Magnesium Therapy Abstracts

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The following is a collection of magnesium therapy abstracts from published scientific research and papers. Integratedhealth.com carries the purest magnesium products from Ancient Minerals, including Magnesium Oil, Magnesium Flakes, Magnesium Gel, and Magnesium Lotion. Magnesium therapy should start with a consultation with your physician.

(REFERENCE 1 OF 20)

Elin RJ

Magnesium metabolism in health and disease.

In: Dis Mon (1988 Apr) 34(4):161-218

Magnesium is an important element for health and disease. Magnesium, the second most abundant intracellular cation, has been identified as a cofactor in over 300 enzymatic reactions involving energy metabolism and protein and nucleic acid synthesis. Approximately half of the total magnesium in the body is present in soft tissue, and the other half in bone. Less than 1% of the total body magnesium is present in blood. Nonetheless, the majority of our experimental information comes from determination of magnesium in serum and red blood cells. At present, we have little information about equilibrium among and state of magnesium within body pools. Magnesium is absorbed uniformly from the small intestine and the serum concentration controlled by excretion from the kidney. The clinical laboratory evaluation of magnesium status is primarily limited to the serum magnesium concentration, 24-hour urinary excretion, and percent retention following parenteral magnesium. However, results for these tests do not necessarily correlate with intracellular magnesium. Thus, there is no readily available test to determine intracellular/total body magnesium status. Magnesium deficiency may cause weakness, tremors, seizures, cardiac arrhythmias, hypokalemia, and hypocalcemia. The causes of hypomagnesemia are reduced intake (poor nutrition or IV fluids without magnesium), reduced absorption (chronic diarrhea, malabsorption, or bypass/resection of bowel), redistribution (exchange transfusion or acute pancreatitis), and increased excretion (medication, alcoholism, diabetes mellitus, renal tubular disorders, hypercalcemia, hyperthyroidism, aldosteronism, stress, or excessive lactation). A large segment of the U.S. population may have an inadequate intake of magnesium and may have a chronic latent magnesium deficiency that has been linked to atherosclerosis, myocardial infarction, hypertension, cancer, kidney stones, premenstrual syndrome, and psychiatric disorders. Hypermagnesemia is primarily seen in acute and chronic renal failure, and is treated effectively by dialysis.

Institutional address: Clinical Pathology Department National Institutes of Health Bethesda Maryland.

 

(REFERENCE 2 OF 20)

Rude RK

Magnesium metabolism and deficiency.

In: Endocrinol Metab Clin North Am (1993 Jun) 22(2):377-95

Magnesium is a prominent intracellular cation required for the function of hundreds of enzyme systems. Magnesium depletion is observed frequently in hospitalized patients and is usually secondary to renal or intestinal magnesium loss. Clinically, magnesium deficiency may present with neuromuscular hyperexcitability, hypocalcemia, hypokalemia, and cardiac arrhythmias. Magnesium therapy appears to improve survival in patients with myocardial infarction. The diagnosis of magnesium deficiency is usually made by a low-serum magnesium concentration, although the magnesium tolerance test may be more indicative of low magnesium states. In acutely ill patients, magnesium is usually give parenterally; oral magnesium may be given for long-term repletion.

Institutional address: Department of Medicine University of Southern California School of Medicine Los Angeles.

 

(REFERENCE 3 OF 20)

Wallach S

Availability of body magnesium during magnesium deficiency.

