Note: Our original copy of this article is defective and some
words and numbers are missing. These are indicated by "[...]".
The missing items will be filled in when we receive our new
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| © Masson, Paris, 1997 |
Ann. Med. Interne, 1997 |
| |
148, nº 6, pp. 440-444 |
| |
Synthèse
|
Magnesium fortification of water
A possible step forward in Preventive Medicine?
Yaron BAR-DAYAN, Yehuda SHOENFELD
|
SUMMARY : Magnesium fortification of water. A
possible step forward in Preventive Medicine?
Magnesium is an essential cation for more than 300
enzymes in our body. Among them, it is a cofactor for ATP
metabolism. Diverse clinical manifestations have been
reported in conjunction with Mg++ deficiencies,
including sudden death, accelerated atherosclerosis,
asthma, neurologic and even psychiatric clinical entities.
Limited previous studies with Mg++
supplementation have shown to be of a large preventive
advantages. We summarize the current literature concerning
Mg++ supplementation and recommend to do so on
national basis adding magnesium to the water supplies of
large areas.
Key words: Hypomagnesemia -- Sudden death --
Magnesium fortification of water.
|
RÉSUMÉ : Supplémentation de
1'eau en magnésium : un progrès en
médecine préventive ?
Le magnésium est un cation essential pour plus de
300 enzymes : il constitue un co-facteur de l'ATP. Diverses
manifestations cliniques dues au déficit en
magnésium ont été rapportées,
dont la mort subite, l'athéroselérose
accélérée, l'asthme, et certaines
maladies neuropsychiatriques. Peu d'études ont
porté sur la supplémentation
magnésienne et démontré ses avantages.
Nous analysons ici la littérature concernant la
supplémentation magnésienne et recommandons
la mise en place de supplementation de 1'eau en
magnésium dans de larges zones
géographiques.
Mots-clés : Hypomagnésémie
-- Mort subite -- Supplémentatioin de l'eau en
magnésium
|
Magnesium is the fourth most abundant cation in the human body
(following calcium, sodium and potassium). The average body
stores of magnesium in an average adult is between 20-28 grams
(1). Approximately 60 % of the magnesium in the body is found in
the bones and most of the remaining 40% are found in muscles and
other soft tissues. Close to one third is intracellular and the
rest is extracellular. The blood contains less than 1% of total
body magnesium stores (2). Magnesium plays an important role as a
cofactor of more than 300 enzymatic reactions, including:
glycolisis, ATP metabolism, transmembrane transport of other
cations such as sodium, potassium and calcium, protein and
nucleic acid synthesis, muscle contraction and nerve reactions
(1).
The National Research Council has recommended a minimal daily
consumption of 400 mg of magnesium for adults (3). The magnesium
content in different common food items is detailed in table
1. The average Western diet does not provide the recommended
daily intake of magnesium and therefore, magnesium deficiency is
very common in the Western society (3-5).
This article will review the mechanisms of magnesium
homeostasis, the cardiovascular manifestations of magnesium
deficiency and discuss the possible implications of magnesium
fortification of drinking water on the prevention of sudden
cardiac deaths in the general population of Israel.
Table 1. - The content of magnesium in different
common food items.
High concentration of magnesium
Moderate concentration of magnesium
fruits
vegetables
meat
fish
Low concentration of magnesium
Homeostatic mechanisms of magnesium
Magnesium homeostasis is regulated by a fine balance between
gastrointestinal absorption and renal excretion (6-10).
Magnesium is absorbed homogeneously throughout the small
intestine (6). The jejunal absorption of magnesium is vitamin D
dependent (7). The percentage of magnesium absorbed is inversely
proportional to the amount of this cation in the diet (6). The
average gastrointestinal tract absorption of magnesium on a
standard diet is [...] mg/day and the average secretion of
magnesium through the gastrointestinal mucosa is approximately
[...] mg/day (6).
The other major site of regulation of magnesium homeostasis is
the kidney. The excretion of magnesium varies between 3% to 25%
of the amount filtered in the glomeruli, depending on the serum
level of magnesium [...]. Magnesium restricted diet causes an
increase in magnesium reabsorption in the loop of Henle before
the occurrence of a detectable change in serum concentration
[...].The most important mechanism of regulation of magnesium
excretion in the kidney are changes in the reabsorption of the
filtered magnesium in the loop of Henle and the proximal tubule
(10). Magnesium reabsorption occurs mainly in the loop of Henle
(65%), and in the proximal tubule (20%-30%) and a smaller
percentage of magnesium is reabsorbed in the distal tubule
(2%-5%) [...]. The endocrine system might also have a role in the
regulation of magnesium homeostasis. Different studies have shown
that aldosteron might either increase or have an effect on
urinary magnesium excretion (11).
