The study by Roman et al revealed that magnesium chloride (MgCl ₂ ) given throughout gestation decreased the incidence of intrauterine growth restriction (intrauterine growth retardation) and significantly decreased interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and Chemokine (C-C motif) ligand 2 (also referred to as monocyte chemotactic protein-1 [MCP-1] and small inducible cytokine A2) levels in amniotic fluid and IL-1β in placental tissues in comparison to the control group that received normal diet with bilateral uterine artery ligation or sham surgery. These results indicate that magnesium has antiinflammatory actions and promotes growth of the fetus despite bilateral uterine artery ligation. It would have been interesting had the authors measured plasma and amniotic fluid endothelial nitric oxide (eNO) and vascular endothelial growth factor levels and placental tissue nitric oxide synthase and vascular endothelial growth factor expression to know whether MgCl ₂ has actions on these indices that could explain its beneficial actions.

Magnesium intake is inversely associated with systemic inflammation and prevalence of the metabolic syndrome in middle-aged and older women that has been attributed to its favorable effects on glucose and insulin homeostasis, lipid metabolism, anticoagulant or antiplatelet action, and increase in endothelium-dependent vasodilation, possibly by increasing eNO generation. Human diploid fibroblasts, when cultured in magnesium-deficient conditions, showed increased senescence and accelerated telomere attrition. MgCl ₂ is not only a cofactor for the synthesis of adenosine triphosphate, polyphosphates such as DNA and RNA, and metabolic enzymes, but also plays a part in intracellular signaling. A rapid transient magnesium influx is induced by antigen receptor stimulation in normal T cells and by growth factor stimulation in nonlymphoid cells. Magnesium transporter gene, MAGT1, deficiency abrogated the magnesium influx, impaired responses to antigen receptor engagement, including defective activation of phospholipase Cγ1 and a markedly impaired calcium influx in T cells but not B cells, suggesting that magnesium functions as an intracellular second messenger coupling cell-surface receptor activation to intracellular effectors.

Magnesium deficiency in rats enhanced plasma total cholesterol, triglycerides levels, and of lipid peroxides. Fatty acid composition of the liver microsomes indicated a decrease in Δ ⁶ desaturase activity, which is the rate-limiting step in the conversion of dietary linoleic acid and α-linolenic acid to their respective long-chain products, in the magnesium-deficient rats compared with control. Thus, magnesium deficiency perturbs essential fatty acid metabolism and decreases cellular membrane polyunsaturated fatty acids that are known to enhance nitric oxide generation, regulate arterial tone via phosphatidylinositol 3-kinase, and inhibit the synthesis of IL-6 and TNF-α cytokines. Based on this evidence, I suggest that increased intake of magnesium ensures formation of adequate amounts of various polyunsaturated fatty acids, eNO, and suppression of inappropriate generation of IL-6 and TNF-α and thus, prevents intrauterine growth restriction and diabetes mellitus, and improves insulin resistance, hyperlipidemia, and possibly, preeclampsia.