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A critical review of Vitamin D and cancer: A report of the IARC Working Group on vitamin D William B. Grant Dermato-Endocrinology. Volume 1, Issue 1 January/February 2009 Pages: 25 - 33 The International Agency for Research on Cancer (IARC) released a report, Vitamin D and Cancer, on November 25, 2008. The report focused on the current state of knowledge and level of evidence of a causal association between vitamin D status and cancer risk. Although presenting and evaluating evidence for the beneficial role of UVB and vitamin D in reducing the risk of cancer, it discounted or omitted important evidence in support of the efficacy of vitamin D. The report largely dismissed or ignored ecological studies on the grounds that confounding factors might have affected the findings. The report accepted a preventive role of vitamin D in colorectal cancer but not for breast cancer.

Vitamin D related articles in "The Heart Scan Blog" by Dr. William Davis

Reducing the Burden of Disease Through Adequate Intake of Vitamin D3. A presentation at University of California, San Diego, April 9, 2008 by William B. Grant, Ph.D

Amsterdam, The Netherlands, May 26, 2009 - There are several risk factors for the development of Alzheimer's disease and vascular dementia. Based on an increasing number of studies linking these risk factors with Vitamin D deficiency, an article in the current issue of the Journal of Alzheimer's Disease (May 2009) by William B. Grant, PhD of the Sunlight, Nutrition, and Health Research Center (SUNARC) suggests that further investigation of possible direct or indirect linkages between Vitamin D and these dementias is needed. Low serum levels of 25-hydroxyvitamin D [25(OH)D] have been associated with increased risk for cardiovascular diseases, diabetes mellitus, depression, dental caries, osteoporosis, and periodontal disease, all of which are either considered risk factors for dementia or have preceded incidence of dementia. In 2008, a number of studies reported that those with higher serum 25(OH)D levels had greatly reduced risk of incidence or death from cardiovascular diseases

Anti-aromatase activity of phytochemicals in white button mushrooms (Agaricus bisporus). Chen S, Oh SR, Phung S, Hur G, Ye JJ, Kwok SL, Shrode GE, Belury M, Adams LS, Williams D. Cancer Res. 2006 Dec 15;66(24):12026-34. PMID: 17178902 doi: 10.1158/0008-5472.CAN-06-2206

Conclusion A low-carbohydrate plant-based diet has lipid-lowering advantages over a high-carbohydrate, low-fat weight-loss diet in improving heart disease risk factors not seen with conventional low-fat diets with animal products. The Effect of a Plant-Based Low-Carbohydrate ("Eco-Atkins") Diet on Body Weight and Blood Lipid Concentrations in Hyperlipidemic Subjects David J. A. Jenkins; Julia M. W. Wong; Cyril W. C. Kendall; Amin Esfahani; Vivian W. Y. Ng; Tracy C. K. Leong; Dorothea A. Faulkner; Ed Vidgen; Kathryn A. Greaves; Gregory Paul; William Singer Arch Intern Med. 2009;169(11):1046-1054. DOI: 10.1001/archinternmed.2009.115

Evolutionary health promotion. Eaton SB, Strassman BI, Nesse RM, Neel JV, Ewald PW, Williams GC, Weder AB, Eaton SB 3rd, Lindeberg S, Konner MJ, Mysterud I, Cordain L. Prev Med. 2002 Feb;34(2):109-18. Review. PMID: 11817903 doi:10.1006/pmed.2001.0876

Ginkgo has many alleged nootropic properties, and is mainly used as memory[25] and concentration enhancer, and anti-vertigo agent. However, studies differ about its efficacy. The largest and longest independent clinical trial to assess ginkgo biloba's ability to prevent memory loss has found that the supplement does not prevent or delay dementia or Alzheimer's disease.[26] Some controversy has arisen over the conclusions drawn by some studies that were allegedly funded by a firm which marketed Ginkgo.[27] In 2002, a long-anticipated paper appeared in JAMA (Journal of the American Medical Association) titled "Ginkgo for memory enhancement: a randomized controlled trial." This Williams College study, sponsored by the National Institute on Aging rather than Schwabe, examined the effects of ginkgo consumption on healthy volunteers older than 60. The conclusion, now cited in the National Institutes of Health's ginkgo fact sheet, said: "When taken following the manufacturer's instructions, ginkgo provides no measurable benefit in memory or related cognitive function to adults with healthy cognitive function." ... The impact of this seemingly damning assessment, however, was ameliorated by the almost simultaneous publication of a Schwabe-sponsored study in the less prestigious Human Psychopharmacology. This rival study, conducted at Jerry Falwell's Liberty University, was rejected by JAMA, and came to a very different-if not exactly sweeping-conclusion: There was ample evidence to support "the potential efficacy of Ginkgo biloba EGb 761 in enhancing certain neuropsychological/memory processes of cognitively intact older adults, 60 years of age and over." According to some studies, in a few cases, Ginkgo can significantly improve attention in healthy individuals.[28][29] Allegedly, the effect is almost immediate and reaches its peak in 2.5 hours after the intake.[30] [edit] In dementia A 2004 conference paper[31] summarizes how various trials indicate that Gi

