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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/m2 (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/m2 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.

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.

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/m2 (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. [ABSTRACT FROM AUTHOR]

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/m2 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. [ABSTRACT FROM AUTHOR]

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.