Environ Health Perspect. 1994 Nov;102 Suppl 7:79-82.
Effects of boron supplementation on bone mineral density and dietary, blood, and urinary calcium, phosphorus, magnesium, and boron in female athletes.
Meacham SL, Taper LJ, Volpe SL.
Department of Human Nutrition, Winthrop University, Rock Hill, South Carolina 29733.

The effects of boron supplementation on blood and urinary minerals were studied in female college students--17 athletes and 11 sedentary controls--over a one-year period. The athletes had lower percent body fat and higher aerobic capacities than sedentary controls. Athletic subjects consumed more boron in their normal diets than sedentary subjects; all other dietary measures were similar between the two groups. The athletes showed a slight increase in bone mineral density, whereas the sedentary group showed a slight decrease. Serum phosphorus concentrations were lower in boron-supplemented subjects than in subjects receiving placebos, and were lower at the end of the study period than during baseline analysis. Activity depressed changes in serum phosphorus in boron-supplemented subjects. Serum magnesium concentrations were greatest in the sedentary controls whose diets were supplemented with boron, and increased with time in all subjects. A group x supplement interaction was observed with serum magnesium; exercise in boron-supplemented subjects lowered serum magnesium. In all subjects, calcium excretion increased over time; in boron-supplemented subjects, boron excretion increased over time. In all subjects, boron supplementation affected serum phosphorus and magnesium, and the excretion of urinary boron.         

Biol Trace Elem Res. 1992 Dec;35(3):225-37.
Studies of the interaction between boron and calcium, and its modification by magnesium and potassium, in rats. Effects on growth, blood variables, and bone mineral composition.
Nielsen FH, Shuler TR.
United States Department of Agriculture, Grand Forks Human Nutrition Research Center, ND 58202-7166.

Two experiments were performed to confirm that boron interacts with calcium, and that this interaction can be modified by dietary magnesium and potassium in the rat. Upon manipulating the dietary variables listed above, it was found that under certain conditions, boron and calcium deprivation similarly affected several variables; for example, they both could be made to elevate plasma alkaline phosphatase activity and to depress femur calcium concentration. Under some dietary conditions, both boron and calcium deprivation affected some variables related to blood or iron metabolism. However, the effects of dietary boron and calcium on spleen weight/body weight ratio, hematocrit, and femur iron concentration generally were not similar. Femur copper, magnesium, phosphorus, and zinc also were affected by an interaction between boron and calcium under some dietary conditions. The findings show that there is a relationship between boron and calcium, but they do not clearly indicate the nature of the relationship. However, the data suggest that boron and calcium act on similar systems in the rat.

Magnes Trace Elem. 1991-92;10(5-6):387-408.
Effects of dietary boron on calcium and mineral metabolism in the streptozotocin-injected, vitamin D3-deprived rat.
Hunt CD, Herbel JL.
USDA, Grand Forks Human Nutrition Research Center, N. Dak.

Dietary boron, in concentrations similar to that found in human diets comprised mainly of fruits and vegetables, affects both mineral and energy metabolism. Therefore, the effects of boron on a model system with a perturbed metabolic insulin-vitamin D3 axis was examined. Weanling male rats were fed a ground corn-high protein casein-corn oil-based diet (0.06 mg B/kg; no supplemental vitamin D3) supplemented with B (as orthoboric acid) at 0 or 2.4 mg/kg. After 55 days, all rats were equilibrated in individual metabolic cages for 6 days. After another 6 days, one half of the rats in both dietary groups were injected intraperitoneally with streptozotocin (STZ). All rats were killed 3 days after STZ treatment. STZ affected many aspects of mineral metabolism as expected. Plasma ionized calcium concentrations fell by approximately 10% in STZ-treated rats. Brain and heart mineral metabolism was spared from the toxic effects of STZ whereas spleen mineral metabolism was especially vulnerable to STZ. Supplemental dietary boron increased urinary excretion of calcium in the non-STZ rats but did not affect the plasma concentrations of alkaline phosphatase, ionized calcium or the concentration of calcium in the brains, lungs, kidneys and spleens of those animals. Supplemental dietary boron temporarily reduced the abnormally elevated renal excretion of albumin, potassium and sodium during the acute phase of diabetes mellitus. On the other hand, physiological amounts of dietary boron exacerbated the abnormally elevated rate of collagen breakdown in the STZ animal. Finally, boron may have indirectly affected heart mineral metabolism because dietary boron did not affect cardiac boron concentrations but did affect cardiac copper, calcium, manganese, molybdenum and phosphorus concentrations, primarily in non-STZ rats. The findings suggest that dietary boron has both protective and regulatory roles in mineral metabolism.      

MAGNESIUM

Magnes Res. 2004 Sep;17(3):197-210.
The alteration of magnesium, calcium and phosphorus metabolism by dietary magnesium deprivation in postmenopausal women is not affected by dietary boron deprivation.
Nielsen FH.
USDA, Agricultural Research Service, Grand Forks Human Nutrition Research Center, Grand Forks, ND, 58202-9034, USA.

A study with human volunteers was conducted to test the hypothesis that naturally occurring inadequate intakes of magnesium induce negative magnesium balance and undesirable changes in calcium metabolism variables, and that these changes are influenced by dietary boron. Diets composed of ordinary Western foods providing approximately 118 and 318 mg Mg/d and approximately 0.25 and 3.25 mg B/d were fed in a double-blind Latin square design to 13 healthy, post menopausal Caucasian women (aged 50-78 years) living in a metabolic unit. Magnesium balance, which was positive when dietary magnesium was 318 mg/d, became negative when dietary magnesium was 118 mg/d. Magnesium deprivation decreased urinary calcium excretion, and significantly increased calcium balance when balance data analyzed came from all collections during the 42-day periods. Urinary phosphorus excretion was increased, but fecal phosphorus excretion was decreased, thus phosphorus balance was not significantly affected by magnesium deprivation. Magnesium deprivation did not affect manganese or zinc balance. The balance data indicated that 700 mg of calcium, 1.0 mg of manganese, and 10 mg of zinc were adequate for post menopausal women. Magnesium deprivation increased serum 25-hydroxycholecalciferol and decreased serum total cholesterol concentrations. Boron deprivation increased but magnesium deprivation decreased urinary potassium excretion. Boron supplementation decreased serum 17beta-estradiol and progesterone when dietary magnesium was low. The dietary treatments did not affect serum calcitonin, parathyroid hormone, osteocalcin or alkaline phosphatase concentrations. One woman placed on consecutive magnesium-low dietary periods exhibited heart ventricular ectopy after consuming the magnesium-low diet for 72 days; the ectopy disappeared upon consuming the magnesium-adequate diet. The findings indicated that consuming an ordinary diet deficient in magnesium, resulting in negative magnesium balance, can affect calcium, potassium, and cholesterol metabolism. Dietary boron did not have an obvious effect on the response to magnesium deprivation.

