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Purpose: Age-related changes affect vitamin D absorption and metabolism. Low 25-hydroxyvitamin D concentrations have been reported as risk factor for the development of metabolic syndrome (MetS). However, recent evaluations suggest this association might be explained by obesity or insulin resistance (IR) in subjects with MetS. Our aim was to analyze associations between vitamin D insufficiency and MetS in a young cohort without diabetes and two senior cohorts with and without diabetes., Methods: Four hundred sixteen young and 1357 older BASE-II participants were analyzed. Type 2 diabetes (T2D) was defined according to European Society of Cardiology (ESC) guidelines, MetS as suggested by International Diabetes Federation/American Heart Association/National Heart, Lung and Blood Institute (IDF/AHA/NHLBI 2009). Vitamin D insufficiency was defined as 25-hydroxyvitamin D concentrations <50 nmol/L. Among other confounders, BMI and IR were taken into account., Results: MetS was prevalent in 7.7% of the young and in 35.6% of the older BASE-II participants and T2D occurred in 12.7% of the older participants. In young subjects without diabetes, vitamin D insufficiency was associated with an independent 3.2-fold increased odds of having MetS (OR: 3.2 CI: 1.0-8.7; p = 0.042). However, in the older participants, this association was lost once BMI was taken into account among those with diabetes, and once IR was taken into account among those without diabetes., Conclusion: Independent associations between vitamin D insufficiency and MetS were only found among young subjects without diabetes. In the older adults, BMI annihilated these associations among subjects without diabetes as did HOMA-IR among subjects with diabetes., (© 2021 The Authors. Diabetes/Metabolism Research and Reviews published by John Wiley & Sons Ltd.)

Only limited information is available on the inter-relationships between genetic and non-genetic factors such as diet and sunlight exposure with serum 25-hydroxyvitamin D [25(OH)D] concentration. This cross-sectional study aimed to examine the independent and interactive associations of season, dietary vitamin D intake, and SNPs of 11 vitamin D-related candidate genes with serum 25(OH)D concentration among 2,721 adults aged ≥40 years at baseline from the Yangpyeong cohort, a part of the Korean Genome Epidemiology Study (KoGES). The interactions between season or dietary vitamin D and 556 SNPs were evaluated using 2-degree of freedom joint tests. Season was strongly (p difference = 1.00 × 10 -12 ) and dietary vitamin D intake was slightly but significantly associated with serum 25(OH)D concentration (p difference = 0.0119). Among five SNPs (rs11723621-GC, rs7041-GC, rs10500804-CYP2R1, rs7129781-CYP2R1, and rs2852853-DHCR7) identified in the screening steps, only one, rs10500804-CYP2R1, significantly interacted with season (p interaction = 8.01 × 10 -5 ). The inverse association between number of minor alleles of rs10500804-CYP2R1 and concentration of 25(OH)D was significant only in summer/fall. Conversely, dietary vitamin D intake was positively associated only in winter/spring. In conclusion, season, dietary vitamin D intake, and four SNPs in GC, CYP2R1, and DHCR7 are independently and rs10500804-CYP2R1 is interactively associated with serum 25(OH)D concentration. Serum 25(OH)D is influenced by genotype of rs10500804-CYP2R1 in summer/fall when sunlight exposure is high, while dietary vitamin D intake is an important determinant of serum 25(OH)D during the seasons with low cutaneous vitamin D synthesis.

