Magnesium is a mineral needed by every cell of your body. About half of your body's magnesium stores are found inside cells of body tissues and organs, and half are combined with calcium and phosphorus in bone. Only 1% is found in the blood. Your body works very hard to keep blood levels of magnesium constant.
Magnesium is needed for more than 300 biochemical reactions in the body. It helps maintain normal muscle and nerve function, keeps heart rhythm steady, and bones strong. It is also involved in energy metabolism and protein synthesis.
Treatment with diuretics (water pills), some antibiotics, and some cancer medicines such as Cisplatin, can increase the loss of magnesium in urine. Poorly-controlled diabetes increases loss of magnesium in urine, causing a depletion of magnesium stores.
Gastrointestinal problems, such as malabsorption disorders, can cause magnesium depletion by preventing the body from using the magnesium in food. Chronic or excessive vomiting and diarrhea may also result in magnesium depletion. The loss of magnesium through diarrhea and fat malabsorption usually occurs after intestinal surgery or infection, but it can occur with chronic malabsorptive problems such as Crohn's disease, gluten sensitive enteropathy, and regional enteritis. Individuals with these conditions may need extra magnesium. The most common symptom of fat malabsorption, or steatorrhea, is passing greasy, offensive-smelling stools.
Many people do not get enough magnesium from their diet for reasons including the following:
Signs of magnesium deficiency include confusion, disorientation, loss of appetite, depression, muscle contractions and cramps, tingling, numbness, abnormal heart rhythms, coronary spasm, and seizures.
Doctors will measure blood levels of magnesium whenever a magnesium deficiency is suspected.
While magnesium deficiency is fairly common, it is frequently overlooked as a source of problems. The reason is that serum magnesium levels (the test most doctors use) do not reflect actual body stores of magnesium. Blood levels are kept within the normal range at the expense of other tissues. When deficiency does occur, it is usually due to excessive loss of magnesium in urine, gastrointestinal system disorders that cause a loss of magnesium or limit magnesium absorption, or a chronically low intake of magnesium.
When levels are mildly depleted, increasing dietary intake of magnesium can help restore blood levels to normal. Eating at least five servings of fruits and vegetables daily, and choosing dark-green leafy vegetables often, as recommended by the Dietary Guidelines for Americans, the Food Guide Pyramid, and the Five-a-Day program, will help adults at-risk of having a magnesium deficiency consume recommended amounts of magnesium. When blood levels of magnesium are very low, an intravenous drip (IV drip) may be needed to return levels to normal. Magnesium tablets also may be prescribed, but some forms, in particular magnesium salts, can cause diarrhea.
What is the health risk of too much magnesium?
Dietary magnesium does not pose a health risk, however very high doses of magnesium supplements, which may be added to laxatives, can promote adverse effects such as diarrhea. Magnesium toxicity is more often associated with kidney failure, when the kidney loses the ability to remove excess magnesium. Very large doses of laxatives also have been associated with magnesium toxicity, even with normal kidney function. The elderly are at risk of magnesium toxicity because kidney function declines with age and they are more likely to take magnesium-containing laxatives and antacids.
Signs of excess magnesium can be similar to magnesium deficiency and include mental status changes, nausea, diarrhea, appetite loss, muscle weakness, difficulty breathing, extremely low blood pressure, and irregular heartbeat.
Magnesium and blood pressure. Evidence suggests that magnesium may play an important role in regulating blood pressure. Diets that provide plenty of fruits and vegetables, which are good sources of potassium and magnesium, are consistently associated with lower blood pressure. The DASH study (Dietary Approaches to Stop Hypertension) suggested that high blood pressure could be significantly lowered by a diet high in magnesium, potassium, and calcium, and low in sodium and fat. In another study, the effect of various nutritional factors on incidence of high blood pressure was examined in over 30,000 U.S. male health professionals. After four years of follow-up, it was found that a greater magnesium intake was significantly associated with a lower risk of hypertension. The evidence is strong enough that the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure recommends maintaining an adequate magnesium intake as a positive lifestyle modification for preventing and managing high blood pressure.
Magnesium and heart disease. Magnesium deficiency can cause metabolic changes that may contribute to heart attacks and strokes. There is also evidence that low body stores of magnesium increase the risk of abnormal heart rhythms, which may increase the risk of complications associated with a heart attack. Population surveys have associated higher blood levels of magnesium with lower risk of coronary heart disease. In addition, dietary surveys have suggested that a higher magnesium intake is associated with a lower risk of stroke. Further studies are needed to understand the complex relationships between dietary magnesium intake, indicators of magnesium status, and heart disease.
Magnesium and osteoporosis. Magnesium deficiency may be a risk factor for postmenopausal osteoporosis. This may be due to the fact that magnesium deficiency alters calcium metabolism and the hormone that regulates calcium. Several studies have suggested that magnesium supplementation may improve bone mineral density, but researchers believe that further investigation on the role of magnesium in bone metabolism and osteoporosis is needed.
