Magnesium Research 2016; 29 (4): 146-53 REVIEW

Magnesium in metabolic syndrome:

a review based on randomized,
double-blind clinical trials
Copyright © 2017 John Libbey Eurotext. Téléchargé par NYU LANGONE MED CTR SCH OF MED HEALTH SCIENCES LIBRARY le 27/05/2017.

Fernando Guerrero-Romero, Francia O. Jaquez-Chairez, Martha Rodríguez-Morán

Biomedical Research Unit, Mexican Social Security Institute, Canoas 100, Col. Los Angeles,
34067 Durango, Dgo. Mexico
Correspondence: F Guerrero-Romero. Biomedical Research Unit, Mexican Social Security Institute, Canoas 100,
Col. Los Angeles, 34067 Durango, Dgo. Mexico
<guerrero.romero@gmail.com>

Abstract. A growing body of evidence shows the effect of magnesium on serum

glucose, HDL-cholesterol, and triglycerides levels, as well as on blood pres-
sure, which strongly suggests that magnesium might play an important role
in metabolic syndrome (MetS), a cluster of risk factors for cardiovascular dis-
ease and type 2 diabetes. We performed a systematic review of clinical evidence
derived from randomized, double-blind, controlled clinical trials, regarding the
efficacy of magnesium supplementation on the components of MetS. Using the
electronic databases of Medline, Embase, and the Cochrane Controlled Trials
Register up to May 2016, we looked for randomized controlled trials focused on
the effects of oral magnesium supplementation on insulin sensitivity, glucose,
triglyceride and HDL-cholesterol levels, as well as its effects on high blood pres-
sure, irrespective of the magnesium salt used, and with a duration of at least four
weeks. Crossover studies, irrespective of blinding criteria, were not included.
Results of this review show that magnesium supplementation in individuals
with hypomagnesemia can be effective in the treatment of MetS.
Key words: magnesium, hyperglycemia, low HDL-cholesterol, triglycerides, insulin
sensitivity

Metabolic syndrome (MetS) is a cluster of
risk factors for cardiovascular disease and type
2 diabetes that include obesity, hyperglycemia,
hypertriglyceridemia, low high-density lipopro-
tein cholesterol (HDL-C) levels, and high blood
pressure (HBP) [1]. Furthermore, insulin resis-
tance has been implicated in the development of
MetS [2, 3].
intake, increases in the prevalence of obesity and
hypomagnesemia have been reported [7].
Magnesium deficiency is involved in the patho-
genesis of dyslipidemia (hypertriglyceridemia and
low HDL-C) through increasing activity of lecithin
cholesterol acyl transferase and HMG-CoA reduc-
tase [9], and decreasing lipoprotein lipase activity
[8].
doi:10.1684/mrh.2016.0404

Given the prevalence of MetS in the general
population worldwide [4, 5], and that it might be
associated with a higher risk of all-cause mortal-
ity [6], strategies focused on its prevention and
treatment, emerge as a public health priority.
Perhaps as consequence of a westernized life-
style that promotes changes in customary dietary
Furthermore, magnesium is involved in more
than 300 enzymatic reactions including: glyco-
gen breakdown and ATP synthesis [10], decreases
in both tyrosine kinase activity at insulin recep-
tors [10, 11] and insulin secretion [12], as well
as in increases in tumor necrosis factor alpha
[13] and C-reactive protein levels [14]. Thus,

146
To cite this article: Guerrero-Romero F, Jaquez-Chairez FO, Rodríguez-Morán M. Magnesium in metabolic syndrome: a review
based on randomized, double-blind clinical trials. Magnes Res 2016; 29(4): 146-53 doi:10.1684/mrh.2016.0404

