Home About us Editorial board Search Ahead of print Current issue Archives Submit article Instructions Subscribe Contacts Login 
Home Print this page Email this page Users Online: 523


 
 Table of Contents  
REVIEW ARTICLE
Year : 2014  |  Volume : 3  |  Issue : 2  |  Page : 66-72

Magnesium: The fifth electrolyte


1 Department of Biochemistry, All India Institute of Medical Sciences, Rishikesh, Uttarakhand, India
2 Department of Home science (Food and Nutrition), Swami Purnanand Technical degree college, Muni ki reti, Tehri Grahwal, India
3 Department of Cardiothoracic and Vascular Surgery, All India Institute of Medical Sciences, Rishikesh, Uttarakhand, India

Date of Web Publication6-May-2014

Correspondence Address:
Jyoti Bharadwaj
23/36 Govind Nagar, Bengali Mandir Road, Rishikesh 249 201, Uttarakhand
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2278-019X.131955

Rights and Permissions
  Abstract 

Among cations of biologic importance, Magnesium (Mg) is the forgotten member, often labeled as "fifth electrolyte" and sometimes even as the body's 'orphan ion', because of an apparent lack of a specific endocrine control. Magnesium is an important co-factor in many enzymatic reactions involving energy metabolism, protein and nucleic acid synthesis. Ionized Mg is the physiologically active form of the element. It has been mentioned in various epidemiological and correlation studies that low Magnesium status is widely prevalent. Data from many studies indicate that in about 60% of adults the Magnesium intakes from food do not meet the estimated average requirement. Recommended dietary allowance especially for Indians are still undefined.

Keywords: Deficiency, magnesium, micronutrients, nutrition


How to cite this article:
Naithani M, Bharadwaj J, Darbari A. Magnesium: The fifth electrolyte. J Med Nutr Nutraceut 2014;3:66-72

How to cite this URL:
Naithani M, Bharadwaj J, Darbari A. Magnesium: The fifth electrolyte. J Med Nutr Nutraceut [serial online] 2014 [cited 2019 Aug 25];3:66-72. Available from: http://www.jmnn.org/text.asp?2014/3/2/66/131955


  Introduction Top


The word Magnesium comes from the name of Greek city, the Magnesia, where large deposits of Magnesium carbonate [MgCO 3 ] were found. Magnesium is the "iron" of the plant world, plays an essential role in a wide range of fundamental biochemical reactions and cellular functions including cell cycle, channel regulation, membrane and nucleic acid stability and is a cofactor for hundreds of enzymes. [1] Chronic changes of Mg status, that may be latent, are poorly understood and require a better knowledge of ionized Mg metabolism. [2] It is a predominant cation but oftentimes is classified under "trace elements," and as such it receives little appreciation for the role of it plays in biologic processes. Magnesium (Mg) is one of the most abundant cation within the cell and the fourth most abundant cation in the body. Among cations of biologic importance, Mg is the forgotten member. [3]

The first report by Kruse et al., inducing Mg deficiency in rats and dogs in 1933, [4] Mg deficiency in humans has been always found to be associated with many clinical disorders. However, limited attention has been drawn to the impact of Mg deficiency till now. The importance of Magnesium in human health is now being taken much more seriously with researchers trying to explain diverse clinical manifestations in conjunction with Magnesium deficiencies as sudden death, accelerated atherosclerosis, asthma, neurologic and psychiatric diseases [Table 1].
Table 1: Manifestations of magnesium depletion

Click here to view


Mg has a stabilizing effect on DNA and chromatin structure [5] and is an essential cofactor in almost all enzymatic systems involved in DNA processing. All components of connective tissue viz collagen and elastin, proteoglycans and glycoproteins are modulated by Magnesium. It is involved at multiple levels in insulin secretion, binding and activity and it serves as a cofactor in the glucose-transporting. It's deficiency has recently been related with age-related diseases through free-radical mechanism also.

Magnesium content and distribution

Magnesium is the most prevalent intracellular divalent cation and the second most prevalent cation in the body. [6],[7] The normal adult body content is approximately 20-25 g and its distribution is between 60 to 70% in bones, 25 to 30% in muscles, 6 to 8% in soft tissues and 1% in the extra cellular fluid. In children about one-third of Mg resides on the surface of bone probably serving as a reservoir to maintain the extracellular concentration but in adults this mostly an integral part of bone crystal structure. [7],[8] In the plasma, 55% of Mg is ionized or free, 15% is complexed to anions and the rest is bound to protein, chiefly albumin. [7],[8] Mg is contained within all intracellular compartments. It is principally bound to ATP (80 to 90%) and other negatively charged molecules. [9] Total cellular Mg ranges from 5-20 mM depending on the metabolic activity of a cell. Mg is actively transported into and out of cells and is influenced by various hormonal and pharmacological factors which perhaps regulate the intracellular Mg 2+ concentration [Figure 1].
Figure 1: Magnesium metabolism in human body

