Book Description

Background: Obesity is an epidemic in the United States, and it is associated with the pathogenesis of many chronic diseases. Individuals who are overweight or obese (Owt/Ob) are at a higher risk of developing cardiometabolic diseases and have a higher prevalence of micronutrient deficiencies when compared to individuals with a healthy weight. Vitamin D and magnesium are two micronutrients that are commonly found to be deficient in the Owt/Ob population, and deficiencies in both nutrients are independently associated with poor cardiometabolic health. Furthermore, magnesium is an essential cofactor that aids in vitamin D metabolism. We theorized that a poor magnesium status may lead to improper vitamin D metabolism, and therefore, leading to an increase of parathyroid hormone (PTH), a hormone that is an independent predictor for elevated systemic inflammation, hypertension, and cardiovascular disease. Parathyroid hormone and vitamin D exhibit a negative relationship in healthy weight individuals. However, this expected negative relationship between vitamin D and parathyroid hormone can potentially be altered in Owt/Ob individuals with magnesium deficiency. This dissertation focused on investigating the role magnesium plays in vitamin D metabolism and the effects of a combined vitamin D and magnesium treatment in the Owt/Ob population and its effect on protecting cardiometabolic health. Methods: A cross-sectional study was first conducted to determine the relationship between magnesium status, serum 25-hydroxyvitamin D (25OHD) concentrations, and serum PTH concentrations. Secondly, we conducted a 12-week double-blinded controlled supplementation trial to determine whether a combined magnesium and vitamin D would increase serum concentrations of 25OHD, and lower serum concentrations of PTH, markers of inflammation and blood pressure. This study had three treatment arms - magnesium + vitamin D (MagD) group, vitamin D only (VitD) group, and a placebo group. Participants in the MagD Group received 360 mg magnesium glycinate + 1000 IU vitamin D3 daily, VitD Group received 1000 IU vitamin D3 daily, and Placebo Group received 10 mg of cellulose. Information such as body composition measurements was collected using Dual-energy X-ray Absorptiometry, systolic and diastolic blood pressures were collected using the American Heart Association In-clinic Guideline for Blood Pressure Measurements, blood biomarkers (serum concentrations of 25-hydroxyvitamin D, parathyroid hormone, markers of inflammation) were assessed through fasting blood samples analyses. Additional information such as anthropometry measurements and diet records were also collected. Results: In our cross-sectional study, a total of 57 Owt/Ob participants were divided into three groups according to dietary magnesium intake percentiles (Low Mg Group = 33 percentile, Medium Mg Group = 33 to 66 percentile, High Mg Group = 66 percentile). Higher serum concentrations of 25OHD were negatively associated with lower serum concentrations of PTH only in the High Mg Intake group (r=-0.472, p=0.041), but not in other groups. For the 12-week double-blinded supplementation trial, a total of 83 Owt/Ob participants were randomized into one of the three study arms. Participants in the MagD Group had a greater increase in serum 25OHD compared to participants in VitD Group, but only for those whose baseline 25OHD were less than 23.49 ng/mL. There were no statistically significant effects on PTH concentrations and markers of inflammation between and within groups. Conclusion: A low dietary magnesium intake may alter PTH response to 25OHD. Furthermore, a combined magnesium and vitamin D treatment may be more effective in raising serum 25OHD concentrations compared to vitamin D supplements alone for individuals whose 25OHD level were insufficient at baseline. However, increase in serum 25OHD concentrations may not influence systemic inflammation and blood pressure.