Numerous research reports and clinical commentaries regarding magnesium deficiency have appeared in recent years. Linkages between magnesium deficiency and insulin resistance, carbohydrate intolerance, accelerated atherosclerosis, dyslipidemia (abnormal blood fats), hypertension, and adverse outcomes in pregnancies complicating diabetes have been observed or postulated. Direct effects of insulin on magnesium metabolism and transport have also been described. Clinical trial results, though limited, have drawn attention to the potential benefits of magnesium replenishment.
To assess the relevancy of these observations to diabetes research and practice, the American Diabetes Association sponsored a consensus conference on magnesium supplementation in the treatment of diabetes on 15-16 May 1992 in Philadelphia. Eight experts in diabetes and related disorders heard 13 presentations from U.S. and European investigators respected in the field of magnesium metabolism and its impact on health and disease. The consensus panel was asked to answer five questions focusing on diagnostic and therapeutic issues regarding magnesium and diabetes.
The following consensus responses were then developed by the panel:
Question 1: What Is the Relationship Between Magnesium Levels and Disease?--Magnesium, the second most abundant intracellular cation, plays a key role in cellular metabolism. It is important for cardiac contractility and conductivity, neurochemical transmission, skeletal muscle excitability, and the maintenance of normal intracellular calcium, potassium, and perhaps sodium levels.
Magnesium is found primarily in bone and muscle tissue, with approximately 1 percent in extracellular fluid. Normal serum concentrations are 1.5-2.0 mEq/L (milliequivalent per liter). Magnesium is found in various foods but particularly good sources include liver, nuts, leafy green vegetables, legumes, and whole grains. The RDA for magnesium is 350 mg for men and 300 mg for non-gravid (not pregnant) women. Although it is estimated that only 30 percent of dietary magnesium is absorbed from the gut, and that the overall intake of dietary magnesium has declined during this century, magnesium deficiency as a result of inadequate dietary intake is unusual in the United States.
There are three main causes of magnesium deficiency: excessive urinary losses (e.g., diuretic therapy, diabetic ketoacidosis), decreased intestinal absorption (e.g., severe diarrhea, small bowel resection), and decreased dietary intake (e.g., prolonged parenteral nutrition). Hypermagnesemia (too much magnesium) may develop in people with renal insufficiency; the levels of toxicity are not clearly defined, but central nervous system depression appears at levels of approximately 8-10 mEq/l.
Available data suggest that magnesium concentrations (both serum and intracellular) are decreased in a number of disease states including hypertension, diabetes, perinatel morbidity (disease at birth) in diabetic pregnancies, arrhythmias, and congestive heart failure. Additionally, there are data relating magnesium deficiency to insulin resistance. Some investigators believe that diminished magnesium concentrations may underlie the "insulin-resistance syndrome."
Data relating magnesium deficiency to human disease are limited. Much of the data has been generated either in nonprimate animal models or in cross-sectional studies in humans involving hospitalized or clinic-based control groups. Carefully designed case control studies involving population-based control subjects, cohort studies, or clinical trials have not been performed. However, a small number of limited clinical trials have been performed examining the effect of magnesium replacement in the peri-infarction period (around time of heart attack) on ventricular arrhythmias and mortality. A recent metaanalysis by Teo et al. (1) suggests a beneficial effect of magnesium replacement in reducing postmyocardial infarction mortality. …