Effects of long-term magnesium supplementation on endothelial function and cardiometabolic risk markers: A randomized controlled trial in overweight/obese adults

Joris, Peter J.; Plat, Jogchum; Bakker, Stephan J. L.; Mensink, Ronald P.

doi:10.1038/s41598-017-00205-9

Cited by 36 publications

(39 citation statements)

References 43 publications

(63 reference statements)

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“…Magnesium could potentially confer protection against CAD by enhancing endothelium-dependent vasodilation and reducing vascular resistance, oxidative stress and oxidised lipids, inflammation and thrombosis, and by anti-arrhythmic effects [ 2 , 4 , 7 , 16 , 17 ]. Several [ 8 , 9 , 13 ] but not all [ 38 , 39 ] randomised trials have shown that magnesium supplementation improves endothelial function and reduces arterial stiffness. The inconsistent results may be related to magnesium status among study participants, as improvement in endothelial function with magnesium supplementation was observed in trials involving patients with low serum magnesium levels [ 9 ] and patients using diuretics [ 8 ], which often cause hypomagnesaemia.…”

Section: Discussionmentioning

confidence: 99%

Serum magnesium levels and risk of coronary artery disease: Mendelian randomisation study

Larsson

Burgess

Michaëlsson

2018

BMC Med

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BackgroundObservational studies have shown that serum magnesium levels are inversely associated with risk of cardiovascular disease, but whether this association is causal is unknown. We conducted a Mendelian randomisation study to investigate whether serum magnesium levels may be causally associated with coronary artery disease (CAD).MethodsThis Mendelian randomisation analysis is based on summary-level data from the CARDIoGRAMplusC4D consortium’s 1000 Genomes-based genome-wide association meta-analysis of 48 studies with a total of 60,801 CAD cases and 123,504 non-cases. Six single-nucleotide polymorphisms associated with serum magnesium levels at genome-wide significance were used as instrumental variables.ResultsA genetic predisposition to higher serum magnesium levels was inversely associated with CAD. In conventional Mendelian randomisation analysis, the odds ratio of CAD was 0.88 (95% confidence interval [CI] 0.78 to 0.99; P = 0.03) per 0.1-mmol/L (about 1 standard deviation) increase in genetically predicted serum magnesium levels. Results were consistent in sensitivity analyses using the weighted median and heterogeneity-penalised model averaging methods, with odds ratios of 0.84 (95% CI 0.72 to 0.98; P = 0.03) and 0.83 (95% CI 0.71 to 0.96; P = 0.02), respectively.ConclusionsThis study based on genetics provides evidence that serum magnesium levels are inversely associated with risk of CAD. Randomised controlled trials elucidating whether magnesium supplementation lowers the risk of CAD, preferably in a setting at higher risk of hypomagnesaemia, are warranted.Electronic supplementary materialThe online version of this article (10.1186/s12916-018-1065-z) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Serum magnesium levels and risk of coronary artery disease: Mendelian randomisation study

Larsson

Burgess

Michaëlsson

2018

BMC Med

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“…A recent study that also found magnesium supplementation did not significantly affect markers of chronic low-grade inflammation can be critiqued in a similar manner. 39 Magnesium was supplemented for 24 weeks in 52 overweight/obese individuals with mean serum magnesium concentrations ranging from 0.84 to 0.87 mmol/L. In these apparently magnesium-adequate individual, magnesium supplementation did not decrease adhesion factors serum VCAM-1, ICAM-1, and E-selectin.…”

Section: Introductionmentioning

confidence: 95%

“…In these apparently magnesium-adequate individual, magnesium supplementation did not decrease adhesion factors serum VCAM-1, ICAM-1, and E-selectin. 39 A recent systematic review and meta-analysis of randomized controlled trials support the suggestion that magnesium supplementation will affect markers of inflammatory stress only when they are elevated. 40 In the overall meta-analysis, magnesium treatment did not significantly affect CRP.…”

Section: Introductionmentioning

confidence: 99%

“…Other studies have found markers of inflammatory stress not elevated in obese or overweight individuals with serum magnesium concentrations indicating adequacy. 38 , 39 Conversely, obesity or being overweight may be significant factors in finding an association between magnesium and chronic low-grade inflammation. Obese and overweight individuals might have a higher magnesium requirement to counteract chronic low-grade inflammation.…”

