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Industry: Email Alert RSS FeedInverse relationship between magnesium intake and risk for type 2 diabetes - Diabetes
Nutrition Research Newsletter, March, 2004
Magnesium is a cofactor in multiple enzymes critical for carbohydrate metabolism. It is believed to play a role in glucose homeostasis, insulin action, and the development of type 2 diabetes. Hypomagnesemia has been shown to occur frequently among patients with diabetes, especially those with poor metabolic control. There is also evidence to support an inverse association between serum or plasma magnesium levels and the risk of type 2 diabetes, indicating a potential role of magnesium status in the pathogenesis of type 2 diabetes. Studies have shown that magnesium supplementation improves insulin-mediated glucose disposal and insulin secretion.
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A prospective investigation to determine whether total magnesium intake from food and supplements is related to the risk of developing type 2 diabetes was performed in a large cohort of US women from the Women's Health Study (WHS). Investigators also conducted a cross-sectional study to examine the relation between magnesium and fasting insulin levels, in a subsample of apparently healthy women randomly selected from the WHS.
A total of 39,876 female health professionals, aged greater than or equal to 45 yrs, and who were free of coronary heart disease, stroke, and cancer were randomized. The subjects provided detailed information about their diet, completing a 131-item semiquantitative food frequency questionnaire. For each food, a commonly used unit or portion size was specified, and each participant was asked how often she had consumed that amount, on average, during the previous year. Data on the use of multivitamin supplements were taken into account to assess the intake of supplemental magnesium. Total magnesium represents the sum of magnesium intake from both dietary and supplemental sources. All subjects were annually asked whether and when they had been diagnosed with type 2 diabetes since completing the previous questionnaire at baseline. A supplemental questionnaire--inquiring about the onset of the disease, symptoms, diagnostic tests, and hypoglycemic treatment--was mailed to all respondents reporting a diagnosis of type 2 diabetes and confirmed type 2 diabetes, according to the guidelines proposed by the American Diabetes Association.
In the cross-sectional analysis, researchers included 349 randomly selected women who had served as control subjects in a previous case-control study nested in the WHS. This subsample comprised healthy, nondiabetic, middle-aged women who remained free of diabetes during the 4-year period subsequent to the assessment of baseline clinical and biochemical parameters. Baseline fasting specimens from these women were assayed for insulin levels.
During 222,523 person-years of follow-up, a total of 918 confirmed incident cases of type 2 diabetes were documented. There was a significant inverse association between magnesium intake and the risk of type 2 diabetes, independent of age, BMI (P=0.007 for trend). After further adjustment for physical activity, alcohol intake, smoking, family history of diabetes, and total calorie intake, the multivariate-adjusted RRs of diabetes from the lowest to highest quintiles of magnesium intake were attenuated at 1.0, 1.06, 0.81, 0.86, and 0.89 (P=0.05 for trend). Among women with BMI greater than or equal to 25 kg/[m.sup.2], the inverse trend was significant; multivariate-adjusted RRs were 1.0, 0.96, 0.76, 0.84, and 0.78 (P=0.02 for trend). Multivariate-adjusted geometric mean insulin levels for overweight women in the lowest quartile of magnesium intake was 53.5 pmol/1 compared with 41.5 pmol/1 among those at the highest quartile (P=0.03 for trend).
These findings suggest that there is a protective role of magnesium in reducing the risk of developing type 2 diabetes, particularly in overweight women.
Y. Song, J. Manson, J. Buring, et al. Dietary magnesium intake in relation to plasma insulin levels and risk of type 2 diabetes in women. Diabetes Care 27:59-65 (January, 2004) [Correspondence: Simin Liu, MD, ScD, Division of Preventive Medicine. Brigham and Women's Hospital, 900 Commonwealth Ave. East, Boston, MA 02215. E-mail: simin.liu@channing.harvard.edu]
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