PerspectivesAre you interested in submitting a Perspective Article? Be sure to read The Science Advisory Board's Editorial Guides for Perspective Articles. Click here. Magnesium Intake: A Balanced View by Tahira Farooqui, Ph.D., Department of Entomology, The Ohio State University Magnesium (symbol, Mg2+; atomic number, 2; atomic weight, 24.312; specific gravity, 1.74) is essential to all living cells. Its salts are essential in human nutrition. Magnesium is the fourth most abundant cation (after calcium, sodium and potassium) in the body. It is a component of both intracellular and extracellular fluids and is excreted in the urine and feces. Normal serum level is in a range of 1.7 to 2.5 mg/dL. The main sources of magnesium include green leafy vegetables, legumes, nuts and animal protein [1]. Magnesium is required as a cofactor in more than 300 enzymic reactions, including enzymes associated with oxidative phosphorylation [1]. Magnesium is essential for all kinase reactions [2]. Magnesium deficiency results in increased insulin resistance, as well as increased smooth muscle and platelet reactivity. It has now been recognized as a clinically important electrolyte. Magnesium acts as a smooth muscle relaxant and is involved in dilating coronary arteries and peripheral vessels. It also exerts antiarrhythmic effects, may have a permissive effect on catecholamine actions, and regulates various thrombogenic conditions. Bone is one of the main magnesium pools (~ half of the total magnesium) in the body; therefore, its deficiency is considered as a risk factor for osteoporosis (3). Dietary magnesium supplementation improves bone formation, bone resorption and bone strength in ovariectomized rats showing a positive link between magnesium intake and bone mineral density but the mechanism still remains unclear [3]. A recent study in newborn piglets has demonstrated that magnesium sulfate administration prior to hypoxia prevents hypoxia-induced increase in calcium/calmodulin-dependent-kinase IV and protein tyrosine kinase activities. This results in inhibition of phosphorylation of cyclic adenosine monophosphate (cAMP), response element-binding proteins (CREB), and pro- and anti-apoptotic proteins (Bcl-2 family) that prevents programmed cell death [4]. In addition to its involvement in enzymic reactions, magnesium is also an important component of cell membranes. Therefore, it plays an important role in regulating ion homeostasis. For example, if magnesium levels in the cell drops below normal, calcium and sodium move inside allowing potassium and magnesium to leak outside of the cell. Calcium and magnesium are both divalent cations, but they react very differently. Therefore, exchange between calcium and magnesium impairs normal cell functions. Hypomagnesemia has been shown to correlate with a number of diseases including osteoporosis, cardiovascular disease, diabetes mellitus, hypertension and hyperlipidemia [3, 5-9] (see Table 1). Alcoholics, and/or patients who are taking diuretics, or patients suffering from diabetic ketoacidosis are most likely to be magnesium deficient. Magnesium plays an important role in regulation of cardiac excitability, neuromuscular transmission, vasomotor tone, and blood pressure, among other functions [8]. Many studies support a pathological role for magnesium in the etiology and development of major coronary risk factors as diabetes mellitus, hypertension, and hyperlipidemia as well as ischemic heart disease [6-8]. Therefore, dietary magnesium supplementation may have a therapeutic value in the management of coronary risk factors and ischemic heart disease [8]. Magnesium is necessary for the activity of enzymes (lecithin cholesterol acyltransferase and lipoprotein lipase), which lowers triglyceride levels and raises High density lipoprotein (HDL) cholesterol levels [7]. Moreover, Mg2+-ATP complex is the controlling factor for the rate-limiting enzyme in the cholesterol biosynthesis that affects cholesterol levels. Therefore, its deficiency results in hyperlipidemia in the bloodstream and liver [7]. Magnesium deficiency frequently occurs in diabetic patients. Several epidemiological studies have also demonstrated a relation between the ingestion of food rich in magnesium and the reduction in diabetes complications, but exact elucidation of magnesium deficiency in diabetes mellitus is not clear [5]. Furthermore, its deficiency is associated with insulin resistance in obese children [9]. Therefore, increased intake of magnesium-rich foods may be an important tool in the prevention of these diseases. Common causes of hypermagnesemia include renal failure and iatrogenic manipulations. Magnesium levels in serum (2-4 mEq/L) are associated with adverse effects including nausea, vomiting, lightheadedness, weakness and skin flushing. A serum magnesium level (5-6 mEq/L) is associated with hypotension and vasodilatation; and serum magnesium level (8-10 mEq/L) results in arrhythmia, intraventricular conduction delay. However, higher serum magnesium level (>10 mEq/L) causes asystole, heart block, coma and death (see Table 