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"Largest-ever meta-analysis finds CRP is unlikely to be causal for CVD December 21, 2009 | Lisa Nainggolan Cambridge, UK - In the largest and most comprehensive meta-analysis to date looking at C-reactive-protein (CRP) levels and risk of coronary heart disease (CHD) and stroke, British researchers conclude that CRP is unlikely to be a causal factor for cardiovascular disease [1]. Although CRP concentration was linearly associated with CHD, stroke, and vascular mortality, as well as nonvascular mortality, statistical adjustment for conventional cardiovascular risk factors "resulted in considerable weakening of associations," note the scientists of the Cambridge-based Emerging Risk Factors Collaboration (ERFC), who report their findings online December 21, 2009 in the Lancet. In an editorial accompanying the paper [2], Drs S Matthijs Boekholdt and John JP Kastelein (Academic Medical Center, Amsterdam, the Netherlands) say the UK authors "are to be commended for this impressive data set." Although the findings "add weight to the evidence of noncausality" for a role of CRP in the development of cardiovascular disease, "the debate can be resolved only by randomized trials with agents that specifically target CRP, and such compounds are currently under development," say the Dutch doctors. Commenting on the new meta-analysis for heartwire, Dr Paul Ridker (Brigham and Women's Hospital, Boston, MA), a long-time advocate of CRP and the lead investigator of the JUPITER trial, said: "Whether or not CRP is 'causal' for heart disease is neither the crucial issue at hand nor relevant for public health. What is crucial is getting international agreement that CRP identifies higher-risk individuals who would not otherwise qualify for a life-saving therapy, and then showing that such individuals clearly benefit from treatment. The new meta-analysis demonstrates the former, and JUPITER demonstrates the latter." "

A systematic review of the evidence supporting a causal link between dietary factors and coronary heart disease. Mente A, de Koning L, Shannon HS, Anand SS. Arch Intern Med. 2009 Apr 13;169(7):659-69. Review. PMID: 19364995 Conclusions The evidence supports a valid association of a limited number of dietary factors and dietary patterns with CHD. Future evaluation of dietary patterns, including their nutrient and food components, in cohort studies and randomized trials is recommended

A systematic review of the evidence supporting a causal link between dietary factors and coronary heart disease. Mente A, de Koning L, Shannon HS, Anand SS. Arch Intern Med. 2009 Apr 13;169(7):659-69. PMID: 19364995

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.

Independent association of low serum 25-hydroxyvitamin d and 1,25-dihydroxyvitamin d levels with all-cause and cardiovascular mortality. Dobnig H, Pilz S, Scharnagl H, Renner W, Seelhorst U, Wellnitz B, Kinkeldei J, Boehm BO, Weihrauch G, Maerz W. Arch Intern Med. 2008 Jun 23;168(12):1340-9. PMID: 18574092 Conclusions Low 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D levels are independently associated with all-cause and cardiovascular mortality. A causal relationship has yet to be proved by intervention trials using vitamin D.

Current impediments to acceptance of the ultraviolet-B-vitamin D-cancer hypothesis. Grant WB, Boucher BJ. Anticancer Res. 2009 Sep;29(9):3597-604. PMID: 19667154 The ultraviolet-B (UVB)-vitamin D-cancer hypothesis was proposed in 1980. There have been numerous ecological, observational and other studies of the hypothesis. There are about 14 types of cancer for which it seems to apply: bladder, breast, colon, endometrial, esophageal, gallbladder, gastric, ovarian, pancreatic, rectal, renal and vulvar cancer and both Hodgkin's and non-Hodgkin's lymphoma. Nonetheless, the hypothesis has not yet been accepted by public health agencies. Some of the reasons for this include a distrust of ecological studies, some mistrust of observational studies, and the existence of just one positive randomized controlled trial, an analysis of a vitamin D and calcium supplementation study involving post-menopausal women in Nebraska. Paradigm shifts such as this generally take time, in part due to opposition from those content with the status quo. In this paper, results of ecological studies in the United States using summertime solar UVB as the index of vitamin D production, which is highly asymmetrical with respect to latitude, and indices for other cancer risk-modifying factors (air pollution, alcohol consumption, dietary iron and zinc, ethnic background, socioeconomic status, smoking and urban/rural residence) are discussed in terms of supporting the hypothesis. These studies were not considered while other ecological studies were examined in recent critiques of the hypothesis. While additional randomized controlled trials would, of course, be helpful, the current evidence seems to satisfy the criteria for causality as outlined by A. Bradford Hill.

