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Blaine Journal, January 1998


Dr. Mildred S. Seelig

Supplementation of Ca to 1.5 grams daily, has recently been recommended by the Food and Nutrition Board of the National Academy of Science.1 Not taken into account is the evidence that this amount of Ca, taken by individuals whose daily Mg intake has been shown by many extensive dietary surveys to be below 300mg,2-7 will intensify the inadequacy of the ingested Mg, with risk of causing Mg deficiency.

In the extensive 1935 study of Ca, Mg and P, 600 mg of Mg/day was recommended, with a Ca/Mg ratio of 2/1,8 a ratio that has long been considered physiologic, on the basis of long-term metabolic studies in young men and women by the Research Division of the United States Department of Agriculture,9 that were analyzed in 1964.10 It was then shown that with Mg intakes of under 5 mg/kg/day (the amount of Mg usually consumed from the diet) an intake of Ca of over 10 mg/kg/day (about 800 mg/day) interfered with Mg retention, causing negative Mg balance in 76% of the balance periods of the young men and in half of the metabolic balance periods of the young women. At Mg intakes of over 6 mg/kg/day, both men and women retained Mg even on high Ca intakes.10 When the Ca intake was further increased to 1000 mg/day, as in a study of young women, whose Mg intake was at the typical American intake of 250-300 mg a day, there was net loss of Mg over a 60 day period.11 A more recent study with eight healthy young women ingesting the recommended dietary allowance (RDA) for Mg and Ca (300 and 800 mg/day respectively), showed that supplementation to 1.5 g Ca/day -- the amount now being recommended -- resulted in markedly increased Mg loss.12 Thus, at Ca intakes of almost twice the early RDA for Ca of 800 mg/day, Mg supplementation was needed to maintain a normal 2/1 ratio of Ca/Mg.

Now that the RDA for Ca has been set at 1500 mg/day, without regard for the inadequacy of the usual diet to provide sufficient Mg to maintain Mg equilibrium, even with lower Ca intakes, the risk of inducing Mg deficiency has been increased. During growth and development, pregnancy, heavy exercise and other stresses, which are anabolic states in which there is increased need for Mg for new tissue formation,13 the likelihood of Mg deficiency is intensified. Nutrients that increase Mg needs (fats, calcium, phosphate, vitamin D and sugar) are ample in the American diet. Even modest intakes of alcohol increase Mg loss, and high fiber intakes interfere with mineral (including Mg) absorption. There is an object example in Finland of the effects of just such a diet, which provides a high Ca/Mg intake of 4/1, as well as high salt and alcohol intakes. Karppanen and his colleagues implicate the high Ca/Mg dietary ratio as being contributory to that country's highest stroke and ischemic heart disease rate in the world, in young and middle aged men 14 (Figure).

bj0198fg - Figure

Since the typical American intake of Mg (by women) is under 300 mg/day, providing a 1500 mg/day intake of calcium would yield a 5/1 Ca/Mg ratio, exceeding the 4/1 ratio in Finland. This high an amount of Ca is particularly recommended for women, to protect against osteoporosis. It is thus of interest that in Finland, where a dietary Ca/Mg ratio of 4/1 is common from childhood throughout life osteoporosis is prevalent.15 Since Mg is a constituent of the organic matrix of bone,13,16 it seems that life-long high Ca intake may not protect against osteoporosis when the Mg intake is inadequate.


Human metabolic studies (cited above) have shown that Ca and Mg, especially when one ispresent in high concentrations, interfere with intestinal absorption and renal tubular reabsorption of the other. Extensive dietary survey studies have shown that most Americans have Mg intakes substantially below that recommended, whereas Ca intakes are at or only slightly below recommended amounts even before the recent increase to 1500 mg/day.2-7

Experimental animal studies have shown that disproportionately large Ca content of Mg deficient diets intensifies the damage caused by subacute and long-term Mg deficiency. These include cardiovascular complications (from arrhythmias, and sudden death) and vascular damage c h a r a c t e r i s t i c o f arteriosclerosis, as well as hypertension, renal tubular microliths and interstitial calcinosis, and bone abnormalities (very hard, brittle bones with abnormal matrix and lacking flexibility).13,16