Section: Introductionmentioning

confidence: 99%

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Magnesium deficiency and increased inflammation: current perspectives

Nielsen

2018

JIR

199

125

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Animal studies have shown that magnesium deficiency induces an inflammatory response that results in leukocyte and macrophage activation, release of inflammatory cytokines and acute-phase proteins, and excessive production of free radicals. Animal and in vitro studies indicate that the primary mechanism through which magnesium deficiency has this effect is through increasing cellular Ca2+, which is the signal that results in the priming of cells to give the inflammatory response. Primary pro-inflammatory cytokines such as tumor necrosis factor-α and interleukin (IL)-1; the messenger cytokine IL-6; cytokine responders E-selectin, intracellular adhesion molecule-1 and vascular cell adhesion molecule-1; and acute-phase reactants C-reactive protein and fibrinogen have been determined to associate magnesium deficiency with chronic low-grade inflammation (inflammatory stress). When magnesium dietary intake, supplementation, and/or serum concentration suggest/s the presence of magnesium deficiency, it often is associated with low-grade inflammation and/or with pathological conditions for which inflammatory stress is considered a risk factor. When magnesium intake, supplementation, and/or serum concentration suggest/s an adequate status, magnesium generally has not been found to significantly affect markers of chronic low-grade inflammation or chronic disease. The consistency of these findings can be modified by other nutritional and metabolic factors that affect inflammatory and oxidative stress. In spite of this, findings to date provide convincing evidence that magnesium deficiency is a significant contributor to chronic low-grade inflammation that is a risk factor for a variety of pathological conditions such as cardiovascular disease, hypertension, and diabetes. Because magnesium deficiency commonly occurs in countries where foods rich in magnesium are not consumed in recommended amounts, magnesium should be considered an element of significant nutritional concern for health and well-being in these countries.

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“…On the other hand, a study examined the effects of Mg 2+ supplementation on the endothelial function of overweight and obese individuals, middle-aged adults, and the elderly, subjected to a daily magnesium supplement of 350 mg for 24 weeks. There was no observed improvement in soluble vascular cell adhesion molecule (sVCAM)-1, soluble intercellular adhesion molecule (sICAM)-1, and soluble endothelial selectin (sE-selectin), along with no change in FMD markers of endothelial function or inflammatory parameters [ 41 ].…”

Section: The Role Of Mg 2+ In Hematopoiesismentioning

confidence: 99%

A Review of the Action of Magnesium on Several Processes Involved in the Modulation of Hematopoiesis

Lima

Fock

2020

IJMS

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Magnesium (Mg2+) is an essential mineral for the functioning and maintenance of the body. Disturbances in Mg2+ intracellular homeostasis result in cell-membrane modification, an increase in oxidative stress, alteration in the proliferation mechanism, differentiation, and apoptosis. Mg2+ deficiency often results in inflammation, with activation of inflammatory pathways and increased production of proinflammatory cytokines by immune cells. Immune cells and others that make up the blood system are from hematopoietic tissue in the bone marrow. The hematopoietic tissue is a tissue with high indices of renovation, and Mg2+ has a pivotal role in the cell replication process, as well as DNA and RNA synthesis. However, the impact of the intra- and extracellular disturbance of Mg2+ homeostasis on the hematopoietic tissue is little explored. This review deals specifically with the physiological requirements of Mg2+ on hematopoiesis, showing various studies related to the physiological requirements and the effects of deficiency or excess of this mineral on the hematopoiesis regulation, as well as on the specific process of erythropoiesis, granulopoiesis, lymphopoiesis, and thrombopoiesis. The literature selected includes studies in vitro, in animal models, and in humans, giving details about the impact that alterations of Mg2+ homeostasis can have on hematopoietic cells and hematopoietic tissue.

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Effects of long-term magnesium supplementation on endothelial function and cardiometabolic risk markers: A randomized controlled trial in overweight/obese adults

Cited by 36 publications

References 43 publications

Serum magnesium levels and risk of coronary artery disease: Mendelian randomisation study

Serum magnesium levels and risk of coronary artery disease: Mendelian randomisation study

Magnesium deficiency and increased inflammation: current perspectives

A Review of the Action of Magnesium on Several Processes Involved in the Modulation of Hematopoiesis

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