breastcancerchoices.org/f.html Breast cancer, fluoride and Vitamin D3 Fluoride is a toxic substance known to inhibit hundreds of enzymes including those that generate ATP to power the cell. Fluoride also affects the iodine transport system and thyroid hormone activation. The recent (2006) National Research Council report on the toxicology of fluoride in drinking water admits it is an “endocrine disruptor”. Fluoride is greatly increased in the modern diet, added to drinking water in nearly every North American large city, and is a large component of air pollution, entering the blood through the lungs. Most North Americans have excessive intake. Up to 80% of intake is retained in the body, accumulating in skeletal tissue from conception. Fluoride is not metabolized and is not a nutrient, but does increase the need for other nutrients, notably calcium, iodine, selenium, C, E and possibly D. Vitamin D3 is an essential nutrient substance and cell function regulator, made in the skin from exposure to UVB radiation from the sun (or tanning lights) and naturally present in some animal and sea foods. There is emerging consensus among researchers that humans need a blood level of 80-100 nmol/L from conception to old age for optimal growth and health including basic protection from infection, autoimmune disease and cancer. Most of the world’s people, all ages, now living indoors and eating processed foods, are deficient. It is theorized that some incidence of some cancers, including breast cancer, could be reduced by up to half with optimization of blood D levels in the general population. However, researchers admit that a fixed supplement dosage does not reliably produce a corresponding optimal level of 25OHD in the blood. Some research points to low thyroid function in cases of stubborn D deficiency. Accuracy of blood tests for 25OHD has also been a problem. breastcancerchoices.org/f.html The role of fluoride as an antagonist to reaching optimal D in the blood has never been examined. Does our increased fluoride intake from food, water and environmental pollution play a role in suppressing vitamin D formation in skin, uptake from food, synthesis and conversion in liver and kidney tissues, and activation in cells? Does it compete with 25OHD to limit vitamin D receptor formation, or affect metabolic degradation of calcitriol (the active hormone-like form of D) leading to a shortage or delay? Is fluoride’s well- known thyroid-suppressive effect part of the D-deficiency picture? Does increased fluoride intake cause dose-related relative deficiency of cancer-protective vitamin D as it does with iodine, selenium and antioxidants like C and E? Could this effect account for part of the increase in cancer incidence and mortality reported in epidemiological and animal studies on artificially fluoridated drinking water? Research throughout the twentieth century found that clinical Vitamin D deficiency disease of the bones can be caused by increased fluoride intake: fluoridealert.org/health/bone/fluorosis/rickets.html Increased fluoride intake also produced deficiency of the active vitamin D metabolites (25OHD and 1,25OHD) normally produced by the liver and kidney. Canadian research correlated higher vitamin D blood levels (25OHD above 100 nmol/L) with better survival odds after breast cancer diagnosis, as well as cancer that is less aggressive. This has given new hope that low-cost dietary supplements, D-enriched foods and sunshine can aid in cancer prevention and improve survival after diagnosis and treatment. British researchers found that breast cancer cells are able to protect themselves against vitamin D’s cancer-fighting chemistry by inhibiting enzymes that activate it from 25OHD (calcidiol) into 1,25OHD (calcitriol) at the cell margins. This effect was most pronounced when levels of 25OHD outside the cell were low. The British researchers concluded that higher levels of 25OHD outside the cell are needed in order to overcome the cancer cell’s defense. When the cancer cell is faced with ample calcidiol, the formation of more vitamin D receptors and activation of more calcitriol tends to promote apoptosis and slow or even stop tumor growth. If vitamin D is as important in fighting breast cancer as it appears to be, and cancer cells have defenses against it, we should know if there are environmental or dietary factors such as increased fluoride intake that inhibit optimal D formation and activation, directly or indirectly. Normal thyroid function is essential for normal D metabolism. Iodine and selenium are required for normal thyroid