OBJECTIVE -To determine the association between serum 25-hydroxyvitamin D (25OHD) and diabetes risk and whether it varies by ethnicity. RESEARCH DESIGN AND METHODS -We performed an analysis of data from participants who attended the morning examination of the Third National Health and Nutrition Examination Survey (1988 -1994), a cross-sectional survey of a nationally representative sample of the U.S. population. Serum levels of 25OHD, which reflect vitamin D status, were available from 6,228 people (2,766 non-Hispanic whites, 1,736 non-Hispanic blacks, and 1,726 Mexican Americans) aged Ն20 years with fasting and/or 2-h plasma glucose and serum insulin measurements.RESULTS -Adjusting for sex, age, BMI, leisure activity, and quarter of year, ethnicityspecific odds ratios (ORs) for diabetes (fasting glucose Ն7.0 mmol/l) varied inversely across quartiles of 25OHD in a dose-dependent pattern .60] for nonHispanic whites and 0.17 [0.08 -0.37] for Mexican Americans) in the highest vitamin D quartile (25OHD Ն81.0 nmol/l) compared with the lowest 25OHD (Յ43.9 nmol/l). This inverse association was not observed in non-Hispanic blacks. Homeostasis model assessment of insulin resistance (log e ) was inversely associated with serum 25OHD in Mexican Americans (P ϭ 0.0024) and non-Hispanic whites (P ϭ 0.058) but not non-Hispanic blacks (P ϭ 0.93), adjusting for confounders.CONCLUSIONS -These results show an inverse association between vitamin D status and diabetes, possibly involving insulin resistance, in non-Hispanic whites and Mexican Americans. The lack of an inverse association in non-Hispanic blacks may reflect decreased sensitivity to vitamin D and/or related hormones such as the parathyroid hormone. Diabetes Care 27:2813-2818, 2004T here is increasing evidence that vitamin D metabolism affects the risk of diabetes. Initial findings from animal studies showed that insulin released from the isolated perfused pancreas of the rat is lower in vitamin D-deficient animals than control animals (1), while pancreatic receptors for 1,25-dihydroxyvitamin D 3 in ␤-cells have been identified in a number of species (2). More recently, human studies have shown that vitamin D supplementation in infancy reduces the risk of type 1 diabetes during early adulthood (3).Vitamin D may also have a role in the development of type 2 diabetes. TaqI vitamin D receptor polymorphisms have been associated with an insulin secretion index among Bangladeshi Asians living in London, who have a high risk of type 2 diabetes (4). The BsmI polymorphism was associated with fasting glucose in inactive German men (5). In the Rancho Bernardo study (6) of older U.S. Caucasians, the ApaI polymorphism was associated with fasting plasma glucose and prevalence of glucose intolerance and the BsmI polymorphism with the homeostatis model assessment (HOMA) of insulin resistance.Given that a number of investigations have shown that vitamin D receptor polymorphisms are associated with various measures of glucose metabolism and diabetes risk, it seems reasonable to conclude t...

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Vitamin D status, which is amenable to intervention by safely increasing sun exposure or vitamin D supplementation, was associated inversely with BP in a large sample representative of the US population.

IMPORTANCE Cohort studies have reported increased incidence of cardiovascular disease (CVD) among individuals with low vitamin D status. To date, randomized clinical trials of vitamin D supplementation have not found an effect, possibly because of using too low a dose of vitamin D. OBJECTIVE To examine whether monthly high-dose vitamin D supplementation prevents CVD in the general population. DESIGN, SETTING, AND PARTICIPANTSThe Vitamin D Assessment Study is a randomized, double-blind, placebo-controlled trial that recruited participants mostly from family practices in Auckland, New Zealand, from April 5, 2011, through November 6, 2012, with follow-up until July 2015. Participants were community-resident adults aged 50 to 84 years. Of 47 905 adults invited from family practices and 163 from community groups, 5110 participants were randomized to receive vitamin D 3 (n = 2558) or placebo (n = 2552). Two participants retracted consent, and all others (n = 5108) were included in the primary analysis.INTERVENTIONS Oral vitamin D 3 in an initial dose of 200 000 IU, followed a month later by monthly doses of 100 000 IU, or placebo for a median of 3.3 years (range, 2.5-4.2 years). MAIN OUTCOMES AND MEASURESThe primary outcome was the number of participants with incident CVD and death, including a prespecified subgroup analysis in participants with vitamin D deficiency (baseline deseasonalized 25-hydroxyvitamin D [25(OH)D] levels <20 ng/mL). Secondary outcomes were myocardial infarction, angina, heart failure, hypertension, arrhythmias, arteriosclerosis, stroke, and venous thrombosis. RESULTSOf the 5108 participants included in the analysis, the mean (SD) age was 65.9 (8.3) years, 2969 (58.1%) were male, and 4253 (83.3%) were of European or other ethnicity, with the remainder being Polynesian or South Asian. Mean (SD) baseline deseasonalized 25(OH)D concentration was 26.5 (9.0) ng/mL, with 1270 participants (24.9%) being vitamin D deficient. In a random sample of 438 participants, the mean follow-up 25(OH)D level was greater than 20 ng/mL higher in the vitamin D group than in the placebo group. The primary outcome of CVD occurred in 303 participants (11.8%) in the vitamin D group and 293 participants (11.5%) in the placebo group, yielding an adjusted hazard ratio of 1.02 (95% CI, 0.87-1.20). Similar results were seen for participants with baseline vitamin D deficiency and for secondary outcomes.CONCLUSIONS AND RELEVANCE Monthly high-dose vitamin D supplementation does not prevent CVD. This result does not support the use of monthly vitamin D supplementation for this purpose. The effects of daily or weekly dosing require further study.

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