In: Magnesium (1988) 7(5-6):262-70

Extensive experimental and clinical studies in animals and humans during the past 25 years have yielded considerable data regarding the availability of internal magnesium (Mg) stores for the maintenance of extracellular and critical tissue concentrations of Mg during periods of Mg deprivation. The bulk of body Mg is present in bone and skeletal muscle, and it is these two sites that provide essentially all the available Mg. In the rat, approximately 15% of bone Mg (equivalent to 1.5 mmol/kg body weight) can be lost, whereas less than one tenth of that amount is available from skeletal muscle. In the human, up to 35% of bone Mg can be lost, but the mean loss in extant studies is 18% (equivalent to 1.2 mmol/kg body weight). In contrast to the rat, up to 40% of human skeletal-muscle Mg can be lost with an average loss of 15% (equivalent to 0.45 mmol/kg). In the human, the bone and skeletal-muscle Mg pools can provide an average of 1.7 mmol/kg body weight equivalent to 15% of total body Mg. Release of Mg from these stores appears to depend on the presence of hypomagnesemia which may also result in small, significant and potentially adverse Mg losses from certain vital organs such as the heart, kidney and brain. The liver and other organs appear not to lose Mg despite Mg deprivation although intracellular Mg shifts of importance cannot be ruled out. These data indicate that the body reserve to combat Mg depletion is not designed to protect the extracellular Mg pool and certain critical organs from Mg deficiency. A continuous optimal intake of Mg is needed for good nutrition and health.

Institutional address: Medical and Medical Research Services Veterans Administration Medical Center Bay Pines Fla.

 

(REFERENCE 4 OF 20)

Dyckner T Wester PO Widman L

Effects of peroral magnesium on plasma and skeletal muscle electrolytes in patients on long-term diuretic therapy.

In: Int J Cardiol (1988 Apr) 19(1):81-7

Twenty patients on long-term diuretic therapy for arterial hypertension and/or congestive heart failure were given a supplementary dose of 15 mmol magnesium aspartate hydrochloride per day for 6 months. Nineteen patients, fulfilling the same admission criteria as the treatment group, served as controls. The addition of magnesium aspartate hydrochloride resulted in a significant rise of the cellular potassium and magnesium content and in a significant decrease of both systolic and diastolic blood pressure. It is concluded that supplementation with magnesium aspartate hydrochloride may effectively prevent the diuretic induced disturbances of electrolyte balance.

Institutional address: Department of Internal Medicine University of Ume~a Sweden.

 

(REFERENCE 5 OF 20)

Dorup I Skajaa K Thybo NK

Oral magnesium supplementation restores the concentrations of magnesium, potassium and sodium-potassium pumps in skeletal muscle of patients receiving diuretic treatment.

In: J Intern Med (1993 Feb) 233(2):117-23

In 76 consecutive patients who had received diuretics for 1-17 years for arterial hypertension or congestive heart failure, muscle concentrations of magnesium, potassium, and sodium-potassium pumps were significantly reduced compared to 31 age- and sex-matched controls. Thirty-six patients with muscle magnesium and/or potassium below the control level received oral magnesium hydroxide supplement for 2-12 weeks (n = 20) or 26 weeks (n = 16). After short-term (2-12 weeks) magnesium supplementation muscle parameters were increased, but far from normalized. After magnesium supplementation for 26 weeks, the muscle concentrations of magnesium, potassium and sodium- potassium pumps were normalized in most cases. Oral magnesium supplementation may restore diuretic-induced disturbances in the concentrations of magnesium, potassium and sodium potassium pumps in skeletal muscle. A supplemental period of at least 6 months seems to be required before complete normalization can be expected.

Institutional address: Institute of Physiology University of Aarhus Denmark.

 

(REFERENCE 6 OF 20)

Schuette SA Lashner BA Janghorbani M

Bioavailability of magnesium diglycinate vs magnesium oxide in patients with ileal resection.