through the reduction of insulin sensitivity and
insulin secretion, and the triggering of the acute
phase reaction, hypomagnesemia is associated
with hyperglycemia.
Finally, also it has been reported that mag-
nesium, by competition for calcium receptors,
inhibits calcium flux into vascular smooth mus-
Copyright © 2017 John Libbey Eurotext. Téléchargé par NYU LANGONE MED CTR SCH OF MED HEALTH SCIENCES LIBRARY le 27/05/2017.
cle sarcoplasmic reticulum [15], attenuates Na-K
ATPase [16], and improves myocardial contractil-
ity [17] and endothelium-dependent vasodilation
[18]. Thus, it is not surprising that magnesium
deficiency contributes to an increase in blood pres-
sure.
Taking all of this into account, it is logical to
suppose that magnesium deficiency might play
a central role in the development of MetS; how-
ever, randomized double-blind controlled clinical
trials (RCTs) specifically designed to demonstrate
the effects that magnesium could exert on compo-
nents of MetS are scarce [19]. Thus, in this study
we reviewed clinical evidence derived from RCTs
regarding the efficacy of magnesium supplemen-
tation on the improvement of components of MetS.
We therefore searched the electronic databases
of Medline, Embase, and the Cochrane Controlled
Trials Register, up to May 2016, according to
RCTs focused on the ability of oral magnesium
supplementation to improve of insulin sensitivity,
glucose, triglycerides and HDL-cholesterol levels,
as well as high blood pressure, irrespective of the
magnesium salt used, and with a duration of at
least four weeks, which were the criteria for iden-
tifying the clinical trials of interest. Crossover
studies, irrespective of blinding criteria, were not
included.
Results
A total of 27 RCTs, focused on the evaluation of
the effects of magnesium supplementation on the
improvement of at least one of the components of
MetS were identified.
With regard to the role of magnesium supple-
mentation in the improvement of fasting glucose
levels, 14 RCTs that enrolled a total of 943 individ-
uals were identified; of these, 483 (49.6%) patients
with type 2 diabetes were enrolled in eight (57.1%)
studies. Only one (7.1%) RCT, that enrolled 62
(6.4%) subjects, was conducted involving individ-
uals with MetS. Finally, five (35.7%) studies were
conducted which involved 428 (44.0%) apparently
Magnesium and metabolic syndrome
healthy individuals. Treatment duration showed a
wide variation, from one month [21] to six months
[29], with an average of 2.7 months (table 1).
Data concerning serum magnesium at baseline
conditions were missing in four (28.6%) studies
[20, 22, 24, 25]. Four (28.6%) RCTs were focused
on patients with normal magnesium levels [27-29,
33], and six (42.9%) on individuals with low serum
magnesium levels [21, 23, 26, 30-32], (table 2).
Concerning the magnesium salt used, six
(42.9%), two (14.3%), two (14.3%), one (7.1%), one
(7.1%), one (7.1%), and one (7.1%), RCTs used
magnesium chloride, magnesium aspartate, mag-
nesium oxide, magnesium lactate-citrate, magne-
sium citrate, magnesium sulfate, and chelated
magnesium, respectively (table 1).
Age and body mass index (BMI) varied from
69.0 ± 5.9 years [22] in type 2 diabetic patients,
and ranging from 31.9 ± 1.0 years in metabol-
ically obese, normal weight individuals [31],
22.4 ± 1.6 kg/m2 in metabolically obese, normal
weight individuals, to 33.7 kg/m2 in individuals
with MetS [19].
Interestingly, no RCTs were found that eval-
uated, as the primary outcome, the efficacy of
magnesium supplementation on the improvement
of low-HDL-C or elevated triglycerides levels; even
the article by de Lordes et al. [21], conducted
among individuals with MetS, clearly states that
the primary trial end point was the change in the
HOMA-IR index.
However, a total of 16 RCTs were found to
have secondarily reported the effect of magne-
sium supplementation on HDL-cholesterol and
triglycerides levels; of these, 11 (68.8%) also
evaluated the effect of magnesium supplementa-
tion on fasting glucose levels [23-33] (table 1).
Thus, evaluation of magnesium supplementation
in improvement of the lipid profile had been per-
formed in 1052 individuals enrolled in 16 RCTs;
of these, 277 (26.3%) subjects, enrolled in five
(31.3%) RCTs, were patients with a diagnosis of
type 2 diabetes. Two (12.5%) studies were con-
ducted in 104 (9.9%) hypertensive individuals, one
(6.3%) in 62 (6.3%) subjects with MetS, one (6.3%)
in 43 (4.1%) individuals with ischemic heart dis-
ease, one (6.3%) in 68 (6.3%) individuals with
non-alcoholic fatty liver disease, and six (37.5%)
RCTs enrolled a total of 498 (47.3%) apparently
healthy individuals (table 1).
Treatment duration varied from two [21] to
six months [29], with an average duration of 3.6
months (table 1).
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 F. GUERRERO-ROMERO, ET AL.