West J Med. 1990 Feb;152(2):145-8.

Low intracellular magnesium in patients with acute pancreatitis and hypocalcemia.
Ryzen E, Rude RK.
Department of Medicine, Los Angeles County-University of Southern California Medical Center.

To determine the role of magnesium deficiency in the pathogenesis of hypocalcemia in acute pancreatitis, we measured magnesium levels in serum and in peripheral blood mononuclear cells in 29 patients with acute pancreatitis, 14 of whom had hypocalcemia and 15 of whom had normal calcium levels. Only six patients had overt hypomagnesemia (serum magnesium < 0.70 mmol per liter [I. 7 mg per dl]). The mean serum magnesium concentration in hypocalcemic patients was not significantly lower than in normocalcemic patients, but the mononuclear cell magnesium content in hypocalcemic patients with pancreatitis was significantly lower than in normocalcemic patients with pancreatitis (P < .Of). The serum magnesium level did not correlate with that of serum calcium or the mononuclear cell magnesium content, but the latter did significantly correlate with the serum calcium concentration (r = .8l, P < .001). Most patients with hypocalcemia had a low intracellular magnesium content. Three normomagnesemic, hypocalcemic patients with alcoholic pancreatitis also underwent low-dose parenteral magnesium tolerance testing and showed increased retention of the magnesium load. We conclude that patients with acute pancreatitis and hypocalcemia commonly have magnesium deficiency despite normal serum magnesium concentrations. Magnesium deficiency may play a significant role in the pathogenesis of hypocalcemia in patients with acute pancreatitis.

J Am Coll Nutr. 1990 Apr;9(2):114-9.
Effect of intravenous epinephrine on serum magnesium and free intracellular red blood cell magnesium concentrations measured by nuclear magnetic resonance.
Ryzen E, Servis KL, Rude RK.
Department of Internal Medicine, University of Southern California, Los Angeles.

Hypomagnesemia is a common clinical finding in hospitalized patients and can cause hypocalcemia, cardiac arrhythmias, muscular weakness, and hypokalemia. Hypomagnesemia usually implies cellular magnesium (Mg) depletion, but stress and some clinical conditions which raise serum catecholamine concentrations may lower serum Mg (sMg) concentrations. To help investigate the mechanism and degree of the effect of catecholamines on sMg concentration, we gave intravenous epinephrine (0.1 microgram/kg/min) to 12 normal volunteers for 2 hours. The sMg concentration fell from 1.86 +/- 0.04 mg/dl to 1.63 +/- 0.05 mg/dl (mean +/- SEM, p less than 0.01). Pre-infusion intracellular free Mg (Mg++) in red blood cells (RBC) as measured by nuclear magnetic resonance spectrophotometry (NMR) was 171 +/- 7.6 microM and did not differ significantly from post-infusion RBC Mg++, 186 +/- 12.6 microM. Total blood mononuclear cell Mg content and urine Mg excretion also did not change. These data suggest that epinephrine has a small but significant effect on the lowering of sMg concentrations. Endogenous catecholamine release during stress or acute illness may therefore contribute to the hypomagnesemia seen in acutely ill patients. Our data also suggest that hypomagnesemia seen under conditions of acute stress may not always imply depleted tissue Mg stores. As no absolute change in cellular Mg or in urinary Mg excretion was demonstrated, acute intracellular shifts of Mg into blood cells and/or urinary Mg losses may not account for the hypomagnesemia. The prevalence and clinical consequences of stress hypomagnesemia require further investigation.

Eur J Clin Nutr. 2004 Feb;58(2):270-6.     ---

Influence of a mineral water rich in calcium, magnesium and bicarbonate on urine composition and the risk of calcium oxalate crystallization.
Siener R, Jahnen A, Hesse A.
Division of Experimental Urology, Department of Urology, University of Bonn, Bonn, Germany.

OBJECTIVE: To evaluate the effect of a mineral water rich in magnesium (337 mg/l), calcium (232 mg/l) and bicarbonate (3388 mg/l) on urine composition and the risk of calcium oxalate crystallization. DESIGN: A total of 12 healthy male volunteers participated in the study. During the baseline phase, subjects collected two 24-h urine samples while on their usual diet. Throughout the control and test phases, lasting 5 days each, the subjects received a standardized diet calculated according to the recommendations. During the control phase, subjects consumed 1.4 l/day of a neutral fruit tea, which was replaced by an equal volume of a mineral water during the test phase. On the follow-up phase, subjects continued to drink 1.4 l/day of the mineral water on their usual diet and collected 24-h urine samples weekly. RESULTS: During the intake of mineral water, urinary pH, magnesium and citrate excretion increased significantly on both standardized and normal dietary conditions. The mineral water led to a significant increase in urinary calcium excretion only on the standardized diet, and to a significantly higher urinary volume and decreased supersaturation with calcium oxalate only on the usual diet. CONCLUSIONS: The magnesium and bicarbonate content of the mineral water resulted in favorable changes in urinary pH, magnesium and citrate excretion, inhibitors of calcium oxalate stone formation, counterbalancing increased calcium excretion. Since urinary oxalate excretion did not diminish, further studies are necessary to evaluate whether the ingestion of calcium-rich mineral water with, rather than between, meals may complex oxalate in the gut thus limiting intestinal absorption and urinary excretion of calcium and oxalate.   

J Intensive Care Med. 2005 Jan-Feb;20(1):3-17.

Magnesium deficiency in critical illness.
Tong GM, Rude RK.
University of Southern California, School of Medicine, Los Angeles, CA 90089-9317, USA.