In: JPEN J Parenter Enteral Nutr (1994 Sep-Oct) 18(5):430-5

BACKGROUND: Patients who have undergone ileal resection are at risk for developing magnesium depletion/deficiency because of poor absorption and decreased intake as well as increased endogenous losses. Magnesium repletion is difficult to accomplish because of the cathartic action of most oral magnesium supplements at therapeutic doses. The results of in vitro and in situ studies show that magnesium diglycinate (chelate) represents a highly available form of magnesium that is absorbed in part as an intact dipeptide in the proximal small intestine. METHODS: We conducted a double-blind, randomized crossover trial with 12 patients who had ileal resections in order to compare the bioavailability of a 100-mg dose of 26Mg- labeled chelate with MgO in this patient population. RESULTS: For the patient group as a whole, 26Mg absorption was low but was not different for the two supplements (23.5% vs 22.8% for magnesium chelate and MgO, respectively). However, 26Mg absorption was substantially greater from the chelate (23.5% vs 11.8%; p < .05) in the four patients who showed the greatest impairment of magnesium absorption with MgO and was better tolerated by all patients. Peak isotope enrichment also occurred significantly earlier after 26Mg chelate than after 26MgO ingestion (mean difference 3.2 +/- 1.3 hours; p < .05), and the area under the enrichment vs time curve was greater after chelate ingestion (p < .05). CONCLUSIONS: Data from this study support the suggestion that some portion of magnesium diglycinate is absorbed intact, probably via a dipeptide transport pathway. Magnesium diglycinate may be a good alternative to commonly used magnesium supplements in patients with intestinal resection.

Institutional address: Department of Medicine University of Chicago IL.

 

(REFERENCE 7 OF 20)

Altura BM Zhang A Cheng TP Altura BT

Ethanol promotes rapid depletion of intracellular free Mg in cerebral vascular smooth muscle cells: possible relation to alcohol-induced behavioral and stroke-like effects.

In: Alcohol (1993 Nov-Dec) 10(6):563-6

The acute effects of ethanol on intracellular free magnesium ions ([Mg2+]i) in cultured canine cerebral vascular smooth muscle cells (VSMCs) were studied by digital imaging microscopy using the Mg2+ fluorescent probe mag-fura-2. In 0 mM ethanol, the basal level of [Mg2+]i was between 500-700 microM with a heterogeneous distribution within the cells; [Mg2+]i was greater in the perinuclear than in the peripheral region. Treatment of the cells with 10, 25, and 100 mM ethanol resulted in rapid (within 30 s) concentration-dependent reduction in [Mg2+]i; the greater the concentration and the greater the duration of acute exposure, the greater the fall in [Mg2+]i. Exposure of cerebral VSMCs to 100 mM ethanol resulted in a 57% reduction in [Mg2+]i (i.e., from 510 +/- 40 to 220 +/- 30 microM). These observations are consistent with the tenet that “binge drinking” of ethanol could result in cerebrovasospasm, ischemia, and rupture of cerebral blood vessels as a consequence of depletion of cerebral VSMC [Mg2+]i. Deficits in [Mg2+]i, O2, and nutrient delivery could account in part for some of the behavioral actions of alcohol.

Institutional address: Department of Physiology State University of New York Brooklyn 11203.

 

(REFERENCE 8 OF 20)

Gullestad L Dolva LO Soyland E Manger AT Falch D Kjekshus J

Oral magnesium supplementation improves metabolic variables and muscle strength in alcoholics.

In: Alcohol Clin Exp Res (1992 Oct) 16(5):986-90

Magnesium deficiency is common among chronic alcoholics, but the knowledge of oral magnesium supplementation to this group is limited. We, therefore, randomized 49 chronic alcoholics, moderate to heavy drinkers for at least 10 years to receive oral magnesium or placebo treatment for 6 weeks according to a double-blind protocol. Effects on metabolic variables and muscle strength were analyzed. Significant reduction of aspartate-aminotransferase (ASAT), alanine- aminotransferase (ALAT) and gamma-glutamyl-transpeptidase (GGT) were seen after magnesium, whereas no change was observed with placebo. Bilirubin decreased in both groups. Serum Na, Ca, and P increased significantly during magnesium therapy compared with no statistically significant change in the placebo group. Serum K and Mg increased slightly after magnesium supplementation and decreased in the placebo group, resulting in a significant difference between the two groups at the end of the study. Muscle strength increased significantly during magnesium treatment, contrasting to no change with placebo. Blood pressure, heart rate, hematological variables, serum lipids (cholesterol, HDL, TG), glucose tolerance, and creatinine were unchanged in the two groups after treatment. Alcohol consumption was similar before and during the trial and does not explain the differences between the two groups The results shows that short-term oral magnesium therapy may improve liver cell function, electrolyte status, and muscle strength in chronic alcoholics.