Table 1. Characteristics of individuals enrolled into randomized, double-blind, placebo-controlled tri-

als to evaluate the role of magnesium supplements on fasting glucose, HDL-cholesterol, and triglyceride
concentrations

Author Target population Treatment N* Mg Salt** Dose level

(months) mg/d†
Gullestad [20] T2D 4 54 Lactate-citrate 15†
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de Lordes Lima [21] T2D 1 163 Oxide 20.7/41.4†

Barragán-Rodríguez [22] T2D & Depression 3 24 Chloride 450
Eibl [23] T2D 3 38 Citrate 30†
De Valk [24] T2D 3 50 Aspartate 15†
Rodriguez-Morán [25] T2D 4 63 Chloride 450
Guerrero-Romero [26] T2D & HBP 4 79 Chloride 450
Solati [27] T2D 3 47 Sulfate 300
Lima de Souza [28] MetS 3 60 Chelated 400
Mooren [29] Ow 6 47 Aspartate 365
Guerrero-Romero [30] Prediabetes 4 116 Chloride 382
Rodríguez-Morán [31] MONW 4 47 Chloride 382
Guerrero-Romero [32] IR 4 63 Chloride 300
Lee et al. [33] Ow or Obese 3 155 Oxide 300
Witteman [34] HBP 6 91 Aspartate 485
Zemel [35] HBP 3 13 Aspartate 20†
Karandish [36] NASH 3 68 Oxide 350
Marken [37] Healthy 2 70 Oxide 400
Rasmussen [38] IHD 3 43 Hydroxide 15†
Kawano Y [39] HBP 2 60 Oxide 20†
Hendersen [40] HBP‡ 6 41 Oxide 500
Doyle [41] Healthy 1 26 Hydroxide 22†
Sacks [42] Normotensive 4 300 Lactate 336
Purvis [43] T2D 4 28 Chloride 384
Hattori [44] HBP‡ 1 20 Oxide 600
Ferrara [45] HBP 6 14 Pidolate 15†
Itoh K [46] Healthy 1 33 Hydroxide 548

T2D, Type 2 diabetes; HBP, hypertension; MetS, metabolic syndrome; MONW, metabolically obese, normal
weight; IR, insulin resistance; Ow, overweight; NASH, non-alcoholic fatty liver disease; IHD, ischemic heart dis-
ease.*Individuals in the intervention/placebo groups**Individuals in the control groups received inert placebo, with
the exception of the study by Barragan-Rodríguez et al. [22] who received imipramine 25-150 mg/d;
†doses of magnesium salt, in mmol/d
‡treatment with diuretics

Data concerning serum magnesium at baseline
conditions are missing in three (18.8%) studies
[24, 25, 37]; six (37.5%) RCTs enrolled individu-
als with low serum magnesium levels [23, 30-32,
35], and seven (43.8%) involved individuals with
normal serum glucose levels [27-29, 33, 34, 36, 38]
(table 2).
As regards the magnesium salt used, five
(31.3%), four (25.0%), three (18.8%), one (6.3%),
one (6.3%), and one (6.3%) of the RCTs used
magnesium chloride, magnesium aspartate, mag-
nesium oxide, magnesium citrate, magnesium
sulfate, and chelated magnesium respectively
(table 1).
As regards the effect of magnesium supple-
mentation on the improvement of high blood
pressure, a total of eight RCTs with the pri-
mary end point being the reduction in systolic
and/or diastolic blood pressure were identified
[39-46]; in addition, the effect of magnesium

148
 Magnesium and metabolic syndrome

Table 2. Biochemical characteristics of individuals enrolled into randomized, double blind, placebo-
controlled trials to evaluate the role of magnesium supplements on fasting glucose, HDL-cholesterol,
and triglyceride concentrations

