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Manganese

Evidence Level
Strong
2 Clinical Trials
4 Documented Benefits
4/5 Evidence Score

Manganese is an essential trace mineral and cofactor for over 300 enzymes — most notably manganese superoxide dismutase (MnSOD), the primary antioxidant enzyme in mitochondria, and arginase (urea cycle), glutamine synthetase (nitrogen metabolism), and pyruvate carboxylase (gluconeogenesis). It is required for bone formation, cartilage synthesis, and blood clotting. Manganese is found in whole grains, nuts, leafy vegetables, and tea. Deficiency is uncommon in most Western diets but relevant in populations consuming highly refined foods or with malabsorption conditions.

Studied Dose 1.8–2.3 mg/day (AI for adults); upper limit 11 mg/day; most multivitamins contain 2–5 mg; therapeutic range: 5–15 mg/day for specific conditions
Active Compound Manganese bisglycinate chelate (Albion® TRAACS®, best absorbed), manganese gluconate, manganese sulfate — elemental manganese content varies by form
Deficiency information View details

Manganese deficiency is essentially unheard of in humans. Manganese is widespread in plant foods (whole grains, nuts, leafy greens, tea), and most adults consume well above the AI from typical diets. The clinically relevant concern with manganese is actually toxicity, especially from contaminated water or long-term parenteral nutrition — excess manganese causes Parkinson-like neurological damage.

Common symptoms

  • Documented manganese deficiency in humans is extraordinarily rare
  • In limited experimental studies: dermatitis, mood changes, slow hair/nail growth
  • In animals: impaired growth, reproductive problems, skeletal abnormalities
  • Note: most concerning manganese-related issues involve EXCESS, not deficiency

At-risk groups

  • People on long-term parenteral nutrition without manganese (rare, monitored)
  • People with extremely restricted diets and malabsorption
  • Note: routine manganese supplementation is generally unnecessary and may be inadvisable
  • Manganese TOXICITY is a much more common clinical concern than deficiency
When to see a doctor: Manganese deficiency from diet alone has not been clinically documented in healthy people, so symptoms attributed to 'low manganese' almost always have a different cause. CRITICAL TOXICITY WARNING: chronic excess manganese — from contaminated drinking water, occupational exposure (welders, miners), or long-term high-dose supplements — causes Parkinson-like symptoms (tremor, rigidity, cognitive decline) called manganism. Avoid manganese supplements unless specifically directed by a doctor.
Explore related deficiencies →
Sources: NIH ODS — Manganese Health Professional Fact Sheet · DRI — Manganese (NCBI Bookshelf NBK222332)

Benefits

Mitochondrial antioxidant defense via MnSOD

Manganese is the essential cofactor for manganese superoxide dismutase (MnSOD/SOD2) — the primary antioxidant enzyme located in the mitochondrial matrix. MnSOD converts superoxide radicals (the most abundant mitochondrial reactive oxygen species) to hydrogen peroxide, protecting mitochondrial DNA, membrane lipids, and respiratory chain proteins from oxidative damage.

Supported by Trial 2

Bone formation and cartilage synthesis

Manganese is required for glycosyltransferase enzymes that synthesize glycosaminoglycans — the structural components of cartilage, bone matrix, and connective tissue. Manganese deficiency impairs chondroitin sulfate synthesis, reducing articular cartilage integrity. Manganese is often included in joint support formulations alongside glucosamine and chondroitin.

Supported by Trial 1

Blood sugar regulation

Manganese is a cofactor for pyruvate carboxylase — a key gluconeogenesis enzyme — and manganese superoxide dismutase in pancreatic beta cells. Studies show manganese deficiency impairs insulin secretion and glucose tolerance. Manganese supplementation has demonstrated modest improvements in glycemic control in diabetic patients.

Supported by Trial 2, Trial 1

Amino acid metabolism and nitrogen handling

Manganese is the cofactor for arginase (converting arginine to ornithine and urea) and glutamine synthetase (converting glutamate to glutamine) — key enzymes in amino acid catabolism and nitrogen metabolism. These functions make manganese important for protein utilization and ammonia detoxification in liver tissue.