Institutional address: Department of Internal Medicine Baerum Hospital Sandvika Norway.

 

(REFERENCE 9 OF 20)

Barbagallo M Resnick LM

The role of glucose in diabetic hypertension: effects on intracellular cation metabolism.

In: Am J Med Sci (1994 Feb) 307 Suppl 1:S60-5

The clinical association of hypertension, obesity, noninsulin- dependent diabetes mellitus (NIDDM), and other cardiovascular risk factors has long been recognized. The recent finding that essential hypertension is also an insulin-resistant state associated with hyperinsulinemia led some authors to attribute a role in mediating this association and in the pathogenesis of hypertension itself to insulin. However, evidence also exists independently of insulin per se that alterations in glucose metabolism in general, and of hyperglycemia in particular, may also contribute to the hypertensive process, especially in the hypertension of diabetes. The authors attempted to understand the relationship between glucose and insulin metabolism, diabetes, and hypertension from a cellular ionic point of view. In vitro it was shown that glucose, in a specific, dose- and time-dependent manner, can directly and coordinately alter intracellular ions, increasing cytosolic free calcium, while suppressing intracellular free magnesium and pH levels. These glucose- induced changes exactly parallel those ionic lesions previously observed in vivo in the fasting hyperglycemia of hypertension associated with NIDDM. These and other data led to the hypothesis that circulating blood glucose, independently of insulin and even at normal levels, is a physiologic determinant of cellular ion homeostasis. Furthermore, the cellular ionic consequences of hyperglycemia may contribute to the increased risk of hypertension and vascular diseases present among subjects with NIDDM, impaired glucose tolerance, or both.

Institutional address: Cardiovascular Center New York Hospital-Cornell Medical Center New York.

 

(REFERENCE 10 OF 20)

Lefebvre PJ Paolisso G Scheen AJ

Magnesium and glucose metabolism

In: Therapie (1994 Jan-Feb) 49(1):1-7 (Published in French)

The interrelationships between magnesium and carbohydrate metabolism have regained considerable interest over the last few years. Insulin secretion requires magnesium: magnesium deficiency results in impaired insulin secretion while magnesium replacement restores insulin secretion. Furthermore, experimental magnesium deficiency reduces the tissues sensitivity to insulin. Subclinical magnesium deficiency is common in diabetes. It results from both insufficient magnesium intakes and increase magnesium losses, particularly in the urine. In type 2, or non-insulin-dependent, diabetes mellitus, magnesium deficiency seems to be associated with insulin resistance. Furthermore, it may participate in the pathogenesis of diabetes complications and may contribute to the increased risk of sudden death associated with diabetes. Some studies suggest that magnesium deficiency may play a role in spontaneous abortion of diabetic women, in fetal malformations and in the pathogenesis of neonatal hypocalcemia of the infants of diabetic mothers. Administration of magnesium salts to patients with type 2 diabetes tend to reduce insulin resistance. Long-term studies are needed before recommending systematic magnesium supplementation to type 2 diabetic patients with subclinical magnesium deficiency.

Institutional address: Departement de Medecine Universite de Liege Belgique.

 

(REFERENCE 11 OF 20)

Rude RK

Physiology of magnesium metabolism and the important role of magnesium in potassium deficiency.

In: Am J Cardiol (1989 Apr 18) 63(14):31G-34G

Magnesium, the second most abundant intracellular cation, has several critically important roles in the body. In addition to energy production and maintaining electrolyte balance, magnesium is essential for normal neuromuscular function as well as calcium and potassium transport. Evidence suggests that a deficit of magnesium is closely interrelated to potassium deficiency and refractory potassium repletion. Although the consequences of hypokalemia are widely documented and recognized, it is only recently that the importance of magnesium deficiency as a cause of potassium depletion has gained clinical attention. Because of the association between hypokalemia and ventricular ectopy/sudden death, familiarity with the causes of magnesium loss, as well as enhanced identification and treatment, appear to be important.

