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Study: Biotin Could Protect Against Manganese-Induced Parkinson Disease
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Key Takeaways
- Biotin may mitigate manganese-induced neurodegeneration, potentially offering protection against Parkinsonism-related symptoms.
- Manganese is essential but toxic at high levels, causing symptoms similar to Parkinson's disease.
Biotin supplementation could mitigate manganese-induced damage caused by manganese deficiency and excessive exposure.
Biotin, a B vitamin that helps the body metabolize carbohydrates, fats, and amino acids may have a protective effect that could mitigate manganese-induced damage caused by manganese deficiency and excessive exposure.1,2
Manganese is an essential mineral that assists enzymes involved in breaking down carbohydrates, proteins, and cholesterol while aiding bone growth and supporting the immune and reproductive systems. The coenzyme is found in a variety of foods, including shellfish, nuts, brown rice, oatmeal, legumes, black tea, black pepper, spinach, and pineapple. The mineral is absorbed in the small intestine, and most is deposited in bone with smaller amounts in the liver, brain, kidney, and pancreas.1,3,4
Manganese levels are challenging to measure; however, high levels of exposure can be toxic to the central nervous system. According to The Nutrition Source, toxic levels of manganese were found in isolated case reports among industrial mining and welding workers that inhaled an abundance of manganese in dust and also in individuals that consumed contaminated water with significantly high levels of manganese. Toxicity symptoms can include tremors, muscle spasms, decreased hand-eye coordination, decreased balance, hearing loss, headache, and depression—presenting symptoms similar to Parkinson disease.1,4
“Exposure to neurotoxic metals like manganese has been linked to the development of Parkinsonism,” Sarkar Souvarish, PhD, an assistant professor at the University of Rochester Medical Center's Departments of Environmental Medicine and Neuroscience, said in a news release. “In this study, we applied untargeted metabolomics using high-resolution mass spectrometry and advanced cheminformatics computing in a newly developed model of parkinsonism, leading us to the discovery of biotin metabolism as a modifier in manganese-induced neurodegeneration.”1
To understand manganese’s damage to the brain, researchers developed a model that resembled occupational manganese exposure in humans on fruit flies. Using a feeding model, the flies were fed MnCl2 solution ad libitum at doses of 1 mM, 10, mM, and 30 mM immediately after eclosion. The researchers observed motor difficulties, damage to cellular structures like mitochondria and lysosomes, neuronal cell death, and a shortened lifespan in the flies. These findings were further supported using human dopamine-producing neurons derived from induced pluripotent stem cells (iPSCs), which demonstrated specific vulnerability to manganese exposure, exhibiting significant damage. The loss of these dopamine-producing cells is a characteristic of Parkinson disease, according to study authors.1,3
However, the study authors noted that changes in biotin metabolism could drive manganese induced neurotoxicity. As a B vitamin, biotin is synthesized by gut bacteria and can be obtained from diet, produced by the gut microbiome, or recycled.1 Foods high in biotin include egg yolks, legumes, nuts and seeds, liver, sweet potatoes, mushrooms, bananas, broccoli, yeast, and avocados.5
Since biotin is crucial for dopamine production, researchers hypothesized that increased biotin metabolism in response to manganese exposure is a compensatory mechanism to counteract early neurodegeneration. To investigate this, they reduced biotin levels in fruit flies by knocking down the expression of the biotinidase gene, which encodes an enzyme essential for biotin utilization. Subsequently, these flies with reduced biotin levels were exposed to manganese. The results demonstrated that biotin supplementation reversed neurotoxicity in the flies and iPSC-derived neurons, which improved mitochondrial function and reduced cell loss, according to study authors.1,3
“Biotin supplementation shows potential as a therapeutic strategy to mitigate manganese-induced neurodegeneration, and the safety and tolerability of biotin in humans make it a promising candidate for further exploration,” Souvarish said in a news release. “Biotin-rich prebiotics or biotin-producing probiotics could provide non-pharmacological intervention options, but more studies have to performed.”1
Despite the need for further research, pharmacists can recommend biotin supplementation for individuals that are impacted by manganese-induced damage or Parkinson disease. However, the study authors noted that future research is necessary to assess the link between gut microbiome dysbiosis, biotin metabolism, environmental neurotoxic exposures, and the development of neurodegenerative diseases.3
