revealed zinc levels were significantly lower in the hypothyroid children before supplementation with thyroxine. The authors suggest that there is an association with zinc deficiency and thyroid function. A study of twelve hyperthyroid and seven hypothyroid patients relative to zinc tolerance found that high levels of zinc excretion were observed in hyperthyroid cases and zinc deficiency was observed in hypothyroid patients leading the authors to conclude that zinc levels were a marker of thyroid function. Zinc and thyroid hormone levels both decline with age and may be related. Children's with Down's syndrome have many symptoms in common with hypothyroidism and are also commonly deficient in zinc, suggesting an association.

    Protein and liver disease
    Protein deficiency, starvation, cirrhosis or other liver disease can reduce the amount of transport proteins available to carry the T4 to the cell. In the case of liver disease, overall nutrition and specifically, glutathione may be helpful in promoting normal liver function.

    Krebs cycle nutrients
    At the level of cellular utillization, CoEnzyme Q10, magnesium and B vitamins may be helpful as they play roles in the Krebs cycle. B vitamins might have more direct roles as well. In animals, B12 deficiency is associated with slight reduction of type I 5'-deiodinase activity and with significant reduction in serum T3. In a study of fifty-two patients under psychiatric care for B-vitamin deficiencies, it was observed that in the female patients where there was depression and a low thyroid index, there was also a deficiency of vitamin B2.
    On the other hand, extreme doses of niacin (mean 2.6 grams daily for an average duration of 1.3 years) revealed significant decreases in serum T4, T3 and TBG with no alterations in free T4 and TSH levels. Similarly, lipoic acid taken with T4 resulted in a 57% reduction in the expected rise in T3 values in just 9 days, suggesting that lipoic acid should not be taken with exogenous T4. Vitamins C and E only improved hepatic 5' Ðdeiodinization in conditions of increased lipid peroxidation due to heavy metal toxicity.
    Most Excellent! gr8 post! (esp the ALA connection w/exogenous T4, very useful)

    There is a searchable post here at IM on reverse T3 if anyone needs more info on it!

    DP

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    So many studies.....so little time.

    Hey Kuso, lay off the tapioca talk there, buddy...You're getting DP all worked up!

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    Originally posted by Dr. Pain


    As far as phylates, didn't one of the studies suggest cooking or fermenting changed that?


    DP
    I

    I don`t know....I believe I asked you to point out any relevent points which you have yet to have done.

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    Originally posted by kuso
    And foods to avoid says

    Soy isoflavones also appear to exert a negative effect on thyroid hormone activity. Animals fed soy protein experienced a decline in T4, free T4 and T3 while experiencing an increase in r-T3. In one study, 37 healthy adults consumed 30 grams of soybeans for 1-3 months. They experienced significantly increased TSH levels and hypometabolic symptoms suggestive of functional thyroid hormone deficiency (malaise, constipation, sleepiness).


    That was important too, as you just answered Nigeepoo's question, cooking negates the negative effect of the Brassicas...and iodine relieves the problem w/raw!

    Soy as I have contended affects the whole thyroid hormonal cascade!

    Good Post!

    DP

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    Originally posted by kuso
    I

    I don`t know....I believe I asked you to point out any relevent points which you have yet to have done.
    I would disagree., respectfully!

    The infornmation flow is exceptional here......I'd like to continue..

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    Originally posted by Dr. Pain
    That was important too, as you just answered Nigeepoo's question, cooking negates the negative effect of the Brassicas...and iodine relieves the problem w/raw!

    Soy as I have contended affects the whole thyroid hormonal cascade!

    Good Post!

    DP
    Not quite, we no not to what extent it negates the effect, nor were any studies mentioned to back it up.

    And also, you posted it was irreversable I believe, where it says it has happened in HALF the cases, all reversed after one month.

    Anyway...I`m too drunk to debate this now, so I`m out til tomorrow or Sunday.

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    Originally posted by Dr. Pain
    I would disagree., respectfully!

    The infornmation flow is exceptional here......I'd like to continue..
    respectively disagree all you like, I`m still waiting for you to answer this...


    Originally posted by kuso
    I have seen NOTHING comparing brassica to soy, nor ANY mention of brassica at all so what was it that caused you to draw this conclusion?

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    Somebody in a post may have said Irreversible, again, FYI....all that is in a post is not my contention!

    Good Job Kuso, let's keep this friendly...I'm learning things and will be able to jhelp more people, I'm excited

    and....NOT into debate

    Thanks for your contributions, you rock!

    DP

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    Originally posted by kuso
    respectively disagree all you like, I`m still waiting for you to answer this...

    I find that information in the conclusions/ideas that I draw from the information...and more!

    Call it my perspective, but I see the effects on thyroid as more negative from soy than from cabbage...

    How about a poll



    DP

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    Originally posted by Dr. Pain
    you rock!
    You`ve only just discovered this? I`ve know it for years

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