"Despite its dubious beginnings, fad-dieting gained mass appeal in the 19th century. In 1829, Presbyterian minister Sylvester Graham touted the Graham Diet - centered on caffeine-free drinks and vegetarian cuisine, and supplemented by the eponymous Graham Cracker - as a cure for not just obesity but masturbation (and the subsequent blindness it was thought to cause.) The diet became so popular that the students of Oberlin College were forced onto it for a brief period in the 1830s before they successfully rebelled through mass dissent in 1841. Thirty-five years later, an English casketmaker named William Banting became famous by pioneering the concept of a low-carbohydrate diet, which helped him lose 50 lbs. He published his results in the 1864 "Letter on Corpulance," and the plan became so popular that "banting" became a synonym for dieting across Britain. "

"Ann Arbor, MI - New laboratory research suggests that the COX-2 inhibitor celecoxib (Celebrex, Pfizer), might impede the action of "baby" aspirin [1]. Dr Gilad Rimon (University of Michigan, Ann Arbor) and colleagues found evidence that this was the case in a dog model and say that "it will be important to determine" whether the same is true in humans. The report was published online December 1, 2009 in the Proceedings of the National Academy of Medicine. Celecoxib is the only COX-2 inhibitor to have remained on the market in the US, and doctors who recommend this painkiller often coprescribe a daily low dose of 81 mg of aspirin (known as a "baby" dose) to counteract any possible prothrombotic effects of the coxib, while minimizing potential gastrointestinal toxicity of the aspirin. Senior author of the new work, Dr William L Smith (University of Michigan, Ann Arbor), explained to heartwire that previous studies in humans have shown that celecoxib does not interfere with the effect of a standard dose of aspirin (325 mg), but any potential interaction of celecoxib with the lower dose has not been examined. Stagger dosing to avoid any potential problems First, Smith explained that he and his colleagues looked in vitro at celecoxib and found that it binds to one of two available sites on the COX-1 enzyme. "This surprised us," he commented. "It appears to interfere with the ability of some other drugs to affect COX-1, most notably aspirin." Second, in beagles, they administered the dog-equivalent of a baby dose of aspirin in humans and then gave some of the animals the equivalent of 100 mg of celecoxib twice daily in addition. "Celecoxib plus aspirin interfered with the normal effect of low-dose aspirin on platelets," he notes. Smith says this observation obviously requires confirmation in humans, but in the meantime he suggests "getting around the problem" by patients taking the low-dose aspirin at least 15 to 30 minutes before the celecoxib is taken, "because

"For what reason I don't know, but this January 2009 editorial by William Faloon of the Life Extension Foundation is making the rounds. Perhaps it just came available on the web. It's a good read, particularly in light of the billions and trillions of dollars the thieves & thugs in DC are about to flush down the crapper on your behalf. Some notable excerpts. A large number of new vitamin D studies have appeared in the scientific literature since I wrote my plea to the federal government. These studies don't just confirm what we knew 16 months ago-they show that optimizing vitamin D intake will save even more lives than what we projected. For instance, a study published in June 2008 showed that men with low vitamin D levels suffer 2.42 times more heart attacks. Now look what this means in actual body counts. Each year, about 157,000 Americans die from coronary artery disease-related heart attacks. Based on this most recent study, if every American optimized their vitamin D status, the number of deaths prevented from this kind of heart attack would be 92,500. To put the number of lives saved in context, tens of millions of dollars are being spent to advertise that Lipitor® reduces heart attacks by 37%. This is certainly a decent number, but not when compared with how many lives could be saved by vitamin D. According to the latest study, men with the higher vitamin D levels had a 142% reduction in heart attacks."

"came across a gem of a study the other day, courtesy of Dr. John Briffa's blog. It's titled "Margarine Intake and Subsequent Coronary Heart Disease in Men", by Dr. William P. Castelli's group. It followed participants of the Framingham Heart study for 20 years, and recorded heart attack incidence*. Keep in mind that 20 years is an unusually long follow-up period. "

"July 9, 2008 | Michael O'Riordan Boston, MA - The consumption of a diet containing vegetable oils rich in alpha-linolenic acid (ALA) is associated with significant reductions in the risk of nonfatal MI, a new study has shown [1]. Investigators say the protective effect of ALA is evident among individuals with low intakes, suggesting the greatest benefit might be in developing countries, where fatty-acid consumption is limited. "The potential for benefit is great when the baseline intake is low," said lead investigator Dr Hannia Campos (Harvard Medical School, Boston, MA). "In countries where people eat very little fish-and some of these countries have almost no sources of omega-3 fatty acids because they cook with corn or sunflower oils-the consumption of vegetable oils with ALA could have a major impact on heart disease." In an editorial accompanying the published study [2], Dr William Harris (University of South Dakota, Sioux Falls) said that the data are suggestive and would be good news for individuals who will not or cannot eat fish, but more studies are still needed. "If ALA were able to do the same 'heavy lifting' that [eicosapentaenoic acid] EPA and [docosahexaenoic acid] DHA do, this would be welcomed news, because the capacity to produce ALA is essentially limitless, whereas there are only so many fish in the sea," he writes. "

