2.413 1 Quantitative importance
Since dietary intake of
magnesium in developed countries is marginal, the
quantity of Mg present in water can, depending on
its level, represent the “critical
factor” that brings the level of dietary
intake from deficiency to an adequate
level (832, 833, 834, 835). Potable water
provides Mg directly when drunk and it also
influences magnesium intake through the amounts
in water used for cooking. A food loses much less
of its magnesium value when cooked in water high
in Mg. One should especially avoid using
artificially softened hot water to cook foods in
order to gain time (272, 391, 402, 560, 848,
849).
2.413 2 Qualitative importance
In the diet, Mg in water has a high level of
bioavailability. Experimental work in severely
deficient mice shows that an intake of 30 mg/L,
i.e., a level available in drinking water from
various distribution systems, is sufficient to
protect against death (1311). In humans, Mg in drinking water is more
rapidly and more highly absorbed than the rest of
dietary Mg (132, 778). Its presence in the diet
thus appears to be of particular importance. It
seems to be necessary, even in the absence of
magnesium deficiency. An insufficient
level of Mg in drinking water leads in the rat
and in humans to the observation — all
other data being equal — of a significant
arterial hypertension with satellite nervous,
endocrine and ion disorders (954). These problems
could derive from continued changes in the
demands made on the neuro-endocrine regulatory
mechanisms of magnesium homeostasis due to a
deficient intake of highly bioavailable Mg (361,
398, 401).
2.414 MD and cardiovascular disease
With the exception of idiopathic mitral valve
prolapse, of the form of MDI that causes
phlebothrombosis and of the rare forms of
cardiomegaly due to magnesium-dependent
hypocalcemia, there exists a large gap between
the information provided by epidemiology and
experimental research and the clinical proof of a
common cardiovascular pathology directly due to
MDI. One describes for example
“idiopathic” problems of cardiac
rhythm that can be cured with magnesium, but
their magnesium dependence has in general been
established only with the positive effects of
parenteral magnesium therapy (405, 633, 1287)
which may only be pharmacodynamic. In contrast,
the verification in a double blind study of
preventive effects obtained by oral magnesium
therapy for arrhythmias observed during open
heart surgery appear much more convincing. The
administration of Mg shows its effects in a
significant shortening of the corrected QT
interval (712). The existence of arrhythmia due
to magnesium deficit appears thus to be
established, but only during the course of this
secondary magnesium deficit.
MD can only be found occasionally in coronary
disease (4, 49, 50). It can only be found during
advanced forms and thus seems to be a secondary
problem with a physiopathology characteristic of
forms with hyperaldosteronism due to left heart
failure, with urinary magnesium wasting due to
salt diuretics (826) or with the release of
catecholamines due to the stress of the
infarction (404, 463, 464). Moreover, magnesium
deficiency in vivo only rarely leads to coronary
lesions (29, 784). It appears rather to be a
factor that favors spasms in the coronary
arteries (29, 200, 1402).
Hypertension is not normally involved in the
hemodynamic problems of experimental magnesium
deficiency (641, 1090). To cause hypertension,
experimental MD must be induced in subjects with
a particular background (31, 125). It may be the
same with humans. We have seen that two forms of
hypertension, labile hypertension and
hypercalcemic hypertension with elevated renin
levels may both be forms of MDI, although here
again the proof is not certain.
Similar reservations, all the more logical in
that cerebral ischemic attacks are themselves
correlated with hypertension, must also be
expressed about the role of MD in ischemic
arterial attacks (33, 323, 324, 346, 359, 402).
The occurrence of transient cerebral ischemic
accidents seems in any case to be favored by the
two major forms of MDI, mitral valve prolapse
(207 399) and latent tetany (447).
It is to be desired that clinical studies,
justified by such remarkable experimental and
epidemiologic research, be systematically
undertaken to determine the place of MDI among
cardiovascular risk factors. It certainly
deserves such a place, but new studies are
required to establish where it ranks in
importance among these factors.
Healthy Water
Association--USA