function. According to the National Research Council 2006 report, chronic hypothyroidism is reliably induced with fluoride dosage from 0.01 mg/kg/day (exceeded with consumption of fluoridated drinking water) when iodine or selenium is deficient. Selenium deficiency can also cause hypothyroidism, and selenium deficiency is known to increase risk of cancer incidence and death. The body’s major detoxification pathways that protect against cancer require selenium. Fluoride-induced thyroid suppression may be one aspect of D deficiency despite supplementation, and may be related to this fluoride-induced iodine and selenium deficiency. Lastly, Vitamin D deficiency is one aspect of hypothyroidism and autoimmune thyroid disease, which increase risk of both breast and thyroid cancers. Supplementation with D can be therapeutic for both hypothyroidism and autoimmune thyroid disease. Reducing fluoride intake should therefore be considered as part of the clinical strategy for prevention and treatment of breast cancer and thyroid disease, and for optimization of vitamin D levels in the blood as well as optimization of iodine and selenium intake. References Anticancer Res. 2006 Jul-Aug;26(4A):2573-80. Colston KW, Lowe LC, Mansi JL, Campbell MJ. Vitamin D Status and Breast Cancer Risk BACKGROUND: Local synthesis of 1alpha,25(OH)D3 in breast tissue may contribute to maintenance of normal cell function and could be impaired with low circulating levels of the precursor 25hydroxyvitamin D. The aims of this study were to: i) assess the association between breast cancer risk and plasma 25OHD3 concentration and ii) define the significance of expression of the 25OHD activating enzyme CYP27b1 in non-malignant and malignant models of breast epithelial cells. MATERIALS AND METHODS: Breast cancer patients and control women were recruited and their 25OHD levels measured by enzyme-linked immunosorbent assay (ELISA). MRNA expression of CYP271b and the 1,25(OH)2D3 inactivating enzyme CYP24 were measured in breast cancer cell lines by RT-PCR and correlated with immunoblotting approaches to the translated proteins. RESULTS: For women with 25OHD < 50 nM the odds ratio for breast cancer compared with women with 25OHD > 50 nM was 3.54 (CI 1.89-6.61, p < 0.001). CYP271b and CYP24 were detected in non-malignant and malignant cell models. Protein levels of 24OHase but not 1alphaOHase were decreased at confluence in the cell lines. CONCLUSION: Impaired local generation of 1,25OHD3 may contribute to the development of breast cancer. Clinch CA. Fluoride Interactions with Iodine and Iodide: Implications for Breast Health. Fluoride April-June 2009:42(2):75-87. fluorideresearch.org/422/files/FJ2009_v42_n2_p00i-iii.pdf Goodwin P. J. et al. Samuel Lunenfeld Research Institute, Toronto, ON, Canada; University of Toronto, Toronto, ON, Canada; Sunnybrook Health Sciences Centre, Toronto, ON, Canada; St. Michaels Hospital, Toronto, ON, Canada. Vitamin D deficiency is common at breast cancer diagnosis and is associated with a significantly higher risk of distant recurrence and death in a prospective cohort study of T1-3, N0-1, M0 BC. Goodwin, P. (2009) Vitamin D in Cancer Patients: Above all, do no harm. Journal of Clinical Oncology, Vol 27, No 13 (May 1), 2009: pp. 2117-2119 Graham, J.R., Burk, O., and Morin, P. (1987). A current restatement and continuing reappraisal concerning demographic variables in American time-trend studies on water fluoridation and human cancer. Proc Pennsylvania Academy of Sci. 61:138-146. Johnson W, et al. (1979). Fluoridation and bone disease in renal patients. In: E Johansen, DR Taves, TO Olsen, Eds. Continuing Evaluation of the Use of Fluorides. AAAS Selected Symposium. Westview Press, Boulder, Colorado. pp. 275-293. National Research Council. (2006). Fluoride in Drinking Water: A Scientific Review of EPAs Standards. National Academies Press, Washington D.C. Susheela, A.K. (2007) A Treatise on Fluorosis. Fluorosis Research and Rural Development Foundation. Delhi, India. Taylor A., Taylor N. (1965). Effects of Fluoride on Tumor Growth. Proceedings of Society of Experimental Biol. and Medicine, Vol. 65 pp252-255. Yiamouyiannis JA. (1993). Fluoridation and cancer: the biology and epidemiology of bone and oral cancer related to fluoridation. Fluoride. 26(2):83-96. Full study at fluoridealert. org/re/yiamouyiannis-1993.pdf Yiamouyiannis J., Burk D. (1977) Fluoridation and cancer age-dependence of cancer mortality related to artificial fluoridation, Fluoride 10: 102-124. breastcancerchoices.org/f.html
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