SCIENTIFIC RESEARCH ARTICLES ON MINERALS

Skip Navigation Links.
Expand <div style='padding: 5px;' ><a style='font-size:13px !important; text-decoration:none;'>View our collection of articles on Trace Minerals</a></div>
Expand <div style='padding: 5px;' ><a style='font-size:13px !important; text-decoration:none;'>View articles by Dr. Meletis on Trace Minerals</a></div>
Expand <div style='padding: 5px;' ><a style='font-size:13px !important; text-decoration:none;'>View articles by Dr. Schauss On Trace Minerals</a></div>
Collapse <div style='padding: 5px;' ><a style='font-size:13px !important; text-decoration:none;'>View our Scientific Articles</a></div>

Magnesium

Magnesium The mineral magnesium functions as an essential cofactor for more than 300 enzymes. It is essential for all energy-dependent transport systems, glycolysis, oxidative energy metabolism, biosynthetic reactions, normal bone metabolism, neuromuscular activity, electrolyte balance, and cell membrane stabilization. The kidney primarily regulates magnesium homeostasis. Magnesium deficiency has been associated with hypertension, insulin resistance, glucose intolerance, dyslipidemia, increased platelet aggregation, cardiovascular disease, complications of diabetes, and complications of pregnancy. Whether poor magnesium status plays a causal role in these disorders or is simply associated with them has not been determined. Less than 0.3% of the body’s magnesium pool is found in serum, and extracellular magnesium levels do not reflect functionally important body pools. This makes assessment of magnesium status difficult. Serum magnesium is a specific, but not sensitive, indicator of magnesium deficiency; low serum magnesium levels indicate low magnesium stores, but a deficiency must be severe before serum levels decline. More sensitive assays are being developed. Magnesium is one of the more common micronutrient deficiencies in diabetes. Decreased magnesium levels and increased urinary magnesium losses have been documented in both type 1 and type 2 diabetic patients. Low dietary magnesium intake has been associated with increased incidence of type 2 diabetes in some, but not all, studies. Hypomagnesemia in diabetes is most likely due to increased urinary losses. Additional risk factors include ketoacidosis, use of certain medications including digitalis and diuretics, malabsorption syndromes, congestive heart failure, myocardial infarction (MI), electrolyte disturbances, acute critical illness, alcohol abuse, and pregnancy. Low-calorie and poor-quality diets are more likely to be inadequate in magnesium. People with diabetes may have diets low in magnesium. Hypermagnesemia may occur with renal insufficiency that impairs magnesium clearance. The RDA is 400 mg/day for men under age 30, 420 mg/day for men over age 30, 310 mg/day for women under 30, and 320 mg/day for women over age 30. The UL is 350 mg/day as supplemental magnesium. Daily intake from food and water is not included in the UL. Mechanism of action. The mechanisms by which magnesium affects insulin resistance, hypertension, and cardiovascular disease are unknown. However, the widespread use of magnesium in normal metabolism of macronutrients, cellular transport systems, intracellular signaling systems, platelet aggregation, vascular smooth muscle tone and contractility, electrolyte homeostasis, and phosphorylation and dephosphorylation reactions1 suggests that these effects are multifactorial. Evidence-based research. Research has focused on the following areas: • Glycemic control. An inverse relationship between plasma magnesium levels and indices of glycemic control has been noted in both type 1 and type 2 diabetes. Clinical studies evaluating the effect of supplemental magnesium on glycemic control are mixed, with some studies reporting improvementsand others showing no improvement. • Insulin sensitivity. Diets low in magnesium are associated with increased insulin levels, and clinical magnesium deficiency is strongly associated with insulin resistance. It is not known if low magnesium levels play a role in the development of insulin resistance, are a result of insulin resistance, or are simply a coexisting condition. In vitro evidence suggests that insulin plays a role in magnesium transport, and insulin resistance has been shown to decrease magnesium uptake in type 2 diabetes. Conversely, magnesium supplementation has a mild positive effect on insulin sensitivity. Animal models show decreased insulin receptor tyrosine kinase activity and decreased glucose uptake and oxidation in magnesium deficiency. Supplement-ation trials have primarily focused on type 2 diabetes. • Hypertension. Observational studies indicate an inverse relationship between magnesium levels and hypertension in people with and without diabetes. Clinical trials have produced inconsistent results. • Cardiovascular disease. Magnesium deficiency is associated with dyslipidemias, atherosclerosis, acute MI, and cardiovascular disease (CVD) and has been shown to alter platelet aggregation and activity. Most trials in type 2 diabetes have shown little effect of supplementation on lipid levels, although improvement in the magnesium status of subjects with type 1 diabetes was associated with mild improvements in triglycerides. • Complications. Some, but not all, research suggests that subjects with common microvascular complications of diabetes have lower serum magnesium levels than subjects without complications. Patients with retinopathy have been found to have lower magnesium levels than control subjects or diabetic subjects without retinopathy. Intracellular magnesium levels were lower in patients with neuropathy. In type 2 diabetic subjects, micro- and macroalbuminuria were associated with lower serum ionized magnesium levels than was normoalbuminuria. When evaluating these studies, one should pay particular attention to the characteristics of the population studied; the etiology of diabetes; the presence of obesity; subjects’ age, renal function, diet composition, oral hypoglycemic or insulin use, and degree of glycemic control; the dose and form of magnesium, subjects’ baseline magnesium status and response to supplementation; assessment methods; length of trial; and the study design and ability to identify causality.