Institutional address: University of Southern California School of Medicine Los Angeles 90033.

 

(REFERENCE 12 OF 20)

Dorup I Skajaa K Clausen T Kjeldsen K

Reduced concentrations of potassium, magnesium, and sodium-potassium pumps in human skeletal muscle during treatment with diuretics.

In: Br Med J (Clin Res Ed) (1988 Feb 13) 296(6620):455-8

Animal studies have shown that potassium depletion induced by diuretics or potassium deficient fodder leads to a selective decrease in the concentrations of potassium and in the concentration of sodium- potassium pumps in skeletal muscle. In 25 patients who had received diuretics for 2-14 years the mean concentrations of potassium, magnesium, and sodium-potassium pumps were measured in skeletal muscle biopsy specimens and were significantly lower than in those from a group of age matched controls. The reductions in all three variables were significant in those patients receiving diuretics for arterial hypertension as well as in those being treated for congestive heart failure. In 14 patients the mean muscle potassium concentration was below the control range, but only one of those was hypokalaemic (3.4 mmol/l), and 13 were receiving potassium supplements. In 15 patients the mean muscle magnesium concentration was below normal, and the mean muscle potassium and magnesium concentrations showed a linear correlation. In 12 patients in whom the mean muscle potassium concentration was below 80 mumol/g wet weight there was a linear correlation between the cellular potassium:sodium ratio and the concentration of 3H-ouabain binding sites indicating that potassium deficiency also leads to a down regulation of sodium-potassium pumps in human skeletal muscle. In spite of potassium supplements long term treatment with diuretics may lead to potassium and magnesium deficiencies, which are not detectable using the standard methods of serum analysis. The changes in concentrations of electrolytes and sodium-potassium pumps associated with treatment with diuretics may impair muscle function and potassium homoeostasis and interfere with the distribution of digitalis glycosides.

Institutional address: Department of Internal Medicine Odder Hospital Denmark.

 

(REFERENCE 13 OF 20)

Wu F Altura BT Gao J Barbour RL Altura BM

Ferrylmyoglobin formation induced by acute magnesium deficiency in perfused rat heart causes cardiac failure.

In: Biochim Biophys Acta (1994 Jan 11) 1225(2):158-64

The oxidation states of intracellular myoglobin and cytochrome oxidase aa3 were monitored by reflectance spectrophotometry in isolated perfused rat hearts subjected to an acutely magnesium deficient environment. After exposure to low extracellular [Mg2+]o (i.e., 0.3 mM) for 30 min, more than 80% of the oxymyoglobin converted to its deoxygenated form. The level of reduced cytochrome oxidase aa3 also increased about 80% in low [Mg2+]o. The deoxymyoglobin was converted further to a species identified as ferrylmyoglobin by its reaction with Na2S to form ferrous sulfmyoglobin which was optically visible. This process, set into motion by acute Mg deficiency, resulted from a direct accessibility of the exogenous peroxide to the cytosolic protein. The results suggest that a pathway leading to cardiac tissue damage, induced by magnesium deficiency, is probably involved in the generation of a ferrylmyoglobin radical which could be prevented by addition of ascorbate, which is known to be a one-electron reductant of this hypervalent form of myoglobin. In further studies, we also investigated whether addition of different concentrations of ascorbic acid (AA) to the perfusate could enhance myocardial function after exposure to low [Mg2+]o perfusion. Four concentrations of AA (0.5, 1, 5, 10 mM) were tested, and the results indicate that they exert their effects in a concentration-dependent manner; 1 mM AA was the most effective dose in improving aortic output in a Mg-deficient heart. Ferrylmyoglobin formation was found to be formed considerably before intracellular release of either creatine phosphokinase or lactic dehydrogenase. These studies may have wide implications as a new mechanism by which low extracellular Mg2+ can induce myocardial injury and subsequent cardiac failure.