Magnesium (Mg) deficiency commonly occurs in critical illness and correlates with a higher mortality and worse clinical outcome in the intensive care unit (ICU). Magnesium has been directly implicated in hypokalemia, hypocalcemia, tetany, and dysrhythmia. Moreover, Mg may play a role in acute coronary syndromes, acute cerebral ischemia, and asthma. Magnesium regulates hundreds of enzyme systems. By regulating enzymes controlling intracellular calcium, Mg affects smooth muscle vasoconstriction, important to the underlying pathophysiology of several critical illnesses. The principle causes of Mg deficiency are gastrointestinal and renal losses; however, the diagnosis is difficult to make because of the limitations of serum Mg levels, the most common assessment of Mg status. Magnesium tolerance testing and ionized Mg2+ are alternative laboratory assessments; however, each has its own difficulties in the ICU setting. The use of Mg therapy is supported by clinical trials in the treatment of symptomatic hypomagnesemia and preeclampsia and is recommended for torsade de pointes. Magnesium therapy is not supported in the treatment of acute myocardial infarction and is presently undergoing evaluation for the treatment of severe asthma exacerbation, for the prevention of post-coronary bypass grafting dysrhythmias, and as a neuroprotective agent in acute cerebral ischemia

Ann Acad Med Stetin. 1997;43:225-38.
[Behavior of selected bio-elements in women with osteoporosis]
Kotkowiak L.                             [Article in Polish]
Z Zakladu Medycyny Rodzinnej Pomorskiej Akademii Medycznej w Szczecinie, Szczecin.

The purpose of this study was to evaluate the concentration of calcium, magnesium, zinc and copper in serum, urine and hair in women with osteoporosis, and to find out whether deficiency of these bioelements correlates with BMD. The concentration of calcium, magnesium, zinc and copper was assessed in 80 women aged 40-68 years. The women had been menopausal for 9.3 years and had never undergone hormone replacement, drugs therapy or mineral supplementation. The bone mass density (BMD) in lumbar spine L2-L4 was measured in 80 postmenopausal women using dual energy X-ray absorptiometry. According to BMD values all women were divided into two groups. The first group (50 persons) comprised women with osteoporosis. The second group included 30 women without osteoporosis. After an overnight fasting the levels of calcium, magnesium, zinc and copper in serum, in urine and in hair were measured by AAS. Concentration of osteocalcin and ionized calcium as well as magnesium was also measured in serum. Calcium, magnesium, zinc and copper excretions were expressed as a ratio of urinary creatine. Data were compared with Wilcoxon-Mann-Whitney's test and significance was assessed at p < 0.05. The regression and correlation analysis was performed between BMD and level of bioelements. It was determined that the mean serum osteocalcin in the examined group (2.067 ng/ml) was higher than in the control group (1.602 ng/ml). It was also disclosed that there was a lower level of total (Tab. 1) and ionized magnesium in serum (Tab. 2) and reduced excretion of this element in urine (Tab. 4) of fasting women with osteoporosis. The concentrations of calcium, zinc and copper in serum (Tab. 1) and in urine (Tab. 4) in both groups were similar to laboratory normal range. Hair calcium and magnesium levels in examined group were lower in comparison with the control group (Tab. 3). Concentrations of zinc and copper in hair were similar in both groups (Tab. 3). The study found out that women with osteoporosis displayed magnesium deficiency. The results showed that highly significant correlation existed between magnesium and calcium. No significant relationship between BMD and the concentration of bioelements was observed.

Intern Med. 2004 May;43(5):410-4.
Depressive state and paresthesia dramatically improved by intravenous MgSO4 in Gitelman's syndrome.
Enya M, Kanoh Y, Mune T, Ishizawa M, Sarui H, Yamamoto M, Takeda N, Yasuda K, Yasujima M, Tsutaya S, Takeda J.
Third Department of Internal Medicine, Gifu University School of Medicine, 40 Tsukasa-machi, Gifu 500-8705.

A 69-year-old woman was referred to our department for evaluation of hypokalemia, which had been treated by oral potassium for more than ten years. She complained of headache, knee joint pain, sleeplessness and paresthesia in extremities and, most prominently, depression. Laboratory data suggested Gitelman's syndrome, which is caused by mutations in the gene encoding the thiazide-sensitive Na-Cl cotransporter. Direct sequencing of the gene in this patient revealed homozygous mutation R964Q in exon 25. Intravenous supplement of MgSO4 dramatically improved both the depression and the paresthesia, suggesting that hypomagnesemia played a role in the clinical manifestations.

Arch Intern Med. 1988 Aug;148(8):1801-5.
The effect of intravenous magnesium therapy on serum and urine levels of potassium, calcium, and sodium in patients with ischemic heart disease, with and without acute myocardial infarction.
Rasmussen HS, Cintin C, Aurup P, Breum L, McNair P.
Medical Department P/Chest Clinic, Bispebjerg Hospital.

Serum concentrations of magnesium, potassium, calcium, and sodium were determined on admission of 224 patients to the hospital and after 2, 4, and 6 days in hospital; all were admitted to the hospital with suspected acute myocardial infarction (AMI). On admission, the patients were randomly allocated to 48 hours of treatment with magnesium intravenously or placebo. One hundred twenty-three patients had AMI (of whom 53 [43%] were treated with magnesium) and 101 had their suspected AMI disproven (of whom 51 [50%] were treated with magnesium). In a supplementary study, serum and urine levels of magnesium, potassium, calcium, and sodium, together with serum levels of parathyroid hormone, were determined before and after intravenous magnesium treatment in six patients with AMI and six patients with ischemic heart disease but without AMI. In both studies, magnesium therapy was associated with significant alterations in extracellular ion homeostasis. Serum concentrations of potassium decreased during the initial days of hospitalization in the patients treated with placebo, but increased slightly in the patients treated with magnesium infusions. These increments in the serum concentrations of magnesium and potassium correlated significantly. The increase in the serum concentration of potassium after magnesium infusions was due to a reduced renal potassium excretion level (from 71.3 to 49.4 mmol/24 h), indicating the existence of a divalent-monovalent cation exchange mechanism in the nephron. This hypothesis was supported by the observation that renal sodium excretion likewise decreased after magnesium infusions (from 83.2 to 59.2 mmol/24 h). Serum concentration of calcium decreased significantly after magnesium treatment (from 2.35 mmol/L on admission to 2.15 mmol/L after 24 hours in the hospital) in the AMI group, in contrast to the placebo-treated patients, where no significant fluctuations in serum concentration of calcium were detected during the initial six days. This decrease in serum concentration of calcium was due to a marked increase in renal calcium excretion (from 3.43 mmol/24 h before to 6.59 mmol/24 h after magnesium infusion). A correlation between increments in serum magnesium concentration and decrements in serum calcium concentration was detected. No change in serum levels of parathyroid hormone was found before and after magnesium infusions. Both serum and urine levels of magnesium significantly increased after magnesium treatment to levels above the upper normal limits (serum magnesium concentration increased from 0.81 to 1.21 mmol/L, urine magnesium excretion levels from 3.57 to 16.57 mmol/24 h for both serum and urine changes.(

Clin Endocrinol (Oxf). 1976 May;5(3):209-24.
Functional hypoparathyroidism and parathyroid hormone end-organ resistance in human magnesium deficiency.
Rude RK, Oldham SB, Singer FR.

