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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OBJECTIVES:To evaluate the association between serum 25-hydroxyvitamin D (25(OH)D) levels and mortality in a representative U.S. sample of older adults. DESIGN: Prospective cohort from the Third National Health and Nutrition Examination Survey (NHANES III) and linked mortality files. SETTING: Noninstitutionalized U.S. civilian population. PARTICIPANTS: Three thousand four hundred eight NHANES III participants aged 65 and older enrolled from 1988 to 1994 and followed for mortality through 2000. MEASUREMENTS: Primary exposure was serum 25(OH)D level at enrollment. Primary and secondary outcomes were all-cause and cardiovascular disease (CVD) mortality, respectively. 1 Vitamin D insufficiency has been associated with higher incidences of many medical conditions that affect mortality risk, including hypertension, 2,3 diabetes mellitus, 4-7 cardiovascular disease (CVD), [8][9][10][11][12] cancer, 13-17 and infection. [18][19][20][21] Vitamin D supplementation appears to mitigate incidence of, and adverse outcomes from, these various diseases. 17,22,23 Accordingly, recent evidence suggests that vitamin D may play a role in mortality risk. 11,24,25 Low serum levels of 25-hydroxyvitamin D (25(OH)D), the major circulating form of vitamin D, have been associated with all-cause mortality in individuals with end-stage renal disease 24 and coronary artery disease 11 and even in the general population. 25 Further evidence suggests that vitamin D supplementation may lower mortality. [26][27][28][29] Although older adults are at high risk for lower 25(OH)D levels 1 and mortality, 30 the association between vitamin D insufficiency and mortality risk has not been specifically evaluated in older adults.Older adults are at high risk for vitamin D insufficiency because of a reduction of 7-dehydrocholesterol, the

New Zealand children, particularly those of Māori and Pacific ethnicity, may be at risk for low vitamin D status because of low vitamin D intakes, the country's latitude (35-46 degrees S), and skin color. The aim of this study was to determine 25-hydroxyvitamin D concentrations and their determinants in a national sample of New Zealand children aged 5-14 y. The 2002 National Children's Nutrition Survey was designed to survey New Zealand children, including oversampling of Māori and Pacific children to allow ethnic-specific analyses. A 2-stage recruitment process occurred using a random selection of schools, and children within each school. Serum 25-hydroxyvitamin D concentration [mean (99% CI) nmol/L] in Māori children (n = 456) was 43 (38,49), in Pacific (n = 646) 36 (31,42), and in New Zealand European and Others (NZEO) (n = 483) 53 (47,59). Among Māori, Pacific, and NZEO, the prevalence (%, 99% CI) of serum 25-hydroxyvitamin D deficiency (<17.5 nmol/L) was 5 (2,12), 8 (5,14), and 3 (1,7), respectively. The prevalence of insufficiency (<37.5 nmol/L) was 41 (29,53), 59 (42,75), and 25 (15,35), respectively. Multiple regression analysis found that 25-hydroxyvitamin D concentrations were lower in winter than summer [adjusted mean difference (99% CI) nmol/L; 15 (8,22)], lower in girls than boys [5 (1,10)], and lower in obese children than in those of "normal" weight [6 (1,11)]. Relative to NZEO, 25-hydroxyvitamin D concentrations were lower in Māori [9 (3,15)] and Pacific children [16 (10,22)]. Ethnicity and season are major determinants of serum 25-hydroxyvitamin D. There is a high prevalence of vitamin D insufficiency in New Zealand children, which may or may not contribute to increased risk of osteoporosis and other chronic disease. There is a pressing need for more convincing evidence concerning the health risks associated with the low vitamin D status in New Zealand children.