Author Magnesium* Glucose* HDL c* Triglycerides* SBP mmHg** DBP mmHg**

Gullestad [20] NA 8.8 ± 2.3 NA NA NA NA
de Lordes Lima 0.70 ± 0.18 10.3 ± 3.3 NA NA 134.0 ± 15.0 85.0 ± 8.0
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[21]
Barragán- NA 194.3 ± 59.0 45.6 ± 20.6 169.0 ± 53.8 134.1 ± 19.2 77.2 ± 3.9
Rodríguez
[22]
Eibl [23] 0.73 ± 0.8 8.5 ± 0.9 1.5 ± 0.4 2.0 ± 1.0 140 ± 18 83 ± 8
De Valk [24] NA 11.8 ± 3.6 1.28 ± 0.38 1.63 (1.32-2.02) 162.6 ± 23.3 84.0 ± 11.5
Rodriguez- NA 12.8 ± 5.6 0.9 ± 0.2 2.4 ± 1.4 148.3 ± 32.3 86.3 ± 17.0
Morán
[25]
Guerrero- 0.62 ± 0.10 13.6 ± 3.7 1.0 ± 0.4 2.9 ± 1.4 161.1 ± 26.0 88.4 ± 14.5
Romero
[26]
Solati [27] 0.88 ± 0.13 10.2 ± 0.8 1.14 ± 0.26 1.83 ± 0.77 117.9 ± 15.0 72.9 ± 8.1
Lima de Souza 0.74 ± 0.05 5.7 ± 0.8 1.20 ± 0.23 1.43 ± 0.49 134 ± 15.0 85.0 ± 8.0
[28]
Mooren [29] 0.89 ± 0.08 5.0 ± 0.6 1.36 ± 0.31 2.17 ± 1.13 137.7 ± 14.9 85.3 ± 9.4
Guerrero- 0.60 ± 0.08 6.3 ± 0.4 1.05 ± 0.40 2.49 ± 2.09 112.8 ± 16.0 74.7 ± 9.8
Romero
[30]
Rodríguez- 0.55 ± 0.10 6.1 ± 0.3 1.15 ± 0.28 3.99 ± 2.70 111.3 ± 14.5 71.5 ± 6.6
Morán
[31]
Guerrero- 0.61 ± 0.08 5.8 ± 0.9 0.9 ± 0.4 2.8 ± 2.1 110.0 ± 8.4 73.0 ± 7.5
Romero
[32]
Lee et al. [33] 0.94 ± 0.06 5.0 ± 0.5 1.13 ± 0.24 1.61 ± 0.85 124.4 ± 12.3 83.5 ± 9.7
Witteman [34] 0.86 ± 0.01 NA 1.41 ± 0.27 NA 146.4 ± 13.6 89.4 ± 6.7
Zemel [35] 0.72 ± 0.01 NA 1.55 ± 0.74 1.97 ± 2.35 136.0 ± 6.0 90.0 ± 2.0
Karandish [36] 2.06 ± 0.13 5.1 ± 0.8 1.06 ± 0.18 2.15 ± 0.93 NA NA
Marken [37] NA NA 1.19 ± 0.34 1.16 ± 0.87 NA NA
Rasmussen [38] 0.80 ± 0.1 NA 1.20 ± 0.3 2.41 ± 1.6 NA NA
Kawano Y [39] 0.89 ± 0.01 NA NA NA 148.6 ± 1.6 90.0 ± 0.9
Hendersen [40] 0.78 ± 0.07 NA NA NA 157 ± 24 93 ± 8
Doyle [41] 0.77 ± 0.11 NA NA NA 111.5 ± 8.7 75.4 ± 7.9
Sacks [42] NA NA NA NA 116 ± 8 73 ± 6
Purvis [43] NA 11.79 ± 0.63 1.04 ± 0.08 2.89 ± 0.59 141.5 ± 4.6 80.0 ± 2.4
Hattori [44] NA NA NA NA 138.1 ± 4.2 86.8 ± 2.3
Ferrara [45] 0.9 ± 0.1 NA NA NA 156 ± 12 97 ± 4
Itoh K [46] 0.86 ± 0.07 NA NA NA 130 ± 14 77 ± 9

Values are expressed as mean ± SD

NA, not available
*Serum levels, at baseline conditions in the intervention group, in mmol/L

supplementation on blood pressure was secon- that enrolled 1337 subjects; of these, seven (33.3%)
darily analyzed in 13 RCTs (table 2). Hence, the studies involved subjects with high blood pres-
effect of magnesium supplementation on high sure, four (19.0%) subjects with type 2 diabetes,
blood pressure was evaluated in a total of 21 RCTs three (14.3%) healthy individuals, two (9.5%)

149
 F. GUERRERO-ROMERO, ET AL.

Table 3. Effects of magnesium supplementation on the components of metabolic syndrome

Author IS Hyperglycemia Low HDL-c HTg HBP

Gullestad [20] –
de Lordes Lima [21] ±
Barragán-Rodríguez [22] – – + –
Eibl [23] –
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De Valk [24] – – – ±
Rodriguez-Morán [25] + + –
Guerrero-Romero [26] – + – +
Solati [27] + + + +
Lima de Souza [28] – – – –
Mooren [29] + –
Guerrero-Romero [30] + +
Rodríguez-Morán [31] + + + + +
Guerrero-Romero [32] + –
Lee et al. [33] + ±
Witteman [34] – – +
Zemel [35] – – –
Karandish [36] + – – –
Marken [37] – –
Rasmussen [38] + +
Kawano Y [39] ±
Hendersen [40] –
Doyle [41] –
Sacks [42] –
Purvis [43] +
Hattori [44] ±
Ferrara [45] –
Itoh K [46] +

