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Thyroid disease is defined as a condition of malfunction of thyroid. Hyperthyroidism is a condition in which the thyroid gland is over active and produces too much thyroid hormones.
Thyroid adenoma is a benign tumor started in the layer of cell lined the inner surface of the thyroid gland. The disease are relatively common among adults living in the United States. According to the study by the Mayo Clinic and Mayo Foundation, there is a report of 4 patients described in whom a follicular carcinoma developed following thyroidectomy for a benign follicular neoplasm. Most thyroid nodules are Thyroid adenoma.
Diet to prevent Thyroid adenoma
1. Legumes, soy and peanut
Daidzein is a phytochemical in the Isoflavones, belonging to the group of Flavonoids (polyphenols), found abundantly in food of the family of legumes, soy, peanut, etc..In the study to explore whether or not human thyroid cancer cell growth can be curbed by a novel isoflavone derivative generated in our laboratory, the N-t-Boc-hexylenediamine derivative of 7-(O)-carboxymethyl daidzein (cD-tboc), showed that when nude mice carrying ARO thyroid xenografts were treated with cD-tboc, tumor volume decreased significantly, and no apparent toxicity was observed. These results suggest that cD-tboc may be a promising agent for therapy of thyroid carcinoma either alone or in combination with existing cytotoxic drugs(28).
In the study to observe that an acidic methanolic extract of soybeans contains compounds that inhibit thyroid peroxidase-(TPO) catalyzed reactions essential to thyroid hormone synthesis, showed that 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(29).
3. Green tea
Epigallocatechin-3-gallate (EGCG), a major catechin in green tea, was shown to possess remarkable therapeutic potential against various types of human cancer cells in in vitro and in vivo models. In the study to investigate the effect of EGCG on the proliferation and apoptosis of ARO cells–human ATC cells, showed that EGCG treatment inhibited the growth of ARO cells in a dose-dependent manner. Furthermore, EGCG suppressed phosphorylation of EGFR, ERK1/2, JNK, and p38. These changes were associated with increased p21 and reduced cyclin B1/CDK1 expression. In addition, EGCG treatment increased the accumulation of sub-G1 cell, activated caspase-3 and cleaved PARP(30).
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