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Sunday, April 7, 2013

Soy and congenital hypothyroidism

Posted by Chantel M. research contributed  US National Library of Medicine National Institutes of Health  
Genistein aglycone, one of the soy isoflavones, has been reported to be beneficial in the treatment of menopausal vasomotor symptoms, osteoporosis, and cardiovascular diseases, as well as in a variety of cancers. However, issues of potential harm on thyroid function resulting from soy isoflavones consumption have been raised. Much of the evidence for the goitrogenic effects of isoflavones is derived from experimental in vitro and in vivo studies. Goitrogenic effects were also noted in infants fed non-iodine-fortified, soy-based formula, a problem that was easily solved with iodine fortification. According to the study by the Physiological and Nutritional Sciences, University of Messina, in the study of Update on genistein and thyroid to review of above studies, posted in PubMed, concluded that
Overall, there is a scarcity of information about the effect of pure isoflavones, such as genistein, on thyroid safety in humans. Results of intervention trials are not easily comparable because the researchers have used (i) mixed isoflavones or isoflavone and protein mixtures with different dosage regimens, soy foods or supplements as the active treatment; (ii) the quality and amount of genistein varied widely in all of these previous studies; and (iii) the trials were of different duration. Although the overall evidence suggests that isoflavone genistein does not affect adversely thyroid function in euthyroid, iodine-replete individuals, further studies are warranted to better define the relationship between genistein and thyroid.
Infants and women deserve particular attention in order to assess the safety of genistein and/or other isoflavones on thyroid function, also considering that thyroid disorders are age- and gender-related,
 posted in PubMed, showed that the combination of red pepper and fermented soybeans in kochujang improves glucose homeostasis by reducing insulin resistance, not by enhancing beta-cell function, in diabetic rats. The improvement is associated with decreased hepatic fat storage by the activation of adenosine monophosphate kinase.

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