Click here to view


Magnesium homeostasis

Magnesium is widely distributed in foods. As it is the metal ion in chlorophyll, plant products that form major source of Magnesium. Legumes and cereals are good source of Magnesium. Animal products also contain sufficient quantity. Efficient mechanisms in both the gastrointestinal tract and the kidney closely regulate Mg homeostasis. Though it is absorbed along the entire intestinal tract, it appears to be most efficiently absorbed in the distal small bowel. In the intestine, an active Mg-transport system accounts for greater fractional absorption at low dietary intake while at high dietary intakes Mg absorption occurs at a lower fractional absorption rate and is due to a passive absorption. [10] At a normal dietary Mg intake of approximately 300 to 350 mg/day, fractional absorption is 30 to 50%. [11] This variation may be due to the presence of other nutrients interacting with Mg in the gut including high dietary fiber, phytate, oxalate, phosphate and dietary protein diets of <30 g/day which reduce Mg absorption by binding the cation or hindering absorption. [12],[13],[14],[15]

The kidney most closely regulates Mg metabolism. [16] There exists a threshold of filtered Mg [17] which is close to the normal plasma Mg concentration. Excessive Mg, either dietary or parenterally administered, is almost totally excreted. In contrast, at the time of Mg deprivation, the kidney avidly conserves Mg. Diet also affects renal Mg excretion, high sodium, calcium and protein diets, caffeine as well as alcohol may increase renal Mg excretion. [18],[19],[20],[21] The major site of Mg re-absorption is the thick ascending limb of Henle, which handles about 65% of the filtered load. [16] Re-absorption in the proximal tubule, 20-30% of filtered load, is linked to sodium and water as well as calcium transport. The mechanisms of Mg transport in the intestine and kidney is still unclear.

Despite early proposals for the existence of a specific hormonal control of Magnesium homeostasis, no single endocrine factor that controls circulating or urinary Magnesium has been identified. It has been described as the body's 'orphan ion', because of an apparent lack of a specific endocrine control similar to that existing for calcium, sodium and potassium. [22] A number of hormones, including parathyroid hormone and calcitonin, vitamin D, insulin, glucagon, antidiuretic hormone, aldosterone and sex steroids have been reported to influence Magnesium balance, notwithstanding the possibility that these may not be primary regulators of magnesium homeostasis. [23],[24] Recent observations suggest that these hormones act through a common second messenger, adenosine 3', 5'- cyclic mono-phosphate to enhance magnesium transport and modulate magnesium excretion at that nephron site. [25]

Biological effects

The physiological role of Mg is principally related to enzyme activity; over 300 enzyme systems particularly Kinases are dependent on the presence of this Cation. [26] This includes all enzyme utilizing ATP, they requires Mg for substrate formation. Intracellular free Mg 2 + also acts as an allosteric activator of enzyme action including critical enzyme systems such as adenylate cyclase, phospholipase C and Na/K-ATPase. [27],[28],[29],[30] It is established that Mg is critical for a number of cellular functions including oxidative phosphorylation, glycolysis, DNA transcription and protein synthesis and the clinical complications of Mg depletion are may be due to perturbation of Mg-requiring enzyme systems. Magnesium is fundamentally required for the energy transfer reactions involving high energy compounds like ATP and creatine phosphate and thus muscle contraction. Thus, it plays vital role in heart and skeletal system function.

Transport of potassium and calcium across the plasma membrane may also require the presence of Mg. Mg has been also termed as nature's physiologic calcium channel blocker. [31],[32] During Mg depletion, intracellular potassium decreases while calcium and sodium increase. [33] In view of close association of occurrence and functions of Ca and Mg, there is evidence of mutually synergistic as well as contraindicative roles of these two divalent anions, particularly in bone health and hypertension.

Requirement of magnesium

An expert consultation for the Food and Agriculture Organization/World Health Organization [FAO/WHO] concluded that evidence was lacking for nutritional magnesium deficiency occurring with consumption of diets supplying a range of magnesium intakes, some of which contain considerably less than the Recommended dietary allowance  RDA for the United States and Canada as well as for the United Kingdom in 2004. [34] But contrary to the above fact, epidemiological and correlation studies indicate that a low magnesium status is widely prevalent. Data from the 2005 to 2006 National Health and Nutrition Examination Survey in the United States and other studies [35] indicated that in about 60% of adults the magnesium intakes from food do not meet the estimated average requirement. Despite such data, widespread pathological conditions attributed to dietary magnesium deficiency have not been reported. In India, initially the Indian Council of Medical Research [ICMR] Committee did not suggest any RDA for magnesium as it was thought that there was no possibility of any Mg deficiency, in our population. Magnesium intake in different regions of India was found to range from 540 mg to 1002mg and average absorption in range of 13 to 50%. In a report by Singh et al. [36] the dietary intake of magnesium was 430mg and 370 mg/d in the rural and urban population, respectively, confirming the earlier data of Rao and Rao collected in 1980. [37] These are further confirmed by reports from North India by Kapil and others. [38],[39],[40] Taking absorption of magnesium as 50%, FAO/WHO has recommended desirable intake of Mg as 4 mg/kg/day for international use. ICMR Committee has decided to use FAO/WHO recommendation for all age groups except adults where 340 mg/day for men and 310 mg/day for females has been recommended.

