Estimated Allowances of Magnesium

Reference from the joint report of FAO/WHO expert consultation on Human Vitamins and Minerals verbatim.

21. Department of Health. 1991. Dietary Reference Values for Food Energy and Nutrients for the United Kingdom. Report on Health and Social Subjects No. 41. London. HMSO.

The scarcity of studies from which to derive estimates of dietary allowances for magnesium has been emphasised by virtually all the agencies faced with this task. One United Kingdom agency commented particularly on the scarcity of studies with young subjects, and circumvented the problem of discordant data from work with adolescents and adults by restricting the range of studies considered (21).

27. Food and Nutrition Board/ National Research Council. 1989. Recommended Dietary Allowances. 10th edition. Washington, National Academy Press.

46. Scientific Committee for Foods. 1993. Nutrient and Energy Intakes for the European Community. Report of the Scientific Committee for Food, Thirty First Series. European Commission, Brussels.

Using experimental data virtually identical to those used for a detailed critique of the basis for US estimates (27), the Scientific Committee for Food of the European Communities (46) did not propose magnesium allowances (or population reference intakes, PRIs) because of inadequate data. Instead, they offered an acceptable range of intakes for adults of 150–500 mg/day and described a series of quasi-PRI values for specific age groups, including an increment of 30 percent to allow for individual variations in growth.

14. Nichols, B.L., Alvarado J., Hazelwood C.F. & Viteri F. 1978. Magnesium supplement in protein-calorie malnutrition. Am. J. Clin. Nutr., 31: 176-188. 

Statements of acceptable intakes leave uncertainty as to the extent of overestimation of derived recommended intakes. It is questionable whether more reliable estimates of magnesium requirements can be made until data from balance studies are supported by the use of biochemical indexes of adequacy that could reveal the development of manifestations of sub-optimal status. 

Such indexes have been examined, for example, by Nichols et al. (14) in their studies of the metabolic significance of magnesium depletion during PEM. A loss of muscle and serum magnesium resulted if total body magnesium retention fell below 2 mg/kg/day and was followed by a fall in the myofibrillar nitrogen-collagen ratio of muscle and a fall in muscle potassium content.

47. Montgomery, R.D. 1960. Magnesium metabolism in infantile protein malnutrition.

Lancet, 2:74-75.

48. Linder, G.C., Hansen,D.L. & Karabus, C.D. 1963. The metabolism of magnesium and other inorganic cations and of nitrogen in acute kwashiorkor. Pediatrics, 31: 552-568.

49. Caddel, J.L. 1969. Magnesium deficiency in protein-calorie malnutrition; a follow-up

study. Ann N Y Acad Sci., 162: 874-890.

Repletion of tissue magnesium status preceded a threefold increase in muscle potassium content. It accelerated by 7–10 days at the rate of recovery of muscle mass and composition initiated by restitution of nitrogen and energy supplies to infants previouslydeficient. Neurologic signs such as hyper-irritability, apathy, tremors, and occasional ataxia accompanied by low concentrations of potassium and magnesium in skeletal muscle and strongly negative magnesium balances were reported by many other studies of protein calorie deficiency in infants (47–49).

49. Caddel, J.L. 1969. Magnesium deficiency in protein-calorie malnutrition; a follow-up study. Ann N Y Acad Sci., 162: 874-890. 

31. Spencer, H., Lesniak, M. & Gatza, C.A., Osis, D. & Lender, M. 1980. Magnesium

absorption and metabolism in patients with chronic renal failure and in patients with

normal renal function. Gastroenterol., 79: 26-34.

50. Caddell, J.L. & Goodard, D.R. 1967. Studies in protein calorie malnutrition: I. Chemical evidence for magnesium deficiency. N. Engl. J. Med., 276: 533-535.

Particularly noteworthy is evidence that all these effects are ameliorated or eliminated by increased oral magnesium, as were specific anomalies in the electrocardiographic T-wave profiles of such malnourished subjects (49). Evidence that the initial rate of growth at rehabilitation is influenced by dietary magnesium intake indicates the significance of this element for those involved in the aetiology of the PEM syndromes (31, 50).

47. Montgomery, R.D. 1960. Magnesium metabolism in infantile protein malnutrition.

Lancet, 2:74-75.

48. Linder, G.C., Hansen,D.L. & Karabus, C.D. 1963. The metabolism of magnesium and other inorganic cations and of nitrogen in acute kwashiorkor. Pediatrics, 31: 552-568.

49. Caddel, J.L. 1969. Magnesium deficiency in protein-calorie malnutrition; a follow-up study. Ann N Y Acad Sci., 162: 874-890.

Neurologic signs such as hyper-irritability, apathy, tremors, and occasional ataxia accompanied by low concentrations of potassium and magnesium in skeletal muscle and strongly negative magnesium balances were reported by many other studies of protein calorie deficiency in infants (47–49).

49. Caddel, J.L. 1969. Magnesium deficiency in protein-calorie malnutrition; a follow-up
study. Ann N Y Acad Sci., 162: 874-890.

31. Spencer, H., Lesniak, M. & Gatza, C.A., Osis, D. & Lender, M. 1980. Magnesium absorption and metabolism in patients with chronic renal failure and in patients with normal renal function. Gastroenterol., 79: 26-34.

50. Caddell, J.L. & Goodard, D.R. 1967. Studies in protein calorie malnutrition: I. Chemical
evidence for magnesium deficiency. N. Engl. J. Med., 276: 533-535.

Particularly noteworthy is evidence that all these effects are ameliorated or eliminated by increased oral magnesium, as were specific anomalies in the electrocardiographic T-wave profiles of such malnourished subjects (49). Evidence that the initial rate of growth at rehabilitation is influenced by dietary magnesium intake indicates the significance of this element for those involved in the aetiology of the PEM syndromes (31,50).