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Diagnosis and treatment of vitamin D deficiency. Cannell JJ, Hollis BW, Zasloff M, Heaney RP. Expert Opin Pharmacother. 2008 Jan;9(1):107-18. PMID: 18076342 The recent discovery - in a randomised, controlled trial - that daily ingestion of 1100 IU of colecalciferol (vitamin D) over a 4-year period dramatically reduced the incidence of non-skin cancers makes it difficult to overstate the potential medical, social and economic implications of treating vitamin D deficiency. Not only are such deficiencies common, probably the rule, vitamin D deficiency stands implicated in a host of diseases other than cancer. The metabolic product of vitamin D is a potent, pleiotropic, repair and maintenance, secosteroid hormone that targets > 200 human genes in a wide variety of tissues, meaning it has as many mechanisms of action as genes it targets. A common misconception is that government agencies designed present intake recommendations to prevent or treat vitamin D deficiency. They did not. Instead, they are guidelines to prevent particular metabolic bone diseases. Official recommendations were never designed and are not effective in preventing or treating vitamin D deficiency and in no way limit the freedom of the physician - or responsibility - to do so. At this time, assessing serum 25-hydroxy-vitamin D is the only way to make the diagnosis and to assure that treatment is adequate and safe. The authors believe that treatment should be sufficient to maintain levels found in humans living naturally in a sun-rich environment, that is, > 40 ng/ml, year around. Three treatment modalities exist: sunlight, artificial ultraviolet B radiation or supplementation. All treatment modalities have their potential risks and benefits. Benefits of all treatment modalities outweigh potential risks and greatly outweigh the risk of no treatment. As a prolonged 'vitamin D winter', centred on the winter solstice, occurs at many temperate latitudes, ≤ 5000 IU (125 μg) of vitamin D/d

Docosahexaenoic acid inhibits superoxide dismutase 1 gene transcription in human cancer cells: the involvement of peroxisome proliferator-activated receptor alpha and hypoxia-inducible factor-2alpha signaling. Tuller ER, Beavers CT, Lou JR, Ihnat MA, Benbrook DM, Ding WQ. Mol Pharmacol. 2009 Sep;76(3):588-95. Epub 2009 Jun 15. PMID: 19528198

"(NaturalNews) New research published in The Journal of the Federation of American Societies for Experimental Biology (FASEB) has found that the "Western" diet, typically high in sugar and fat, may be responsible for activating genes that signal the body to become fatter. According to scientists, the body's response to high amounts of energy-dense food is to activate the kappa opioid receptor which triggers increased fat storage. Researchers arrived at this conclusion by conducting an experiment on two groups of mice. One group had its kappa opioid receptors genetically deactivated while the other remained intact. Both groups were fed diets high in fat and sugar for 16 weeks. At the end of 16 weeks, the group with the deactivated receptor remained lean while the control group gained significant weight. Besides limiting their bodies' ability to store energy-dense food in their fat stores, the mice whose receptors had been deactivated were noted to also have a limited ability to assimilate and store nutrients from the foods they ingested. Traci Ann Czyzyk-Morgan, one of the study's researchers, indicated that the findings prove the hypothesis long held by many in the scientific community that the kappa opioid receptor may be responsible for causing widespread obesity in Western countries. She and others continue to encourage people to avoid diets high in fat and sugar. "