Magnesium deficit

Magnesium deficiency is common and multifactorial in nature [41],[42] but health implications are still debatable due to with limited number of research reports and clinical commentaries on this topic. Magnesium deficit can be categorized into two types: Magnesium deficiency and magnesium depletion. Dietary amounts of magnesium are marginal in the whole population and little alteration in magnesium intake may increase the prevalence of magnesium deficiency. Magnesium depletion may be due to deregulation of factors controlling magnesium status. This depletion especially when moderate to severe is almost always related to either gastrointestinal or renal Mg loss.

Magnesium deficiency

Despite claims of adequate magnesium in diets, dietary surveys have found to the contrary suboptimal magnesium and low magnesium status is prevalent. Data from nationwide population-based nutrition surveys in Taiwan were used to investigate trends and nutritional status for magnesium from 1993 to 2008. In this survey 74-81% of adult subjects' dietary magnesium was estimated as sub-optimal. The prevalence of low serum magnesium (<0.8mmol/L) was 12.3 and 23.7% for the males and females, respectively. [42] In adult German population, prevalence of magnesium deficiency was found to be 14.5%. [43] In Another study conducted in Mexico, the overall prevalence of low serum magnesium was 37.6%, much higher than that reported for German individuals (14.5%). It was concluded that an insufficient diet in Mexico, especially in animal tissue may explain such a difference. [44] The suboptimal magnesium status seems equally prevalent in pediatric population with studies giving findings which are alarming since overweight children have low serum magnesium levels. In one study, by Huerta et al., overweight children had lower serum levels as well as lower calorie-adjusted intake of magnesium compared to normal weight children. [45] In another study conducted in India, it was found that the unadjusted as well as calorie-adjusted dietary intake of magnesium to be higher in the overweight group, still such overweight children had lower serum levels of magnesium. [46] It was postulated that this might be due to either decreased absorption or increased excretion of magnesium. Association of lower serum magnesium levels with BMI, systolic and diastolic BP and serum insulin level in this study suggests that the origin of the association of insulin resistant state with low serum magnesium starts in childhood itself. [47] Some studies have indicated a different trend that children are now consuming diets poor in magnesium content. The studies have also indicated that affluent family children may also have low magnesium status. Analysis of minerals in the diet of 200 school going children in a recent study show that they consume low magnesium. [48]

Magnesium depletion

Magnesium depletion as already mentioned is due to dysregulation of factors controlling magnesium status. This depletion especially when moderate to severe is almost always related to either gastrointestinal or renal Mg loss or it may be an on effect of drugs on its homeostasis.

Gastrointestinal disorders: Disorders of the intestinal tract may result in profound Mg depletion. Any chronic and/or acute diarrheal syndrome or fistual drainage may result in Mg depletion since the content of Mg in diarrheal fluids may be quite high. [49] Mal-absorption syndromes will result in Mg mal-absorption, presumably as a result of intestinal mucosal damage and/or steatorrhea through formation of non absorbable Mg-lipid salts. [50] Intestinal resection, infarction and specific defects in Mg absorption will also result in Mg deficiency. [51],[52],[53],[54],[55] Acute pancreatitis is associated with low serum Mg levels in up to 20% of cases [56],[57],[58] probably due to a predisposing conditions (e.g. alcoholism) or soaponification of Mg in necrotic parapancreatic fat

Renal magnesium wasting: Renal Mg wasting underlies the basis for Mg depletion in many patients. Decreased proximal tubule Mg re-absorption occurs in osmotic diuresis, increased sodium excretion and increased calcium excretion. [59],[60],[61] Hypercalcemia limits Mg re-absorption in the ascending limb of Henle as it was demonstrated by micro-puncture studies in the rat [62] Loop diuretics like frusemide will also cause decreased Mg re-absorption in this segment of the nephron. [63]

A number of commonly used medications may result in renal Mg wasting by unclear mechanisms. Aminoglycosides have been reported to cause hypermagnesuria and hypomagnesemia. [64],[65] Cisplatin causes a dose-related renal Mg loss in up to 100% of patients that may persist for months to years after therapy. [66],[67],[68] Cyclosporine given for immunosuppression is also known to result in tubular damage leading to renal Mg wasting. [69],[70] Alcohol, acidosis and a variety of renal disorders may also impair the ability of the kidney to conserve Mg and contribute to Mg depletion. [71],[72] Apart from diseased conditions increased fractional excretion is also reported related to type- 2 Diabetes mellitus, hypertension and obesity in adults. [73] [Table 2].
Table 2: Causes of magnesium defi ciency

Click here to view


Assessment of magnesium status

The tests for the assessment of magnesium status can be divided into three functional categories: Physiological assessment of magnesium, Tissue Magnesium and Serum/plasma magnesium.