Hypocalcaemia is a well-recognized manifestation of magnesium deficiency. We have studied seventeen patients with this syndrome in an attempt to determine the pathogenesis of the hypocalcaemia. Mean initial serum calcium concentration was 5-6 mg/dl and mean initial serum magnesium concentration was 0-75 mg/dl. Serum immunoreactive parathyroid hormone (IPTH) was measured in sixteen patients in the untreated state. Despite severe hypocalcaemia, serum IPTH was either undetectable (less than 150 pg/ml) or normal (less than 550 pg/ml) in all but two patients. Serial measurements made during the initial 4 days of magnesium therapy in four patients showed an increase in serum IPTH within 24h, but a delayed increase in serum calcium, which required approximately 4 days to reach normal values. The effect of the rapid normalization of serum magnesium on serum IPTH and serum calcium concentration was studied in three patients. Within 1 min after 144-300 mg of elemental magnesium was administered i.v., serum IPTH had risen from undetectable to 3600 pg/ml and 1725 pg/ml in two patients and from 425 pg/ml to 937 pg/ml in the third. Serum calcium concentrations were unchanged after 30-60 min. These data provide evidence for impaired parathyroid gland function in most of the magnesium deficient patients. The rapidity with which serum IPTH rose in response to magnesium therapy indicates that this may reflect a defect in parathyroid hormone (PTH) secretion rather than its biosynthesis. The failure of serum calcium concentration to increase during the initial days of magnesium repletion, at a time when serum IPTH concentrations were normal or elevated, suggests end-organ resistance to PTH in these patients. The renal response to PTH was examined in two magnesium deficient patients by measurement of urinary cyclic AMP excretion following administration of parathyroid extract. In both patients there was a minimal increase in urinary cyclic AMP concentrations. In contrast, when the hepatic response to glucagon was tested on the same patients by measurement of plasma cyclic AMP concentrations following administration of glucagon, normal increases were observed. These results suggest that adenylate cyclase systems of various organs may be affected differentially by a state of magnesium deficiency. It is suggested that magnesium deficiency may result in defective cyclic AMP generation in the parathyroid glands and in the PTH target organs. This could be the principal mechanism operative in both impaired PTH secretion and end-organ resistance

J Clin Endocrinol Metab. 1969 Jun;29(6):842-8.
Hypocalcemia due to hypomagnesemia and reversible parathyroid hormone unresponsiveness.
Estep H, Shaw WA, Watlington C, Hobe R, Holland W, Tucker SG.

Acta Med Scand Suppl. 1981;647:139-44.
Magnesium and potassium interrelationships, experimental and clinical.
Whang R, Oei TO, Aikawa JK, Ryan MP, Watanabe A, Chrysant SG, Fryer A.

1) Coexisting Mg and K deficiency may occur with greater frequency than has been previously appreciated. 2) Profound hypokalemia, or refractoriness to K repletion or coexisting hypokalemia and hypocalcemia should suggest the possibility of concurrent Mg and K depletion. 3) The identification and treatment of concurrent K and Mg depletion is especially important in patients with congestive heart failure because of problem of digitalis toxicity. 4) We believe that the role of magnesium in optimizing cardiac function remains to be elucidated, identification and treatment of coexisting Mg and K depletion will be facilitated by making serum Mg a routine electrolyte determination together with Na, K, Cl, CO2.

Arch Intern Med. 1988 Nov;148(11):2415-20.
Magnesium metabolism. A review with special reference to the relationship between intracellular content and serum levels.
Reinhart RA.
Marshfield Clinic, WI 54449.

Magnesium (Mg++) is a ubiquitous element in nature, playing a role in photosynthesis and many metabolic functions in humans. All enzymatic reactions that involve adenosine triphosphate have an absolute requirement for Mg++. Levels of Mg++ are controlled by the kidneys and gastrointestinal tract and appear closely linked to calcium, potassium, and sodium metabolism. The clinical manifestations and causes of abnormal Mg++ status are protean. Testing for altered Mg++ homeostasis is problematic. Serum levels, which are those generally measured, reflect only a small part of the total body content of Mg++. The intracellular content can be low, despite normal serum levels in a person with clinical Mg++ deficiency. Future directions in research related to intracellular content of Mg++ are discussed. Treatment of altered Mg++ status depends on the clinical setting and may include the addition of a potassium/Mg++-sparing drug to an existing diuretic regimen. Guidelines for therapy are given.

J Clin Endocrinol Metab. 1985 Nov;61(5):933-40.
Low serum concentrations of 1,25-dihydroxyvitamin D in human magnesium deficiency.
Rude RK, Adams JS, Ryzen E, Endres DB, Niimi H, Horst RL, Haddad JG Jr, Singer FR.

