Mg – Magnesium is found in igneous rocks at 23,300 ppm; in shale at 15,000 ppm; sandstone 10,700 ppm; limestone at 2,700 ppm; fresh water at 4.1 ppm; sea water at 1,350 ppm; soil at 5,000 ppm (highest in soil derived from basalt, serpentine or dolomite) -Mg is the second most common exchangeable cation in most soils; marine plants at 5,200 ppm; land plants at 3,200 ppm; marine animals at 5,000 ppm; land animals at 1,000 ppm (accumulates in mammalian bone).
Magnesium is essential to all living organisms and has electrochemical, catalytic and structural functions, activates numerous enzymes and is a constituent of all chlorophyll.
The adult human contains 20 to 28 grams of total body magnesium. Approximately 60 % is found in bone, 26 % is associated with skeletal muscle and the balance is distributed between various organs and body fluids. Serum levels of Mg range from 1.5 to 2.1 mEq/L; it is second to K as an intracellular cation – half of the Mg, including most that is bound in the bone, is not exchangeable.
Magnesium is required for the production and transfer of energy for protein synthesis, for contractility of muscle and excitability of nerves, and as a cofactor in myriads of enzyme systems. AN EXCESS OF MG WILL INHIBIT BONE CALCIFICATION. Calcium and Mg have antagonistic roles in normal muscle contraction, calcium acting as the stimulator and Mg as the relaxer. An excessive amount of Ca can induce signs of Mg deficiency.
The rate of absorption of Mg ranges from 24 to 85 %. The lesser absorption rate is for metallic sources of Magnesium, the higher levels are associated with plant derived colloidal sources. Vitamin D has no effect on Mg absorption; the presence of fat, phytates and calcium reduces the efficiency of absorption. High performance athletes lose a considerable amount of Mg in sweat.
Deficiency Diseases of Magnesium
- Menstrual migraines
- Growth failure
- ECG changes
- Neuromuscular problems
- Tetany (Convulsions)
- Muscular weakness
- Muscle “Ties”
- Calcification of small arteries
- Malignant’ calcification of soft tissue
The RDA for Mg is 350mg/day for adult males, 300mg/day for adult females and 450 mg/day for pregnant and lactating females. If kidneys are healthy there is no evidence of toxicity at up to 6,000 mg per day.
Deficiencies of Mg result in a wide variety of deficiency diseases and symptoms.
Magnesium a major mineral nutrient. The body contains 20 to 28 g of magnesium; 40% is found in tissues like MUSCLE and 60% occurs in BONE and teeth, where it is combined with phosphate. Among soft tissues the liver and muscles contain the highest levels. Within cells magnesium is the second most prevalent type of positively charged ion (cation) after potassium. Magnesium is required for all major metabolic processes involving ATP, the chemical energy currency of the cell. Magnesium and magnesium-ATP complexes activate more than 300 enzymes. It functions in energy-consuming processes like biosynthesis of protein and of DNA and RNA; sugar breakdown (glycolysis); and ATP-dependent transport of materials into the cell. Magnesium is essential for the transmission of nerve impulses; for electrical potentials of cell membranes; muscle contraction; ATP formation; and maintenance of blood vessels.
Possible Roles in Maintaining Health
Magnesium is essential for normal calcium metabolism. In muscle contraction, magnesium balances the effects of calcium, which stimulates contraction. Thus magnesium regulates calcium uptake by cells to activate functions like heartbeat. Magnesium may also:
- protect against cardiovascular disease. It can help reduce high blood pressure, lower cholesterol as low-density lipoprotein (LDL) and increase HDL (high-density lipoprotein) cholesterol;
- protect against lead poisoning;
- protect against migraine and depression;
- help maintain normal heart function and prevent irregular heartbeat (cardiac dysrythmia); The imbalance
between calcium and magnesium may increase the risk of
cardiovascular disease, and magnesium deficiency increases the risk of severe disruptions of cardiac rhythm;
- help alleviate premenstrual syndrome, when used with zinc and vitamin B6 in certain cases;
- prevent kidney stones;
- alleviate preeclampsia and eclampsia, a syndrome in pregnancy characterized by high blood pressure and protein in the urine. In serious cases eclampsia can lead to convulsions and coma.