Institutional address: Department of Physiology State University of New York Health Science Center at Brooklyn 11203.

 

(REFERENCE 14 OF 20)

Taubert K

Magnesium in migraine. Results of a multicenter pilot study

In: Fortschr Med (1994 Aug 30) 112(24):328-30 (Published in German)

BACKGROUND: Numerous experiments and clinical observations have credited magnesium with a positive influence on the incidence of migraine attacks. METHODS: With the aim of testing this hypothesis, a doubleblind, cross-over multicenter pilot study was initiated. The study contained 43 migraine patients who met the criteria of the international Headache Society. INTERVENTIONS: Administration of 600 mg magnesium/day in the form of trimagnesium dicitrate for prophylaxis. RESULTS: Under this medication, a significant reduction in the incidence of migraine attacks was observed. Although the level of effectiveness of the regimen does not appear to be as high as that of presently approved migraine prophylactic substances, a very low rate of side effects can be expected. CONCLUSION: The working hypothesis to the effect that magnesium may be useful in the prevention of migraine attacks has been confirmed by the pilot study. Further studies aimed at determining dosage and enabling a further differentiation of patient material are in preparation.

Institutional address: Klinikum Neubrandenburg.

 

(REFERENCE 15 OF 20)

Singh RB Rastogi SS Sharma VK Saharia RB Kulshretha SK

Can dietary magnesium modulate lipoprotein metabolism?

In: Magnes Trace Elem (1990) 9(5):255-64

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.

Institutional address: Medical Hospital and Research Center Moradabad India.

 

(REFERENCE 16 OF 20)

Toninello A Di Lisa F Siliprandi D Siliprandi N

On the mechanism of citrate and isocitrate protective action on rat liver mitochondria.

In: Biochem Biophys Res Commun (1983 Sep 15) 115(2):749-55

Both citrate and isocitrate prevent the damage (efflux of endogenous Mg2+ and pyridine nucleotides, decay of delta psi and release of accumulated Ca2+) induced in rat liver mitochondria by Ca2+ and phosphate fluxes. Addition of fluorocitrate suppresses the action of isocitrate, but not that of citrate. The same results have been obtained with mitochondria isolated from animals treated with fluoroacetate. It is suggested that citrate directly and isocitrate by prior conversion into citrate exert the protective action by chelating and retaining Mg2+ within the mitochondria.

 

(REFERENCE 17 OF 20)

Lindberg J Harvey J Pak CY

Effect of magnesium citrate and magnesium oxide on the crystallization of calcium salts in urine: changes produced by food- magnesium interaction.

In: J Urol (1990 Feb) 143(2):248-51

The effect of magnesium citrate and magnesium oxide on urinary biochemistry and on the crystallization of calcium salts was examined in 7 normal subjects and 4 patients with recurrent calcium oxalate nephrolithiasis. When magnesium citrate or magnesium oxide was administered on an empty stomach (10 mEq. 4 times per day or 486 mg. magnesium per day for 2 weeks) urinary magnesium increased by only 77 to 79 mg. per day and urinary citrate increased by 98 to 142 mg. per day. However, urinary calcium increased by 21 to 25 mg. per day. No significant changes were noted in urinary saturation of calcium oxalate or brushite or in the limit of metastability (formation product) of these salts. However, when magnesium salts were provided with meals there were more prominent increases in urinary magnesium (by 92 to 96 mg. per day) and in citrate (by 218 to 226 mg. per day). Moreover, urinary oxalate decreased. Owing to these changes the urinary saturation of calcium oxalate decreased and the formation product increased. If magnesium citrate and magnesium oxide are to be used in the management of recurrent calcium oxalate nephrolithiasis, they should be administered with meals.

Institutional address: Southwestern Medical School University of Texas Southwestern Medical Center Dallas.

 

(REFERENCE 18 OF 20)

Dhingra S Solven F Wilson A McCarthy DS

Hypomagnesemia and respiratory muscle power.

