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FRANZ KBa, SEELIG MSb aBrigham Young University, Provo, UT, USA; bUniversity of North Carolina, School of Medicine, Chapel Hill, NC, USA

Key Words: magnesium, calcium, phosphorus, vitamin D, DRI, RDA, AI, UL, eclampsia, syndrome X, hypertension, cardiovascular disease, diabetes mellitus

New dietary standards are being developed in the United States, and Canada to replace the Recommended Dietary Allowances (RDAs) of 19801, that were revised in 19892, and the 1990 recommendations from Health Canada. The RDAs were established to prevent deficiency diseases; the new standards, termed Dietary Reference intakes (DRIs), are intended to provide amounts of nutrients that will help in achieving and maintaining optimum health and limit chronic disease. The Food and Nutrition Board (of the Institute of Medicine, National Academy of Sciences, the United States) presented DRIs for magnesium (Mg), calcium (Ca), phosphorus (P), and vitamin D in August 1997.3

The New Dietary Standards (Table 1): As part of the new DRIs, additional terms are introduced. Adequate Intake (AI) is a new term that is similar to the RDA, but that is based on less extensive evidence. The new term, the Estimated Average Requirement (EAR) is a median requirement to meet the needs of 50% of an age and gender group. RDAs were set for Mg and P based on their EARs. Since there were too few data to set EARs for Ca and vitamin D, only AIs were designated. A third new term is the Tolerable Upper Intake Levels (UL), from both food and supplements, that applies to Ca, P, and vitamin D. The UL for Mg is the intake only from supplements. The UL designates the maximum amount that is unlikely to pose risks of adverse health effects. It is not the recommended level of intake.


Table I. The 1997 DRIs for magnesium, calcium, phosphorus, and vitamin D.





Vitamin D-AI(ug)





























































*Above 1989 RDA; **Below 1989 RDA; ***Above 1989 but below 1980 RDA


DRIs are higher for Mg, than they were in the 1989 RDAs, but lower than in the 1980 RDAs for pregnant women. For Ca and P, the DRIs are lower than the RDAs for some but higher for others. Adult Ca intake is increased from 800 mg to 1000 mg for adults up to the age of 50 years, and further increased to 1200 mg for those older than 50. Adult DRIs for vitamin D are similar to the previous RDAs for young adults, but are higher for those older than 50. Ca and vitamin D recommendations for older adults were increased largely to prevent osteoporosis. ULs (Table II) were developed to provide guidelines for supplements and for nutritional fortification of foods.


Table II. The tolerable upper limits (UL) for magnesium, calcium, phosphorus, and vitamin D.





Vitamin D*






All ages





For Mg, UL is intake only from supplements; does not include Mg in food and water.
For Ca, P, and vitamin D, includes the total intake from food, water, and supplements.


Some Concerns: The UL of Mg was estimated as the amount that will cause the least diarrhea, even in the minority with intestinal sensitivity to Mg supplementation.3 This low UL for Mg may induce some in the medical community to restrict Mg supplementation to the UL for all individuals, even though higher amounts are needed by some, certainly during pregnancy, by those with familial predisposition to cardiovascular diseases in which low intracellular (i.c.) Mg has been identified, and by normal persons undergoing stress.4-6 This has recently been illustrated by the beneficial effect of 411-548 mg Mg/day on blood pressure and HDL-cholesterol, in apparently healthy individuals.7

In contrast to the low UL for Mg supplements (350mg), the UL for Ca is high (2500 mg). Allowing for addition of the supplemental Mg to the customary Mg intake of about 300, the intake of some could reach ratios exceeding 5:1 by those ingesting the UL for Ca. Might the ULs of Ca and vitamin D be interpreted by some in the medical community as more desired intakes than the AIs for these nutrients, even though this was not the intent of these recommendations? More information is needed about the impact of UL levels of intake of Ca and vitamin D upon intestinal Mg absorption, distribution in the body, and renal excretion, particularly by those with low Mg intake.

Although the RDA for P was decreased for adults, dietary intakes of P are usually much higher. P can come in several different forms in the diet; some are better absorbed by the intestines than others. About 65% of food P is absorbed, but phytic acid8 or polyphosphate additives to food,9 are poorly absorbed. The unabsorbed P binds to Ca and Mg ions and decreases their absorption.8 If 3500 mg of P were consumed in the diet and 65% was absorbed, this would result in 1225 mg of fecal P. If dietary Mg were low, its decreased absorption through binding to P, could result in increased risk of Mg deficiency, as a result of fecal excretion of more Mg than was ingested. With poorly absorbed P compounds, critical levels of stool P that adversely affect intestinal Mg absorption could be achieved with P intakes lower than the UL.

