the government is the biggest mystery to me.


http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=314438


from the link:

"Abstract

A renewal of the search for a link between Breast Cancer and thyroid disease has once again demonstrated an increased prevalence of autoimmune thyroid disease in patients with breast cancer. This is the most recent of many studies showing an association between a variety of thyroid disorders and breast cancer. Such an association is not surprising as both diseases are female predominant with a similar postmenopausal peak incidence. The significance of the presence of thyroid autoantibodies, particularly thyroid peroxidase antibodies, in serum from patients with Breast Cancer is unknown, but it has been suggested that antibody positivity is associated with better prognosis. One area in which thyroid and breast functions overlap is in the uptake and utilization of dietary iodide. Experimental findings showing the ability of Iodine or iodine-rich seaweed to inhibit breast tumour development is supported by the relatively low rate of Breast Cancer in Japanese women who consume a diet containing iodine-rich seaweed. However, there is as yet no direct evidence that iodine, iodinated compounds, or a combination of Iodine and selenium is the antimammary carcinogenic element in the Japanese diet. It remains to be resolved whether the perceived breast cancer–thyroid disease relationship is thyroid or Iodine related or, in the case of thyroid autoantibodies, is the consequence of an immune response to the carcinoma. Is this response breast specific and does it relate to iodine status? These and many other questions await resolution before a definitive role in the natural history of breast carcinoma can be assigned to the thyroid."


and here is some juice:

"One area in which thyroid and breast functions overlap is in the uptake and utilization of iodide. In the thyroid, I- is required for thyroid hormonogenesis whereas in the breast I- is needed in breast milk as a source of neonatal nutrition. Both organs require a method of oxidizing I- to I2 (organification) in order to produce iodoproteins [23,24]. This involves the presence of H2O2 (Hydrogen-Peroxid) as an oxidizing agent catalyzed by TPO in the thyroid and by lactoperoxidases in the breast. Apart from the requirement for Iodide as a nutrient in breast milk, there is no known role for iodine in the normal or diseased breast. However, a breast requirement for I2 rather than I- has been suggested [25]. It has been postulated that formation of iodolipids such as iodolactones or iodoaldehydes represents a form of thyroidal autoregulation [26], which may be the mode of action of Iodide inhibition of thyroid function in the Wolff–Chaikoff effect [27-29].

In addition to their role in inhibiting thyroid function, these compounds may act as antiproliferative agents in the thyroid [26]. Iodinated compounds (so-called XI) may exert inhibitory effects on adenylate cyclase, NADPH (nicotinamide adenine dinucleotide phosphate, reduced form)-oxidase and TPO activities [27]. This effect seems to require oxidation of I- to I2 because inhibitors of TPO or I- trapping can reverse the inhibitory effect [29]. It has also been suggested that such inhibitory actions of iodo-compounds on cell proliferation might play a role in the breast [30,31]. Some support for a role for iodine in the human breast is provided by our own findings [20], which showed that tissue iodine levels were relatively low in patients with breast cancer as compared with normal tissues or benign breast tumours (fibroadenomata). We have also recently shown 125I uptake blocking effects in sera from 19% of 105 patients with breast cancer [20], as compared with a published prevalence of 30.7% of such blocking activity, believed to be of immunogenic origin, in Graves' disease [32]. The ability of the breast to express sodium–iodide symporter [20-22] and, at least in lactation, to take up significant amounts of Iodide has led to studies of the potential for use of 131I ablative therapy in breast cancer, analogous to that employed in the treatment of hyperthyroidism or thyroid cancer.

An anticarcinogenic role for iodine in experimental animals was suggested by the work of Funahashi and coworkers [33], who found that administration of Lugol's iodine or iodine-rich Wakame seaweed to rats treated with the carcinogen dimethyl benzanthracene suppressed the development of mammary tumours. In further studies [34], the same group demonstrated that seaweed induced apoptosis in human breast cancer cells with greater potency than that of fluorouracil, a chemotherapeutic agent used to treat breast cancer. This finding led the authors to speculate that 'seaweed may be applicable for prevention of breast cancer'.

This hypothesis is in accord with the relatively low breast cancer rate reported in Japan [35], where the normal diet is seaweed rich, and with increasing breast cancer rates in Japanese women who emigrate [36] or consume a western style diet [37]. Interestingly this finding applies to rates of breast cancer in both males and females [38]. This evidence favours the low rate of breast cancer being environmental rather than genetic in origin. One of the main dietary differences between Japanese and western women is the consumption of large amounts of iodine-rich seaweeds by the former, yielding a dietary iodine intake of several milligrams per day in Japanese women as compared with microgram quantities in western women [31]. Of course it must be stressed that all this evidence is circumstantial because the contribution, if any, of dietary iodine intake to these findings is unknown. Equally, the possibility that this protective effect may be lost in patients with AITD [8] remains to be explored.

The frequent coexistence of iodine and selenium deficiencies and the importance of replacing both to maintain thyroid function is well established [39]. It has also been suggested that a combined iodine–selenium deficiency may facilitate the development of breast cancer [31]. Selenium deficiency results in diminution of selenium-containing antioxidative enzymes such as glutathione peroxidase, deiodinases and thioredoxine reductases [39,40], leading to increased levels of reactive oxygen species. These oxidants can inactivate many enzymes, are a feature of lipid peroxidation and DNA damage, and have been shown to be associated with carcinogenesis in the breast [41]. On the other hand, increased serum levels of antioxidants have been associated with reductions in breast cancer risk [42]. There is also some evidence that iodide itself may act as an antioxidant [43]. Selenium deficiency is associated with AITD perhaps as a result of increased inflammatory activity arising from decreased activity of selenium containing antioxidative enzymes such as glutathione peroxidase [39], whereas increasing dietary selenium or administration of selenomethionine have also been reported to diminish TPO antibody levels [44,45]."


read it all. its hard to believe the fear mongering regarding breast cancer when the answer is right in front of us.