For both healthy patients and those with metabolic impairment, risk decreased when participants took the recommended daily allowance of magnesium….
Studies have shown that those with higher magnesium intake are 10-47% less likely to develop type 2 diabetes. In the U.S., however, only about 50% of the population achieve the recommended dietary allowance of magnesium, which is 400-420 mg/day for men and 300-310 mg/day for women. A meta-analysis of 9 trials studying magnesium supplements in those with type 2 diabetes found that 360 mg/day resulted in lower fasting glucose levels, while another smaller and more recent trial studying obese, nondiabetic, insulin-resistant patients found that 365 mg/day for 6 months not only lowered fasting glucose values, but also lowered fasting insulin and insulin resistance, and improved insulin sensitivity. In patients with other risk factors, such as mild hypertension, 3-month supplementation with magnesium was found to improve insulin sensitivity and pancreatic β-cell function. Low magnesium diets, meanwhile, have been shown to impair insulin sensitivity in just 3 weeks in otherwise healthy patients.
Few studies exist that evaluate magnesium intake long term (>5 years) in patients in various different stages of health (whether they are in a normal or impaired state). There is also little research examining magnesium’s association with the progression from baseline impaired states to type 2 diabetes. The purpose of this particular study was to evaluate the association between magnesium intake and incidence of metabolic impairment in a prospective nature. Metabolic impairment is defined as impaired fasting glucose (IFG), impaired glucose tolerance (IGT), insulin-resistance (IR), or hyperinsulinemia in other otherwise healthy individuals. Also, for those with baseline metabolic impairment, this study examined whether magnesium intake is associated with incident diabetes.
Study participants were obtained from The National Heart, Lung, and Blood Institute’s Framingham Heart Study (FHS) Offspring cohort, a longitudinal study of CV disease. In the 5th examination cycle, occurring from 1991-1995, study participants were required to undergo standard medical examinations, including laboratory and anthropometric measurements and dietary assessments. The participants were followed from the 5th through the 7th assessments (ending in 2001). Patients were excluded if they had a history of diabetes or if they were identified to have diabetes at baseline, were absent at follow-up, or had invalid or missing dietary data. A total of 2,582 patients were included in the baseline assessment. The average age was 54 years, with 55% being female, 42% overweight, and 21% obese. Regarding dietary intake, the Harvard semiquantitative, 126-item food frequency questionnaire was administered at each exam. This questionnaire asked patients to report their consumption of various food items over the previous year according to nine consumption frequency categories. The consumption of interest was magnesium, whether from dietary or non-dietary sources. FG, 2-h OGTT glucose, fasting insulin, and 2-h OGTT insulin were measured at baseline (exam 5) and again at exam 7. Energy-adjusted quintile categories of averaged magnesium intake were generated from the above questionnaire results, with patient characteristics adjusted for age, sex, and energy (in regards to food and nutrients). These quintile categories along with measured lab values were then used in a multitude of statistical tests to determine magnesium’s association with progression from normal to metabolic impairment, and with incident type 2 diabetes among participants who had baseline metabolic impairment.
Data showed that baseline characteristics of almost all glucose and insulin parameters tended to be lower in patients with higher magnesium intake. Among those with normal status at baseline, higher magnesium intake was associated with 37% lower risk of incident metabolic impairment, though this was attenuated after adjusting for dietary fiber and risk factors. For those that were metabolically impaired at baseline, 16.6% of patients developed diabetes over the seven year follow-up. After adjusting for confounders, higher magnesium intake was associated with 38% lower risk of incident diabetes when compared to the lowest category of magnesium intake. These results support previously reported associations between high magnesium intake and lower risk of type 2 diabetes. Other clinical studies say that magnesium supplementation in those with and without diabetes can also improve glycemic control, insulin sensitivity, and β-cell function. In animals fed magnesium-deficient diets, hypomagnesemia caused insulin sensitivity of peripheral tissues to decrease, and is thought to affect insulin production by impacting the proliferation and mass of beta cells.
While this study found that higher magnesium intake was inversely associated with long-term changes in fasting glucose and insulin resistance in those without incident diabetes, it did not find any significant trends relating magnesium intake with fasting insulin, glucose clearance, insulin metabolism or insulin sensitivity. One potential confounder of this study that was not completely accounted for was that higher magnesium intake may be reflective of better overall health awareness, which could also affect a patient’s likelihood of developing metabolic impairment or type 2 diabetes.
The results of this study and others like it suggest that meeting the recommended daily allowance of magnesium each day may lower the risk of progression to type 2 diabetes in those at high risk.
Higher magnesium intake may help offset the risk of developing metabolic impairment in those with normal baseline glucose and insulin homeostasis.
In patients who already had some sort of metabolic impairment, magnesium was associated with a lower risk of type 2 diabetes.
Hruby, A. et al. "Higher Magnesium Intake Reduces Risk of Impaired Glucose and Insulin Metabolism and Progression From Prediabetes to Diabetes in Middle-Aged Americans" Diabetes Care. 2014: 37(2): 419-427.