Prader-Willi syndrome (PWS) is a genetic disorder characterized by hyperphagia with progressive, severe obesity, and an increased risk of obesity-related comorbidities in adult life. Although low dietary vitamin D intake and low 25-hydroxy vitamin D (25OHD) levels are commonly reported in PWS in the context of bone metabolism, the association of low 25OHD levels with fat mass has not been extensively evaluated in PWS adults. The aims of this study were to investigate the following in PWS adults: (1) 25OHD levels and the dietary vitamin D intake; (2) associations among 25OHD levels with anthropometric measurements and fat mass; (3) specific cut-off values for body mass index (BMI) and fat mass predictive of the 25OHD levels. In this cross-sectional, single-center study we enrolled 30 participants, 15 PWS adults (age 19-41 years and 40% males) and 15 control subjects matched by age, sex, and BMI from the same geographical area (latitude 40° 49' N; elevation 17 m). Fat mass was assessed using a bioelectrical impedance analysis (BIA) phase-sensitive system. The 25OHD levels were determined by a direct competitive chemiluminescence immunoassay. Dietary vitamin D intake data was collected by three-day food records. The 25OHD levels in the PWS adults were constantly lower across all categories of BMI and fat mass compared with their obese counterpart. The 25OHD levels were negatively associated with BMI ( p = 0.04), waist circumference ( p = 0.03), fat mass ( p = 0.04), and dietary vitamin D intake ( p < 0.001). During multiple regression analysis, dietary vitamin D intake was entered at the first step ( p < 0.001), thus explaining 84% of 25OHD level variability. The threshold values of BMI and fat mass predicting the lowest decrease in the 25OHD levels were found at BMI ≥ 42 kg/m 2 ( p = 0.01) and fat mass ≥ 42 Kg ( p = 0.003). In conclusion, our data indicate that: (i) 25OHD levels and dietary vitamin D intake were lower in PWS adults than in the control, independent of body fat differences; (ii) 25OHD levels were inversely associated with BMI, waist circumference, and fat mass, but low dietary vitamin D intake was the major determinant of low vitamin D status in these patients; (iii) sample-specific cut-off values of BMI and fat mass might help to predict risks of the lowest 25OHD level decreases in PWS adults. The presence of trained nutritionists in the integrated care teams of PWS adults is strongly suggested in order to provide an accurate nutritional assessment and tailored vitamin D supplementations.

Our objective was to investigate the relationship between dietary vitamin D intake and serum concentration of vitamin D (25(OH)D) on changes in body weight, waist circumference (WC), and body mass index (BMI), and to determine if this relationship changes between obese and non-obese individuals at baseline and those who have or do not have 25(OH)D deficiency. This was a prospective study with a sample of 572 individuals aged 25-65 years, who were participants in the cohort study EpiFloripa Adults. Changes in weight (in kg), BMI, and WC between 2012 and 2014 were evaluated as outcomes. The main exposure was the dietary intake of vitamin D (2012), and the 25(OH)D serum concentration was secondary. When the analyses were stratified by the presence of obesity in the baseline, among obese individuals it was observed that those in the extreme categories of vitamin D intake had an average gain of 3.0 kg in weight, 0.9 kg/m 2 in BMI, and 1.7-2.7 cm in WC. When 25(OH)D serum concentration were incorporated into the analyses, it was observed that non-obese subjects not having 25(OH)D deficiency had a mean reduction of 2.3 cm in WC. In conclusion, the increases in body weight, BMI, and WC were higher over time in obese patients with deficient 25(OH)D serum concentration, regardless of dietary vitamin D intake., Competing Interests: The authors declare no conflict of interest.

We examined the association of vitamin D deficiency to risk of cesarean delivery using prospective data in a cohort of 1153 low income and minority gravidae. Circulating maternal 25-hydroxyvitamin D and intact parathyroid hormone were measured at entry to care 13.73 ± 5.6 weeks (mean ± SD). Intake of vitamin D and calcium was assessed at three time points during pregnancy. Using recent Institute of Medicine guidelines, 10.8% of the gravidae were at risk of vitamin D deficiency, and 23.8% at risk of insufficiency. Maternal 25-hydroxyvitamin D was related positively to vitamin D and calcium intakes and negatively to circulating concentrations of parathyroid hormone. Risk for cesarean delivery was increased significantly for vitamin D deficient women; there was no increased risk for gravidae at risk of insufficiency. When specific indications were examined, vitamin D deficiency was linked to a 2-fold increased risk of cesarean for prolonged labor. Results were the similar when prior guidelines for vitamin D deficiency (25(OH)D < 37.5nmol/L) and insufficiency (37.5-80 nmol/L) were utilized.