  • Physiological assessment of magnesium: Magnesium balance studies (after oral or parenteral administration) though very accurate have a very demanding protocol and require a dedicated staff therefore it can be done in only a few research centers in the world. Such studies have answered important questions about absorption and excretion of magnesium. [74] but practically not possible and unavailable
  • Oral administration of magnesium is used to assess intestinal absorption, tissue uptake and excretion. [75] Parenteral administration of magnesium avoids the variability of intestinal absorption. Isotope studies have been used to assess absorption but it also imposes various restrictions on the investigator. [76] Studies with isotopes of magnesium are currently limited to research only
  • Tissue magnesium: Data on magnesium concentration for a particular tissue may be limited to that tissue, as various separate studies have shown no correlation among serum, erythrocyte and MBC concentrations of magnesium in humans. [77],[78],[79] Magnesium level in Blood has been determined most frequently than in any other tissues. Magnesium is usually determined in serum rather than plasma, because the anticoagulant for plasma could be contaminated with magnesium and it will affect the assay procedure. Some investigators view the magnesium content in serum as "the fifth electrolyte". [80] Others advocate that the most productive strategy is to determine the concentration of magnesium in serum in selected patients only. [81] Blood magnesium has to be maintained in a narrow range. For assessing acute changes in magnesium status, measurement of the magnesium concentration in serum is of value (Normal value -0.75-1.2 mmol/L OR 1.7 to 2.2 mg/dL, Critical value: <0.5 mmol/L and >2.35 mmol/L). A high prevalence of hypomagnesemia (11%) and hypermagnesemia (9.3%) has been documented in hospitalized patients. [82] But on the contrary, Serum magnesium test may not accurately measure magnesium levels because less than one percent of body's magnesium is in Serum this means the magnesium levels in serum are not necessarily representative of overall magnesium levels
  • As with serum, the concentration of magnesium in erythrocytes has not been shown to correlate significantly with other tissue pools of magnesium. The usefulness of determining erythrocytic magnesium content for clinical medicine is unclear
  • Mononuclear blood cells [MBC] have been studied for magnesium levels and investigators agree relatively well on the mean value for magnesium in MBC. [83] The magnesium content of MBC reportedly is a better indicator for cardiac arrhythmias associated with magnesium deficiency than serum magnesium concentration. [84] The correlation for magnesium concentrations between MBC and muscle or other body tissues, particularly bone, needs to be better defined to make this a clinically useful assay
  • Muscle tissue represents approximately 43% of the body weight and contains approximately 27% of the total body magnesium. Thus, it is an appropriate and important tissue for the assessment of magnesium status. Three studies have shown a lack of correlation between the concentrations of magnesium in serum and muscle. [85],[86],[87],[88],[89] However, in patients with Type I diabetes mellitus, the concentration of magnesium in muscle correlated significantly (P < 0.001) with that of MBC. [90] Needle biopsy of muscle has been used successfully to determine the magnesium concentration of this tissue [91] but this procedure requires special skills and the assay is tedious
  • Serum/plasma magnesium: As described serum magnesium test may not accurately measure overall magnesium levels. [92] This also includes free and total magnesium levels. Free magnesium can be determined in biological fluids and tissue by indirect or direct methods. The indirect method is based on the separation of free and complexed magnesium fractions from the protein-bound fraction by ultracentrifugation or equilibrium dialysis and this requires rigid analytical conditions for accuracy and not feasible. Direct methods like dye binding or an ion-selective electrode are also both in the developmental stage.


There is limited information on the total body's mineral status of magnesium and in light of the fact that none of the tests clearly defines magnesium status. It is requirement of day to conduct more studies. Future research is needed to establish the complex relations between dietary magnesium, other dietary factors affecting inflammation, oxidative stress and chronic diseases. The magnesium deficiency may be that undiscovered key which would solve the problem of chronic disorders like insulin deficiency, hypertension and atherosclerosis.