Magnesium Status and Health
Ivor E. Dreosti, PhD., D.Sc.
Nutrition Reviews, Vol. 53, No. 9
Magnesium is found in the body principally in the cells and the skeleton. Many biological processes are dependent on magnesium. Magnesium is involved in the functioning of more than 200 enzymes and the utilization of energy-rich ATP Not surprisingly, magnesium deficiency gives rise to a very broad syndrome, with symptoms including growth failure, pallor, weakness, tremor, muscle and nerve irritability, electromyographic changes, hypocalcemia, and hypokalemia.
Overall, nutritionists believe that the principal physiological functions of magnesium are known and can be met by the current world average Recommended Dietary Intake (RDI) of 4.5 mg/kg body weight per day. Indeed, it would seem that magnesium deficiency rarely occurs for purely dietary reasons. The condition, when it exists, is generally associated with gastrointestinal malabsorption, excessive fluid and electrolyte loss, renal dysfunction, general malnutrition associated with alcoholism, and several iatrogenic causes.
Nevertheless, a large number of research nutritionists strongly believe that many important aspects of magnesium deficiency remain to be recognized and evaluated, and that the condition occurs more widely than is currently recognized. The present review will concentrate on several aspects of these views.
Magnesium and Osteoporosis
Estrogen, Calcium, and Osteoporosis
In postmenopausal women loss of estrogen and the attendant lack of control of parathyroid hormone are important factors underlying the development of osteoporosis. Estrogen replacement, supplementation with calcium and vitamin D, or both, are widely applied prophylactic strategies with respect to osteoporosis, yet little attention is paid to the important involvement of magnesium in ensuring bone integrity.
Magnesium Status and Osteoporosis
Repeated studies have demonstrated that osteoporotic trabecular bone has significantly lower levels (12%) of magnesium than controls; these levels are similar to those that occur in magnesium deficiency. Dietary magnesium intakes have been reported to be lower (15%) in osteoporotic patients than in normal women, and markedly increased retention of magnesium (up to 90%) has been noted in osteoporotic postmenopausal women following a parenteral magnesium load. Serum magnesium levels are often slightly reduced, but red blood cell magnesium appears to be significantly lower in osteoporotic patients.
Magnesium in the Treatment of Osteoporosis
Several recent studies have reported on magnesium supplements in the treatment of osteoporosis-with favorable results. In a group of postmenopausal women in Israel suffering from osteoporosis who received magnesium supplements in the range 250-750 mg/day for 24 months, either trabecular bone density increased (up to 8%) or bone loss was arrested (in 87%); in some cases both an increase in bone density and arrested bone loss occurred. Untreated controls, on the other hand, lost bone density at an average of I % a year. Similarly, a group of postmenopausal osteoporotic patients in Czechoslovakia who received magnesium at levels ranging from 1500 to 3000 mg of magnesium lactate per day for 2 years. Nearly 65% were classified totally free of pain and with no further deformity of vertebrae, with the condition in the remainder either arrested or slightly improved.
Magnesium and Heart Disease
Much has been written over the last decade in relation to magnesium and heart disease. At pharmacological levels there is some evidence that infusion of magnesium ions may help in the treatment of cardiac arrhythmia, possibly due to its role as a physiological calcium blocker. Several epidemiological studies with humans and experiments with animals suggest a degree of protection associated with replete magnesium status with respect to atherogenesis. In addition, a limited number of experimental studies with humans point to an improved blood lipid profile in patients supplemented with dietary magnesium. Most recently, studies with rats have indicated that dietary magnesium deficiency increases the susceptibility of lipoproteins and tissues to peroxidation, which suggests that the mechanism responsible for the pathology associated with several aspects of magnesium deficiency may involve lipid peroxidation.