The effect of magnesium deficiency on vitamin D metabolism was assessed in 23 hypocalcemic magnesium-deficient patients by measuring the serum concentrations of 25-hydroxyvitamin D (25OHD) and 1,25-dihydroxyvitamin D [1,25-(OH)2D] before, during, and after 5-13 days of parenteral magnesium therapy. Magnesium therapy raised mean basal serum magnesium [1.0 +/- 0.1 (mean +/- SEM) mg/dl] and calcium levels (7.2 +/- 0.2 mg/dl) into the normal range (2.2 +/- 0.1 and 9.3 +/- 0.1 mg/dl, respectively; P less than 0.001). The mean serum 25OHD concentration was in the low normal range (13.2 +/- 1.5 ng/ml) before magnesium administration and did not significantly change after this therapy (14.8 +/- 1.5 ng/ml). Sixteen of the 23 patients had low serum 1,25-(OH)2D levels (less than 30 pg/ml). After magnesium therapy, only 5 of the patients had a rise in the serum 1,25-(OH)2D concentration into or above the normal range despite elevated levels of serum immunoreactive PTH. An additional normocalcemic hypomagnesemic patient had low 1,25-(OH)2D levels which did not rise after 5 days of magnesium therapy. The serum vitamin D-binding protein concentration, assessed in 11 patients, was low (273 +/- 86 micrograms/ml) before magnesium therapy, but normalized (346 +/- 86 micrograms/ml) after magnesium repletion. No correlation with serum 1,25-(OH)2D levels was found. The functional capacity of vitamin D-binding protein to bind hormone, assessed by the internalization of [3H]1,25-(OH)2D3 by intestinal epithelial cells in the presence of serum was not significantly different from normal (11.42 +/- 1.45 vs. 10.27 +/- 1.27 fmol/2 X 10(6) cells, respectively). These data show that serum 1,25-(OH)2D concentrations are frequently low in patients with magnesium deficiency and may remain low even after 5-13 days of parenteral magnesium administration. The data also suggest that a normal 1,25-(OH)2D level is not required for the PTH-mediated calcemic response to magnesium administration. We conclude that magnesium depletion may impair vitamin D metabolism.

Alcohol Clin Exp Res. 1992 Oct;16(5):986-90.
Oral magnesium supplementation improves metabolic variables and muscle strength in alcoholics.
Gullestad L, Dolva LO, Soyland E, Manger AT, Falch D, Kjekshus J.
Department of Internal Medicine, Baerum Hospital, Sandvika, Norway.

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.

Br J Nutr. 1996 Dec;76(6):821-3

The effect of long-term calcium supplementation on indices of iron, zinc and magnesium status in lactating Gambian women.

Yan L, Prentice A, Dibba B, Jarjou LM, Stirling DM, Fairweather-Tait S.

Medical Research Council Dunn Nutrition Unit, Cambridge, The Gambia.

The effect of long-term supplementation with CaCO3 on indices of Fe, Zn and Mg status was investigated in a randomized, double-blind intervention study of sixty lactating Gambian women. The supplement contained 1000 mg Ca and was consumed between meals 5 d/week, for 1 year starting 1.5 weeks postpartum. Compliance was 100%. Plasma ferritin concentration, plasma Zn concentration and urinary Mg output were measured before, during and after supplementation at 1.5, 13, 52 and 78 weeks postpartum. No significant differences in mineral status were observed at any time between women in the supplement and placebo groups. Analysis of the longitudinal data series showed that plasma ferritin and Mg excretion were characteristic of the individual (P < 0.001). Within individuals, ferritin concentration was higher at 1.5 weeks postpartum than later in lactation (P = 0.002). Plasma Zn concentration was lower at 1.5 weeks postpartum than at other times (P < 0.001), an effect which disappeared after albumin correction. Low plasma concentrations of ferritin and Zn indicated that the Gambian women were at high risk of Fe and Zn deficiency. Measurements of alpha 1-antichymotrypsin suggested that the results were not confounded by acute-phase responses. The results of the present study indicate that 1000 mg Ca as CaCO3 given between meals does not deleteriously affect plasma ferritin and Zn concentrations or urinary Mg excretion in women who are at risk of Fe and Zn deficiency.

PIP: During March 1990-March 1991, 60 lactating mothers were recruited into a randomized, placebo-controlled trial designed to examine the effect of calcium (Ca) supplementation on plasma zinc (Zn) and ferritin (Fe) concentrations and on magnesium (Mg) excretion during and after Ca supplementation. The women lived in Keneba and Manduar villages in rural Gambia. They consumed 1000 mg Ca or the placebo (2 tablets of dextrose) between meals 5 days/week for 12 months beginning 1-5 weeks postpartum. All women complied. At no time were there significant differences in the indices used to determine Zn, Fe, and Mg status between lactating women on Ca supplements and those receiving the placebo. In fact, the mean differences were less than 10% of the total value. Many women (33-50%), regardless of supplementation group, had a plasma Fe concentration lower than 12 mcg/l, indicating depleted Fe stores. Many women also had low plasma Zn levels. Within individuals, plasma Zn concentrations were 15% lower at day 9 than later in lactation (p 0.001), while plasma Fe levels were 10% higher (p = 0.002). Plasma Zn levels were associated with plasma albumin levels (p 0.001). When adjusted for albumin, the effect of lactation on Zn disappeared. When compared with British women, Gambian women had a lower plasma Zn concentration (p 0.001). Within individuals and after adjustment for lactation stage and for albumin, plasma Zn levels varied between seasons (i.e., hot season values higher than other seasons) (p = 0.004). Women were more likely to excrete Mg during the hot season (p 0.001). These findings indicate that ingestion of 1000 mg Ca between meals has no adverse effect on plasma Fe and Zn levels or urinary Mg excretion in women at risk of Zn and Fe deficiency.

West J Med. 1990 Feb;152(2):145-8.

Low intracellular magnesium in patients with acute pancreatitis and hypocalcemia.
Ryzen E, Rude RK.
Department of Medicine, Los Angeles County-University of Southern California Medical Center.

To determine the role of magnesium deficiency in the pathogenesis of hypocalcemia in acute pancreatitis, we measured magnesium levels in serum and in peripheral blood mononuclear cells in 29 patients with acute pancreatitis, 14 of whom had hypocalcemia and 15 of whom had normal calcium levels. Only six patients had overt hypomagnesemia (serum magnesium < 0.70 mmol per liter [I. 7 mg per dl]). The mean serum magnesium concentration in hypocalcemic patients was not significantly lower than in normocalcemic patients, but the mononuclear cell magnesium content in hypocalcemic patients with pancreatitis was significantly lower than in normocalcemic patients with pancreatitis (P < .Of). The serum magnesium level did not correlate with that of serum calcium or the mononuclear cell magnesium content, but the latter did significantly correlate with the serum calcium concentration (r = .8l, P < .001). Most patients with hypocalcemia had a low intracellular magnesium content. Three normomagnesemic, hypocalcemic patients with alcoholic pancreatitis also underwent low-dose parenteral magnesium tolerance testing and showed increased retention of the magnesium load. We conclude that patients with acute pancreatitis and hypocalcemia commonly have magnesium deficiency despite normal serum magnesium concentrations. Magnesium deficiency may play a significant role in the pathogenesis of hypocalcemia in patients with acute pancreatitis.