 
  References Top

1.
Chaudhary DP, Sharma R, Bansal DD. Implications of magnesium deficiency in type 2 diabetes: A review. Biol Trace Elem Res 2010;134:119-29.  Back to cited text no. 1
    
2.
Elin RJ. magnesium: The fifth but forgotten electrolyte. Am J Clin Pathol 1994:102:616-22.  Back to cited text no. 2
    
3.
Aikawa JK. Magnesium. West J Med 1980;133:333-4.  Back to cited text no. 3
    
4.
Kruse HD, Schmidt MM, McCollum EV. Studies on magnesium deficiency in animals: V. Changes in the mineral metabolism of animals following magnesium deprivation. J Biol Chem 1934;106:553-72.  Back to cited text no. 4
    
5.
Hartwig A. Role of magnesium in genomic stability. Mutat Res 2001;475:113-21.  Back to cited text no. 5
    
6.
Rude RK, Oldham SB. Disorders of magnesium metabolism. In: Cohen RD, Lewis B, Alberti KG, Denman AM, editors. The Metabolic and Molecular Basis of Acquired Diseases. London: Bailliere Tindall; 1990. p. 1124-48.  Back to cited text no. 6
    
7.
Elin RJ. Assessment of magnesium status. Clin Chem 1987;33:1965-70.  Back to cited text no. 7
    
8.
Wallach S. Availability of body magnesium during magnesium deficiency. Magnesium 1988;7:262-70.  Back to cited text no. 8
    
9.
Arinzon Z, Peisakh A, Schrire S, Berner YN. Prevalence of hypomagnesemia (HM) in a geriatric long-term care (LTC) setting. Arch Gerontol Geriatr 2010;51:36-40.  Back to cited text no. 9
    
10.
Kayne LH, Lee DB. Intestinal magnesium absorption. Miner Electrolyte Metab 1993;19:210-7.  Back to cited text no. 10
    
11.
Fine KD, Santa Ana CA, Porter JL, Fordtran JS. Intestinal absorption of magnesium from food and supplements. J Clin Invest 1991;88:396-402.  Back to cited text no. 11
    
12.
Schwartz R, Spencer H, Welsh JJ. Magnesium absorption in human subjects from leafy vegetables, intrinsically labeled with stable Mg. Am J Clin Nutr 1984;39:571-6.  Back to cited text no. 12
    
13.
Franz KB. Influence of phosphorus on intestinal absorption of calcium and magnesium. In: Itokawa Y, Durlach J, editors. Magnesium in Health and Disease. London, UK: John Libbey and Co.; 1989. p. 71-8.  Back to cited text no. 13
    
14.
Wisker E, Nagel R, Tanudjaja TK, Feldheim W. Calcium, magnesium, zinc and iron balances in young women: Effects of a low-phytate barley-fiber concentrate. Am J Clin Nutr 1991;54:553-9.  Back to cited text no. 14
    
15.
Siener R, Hesse A. Influence of a mixed and a vegetarian diet on urinary magnesium excretion and concentration. Br J Nutr 1995;73:783-90.  Back to cited text no. 15
    
16.
Hunt SM, Schofield FA. Magnesium balance and protein intake level in adult human female. Am J Clin Nutr 1969;22:367-73.  Back to cited text no. 16
    
17.
Quamme GA, Dirks JH. The physiology of renal magnesium handling. Ren Physiol 1986;9:257-69.  Back to cited text no. 17
    
18.
Rude RK, Ryzen E. TmMg and renal Mg threshold in normal man in certain pathophysiologic conditions. Magnesium 1986;5:273-81.  Back to cited text no. 18
    
19.
Mahalko JR, Sandstead HH, Johnson LK, Milne DB. Effect of a moderate increase in dietary protein on the retention and excretion of Ca, Cu, Fe, Mg, P and Zn by adult males. Am J Clin Nutr 1983;37:8-14.  Back to cited text no. 19
    
20.
Martinez ME, Salinas M, Miguel JL, Herrero E, Gomez P, Garcia J, et al. Magnesium excretion in idiopathic hypercalciuria. Nephron 1985;40:446-50.  Back to cited text no. 20
    
21.
Massey LK, Whiting SJ. Caffeine, urinary calcium, calcium metabolism and bone. J Nutr 1993;123:1611-14.  Back to cited text no. 21
    
22.
Kelepouris E, Agus ZS. Hypomagnesemia: Renal magnesium handling. Semin Nephrol 1998;18:58-73.  Back to cited text no. 22
    
23.
Toromanoff A, Ammann P, Mosekilde L, Thompson JS, Riond JL. Parathyroid hormone increases bone formation and improves mineral balance in vitamin D-deficient female rats. Endocrinology 1997;138:2449-57.  Back to cited text no. 23
    
24.
Romani A, Marfella C, Lakshmanan M. Mobilization of Mg2 + from rat heart and liver mitochondria following the interaction of thyroid hormone with the adenine nucleotide translocase. Thyroid 1996;6:513-9.  Back to cited text no. 24
    
25.
Quamme GA. Renal magnesium handling: New insights in understanding old problems. Kidney Int 1997;52:1180-95.  Back to cited text no. 25
    
26.
Nadler JL, Rude RK. Disorders of magnesium metabolism. Endocrinol Metab Clin North Am 1995;24:623-41.  Back to cited text no. 26
    