The adult Recommended Dietary Allowance (RDA) for magnesium is 350 mg per day for men and 280 mg for women. The typical American diet provides about 120 mg per 1,000 calories. Thus a person consuming 1,500 calories or less is likely to be magnesium deficient. Factors that increase the need for magnesium due to limited uptake or increased losses include high dietary fiber; too much phosphate (as soft drinks) and alcoholic beverages; high psychological stress; some diuretics (water pills) and regular, strenuous exercise. Excessive calcium in supplements may compete with magnesium. Diseases and conditions that cause magnesium depletion include malabsorption, malnutrition, alcoholism and intravenous feeding using nutrient mixtures that do not contain enough magnesium. Marginal deficiency is very common among teenagers and people who diet; diabetics; pregnant and lactating women; those who drink heavily; elderly persons with poor eating habits; those taking diuretics and digitalis; athletes; women with osteoporosis; and individuals with severe kidney disease and severe diarrhea.
Early symptoms of magnesium deficiency, including a loss of appetite, upset stomach and diarrhea, are vague, making diagnosis of a mild deficiency difficult. Symptoms of long-term deficiency relate to the nervous system: confusion, apathy, depression, irritability, irregular heartbeat, muscle weakness, tremors, convulsions and poor coordination, as well as a lack of appetite, listlessness, nausea and vomiting. Measurement of white blood cell magnesium can be used to help assess the nutritional status of this mineral.
Excessive use of the home remedies Epsom salts and milk of magnesia leads to deficiencies of other minerals, even toxicity. Overdose with magnesium antacids (1,500 mg or more daily) is indicated by low blood pressure, drowsiness, nausea, slurred speech and unsteadiness. Magnesium toxicity can occur when the kidneys cannot clear large overloads. While magnesium appears to be safe, patients should not take it with kidney disease or by those with heart problems (atrioventricular blocks). A physician should be consulted prior to using supplements.
Altura,, Burton M., “Magnesium: Growing in Clinical Importance, Patient Care 28:1 (January 15, 1994), pp. 130-36.
Biol Trace Elem Res 1997 Oct;60(1-2):139-144
Depressed antioxidant defense in rat heart in experimental magnesium deficiency. Implications for the pathogenesis of myocardial lesions.
Kumar BP, Shivakumar K
Division of Cellular and Molecular Cardiology, Sree Chitra Tirunal Institute for Medical Sciences & Technology, Trivandrum, India.
Magnesium (Mg) deficiency has been shown to produce myocardial lesions in different experimental models. Based on several lines of evidence, it has been proposed that oxidative injury to the cardiac muscle may explain the pathobiology of such lesions. In pursuance of this postulation, the present study examined the effect of dietary deficiency of Mg on the activity of the antioxidant enzymes, superoxide dismutase (SOD) and catalase, in rat heart. This article reports a significant lowering of the activity of both these enzymes in the cardiac tissue in Mg-deficient rats. Since depressed antioxidant defense in the heart may enhance myocardial susceptibility to oxidative injury, the observation is of possible relevance to the pathogenesis of cardiac lesions in Mg deficiency.
Influence of magnesium supplementation on atherogenic risk factors by K. Kisters, W. Zidek, C. Karoff, K.H. Rahn in Metal Ions in Biology and Medicine. Eds. Ph. Collery, LA. Poirier, M. Monfait, J.C. Etienne. John Libbey Eurotext, Paris 0 1990, pp. 165-167. Medizinische Poliklinik der Universitat 4400 Munster, Albert-Schweitzer-Str 33, West Germany
In the present study the effect of oral magnesium supplementation on serum lipids in patients with hyperlipidemia of Frederickson type IV and IIb and on blood pressure was examined. In 65 patients with normal renal function, on cholesterol-poor and calorie restricted diet, blood pressure, serum cholesterol, triglyceride, HDL-and LDL-cholesterol as well as plasma and intracellular magnesium concentration were measured before and 4 weeks after therapy. 35 patients received 500 mg of Mg daily additionally.
The results of our study show that magnesium supplementation in addition to the usual dietary measures is beneficial with regard to serum triglycerides, but exerts no positive effect on blood pressure and serum cholesterol. Furthermore intracellular magnesium concentration increased significantly under magnesium supplementation.