J Am Coll Nutr. 1990 Apr;9(2):114-9.
Effect of intravenous epinephrine on serum magnesium and free intracellular red blood cell magnesium concentrations measured by nuclear magnetic resonance.
Ryzen E, Servis KL, Rude RK.
Department of Internal Medicine, University of Southern California, Los Angeles.

Hypomagnesemia is a common clinical finding in hospitalized patients and can cause hypocalcemia, cardiac arrhythmias, muscular weakness, and hypokalemia. Hypomagnesemia usually implies cellular magnesium (Mg) depletion, but stress and some clinical conditions which raise serum catecholamine concentrations may lower serum Mg (sMg) concentrations. To help investigate the mechanism and degree of the effect of catecholamines on sMg concentration, we gave intravenous epinephrine (0.1 microgram/kg/min) to 12 normal volunteers for 2 hours. The sMg concentration fell from 1.86 +/- 0.04 mg/dl to 1.63 +/- 0.05 mg/dl (mean +/- SEM, p less than 0.01). Pre-infusion intracellular free Mg (Mg++) in red blood cells (RBC) as measured by nuclear magnetic resonance spectrophotometry (NMR) was 171 +/- 7.6 microM and did not differ significantly from post-infusion RBC Mg++, 186 +/- 12.6 microM. Total blood mononuclear cell Mg content and urine Mg excretion also did not change. These data suggest that epinephrine has a small but significant effect on the lowering of sMg concentrations. Endogenous catecholamine release during stress or acute illness may therefore contribute to the hypomagnesemia seen in acutely ill patients. Our data also suggest that hypomagnesemia seen under conditions of acute stress may not always imply depleted tissue Mg stores. As no absolute change in cellular Mg or in urinary Mg excretion was demonstrated, acute intracellular shifts of Mg into blood cells and/or urinary Mg losses may not account for the hypomagnesemia. The prevalence and clinical consequences of stress hypomagnesemia require further investigation.

Eur J Clin Nutr. 2004 Feb;58(2):270-6.     ---

Influence of a mineral water rich in calcium, magnesium and bicarbonate on urine composition and the risk of calcium oxalate crystallization.
Siener R, Jahnen A, Hesse A.
Division of Experimental Urology, Department of Urology, University of Bonn, Bonn, Germany.

OBJECTIVE: To evaluate the effect of a mineral water rich in magnesium (337 mg/l), calcium (232 mg/l) and bicarbonate (3388 mg/l) on urine composition and the risk of calcium oxalate crystallization. DESIGN: A total of 12 healthy male volunteers participated in the study. During the baseline phase, subjects collected two 24-h urine samples while on their usual diet. Throughout the control and test phases, lasting 5 days each, the subjects received a standardized diet calculated according to the recommendations. During the control phase, subjects consumed 1.4 l/day of a neutral fruit tea, which was replaced by an equal volume of a mineral water during the test phase. On the follow-up phase, subjects continued to drink 1.4 l/day of the mineral water on their usual diet and collected 24-h urine samples weekly. RESULTS: During the intake of mineral water, urinary pH, magnesium and citrate excretion increased significantly on both standardized and normal dietary conditions. The mineral water led to a significant increase in urinary calcium excretion only on the standardized diet, and to a significantly higher urinary volume and decreased supersaturation with calcium oxalate only on the usual diet. CONCLUSIONS: The magnesium and bicarbonate content of the mineral water resulted in favorable changes in urinary pH, magnesium and citrate excretion, inhibitors of calcium oxalate stone formation, counterbalancing increased calcium excretion. Since urinary oxalate excretion did not diminish, further studies are necessary to evaluate whether the ingestion of calcium-rich mineral water with, rather than between, meals may complex oxalate in the gut thus limiting intestinal absorption and urinary excretion of calcium and oxalate.   

J Intensive Care Med. 2005 Jan-Feb;20(1):3-17.

Magnesium deficiency in critical illness.
Tong GM, Rude RK.
University of Southern California, School of Medicine, Los Angeles, CA 90089-9317, USA.

Magnesium (Mg) deficiency commonly occurs in critical illness and correlates with a higher mortality and worse clinical outcome in the intensive care unit (ICU). Magnesium has been directly implicated in hypokalemia, hypocalcemia, tetany, and dysrhythmia. Moreover, Mg may play a role in acute coronary syndromes, acute cerebral ischemia, and asthma. Magnesium regulates hundreds of enzyme systems. By regulating enzymes controlling intracellular calcium, Mg affects smooth muscle vasoconstriction, important to the underlying pathophysiology of several critical illnesses. The principle causes of Mg deficiency are gastrointestinal and renal losses; however, the diagnosis is difficult to make because of the limitations of serum Mg levels, the most common assessment of Mg status. Magnesium tolerance testing and ionized Mg2+ are alternative laboratory assessments; however, each has its own difficulties in the ICU setting. The use of Mg therapy is supported by clinical trials in the treatment of symptomatic hypomagnesemia and preeclampsia and is recommended for torsade de pointes. Magnesium therapy is not supported in the treatment of acute myocardial infarction and is presently undergoing evaluation for the treatment of severe asthma exacerbation, for the prevention of post-coronary bypass grafting dysrhythmias, and as a neuroprotective agent in acute cerebral ischemia

Ann Acad Med Stetin. 1997;43:225-38.
[Behavior of selected bio-elements in women with osteoporosis]
Kotkowiak L.                             [Article in Polish]
Z Zakladu Medycyny Rodzinnej Pomorskiej Akademii Medycznej w Szczecinie, Szczecin.