27.
Arnaud MJ. Update on the assessment of magnesium status. Br J Nutr 2008;99 Suppl 3:S24-36.  Back to cited text no. 27
    
28.
Rude RK. Magnesium homeostasis. In: Bilezikian JP, Raisz LG, Rodan GA, editors. Principles of Bone Biology. California: Academic Press; 2002. p. 339-58.  Back to cited text no. 28
    
29.
Da Silva JF, Williams RJ. The Biological Chemistry of the Elements: The Inorganic Chemistry of Life. Oxford University Press; 2001.  Back to cited text no. 29
    
30.
Schweigel M, Martens H. Magnesium transport in the gastrointestinal tract. Front Biosci 2000;5:D666-77.  Back to cited text no. 30
    
31.
Iseri LT, French JH. Magnesium: Nature's physiologic calcium blocker. Am Heart J 1984;108:188-93.  Back to cited text no. 31
    
32.
Turlapaty PD, Altura BM. Magnesium deficiency produces spasms of coronary arteries: Relationship to etiology of sudden death ischemic heart disease. Science 1980;208:198-200.  Back to cited text no. 32
    
33.
Dunn MJ. Red blood cell calcium and magnesium: Effects upon sodium and potassium transport and cellular morphology. Biochim Biophys Acta 1974;352:97-116.  Back to cited text no. 33
    
34.
Food and Agriculture Organization/World Health Organization. Vitamin and Mineral Requirements in Human Nutrition. 2 nd ed. Geneva: Food and Agriculture Organization/World Health Organization; 2004. p. 217-28.  Back to cited text no. 34
    
35.
Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D and Fluoride. Washington DC: National Academy Press; 1997. p. 190-249.  Back to cited text no. 35
    
36.
Singh RB, Niaz MA, Rastogi SS, Bajaj S, Gaoli Z, Shoumin Z. Current zinc intake and risk of diabetes and coronary artery disease and factors associated with insulin resistance in rural and urban populations of North India. J Am Coll Nutr 1998;17:564-70.  Back to cited text no. 36
    
37.
Rao CN, Rao BS. Absorption and retention of magnesium and some trace elements by man from typical Indian diets. Nutr Metab 1980;24:244-54.  Back to cited text no. 37
    
38.
Pathak P, Kapil U, Kapoor SK, Saxena R, Kumar A, Gupta N, et al. Prevalence of multiple micronutrient deficiencies amongst pregnant women in a rural area of Haryana. Indian J Pediatr 2004;71:1007-14.  Back to cited text no. 38
    
39.
Kapil U, Verma D, Goel M, Saxena N, Gnanasekaran N, Goindi G, et al. Dietary intake of trace elements and minerals among adults in underprivileged communities of rural Rajasthan, India. Asia Pac J Clin Nutr 1998;7:29-32.  Back to cited text no. 39
    
40.
Tong GM, Rude RK. Magnesium deficiency in critical illness. J Intensive Care Med 2005;20:3-17.  Back to cited text no. 40
    
41.
Parikh M, Webb ST. Cations: Potassium, calcium and magnesium. CEACCP 2012;12:195-8.  Back to cited text no. 41
    
42.
Wang JL, Weng YL, Pan WH, Kao MD. Trends and nutritional status for magnesium in Taiwan from NAHSIT 1993 to 2008. Asia Pac J Clin Nutr 2011;20:266-74.  Back to cited text no. 42
    
43.
Schimatschek HF, Rempis R. Prevalence of hypomagnesemia in an unselected German population of 16,000 individuals. Magnes Res 2001;14:283-90.  Back to cited text no. 43
    
44.
De la Cruz-Góngora V, Gaona B, Villalpando S, Shamah-Levy T, Robledo R. Anemia and iron, zinc, copper and magnesium deficiency in Mexican adolescents: National Health and Nutrition Survey 2006. Salud Publica Me×2012;54:135-45.  Back to cited text no. 44
    
45.
Huerta MG, Roemmich JN, Kington ML, Bovbjerg VE, Weltman AL, Holmes VF, et al. Magnesium deficiency is associated with insulin resistance in obese children. Diabetes Care 2005;28:1175-81.  Back to cited text no. 45
    
46.
Jose B, Jain V, Vikram NK, Agarwala A, Saini S. Serum magnesium in overweight children. Indian Pediatr 2012;49:109-12.  Back to cited text no. 46
    
47.
Dholpuria R, Raja S, Gupta BK, Chahar CK, Panwar RB, Gupta R, et al. Atherosclerotic risk factors in adolescents. Indian J Pediatr 2007;74:823-6.  Back to cited text no. 47
    
48.
Thoren L. Magnesium deficiency in gastrointestinal fluid loss. Acta Chir Scand Suppl 1963;306 (Suppl):1-65.  Back to cited text no. 48
    
