Manganese

What it is

Manganese is a trace mineral that is both needed in small amounts and toxic in excess. It is part of enzymes such as manganese superoxide dismutase, the main antioxidant enzyme in mitochondria, and arginase, which the liver uses in the urea cycle.

What the research says

Manganese is essential, but deficiency is not a concern in people eating normal diets. Trials of manganese alone are almost absent: benefits reported for bone and knee osteoarthritis come from combination products, so manganese's own role cannot be separated, and an acute dose did not improve glucose tolerance. The clearer evidence is of harm: inhaled or intravenous manganese, manganese in long-term intravenous nutrition, and possibly very high levels in drinking water are linked to parkinsonism-like brain injury, and higher exposure in children is associated with poorer neurodevelopment in observational studies.

Evidence grade: Limited evidence.

What goes wrong

A systematic review and meta-analysis of observational studies found higher manganese exposure associated with poorer cognitive, motor and behavioural development in children. (Source 1)

• Meta-analysis, Low certainty.
• Size: observational studies (number not captured)
• Who: children 0 to 18 years.
• How long: not applicable.
• Result: negative association; sex differences unclear.
• Funding: not stated.

Higher manganese exposure is negatively associated with childhood neurodevelopment, especially cognitive and motor skills for children under 6 years old and cognitive and behavioral performance for children aged 6–18 years old.

A 73-year-old man reached toxic blood manganese after 31 days of 300 μg/day in intravenous nutrition and later developed choreiform movements with manganese deposits in the brain. (Source 2)

• Case report, Very low certainty.
• Size: 1 patient.
• Who: 73-year-old ICU patient with liver dysfunction and iron deficiency.
• How long: 31 days of parenteral nutrition; symptoms 223 days later.
• Result: whole-blood manganese 34 µg/L (reference below 13 µg/L)
• Funding: not applicable.

Our patient showed toxic Mn concentrations in whole blood after 31 days of receiving 300 μg·d−1 of Mn in PN, a shorter duration than typically reported.

A woman on chronic intravenous nutrition without known liver disease developed parkinsonian features with the typical MRI pattern of manganese deposition. (Source 3)

• Case report, Very low certainty.
• Size: 1 patient.
• Who: 38-year-old woman on chronic TPN.
• How long: chronic.
• Result: symmetric T1 hyperintensities in the globus pallidi.
• Funding: not applicable.

Manganese accumulation in the central nervous system creates clinical symptoms of cognitive dysfunction, behavioral changes, and movement disorders resembling Parkinson's disease.

Manganese-contaminated methcathinone (ephedrone) injected intravenously causes lasting parkinsonism, a contamination harm. (Source 4)

• Case series, Low certainty.
• Size: not stated.
• Who: people injecting home-made methcathinone.
• How long: not stated.
• Result: lasting neurological damage.
• Funding: not applicable.

Intravenous use of manganese-contaminated methcathinone (i.e., when the drug is synthesized with potassium permanganate as the oxidant) can cause lasting neurological damage and a parkinsonism disorder.

Iron supplements (60 mg/day for four months) were associated with lower blood manganese and lower MnSOD activity, and magnesium antacids and tetracycline may reduce manganese absorption. (Source 4)

• Randomized trial, Low certainty.
• Size: not stated.
• Who: not stated.
• How long: 4 months.
• Result: lower blood manganese and leukocyte MnSOD activity.
• Funding: not stated.

Iron supplementation (60 milligrams mg/day for four months) has been associated with decreased blood manganese concentrations and decreased MnSOD activity in leukocytes, indicating a reduction in manganese nutritional status.

Position, NIH ODS (consumer sheet, updated 22 March 2021): no harm shown from manganese in food, but toxicity has occurred from water with very high manganese. (Source 5)

• Official position, Certainty not rated.
• Size: not applicable.
• Who: general population.
• How long: not applicable.
• Result: not applicable.
• Funding: government.

Studies have not shown any harm from the manganese in food and beverages, but some people have developed manganese toxicity by consuming water containing very high levels of manganese.

What the evidence supports

In a small crossover RCT, a combination of glucosamine, chondroitin and manganese ascorbate relieved knee osteoarthritis symptoms versus placebo; this supports the combination, not manganese alone. (Source 6)

• Randomized trial, Low certainty.
• Size: 34 men.
• Who: US Navy divers and special warfare personnel with knee or low-back degenerative joint disease.
• How long: 16 weeks (crossover)
• Result: summary disease score -16.3% (p = 0.05); pain VAS -26.6% (p = 0.05); no change in running times.
• Funding: not stated.

Knee osteoarthritis symptoms were relieved as demonstrated by the summary disease score (-16.3%; p = 0.05)

What the evidence does not support

The same trial found no change in running times and could neither show nor exclude a benefit for low-back disease. (Source 6)

• Randomized trial, Low certainty.
• Size: 34 men.
• Who: US Navy personnel with knee or low-back degenerative joint disease.
• How long: 16 weeks (crossover)
• Result: running times unchanged; spinal benefit neither demonstrated nor excluded.
• Funding: not stated.

Running times did not change. The study neither demonstrated, nor excluded, a benefit for spinal DJD.