This study indicates that long-term peroral magnesium supplementation changes blood lipid composition. In addition to dietary measures magnesium supplementation causes a significant decrease in triglycerides, whereas no positive effect on serum cholesterol and blood pressure was noted in patients with normal renal function and hyperlipidemia of Frederickson type IV and IIb Only a few studies have evaluated the effect of peroral magnesium therapy on blood lipid composition in humans. Haywood and Sylvester, 1962, found that treatment over a period of 19 months with a magnesium combined therapy lowered 2 factions of the lipoproteins. Davis et al., 1984, found that treatment of 16 patients with hyperlipidemia for a period of 118 days significantly reduced total cholesterol. The physiologic and biochemical background of the effect of an oral magnesium supplementation has not been studied in detail yet. Two enzymes, both of which are essential in lipid metabolism may be involved, namely the lecithin cholesterol acyl transferase (LCAT) and the lipoprotein lipase. From animal studies, it has been suggested that magnesium is an important cofactor for both of these enzymes (Gueux et al., 1984). This study has shown that peroral magnesium therapy can alter blood lipid composition and therefore be of use in reducing atherogenic risk factors,but further investigations, especially with regard to a long-term magnesium therapy, still remain to be settled
Magnes Trace Elem 1990;9(1):1-14
Effects of magnesium on skeletal metabolism.
Medical Service, Veterans Administration Medical Center, Bay Pines, Fla.
Magnesium (Mg) makes up 0.5-1% of bone ash and is therefore not a trace element in the skeleton. Mg influences both mineral and matrix metabolism in bone by a combination of effects on hormones and other factors that regulate skeletal and mineral metabolism, and by direct effects on bone itself. The skeletal content of Mg is very variable both between and within species, and reported values range between 150 and 440 mmol/kg ash weight (AW). Dietary Mg has a direct influence and age an inverse influence on skeletal Mg content. It is unclear whether skeletal Mg content varies from region to region. In humans, reported values cluster around the 200 mmol/kg AW level, 30-40% lower than most rat data. Human iliac crest cortical bone has 10-20% less Mg per unit weight than iliac crest trabecular bone. Mg depletion adversely affects all phases of skeletal metabolism. In the rat, cessation of bone growth is noted with a decrease in both osteoblast and osteoblast activity, decreased bone formation, osteopenia, increased fragility and development of a form of ‘aplastic bone disease’. The epiphyseal growth plate is thinned and the percent ash weight of the growth plate is increased, possibly due to enhanced crystallization of bone salt under conditions of Mg depletion. In contrast, in chicks and in rats with severe Mg deficiency, these ‘antianabolic’ effects are not observed but instead, predominant inhibition of bone resorption occurs with increased cortical thickness rather than osteopenia, and the occasional development of subperiosteal hyperplasia or of fibrous tumors of the periosteum. It is probable that this unusual response under conditions of severe Mg deficiency is in part an indirect effect secondary to a defect in secretion and/or skeletal responsiveness to parathyroid hormone (PTH) and vitamin D metabolites. Mg excess also has adverse biologic effects on bone. Crystallization of bone salt is severely impaired and an osteomalacia-like picture may be produced with decreased osteoblastic activity, widened growth plates, excessive osteoid seams and short, thickened bones. In some studies, especially in mice, Mg excess stimulates bone resorption, independently of PTH. The role of Mg deficiency and excess in human skeletal conditions requires more extensive investigation. Bone Mg is uniformly increased in renal insufficiency and may play a role in renal osteodystrophy since improvement has been noted in the osteomalacic component by normalizing the serum Mg. Decreased bone Mg has been reported in alcoholic patients, diabetes and in osteoporosis.
Magnes Trace Elem 1990;9(2):61-69
Studies on the relationship between boron and magnesium which possibly affects the formation and maintenance of bones.
United States Department of Agriculture, Grand Forks Human Nutrition Research Center, N. Dak.
