| The Iodine Group | ||
|
Home | Orthoiodosupplementation | Body | Disease | Special | Overviews |
||
|
|
CANN
Hypothesis: Iodine, selenium and the development of breast cancer.Cann SA, van Netten JP, van Netten C.
"Background: In this paper we examine some of the evidence linking iodine and selenium to breast cancer development. Seaweed is a popular dietary component in Japan and a rich source of both of these essential elements. We hypothesize that this dietary preference may be associated with the low incidence of benign and malignant breast disease in Japanese women. In animal and human studies, iodine administration has been shown to cause regression of both iodine-deficient goiter and benign pathological breast tissue. Iodine, in addition to its incorporation into thyroid hormones, is organized into anti-proliferative iodolipids in the thyroid; such compounds may also play a role in the proliferative control of extrathyroidal tissues. Selenium acts synergistically with iodine. All three mono-deiodinase enzymes are selenium-dependent and are involved in thyroid hormone regulation. In this way selenium status may affect both thyroid hormone homeostasis and iodine availability.
"Conclusion: Although there is suggestive evidence for a preventive role for iodine and selenium in breast cancer, rigorous retrospective and prospective studies are needed to confirm this hypothesis."
"In recent years a second pathway for iodine organification has been described, and involves iodine incorporation into lipid molecules. These iodolipids have been isolated from thyroid tissue and have been shown to be key regulators of thyroid cell proliferation and metabolism [53]. Iodide peroxidases (i.e., thyro/lactoperoxidase) catalyze the iodination of lipids [54]. One such com-pound derived from arachidonic acid, 6-iodo-5-hy-droxy-eicosatrienoic acid (d-iodolactone), was found to be a potent inhibitor of human thyroid follicular cell proliferation in vitro [55] and to induce goiter regression in rats in vivo [56]. These or similar compounds may also play a role in the proliferative control of breast tissue."
Iodide accumulation in extrathyroidal tissues.Cann SA, van Netten JP, Glover DW, van Netten C. J Clin Endocrinol Metab. 1999 Feb;84(2):821-2.
"We read with interest the paper by Spitzweg et al. on human sodium iodide symporter (hNIS) gene expression in nonthyroidal tissues. The authors state that extrathyroidal tissues are not able to organify accumulated iodide; however, there are exceptions to this rule. In addition to thyroperoxidase, other peroxidases found in nonthyroidal tissues such as lacto-, myelo-, and eosinophil peroxidase have been shown to efficiently organify iodide. In the mammary gland, iodide is bound to tyrosyl residues of caseins and other milk proteins, and this organification has been shown to correlate with peroxidase activity. In addition, there is evidence that iodoprotein formation may occur in inactive mammary tissue as well."
"Although iodide uptake in nonthyroidal tissues does not appear to be influenced by TSH, a number of other hormones are known to augment its accumulation. In mice, prolactin has been shown to enhance mammary iodide uptake during pregnancy. In nonpregnant rats, estradiol has been shown to significantly enhance mammary iodide accumulation. Conversely, estradiol has been shown to inhibit, while progesterone enhances, iodide uptake in the rat uterus and oviduct. Thus, a dynamic iodide balance may be maintained in these nonthyroidal tissues depending on the hormonal milieu and dietary iodine levels."
|
|
Home | Orthoiodosupplementation | Body | Disease | Special Topics | OverviewsThe Iodine Group | Books | Disclaimers | Contact Us | SearchCopyright: Zoe, 2006. |
||