See corresponding editorial on page 269.
Dietary magnesium intake and risk of stroke: a meta-analysis of
Susanna C Larsson, Nicola Orsini, and Alicja Wolk
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 summa-
rize the evidence regarding the association between magnesium in-
take and stroke risk.
Design: Relevant studies were identified by searching PubMed and
EMBASE from January 1966 through September 2011 and review-
ing 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 com-
bined 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-analy-
sis. We observed a modest but statistically significant inverse asso-
ciation 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%). Magne-
sium 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.
Am J Clin Nutr
Dietary magnesium intake has been inversely associated with
risk factors for stroke such as hypertension (1, 2), metabolic
syndrome (3), and type 2 diabetes (2, 4). Randomized clinical
trials have shown that magnesium supplementation modestly
reduces diastolic blood pressure (5) as well as fasting C-peptide
studies have shown that high-magnesium diets have favorable
effects on plasma glucose and blood lipid concentrations (7), and
magnesium deficiency increases the susceptibility of lipoproteins
to peroxidation (8). Hence, a high dietary magnesium intake may
potentially reduce risk of stroke.
To our knowledge, the epidemiologic evidence on the relation
between dietary magnesium intake and risk of stroke has not yet
been summarized. Therefore, we performed a systematic review
and dose-response meta-analysis to assess the association be-
tween magnesium intake and risk of total stroke and stroke
Literature search and selection
We followed standard criteria for conducting and reporting
of meta-analyses of observational studies (9). We conducted
a literature search of PubMed (http://www.ncbi.nlm.nih.gov/
pubmed) and EMBASE (http://www.embase.com) from January
1966 through September 2011 by using the key words “mag-
nesium intake”combined with“stroke.” Inaddition, we reviewed
reference lists of retrieved articles to identify additional relevant
studies. No language restrictions were imposed.
Studies were included in this meta-analysis if they fulfilled the
following criteria: 1) had a prospective design, 2) the exposure
of interest was magnesium intake, 3) the outcome was stroke,
and 4) the studies reported RRs with 95% CIs for ?3 quanti-
tative categories of magnesium intake. RRs had to at least be
adjusted for age and sex (if applicable).
The following data were extracted from each study: first
author’s last name, publication year, name of the cohort study,
study location, years of follow-up, sex, age, sample size (number
of cases and total number of participants), magnesium intake
categories, covariates adjusted for in the multivariable analysis,
and RRs with their 95% CIs for each category of magnesium
intake. We extracted RRs that reflected the greatest degree of
adjustment for potential confounders. Data extraction was con-
ducted independently by 2 investigators (SCL and NO) with
disagreements resolved by consensus.
1From the Division of Nutritional Epidemiology, National Institute of
Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
2Funding sources had no role in the design and conduct of the study;
collection, management, analysis, and interpretation of the data; or prepara-
tion, review, or approval of the manuscript.
3Supported by a research grant from the Swedish Council for Working
Life and Social Research and a Research Fellow grant from Karolinska
4Address correspondence to SC Larsson, Division of Nutritional Epide-
miology, National Institute of Environmental Medicine, Karolinska Institutet,
Box 210, SE-17177 Stockholm, Sweden. E-mail: email@example.com.
Received June 23, 2011. Accepted for publication October 24, 2011.
First published online December 28, 2011; doi: 10.3945/ajcn.111.022376.
Am J Clin Nutr 2012;95:362–6. Printed in USA. ? 2012 American Society for Nutrition
by guest on October 26, 2015