Recent findings are reviewed indicating that changes in dietary boron and magnesium affect calcium, and thus bone, metabolism in animals and humans. In animals, the need for boron was found to be enhanced when they needed to respond to a nutritional stress which adversely affected calcium metabolism, including magnesium deficiency. A combined deficiency of boron and magnesium caused detrimental changes in the bones of animals. However, boron deprivation did not seem to enhance the requirement for magnesium. In two human studies, boron deprivation caused changes in variables associated with calcium metabolism in a manner that could be construed as being detrimental to bone formation and maintenance; these changes apparently were enhanced by low dietary magnesium. Changes caused by boron deprivation included depressed plasma ionized calcium and calcitonin as well as elevated plasma total calcium and urinary excretion of calcium. In one human study, magnesium deprivation depressed plasma ionized calcium and cholesterol. Because boron and/or magnesium deprivation causes changes similar to those seen in women with postmenopausal osteoporosis, these elements are apparently needed for optimal calcium metabolism and are thus needed to prevent the excessive bone loss which often occurs in postmenopausal women and older men.
Magnes Trace Elem 1990;9(5):255-264
Can dietary magnesium modulate lipoprotein metabolism?
Singh RB, Rastogi SS, Sharma VK, Saharia RB, Kulshretha SK
Medical Hospital and Research Center, Moradabad, India.
In a randomized, single-blinded, controlled study (430 patients aged 25-63 years, 394 males), 214 subjects were administered a magnesium-rich diet and 216 subjects were administered a usual diet for 12 weeks. Age, sex, body weight, hypertension, diabetes, hyperlipidemia, smoking, obesity, diuretic therapy and hypomagnesemia were comparable between the two groups as were laboratory data at entry to the study. The intervention group A received a significantly higher amount of dietary magnesium (1,142.0 +/- 225 mg/day) compared to group B which received the usual diet (438 +/- 118 mg/day). After 12 weeks, there was a significant decrease in total serum cholesterol (10.7%), low-density-lipoprotein (LDL) cholesterol (10.5%) and triglyceride (10.1%) in group A compared to the values at entry to the study; no such changes were evident in group B subjects. HDL-cholesterol showed a marginal mean decrease of 0.8 mg/dl in group B and 2.0 mg/dl increase in group A. However, in hypomagnesemic patients (26 cases) of the intervention group, there was a 10.9% increase in high-density-lipoprotein (HDL) cholesterol in association with a decrease in other lipids. Although a general blood-lipid-reducing effect of a high-fiber, low-cholesterol diet cannot be excluded, dietary magnesium may have contributed to the reduction of total serum cholesterol, LDL-cholesterol, and triglyceride as well as to the marginal rise in HDL-cholesterol. More studies with a longer follow-up are needed in order to confirm the role of magnesium in preventing a decrease in HDL-cholesterol in association with reduction in other lipoproteins.
Magnes Trace Elem 1991;10(2-4):220-228
The role of magnesium in lung diseases: asthma, allergy and pulmonary hypertension.
Mathew R, Altura BM
New York Medical College, Valhalla.
Magnesium is the fourth most abundant metal found in the body. It plays a crucial role in numerous biological processes. It is a natural calcium blocker. It can block or compete with Ca2+ at voltage-dependent, receptor- or leak-operated channels and result in translocation of intracellular Ca2+. Mg2+ inhibits Ca2+ release from the sarcoplasmic reticulum. Intracellular Mg2+ is thought to modulate smooth muscle contractions and the rate of relaxation. Mg2+ is a cofactor of numerous enzymes and is coupled with cellular use of phosphate as an activator and energy source. cAMP-dependent protein and adenylate cyclase are among many enzymes that require Mg2+ for their function. Mg2+ has been used successfully in treating asthma. There is experimental evidence that Mg2+ is required for various immune responses, and in rats, Mg2+ treatment has been shown to attenuate chemically induced pulmonary hypertension. It is not clear if Mg2+ deficiency plays a role in development of some of these diseases, but Mg2+ salts appear to have therapeutic value and certainly it has a role as an adjunct to traditional therapy in various lung diseases.
Magnes Trace Elem 1991;10(2-4):215-219
Magnesium deficiency and diabetes mellitus.
Case Western Reserve University Cleveland, Ohio.
Hypomagnesemia is the commonest electrolyte abnormality in the ambulatory diabetic patient and is also a frequent finding in patients with diabetic ketoacidosis. Excessive urinary magnesium loss associated with glycosuria is probably the most important factor in the genesis of hypomagnesemia in the diabetic patient. The clinical consequences of magnesium deficiency include impairment of insulin secretion, insulin resistance and increased macrovascular risk. The role of magnesium deficiency in microvascular complications has yet to be clearly defined.
