Low Serum 25-Hydroxyvitamin D Is Associated with Increased Risk of the Development of the Metabolic Syndrome at Five Years: Results from a National, Population-Based Prospective Study (The Australian Diabetes, Obesity and Lifestyle Study: AusDiab)
ABSTRACT Serum 25-hydroxyvitamin D [25(OH)D] concentration has been inversely associated with the prevalence of metabolic syndrome (MetS), but the relationship between 25(OH)D and incident MetS remains unclear.
We evaluated the prospective association between 25(OH)D, MetS, and its components in a large population-based cohort of adults aged 25 yr or older.
We used baseline (1999-2000) and 5-yr follow-up data of the Australian Diabetes, Obesity, and Lifestyle Study (AusDiab).
Of the 11,247 adults evaluated at baseline, 6,537 returned for follow-up. We studied those without MetS at baseline and with complete data (n = 4164; mean age 50 yr; 58% women; 92% Europids).
We report the associations between baseline 25(OH)D and 5-yr MetS incidence and its components, adjusted for age, sex, ethnicity, season, latitude, smoking, family history of type 2 diabetes, physical activity, education, kidney function, waist circumference (WC), and baseline MetS components.
A total of 528 incident cases (12.7%) of MetS developed over 5 yr. Compared with those in the highest quintile of 25(OH)D (≥34 ng/ml), MetS risk was significantly higher in people with 25(OH)D in the first (<18 ng/ml) and second (18-23 ng/ml) quintiles; odds ratio (95% confidence interval) = 1.41 (1.02-1.95) and 1.74 (1.28-2.37), respectively. Serum 25(OH)D was inversely associated with 5-yr WC (P < 0.001), triglycerides (P < 0.01), fasting glucose (P < 0.01), and homeostasis model assessment for insulin resistance (P < 0.001) but not with 2-h plasma glucose (P = 0.29), high-density lipoprotein cholesterol (P = 0.70), or blood pressure (P = 0.46).
In Australian adults, lower 25(OH)D concentrations were associated with increased MetS risk and higher WC, serum triglyceride, fasting glucose, and insulin resistance at 5 yr. Vitamin D supplementation studies are required to establish whether the link between vitamin D deficiency and MetS is causal.
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ABSTRACT: Abstract: Vitamin D is a steroid prohormone synthesized in the skin following ultraviolet exposure and also achieved through supplemental or dietary intake. While there is strong evidence for its role in maintaining bone and muscle health, there has been recent debate regarding the role of vitamin D deficiency in hypertension based on conflicting epidemiological evidence. Thus, we conducted a scoping systematic literature review and meta-analysis of all observational studies published up to early 2014 in order to map trends in the evidence of this association. Mixed-effect meta-analysis was performed to pool risk estimates from ten prospective studies (n=58,262) (pooled risk for incident hypertension, relative risk [RR] =0.76 (0.63–0.90) for top vs bottom category of 25-hydroxyvitamin D [25OHD]) and from 19 cross-sectional studies (n=90,535) (odds ratio [OR] =0.79 (0.73–0.87)). Findings suggest that the better the assessed quality of the respective study design, the stronger the relationship between higher 25OHD levels and hypertension risk (RR =0.67 (0.51–0.88); OR =0.77 (0.72–0.89)). There was significant heterogeneity among the findings for both prospective and cross-sectional studies, but no evidence of publication bias was shown. There was no increased risk of hypertension when the participants were of older age or when they were vitamin D deficient. Younger females showed strong associations between high 25OHD levels and hypertension risk, especially in prospective studies (RR =0.36 (0.18–0.72); OR =0.62 (0.44–0.87)). Despite the accumulating evidence of a consistent link between vitamin D and blood pressure, these data are observational, so questions still remain in relation to the causality of this relationship. Further studies either combining existing raw data from available cohort studies or conducting further Mendelian analyses are needed to determine whether this represents a causal association. Large randomized controlled trials are also needed to determine whether vitamin supplementation may be beneficial in the prevention or the treatment of hypertension. Keywords: 25OHD, high blood pressure, meta-analysis, prospective, cross-sectional, blood pressureIntegrated Blood Pressure Control 04/2015; 8:13-35. DOI:10.2147/IBPC.S49958
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ABSTRACT: To determine the dose-response of vitamin D3 supplementation on serum 25-hydroxyvitamin D [25(OH)D] among Chinese adults. In this 5-arm, randomized, double-blinded controlled trial, 76 healthy participants were assigned to orally administrate 0, 400, 800, 1200 or 2000 IU/d of vitamin D3 for 16 weeks. Serum 25(OH)D, parathyroid hormone, calcium, biomarkers of liver and renal function were measured at multiple time points. The mean (SD) serum 25(OH)D at baseline was 31.6 (8.7) nmol/L, and the dose-response relationship was curvilinear with a plateau around 6 weeks for all doses. At week 16, 25(OH)D was increased by 6.0 (6.5), 21.7 (15.8), 26.3 (12.6), 32.0 (12.8) and 36.3 (26.0) nmol/L for 0, 400, 800, 1200 and 2000 IU/d (all P ≤ 0.002), corresponding to approximately 19, 53, 67, 77 and 80 % of reversion of vitamin D deficiency, respectively. Daily intake of 800 IU vitamin D3 reached a targeted 25(OH)D ≥ 30 nmol/L in at least 97.5 % of Chinese, but not a targeted 25(OH)D ≥ 50 nmol/L even with 2000 IU/d. Change of 25(OH)D was inversely associated with change of PTH concentration (r = -0.39, P < 0.001) after controlling for age and sex. No between-group differences were observed in terms of the change in serum calcium, alanine transaminase, aspartate aminotransferase, gamma-glutamyltransferase and creatinine (P ≥ 0.22). Supplementation with 400, 800, 1200 or 2000 IU/d vitamin D could improve the vitamin D deficiency with various degrees. Whether 2000 IU/d vitamin D3 would generate a better result without side effect requires more studies with larger samples in future.European Journal of Nutrition 02/2015; DOI:10.1007/s00394-015-0859-4 · 3.84 Impact Factor
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