Combined vitamin D and magnesium supplementation does not influence markers of bone turnover or glycemic control: A randomized controlled clinical trial.

High-dose vitamin D supplementation can increase total osteocalcin concentrations that may reduce insulin resistance in individuals at risk for prediabetes or diabetes mellitus. Magnesium is a cofactor in vitamin D metabolism and activation. The purpose of this study was to determine the combined effect of vitamin D and magnesium supplementation on total osteocalcin concentrations, glycemic indices, and other bone turnover markers after a 12-week intervention in individuals who were overweight and obese, but otherwise healthy. We hypothesized that combined supplementation would improve serum total osteocalcin concentrations and glycemic indices more than vitamin D supplementation alone or a placebo. A total of 78 women and men completed this intervention in 3 groups: a vitamin D and magnesium group (1000 IU vitamin D3 and 360 mg magnesium glycinate), a vitamin D group (1000 IU vitamin D3), and a placebo group. Despite a significant increase in serum 25-hydroxyvitamin D concentrations in the vitamin D and magnesium group compared with the placebo group (difference = 5.63; CI, -10.0 to -1.21; P = .001) post-intervention, there were no differences in serum concentrations of total osteocalcin, glucose, insulin, and adiponectin or the homeostatic model assessment of insulin resistance (HOMA-IR) among groups (P > .05 for all). Additionally, total osteocalcin (ß = -0.310, P = .081), bone-specific alkaline phosphatase (ß = 0.004, P = .986), and C-terminal cross-linked telopeptide (ß = 0.426, P = .057), were not significant predictors of HOMA-IR after the intervention. Combined supplementation was not associated with short-term improvements in glycemic indices or bone turnover markers in participants who were overweight and obese in our study. This trial was registered at clinicaltrials.gov (NCT03134417).

The effect of combined magnesium and vitamin D supplementation on vitamin D status, systemic inflammation, and blood pressure: A randomized double-blinded controlled trial.

OBJECTIVE: Poor vitamin D and magnesium status is observed in individuals who are overweight and obese (Owt/Ob) and is often associated with a heightened risk of cardiovascular disease. Magnesium is a cofactor that assists vitamin D metabolism. We aimed to determine the efficacy of a combined magnesium and vitamin D regimen compared with vitamin D only on increasing serum 25-hydroxyvitamin D (25OHD) concentrations and the effects of these supplements on cardiometabolic outcomes. METHODS: This 12-week double-blinded randomized controlled trial had three treatment arms: magnesium + vitamin D (MagD; 360 mg magnesium glycinate + 1000 IU vitamin D 3 × daily), vitamin D only (VitD; 1000 IU vitamin D 3 × daily), and placebo. A total of 95 Owt/Ob participants were randomized into one of these three study arms. Anthropometry, dietary intake, concentrations of serum 25OHD, serum parathyroid hormone (PTH), serum inflammatory markers, and blood pressure were obtained at baseline and week 12. RESULTS: The MagD group experienced the greatest increase in serum 25OHD concentrations (6.3 ± 8.36 ng/mL; P < 0.05). There was a decrease in systolic blood pressure (7.5 ± 8.26 mmHg; P < 0.05) for individuals who had a baseline systolic blood pressure of >132 mmHg in the MagD group. There were no statistically significant treatment effects on serum PTH concentrations and markers of inflammation. CONCLUSIONS: A combined MagD treatment may be more effective in increasing serum 25OHD concentrations compared with VitD supplementation alone in Owt/Ob individuals.

Dietary magnesium intake in relation to body mass index and glycemic indices in middle school students from the HEALTHY Study.

BACKGROUND: Data on dietary magnesium intake on the risk of type 2 diabetes mellitus (T2DM) among children and adolescents is limited. AIM: We examined whether dietary magnesium intake was related to body mass index (BMI) percentile, and glycemic indices at baseline and at end of the HEALTHY Study for both intervention and control schools. The HEALTHY Study was a multi-component, school-based intervention, to prevent T2DM in children and adolescents from 6th to 8th grades. METHODS: A secondary data analyses of 2181 ethnically diverse students with completed dietary records, BMI percentile, and plasma insulin and glucose concentrations at baseline (6th grade) and end of study (8th grade) were included from the HEALTHY Study. Dietary magnesium intake was self-reported using the Block Kids Food Frequency Questionnaire. A hierarchical multiple regression model was used to determine the relationships between dietary magnesium intake, BMI percentile, and glycemic indices at baseline and end of the HEALTHY Study, adjusting for magnesium intake from supplements, total energy intake, and fitness level. RESULTS: Dietary magnesium intake was related to BMI percentile at baseline and at end of the HEATHY Study (ß = -0.05, 95% CI = -0.02 to 0, p = 0.04; ß = -0.06, 95% CI = -0.02 to -0.003, p = 0.004); R 2 [regression coefficient effect size] = 0.03; R 2 = 0.06). Dietary magnesium intake was not related to plasma insulin and glucose concentrations at baseline and end of the HEALTHY Study. CONCLUSION: Dietary magnesium intake was inversely related to BMI percentile among middle school students from the HEALTHY Study. Research is required to evaluate the dose-response relationship between fruit and vegetable consumption (good sources of magnesium) and risk of T2DM in children and adolescents. This relationship also needs to be explored among different BMI categories.

Three Doses of Vitamin D and Cognitive Outcomes in Older Women: A Double-Blind Randomized Controlled Trial.

