Contemporary Nutrition, January, 1982, Vol. 7 No. 1
It is generally assumed that most American diets are adequate in magnesium (Mg). However, metabolic balance studies indicate that certain nutrients and stress conditions increase the need for Mg.1 Furthermore, dietary surveys show that self-selected diets often contain 200-250 mg of Mg/day. which is below the Recommended Dietary Allowances (RDA) of 300-400 mg per day for adults.2,3,4 Since Mg is an activator of numerous enzyme systems which control carbohydrate, fat and electrolyte metabolism, nucleic acid and protein synthesis, and membrane transport and integrity,5,6 this level of intake may have serious risks.
A Mg deficiency that is severe enough to result in low plasma levels is marked by well-known symptoms, such as convulsions and cardiac arrhythmia. Marginal deficiencies are associated with a variety of other acute and chronic disorders.5,6,7,8,9
The RDAs for Mg are 300 mg for young women and 350 mg for young men (4.5-5 mg/kg/day).4 The RDAs for 15- to 18-year-old boys and pregnant and lactating women are estimated at 400 and 450 mg. respectively. The recommendation for older children is that sufficient Mg be consumed to provide for needs during growth. Balance studies, however, indicate that adolescent girls require 6-10 mg/kg/day, while adolescent boys seem to need even more.2,10 The RDAs for infants (50-70 mg or 4-10 mg/kg/day) are based on the amounts in human milk and infant formulas and are presumed to provide an infant’s entire need. But, infants may need as much as 15-20 mg/kg/day. depending on their rates of growth and composition of their diets.2 While it is also assumed that infant formulas provide enough Mg to meet an infant’s need, it is significant that the formula-fed infants studied were barely in Mg equilibrium rather than in positive balance necessary for growth.2,4 It is noteworthy that although infant formulas contain higher levels of Mg than mother milk, plasma Mg levels of bottle-fed infants were lower than breast-fed.2,7,11
The RDAs for Mg may not be optimal for most people. Attempts to redefine Mg requirements should take into account factors known to increase the need for Mg, such as excesses of some nutrients and of stress. Thus, studies conducted in metabolic units may yield misleading results because subjects are protected from uncontrolled dietary and stress factors.
Mg intakes have not decreased significantly during this century, but the intake of major nutrients that increase the requirement for Mg have risen substantially.1,2,7 Animal experiments show that high dietary ratios of Ca/Mg and PO4/Mg and Vitamin D excess, either alone or in combination, cause Mg loss.2,7,12 Human metabolic balance studies have examined the effects of increasing the ratios of Ca/Mg and PO4/Mg within the limits of normal dietary intakes. When the dietary intake of Mg was maintained at 250 mg/day, and Ca was increased from low (200 mg/day) to high (1400 mg/day), negative Mg balance was observed.13 However, when Mg intake was increased to 500 mg/day, Mg balance was restored. Similarly. a negative Mg balance was produced when PO4 was increased from the near RDA level of 975 mg/day to 1500 mg/day. Even greater dietary PO4 intakes are common in the U.S. diet.7 The most dramatic human example of Mg deficiency precipitated by PO4 is a report of convulsive hypomagnesemia in formula-fed young infants. This form of induced hypomagnesemia can also cause hypocalcemia in humans, a condition often treated with Ca and calcemic agents, but with less effectiveness than when treated with Mg. Finally, during three consecutive 20-day balance periods, 15 young women were fed diets with Mg controlled at the RDA level and normal intakes of Ca and PO4. Results showed all women were in strongly negative Mg balance. This study suggests that at these levels of intake, the dietary ratios of Ca/Mg and PO4/Mg are high and supports earlier work indicating that Mg intake for adults should not be less than 6 mg/kg/day.
A provocative finding in diets with high Ca/Mg and PO4/Mg ratios was a gradual rise in serum cholesterol despite low fat in the diet.14 Moreover, the calcemic agent Vitamin D, in addition to decreasing Mg retention when given in excess, also causes hypercholesterolemia.7,15
High levels of fat in the intestinal lumen derived from fatty food ingestion or intestinal dysfunction, such as steatorrhea or short bowel, interfere with Mg absorption because soaps that are formed from fat and divalent cations like Mg are not absorbed.2
Adequate protein intake is necessary for optimal Mg retention. When protein intake was increased from low to normal levels in young and adolescent boys and in girls and women on diets marginal in Mg, improved Mg retention was observed.2,10 Diets containing sufficient Mg for growth and development(10-16 mg/kg/day) resulted in positive balances regardless of the protein intake.10 High Mg intakes also improve nitrogen (N) balance in persons consuming a high protein diet.
