Manganese
Manganese is an essential cofactor, but dietary deficiency in humans has essentially never been documented outside experimental depletion — while manganese excess is a well-characterised neurotoxic syndrome. This is a nutrient almost nobody should be supplementing.
What the science says
- Deficiency is a non-problem; toxicity is the real one Moderate evidence
Manganese is required for mitochondrial superoxide dismutase, arginase and several glycosyltransferases, but human dietary deficiency has never been convincingly demonstrated outside controlled depletion experiments — grains, nuts, tea and legumes supply it abundantly. The clinical literature on manganese is overwhelmingly about excess, and the same transport biology that makes it essential is what makes it neurotoxic above a threshold.
- Excess causes manganism, a parkinsonian syndrome Moderate evidence
Chronic overexposure — welding fume, contaminated drinking water, long-term parenteral nutrition, liver failure — accumulates manganese in the globus pallidus and produces manganism: dystonia, bradykinesia, gait disturbance, tremor and psychiatric change. It resembles Parkinson's disease but responds poorly to levodopa, and unlike most nutrient toxicities it is often only partially reversible after exposure stops.
- Cognitive effects appear biphasic, not linear Limited evidence
Reviews of manganese exposure across the lifespan describe an inverted-U dose-response, in which both unusually low and elevated exposures associate with poorer cognitive and motor performance, most consistently in children. The studies are observational with inconsistent exposure assessment, and no supplementation trial has demonstrated cognitive benefit at any dose in anyone.
Dosage & safety
Scientific references
Where to buy
Solgar, Chelated Manganese, 100 Tablets (8 mg per Tablet)
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