G'day G'day Folks,  Diets high in isoflavones are reputed by some to exacerbate hypothyroidism.  The Japanese diet is high is isoflavones.   What else, if anything, does it contain that allows Japanese to avoid hypothyroidism? Thanks,

hello ya'll, The most common type of hypothyroidism is called Hashimoto's thyroiditis. It's autoimmune in nature. Jorge Good pickup, Hashimoto's is common in women (in Australia at least) as they approach middle age (a friend has it). I always wondered about the origin of the name. . . and I just looked it up: 'Named after the Japanese physician, Hakaru Hashimoto . . . first described in 1912.' To get back to Quentin's original question: maybe the Japanese don't avoid hypothyroidism. That could mean soy is a predisposing agent in Japanese diet . . . or it could mean nothing of the sort. As Mark Twain said: There is something fascinating about science. One gets such a wholesale return of conjecture for such a trifling investment of fact. Paul R

'Named after the Japanese physician, Hakaru Hashimoto . . . first described in 1912.' To get back to Quentin's original question: maybe the Japanese don't avoid hypothyroidism. Of course they don't.

To get back to Quentin's original question: maybe the Japanese don't avoid hypothyroidism. Of course they don't. But note that Iodine deficiency is an important factor in thyroid disease, and the Japanese diet is Iodine-rich because of the large amount of shellfish and other seafood consumed. Perhaps that explains why thyroid disease is no more common here in Japan than in countries where soy is not eaten in similar quantities. Here's the other side of the story:     There is no convincing evidence that soy protein has an adverse   effect on thyroid function, particularly at the moderate level of   consumption (25 grams) that would occur due to the approval of a   health claim for coronary heart disease.     There is evidence that animals exposed to large amounts of soy   protein (e.g., 40%) will develop goiter, particularly when fed an   iodine deficient diet (Kimura et al., 1976; Filisetti and Lajolo, 1981).    The mechanism for this effect can be explained by the fact that the   principal isoflavones in soy, genistein and daidzein, have been shown   to inhibit thyroid peroxidase (Divi et al., 1997) and 5'-deiodinase   (Cody et al., 1989), key enzymes involved in thyroid hormone   biosynthesis. The inhibition of these enzymes results in decreased   levels of circulating thyroid hormones (e.g., T4 and T3) which leads   to increased secretion of thyroid stimulating hormone (TSH) by the   anterior pituitary. The increased levels of TSH provides a growth   stimulus to the thyroid, resulting in goiter. It must be emphasized,   however, that this occurs only with large amounts of soy isoflavones   in the diet and/or when the diet is low in iodine. Furthermor, soy   isoflavones are not the only dietary flavonoids that can inhibit   thyroid peroxidase. A variety of other flavonoids have also been shown   to be even more potent in inhibiting the activity of this enzyme,   including kaempferol, naringenin, and quercetin (Divi and Doerge, 1996).    Such flavonoids are widely distributed in plant-derived foods and   would be consumed daily at relatively high levels (possibly up to 1   gram or more per day) by vegetarians or semi-vegetarians, yet such   individuals do not have a significant increased incidence of goiter.   Goiter has also been reported in infants where soy has served as the   sole source of food (Hydovitz, 1960). However, this situation is   hardly comparable to adults consuming soy protein in moderate amounts   as a means to lower total or LDL cholesterol levels.     In sum, soy products have been consumed as a dietary staple in Asian   countries for hundreds of years with no significant occurrence of   goiter in that population. Goiter is primarily due to a deficiency of   dietary iodine, not the consumption of moderate amounts of soy protein   incorporated into a nutritionally sound diet. That goiter would result   in adults consuming 25 grams of soy protein per day in response to an   approved health claim for coronary heart disease is ludicrous. References: Cody V, Koehrle J and Hesch RD. Structure-activity relationships of flavonoids as inhibitors of iodothyronine deiodinase. In: Environmental Goitrogenesis, Gaitan, E. (ed), pp. 57-69, CRC Press, Boca Raton, FL, 1989. Divi RL, Chang HC and Doerge DR. Anti-thyroid isoflavones from soybean. Biochem. Pharmacol 54:1087-1096, 1997. Divi RL and Doerge DR. Inhibition of thyroid peroxidase by dietary flavonoids. Chem. Res. Toxicol. 9:16-23, 1996. Filisetti TM and Lajolo FM. Effect of the ingestion of soybean fractions, raw or autoclaved, on the rat thyroid. Arch. Latinoam. Nutr. 31:287-302, 1981. Hydovitz JD. Occurrence of goiter in an infant on a soy diet. N Engl. J. Med. 262:351-353, 1960. Kimura S, Suwa J, Ito B and Sato H. Development of malignant goiter by defatted soybean with iodine-free diet in rats. Gann 67:763-765, 1976.

hypothyroidism. Of course they don't. But note that Iodine deficiency is an important factor in thyroid disease, and the Japanese diet is Iodine-rich because of the large amount of shellfish and other seafood consumed. Perhaps that explains why thyroid disease is no more common here in Japan than in countries where soy is not eaten in similar quantities. Sorry, but that's not it. Hypothyroidism is most common in Japanese coastal areas where iodine intake is HIGHEST. One of my beefs with the orthopathic weenies is that they simply look at a problem and throw whatever nutrient they can think of at it. Alas, iodine/iodide supplementation is useful only for one small (now rare) kind of hypothyroidism. All the other kinds it does either nothing for, or else causes it to get worse (since iodine actually suppresses thyroid function at high doses). The last is probaby what is happening in Japan with the Hashimoto's disease