Protein loading (e.g.. large gelatin doses added to a normal diet) causes urinary Mg loss.12 In this respect. hypomagnesemia was detected in a patient who experienced fatal cardiac arrhythmia during re-feeding, subsequent to consuming a liquid protein diet for weight reduction.18 This recalls the Mg-responsive cardiac arrhythmias observed in infants suffering from protein-calorie malnutrition during re-feeding with diets low in Mg and high in protein, Ca and PO4.19 Thus, with protein intakes common to liquid protein-reducing diets, Mg depletion is a risk. The results of these studies indicate that a low Mg/protein ratio can jeopardize Mg balance and that increasing the Mg/protein ratio improves N balance Therefore, Mg intake should be high enough to permit optimal Mg and N retention.10
High intakes of sugar also appear to increase the need for Mg.2,20 The urinary excretion of Mg more than doubled in young men after ingesting 100g of glucose.12
Alcohol consumed with or without food increases Mg requirements. Even moderate alcohol consumption increases the urinary excretion of Mg.12 Poor diet and urinary loss during alcoholism contribute to severe Mg depletion. This was one of the first clinically recognized conditions involving a Mg deficit.12,21
Stress causes secretion of epinephrine (adrenalin) and corticosteroids and results in Mg loss in animals and in humans.2,7 The types of stresses that can increase Mg needs can be physical (exhausting or competitive exercise, extremes of temperature, and accidental or surgical trauma), or psychological (anger, fear, anxiety, overwork and crowding). Subjects exposed to the vicissitudes of life may need more than the RDAs for Mg.
Mg deficiency causes cardiovascular damage, and its administration is therapeutic in cardiac arrhythmia.7,22,23 Its suboptimal supply can have serious immediate and long-term consequences. For example, hyperirritability and convulsions mark acute Mg depletion in experimental animals.7,8,9 Similar dysfunctions have been diagnosed in humans with hypomagnesemia.21,22,23 Deficiency studies, which create less severe deficiencies but impose them for longer periods, cause myocardial necrosis and lesions of small arteries.7,24 In experimental animal models, high-fat atherogenic diets are more vasopathic when the diet is low in Mg and even more so with high dietary Ca, PO4 and/or Vitamin D.7,24 When the diet also provides protein and sodium in amounts similar to the levels consumed in the U.S. diet, it becomes cardiovasopathic(CVP), causing arteriosclerosis, hypertension, hypercholesterolemia, and myocardial infarction (MI) in 80-90% of the animals.7,24,25 When either the excess fat or Vitamin D was removed from the diet, the MI incidence was reduced by 20% and 40% respectively, while providing a normal mineral mixture lowered it by 70%. However, increasing the Mg in the diet 5-fold, without otherwise changing the CVP diet, nearly eliminated the incidence of MI.25
Epidemiologists have noted the experimental evidence linking Mg deficiency and heart disease and the clinical evidence that Mg is also useful in treating cardiac arrhythmias.7,22,24 The incidence of sudden cardiac death is lower among people living in hard water areas than among those drinking soft water.23,26 Hence, the higher Mg levels in hard water have been suggested as a factor that may protect against sudden cardiac deaths.
An important study with animals has illustrated the body’s ability to adapt to low Mg intake.27 Weanling rats that survived symptom-provoking hypomagnesemia gradually became free of overt signs of deficiency, and plasma Mg returned to normal levels. However, their ability to withstand induced stress conditions was reduced and their life spans were shortened, when compared with control animals consuming identical diets adequate in Mg.
Plasma Mg is normally maintained within a narrow range as the result of homeostatic control, even during periods of dietary restriction.8,9 Thus, plasma hypomagnesemia is a clear indication of severe Mg deficiency. However, normal plasma values are not necessarily a reliable indicator of normal tissue levels. The adaptation of rats to low intakes suggests that better means of diagnosing Mg deficiency are needed.27 The amount of Mg retained over a 24-hour period after a parenteral load is given is a better index, but is cumbersome and applicable only to those with normal renal Mg clearance.7 The most valuable index is to determine soft tissue levels. The heart, particularly vulnerable to Mg inadequacy, has more rapid Mg turnover than skeletal muscle or red blood cells, usually used for biopsies. A simplified test is currently being developed using white blood cells, which are actively metabolizing cells that may accurately reflect the Mg status in soft tissues.