The negative impact of high dietary Ca: Mg ratios on Mg in the body, which has been implicated in the high cardiovascular disease morbidity and mortality in Finland,10 might be contributed to by the P that often accompanies high Ca intake, with subsequent impact on intestinal Mg absorption.8 A liter of skim milk contains about 1270 mg Ca, 135 mg Mg, and 1035 mg P. The dietary P:Mg ratio may be as important as, or in those with high milk diets or with intake of other high P foods or drinks, be even more significant than the dietary Ca-Mg ratio because of the greater impact of P on Mg intestinal absorption.

On the other hand, increasing use of high dose Ca supplements (e.g. to prevent or limit progression of osteoporosis11,12), or as reflected by a recent large study of administration of 2 grams of supplemental Ca to see if it would prevent eclampsia,13 puts the emphasis on potential risks of high Ca:Mg intakes. Ca supplementation did not prevent eclampsia among the 2295 women given the Ca, as compared with 2294 given placebo. Data were provided in tables that indicate somewhat worse outcomes in Ca supplemented than in control mothers. Occurring more often in the Ca-group than in the controls were: 1.) HELLP, an uncommon severe toxemic -syndrome comprising hemolysis, elevated hepatic enzymes, and low platelet count (7 versus 2); 2.) small for gestational age infants (124 versus 105); 3.) preterm births (344 versus 314); 4.) infants requiring intensive care (343 versus 315); and 5.) neonatal deaths (12 versus 6). No data were given as to Mg intakes or status. Low dietary Mg intakes are common in the U.S.A. both in low and average income pregnant women.14 In Hungary, there is high prevalence of spontaneous abortions and preterm births in low Mg areas;15, 16 and early Mg supplementation during pregnancy has been beneficial,15 a finding also in a double-blind study in Germany.17

Insight into why Mg supplementation during pregnancy protects both mother and fetus, while high Ca intake does not, is provided by elucidation of pathogenic mechanisms of eclampsia, which involve placental pathology - caused by platelet aggregation and adhesion and enhancement of the coagulation cascade, which enhance likelihood of thrombosis, and by endothelial damage with release of vasoconstricting thromboxane.18,19 These reactions are inhibited by Mg,20-22 while Ca has reciprocal effects.21 It has been hypothesized that low Mg is the unifying factor in pregnancy pathologies, and that early Mg supplementation might prevent much pregnancy-induced disease.24

An ionic hypothesis attributes to low i.c. free Mg and excess cytosolic free Ca, such clinically disparate disorders as Syndrome X, which includes obesity, insulin-resistance, hyperinsulinemia, non-insulin-dependent diabetes mellitus and left ventricular hypertrophy, as well as hypertension and atherosclerosis.25 Higher ionized Ca:Mg ratio in cells, in comparison with that in normal individuals, has been reported in atherosclerosis and essential hypertension,26,27 hypertension associated with preeclampsia28,29 and during labor,30 and diabetes mellitus whether or not associated with pregnancy.25, 28, 31 Usually, ionized Ca is increased or normal as ionized Mg is decreased. Is this cellular imbalance due to chronic Mg deficiency in the body or factors that directly increase Ca uptake - be they dietary, from use of supplements, hormonal, or other? If cellular ionized Ca is increased or normal and ionized Mg is decreased, increasing dietary Ca, or providing large Ca supplements without a concomitant increase in Mg intake seems imprudent.



1. Food & Nutrition Board, National Research Council. Recommended Dietary Allowances, 9th ed. Washington, D.C., National Academy Press, 1990.

2. Food & Nutrition Board, National Research Council. Recommended Dietary Allowances, 10th ed. Washington, D.C., National Academy Press, 1999.

3. Food & Nutrition Board, Inst of Mod. Dietary Reference Intakes: Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride. Washington, D.C., Natl Acad Press, 1997.

4. Seelig MS. Magnesium in the Pathogenesis of Disease: Early Roots of Cardiovascular, Skeletal and Renal Abnormalities, Publ: Plenum Press, NY, 1980.

5. Seelig MS. Nutritional status and requirements of magnesium, with consideration of individual differences and prevention of cardiovascular disease. Magnesium Bull 1986; 8:170-185.

6. Seelig MS: Consequences of magnesium deficiency enhancement of stress reactions-, preventive and therapeutic implications. J Am Coll Nutr 1994, 12:429-446.

7. Itoh K, Kawasaki T, Nakamura M, The effects of high oral magnesium supplementation on blood pressure, serum lipids and related variables in apparently healthy Japanese subjects, Brit J Nutr 1997; 78:737-650.