Glucose restriction can extend normal cell lifespan and impair precancerous cell growth through epigenetic control of hTERT and p16 expression. Li Y, Liu L, Tollefsbol TO. FASEB J. 2009 Dec 17. [Epub ahead of print] PMID: 20019239 doi: 10.1096/fj.09-149328 Cancer cells metabolize glucose at elevated rates and have a higher sensitivity to glucose reduction. However, the precise molecular mechanisms leading to different responses to glucose restriction between normal and cancer cells are not fully understood. We analyzed normal WI-38 and immortalized WI-38/S fetal lung fibroblasts and found that glucose restriction resulted in growth inhibition and apoptosis in WI-38/S cells, whereas it induced lifespan extension in WI-38 cells. Moreover, in WI-38/S cells glucose restriction decreased expression of hTERT (human telomerase reverse transcriptase) and increased expression of p16(INK4a). Opposite effects were found in the gene expression of hTERT and p16 in WI-38 cells in response to glucose restriction. The altered gene expression was partly due to glucose restriction-induced DNA methylation changes and chromatin remodeling of the hTERT and p16 promoters in normal and immortalized WI-38 cells. Furthermore, glucose restriction resulted in altered hTERT and p16 expression in response to epigenetic regulators in WI-38 rather than WI-38/S cells, suggesting that energy stress-induced differential epigenetic regulation may lead to different cellular fates in normal and precancerous cells. Collectively, these results provide new insights into the epigenetic mechanisms of a nutrient control strategy that may contribute to cancer therapy as well as antiaging approaches.

"Hi! This is Amy Proal. I wrote the article referenced at the start of the thread about vitamin D. Dr. Marshall is not concerned with vitamin D toxicity. Rather his molecular modeling research has clarified the actions of the two vitamin D metabolites 25-D and 1,25-D. The Vitamin D Receptor (VDR) is a fundamental receptor of the body - it controls the expression thousands of genes, as well as the activity of the innate immune system and the antimicrobial peptides. If you think of the VDR as a switch, 25-D (which is a corticosteroid) turns it off (inactivates it) and 1,25-D turn it on (activates it). What is commonly believed among vitamin D researchers is that if people supplement with extra vitamin D it will be converted into 1,25-D and activate the VDR. Unfortunately, Marshall's work revealed that the type of vitamin D derived from supplements and sun remains, for the most part, in it's precursor form 25-D. This means that the extra vitamin D we get from fortified food products and supplements is turning the VDR off, not on. That causes a decrease in immune function and gene transcription."

"Vitamin D is not just a sun-derived vitamin, but is a crucial steroid precursor that is transformed into one of the most potent hormones in the human body for strength, power, lung function and regulating gene expression in every organ system. Athletes need Vitamin D. Dr. Cannell has written quite extensively about the role of vitamin D in athletes"

Conjugated linoleic acid promotes human adipocyte insulin resistance through NFkappaB-dependent cytokine production. Chung S, Brown JM, Provo JN, Hopkins R, McIntosh MK. J Biol Chem. 2005 Nov 18;280(46):38445-56. Epub 2005 Sep 9. PMID: 16155293 doi: 10.1074/jbc.M508159200 Collectively, these data demonstrate for the first time that trans-10, cis-12 CLA promotes NFkappaB activation and subsequent induction of IL-6, which are at least in part responsible for trans-10, cis-12 CLA-mediated suppression of peroxisome proliferator-activated receptor gamma target gene expression and insulin sensitivity in mature human adipocytes. In summary, our in vitro data demonstrate that a physiological level of trans-10, cis-12 CLA activates NFκB- and ERK1/2-dependent cytokine production, which together suppress PPARγ and Glut4 levels and lead to impaired glucose uptake. Studies are currently under way examining 1) how CLA regulates PPARγ and the expression of its target genes, 2) the specific signaling role of SV cells and adipocytes in mediating the TG-lowering actions of CLA, and 3) the CLA-induced, upstream signal that activates NFκB and ERK1/2.

"In an article published in the December 29, 2005, issue of the journal Cell, the researchers report that knocking out a single gene encoding the enzyme GnT-4a glycosyltransferase (GnT-4a ) disrupts insulin production. Importantly, the scientists showed that a high-fat diet suppresses the activity of GnT-4a and leads to type 2 diabetes due to failure of the pancreatic beta cells. "We have discovered a mechanistic explanation for beta cell failure in response to a high-fat diet and obesity, a molecular trigger which begins the chain of events leading from hyperglycemia to insulin resistance and type 2 diabetes," said Jamey Marth, a Howard Hughes Medical Institute investigator at the University of California, San Diego (UCSD). Marth and first author Kazuaki Ohtsubo at UCSD collaborated on the studies with researchers from the Kirin Brewery Co. Ltd., and the University of Fukui, both in Japan."

