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(VIDEO) Shedding light on the vitamin D deficiency 'crisis' By GrassRootsHealth.com Oct 11, 2009 - 4:49:39 PM San Diego, CA - Can vitamin D prevent 80% of the incidence of breast cancer? What is its affect on colon cancer and other major illnesses? These questions and more will be addressed when some of the most prominent vitamin D researchers in North America participate in the " Diagnosis & Treatment of Vitamin D Deficiency" seminar presented by GrassrootsHealth at the University of Toronto on Tuesday, November 3 from 8 a.m. - 5 p.m. GrassrootsHealth is the founder of D*action, an international public health project whose goal is to solve the vitamin D deficiency epidemic. GrassrootsHealth and D*action work with over 30 scientists, institutions and individuals committed to educate, test, and study vitamin D levels worldwide. At the conference, a group of physicians and researchers in the vitamin D field will discuss vitamin D's role in the potential prevention of many diseases, including breast cancer, colon cancer, type 1 diabetes and multiple sclerosis, the ultimate reduction in the incidence of infectious diseases and the economic impact of such action

The vitamin D craze has been building over the last few years, with low levels of the supplement being the blamed as a source of many of our ills. Depression? D can ease it. Chronic pain? Take D. It is said to prevent kidney disease, diabetes, osteoporosis, colon and breast cancer, cardiovascular disease, or even the common cold. Recently, a study linked low vitamin D levels to the rise in Caesarean births.

Induction of ovarian cancer cell apoptosis by 1,25-dihydroxyvitamin D3 through the down-regulation of telomerase. Jiang F, Bao J, Li P, Nicosia SV, Bai W. J Biol Chem. 2004 Dec 17;279(51):53213-21. Epub 2004 Oct 12. PMID: 15485861 doi: 10.1074/jbc.M410395200 Overall, the study suggests that the down-regulation of telomerase activity by 1,25(OH)2VD3 and the resulting cell death are important components of the response of OCa cells to 1,25(OH)2VD3-induced growth suppression. Progressive shortening of telomere associated with cell divisions limits the life span of normal cells and eventually leads to senescence. To become immortal, human cancers including OCa are invariably associated with activation of mechanism that maintains telomere length. Approximately 85-90% of cancers show reactivation of telomerase. The present study shows that telomerase in OCa cells is down-regulated by 1,25(OH)2VD3. Down-regulation of telomerase is due to decreased stability of hTERT mRNA rather than VDRE-mediated transcriptional repression through the putative VDRE present in the regulatory region of the hTERT gene. It is known that the inhibition of telomerase may lead to a phenotypic lag during which cells would continue to divide until the point at which the telomeres became critically short. This phenomenon may explain why the apoptotic induction by 1,25(OH)2VD3 needs the treatment for more than 6 days. As mentioned in the results, no detectable shortening of telomeric repeats was observed in parental OVCAR3 cells after 9 days of treatment with 1,25(OH)2VD3 (Fig. 4D). This is likely due to the fact that the short telomere (about 3 kb) in OVCAR3 cells is very close to the minimal length required for survival and that cells with detectably shorter telomere may have been selected against apoptosis. It has been shown that transformed human cells enter crisis once the terminal restriction fragment of the telomere reaches a length of about 4 kb. This is insufficient to protect chro