49.
LaSala MA, Lifshitz F, Silverberg M, Wapnir RA, Carrera E. Magnesium metabolism studies in children with chronic inflammatory disease of the bowel. J Pediatr Gastroenterol Nutr 1985;4:75-81.  Back to cited text no. 49
    
50.
Nyhlin H, Dyckner T, Ek B, Wester PO. Plasma and skeletal muscle electrolytes in patients with Chron's disease. J Am Coll Nutr 1985;4:531-8.  Back to cited text no. 50
    
51.
Heaton FW, Fourman P. Magnesium deficiency and hypocalcemia in intestinal malabsorption. Lancet 1965;2:50-2.  Back to cited text no. 51
    
52.
Booth CC, Babouris N, Hanna S, Macintyre I. Incidence of hypomagnesemia in intestinal malabsorption. Br Med J 1963;2:141-4.  Back to cited text no. 52
    
53.
Goldman AS, Van Fossan DD, Baird EE. Magnesium deficiency in celiac disease. Pediatrics 1962;29:948-52.  Back to cited text no. 53
    
54.
Smith GA, Tompkins RK. Biliary magnesium loss in the postoperative patient. Arch Surg 1974;109:77-9.  Back to cited text no. 54
    
55.
Dyckner T, Hallberg D, Hultman E, Wester PO. Magnesium deficiency following jejunoileal bypass operations for obesity. J Am Coll Nutr 1982;1:239-46.  Back to cited text no. 55
    
56.
Swenson SA Jr, Lewis JW, Sebby KR. Magnesium metabolism in man with special reference to jejunolileal bypass for obesity. Am J Surg 1974;127:250-5.  Back to cited text no. 56
    
57.
Van Gaal L, Delvigne C, Vandewoude M, Cogge E, Vaneerdeweg W, Schoofs E, et al. Evaluation of magnesium before and after jejuno-ileal versus gastric bypass surgery for morbid obesity. J Am Coll Nutr 1987;6:397-400.  Back to cited text no. 57
    
58.
Strømme JH, Steen-Johnsen J, Harnaes K, Hofstad F, Brandtzaeg P. Familial hypomagnesemia-a follow-up examination of three patients after 9 to 12 years of treatment. Pediatr Res 1981;15:1134-9.  Back to cited text no. 58
    
59.
Weir GC, Lesser PB, Drop LJ, Fischer JE, Warshaw AL. The hypocalcemia of acute pancreatitis. Ann Intern Med 1975;83:185-9.  Back to cited text no. 59
    
60.
Haldiman B, Goldstein DA, Akmal M, Massry SG. Renal function and blood levels of divalent ions in acute pancreatitis. Miner Electrolyte Metab 1980;3:190-9.  Back to cited text no. 60
    
61.
Ryzen E, Rude RK. Low intracellular magnesium in patients with acute pancreatitis and hypocalcemia. West J Med 1990;152:145-8.  Back to cited text no. 61
    
62.
Massry SG, Coburn JW, Chapman LW, Kleeman CR. Effect of NaCl infusion on urinary Ca++ and Mg++ during reduction in their filtered loads. Am J Physiol 1967;213:218-24.  Back to cited text no. 62
    
63.
Coburn JW, Massry SG, Kleeman CR. The effect of calcium infusion on renal handling of magnesium with normal and reduced glomerular filtration rate. Nephron 1970;7:131-43.  Back to cited text no. 63
    
64.
McNair P, Christensen MS, Christiansen C, Madsbad S, Transbøl IB. Renal hypomagnesaemia in human diabetes mellitus: Its relation to glucose homeostasis. Eur J Clin Invest 1982;12:81-5.  Back to cited text no. 64
    
65.
Quamme GA. Control of magnesium transport in the thick ascending limb. Am J Physiol 1989;256:F197-210.  Back to cited text no. 65
    
66.
Quamme GA. Effect of furosemide on calcium and magnesium transport in the rat nephron. Am J Physiol 1981;241:F340-7.  Back to cited text no. 66
    
67.
Zaloga GP, Chernow B, Pock A, Wood B, Zaritsky A, Zucker A. Hypomagnesemia is a common complication of aminoglycoside therapy. Surg Gynecol Obstet 1984;158:561-5.  Back to cited text no. 67
    
68.
Kes P, Reiner Z. Symptomatic hypomagnesemia associated with gentamicin therapy. Magnes Trace Elem 1990;9:54-60.  Back to cited text no. 68
    
69.
Rude RK. Magnesium disorders. In: Kokko JP, Tannen RL, editors. Fluids and Electrolytes. 3 rd ed. Philadelphia, PA: WB Saunders Co.; 1996. p. 421-45.  Back to cited text no. 69
    
70.
Meyer KB, Madias NE. Cisplatin nephrotoxicity. Miner Electrolyte Metab 1994;20:201-13.  Back to cited text no. 70
    
71.
Buckley JE, Clark VL, Meyer TJ, Pearlman NW. Hypomagnesemia after cisplatin combination chemotherapy. Arch Inter Med 1984;144:2347-8.  Back to cited text no. 71
    
