In parts 1, 2, and 3 of this series, I wrote about the basics of supplementation, the effects of too much iodine in the body, and the possibility of vitamin D overdose, specifically in pregnancy. In this blog, I’ll explore the causes of manganese toxicity and the resulting symptoms.

“Manganese” comes from the Greek word mangania, meaning “magic.” It is technically a heavy metal that is also an essential biological mineral.* We need manganese in very specific amounts for the formation of healthy cartilage and bone, antioxidant function in the mitochondria, metabolism of carbohydrates, amino acids, and cholesterol, and proper wound healing. It also plays critical roles in the body’s response to bacterial infection (1,2).

The human body contains about 10 to 20 milligrams of manganese, with concentrations occurring in the skeletal system, liver, pancreas, kidney, and brain. Importantly, more than 90% of the manganese we take in is excreted via the bile into the feces, with minimal resorption.

The Tolerable Upper Limit of manganese ranges from 2 milligrams in early childhood to 11 milligrams for those 19 years and older, including pregnant and lactating individuals. There are no ULs for infants and babies—milk, formula, and food should be their only source (3). The National Institutes of Health Fact Sheet notes that the UL ranges do not apply to those taking supplemental manganese under medical supervision.

Trace amounts of manganese are present in drinking water, though tight controls are kept on the amount in municipal water sources in order to prevent toxicity. Food sources include grains, nuts, fruits, vegetables, and tea. Blue mussels, hazelnuts, pecans, oysters, almonds, brown rice, pineapple, and spinach contain especially high amounts of manganese.

Infant formula and some supplements also contain manganese. Bone and joint and adrenal support complexes generally contain more manganese than other supplements (4). The amount of manganese in some supplements, such as this one, is much higher than the recommended UL.

So, what causes manganese toxicity? And, what are the symptoms?

Sources of excessive manganese include work exposures from jobs such as smelting, welding, mining, or the production of batteries. Overexposure to gasoline can also be a concern. Well water manganese levels are generally not regulated and may contribute to total intake. Infant formulas, overconsumption of manganese-rich foods, and supplements may create toxicity. Finally, parenteral nutrition, especially in children, may cause manganese toxicity (5).

I became concerned about manganese toxicity, called manganism, after seeing a client with neurological symptoms that I believe were associated with altered manganese levels. This client was a woman in her early 30s who experienced tremors, mood shifts, and overarching psychiatric problems. These symptoms came on suddenly with no personal or family history to explain the change.

I reviewed her supplement regimen.

She was taking several adrenal support complexes and a multi-vitamin. Her daily supplemental manganese intake was 45 milligrams, over four times the Tolerable Upper Limit for manganese.

She was consuming approximately five more milligrams per day from her diet. The tremors and mood issues went away within a few weeks of discontinuing the manganese-containing supplements.

Another client had high manganese and copper on a mineral hair test that was consistent with the overconsumption of nuts on her food log. She was eating a lot of nuts and seeds! It was an unusual eating pattern for her that she was happy to change. Her hair tests normalized after she re-balanced her nut and seed intake.

Finally, I’ve noticed high manganese on mineral hair tests from people who drink well water. I recommend that people test their water every year for microbial and mineral markers—manganese and lithium can sometimes be very high.

Thankfully, my clients’ symptoms normalized after dietary shifts. But manganism can lead to severe neurological symptoms such as tremors and aggressiveness, insomnia, delusions, reduced hand-eye coordination, and affected gait and balance. Toxicity may even progress beyond manganism and contribute to the etiology of neurological illnesses. A review from 2020 explored the possible connections between manganese toxicity and Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, prion disease, and ALS (6).

Other symptoms of manganese toxicity include reproductive disturbances via manganese-induced effects on the brain-pituitary-testicular axis and cognitive and behavioral issues in children (7).

Some people are more susceptible to manganism than others. Interestingly, dietary iron and serum iron stores (ferritin) are inversely related to manganese absorption. This means that if dietary iron is low, such as in iron-deficiency anemia, then manganese has a greater chance of becoming elevated. Additionally, women tend to have higher manganese levels compared to men, and pregnant people have higher levels compared to non-pregnant people. The relatively lower levels of iron in women’s blood may explain this interesting, and clinically important, pattern.

Other populations that have greater chances of manganese toxicity include infants, children, and the elderly. Older people, especially, are susceptible to manganese’s neurotoxic effects. Finally, those with liver or gallbladder dysfunction risk manganese toxicity due to its storage in the liver and excretion through the bile. If the balance of storage and excretion becomes altered then manganism may result.

*In addition to manganese, chromium, selenium, iron, and zinc are other heavy metals that are essential for biological function.

References

  1. https://lpi.oregonstate.edu/mic/minerals/manganese
  2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4631260/pdf/nihms733624.pdf
  3. https://ods.od.nih.gov/factsheets/Manganese-HealthProfessional/
  4. https://link.springer.com/article/10.1007/BF02739775
  5. https://www.ncbi.nlm.nih.gov/books/NBK560903/
  6. https://pubmed.ncbi.nlm.nih.gov/32799578/
  7. https://pubmed.ncbi.nlm.nih.gov/28040552/