Because the osteoarthritis trials did not test the combination without manganese, manganese's own contribution is unknown. (Source 4)

• Official position, Low certainty.
• Size: 2 trials.
• Who: people with knee osteoarthritis.
• How long: not applicable.
• Result: not applicable.
• Funding: not stated.

Neither study compared the treatment containing manganese ascorbate to a treatment containing glucosamine hydrochloride and chondroitin sulfate without manganese ascorbate, so it is impossible to determine whether the supplement would have resulted in the same benefit without high doses of manganese.

A single oral dose of 15 or 30 mg manganese, given with an oral glucose challenge, did not improve glucose tolerance in people with or without diabetes. (Source 4)

• Randomized trial, Low certainty.
• Size: not stated.
• Who: people with and without diabetes.
• How long: single dose.
• Result: no improvement in glucose tolerance.
• Funding: not stated.

When given at the same time as an oral glucose challenge, an acute oral dose of 15 mg or 30 mg manganese did not improve glucose tolerance in subjects with diabetes or in controls without diabetes.

Where the evidence is mixed

A two-year trial found calcium plus manganese, copper and zinc slowed spinal bone loss more than calcium alone, but manganese's own effect cannot be isolated. (Source 4)

• Randomized trial, Low certainty.
• Size: not stated.
• Who: not stated in source.
• How long: 2 years.
• Result: better than calcium alone for spinal bone loss.
• Funding: not stated.

the presence of other trace elements in the supplement makes it impossible to determine whether manganese supplementation was the beneficial agent for maintaining bone mineral density.

How much

• Reference intake: US Food and Nutrition Board Adequate Intakes for adults: 2.3 mg/day men, 1.8 mg/day women (NIH ODS consumer sheet, updated 2021). (Source 5)
• Upper limit: US Food and Nutrition Board (2001 DRIs) UL for adults 19+: 11 mg/day from all sources. EFSA published a 2023 opinion on manganese upper intake that could not be fetched. (Source 4)
• Studied: Manganese ascorbate 228 mg/day with glucosamine 1,500 mg and chondroitin 1,200 mg for 16 weeks in knee or low-back joint disease. (Source 6)
• Studied: 5 mg/day manganese with copper 2.5 mg, zinc 15 mg and calcium 1,000 mg over two years for bone loss. (Source 4)

A common belief, and what the research shows

The belief: Manganese in joint supplements is proven to help arthritis.

What the research shows: The trials used a combination, and 'Neither study compared the treatment containing manganese ascorbate to a treatment containing glucosamine hydrochloride and chondroitin sulfate without manganese ascorbate'.

Questions and answers

What is it?

Manganese is a trace mineral the body needs in small amounts but that is toxic in excess. (Source 4)

What does it do in the body?

It is part of enzymes that protect cells from oxidative damage and that help the liver clear ammonia, and it supports bone, reproduction, blood clotting and immunity. (Source 4)

Is it good or bad for you?

Needed in small amounts from food, but excess exposure damages the brain and can cause a Parkinson's-like disorder. Inhaled dust, intravenous nutrition and contaminated drugs are the best documented routes. (Source 4)

How do you get more of it?

Manganese comes from whole grains, legumes, nuts, leafy vegetables and tea. Iron in a meal lowers manganese absorption. (Source 4)

If it is harmful, what reduces it?

Manganese leaves the body mainly in bile, so exposure is reduced by removing the source; in reported intravenous-nutrition cases, symptoms improved after stopping TPN. (Source 4)

Why might someone be low in it or missing it?

Deficiency is not a practical concern in people eating normal diets; it has been produced only in experimental low-manganese diets. (Source 4)

Which whole foods contain it or feed it?

Whole grains, legumes, nuts, leafy vegetables and tea, with pecans, brown rice, pineapple and spinach among good sources. Tannins in tea may reduce how much is absorbed. (Source 4)

What happens if you do not have it?

In experiments where young men ate a low-manganese diet, they developed lower cholesterol and a short-lived skin rash. No natural deficiency disease is recognised. (Source 4)

How can you test for it?

Whole-blood manganese is measured when toxicity is suspected, and MRI of the globus pallidus shows brain build-up, but MRI is not practical routinely. No validated test of manganese adequacy was found. (Source 2)

References

1. Environmental Health. Biomarkers of environmental manganese exposure and associations with childhood neurodevelopment: a systematic review and meta-analysis. 2020. PMID 33008482, DOI 10.1186/s12940-020-00659-x. Read the source
2. Diagnostics (MDPI). Manganese Intoxication Induced by Total Parenteral Nutrition in the Intensive Care Unit: A Case Report. 2025. DOI 10.3390/diagnostics15111346. Read the source
3. Case Reports in Neurological Medicine. Manganese Neurotoxicity as a Complication of Chronic Total Parenteral Nutrition. 2020. DOI 10.1155/2020/9484028. Read the source
4. Linus Pauling Institute Micronutrient Information Center, Oregon State University. Manganese. n.d.. Read the source
5. NIH Office of Dietary Supplements. Manganese: Fact Sheet for Consumers (updated March 22, 2021). 2021. Read the source
6. Military Medicine. Glucosamine, Chondroitin, and Manganese Ascorbate for Degenerative Joint Disease of the Knee or Low Back: A Randomized, Double-Blind, Placebo-Controlled Pilot Study. 1999. PMID 10050562. Read the source