Circulating Vitamin D, Supplement Use, and Cardiovascular Disease Risk: The MrOS Sleep Study
The Journal of Clinical Endocrinology and Metabolism (Impact Factor: 6.21). 03/2014; 99(9):jc20134178. DOI: 10.1210/jc.2013-4178
Context: Evidence suggests an inverse association between circulating 25(OH) vitamin D and cardiovascular disease (CVD). Objective: Determine the association between serum 25(OH) vitamin D and risk for CVD events. Design: From March 2000 to April 2002, participants were recruited for the Osteoporotic Fractures in Men (MrOS) study; between December 2003 and March 2005, members of the MrOS cohort were invited to participate in the MrOS Sleep Study. We followed participants from the sleep study cohort for a mean of 5.9 years. Setting: Clinical centers at six recruitment sites across the United States. Patients: 3,135 men aged 65 and older from the MrOS cohort, of whom 116 were excluded for missing vitamin D or CVD data. Interventions: Participants were divided into two groups based on serum 25(OH) vitamin D levels: <20 ng/mL and ≥20 ng/mL. Main Outcome Measure: Participants were followed for CVD endpoints: coronary heart disease (CHD) and cerebrovascular events. We calculated age- and multivariable adjusted hazard ratios and stratified by use of vitamin D containing supplements. Results: We observed no significant association between circulating 25(OH) vitamin D and risk of CVD event (HR=0.91, 95% CI=0.73-1.13) and CHD event (HR=0.81, 95% CI=0.61-1.07). For cerebrovascular events, men with vitamin D deficiency appeared to exhibit a higher risk (HR=1.44, 95% CI=1.00-2.08) using the minimally adjusted model and after excluding supplement users (HR=1.70, 95% CI=1.02-2.83). Conclusions: 25(OH) vitamin D was not associated with risk of CVD and CHD events. However, vitamin D deficiency may be associated with an increased risk of cerebrovascular events.
Article: Deaths: Preliminary Data for 2011[Show abstract] [Hide abstract]
ABSTRACT: Objectives-This report presents preliminary U.S. data on deaths, death rates, life expectancy, leading causes of death, and infant mortality for 2011 by selected characteristics such as age, sex, race, and Hispanic origin. Methods-Data in this report are based on death records comprising more than 98 percent of the demographic and medical files for all deaths in the United States in 2011. The records are weighted to independent control counts for 2011. Comparisons are made with 2010 final data. Results-The age-adjusted death rate decreased from 747.0 deaths per 100,000 population in 2010 to 740.6 deaths per 100,000 population in 2011. From 2010 to 2011, age-adjusted death rates decreased significantly for 5 of the 15 leading causes of death: Diseases of heart, Malignant neoplasms, Cerebrovascular diseases, Alzheimer's disease, and Nephritis, nephrotic syndrome and nephrosis. The age-adjusted death rate increased for six leading causes of death: Chronic lower respiratory diseases, Diabetes mellitus, Influenza and pneumonia, Chronic liver disease and cirrhosis, Parkinson's disease, and Pneumonitis due to solids and liquids. Life expectancy remained the same in 2011 as it had been in 2010 at 78.7 years.
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ABSTRACT: Imbalancing nutritionally adequate diets with an excessive amount of fat calories and cholesterol has obscured the fact that intimal thickening occurs spontaneously in time on low-fat cholesterol-free diets during the aging process, and that intimal thickening can be accelerated by dietary angiotoxic "risk factors." Electron microscopy of arterial tissue from animal models identified degenerated smooth muscle cells in the fetus from sows kept on low-fat cholesterol-free diets. After birth, the degenerated smooth muscle cells increased in number with age. The presence of angiotoxic "risk factors" such as oxidized cholesterol and vitamin D3 (cholecalciferol) in the diet of such animal models increased the frequency of smooth muscle cell death in their arteries. Two types of pathology could be developed in the thoracic aorta by continuous or short term feeding of 12.5 times more vitamin D than normally present in commercial rations: 1) a diffuse fibroelastic intimal thickening in the thoracic aorta (arteriosclerosis) with no evidence of lipid deposition by continuous feeding of vitamin D or 2) an initimal thickening in the thoracic aorta and intimal thickening with foam cells and extracellular lipid deposits (atherosclerosis) in the coronary arteries after a short period of supplemental vitamin D followed by 3 to 4 months of supplement-free diets. These two types of arterial damage were identical to that in the plugs of thoracic aorta obtained as a by-product of elective coronary bypass surgery. Although all of the possible sources of oxidized cholesterol in the diet have as yet not been identified, laboratory studies have identified oxidized cholesterol as an angiotoxic factor. Since population groups that consume less vitamin D-supplemented foods, less deep fat fried cholesterol-containing foods, and less hydrogenated fats have a lower incidence of coronary heart disease than Americans, it seems judicious for food processors to reduce these previously unconsidered risk factors to a minimum. This could be done by eliminating vitamin D2 and D3 from all vitamin supplements, from all food and cereal products and from the diet of livestock 1 month before they were killed so that the intake of vitamin D is no larger than the 400 IU/quart in milk which is necessary to prevent rickets in children. Deep fat fryers, which are kept at almost 200 C for 24 hr/day, could perhaps be replaced with microwave ovens in fast food chain outlets. Processors could hydrogenate vegetable oils to a minimum trans fatty acid content and rearrange this fat with polyunsaturated fats to produce high polyunsaturated fats trans-free margarines and shortenings.American Journal of Clinical Nutrition 02/1979; 32(1):58-83. · 6.77 Impact Factor
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ABSTRACT: Background: Vitamin D status has been linked to the risk of cardiovascular disease (CVD). However, the optimal 25-hydroxy-vitamin D (25[OH]-vitamin D) levels for potential cardiovascular health benefits remain unclear. Methods and results: We searched MEDLINE and EMBASE from 1966 through February 2012 for prospective studies that assessed the association of 25(OH)-vitamin D concentrations with CVD risk. A total of 24 articles met our inclusion criteria, from which 19 independent studies with 6123 CVD cases in 65 994 participants were included for a meta-analysis. In a comparison of the lowest with the highest 25(OH)-vitamin D categories, the pooled relative risk was 1.52 (95% confidence interval, 1.30-1.77) for total CVD, 1.42 (95% confidence interval, 1.19-1.71) for CVD mortality, 1.38 (95% confidence interval, 1.21-1.57) for coronary heart disease, and 1.64 (95% confidence interval, 1.27-2.10) for stroke. These associations remained strong and significant when analyses were limited to studies that excluded participants with baseline CVD and were better controlled for season and confounding. We used a fractional polynomial spline regression analysis to assess the linearity of dose-response association between continuous 25(OH)-vitamin D and CVD risk. The CVD risk increased monotonically across decreasing 25(OH)-vitamin D below ≈60 nmol/L, with a relative risk of 1.03 (95% confidence interval, 1.00-1.06) per 25-nmol/L decrement in 25(OH)-vitamin D. Conclusions: This meta-analysis demonstrated a generally linear, inverse association between circulating 25(OH)-vitamin D ranging from 20 to 60 nmol/L and risk of CVD. Further research is needed to clarify the association of 25(OH)-vitamin D higher than 60 nmol/L with CVD risk and assess causality of the observed associations.Circulation Cardiovascular Quality and Outcomes 11/2012; 5(6). DOI:10.1161/CIRCOUTCOMES.112.967604 · 5.66 Impact Factor
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