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Human cathelicidin antimicrobial peptide (CAMP) gene is a direct target of the vitamin D receptor and is strongly up-regulated in myeloid cells by 1,25-dihydroxyvitamin D3.\nGombart AF, Borregaard N, Koeffler HP.\nFASEB J. 2005 Jul;19(9):1067-77.\nPMID: 15985530

WEST LAFAYETTE, Ind. - Researchers have uncovered new evidence suggesting factors other than genes could cause obesity, finding that genetically identical cells store widely differing amounts of fat depending on subtle variations in how cells process insulin. Learning the precise mechanism responsible for fat storage in cells could lead to methods for controlling obesity. "Insights from our study also will be important for understanding the precise roles of insulin in obesity or Type II diabetes, and to the design of effective intervention strategies," said Ji-Xin Cheng, an assistant professor in Purdue University's Weldon School of Biomedical Engineering and Department of Chemistry. Findings indicate that the faster a cell processes insulin, the more fat it stores.

Fish oil and treatment of cancer cachexia. Giacosa A, Rondanelli M. Genes Nutr. 2008 Apr;3(1):25-8. PMID: 18850196

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.

View Michael Mullan's professional profile on LinkedIn. Dr Michael Mullan, CEO and President of the Roskamp Institute, Sarasota, FL. He research to cure Alzheimer's Disease. He discovered Swedish Mutation in the Amyloid Precursor Protein gene that is widely used in Alzheimer's research today.

Michael Mullan, CEO and President of the Roskamp Institute, Sarasota, FL. He research to cure Alzheimer's Disease. He discovered Swedish Mutation in the Amyloid Precursor Protein gene that is widely used in Alzheimer's research today. Michael Mullan is a leading expert in Alzheimers Research and other neurodegnerative disorder.

ScienceDaily (Feb. 22, 2009) - Cancer cells need a lot of nutrients to multiply and survive. While much is understood about how cancer cells use blood sugar to make energy, not much is known about how they get other nutrients. Now, researchers at the Johns Hopkins University School of Medicine have discovered how the Myc cancer-promoting gene uses microRNAs to control the use of glutamine, a major energy source. The results, which shed light on a new angle of cancer that might help scientists figure out a way to stop the disease, appear Feb. 15 online at Nature

Blueberry Punch is an Australian product but is available for sale on the internet at £16 a bottle.\n\nIt also includes a host of other natural ingredients thought to boost health, including green tea, olive leaves, the herb tarragon and the spices turmeric and ginger.\n\nIt is thought the ingredients act together to cut inflammation and block a cancer gene.\n\nDr Jas Singh, who conducted the research on mice at Sydney University, said: "We have undertaken efficacy studies on individual components of Blueberry Punch in the same laboratory setting and found these effective in suppressing cell growth in culture.\n\n"We reasoned that synergistic or additive effects are likely to be achieved when they are combined."\n\nThe researchers looked at the effect of Blueberry Punch on both cancer cell cultures in the laboratory and genetically engineered mice with human prostate tumours. After only two weeks of having the syrupy solution added to their drinking water, their tumours had shrunk by

ScienceDaily (Feb. 12, 2009) - Diet - and how it has shaped our genome - occupies much of an evolutionary scientist's time. Anne Stone, associate professor of anthropology in Arizona State University's School of Human Evolution and Social Change, will discuss how diet holds keys to understanding who we are, how we live and form societies, and how we evolved from hunter-gatherers to agriculturists, all the way to modern urban dwellers, at the American Association for the Advancement of Science annual meeting.