Magnesium and diabetes. Magnesium is important to carbohydrate metabolism. It may influence the release and activity of insulin, the hormone that helps control blood glucose levels. Elevated blood glucose levels increase the loss of magnesium in the urine, which in turn lowers blood levels of magnesium. This explains why low blood levels of magnesium (hypomagnesemia) are seen in poorly controlled type 1 and type 2 diabetes.
In 1992, the American Diabetes Association issued a consensus statement that concluded: "Adequate dietary magnesium intake can generally be achieved by a nutritionally balanced meal plan as recommended by the American Diabetes Association." It recommended that "... only diabetic patients at high risk of hypomagnesemia should have total serum (blood) magnesium assessed, and such levels should be repleted (replaced) only if hypomagnesemia can be demonstrated".
Myocardial magnesium was measured in 8 young patients (mean age 32) with ventricular tachycardia of less than 30 seconds in duration who underwent endomyocardial biopsy. Histologically, 4 had myocarditis and 1 had right-ventricular dysplasia. The other 3 patients had a cardiomyopathy with electron microscopic findings consistent with intracellular calcium overload, possibly due to reduced intracellular magnesium. Myocardial magnesium content was lower in the 4 with cardiomyopathic and dysplastic lesions than in the 4 with inflammatory lesions (myocarditis) and 8 controls. 10gm magnesium over 24 hours caused a resolution of ventricular tachycardias and a greater than 80% reduction in ventricular extrasystoles. No response was seen in the 4 patients with inflammatory lesions. [Lancet: 1019, 1987]
Myocardial magnesium was measured in 8 young patients (mean age 32) with ventricular tachycardia of less than 30 seconds in duration who underwent endomyocardial biopsy. Myocardial magnesium content was lower in the 4 with cardiomyopathic and dysplastic lesions than in the 4 with inflammatory lesions (myocarditis) and 8 controls. 10gm magnesium over 24 hours caused a resolution of ventricular tachycardias and a greater than 80% reduction in ventricular extrasystoles. No response was seen in the 4 patients with inflammatory lesions. [Lancet: 1019, 1987]
According to Ploceniak, prolonged magnesium administration nearly always provides a cure for bruxism. This confirms an earlier report which claimed remarkable reductions and sometimes disappearance in the frequency and duration of grinding episodes in six patients who took assorted vitamins and minerals (which included 100mg of magnesium) for at least five weeks. When the supplement intake stopped, the symptoms returned. [Bruxism and Magnesium, My Clinical Experiences Since 1980, by C. Ploceniak (Translated from the French by James Michels)]
Magnesium deficiency is strongly implicated as a causative factor in PMS. Red Blood Cell magnesium levels in PMS patients have been shown to be significantly lower than in normal subjects. The deficiency is characterized by a generalized hyperesthesia syndrome (with generalized aches and pains), and a lower premenstrual pain threshold. One clinical trial of magnesium in PMS showed a reduction of nervousness in 89%, mastalgia in 96%, and weight gain in 95%.
Early symptoms of magnesium deficiency can include fatigue, anorexia, irritability, insomnia, and muscle tremors or twitching. Many cases of muscle cramps are caused by low concentrations of magnesium. [Muscle cramps and magnesium deficiency: case reports. Canadian Family Physician. July 1996: 42; pp.1348-1351]
People who abuse alcohol are at high risk for magnesium deficiency because alcohol increases urinary excretion of magnesium. Low blood levels of magnesium occur in 30-60% of alcoholics, and in nearly 90% of patients experiencing alcohol withdrawal. In addition, alcoholics who substitute alcohol for food will usually have lower magnesium intakes. Medical doctors routinely evaluate the need for extra magnesium in this population.
In evaluating magnesium levels in patients with small bowel resection, it was found that while serum magnesium was not abnormally low, but both urinary and muscle magnesium concentration decreased with increasing resection length. Muscular fatigue was also positively correlated to a pathologically low muscle magnesium concentration. Results suggest that clinically important magnesium deficiency occurs in patients with resections exceeding 75cm.
Hypomagnesemia has been demonstrated in both insulin-dependent and non-insulin-dependent diabetic patients. A low intake of magnesium, which is a common deficiency, has been associated with insulin resistance and diabetes in several studies. Magnesium deficiency in diabetes is most likely the result of increased urinary magnesium losses secondary to chronic glycosuria. However, short-term improvement in glycemic control has not been shown to restore the serum magnesium level. Long-term studies may be needed to resolve this discrepancy.
Experimental studies have demonstrated a correlation between magnesium deficiency and atherosclerosis, but without any clear evidence to determine the mechanisms involved. Magnesium deficiency may affect the atherosclerosis process through several different mechanisms.
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