Penland JG. Quantitative analysis of EEG effects following experimental marginal magnesium and boron deprivation. Magnesium Research 8:341-58, 1995.
Severe magnesium deficiency is frequently accompanied by excessive electrical activity in the brain, including seizure-like activity. This controlled, double-blind study investigated whether marginal intakes of dietary magnesium, similar to those consumed by many Americans, would also result in increased brain electrical activity. Because previous studies have shown that the mineral boron may affect biological response to magnesium, dietary intakes of boron were also examined. Compared to when they ate more than 300 mg magnesium daily, postmenopausal women eating approximately 115 mg magnesium daily for six weeks showed increases in brain electrical activity very similar to but not as extreme as those found with severe magnesium deficiency. Some changes in brain electrical activity were also found when these women ate less than 1 mg of boron daily, compared to when they ate more than 3 mg of boron daily. The effect of low dietary boron was to decrease the type of electrical activity associated with alertness. In very few instances did the amount of boron eaten affect the response to the amount of magnesium eaten. These findings are important to gaining a better understanding of the functional consequences of marginal as well as severe deficiencies of magnesium and boron in the diet.
Grand Forks Human Nutrition Research Center
A Healthy Heart – the Mineral Connection
David B. Milne
Coronary heart disease is this nation’s number one killer. World wide it is estimated to kill 800,000 annually.
Considerable attention has been focused on factors that increase risk, such as diets containing high amounts of fat and saturated fat, and on increasing nutrients thought to reduce risk. These include folic acid and antioxidant vitamins, such as beta carotene, and vitamins C and E.
Research at the Grand Forks Human Nutrition Research Center and at several laboratories around the world has demonstrated the importance of two essential elements, magnesium and copper in maintaining a healthy heart.
A recent review relates low magnesium intake to a high incidence of cardiac deaths, particularly in soft water areas where magnesium in the water is low. Chronic magnesium deficiency in both humans and animals is known to produce hypertension, atherosclerosis, abnormal heart rhythms and electrocardiograms, damaged heart tissue, and sudden cardiac death.
The body needs magnesium in a variety of body processes, including normal muscle contraction and nerve function.
Research suggests that mild copper deficiency also contributes to all stages of atherosclerosis and increased risk of heart disease. Abnormal electrocardiograms, high blood cholesterol, and elevated blood pressures have been seen in both humans and animals experimentally depleted of copper.
The body needs copper to maintain the elasticity of the heart and blood vessels as well as the activity of an important antioxidant enzyme in the blood.
Surveys of daily diets in North America and Europe indicate that more than 30 percent contain less than 1 milligram of copper. That’s insufficient for adults based on studies conducted at the Grand Forks center.
Foods that are rich in magnesium are generally high in copper and vice versa. Good sources of both minerals include seeds, nuts, legumes, and cereal grains. Dark green vegetables are an additional source of magnesium. Other foods that are high in copper are oysters, liver, chocolate, and shell fish. Adding sunflower seeds to a copper and magnesium-poor lettuce and dressing salad can change it into to one that is a good source of both copper and magnesium.
By contrast, diets high in refined foods, meat, and dairy products are usually lower in both copper and magnesium than diets rich in vegetables and unrefined grains. Following the guidelines of the USDA’s food pyramid provides diets that contain healthy amounts of both copper and magnesium, as well as antioxidant vitamins and other nutrients needed for maintaining good health.
The heart has held special significance throughout history as a symbol of life and disease, as the place of the soul, as the source of feelings of love. Attention to the foods we eat is an important part of a healthy life style needed to maintain a healthy heart and quality of life.
Magnes Trace Elem 1990;9(4):198-204
Magnesium and potassium administration in acute myocardial infarction.
Singh RB, Sircar AR, Rastogi SS, Garg V
Medical Hospital and Research Centre, Moradabad, UP, India.