Magnesium deficiency
The serum level of magnesium does not necessarily [...] with
total body stores and patients with magnesium deficiency are
frequently asymptomatic, therefore, magnesium deficiency might be
difficult to diagnose (1). [...] of magnesium deficiency should
exist, regardless of measured serum level, in those conditions
which are accompanied by magnesium deficiency (11), such as:
[...] use of drugs which cause renal wasting of magnesium (e.g.
digoxin, gentamycin, loop. diuretics), [...], alcoholism,
hypokalemia and hypocalcemia or patients with diabetes
mellitus.
It is necessary to discriminate between magnesium deficiency
due to an insufficient magnesium intake which [...] requires oral
physiological supplementation and magnesium depletion related to
a dysregulation of the [...] mechanisms of magnesium status which
requires [...] or less specific regulation of its causal
dysregulation. (12). The average intake of magnesium in the
western diet is often barely adequate to meet daily requirements
and therefore, magnesium deficiency is very [...] in these
countries.
Hypomagnesemia is a common disorder found in 65% of an
intensive care unit population (14) and 11% of a [...] in-patient
population (15). Other investigators have shown that the
prevalence of hypomagnesemia in acute care patients in two
divisions of a consolidated medical center was 26.1% to 41.4%
compared to a frequency of 3.5% and 12.5% in the chronic care
population (16).
Magnesium deficiency might be asymptomatic even in severe
cases. If present, the clinical manifestations of magnesium
deficiency generally fall within one of five categories :
cardiovascular effects, respiratory function, neurologic and
neuromascular effects, psychiatric disturbances or metabolic
abnormalities (17).
Magnesium deficiency affects different targets in the
cardiovascular system :
Magnesium dietary intake modulates blood lipid levels,
atherogenesis and atherosclerosis (18, 19). Magnesium deficiency
enhances the uptake and metabolism of LDL by cultured human
endothelial cells (20). Magnesium modulates serum lipid uptake in
macrophages, smooth muscle cells and arterial wall (21).
Magnesium supplementation markedly attenuates the
artheroselerotic process, while dietary deficiency of magnesium
augments atherogenesis. Both magnesium aspartate and magnesium
sulfate were equipotent in preventing the development of
atherosclerosis and the rise in serum triglycerides caused by
cholesterol loading, although only magnesium aspartate lowered
the serum cholesterol levels (19). Magnesium deficiency might be
a contributing factor to ischemic heart disease and to variant
angina (22-24).
Magnesium has antiarrythmic effect. It prolongs the PR
interval, prolongs the sinuatrial conduction time, increases the
AV nodal refractory period, reduces automaticity and has no
effect on atrial or ventricular refractoriness or conduction
(11). Magnesium is a crucial cofactor in the Na-K-ATPase enzyme.
Thus, magnesium deficiency reduces the ability of the cell to
accumulate potassium against a concentration gradient. The
lowered intracellular potassium concentration leads to a less
negative resting membrane potential, which may make the cell more
easily depolarized and increases cellular excitability (11).
Magnesium therapy prevented ventricular premature beats in
patients with congestive heart failure (25), terminated
supraventricular tachyeardia (26, 27), multifocal atrial
tachycardia (28), atrial fibrillation (29), intractable
ventricular arrythmia (30) and torsades de pointes (31-35).
Patients with congestive heart failure are usually treated by
digitalis and loop diuretics which are well known causes of
magnesium deficiency (11). This fact is important because
magnesium deficiency enhances the arrythmogenic effect of
digitalis (36).
Magnesium deficiency is associated with myocardial injury
(cell degeneration, fibrosis, necrosis and calcifications).
Magnesium deficiency decreases the body's antioxidant capacity
and the resistance of the tissues to free radicals. This might be
the mechanism which associates magnesium deficiency with
cardiomyopathy (37).
Substantial evidence suggests that magnesium deficiency is
associated with sudden death (22). This fact is important because
sudden death is the major cause of mortality in the USA and it
accounts for over 300,000 deaths per year (38).