Manifestations of toxemias of pregnancy, and of adverse effects of abnormal pregnancy on the fetus are very likely to reflect Mg deficiency. The recognized efficacy of parenteral Mg for severe eclampsia (hypertension and convulsions) and; the newer use to delay preterm delivery (tocolysis), reflect repair of Mg deficiency, as well as pharmacologic effects of its parenteral administration. The growing evidence that much of the disorder (of eclampsia) stems from platelet aggregation and fibrin-related problems (from microthrombi -- especially placental), and fibrin deposition in renal glomeruli, and the anticoagulant activity of Mg links Mg deficiency to the pathogenesis of these serious diseases of pregnancy.17 Since a high Ca/Mg ratio enhances both the coagulation cascade and platelet aggregation directly and through their reciprocal effects on platelet and endothelial derived substances,18,19 substantially increasing the Ca intake without supplementing with Mg during pregnancy should be undertaken only with concern for the effect on Mg and Ca on thrombogenic and vasoconstrictive parameters.


Studies with catecholamine-secreting granules from the adrenal medulla or from nerve endings, suspended in solutions providing low Mg/Ca ratios or high Mg/Ca ratios have shown that low Mg increases catecholamine release, and that high Mg decreases it, whereas high Ca increases catecholamine secretion especially when Mg is low.20 Since increased Ca stimulates catecholamine release, the effect of verapamil, a Ca channel-blocker, on catecholamine release has been compared with that of Mg, which is a physiologic Ca-blocker. Cerebral arterial contractions of the cat, induced by norepinephrine, were enhanced by low and inhibited by high Mg concentrations, the effect being attributed partly to inhibition of Ca uptake.21

Pertinent to the effect of is a study of college students who retained Mg throughout a month-long metabolic balance study, while on Mg supplementation of 9 mg/kg/day, except for one week in which one of the students was taking final exams. During that week he lost Mg; and his sustained positive Mg balance during his high Mg intake became negative.22 This loss can be attributed to increased epinephrine secretion, since hypomagnesemia has been reported in patients in clinical situations where blood catecholamines are raised, and after epinephrine infusions to normal volunteers.23


Hypertension has long been recognized as a consequence of emotional stress, such as hostility, anxiety, frustration, worry, and tension, which evoke acute and sustained elevations of blood pressure. Resnick and his colleagues have demonstrated that regardless of whether clinical hypertension is associated with low or high plasma renin activity (PRA), free intracellular (i.c.) Mg is depressed in hypertensive patients.24,25 Their work has solved the puzzle of lack of uniformity of response of hypertensive patients to Ca, Mg, and Ca-channel blocking agents. Those with low PRA, have a hypotensive response to Ca supplementation; those with high PRA respond better to Mg supplementation. It is important to note that Mg deficiency increases renin secretion (causing high PRA). They found a continuous negative correlation of PRA with serum Mg levels. However, they found that in both PRA groups the free i.c. Mg was closely and inversely correlated with the degree of hypertension. This finding was also true for experimental hypertension of rats -- whether caused by mineralo-corticosteroid and salt loading, or whether by nephrectomy or renal ischemia. Their observations have led them to postulate that it is the low i.c. free rbc Mg, common to thin and obese hypertensive patients, and to hypertensives with abnormal glucose tolerance, that explains the common coincidence of hypertension in obese patients with or without diabetes mellitus, and in diabetics, whether or not they are obese. In a study of total rbc Mg levels (a less sensitive parameter than the free ionic Mg, but more accurate than serum Mg) of middle-aged patients with labile hypertension, those who had low total rbc Mg had their blood pressure lowered by three months of Mg supplementation.26


Metabolic balance studies of patients with osteopathies and/or hypercalciuria, whose Mg intakes were below 300 mg/day, showed that Ca supplementation intensified their negative Mg balances. Middle-aged and elderly recovering alcoholics (who are prone to Mg deficiency) and patients receiving Mg-wasting corticosteroids for rheumatoid arthritis, who were given 2 g/day Ca, showed increased Mg and Ca retention after receiving Mg supplements of 1 g/day for 3 weeks. The improvement of Ca. utilization resulting from increased Mg intake, might result from the effect of Mg on parathyroid secretion and on synthesis of the hormonal forms of vitamin D.31


It is important to keep in mind that nutritional recommendations designed to protect against one disease (i.e. osteoporosis), should not increase the risk of another (i.e. ischemic heart disease). Japan, which had the most favorable Ca/Mg ratio with the lowest heart disease prevalence in the figure, has been increasingly adopting a Western dietary pattern which includes a rise in the Ca/Mg ratio. Urban Japanese have experienced a rise of cardiovascular disease prevalence approximately equivalent to that in the Occident.32

Dietary surveys have indicated that the customary dietary intake of Mg in the United States is often below 300 mg, providing less than 5 mg/kg/day.2-7 Administration of Ca supplements should be accompanied by appropriate Mg supplementation. Increasing the Mg intake protects against high Ca-intensification of the risk of Mg deficiency. Positive Ca balance of subjects who are Mg deficient, and who are given Ca supplements, is difficult to interpret, since it may reflect deposition not only in bone, but also in soft tissue as calcinosis (characteristic of low Mg and high Ca intakes), or in arteries as arteriosclerosis, as has been demonstrated in many species (to be discussed in a future Blaine Journal).