Association of n-3 polyunsaturated fatty acids with stability of atherosclerotic plaques: a randomised controlled trial. Thies F, Garry JM, Yaqoob P, Rerkasem K, Williams J, Shearman CP, Gallagher PJ, Calder PC, Grimble RF. Lancet. 2003 Feb 8;361(9356):477-85. PMID: 12583947 doi:10.1016/S0140-6736(03)12468-3 Interpretation Atherosclerotic plaques readily incorporate n-3 PUFAs from fish-oil supplementation, inducing changes that can enhance stability of atherosclerotic plaques. By contrast, increased consumption of n-6 PUFAs does not affect carotid plaque fatty-acid composition or stability over the time course studied here. Stability of plaques could explain reductions in non-fatal and fatal cardiovascular events associated with increased n-3 PUFA intake

Conjugated linoleic acid impairs endothelial function. Taylor JS, Williams SR, Rhys R, James P, Frenneaux MP. Arterioscler Thromb Vasc Biol. 2006 Feb;26(2):307-12. Epub 2005 Dec 8. PMID: 16339498 CONCLUSIONS: A CLA isomeric mixture had at most modest effects on adiposity and worsened endothelial function. On the basis of these results, the use of the isomeric mixture of CLA as an aid to weight loss cannot be recommended

Opposing effects of cis-9,trans-11 and trans-10,cis-12 conjugated linoleic acid on blood lipids in healthy humans. Tricon S, Burdge GC, Kew S, Banerjee T, Russell JJ, Jones EL, Grimble RF, Williams CM, Yaqoob P, Calder PC. Am J Clin Nutr. 2004 Sep;80(3):614-20. PMID: 15321800 Conclusion: Divergent effects of cis-9,trans-11 CLA and trans-10,cis-12 CLA appear on the blood lipid profile in healthy humans: trans-10,cis-12 CLA increases LDL:HDL cholesterol and total:HDL cholesterol, whereas cis-9,trans-11 CLA decreases them.

The effects of conjugated linoleic acid on human health-related outcomes. Tricon S, Burdge GC, Williams CM, Calder PC, Yaqoob P. Proc Nutr Soc. 2005 May;64(2):171-82. Review. PMID: 15960862 Conjugated linoleic acid (CLA) is a collective term for a mixture of positional and geometric isomers of conjugated dienoic derivatives of linoleic acid. CLA has received considerable attention as a result of animal experiments that report anti-carcinogenic, anti-atherogenic and anti-diabetic properties, and modulation of body composition and immune function. Several studies of CLA supplementation in human subjects have now been published, but in contrast to animal studies there has been marked variation between reports on the health-related outcomes. The consensus from seventeen published studies in human subjects is that CLA does not affect body weight or body composition. Some detrimental effects of the trans-10,cis-12 CLA isomer have also been reported in terms of altered blood lipid composition and impaired insulin sensitivity. Finally, CLA has only limited effects on immune functions in man. However, there have been reports of some interesting isomer-specific effects of CLA on the blood lipid profile, but not on immune function. These isomer-specific effects need further investigation. Until more is known, CLA supplementation in man should be considered with caution.

Effects of dairy products naturally enriched with cis-9,trans-11 conjugated linoleic acid on the blood lipid profile in healthy middle-aged men. Tricon S, Burdge GC, Jones EL, Russell JJ, El-Khazen S, Moretti E, Hall WL, Gerry AB, Leake DS, Grimble RF, Williams CM, Calder PC, Yaqoob P. Am J Clin Nutr. 2006 Apr;83(4):744-53. PMID: 16600923 CONCLUSION: Dairy products naturally enriched with cis-9,trans-11 CLA and trans-11 18:1 do not appear to have a significant effect on the blood lipid profile

Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia -- Krauss et al. 83 (5): 1025 -- American Journal of Clinical Nutrition Changes in peak LDL diameter (Table 2) and mass concentrations of LDL subfractions (Table 3) induced by each of the diets were reflected by changes in the proportions of subjects exhibiting LDL subclass pattern B (Figure 2). There were linear reductions in the prevalence of pattern B as a function of reduced carbohydrate intake after both the stable-weight and weight-loss periods. However, the slopes of these relations differed (P = 0.04) such that the magnitude of the reduction in expression of pattern B induced by weight loss increased in association with the percentage of carbohydrate intake. Conclusions: Moderate carbohydrate restriction and weight loss provide equivalent but nonadditive approaches to improving atherogenic dyslipidemia. Moreover, beneficial lipid changes resulting from a reduced carbohydrate intake were not significant after weight loss. Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia. Krauss RM, Blanche PJ, Rawlings RS, Fernstrom HS, Williams PT. Am J Clin Nutr. 2006 May;83(5):1025-31; quiz 1205. Erratum in: Am J Clin Nutr. 2006 Sep;84(3):668. PMID: 16685042

Prostate cancer prevention and treatment by nutrition and supplements. LEF Magazine February 2007.