72.
Allen RD, Hunnisett AG, Morris PJ. Cyclosporin and magnesium. Lancet 1985;325:1283-4.  Back to cited text no. 72
    
73.
Bennett WM, Burdmann E andoh T, Elzinga L, Franceschini N. Nephrotoxicity of immunosuppressive drugs. Miner Electrolyte Metab 1994;20:214-20.  Back to cited text no. 73
    
74.
Mendelson JH, Ogata M, Mello NK. Effects of alcohol ingestion and withdrawal on magnesium states of alcoholics: Clinical and experimental findings. Ann N Y Acad Sci 1969;162:918-33.  Back to cited text no. 74
    
75.
Lau K, Rodriguez Nichols F, Tannen RL. Renal excretion of divalent ions in response to chronic acidosis: Evidence that systemic pH is not the controlling variable. J Lab Clin Med 1987;109:27-33.  Back to cited text no. 75
    
76.
Sjögren A, Florén CH, Nilsson A. Magnesium, potassium and zinc deficiency in subjects with type II diabetes mellitus. Acta Med Scand 1988;224:461-6.  Back to cited text no. 76
    
77.
Spencer H, Friedland JA, Ferguson V. Human balance studies in mineral metabolism. In: Zipkmn I, editor. Biological Mineralization. New York: John Wiley and Sons Inc; 1973. p. 689-724.  Back to cited text no. 77
    
78.
Nicar MJ, Pak CY. Oral magnesium load test for the assessment of intestinal absorption. Application in control subjects, absorptive hypercalciuria, primary hyperparathyroidism and hypoparathyroidism. Minor Electrolyte Metab 1982;8:44-51.  Back to cited text no. 78
    
79.
Schwartz R, Spencer H, Wentworth RA. Measurement of magnesium absorption in man using stable 26Mg as a tracer. Clin Chim Acta 1978;87:265-73.  Back to cited text no. 79
    
80.
Elin RJ, Hosseini JM. Magnesium content of mononuclear blood cells. Clin Chem 1985;31:377-80.  Back to cited text no. 80
    
81.
Elin RJ, Johnson E. A method for the determination of the Magnesium content of blood mononuclear cells. Magnesium 1982;1:115-21.  Back to cited text no. 81
    
82.
Millart H, Collery P, Lambliale D, Hioco D, Pechery C, Choisy H. The determination of lymphocyte magnesium content as a reliable laboratory test with regard to magnesium status. J Am Coll Nutr 1985;4:397.  Back to cited text no. 82
    
83.
Whang R. Routine serum magnesium determination-a continuing unrecognized need. Magnesium 1987;6:1-4.  Back to cited text no. 83
    
84.
Croker JW, Walmsley RN. Routine plasma magnesium estimation: A useful test? Med J Aust 1986;145:71, 74-6.  Back to cited text no. 84
    
85.
Wong ET, Rude RK, Singer FR, Shaw ST Jr. A high prevalence of hypomagnesemia and hypermagnesemia in hospitalized patients. Am J Clin Pathol 1983;79:348-52.  Back to cited text no. 85
    
86.
Elin RJ. Status of the mononuclear blood cell magnesium assay. J Am Coll Nutr 1987;6:105-7.  Back to cited text no. 86
    
87.
Cohen L, Kitzes R. Magnesium sulfate and digitalis-toxic arrhythmias. JAMA 1983;249:2808-10.  Back to cited text no. 87
    
88.
Martindale L, Heaton FW. The relation between skeletal and extracellular-fluid magnesium in vitro. Biochem J 1965;97:440-3.  Back to cited text no. 88
    
89.
Lim P, Jacob E. Magnesium deficiency in patients on long-term diuretic therapy for heart failure. Br Med J 1972;3:620-2.  Back to cited text no. 89
    
90.
Sjögren A, Florén CH, Nilsson A. Magnesium deficiency in IDDM related to level of glycosylated hemoglobin. Diabetes 1986;35:459-63.  Back to cited text no. 90
    
91.
Dyckner T, Wester PO. Skeletal muscle magnesium and potassium determinations: Correlation with lymphocyte contents of magnesium and potassium. J Am Coll Nutr 1985;4:619-25.  Back to cited text no. 91
    
92.
Wester PO, Dyckner T. Diuretic treatment and magnesium losses. Acta Med Scand Suppl 1981;647:145-52.  Back to cited text no. 92
    


    Figures

  [Figure 1]
 
 
    Tables

  [Table 1], [Table 2]



 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
Abstract
Introduction
References
Article Figures
Article Tables

 Article Access Statistics
    Viewed3782    
    Printed116    
    Emailed1    
    PDF Downloaded278    
    Comments [Add]    

Recommend this journal