There is substantial evidence suggesting that Mg intake in the U.S. is marginal. Why, then, is so little attention paid to the possibility of marginal Mg deficiency? Methodological difficulties contribute, as does the interpretation of findings from nutritional studies. A definition of optimal Mg requirement is needed. Instead of focusing on studies to determine minimal Mg requirements, it is preferable to know how much of a moderately high intake is necessary to establish equilibrium. The safety of even pharmacologic doses of Mg (except for those with immature or defective renal function) is attested to by the time-honored use of megadoses of Mg as a cathartic and as an anticonvulsant.
A number of diseases have characteristics resembling experimental Mg deficiency, some of which respond to Mg therapy. It remains to be determined whether increased intakes of Mg will reduce the incidence and severity of these diseases.
1. Seelig, M.S. Am. J. Clin. Nutr. 14:342-390, 1964.
2. Seelig, M.S. Magnesium Bulletin 3(1a) 27-47, 1981.
3. U.S. Department of Agriculture. Nationwide Food Consumption Survey. 1977-78. Preliminary Report No. 2. Washington, DC., 1980.
4. Food and Nutrition Board. Recommended Dietary Allowances. Edition No. 9. National Academy of Sciences. 1980.
5. Wacker, W.E.C. Magnesium and Life. Harvard University Press. Cambridge, MA, 1980.
6. Aikawa, J.K. Magnesium, Its Biological Significance CRC Press, Boca Raton, FL, 1981.
7. Seelig, M.S. Magnesium Deficiency in the Pathogenesis of Disease. Plenum Books Company. New York, NY. 1980.
8. Cantin, M.; Seelig, M.S. Editors Magnesium in Health and Disease. Proc. 2nd International Symposium on Mg. SP Medical and Science Books. Jamaica, NY, 1980
9. Magnesium Bulletin No.3 (Suppl 1a & b). Proc 3rd International Symposium on Mg. Baden Baden, W. Germany, 1981.
10. Schwartz, R. et al., Am. J. Clin. Nutr. 26:510-518, 1973.
11. Cockburn, R. et al., Arch. Dis. Child. 48:99-108, 1973.
12. Lindeman, R.D. at al. Magnesium in Health and Disease. pp 236-245. SP Medical and Science Books. Jamaica NY. 1980.
13. Spencer, H. et al. Magnesium in Health and Disease. pp 911-919. SP Medical and Science Books. Jamaica, NY, 1980.
14. Irwin, M.I., Feeley, R.M. Am.J. Clin. Nutr. 20:816-824, 1967.
15. Linden, V., In: Nutritional imbalances in Infant and Adult Disease. pp 23-42. SP Medical and Science Books. Jamaica, NY, 1977
16. Seelig, M.S. NY Acad. Science. 147:537-582, 1969.
17. Sandstead, H.H. et al. In: Dietary Fibers Chemistry and Nutrition pp 751-756. Academic Press. NY, 1979
18. Michiel, R.P. et al. New Engl. J. Med. 198:1005-1007, 1976.
19. Caddell, J.L. Pediatrics 66:392-413, 1965.
20. Durlach, J. Le Diabete. 19:99-113, 1971
21. Flink, E.B. JAMA. 160:1406-1409 1956.
22. Iseri, L.I.; Bures, A.R. Am. J. Med. 58:837-846, 1975.
23. Chadda, K.D. et al. Am. J. Cardiol. 31:98-100, 1973
24. Seelig, M.S.; Heggtveit, H.A. Am. J. Clin. Nutr. 27:59-79. 1974.
25. Sos, J. In: Electrolytes and Cardiovascular Diseases. pp. 161-182. S. Karger and Williams and Wilkins Baltimore, MD. 1965
26. Anderson, T.W. et al, In: Magnesium in Health and Disease. SP Medical and Science Books. Jamaica, NY. 1980.
27. Herous, O. et al. J. Nutr. 107:1640-1652, 1977.
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