Magnesium: Biochemistry, Nutrition, Detection, and Social Impact of Diseases Linked to Its Deficiency Original paper

What was reviewed?

This paper reviewed magnesium from four clinician-relevant angles: core biochemistry and cellular roles, diet sources and real-world reasons intake runs low in Western patterns, practical challenges in measuring magnesium status, and the disease burden tied to deficiency. It emphasized that magnesium supports hundreds of enzymes, ATP-dependent metabolism, DNA/RNA stability, neuromuscular signaling, and vascular function. It also highlighted that serum magnesium can stay “normal” even when intracellular and bone stores are depleted, which can mask chronic insufficiency in routine care.

Who was reviewed?

Because this was a review, it did not enroll a single cohort; it synthesized prior human and preclinical research across broad populations and high-risk clinical groups. The reviewed evidence included adults with cardiometabolic risk, people with type 2 diabetes or insulin resistance, postmenopausal and older adults at fracture risk, and patients affected by neurological conditions where excitability pathways matter. It also incorporated data on groups prone to low magnesium because of losses or malabsorption, including older adults, people with gastrointestinal diseases such as Crohn’s disease, inflammatory bowel disease, and celiac disease, and individuals exposed to medications that can lower magnesium.

What were the most important findings?

The review argued that chronic, subclinical magnesium deficiency is common and clinically meaningful because it shifts multiple pathways toward inflammation and dysfunction. Mechanistically, magnesium acts as a physiological calcium antagonist, modulates L-type calcium channels in the heart and vessels, supports endothelial nitric oxide biology, and stabilizes neuronal excitability through NMDA receptor gating, so low magnesium plausibly links to hypertension, arrhythmias, cramps, migraines, and neuropsychiatric symptoms.

What are the greatest implications of this review?

Clinicians should treat magnesium as a systems-level modifier rather than a minor electrolyte, especially when symptoms cluster across cardiometabolic, neuromuscular, and inflammatory domains. The review supports a practice shift toward risk-based assessment because serum magnesium alone may miss depleted tissue stores, and it strengthens the rationale for addressing diet quality and absorption barriers alongside supplementation when appropriate. For microbiome-aware care, the key implication is directional: gut health and fermentable fiber patterns can move magnesium bioavailability, and low magnesium can amplify low-grade inflammation that may worsen gut-related symptom loops, making magnesium a practical lever in integrative management.