The purpose of this study was to evaluate the concentration of calcium, magnesium, zinc and copper in serum, urine and hair in women with osteoporosis, and to find out whether deficiency of these bioelements correlates with BMD. The concentration of calcium, magnesium, zinc and copper was assessed in 80 women aged 40-68 years. The women had been menopausal for 9.3 years and had never undergone hormone replacement, drugs therapy or mineral supplementation. The bone mass density (BMD) in lumbar spine L2-L4 was measured in 80 postmenopausal women using dual energy X-ray absorptiometry. According to BMD values all women were divided into two groups. The first group (50 persons) comprised women with osteoporosis. The second group included 30 women without osteoporosis. After an overnight fasting the levels of calcium, magnesium, zinc and copper in serum, in urine and in hair were measured by AAS. Concentration of osteocalcin and ionized calcium as well as magnesium was also measured in serum. Calcium, magnesium, zinc and copper excretions were expressed as a ratio of urinary creatine. Data were compared with Wilcoxon-Mann-Whitney's test and significance was assessed at p < 0.05. The regression and correlation analysis was performed between BMD and level of bioelements. It was determined that the mean serum osteocalcin in the examined group (2.067 ng/ml) was higher than in the control group (1.602 ng/ml). It was also disclosed that there was a lower level of total (Tab. 1) and ionized magnesium in serum (Tab. 2) and reduced excretion of this element in urine (Tab. 4) of fasting women with osteoporosis. The concentrations of calcium, zinc and copper in serum (Tab. 1) and in urine (Tab. 4) in both groups were similar to laboratory normal range. Hair calcium and magnesium levels in examined group were lower in comparison with the control group (Tab. 3). Concentrations of zinc and copper in hair were similar in both groups (Tab. 3). The study found out that women with osteoporosis displayed magnesium deficiency. The results showed that highly significant correlation existed between magnesium and calcium. No significant relationship between BMD and the concentration of bioelements was observed.

Intern Med. 2004 May;43(5):410-4.
Depressive state and paresthesia dramatically improved by intravenous MgSO4 in Gitelman's syndrome.
Enya M, Kanoh Y, Mune T, Ishizawa M, Sarui H, Yamamoto M, Takeda N, Yasuda K, Yasujima M, Tsutaya S, Takeda J.
Third Department of Internal Medicine, Gifu University School of Medicine, 40 Tsukasa-machi, Gifu 500-8705.

A 69-year-old woman was referred to our department for evaluation of hypokalemia, which had been treated by oral potassium for more than ten years. She complained of headache, knee joint pain, sleeplessness and paresthesia in extremities and, most prominently, depression. Laboratory data suggested Gitelman's syndrome, which is caused by mutations in the gene encoding the thiazide-sensitive Na-Cl cotransporter. Direct sequencing of the gene in this patient revealed homozygous mutation R964Q in exon 25. Intravenous supplement of MgSO4 dramatically improved both the depression and the paresthesia, suggesting that hypomagnesemia played a role in the clinical manifestations.

Arch Intern Med. 1988 Aug;148(8):1801-5.
The effect of intravenous magnesium therapy on serum and urine levels of potassium, calcium, and sodium in patients with ischemic heart disease, with and without acute myocardial infarction.
Rasmussen HS, Cintin C, Aurup P, Breum L, McNair P.
Medical Department P/Chest Clinic, Bispebjerg Hospital.

Serum concentrations of magnesium, potassium, calcium, and sodium were determined on admission of 224 patients to the hospital and after 2, 4, and 6 days in hospital; all were admitted to the hospital with suspected acute myocardial infarction (AMI). On admission, the patients were randomly allocated to 48 hours of treatment with magnesium intravenously or placebo. One hundred twenty-three patients had AMI (of whom 53 [43%] were treated with magnesium) and 101 had their suspected AMI disproven (of whom 51 [50%] were treated with magnesium). In a supplementary study, serum and urine levels of magnesium, potassium, calcium, and sodium, together with serum levels of parathyroid hormone, were determined before and after intravenous magnesium treatment in six patients with AMI and six patients with ischemic heart disease but without AMI. In both studies, magnesium therapy was associated with significant alterations in extracellular ion homeostasis. Serum concentrations of potassium decreased during the initial days of hospitalization in the patients treated with placebo, but increased slightly in the patients treated with magnesium infusions. These increments in the serum concentrations of magnesium and potassium correlated significantly. The increase in the serum concentration of potassium after magnesium infusions was due to a reduced renal potassium excretion level (from 71.3 to 49.4 mmol/24 h), indicating the existence of a divalent-monovalent cation exchange mechanism in the nephron. This hypothesis was supported by the observation that renal sodium excretion likewise decreased after magnesium infusions (from 83.2 to 59.2 mmol/24 h). Serum concentration of calcium decreased significantly after magnesium treatment (from 2.35 mmol/L on admission to 2.15 mmol/L after 24 hours in the hospital) in the AMI group, in contrast to the placebo-treated patients, where no significant fluctuations in serum concentration of calcium were detected during the initial six days. This decrease in serum concentration of calcium was due to a marked increase in renal calcium excretion (from 3.43 mmol/24 h before to 6.59 mmol/24 h after magnesium infusion). A correlation between increments in serum magnesium concentration and decrements in serum calcium concentration was detected. No change in serum levels of parathyroid hormone was found before and after magnesium infusions. Both serum and urine levels of magnesium significantly increased after magnesium treatment to levels above the upper normal limits (serum magnesium concentration increased from 0.81 to 1.21 mmol/L, urine magnesium excretion levels from 3.57 to 16.57 mmol/24 h for both serum and urine changes.(

Clin Endocrinol (Oxf). 1976 May;5(3):209-24.
Functional hypoparathyroidism and parathyroid hormone end-organ resistance in human magnesium deficiency.
Rude RK, Oldham SB, Singer FR.