This study included 264 patients with proven acute myocardial infarction who were randomized to either magnesium sulphate, potassium chloride, 10% glucose solution or a placebo containing 200 ml of 2% glucose solution given intravenously, slowly, daily for 3 days in a double-blind, placebo-controlled fashion. The ages varied between 30 and 65 years and 230 were males. Laboratory data such as enzymes, sodium, potassium, calcium and magnesium were obtained in all the patients before and after the therapy. Age, sex, risk factors and drug therapy were comparable between all the groups of patients. After 4 weeks of follow-up, there was a significant decrease in the total number of complications in group A (52%) and B (30%) patients, who were given magnesium and potassium compared to group C and D, who were administered only 10% glucose and placebo. There was a significant rise in mean serum magnesium and potassium levels in group A and B, respectively, after therapy compared to their mean concentrations before therapy. Although mortality was less in groups A and B, a firm statistical conclusion is not possible due to a lesser number of cases. However, it is possible that magnesium and potassium ions have beneficial effects on ischemia-induced alterations and myocardial metabolism resulting in less complications and mortality in group A and B patients.
Magnes Trace Elem 1991;10(2-4):193-204
Magnesium-potassium interactions in cardiac arrhythmia. Examples of ionic medicine.
Iseri LT, Ginkel ML, Allen BJ, Brodsky MA
College of Medicine University of California, Irvine.
Ionic biology involving Ca2+, Na+, K+ and Mg2+ across the cell membrane and in the development of the action potential is reviewed with reference to cardiac arrhythmia. K+ and Mg2+ deficiency which frequently occur together lead to abnormal ionic transfer of Na+, K+ and Ca2+ with development of automaticity, triggered impulses and reentrant tachycardia. Tachycardia occurring in acute myocardial ischemia, congestive heart failure, hypertensives on diuretics and digitalis toxicity is examined according to the concept of ionic imbalance. A protocol for prevention and treatment of cardiac tachyarrhythmia is proposed with this concept in mind.
Magnes Trace Elem 1991;10(2-4):182-192
Cardiovascular risk factors and magnesium: relationships to atherosclerosis, ischemic heart disease and hypertension.
Altura BM, Altura BT
Department of Physiology, State University of New York Health Science Center, Brooklyn.
Hypertension and atherosclerosis are well-known precursors of ischemic heart disease, stroke and sudden cardiac death. Although there is general agreement that the atheroma is the hallmark of atherosclerosis and is found in coronary obstruction, there is no agreement as to its etiology. It is now becoming clear that a lower than normal dietary intake of Mg can be a strong risk factor for hypertension, cardiac arrhythmias, ischemic heart disease, atherogenesis and sudden cardiac death. Deficits in serum Mg appear often to be associated with arrhythmias, coronary vasospasm and high blood pressure. Experimental animal studies suggest interrelationships between atherogenesis, hypertension (both systemic and pulmonary) and ischemic heart disease. Evidence is accumulating for a role of Mg2+ in the modulation of serum lipids and lipid uptake in macrophages, smooth muscle cells and the arterial wall. Shortfalls in the dietary intake of Mg clearly exist in Western World populations, and men over the age of 65 years, who are at greatest risk for development and death from ischemic heart disease, have the greatest shortfalls in dietary Mg. It is becoming clear that Mg exerts multiple cellular and molecular effects on cardiac and vascular smooth muscle cells which explain its protective actions.
Magnes Trace Elem 1990;9(3):143-151
Effect of dietary magnesium supplementation in the prevention of coronary heart disease and sudden cardiac death.
Medical Hospital and Research Centre, Moradabad, India.