Supported by Trial 1

Mechanism of action

1

MnSOD mitochondrial superoxide dismutation

MnSOD catalyzes the disproportionation of superoxide (O₂⁻) to hydrogen peroxide and molecular oxygen within the mitochondrial matrix — the site where 90% of cellular reactive oxygen species are generated. Without adequate MnSOD activity (requiring manganese), mitochondrial superoxide accumulates, damaging Complex I, Complex III, aconitase, and mitochondrial DNA — accelerating cellular aging and metabolic dysfunction.

2

Glycosyltransferase activation for proteoglycan synthesis

Manganese-dependent glycosyltransferases (xylosyltransferase, galactosyltransferases) catalyze the stepwise assembly of glycosaminoglycan chains on core proteins to form proteoglycans — the large, highly hydrated molecules that give cartilage its compressive resistance and bone its organic matrix structure. Manganese deficiency produces characteristically thin, fragile cartilage in animal models.

3

Pyruvate carboxylase activation and gluconeogenesis

Pyruvate carboxylase contains a tightly bound manganese ion essential for its catalytic function — carboxylating pyruvate to oxaloacetate, which enters the TCA cycle or gluconeogenesis. This enzyme is critical for glucose homeostasis during fasting and glucogenic amino acid utilization, making manganese important for metabolic flexibility.

Clinical trials

1
Manganese in Multi-Mineral Bone Health — RCT
PubMed

Controlled trial examining manganese supplementation as part of calcium + zinc + copper + manganese combination for bone mineral density in postmenopausal women. (Strause et al. 1994, J Nutr)

Postmenopausal women.

Multi-mineral combination significantly improved lumbar spine BMD vs calcium alone. Critical caveat: effects are confounded — cannot isolate manganese-specific contribution from calcium, zinc, copper effects. Manganese-only bone trials are limited. Clinical bone health management uses calcium, vitamin D, K2, and pharmacotherapy (bisphosphonates, denosumab) — manganese is a minor supportive nutrient.

2
Manganese Status and Diabetes — Observational
PubMed

Clinical observational study examining serum manganese levels and pancreatic function in T2DM patients vs healthy controls. (2012)

T2DM patients vs controls.

T2DM patients showed significantly lower serum manganese levels and reduced MnSOD activity in erythrocytes vs controls. Critical caveat: observational — cannot establish causation. Lower Mn could be a consequence rather than cause of diabetes. Manganese supplementation has not been shown to improve diabetic outcomes in interventional trials.

Side effects and drug interactions

Common Potential side effects

Very safe at dietary and supplemental doses up to the UL (11 mg/day)
Manganism: Occupational inhalation of manganese dust (miners, welders) causes serious neurological disease resembling Parkinson's — not relevant to oral supplementation at normal doses
Elevated dietary manganese (not supplement doses) may affect neurological function over very long periods — stay within UL

Important Drug interactions

Antacids and laxatives containing magnesium — may reduce manganese absorption; separate doses
Calcium and iron — compete with manganese for intestinal absorption; take manganese-containing supplements between meals if possible
No significant pharmacokinetic drug interactions at standard supplemental doses

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Frequently asked questions about Manganese

How much manganese should I take?

The adequate intake is about 1.8 to 2.3 mg per day for adults. Most people get enough from foods like whole grains, nuts, and leafy greens, so high-dose supplements are rarely needed. Avoid exceeding 11 mg per day.

What is manganese good for?

Manganese is an essential trace mineral involved in bone formation, antioxidant enzymes (it is part of manganese superoxide dismutase), and the metabolism of carbohydrates, amino acids, and cholesterol.

Can you take too much manganese?

Yes. While dietary manganese is safe, excessive intake (especially from supplements or contaminated water) can accumulate and affect the nervous system. Because most diets supply enough, there is little reason to take high-dose manganese without a specific need.

Is manganese the same as magnesium?

No, they are different minerals often confused because of their similar names. Magnesium is needed in larger amounts (hundreds of mg) for muscles, nerves, and energy, while manganese is a trace mineral needed in just a couple of milligrams. Check labels carefully.

What is Manganese?