1. Food Nutrition Board, Natl Acad Sci., Chapter3.1997.

2. Pao E.M, Mickle S.J. (1981) Food Technology35:58

3. Lakshmanan F.L., Rao R.B., Kim W.W., Kelsay J.L. (1984). Am J Clin Nutr.40:1380

4. Morgan K.J., Stampley G.L. (1988). Magnesium, 7:225

5. Morgan K.J., Stampley G.L., Zabik M.E., Fischer D.R. (I 985), J Am Coll Nutr.4: 195

6. Abdulla M., Behbehani A., Dashti H. (I 989) ed Itokawa Y., and Durlach J., Magnesium in Health and Disease, Publ. J. Libbey, London: III.

7. Pennington J.A., Young B.E. (1991). J Am Diet Assoc 91:179183.

8. Schmidt C.L.A., Greenberg D.M., Physiol Rev, 15: 297.

9. Hathaway F.W., Home Economics Research Report #19, Agricultural Research Service, Washington D.C., 1962.

10. Seelig M. S. (1964). Am 3 Clin Nutr 14:342.

11. Irwin M.I., Feeley R.M. (1967) Am J Clin Nutr,20:816.

12. Spiller G.A., Jensen C.D., Whittam J.H. (1988). FASEBJ.,2:A1099.

13. Seelig M.S. (1980). Magnesium Deficiency in the pathogenesis of disease. Early Roots of Cardiovascular, Skeletal, and Renal Abnormalities. Pub] Plenum Press, NY, pp

14. Karppannen H. (1990). Magnesium Bulletin 12:80-86.

15. Simonen H. (1991). Calcif Tiss Res (Suppl) 49:S8.

16. Seelig M.S. (1990). Magnesium Res 3:197.

17. Weaver K. (1986).Magnesium 5:191200.

18. Hwang DL, Yen CF, Nadler JL (1992). Am J Hypertens 5:700.

19. Seelig M.S. (1993). J Am Coll Nutr 12:442- 458.

20. Seelig M.S. (1994). J Am Coll Nutr 12:429.

21. Farago, M., Szabo, C., Dora, E., et al (1991). J Cerebr Blood Flow Metab 11:161.

22. Gormican A, Catli, E [1971] Nutr Metab 13:364-377.

23. Whyte K.F., Addis G.J., Whitesmith R., Reid J.L. (1987). Clin Sci 72:135.

24. Resnick L.M. (1992). Am J Med 93(2A): 11S20S.

25. Barbagallo M., Novo S., Licata G., Resnick L.M. (1993). Intl Angiol 12:365370.

26. Rueddel H., Baehr M., Schaechinger H., Schmieder R., Ising G. (1989). Magnesium Bulletin 11:9398.

27. Parlier R., Hioco D., LeBlanc R. (I 963). Rev Franc Endocr Clin, 4:93.31

28. Leichsenring J.M., Norris L.M., Lamison S.A. (1951) J Nutr 45:477.

29. Briscoe A.M., Ragan C. (1966). Am J Clin Nutr, 19:296.

30. Lichton, J (1989). Magnesium 8:117.

31. Fatemi S, Ryzen E, Flores J, Endres DB, Rude RK (1991). J Clin Endocrinol Metab 73:1067.

32. Kimura M., Nagai, K, Itokawa, Y. (1989). In Magnesium in Health and Disease. eds Itokawa Y, Durlach J, Publ J. Libbey, London: 63.

The above article is from the January 1998 , Blaine Journal, "A Medical Publication for Today's Healthcare Providers." Blaine Pharmaceuticals is the manufacturer of Mag-Ox 400 and Uro-Mag magnesium supplements. Their website includes sections on products, magnesium education, The Magnesium Report, medical advisory board, research, medical meetings, and a magnesium library. As of this date, March 2002, parts of the site are still under construction.
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Blaine Pharmaceuticals publishes The Magnesium Report, a newsletter of clinical, research, and laboratory news for cardiologists. Articles now available in on this site include:

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