Magnesium toxicity and adverse reactions
Two different types of therapy with magnesium are used :
physiological oral magnesium supplementation which is totally
atoxic since it palliates magnesium deficiencies by simply
normalizing the magnesium intake and the high pharmacological
magnesium doses which may induce iatrogenic magnesium overload
(12). Clinically significant states of magnesium excess as a
result of oral physiologic dose of magnesium therapy are very
rare. In the presence of normal renal function, excess dietary
magnesium is virtually never a cause of toxicity (39). The risk
of hypermagnesemia is significant mainly in patients with renal
failure (1). The early symptoms of magnesium toxicity include
nausea, vomiting, and cutaneous flashing. In patients with severe
hypermagnesemia there is muscle weakness and reduction of deep
tendon reflexes (1). Table 2 summarize the various
symptoms of hypermagnesemia stratified by the blood levels of
magnesium (1). Case reports have demonstrated that patients with
normal renal function who develop magnesium toxicity, resulting
in refractory hypertension and even cardiac arrest, have all been
subjected to multiple frequent oral doses of magnesium containing
cathartics or antacids in massive total amounts ranging from 18
to 90 g of magnesium (39-41). No cases of hypermagnesemia have
been reported in patients with normal renal function with
appropriate use of magnesium containing cathartics (40).
Table 2. - The various symptoms of hypermagnesemia stratified
by the magnesium blood levels.
| Magnesium blood level |
The associated side-effect |
|
| 5-10 mEq/L |
Prolongation of PR interval |
| |
Prolongation of QRS duration |
| |
|
| 10 mEq/L |
Loss of reflexes |
| |
|
| 15 mEq/L |
Respiratory paralysis |
| |
|
| 25 mEq/L |
Cardiac arrest |
Magnesium supplementation
Magnesium supplementation has been proposed as a possible
preventive treatment for reducing the risk of sudden death. The
suggested ways of supplementing magnesium include public
education to change dietary habits, fortification of foods, oral
supplementation and addition of magnesium to water supplies (22).
In the general population the major portion of magnesium intake
is via food, and to a lesser extent via drinking water. However,
previous studies support the hypothesis that magnesium in
drinking water can be critical for the magnesium content of the
body. In the Western diet, in take of dietary magnesium is often
lower than the recommended dietary amounts (6 mg/kg/day) (42).
Water magnesium has a higher bioavailability because magnesium in
the water appears as hydrated ions which are absorbed 30% better
and much faster than magnesium in food. Magnesium in cooked food
is lost to the water and this reduces its bioavailability. Thus,
magnesium in the drinking water can make an important
contribution to the total daily intake (43). Magnesium and
calcium are the principal minerals that determine water hardness,
but the proportion of these minerals may very substantially. In
North America, Mg: Ca ratios generally range from 1 : 1 to 1 : 5,
but in certain areas of Western Europe, they may be two orders of
magnitude lower. Knowledge of Mg and Ca contributions to water
hardness is important when assessing studies relating Mg
deficiency and sudden death (22). Relations have been show,
between water magnesium and magnesium content in heart muscle
(44), coronary arteries (45), and skeletal muscles (46).
Epidemiological studies have demonstrated an inverse relation
between water hardness and death from cardiovascular disease,
primarily among men (47-54). A higher cardiac mortality rate was
seen in regions with "softer" water (47), with follow-up autopsy
studies in the same regions showing there were differences in
myocardial magnesium content between regions with "soft" or
"hard" water as well as greater differences in myocardial
magnesium between those who died from ischemic heart disease and
those who died accidentally (44). Little relationship was found
with non-acute heart disease (50). In hard water areas the
incidence of sudden cardiac death was 120 in 100,000, while in
soft water areas the incidence was 195 in 100,000 (22). The lower
death rate from ischemic heart disease in Japan, China, India,
Italy and Greece compared to the higher death rates from ischemic
heart disease in the USA and Europe was partially attributed by
some investigators to the differences in composition of dietary
salt (54). The salt used in Japan China, India, Italy, and Greece
is obtained by evaporating sea water, and therefore contains
calcium, potassium and large amounts of magnesium and sodium. The
table salt available in Northern Europe and the USA, however, is
obtained from salt mines. As a result of washing with
hydrochloric acid and recrystalization, this purified salt is
almost 100 % sodium chloride. Therefore, the average magnesium
intake in Japan China, India, Italy, and Greece is more than five
times the magnesium consumption for average adult in the USA and
Europe. Interestingly, the death rate from heart disease hast
almost doubled between 1975 and 1985 in Japan. This coincides
with the change, in 1972, from sea salt to pure sodium chloride
(54). It was reported that within a few years after drinking
water changes there was a reduction in death rate (55). A few
studies have found no correlation between magnesium intake and
cardiovascular mortality (56-58). However, the lack of
correlation between water hardness and sudden death in these
reports was later explained by the inclusion of hard water areas
with unusually low Mg concentration (22, 59). The recommended
level of magnesium in the water in Israel is limited to 50 mg/L.