8. Franz, KB. Influence of phosphorus on intestinal absorption of calcium and magnesium, In Itokawa Y, Durlach J, eds. Magnesium in Health and Disease London, John Libbey: 1989:71-8.

9. Zemel MB, Linkswiler HM, Calcium metabolism in the young adult male as affected by level and form of phosphorus intake and level of calcium intake. J Nutr 1991; 111:315-24.

10. Karppannen H, Pennanen R, Passinen L. Minerals, coronary heart disease and sudden coronary death. Adv Cardiol 1978; 25:9-24.

11. Seelig MS. Increased magnesium need with use of combined estrogen and calcium for osteoporosis. Magnesium Research 1990; 3:197-215.

12. Elders PJ, Lips P, Netelenbos JC, et al. Long-term effect of calcium supplementation on bone loss in perimenopausal women. J Bone Miner Res 1904; 9:963-970.

13. Levine RJ, Hauth JC, Curet LB, et al. Trial of calcium to prevent preeclampsia. New Engl J Med 1997. 337:69-76

14. Franz KB- Magnesium deficiency during pregnancy, Magnesium 6:18-27, 1997,

15. Kuti V, Balazs M, Morvay F, et al. Effect of maternal magnesium supply on spontaneous abortion and premature birth and on intrauterine foetal development: experimental epidemiological study. Magnesium Bul 3; 73-79, 1991.

16. Losonczy J, Adorjan G, Novak M, Toth MO. Correlation between the incidence of preterm delivery and the concentration of magnesium in drinking water in Szabolcs-Szatmar County, Northeast Hungary. Magnesium Res 1989; 2:229-230.

17. Spaetling L, Spaetling G. Magnesium supplementation in pregnancy. A double blind study. Br J Obstet Gynec 95:120-125, 1988

18. Roberts JM, Taylor RN, Musci TJ, et al. Preeclampsia: an endothelial disorder. Am J Obstet Gynecol 1989, 161:1200-1204, 1989).

19. Wang Y, Walsh S. hormonal and related mechanisms for preeclampsia of pregnancy. Endocrinologist 1997; 7:239-244.

20. Weaver K, Pregnancy-induced hypertension and low birth weight in magnesium-deficient ewes. Magnesium 1986; 5-191-200.

21. Briel RC, Lippert TH, Zahradnik HP. [Changes in blood coagulation, thrombocyte function and vascular prostacyclin synthesis caused by magnesium sulfate]. Geburtshilfe Frauenheilkd 1987; 47:332-336. (in GERMAN)

22. Watson KV, Moldow CF, Ogburn PL, Jacob HS. Magnesium sulfate: rationale for its use in preeclampsia. Proc Natl Acad Sci USA 1986; 83:1075-1078

23. Seelig MS. Interrelationship of magnesium and estrogen in cardiovascular and bone disorders, eclampsia, migraine, and premenstrual syndrome. J Am Coll Nutr 1993, 12:442-458.

24. Newman JC, Amarasingham JL: The pathogenesis of eclampsia: the magnesium ischaemia hypothesis. Med Hypotheses 40; 250-2,56, 1993.

25. Resnick LR. Ionic disturbances of calcium and magnesium metabolism in essential hypertension, in "Hypertension: Pathophysiology, Diagnosis, and Management" Eds JH Laragh & BM Brenner, Publ Raven Press Ltd, NY, 2nd Ed, 1995: pp 1169-1191.

26. Delva PT, Pastori C, Degan M, Montesi GD, Lechi A. Intralymphocyte free magnesium in a group of subjects with essential hypertension. Hypertension 1996; 28:433-43.

27. Altura BM, Zhang A, Altura BT, Magnesium, hypertensive vascular diseases, atherogenesis, subcellular compartmentation of Ca2+ and Mg 2+ and vascular contractility. Miner Electrolyte Metab 1993; 19:323-336.

28. Bardicef M, Bardicef O, Sorokin Y, et al. Extracellular and intracellular magnesium depletion in pregnancy and gestational diabetes. Am J Obstet Gyncol 1995; 172, 1009-1013.

29. Standley CA, Whitty JE, Mason BA, Conon DB. Serum ionized magnesium levels in normal and preeclamptic gestation. Obstet Gynecol 1997-89:24-27.

30. Handwerker SM, Altura BT, Royo R, Altura BM. Ionized magnesium and calcium levels in umbilical cord serum of pregnant women with transient hypertension during labor. Am J Hypertens 1993, 6(Pt 1); 542-545.

31. Resnick LM, Altura BT, Gupta RK, et al, Intracellular and extracellular magnesium depletion in type 2 (non-insulin-dependent) diabetes mellitus. Diabetologia 1993; 36:767-770.

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