Vitamin D may affect cognitive performance, but previous studies are either short term or observational. We conducted a randomized controlled trial of vitamin D supplementation on domain-specific cognitive measures in postmenopausal women. Overweight/obese women with serum 25-hydroxyvitamin D (25OHD) levels less than 30 ng/mL were recruited. Vitamin D3 supplementation (600, 2,000, or 4,000 IU/d) was randomly assigned in a double-blinded manner for 1 year. Serum 25-hydroxyvitamin D, osteocalcin (total and undercarboxylated), amyloid beta, parathyroid hormone, and estradiol were analyzed before and after supplementation. Cognitive tests were administered after treatment. The women (58 ± 6 years; body mass index, 30.0 ± 3.5 kg/m2) had a baseline serum 25-hydroxyvitamin D level of 22.6 ± 5.8 ng/mL that increased to 30.2 ± 5.6, 36.0 ± 4.9, and 40.8 ± 7.0 ng/mL in the 600, 2,000, and 4,000 IU/d groups, respectively (p < .001). Participants taking 2,000 IU/d compared to other doses performed better in learning and memory tests (p < .05), yet the 4,000 IU/d group had a slower reaction time compared to the 600 IU/d group. Multiple regression indicated that serum undercarboxylated osteocalcin predicted tasks associated with reaction time and executive function, whereas body mass index and parathyroid hormone negatively predicted reaction time and executive function (p ≤ .01). These data suggest that vitamin D has differential effects on domain-specific cognitive measures and that a higher dose may negatively affect reaction time.

Serum Parathyroid Hormone Responses to Vitamin D Supplementation in Overweight/Obese Adults: A Systematic Review and Meta-Analysis of Randomized Clinical Trials.

Obesity is often associated with vitamin D deficiency and secondary hyperparathyroidism. Vitamin D supplementation typically leads to the reductions in serum parathyroid hormone (PTH) levels, as shown in normal weight individuals. Meanwhile, the dose of vitamin D supplementation for the suppression of PTH may differ in overweight and obese adults. We conducted a systematic review and meta-analysis of randomized controlled trials to determine the dose of vitamin D supplementation required to suppress PTH levels in overweight/obese individuals. We identified 18 studies that examined overweight or obese healthy adults who were supplemented with varying doses of vitamin D3. The primary outcomes examined were changes in PTH and serum 25-hydroxyvitamin D (25OHD) levels from baseline to post-treatment. The results of the meta-analysis showed that there was a significant treatment effect of vitamin D supplementation on PTH, total standardized mean difference (SMD) (random effects) = -0.38 (95% CI = -0.56 to -0.20), t = -4.08, p < 0.001. A significant treatment effect of vitamin D supplementation was also found on 25OHD, total SMD (random effects) = 2.27 (95% CI = 1.48 to 3.06) t = 5.62, p < 0.001. Data from available clinical trials that supplemented adults with D3 ranging from 400 IU to 5714 IU, showed that 1000 IU of vitamin D supplementation best suppressed serum PTH levels, total SMD = -0.58, while vitamin D supplementation with 4000 IU showed the greatest increase in serum 25OH levels. Vitamin D and calcium supplementation of 700 IU and 500 mg, respectively, also showed a significant treatment effect on the suppression of PTH with a total SMD = -5.30 (95% CI = -9.72 to -0.88). In conclusion, the meta analysis of available clinical trials indicates that 1000 IU vitamin D supplementation can suppress serum PTH levels, while 4000 IU of vitamin D was associated with the largest increase in serum 25OHD levels in the overweight and obese population.

Vitamin D supplementation and calcium absorption during caloric restriction: a randomized double-blind trial.

BACKGROUND: Weight loss (WL) is associated with a decrease in calcium absorption and may be one mechanism that induces bone loss with weight reduction. OBJECTIVE: Because vitamin D supplementation has been shown to increase true fractional calcium absorption (TFCA), the goal of this study was to examine the effect of vitamin D during WL or weight maintenance (WM). DESIGN: A randomized, placebo-controlled, double-blind 6-wk study was conducted in 82 postmenopausal women [BMI (in kg/m(2); ±SD): 30.2 ± 3.7] with 25-hydroxyvitamin D [25(OH)D] concentrations <70 nmol/L during either WL or WM. All women were given 10 µg vitamin D(3)/d and 1.2 g Ca/d and either weekly vitamin D(3) (375 µg) or a placebo equivalent to 63 µg (2500 IU)/d and 10 µg (400 IU)/d, respectively. We measured TFCA with the use of dual-stable isotopes, 25(OH)D, parathyroid hormone, estradiol, calcitriol, and urinary calcium at baseline and 6 wk in weight loss and vitamin D(3)-supplementation (WL-D; n = 19), weight maintenance and vitamin D(3)-supplementation (WM-D; n = 20), weight loss and placebo (n = 22), and weight maintenance and placebo (n = 21) groups. RESULTS: WL groups lost 3.8 ± 1.1% of weight with no difference between vitamin D(3) supplementation and the placebo. The rise in serum 25(OH)D was greatest in the WL-D group (19.8 ± 14.5 nmol/L) compared with in WM-D (9.1 ± 10.3 nmol/L) and placebo groups (1.5 ± 10.9 nmol/L). TFCA increased with vitamin D(3) supplementation compared with placebo treatment (P < 0.01) and decreased during WL compared with WM. Serum 25(OH)D or 1,25-dihyroxyvitamin D did not correlate with TFCA. CONCLUSION: These data show that vitamin D supplementation increases TFCA and that WL decreases TFCA and suggest that, when calcium intake is 1.2 g/d, either 10 or 63 µg vitamin D/d is sufficient to maintain the calcium balance. This trial was registered at clinicaltrials.gov as NCT00473031.