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BACKGROUND: To determine the effect of vitamin D binding protein (DBP) genotypes on 25-hydroxyvitamin D [25(OH)D] changes with vitamin D supplements, we studied 98 adults receiving 600 or 4000 IU/d vitamin D(3) for one year. METHODS: The DBP functional variant, T436K, was genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). RESULTS: Mean 25(OH)D increases were 97% for TT (n=48), 151% for TK (n=31) and 307% (n=6) for KK genotypes (p=.004). CONCLUSIONS: As with baseline 25(OH)D, T436K genotype predicts 25(OH)D changes after long-term vitamin D supplementation. Common genetic variants of the vitamin D binding protein (DBP) predict differences in response of serum 25-hydroxyvitamin D [25(OH)D] to vitamin D supplementation. Fu L, Yun F, Oczak M, Wong BY, Vieth R, Cole DE. Clin Biochem. 2009 Jul;42(10-11):1174-7. Epub 2009 Mar 18. PMID: 19302999

"THURSDAY, Dec. 3 (HealthDay News) -- New research points to the possibility of a genetic link between vitamin D and heart disease. People with high blood pressure who had a gene variant that reduces vitamin D activation in the body were found to be twice as likely as those without the variant to have congestive heart failure, the study found. The finding may lead to a way to identify people at increased risk for heart disease, according to Robert U. Simpson, an assistant professor of pharmacology at the University of Michigan Medical School and his research colleagues. They analyzed the genetic profiles of 617 people. One-third had hypertension, one-third had hypertension and congestive heart failure, and the remaining third served as healthy controls. The researchers found that a variant in the CYP27B1 gene was associated with congestive heart failure in people with hypertension. The study is in the November issue of Pharmacogenomics."

Vitamin D receptor (VDR) gene polymorphisms and haplotypes, interactions with plasma 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D, and prostate cancer risk. Mikhak B, Hunter DJ, Spiegelman D, Platz EA, Hollis BW, Giovannucci E. Prostate. 2007 Jun 15;67(9):911-23. PMID: 17440943 DOI: 10.1002/pros.20570 RESULTS No association was found between these SNPs or their associated haplotypes and all PC subtypes except that haplotype 2 (A-f-b) with Cdx2 A, Fok1 f, and Bsm1 b alleles and haplotype 3 (A-F-B) with Cdx2 A, Fok1 F and Bsm1 B alleles compared to the most common haplotype (A-F-b), were associated with reduced risk of aggressive PC (high stage or Gleason sum 7; P = 0.02), both with two alleles suspected of being low risk. Carriers of the variant Cdx2 A allele who were deficient in plasma 25-hydroxyvitamin D (15 ng/ml) compared to non-carriers with normal 25-hydroxyvitamin D, had a lower risk of total and poorly differentiated PCs (Gleason sum 7) (P for interaction = 0.02 and 0.04, respectively). Plasma 1,25-dihydroxyvitamin D deficiency (26 pg/ml) was associated with a threefold risk of poorly differentiated PC (P for interaction = 0.01) when comparing carriers of the Cdx2 A allele to non-carriers with normal 1,25-dihydroxyvitamin D. CONCLUSION In this population of men, none of the VDR polymorphisms studied was associated with susceptibility to PC. Carriers of the variant Cdx2 A allele with low plasma 25-hydroxyvitamin D may experience a reduction in risk of total and poorly differentiated prostate cancers compared to non-carriers with adequate 25-hydroxyvitamin D.

Research finds people with gene variant who lack vitamin D, produced from sun exposure, can develop condition

The Author The author of this site is the British writer, John Davidson. Please note that the author is neither a doctor, nor a qualified health practitioner. Every cancer patient should always consult his or her medical practitioner with regard to the use of complementary remedies or treatments, and nothing on this site should be construed in any way as medical or therapeutic advice. It is simply the result of one person's search for solutions. Please read our disclaimer. About This Site Internet searches trawl up vast amounts of information about cancer, from a broad spectrum of viewpoints. The information and internet links on this site are for those seeking to augment the treatment offered by their hospital oncology (cancer) unit. Of course, a great many other internet sites concerning cancer can be found by keying the requisite search words into any of the major search engines. The content of this site was initially prepared, at the request of medical and nursing staff and others, some weeks after I had had an emergency operation for the removal of a colon cancer, and while undergoing chemotherapy in case any cancer cells had gone AWOL. There had been some escape of cancer cells into associated lymph nodes (3 out of 17, including the most distal), but no other tumours had been picked up by a CT scan. When I returned home from hospital in September 2005, with the help of friends, I started doing some research on cancer. I was amazed to discover that despite the billions of pounds/euros/dollars etc. spent on cancer research, and the many advances in understanding the numerous variants of the disease, the standard treatment for my stage of colon cancer is still a drug (fluorouracil, also called 5FU) that has been in use for more than forty years, has uncomfortable side effects, and which only increases the chances of survival after five years by 5 to 10%.

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