Understanding How Minerals Contribute to Optimal Immune Function Original paper

What was reviewed?

This paper reviewed how key dietary minerals support immune function and regulate inflammation, with a practical focus on magnesium, zinc, copper, iron, and selenium. The authors summarized mechanisms that shape innate immunity, adaptive immunity, and long-term inflammatory balance, and they paired these mechanisms with nutrition guidance and cautions about excessive supplementation. The review also described how mineral status can shift infection risk and chronic disease trajectories by altering immune cell signaling, cytokine production, oxidative stress control, and mucosal barrier stability.

Who was reviewed?

This was a narrative review, so it did not study one enrolled patient group; it reviewed previously published evidence across human studies, clinical trials, and relevant animal and mechanistic work. The reviewed literature covered general adult populations and higher-risk groups such as older adults, pregnant individuals, people with chronic disease or restricted diets, and those with mineral insufficiency that can weaken immune competence. The evidence base also included immune cell and tissue models that clarify mineral-driven effects on macrophages, neutrophils, lymphocytes, and inflammatory signaling pathways.

What were the most important findings?

The review argued that mineral adequacy protects immune performance by preventing a predictable pattern: overactive innate inflammation paired with weaker adaptive responses. For magnesium, it described immunoregulatory control of inflammatory signaling, including reduced cytokine output after immune stimulation through inhibition of NF-κB activation, and it emphasized magnesium’s role in T-cell development through Mg2+ transporters like TRPM7. For a microbiome signatures database, the strongest direct microbial association appeared under magnesium deficiency, where the review linked low magnesium to compromised intestinal barrier integrity and reduced bifidobacteria, alongside higher proinflammatory cytokines such as TNF and IL-6 in gut and liver. For zinc, it emphasized that deficiency impairs innate killing capacity and adaptive T-cell balance, while excessive zinc can suppress immunity. For copper, iron, and selenium, it highlighted that both low and high status can distort host defense, with iron and selenium tightly tied to oxidative stress and infection outcomes.

What are the greatest implications of this review?

Clinicians should treat mineral status as a modifiable immune driver, not a minor nutrition detail, especially when patients show recurrent infections, chronic low-grade inflammation, slow recovery, or diet and absorption risks. The review supports a food-first approach and targeted supplementation only when deficiency risk is clear, because oversupplementation can backfire and worsen immune regulation. For microbiome-informed care, the magnesium section provides a clinically useful bridge: magnesium deficiency can weaken the gut barrier and reduce beneficial bifidobacteria, which can amplify inflammatory signaling beyond the intestine and reinforce systemic immune dysregulation.