A sample of drinking water from Tel-Aviv was taken in 1996 and
the magnesium concentrations of the samples were between 30-40
mg/L (unpublished data). This level is similar to the level found
in a previous study which was conducted in Israel 1970 (60),
although higher levels of magnesium (99-149 mg/L) were found in
the water of Eilat (60). Such differences in the concentration of
magnesium in the drinking water in two different areas of the
same country enables the comparison between the cardiac mortality
of these populations. Finally, it is becoming clear that a large
body of epidemiological data supports the idea that magnesium
deficiency can be a strong risk factor for hypertension, cardiac
arrythmias, ischemic heart disease and sudden cardiac death, but
most data come from observational rather than intervention
studies. Proof that magnesium supplementation reduces the risk of
sudden cardiac death is needed before efforts to increase Mg
intake are undertaken. A large, randomized, placebo controlled
study is needed in order to estimate the effect of magnesium
supplementation on primary prevention of sudden cardiac death in
the general population of Israel. If such a study demonstrates
that Mg supplementation reduces both sudden death and overall
mortality rates, magnesium fortification of water could lead to
another step forward in preventive medicine.
References
1. WAKER WEC, PARISI AF: Magnesium metabolisms. N Engl J
Med 1968; 278: 658-63, 712-7, 772-6.
2. REINHART RA : Magnesium metabolisms. Arch Intern
Med 1988; 148: 2415-20.
3. RYAN MF : The role of magnesium in clinical biochemistry :
an overview. Ann Clin Biochem 1991; 28:
19-26.
4. WHANG R : Routine serum magnesium determination--a
continuing unrecognized need. Magnesium 1987;
6: 1-4.
5. KARPANNEN H : Epidemiological studies on the relationship
between magnesium intake and cardiovascular diseases.
Artery 1981; 9: 190-9.
6. GRAHAM LA, CAESAR JJ, BURGEN ASV : Gastrointestinal
absorption and excretion of magnesium in 38 man. Metab Clin
Exp ; 1960; 9: 646-59.
7. SCHMULEN AC, LERMAN M, PAK CYC et al. : Effect of
1,25- (OH) 2D3 on jejunal absorption of magnesium in patients
with chronic renal disease. Am J Physiol 1980;
238: G349- 52.
8. BARKER ES, ELKINTON JR, CLARK JK : Studies of the renal
excretion of magnesium in man. J Clin Invest 1959;
38 : 1733-45.
9. SHAFIK IM, QUAMME GA : Early adaptation of renal magnesium
resorption in response to magnesium restriction. Am
J Physiol 1989; 257: F974-7.
10. QUAMME GA, DIRKS JH : The physiology of renal magnesium
handling. Renal Physiol 1986; 9 : 257-69.
11. Mc LEAN RM : Magnesium and its therapeutics uses : a
review. Am J Med 1994; 96: 63-76.
12. DURLACH J, DURLACH V, BAC P et al. : Magnesium
and therapeutics. Magnes Res 1994; 7:
313-28.
13. JONES JE, MANALO R, FLINK EB : Magnesium requirements in
adults. Am J Clin Nutr 1967; 20: 632-5.
14. RYZEN E, WAGERS PW, SINGER FR et al. : Magnesium
deficiency in a medical ICU population. Crit Care Med
1985; 13: 19-21.
15. WONG ET, RUDE RK, SINGER FR et al. : A high
prevalence of hypomagnesemia in hospitalized patients, Am J
Clin Pathol 1983; 79: 348-52.
16. LUM G: Hypomagnesemia in acute and chronic patient care
population. Am J Clin Pathol 1992; 97: 827-30.
17. FLINK EB : Magnesium deficiency. Etiology and clinical
spectrum. Acta Med Scand 1981 ; 647 (Suppl) :
125-37.
18. OUCHI Y, TABATA RE, STERGIOPOULOS K et al. :
Effect of dietary magnesium on development of atherosclerosis in
cholesterol fed rabbits. Arteriosclerosis 1990;
10: 732-7.
19. ALTURA BT, BURST M, BLOOM S et al. : Magnesium
dietary intake modulates blood lipid levels and atherogenesis.
