Background: Prospective studies of dietary magnesium intake in relation to risk of stroke have yielded inconsistent results.
Objective: We conducted a dose-response meta-analysis to summarize the evidence regarding the association between magnesium intake and stroke risk.
Design: Relevant studies were identified by searching PubMed and EMBASE from January 1966 through September 2011 and reviewing reference lists of retrieved articles. We included prospective studies that reported RRs with 95% CIs of stroke for ≥3 categories of magnesium intake. Results from individual studies were combined by using a random-effects model.
Results: Seven prospective studies, with 6477 cases of stroke and 241,378 participants, were eligible for inclusion in the meta-analysis. We observed a modest but statistically significant inverse association between magnesium intake and risk of stroke. An intake increment of 100 mg Mg/d was associated with an 8% reduction in risk of total stroke (combined RR: 0.92; 95% CI: 0.88, 0.97), without heterogeneity among studies (P = 0.66, I2 = 0%). Magnesium intake was inversely associated with risk of ischemic stroke (RR: 0.91; 95% CI: 0.87, 0.96) but not intracerebral hemorrhage (RR: 0.96; 95% CI: 0.84, 1.10) or subarachnoid hemorrhage (RR: 1.01; 95% CI: 0.90, 1.14).
Conclusion: Dietary magnesium intake is inversely associated with risk of stroke, specifically ischemic stroke.
Seven
randomised
clinical
trials
in
a
total
of
over
1,300
patients
have
examined
the
effects
of
intravenous
magnesium
salts
(chloride
or
sulphate)
given
early
after
acute
myocardial
infarction.
Five
of
them
(Abraham
et
al.,
1987;
Ceremuzynski
et
al.,
1989;
Rasmussen
et
al.,
1986,
1987,
1988a;
Schechter
et
al.,
1990;
Smith
et
al.,
1986)
reported
a
reduction
in
mortality,
in
frequency
of
arrhythmias
or
both
in
those
patients
who
received
magnesium.
Two
(Feldstedt
et
al.,
1988;
Morton
et
al.,
1984)
were
negative;
the
first
of
these
included
only
76
patients.
Rasmussen
et
al.
(1986,
1988a)
randomised
273
patients
with
suspected
acute
myocardial
infarction
to
receive
62
mmol
magnesium
chloride
or
saline
over
48
h.
Significantly
fewer
patients
had
infarction
confirmed
in
the
magnesium
group
and
mortality
at
1
year
was
32%
in
the
placebo
group
and
20%
in
the
magnesium
group
(P
<
0.02).
Although
none
of
the
trials
had
sufficient
statistical
power
to
be
conclusive,
collectively
they
strongly
suggest
a
beneficial
effect
of
intravenous
magnesium
and
this
interpretation
is
supported
by
a
formal
meta-
analysis
of
all
the
available
data
(Teo
et
al.,
1990).
A
further
trial
with
a
sample
size
of
2,500
patients,
due
to
be
completed
in
early
1992,
is
described
in
a
later
section.
Magnesium
antagonises
the
effects
of
calcium
in
a
range
of
important
cellular
processes
and
many
of
its
cardiovascular
effects
can
be
described
as
those
of
‘Nature’s
physiological
calcium
blocker’
(Altura
et
al.,
1987;
Iseri
&
French
1984).
In
addition
magnesium
is
important
for
the
function
of
many
key
enzymes,
including
adenylate
cyclase
(Bockaert
et
al.,
1984).
The
main-
tenance
of
free
intracellular
magnesium
concentration
([Mg2+],)
within
narrow
limits
suggests
that
the
cation
has
a
regulatory
role
(Maguire,
1984;
White
&
Hartzell,
1989).
Developments
in
3
P
nuclear
magnetic
resonance
spectroscopy
and
in
fluorescence
spectrophotometry
for
the
measurement
of
[Mg2+]i
are
rapidly
expanding
our
understanding
of
basic
mechanisms
and
it
is
opportune
to
draw
together
the
clinical
and
laboratory
data
which
might
have
relevance
to
the
therapeutic
use
of
magnesium
in
myocardial
infarction.
This
paper
reviews
the
pharmacological
effects
on
the
cardiovascular
system
which
occur
when
serum
magnesium
concentration
is
raised
above
the
physio-
logical
range
(0.7-0.95
mM),
and
considers
how
the
clinical
course
of
acute
myocardial
infarction
might
be
modified
in
consequence
