A narrative review on the role of magnesium in immune regulation, inflammation, infectious diseases, and cancer Original paper

What was reviewed?

This narrative review examined how magnesium supports immune regulation and how magnesium deficiency drives inflammation, oxidative stress, infection risk, and cancer biology. The authors synthesized evidence on magnesium’s core roles in immune cell signaling, cytokine control, antibody and complement activity, and cellular energy and nucleic-acid stability. They also reviewed how magnesium intake, absorption, and renal handling shape systemic magnesium status, then connected magnesium biology to clinical patterns such as chronic low-grade inflammation, impaired antiviral defense, and tumor progression.

Who was reviewed?

The review covered a mix of animal experiments, human observational studies, mechanistic cell work, and selected clinical research, rather than one single patient cohort. The “who” therefore included rodents fed magnesium-deficient diets to model immune and inflammatory changes, cultured human and animal immune or endothelial cells used to map signaling pathways, and human populations studied for links between dietary or serum magnesium and outcomes. These human groups included older adults, post-menopausal women, hospitalized or critically ill patients, people with asthma, and patients studied during COVID-19 waves for associations between magnesium status and inflammatory burden.

What were the most important findings?

The review concluded that magnesium acts as a required immune cofactor and a gatekeeper of inflammatory tone. Magnesium deficiency repeatedly aligned with higher baseline inflammation, including higher pro-inflammatory cytokine signaling and oxidative stress, while also impairing adaptive responses such as cell-mediated immunity and immunoglobulin-related functions. Mechanistically, magnesium supported CD8+ T-cell effector function through magnesium-dependent regulation of LFA-1 activity, and magnesium flux through transport systems such as MAGT1 helped sustain signaling needed for immune activation. For microbiome-signature context, the review linked magnesium insufficiency to “inflammaging” and gut microbiota–related inflammatory stimuli, but it did not define consistent taxon-level microbial markers as major microbial associations.

What are the greatest implications of this review?

Clinically, this review positions magnesium status as a modifiable upstream variable that can shape immune competence, inflammation, and vulnerability to infection and malignancy. It supports screening for deficiency in higher-risk settings where low magnesium is common, including older age, critical illness, and chronic inflammatory states, because deficiency can amplify inflammatory cascades and weaken antiviral or antitumor immune responses. At the same time, the review emphasizes that excessive supplementation can be harmful, so clinicians should individualize dosing and monitor risk, especially in patients with altered renal handling.