IS, insulin sensitivity; HTg, hypertriglyceridemia; HBP, high blood pressure

+, improvement; ± , little to modest effect; –, no effect

overweight or obese, apparently healthy subjects,
one (4.8%) individuals with MetS, one (4.8%)
subjects with prediabetes, one (4.8%) involving
metabolically obese, normal weight individuals,
and one (4.8%) individuals with insulin resistance
(table 1).
Treatment duration showed a wide variation,
from one month [41] to six months [29, 34, 40, 45],
with an average of 3.6 months (table 1).
Data concerning serum magnesium at baseline
conditions are missing in six (28.6%) studies [22,
24, 25, 39, 42, 44]; nine (42.9%) studies enrolled
patients with normal magnesium levels [27-29,
33, 34, 40, 41, 45, 46], and six (28.6%) included
individuals with low serum magnesium levels [21,
26, 30-32, 35] (table 2).
As regards the magnesium salt used, seven
(33.3%), four (19.0%), four (9.0%), two (9.5%),
one (6.3%), one (4.8%) one (4.8%), and one
(4.8%) RCTs used magnesium chloride, magne-
sium aspartate, magnesium oxide, magnesium
hydroxide, magnesium sulfate, chelated mag-
nesium, and magnesium pidolate, respectively
(table 1).
Although a total of 27 RCTs had been conducted
to evaluate the effect of magnesium supplemen-
tation on the components of MetS, data for
evaluating the effect on insulin sensitivity, hyper-
glycemia, low HDL-c, hypertriglyceridemia, and
HBP are available in only six (22.2%), 12 (44.4%),
11 (40.7%), 11 (40-.7%), and 21 (77.8%), studies,
respectively (table 3).

150

The six studies that evaluated the effect of mag-
nesium supplementation on the improvement of
insulin sensitivity showed its efficacy in the reduc-
tion of HOMA-IR. As regards hyperglycemia, four
(33.3%) RCTs reported a significant decrease in
glucose levels. An improvement in HDL-C and
triglyceride levels was reported in four (36.4%)
Copyright © 2017 John Libbey Eurotext. Téléchargé par NYU LANGONE MED CTR SCH OF MED HEALTH SCIENCES LIBRARY le 27/05/2017.
and four (36.4%) RCTs, respectively. Finally, an
improvement in blood pressure was reported in
seven (33.3%) of the RCTs analyzed (table 3). A
small to modest effect was reported in one (8.3%)
and four (19.0%) of the RCTs evaluating improve-
ment in glucose levels (21) and high blood pressure
[24, 33, 39, 44], respectively
The studies by Rodriguez et al. [31] and Solati et
al. [27] reported an improvement in five and four
components of MetS respectively; in addition, five
(18.5%) studies showed an improvement in two
components [25, 30, 32, 33, 38] and 10 (37.0%)
studies in one component of MetS [21, 22, 24, 26,
29, 34, 36, 39, 45, 46]. Finally, nine (33.3%) of the
studies [20, 23, 28, 35, 37, 40-42, 45] showed no
effect of magnesium supplementation on the com-
ponents of MetS.
Conclusions
The results of this review show that, out of a total
of 18 (66.7%) RCTs, magnesium supplementation
is effective in the improvement of at least one com-
ponent of MetS; results that strongly suggest that
magnesium could be an alternative adjuvant in
the management of MetS
According to the recommendations of the
International Diabetes Federation [47], once a
diagnosis of MetS has been established, manage-
ment of the condition should be uncompromising
in its aim to reduce the risk of future disease; in
this regard, the promotion of a healthy lifestyle
is mandatory. Albeit evidence derived from RCTs
concerning the benefits of including magnesium
supplements in the pharmacological treatment of
MetS is not conclusive, it seems logical to make
every effort pursue a healthy lifestyle and to main-
tain appropriate serum magnesium levels.
A total of 18 (66.7%) RCTs showed improvement
in at least one component of MetS: accordingly,
magnesium supplements could be of benefit to
those individuals with MetS.
Of the 9 (33.3%) RCTs that showed no effect of
magnesium supplementation on the components
Magnesium and metabolic syndrome
of MetS, it is necessary to point out that seven
(77.8%) studies were conducted in healthy indi-
viduals [37, 41, 42] or, in whom at baseline, serum
magnesium levels were normal [28, 40, 41, 45], or
in those where data concerning magnesium sta-
tus at baseline are missing [20, 37, 42]. Given
that magnesium is strictly controlled within the
body, it is to be expected that administration of
magnesium supplements, under conditions of nor-
momagnesemia, would be rapidly regulated by
renal excretion, avoiding any additional biological
effect.
In addition, the heterogeneity related to the
bioavailability of the magnesium salt used, the
duration of treatment, and the health status of the
target population could also be a source of bias in
the interpretation of results.
In conclusion, the results of this review show
that magnesium supplementation in individu-
als with hypomagnesemia can effectively improve
aspects of MetS.
Disclosure
Financial support: none. Conflict of interest: none.
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