Lady Finger for Diabetes
Magnesium and Diabetes
Magnesium affects carbohydrate metabolism by influencing the release and activity of insulin, the hormone that controls blood sugar levels, by influencing the resistance and sensitivity to insulin. Magnesium for diabetics is critical. At least twenty five percent of diabetics have hypomagnesemia [i] and this is likely an underestimate. One group has recently suggested that the effects of reduced glutathione on glucose metabolism may be mediated, at least in part, by intracellular magnesium levels. [ii]
Dr. Carolyn Dean indicates that magnesium deficiency may be an independent predictor of diabetes and that diabetics both need more magnesium and lose more magnesium than most people. Magnesium is necessary for the production, function & transport of insulin. Magnesium deficiency is associated with insulin resistance and increased platelet reactivity. According to Dr. Jerry L. Nadler, “The link between diabetes mellitus and magnesium deficiency is well known. A growing body of evidence suggests that magnesium plays a pivotal role in reducing cardiovascular risks and may be involved in the pathogenesis of diabetes itself. While the benefits of oral magnesium supplementation on glycemic control have yet to be demonstrated in patients, magnesium supplementation has been shown to improve insulin sensitivity. Based on current knowledge, clinicians have good reason to believe that magnesium repletion may play a role in delaying type 2 diabetes onset and potentially in warding off its devastating complications — cardiovascular disease, retinopathy, and nephropathy.”
A separate Gallup survey (in 1995) of 500 adults with diabetes reported that 83 percent of those with diabetes are consuming insufficient magnesium from food, with many by significant margins.[iii] One group has recently suggested that the effects of reduced glutathione on glucose metabolism may be mediated, at least in part, by intracellular magnesium levels. [iv]
The mechanism of hypomagnesemia in diabetic patients still remains unsolved but there is enough evidence to suggest that Mg levels drop in the course of recovery from ketoacidosis, during insulin therapy [v] or with severe retinopathy [vi] or proteinuria. [vii] Diabetic patients, especially those with poor glucose control, develop hypomagnesemia from a glucose-induced osmotic diuresis.
Insulin resistance and magnesium depletion may result in a vicious cycle of worsening insulin resistance and decrease in intracellular Mg(2+) which may limit the role of magnesium in vital cellular processes. Diabetic ketoacidosis (DKA) [viii] is a state of inadequate insulin levels resulting in high blood sugar and accumulation of organic acids and ketones in the blood. Increased blood acids (ketoacidosis) can be an acute complication of diabetes. It occurs when your muscle cells become so starved for energy that your body takes emergency measures and breaks down fat, a process that forms acids known as ketones. [ix]
Hyperglycemia initially causes the movement of water out of cells, with subsequent intracellular dehydration, extracellular fluid expansion and hyponatremia (sodium loss). It also leads to a diuresis in which water losses exceed sodium chloride losses. It is believed that magnesium is also lost by osmotic action. Urinary losses then lead to progressive dehydration and volume depletion, which causes diminished urine flow and greater retention of glucose in plasma. The net result of these alterations is hyperglycemia with metabolic acidosis.[x]
Proteinuria is protein in the urine, caused by damaged kidneys and a declining ability of the kidneys to protect the body from protein loss. This is frequently seen in longstanding diabetes, hypertension, as well as other chronic renal conditions. In the United States, diabetes is the leading cause of end-stage renal disease (ESRD), the result of chronic kidney disease. In both type 1 and type 2 diabetes, the first sign of deteriorating kidney function is the presence of small amounts of albumin in the urine, a condition called microalbuminuria. As kidney function declines, the amount of albumin in the urine increases, and microalbuminuria becomes full-fledged proteinuria. Lower serum magnesium levels are associated with more rapid decline of renal function. During insulin treatment, neither magnesium nor potassium can be metabolized properly, so these essential minerals must be replaced.
Severe symptomatic hypermagnesemia is relatively rare. But high levels of magnesium can develop in people, most commonly those with renal insufficiency or renal failure.[xi] (diabetes, chronic renal insufficiency). Kidney disease, rather than diet, is the usual cause of magnesium overload, because the kidneys lose the ability to remove excess magnesium.
Magnesium is regulated and excreted primarily by the kidneys where various ATPase enzymes are responsible for maintaining homeostasis.[xii] However hypermagnesemia can also occur in people with hypothyroidism, those using magnesium containing medications such as antacids, laxatives, cathartics, and in those with certain types of gastrointestinal disorders, such as colitis, gastroenteritis and gastric dilation, which may cause an increased absorption of magnesium.