Magnesium may be important in the pathogenesis of coronary heart disease and sudden death. To study the role of magnesium, 400 high-risk individuals were asked to volunteer either for a magnesium-rich diet (group A, 206) or for our usual diet (group B, 194) for 10 years in a randomized fashion. The age groups were between 25 and 63 years and the majority (374) of them were males. At entry to the study, age, sex, incidence of hypertension, diabetes, hypercholesterolemia, smoking, coronary disease and diuretic therapy were comparable. Dietary magnesium intake in group A (1,142 +/- 233 mg/day) was higher than in group B (418 +/- 105 mg/day). Total complications in group A (59; 28.6%) were significantly (p less than 0.001) less compared to group B (117; 60.3%). Sudden deaths were one and a half times more common in group B than in group A. Total mortality in group A (22; 10.7%) was significantly (p less than 0.01) less than in group B (34; 18.0%). A greater number of complications and increased mortality in group B subjects was consistent with a higher incidence of hypokalemia, hypomagnesemia and coronary risk factors in group B patients. Mean serum magnesium levels in group B participants were significantly (p less than 0.01) lowered compared to the mean magnesium level in group A participants who were administered the magnesium-rich diet. It is possible that increased intake of dietary magnesium in association with the general effects of a nutritious diet can offer protection against cardiovascular deaths among high-risk individuals predisposed to coronary heart disease.
Magnes Trace Elem 1990;9(5):283-288
Magnesium-deficient diet aggravates anaphylactic shock and promotes cardiac myolysis in guinea pigs.
Ashkenazy Y, Moshonov S, Fischer G, Feigel D, Caspi A, Kusniec F, Sela BA, Zor U
Department of Internal Medicine, Wolfson Hospital, Holon, Israel.
Actively sensitized guinea pigs were rendered Mg(2+)-deficient for 2-3 weeks and then subjected to immune stress. No differences could be seen between treated and control groups prior to immune challenge. 1-2 h after antigen challenge, 95% of the Mg(2+)-deficient animals were observed to be anaphylactic, i.e. apathetic, dyspneic, and they had a rapid pulse rate. Only 4% of the control animals showed signs of anaphylaxis. Serum magnesium concentration, [Mg2+], fell from 1.32 +/- 0.07 mM in control guinea pigs to 0.56 +/- 0.04 mM in those fed a Mg(2+)-deficient diet. Cardiomyolysis (CM) developed in 19% of the anaphylactic animals and in 3% of the controls. We conclude that Mg(2+)-deficient animals continue to function, provided conditions are normal, but they are unable to withstand stress. The heart, however, appears to be better equipped to defend itself against Mg2+ deficiency and low serum [Mg2+], a supposition supported by the fact that heart [Mg2+] is not significantly reduced in hypomagnesemic guinea pigs (0.864 +/- 0.021 microgram/mg dry weight in control and 0.834 +/- 0.062 microgram/mg dry weight in magnesium-deficient animals). The data indicate that hypomagnesemia heightens the intensity of the immune response, thereby exacerbating both anaphylactic shock (AS) and CM. A normal serum [Mg2+] would thus seem essential for protection against immune stress.
Arteriosclerosis 1990 Sep-Oct;10(5):732-7
Effect of dietary magnesium on development of atherosclerosis in cholesterol-fed rabbits.
Ouchi Y, Tabata RE, Stergiopoulos K, Sato F, Hattori A, Orimo H
Department of Geriatrics, Faculty of Medicine, University of Tokyo, Japan.
The effect of dietary magnesium (Mg) on the development of atherosclerosis in cholesterol-fed rabbits was investigated. Male New Zealand White rabbits (n = 31) were placed on five kinds of diets: regular, 1% cholesterol, and 1% cholesterol diets supplemented with either 300, 600, or 900 mg (as Mg) of Mg sulfate. The regular and 1% cholesterol diets contained 400 mg of Mg per 100 g. Each rabbit received 100 g daily of the appropriate diet. Additional Mg was well tolerated and did not affect blood pressure or body weight. The rabbits were sacrificed after 10 weeks, and the oil red O-positive atherosclerotic area that covered the aortic intima and the cholesterol content of the aorta was
measured. Additional Mg decreased both the area of the aortic lesions and the cholesterol content of the aortas in a dose-dependent manner. The 1% cholesterol diet significantly increased plasma cholesterol and triglyceride
concentrations and decreased high density lipoprotein (HDL) cholesterol concentration. Additional Mg had no further effect on cholesterol and HDL cholesterol concentrations, but it slightly decreased the rise in triglyceride concentration. These results indicate that dietary Mg prevents the development of atherosclerosis in cholesterol-fed rabbits by inhibiting lipid accumulation in the aortic wall.