Proc Natl Acad Sci USA 1990; 87:
1840-4.
20. YOKOYAMA S, GU J, KASHIMA K et al. : Combined
effects of magnesium deficiency and an atherogenic level of low
cultured human endothelial cells. II electron microscopic data.
Magnes Res 1994; 7: 97-105.
21. ALTURA EM, ALTURA BT : Cardiovascular risk factors and
magnesium: relationship to atherosclerosis, ischemic heart
disease and hypertension. Magnes Trace Elem 1992;
10 :182-92.
22. EISENBERG MJ : Magnesium deficiency and sudden death.
Am Heart J 1992; 124 : 544-9.
23. RASMUSSEN HS, Mc NAIR P, GORANSSON L et al. :
Magnesium deficiency in patients with ischemic heart disease with
and without acute myocardial infarction uncovered by an
intravenous loading test. Arch Intern Med 1988;
148: 329-32.
24. GOTO K, YASUE H, OKUMURA K et al. : Magnesium
deficiency detected by intravenous loading test in variant angina
pectoris. Am J Cardiol 1990; 65:
709-12.
25. GOTTLIEB S, FISHER ML, PRESSEL MD et al. :
Effects of intravenous magnesium sulfate on arrhythmias in
patients with congestive heart failure. Am Heart J 1993;
125: 1645-50.
26. WESLEY RC, HEINES DE, LERMAN BB et al. : Effect
of intravenous magnesium sulfate on supraventricular tachycardia.
Am J Cardiol 1989; 63: 1128-31.
27. SAGER PT, WIDERHORN J, PETERSON R et al. :
Prospective evaluation of parenteral magnesium sulfate in the
treatment of patients with reentrant AV supraventricular
tachycardia. Am Heart J 1990; 119 : 308-16.
28. ISERI LT, FAIRSHTER RD, HARDEMANN JL et al. :
Magnesium and potassium therapy in multifocal atrial tachycardia.
Am Heart J 1985; 110 : 879-85.
29. DE CARLI C, SPROUSE G, LA ROSA JC: Serum magnesium levels
in symptomatic atrial fibrillation and their relation to rhythm
control by intravenous digoxin. Am J Cardiol 1986; 57:
956-9.
30. ISERI LT, CHUNG P, TOBIS J : Magnesium therapy for intrac-
table ventricular tachyarrythmias in normomagnesemic pa- tients.
West J Med 1983; 138: 823-8.
31. TOPOL EJ, LERMAN BB : Hypomagnesemic torsades de pointes.
Am J Cardiol 1983; 52 : 1367-8.
32. RAMEE SR, WHITE CJ SVINARICH JT et al. : Torsades
de pointes and magnesium deficiency. Am Heart J 1985;
109: 164-6.
33. TZIVONI D, KAREN A, COHEN AN et al. : Magnesium
therapy for torsades de pointes. Am J Cardiol 1984;
53 : 528-30.
34. PERTICONE F, ADINOLFI L, BONADUCE D : Efficacy of
magnesium sulfate in the treatment of torsades de pointes.
Am Heart J 1986; 112 : 847-9.
35. TZIVONI D, BANAI S, SCHUGER C et al. : Treatment
of torsades de pointes with magnesium sulfate.
Circulation 1988; 77: 392-7.
36. SELLER RH, CANGIANO J, KIM KE et al. : Digitalis
toxicity and hypomagnesemia. Am Heart J 1970;
79: 57-68.
37. FREEDMAN AM, ATRACKHI AH, CASSIDY NM et at. :
Magnesium deficiency-induced cardiomyopathy : protection by
vitamin E. Biochem Biophys Res Commun 1990; 170
: 1102-6.
38. LOWN B : Sudden cardiac death : the major challenge
confronting contemporary cardiology. Am J Cardiol 1979;
43: 313-28.
39. FASSLER CA, RODRIGUEZ M, BADESCH DB et al. :
Magnesium toxicity as a cause of hypotension and hypoventilation.
Arch Intern Med 1985; 145: 1604-6.
40. SMILKSTEIN MJ, SMOLINSKE SC, KULIG KW et al. :
Severe hypermagnesemia due to multiple dose cathartic therapy.
West Med J 1988; 148 : 208-11.
41. GERARD SK, HERNANDEZ C, KHAYAM-BASHI H : Extreme
hypermagnesemia caused by an overdose of magnesium containing
cathartics. Ann Emerg Med 1988; 17: 728-31.