In: Am Rev Respir Dis (1984 Mar) 129(3):497-8

Although hypomagnesemia is common and causes weakness in humans, it is not known what effect its correction has on respiratory muscle power. We designed an experiment to test the hypothesis that correction of hypomagnesemia will improve respiratory muscle power. We measured muscle power and lung volumes in 16 control subjects and 17 patients (11 alcoholics, 6 nonalcoholics) on 3 consecutive days. After baseline measurements on Day 1, patients were randomized and the study was double blinded. Patients were given magnesium intravenously or dextrose as placebo. Measurements were repeated on Day 2, and the patients were then given magnesium if they had previously been given placebo, and vice versa. Measurements were done again on Day 3. There was no significant difference in lung volumes in patients or control subjects over the 3 days. There were no changes in respiratory muscle power in control subjects, but there was an improvement in all parameters of muscle power measured after magnesium therapy in patients. Hypomagnesemia should be excluded as a cause of muscle weakness because its replacement may improve muscle power.

 

(REFERENCE 19 OF 20)

Rock E Astier C Lab C Vignon X Gueux E Motta C Rayssiguier Y

Dietary magnesium deficiency in rats enhances free radical production in skeletal muscle.

In: J Nutr (1995 May) 125(5):1205-10

Recent studies suggest that free radicals may be involved in tissue injuries induced by magnesium deficiency. The aim of the present study was to assess the effect of magnesium deficiency on free radical production of skeletal muscle tissue. Male Wistar rats were pair-fed from weaning for 12 d either control or Mg-deficient diets containing 960 or 40 mg magnesium/kg diet, respectively. In the Mg- deficient rats, hypomagnesemia was accompanied by significantly lower magnesium and greater calcium concentrations in skeletal muscle tissue. Electron microscopy of skeletal muscle tissue revealed ultrastructural changes, including swelling mitochondria and disorganization of the sarcoplasmic reticulum network. Using the spin- trapping technique, we showed that significantly more hydroxyl radicals were generated in muscle homogenates of Mg-deficient rats. Moreover, the amount of spin trap adducts was increased in the presence of exogenous iron in both groups. In agreement with these observations, a greater concentration of thiobarbituric acid-reactive substances and a lower concentration of thiol groups were found in skeletal muscle of the Mg-deficient group compared with controls. These results strongly support the hypothesis that free radical- mediated injury could contribute to skeletal muscle lesions resulting from magnesium deficiency.

Institutional address: INRA Laboratoire des Maladies Metaboliques France.

(REFERENCE 20 OF 20)

Weglicki WB

Erythrocytes from magnesium-deficient hamsters display an enhanced susceptibility to oxidative stress.

In: Am J Physiol (1992 Jun) 262(6 Pt 1):C1371-5

Previous studies in our laboratory have indicated a role for free radical participation in magnesium deficiency cardiomyopathy. We have demonstrated the ability of various antioxidant drugs and nutrients to protect against magnesium deficiency-induced myocardial injury. In this study, we have examined erythrocytes from normal and magnesium- deficient animals and compared their susceptibility to an in vitro oxidative stress. Syrian male hamsters were placed on either magnesium-deficient or magnesium-supplemented diets. Animals from each group also received vitamin E in doses of 10 and 25 mg as subcutaneous implants. Erythrocytes obtained after 14 days on the diet were exposed to an exogenous hydroxyl (.OH) radical generating system (dihydroxyfumarate not equal to Fe3+ ADP) at 37 degrees C for 20 min. Erythrocyte crenation was observed and quantified by scanning electron microscopy. Lipid peroxidation, hemolysis (%), and intracellular glutathione levels were determined. In addition, serum lipid changes and membrane phospholipids were characterized. Our data demonstrate that erythrocytes from magnesium-deficient animals are more susceptible to free radical injury, supporting our hypothesis that magnesium deficiency reduces the threshold antioxidant capacity.

Institutional address: Department of Medicine George Washington University Medical Center Washington DC 20037.