2). Hypermagnesemia is a rare cause of coma in a patient with normal renal function [10]. Hypermagnesemia produced from Epsom salt gargles result in subtle neurological and cardiovascular signs to the major life-threatening clinical manifestations of shock, dysrhythmias, coma, and cardiopulmonary arrest despite emergency dialysis [10]. Epsom salt gargling increases serum magnesium to 23.6 mg/dL (9.8 mmol/L). These levels produce a life threatening manifestation such as coma. There are cases when patients were erroneously given intravenous magnesium overdose (20 g of magnesium sulfate). This results in cardiac arrest [11]. Magnesium sulphate provides rapid control of convulsions in eclamptic patients with minimal sedative effects. Therefore, due to neuromuscular blocking action of magnesium and the narrow margin between therapeutic and toxic serum levels, the drug must be given with caution. Based on preclinical results in models, some studies suggest that magnesium sulfate may act as a putative neuroprotective agent after acute brain injury. Due to the blood brain barrier, magnesium ion has limited entry into the central nervous system. Further experimental work is needed to define its neuroprotective threshold in the injured brain [12]. Furthermore, osteopenic effects (damage to bone mass, bone structure, and bone metabolism) have been reported in premature infants whose mothers had prolonged treatment with magnesium sulfate. These infants have hypocalcemia, osteopenia, and fractures [13] (see Table 2). In modern westernized diet, intake of magnesium from food such as grain, barley, vegetables, seaweed, and nuts has been remarkably decreased. Therefore, our generation is facing a risk of developing hypomagnesemia easily. Furthermore, increasing intake of animal fat, exercise insufficiency, and accumulation of various stresses in every day’s busy life has started developing a metabolic syndrome. This syndrome is often complicated with obesity, hypertension, hyperglycemia, and hyperlipidemia, which makes our body more susceptible to chronic diseases [14]. Therefore, the maintenance of normal levels of magnesium by either magnesium-supplementation or increased intake of magnesium-rich foods should be recognized for having good health. Since almost 99% of the body’s magnesium is inside the cells and its function is mainly intracellular, intracellular magnesium in erythrocytes – iMge – is the best magnesium parameter to observe hypo- or hypermagnesemia in both groups of patients [15]. It is timely that both physicians and patients should be aware of advantages and disadvantages of taking additional magnesium supplements. Therefore, patients should first get an analysis done for their serum magnesium to recognize their magnesium status (hypomagnesemia or hypermagnesemia) before starting the supplements.   References: [1] Fox C, Ramsoomair D, Carter C. 2001. Magnesium: its proven and potential clinical significance. South Med J 94: 1196-1201. [2] Mildvan AS. 1987. Role of magnesium and other divalent cations in ATP-utilizing enzymes. Magnesium 6: 28-33. [3] Matsuzaki H. 2006. Prevention of osteoporosis by foods and dietary supplements. Magnesium and bone metabolism. Clin Calcium 16:1655-1660. [4] Mami AG, Ballesteros JR, Fritz KI, Kubin J, Mishra OP, Delivoria-Papadopoulos M. 2006. Effects of magnesium sulfate administration during hypoxia on CaM kinase IV and protein tyrosine kinase activities in the cerebral cortex of newborn piglets. Neurochem Res 31: 57-62. [5] Sales CH, Pedrosa Lde F. 2006. Magnesium and diabetes mellitus: their relation. Clin Nutr. 25:554-562. [6] Kumeda Y, Inaba M. 2005. Metabolic syndrome and magnesium. Clin Calcium 15:97-104. [7] Inoue I. 2005. Lipid metabolism and magnesium. Clin Calcium 15: 65-76. [8] Ueshima K. 2005. Magnesium and ischemic heart disease: a review of epidemiological, experimental, and clinical evidences. Magnes Res 18: 275-284. [9] Huerta MG, Roemmich JN, Kington ML, Bovbjerg VE, Weltman AL, Holmes VF, Patrie JT, Rogol AD, Nadler JL. 2005. Magnesium deficiency is associated with insulin resistance in obese children. Diabetes Care 28: 1175-1181. [10] Birrer RB, Shallash AJ, Totten V. 2002. Hypermagnesemia-induced fatality following Epson salt gargles (1). J Emerg Med 22:185-188. [11] Vissers RJ, Purssell R. 1996. Latrogenic magnesium overdose: two case reports. J Emerg Med 14: 187-191. [12] McKee JA, Brewer RP, Macy GE, Borel CO, Reynolds JD, Warner DS. 2005. Magnesium protection is limited in humans with acute brain injury. Neurocrit Care 2: 342-351. [13] Kaplan W, Haymond MW, Mckay S, Karaviti LP. 2006. Osteopenic effects of MgSO4 in multiple pregnancies. J Pediatr Endocrinol Metab 19: 1225-1230. [14] Kumeda Y, Inaba M. 2005. Metabolic syndrome and magnesium. Clin Calcium 15: 97-104. [15] Malon A, Brockmann C, Fijalkowska-Morawska J, Rob P, Maj-Zurawska M. 2004. Ionized magnesium in erythrocytes—the best magnesium parameter to observe hypo- or hypermagnesemia. Clin Chim Acta 349: 67-73. ### << Previous Next >> [ View All Perspectives ] |
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