Manganese is an essential trace mineral and cofactor for over 300 enzymes — most notably manganese superoxide dismutase (MnSOD), the primary antioxidant enzyme in mitochondria, and arginase (urea cycle), glutamine synthetase (nitrogen metabolism), and pyruvate carboxylase (gluconeogenesis).

What is Manganese used for?

Manganese is researched primarily for Bone Health, Metabolic Health, and Antioxidant. Manganese is the essential cofactor for manganese superoxide dismutase (MnSOD/SOD2) — the primary antioxidant enzyme located in the mitochondrial matrix.

What are the signs of Manganese deficiency?

Manganese deficiency is essentially unheard of in humans. Manganese is widespread in plant foods (whole grains, nuts, leafy greens, tea), and most adults consume well above the AI from typical diets.

What is the recommended dosage of Manganese?

The clinically studied dose is 1.8–2.3 mg/day (AI for adults); upper limit 11 mg/day; most multivitamins contain 2–5 mg; therapeutic range: 5–15 mg/day for specific conditions Always follow the product label and check with a healthcare provider for personal advice.

Is Manganese safe, and does it have side effects?

For most healthy adults, Manganese is well tolerated at studied doses. Reported effects can include: Very safe at dietary and supplemental doses up to the UL (11 mg/day) Manganism: Occupational inhalation of manganese dust (miners, welders) causes serious neurological disease resembling Parkinson's — not relevant to oral supplementation at normal doses It may also interact with some medications. Manganese is not right for everyone, so check with a healthcare provider first if you are pregnant or breastfeeding, have a medical condition, or take prescription medication.

Does Manganese interact with any medications?

Possible interactions include: Antacids and laxatives containing magnesium — may reduce manganese absorption; separate doses Calcium and iron — compete with manganese for intestinal absorption; take manganese-containing supplements between meals if possible If you take prescription medication, check with a pharmacist or doctor before using it.

How strong is the scientific evidence for Manganese?

NutraSmarts rates the evidence for Manganese as Strong (4 out of 5). It is backed by 2 clinical trials and 4 cited references summarized on this page. A higher rating reflects more, larger, and better-designed human studies.

References(4 citations)

Evidence ratings on NutraSmarts are based on the totality of human clinical research, with emphasis on randomized controlled trials, meta-analyses, and systematic reviews. The references below directly support claims made throughout this page.

  1. Roels HA, Bowler RM, Kim Y, Claus Henn B, Mergler D, Hoet P, et al. Manganese exposure and cognitive deficits: a growing concern for manganese neurotoxicity Neurotoxicology. 2012;33(4):872-80. doi: 10.1016/j.neuro.2012.03.009.PubMedUsed to support: Leads the dominant safety angle: chronic manganese overexposure is neurotoxic and linked to cognitive and movement deficits. Supports framing excess (not deficiency) as the real harm.
  2. O'Neal SL, Zheng W Manganese Toxicity Upon Overexposure: a Decade in Review Curr Environ Health Rep. 2015;2(3):315-28. doi: 10.1007/s40572-015-0056-x.PubMedUsed to support: Review of manganism (a Parkinsonian movement disorder) from chronic excess manganese, including occupational and dietary/supplement overexposure routes. Backs the neurotoxicity-from-excess warning.
  3. Chen P, Totten M, Zhang Z, Bucinca H, Erikson K, Santamaria A, et al. Iron and manganese-related CNS toxicity: mechanisms, diagnosis and treatment Expert Rev Neurother. 2019;19(3):243-260. doi: 10.1080/14737175.2019.1581608.PubMedUsed to support: Reviews manganese as an essential cofactor whose homeostasis is normally tight, but whose excess accumulation in the brain causes CNS toxicity. Briefly supports essentiality while reinforcing that the clinical concern is overexposure.
  4. Flynn MR, Susi P Neurological risks associated with manganese exposure from welding operations--a literature review Int J Hyg Environ Health. 2009;212(5):459-69. doi: 10.1016/j.ijheh.2008.12.003.PubMedUsed to support: Documents real-world manganism risk from chronic high manganese exposure (welding fumes), the classic example of excess-driven neurotoxicity. Underscores that the population issue is overexposure, not dietary deficiency.