Contemporary Nutrition, January, 1982, Vol. 7 No. 1
Magnesium Requirements in Human Nutrition
Mildred S. Seelig, M. D., M.P.H., F.A.C.N.
Department of Medicine
Goldwater Memorial Hospital
University Medical Center
New York, New York 10044
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
Are the RDAs for Magnesium Optimal?
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.
Dietary Components that Increase the Requirements of
Magnesium
Calcium(Ca), Phosphate(PO4) and Vitamin D
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
Dietary Fat
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
Protein, Sugar and Alcohol
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
Magnesium Loss Caused by Stress
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.
Cardiovascular and Neuromuscular Risks of Magnesium
Deficiency
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.
Adaptation to Long-Term Low Magnesium
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.
Diagnosis of Magnesium Deficiency
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.
Conclusions
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.
References
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.
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NY. 1980.
13. Spencer, H. et al. Magnesium in Health and
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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,
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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,
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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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