42. DURLACH J : Recommended dietary amounts of magnesium : Mg
RDA. Magnesium Res 1989; 2, 3: 229-32.
43. THEOPHANIDES T, ANGIOBOUST JF, POLISSIOU M et al.
: Possible role of water structure in biological magnesium
systems. Magnesium Res 1990; 3: 5-13.
44. ANDERSON TW, NERI LC, SCHREIBER GB et al. :
Ischemic heart disease, water hardness and myocardial magnesium.
Can Med Assoc J 1975; 113 : 199-203.
45. CRAWFORD T, CRAWFORD MD: Prevalence and pathological
changes of ischemic heart disease in hard water and soft water
area. Lancet 1967; 2 : 229-32.
46. LANDIN K, BONEVIK H, RYLANDER R et al. : Skeletal
muscle magnesium and drinking water magnesium level.
Magnesium Bull 1989; 11 : 177-9.
47. SCHROEDER HA : Relationship between mortality from
cardiovascular disease and treated water supplies. Variations in
states and 163 largest municipalities of the United States.
JAMA 1960; 172: 1902-8.
48. CRAWFORD MD, GARDNER MJ, MORRIS JN : Mortality and
hardness of local water supplies. Lancet 1969;
1 : 827-31.
49. COMSTOCK GW : Water hardness and cardiovascular disease.
Am J Epidemiol 1979; 110 : 375-400.
50. ANDERSON TW; LERICH LH, MAC KAY JS : Sudden death and
ischemic heart disease: correlation with water hardness and local
water supply. N Engl J Med 1969; 280:
805-6.
51. LEARY WP, REYES AJ, LOCKETT CJ et al. : Magnesium
and deaths ascribed to ischemic heart disease in South Africa.
S Afr Med J 1983; 64: 775-6.
52. LUBMA H, AROMAA A, HELMINEN S et al. : Risk of
myocardial infarction in Finnish men in relation to fluoride,
magnesium and calcium concentration in drinking water.
Acta Med Scand 1983; 213: 171-6.
53. RYLANDER R, BONEVIK H, RUBENOWITZ E: Magnesium and calcium
in drinking water and cardiovascular mortality. Scand J Work
Environ Health 1991 ; 17: 91-4.
54. KUMMEROW FA : Hypothesis : possible role of magnesium and
calcium in the development of structure and function of the
plasma membrane in mammalian cells and in human disease. J Am
Coll Nutr 1992; 11 : 410-25.
55. CRAWFORD MD, GARDNER MJ, MORRIS JN et al. :
Changes in water hardness and local death rates. Lancet
1971; 2 : 327-9.
56. NERBAND C, SVERDSUSS K, EK J et al. :
Cardiovascular mortality and morbidity in seven counties in
Sweden in relation to water hardness and geological settings.
Eur Heart J 1992; 13 : 721-7.
57. SHAPER AG, PACKHAM RF, POCOCK SJ : The British Regional
Heart Study : cardiovascular mortality and water quality. J
Environ Pathol Toxicol 1980; 4-2, 3 : 89-111.
58. BJÖRCK G, BOSTRÖM H, WIDSTRÖM A: On the
relationship between water hardness and death rates in
cardiovascular diseases. Acta Med Scand 1965;
178: 239-52.
59. RUBENOWITZ E, AXELSSON G, RYLANDER R: Magnesium in
Drinking water and death from acute myocardial infarction. Am
J Epidemiol 1996; 143 : 456-62.
60. SHILON M, SHAPIRA Y, MAGAZANICK A : Consumption of Arava
water and its effect on urinary calcium and magnesium.
Harefua 1973; 85: 203-6.
The study was supported by the Freda and Leon Schaller and the
Dead-Sea Works.
Department of Medicine 'B', Research Unit of Autoimmune
Diseases, Sheba Medical Center, Tel-Hashomer; and Sackler Faculty
of Medicine, Tel-Aviv University, Tel-Aviv, Israel.
Reprints : Y. SHOENFELD Dept. Medicine 'B', Sheba
Medical Center, Tel Hashomer, 52621 Israel.
Article reçu le 30 janvier 1997; acceptation
définitive le 21 mai 1997.
Related information on gastrointestinal absorption of
magnesium can be found at: Divalent Cation
Metabolism: Magnesium, p. 4.4, Gastrointestinal
Absorption of Magnesium. This is Volume One, Chapter 4,
edited by Tomas Berl and Joseph V. Bonvente, from a series of
books called the Atlas of Diseases of the Kidney, edited by
Robert W. Schrier.
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