Hypocalcaemia is a well-recognized manifestation of magnesium deficiency. We have studied seventeen patients with this syndrome in an attempt to determine the pathogenesis of the hypocalcaemia. Mean initial serum calcium concentration was 5-6 mg/dl and mean initial serum magnesium concentration was 0-75 mg/dl. Serum immunoreactive parathyroid hormone (IPTH) was measured in sixteen patients in the untreated state. Despite severe hypocalcaemia, serum IPTH was either undetectable (less than 150 pg/ml) or normal (less than 550 pg/ml) in all but two patients. Serial measurements made during the initial 4 days of magnesium therapy in four patients showed an increase in serum IPTH within 24h, but a delayed increase in serum calcium, which required approximately 4 days to reach normal values. The effect of the rapid normalization of serum magnesium on serum IPTH and serum calcium concentration was studied in three patients. Within 1 min after 144-300 mg of elemental magnesium was administered i.v., serum IPTH had risen from undetectable to 3600 pg/ml and 1725 pg/ml in two patients and from 425 pg/ml to 937 pg/ml in the third. Serum calcium concentrations were unchanged after 30-60 min. These data provide evidence for impaired parathyroid gland function in most of the magnesium deficient patients. The rapidity with which serum IPTH rose in response to magnesium therapy indicates that this may reflect a defect in parathyroid hormone (PTH) secretion rather than its biosynthesis. The failure of serum calcium concentration to increase during the initial days of magnesium repletion, at a time when serum IPTH concentrations were normal or elevated, suggests end-organ resistance to PTH in these patients. The renal response to PTH was examined in two magnesium deficient patients by measurement of urinary cyclic AMP excretion following administration of parathyroid extract. In both patients there was a minimal increase in urinary cyclic AMP concentrations. In contrast, when the hepatic response to glucagon was tested on the same patients by measurement of plasma cyclic AMP concentrations following administration of glucagon, normal increases were observed. These results suggest that adenylate cyclase systems of various organs may be affected differentially by a state of magnesium deficiency. It is suggested that magnesium deficiency may result in defective cyclic AMP generation in the parathyroid glands and in the PTH target organs. This could be the principal mechanism operative in both impaired PTH secretion and end-organ resistance

J Clin Endocrinol Metab. 1969 Jun;29(6):842-8.
Hypocalcemia due to hypomagnesemia and reversible parathyroid hormone unresponsiveness.
Estep H, Shaw WA, Watlington C, Hobe R, Holland W, Tucker SG.

Acta Med Scand Suppl. 1981;647:139-44.
Magnesium and potassium interrelationships, experimental and clinical.
Whang R, Oei TO, Aikawa JK, Ryan MP, Watanabe A, Chrysant SG, Fryer A.

1) Coexisting Mg and K deficiency may occur with greater frequency than has been previously appreciated. 2) Profound hypokalemia, or refractoriness to K repletion or coexisting hypokalemia and hypocalcemia should suggest the possibility of concurrent Mg and K depletion. 3) The identification and treatment of concurrent K and Mg depletion is especially important in patients with congestive heart failure because of problem of digitalis toxicity. 4) We believe that the role of magnesium in optimizing cardiac function remains to be elucidated, identification and treatment of coexisting Mg and K depletion will be facilitated by making serum Mg a routine electrolyte determination together with Na, K, Cl, CO2.

Arch Intern Med. 1988 Nov;148(11):2415-20.
Magnesium metabolism. A review with special reference to the relationship between intracellular content and serum levels.
Reinhart RA.
Marshfield Clinic, WI 54449.

Magnesium (Mg++) is a ubiquitous element in nature, playing a role in photosynthesis and many metabolic functions in humans. All enzymatic reactions that involve adenosine triphosphate have an absolute requirement for Mg++. Levels of Mg++ are controlled by the kidneys and gastrointestinal tract and appear closely linked to calcium, potassium, and sodium metabolism. The clinical manifestations and causes of abnormal Mg++ status are protean. Testing for altered Mg++ homeostasis is problematic. Serum levels, which are those generally measured, reflect only a small part of the total body content of Mg++. The intracellular content can be low, despite normal serum levels in a person with clinical Mg++ deficiency. Future directions in research related to intracellular content of Mg++ are discussed. Treatment of altered Mg++ status depends on the clinical setting and may include the addition of a potassium/Mg++-sparing drug to an existing diuretic regimen. Guidelines for therapy are given.

J Clin Endocrinol Metab. 1985 Nov;61(5):933-40.
Low serum concentrations of 1,25-dihydroxyvitamin D in human magnesium deficiency.
Rude RK, Adams JS, Ryzen E, Endres DB, Niimi H, Horst RL, Haddad JG Jr, Singer FR.

The effect of magnesium deficiency on vitamin D metabolism was assessed in 23 hypocalcemic magnesium-deficient patients by measuring the serum concentrations of 25-hydroxyvitamin D (25OHD) and 1,25-dihydroxyvitamin D [1,25-(OH)2D] before, during, and after 5-13 days of parenteral magnesium therapy. Magnesium therapy raised mean basal serum magnesium [1.0 +/- 0.1 (mean +/- SEM) mg/dl] and calcium levels (7.2 +/- 0.2 mg/dl) into the normal range (2.2 +/- 0.1 and 9.3 +/- 0.1 mg/dl, respectively; P less than 0.001). The mean serum 25OHD concentration was in the low normal range (13.2 +/- 1.5 ng/ml) before magnesium administration and did not significantly change after this therapy (14.8 +/- 1.5 ng/ml). Sixteen of the 23 patients had low serum 1,25-(OH)2D levels (less than 30 pg/ml). After magnesium therapy, only 5 of the patients had a rise in the serum 1,25-(OH)2D concentration into or above the normal range despite elevated levels of serum immunoreactive PTH. An additional normocalcemic hypomagnesemic patient had low 1,25-(OH)2D levels which did not rise after 5 days of magnesium therapy. The serum vitamin D-binding protein concentration, assessed in 11 patients, was low (273 +/- 86 micrograms/ml) before magnesium therapy, but normalized (346 +/- 86 micrograms/ml) after magnesium repletion. No correlation with serum 1,25-(OH)2D levels was found. The functional capacity of vitamin D-binding protein to bind hormone, assessed by the internalization of [3H]1,25-(OH)2D3 by intestinal epithelial cells in the presence of serum was not significantly different from normal (11.42 +/- 1.45 vs. 10.27 +/- 1.27 fmol/2 X 10(6) cells, respectively). These data show that serum 1,25-(OH)2D concentrations are frequently low in patients with magnesium deficiency and may remain low even after 5-13 days of parenteral magnesium administration. The data also suggest that a normal 1,25-(OH)2D level is not required for the PTH-mediated calcemic response to magnesium administration. We conclude that magnesium depletion may impair vitamin D metabolism.

Alcohol Clin Exp Res. 1992 Oct;16(5):986-90.
Oral magnesium supplementation improves metabolic variables and muscle strength in alcoholics.
Gullestad L, Dolva LO, Soyland E, Manger AT, Falch D, Kjekshus J.
Department of Internal Medicine, Baerum Hospital, Sandvika, Norway.

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.