Strong correlations have been noted between cardiovascular diseases and low bone density / osteoporosis-connections so strong that the presence of one type of pathology is considered a likely predictor of the other. This potentially causal relationship has led to the hypothesis that these conditions share core mechanisms. Recent advances in our understanding of the complimentary roles played by vitamin D3 and vitamin K2 in vascular and bone health provide support for this hypothesis, along with insight into key metabolic dysfunctions underlying cardiovascular disease and osteoporosis. Part I of this review summarizes current research linking vitamin D deficiency to cardiovascular disease, the physiological mechanisms underlying vitamin D's cardiovascular effects, and leading vitamin D researchers' recommendations for significantly higher supplemental doses of the pro-hormone. Part II reviews the vitamin K connection to cardiovascular disease; the ways in which vitamin D and vitamin K pair up to prevent inflammation, vascular calcification and osteoporosis; and the necessity of providing vitamin K along with vitamin D to preclude adverse effects associated with hypervitaminosis D, which include vascular and other soft tissue calcification.

Vitamin D Status and the Risk of Cardiovascular Disease Death. Kilkkinen A, Knekt P, Aro A, Rissanen H, Marniemi J, Heliövaara M, Impivaara O, Reunanen A. Am J Epidemiol. 2009 Sep 17. [Epub ahead of print] PMID: 19762371 doi:10.1093/aje/kwp227 A low vitamin D level may be associated with higher risk of a fatal CVD event, particularly cerebrovascular death. These findings need to be replicated in other populations. To demonstrate a causal link between vitamin D and CVD, randomized controlled trials are required.

Prospective Study of Serum 25-Hydroxyvitamin D Level, Cardiovascular Disease Mortality, and All-Cause Mortality in Older U.S. Adults. Ginde AA, Scragg R, Schwartz RS, Camargo CA Jr. J Am Geriatr Soc. 2009 Jun 22. [Epub ahead of print] PMID: 19549021 DOI: 10.1111/j.1532-5415.2009.02359.x CONCLUSION: In noninstitutionalized older adults, a group at high risk for all-cause mortality, serum 25(OH)D levels had an independent, inverse association with CVD and all-cause mortality. Randomized controlled trials of vitamin D supplementation in older adults are warranted to determine whether this association is causal and reversible.

A diet rich in coconut oil reduces diurnal postprandial variations in circulating tissue plasminogen activator antigen and fasting lipoprotein (a) compared with a diet rich in unsaturated fat in women. Müller H, Lindman AS, Blomfeldt A, Seljeflot I, Pedersen JI. J Nutr. 2003 Nov;133(11):3422-7. PMID: 14608053 In conclusion, our results indicate that a coconut oil-based diet (HSAFA-diet) lowers postprandial t-PA antigen concentration, and this may favorably affect the fibrinolytic system and the Lp(a) concentration compared with the HUFA-diet. The proportions of dietary saturated fatty acids more than the percentage of saturated fat energy seem to have a beneficial influence on Lp(a) levels. The connection between Lp(a) and atherosclerosis is not entirely understood. Different studies have provided strong evidence that Lp(a) level is an independent risk factor for developing coronary artery disease in men (47,48), but the question of causality continues to be debated. Recent data suggest that Lp(a) might be atherogenic (49), in particular when combined with other risk factors. High levels of Lp(a) combined with other risk factors such as the ratio of plasma total/HDL cholesterol have been shown to increase the risk for coronary heart diseases (50). It has also been reported that when substantial LDL cholesterol reductions were obtained in men with coronary heart disease, persistent elevations of Lp(a) were no longer atherogenic or clinically threatening (51). In conclusion, the present results show that the HSAFA-diet lowered postprandial t-PA antigen and thus potentially improved fibrinolysis compared with the HUFA-diet. Diets with either high or low levels of saturated fatty acids from coconut oil beneficially decrease Lp(a) compared with a HUFA-diet. The proportions of dietary saturated fatty acids more than the percentage of saturated fat energy may be of importance if the goal is to decrease Lp(a).

Effects of vitamin D supplementation on symptoms of depression in overweight and obese subjects: randomized double blind trial. Jorde R, Sneve M, Figenschau Y, Svartberg J, Waterloo K. J Intern Med. 2008 Dec;264(6):599-609. Epub 2008 Sep 10. PMID: 18793245 Conclusions. It appears to be a relation between serum levels of 25(OH)D and symptoms of depression. Supplementation with high doses of vitamin D seems to ameliorate these symptoms indicating a possible causal relationship.