Manganese

Optimal result: 0.03 – 1.16 ug/g creat

Individuals with increased susceptibility to manganese toxicity include patients with chronic liver disease, newborns and children, iron, deficient populations, patients on parenteral nutrition, and occupational exposure.

Manganese is neurotoxic and excess levels have been associated with Parkinson's like symptoms.

A blood manganese level may provide the best estimate for brain manganese levels when exposure is recent.

Manganese toxicity is generally due to environmental or occupational exposures, including airborne (inhaled) and drinking water.

Periods of occupation exposure of six months to two years may lead to manganism and the motor and neural psychiatric symptoms may remain several years after the exposure. Symptoms include dystonia, bradykinesia, and rigidity (due  to damage to dopaminergic neurons) and gliosis.

Additional symptoms include tremors, muscle spasms, tinnitus, hearing loss, ataxia, mania, insomnia, depression, delusions, anorexia, headaches, irritability, lower extremity weakness, changes in mood or short-term memory, altered reaction times, and reduced hand eye coordination.

Manganese deficiency is rare and result in impaired growth, poor bone formation, and skeletal defects, abnormal glucose tolerance, altered lipid and carbohydrate, metabolism, dermatitis, slowed hair/nail growth.

Disease is reported with low blood manganese concentrations include epilepsy, Mseleni disease, Down's syndrome, osteoporosis and Perthst disease.

Sources:

Whole grains (wheat germs, oats anda bran), rice, and nuts (hazelnuts, almonds, and pecans) contain the highest amount of Manganese. 

Other food sources include chocolate, tea, mussels, clams, legumes, fruit, leafy vegetables (spinach), seeds (flax, sesame, pumpkin, sunflower, and pine nuts) and spices (chili powder, cloves and saffron). 

Airborne exposure can occur through automobile exhaust, unleaded gasoline and occupational exposire (mining, welding, ferroalloy and steel industry, battery manufacturing). 

It is also present in fungicides, textile bleaching, manufacturing of glass and ceramics, paint, matches and fireworks, leather tanning, hydroquinone, potassium permanganate and other chemical production. Soil manganese concentrations can contaminate well water. 

Absorption:

Only about 1 to 5% of dietary manganese is absorbed in the gut. Absorption is influenced by intestinal pH, the presence of divalent metal transporter DMT1, other divalent metals, competing for absorption (iron, copper, zinc, copper, calcium) and phytic acid.

The absorption of manganese is tightly regulated in the gut, and therefore toxicity from the diet has not been reported.

Iron deficiency increase as manganese absorption.

Supplemental magnesium (200 mg per day) may decrease manganese availability by decreasing absorption or increasing excretion.

Manganese is eliminated mainly via bile.

Biochemical actions:

Required for immune function, regulation of blood, sugar and cellular energy, reproduction, digestion, bone growth, black, coagulation, hemostasis, wound healing, and antioxidant.

Manganese is incorporated into metalloproteins, such as superoxide, dismutase, and others.

Symptoms of imbalance:

Manganese deficiency is rare and result in impaired growth, poor bone formation, and skeletal defects, abnormal glucose tolerance, altered lipid and carbohydrate, metabolism, dermatitis, slowed hair/nail growth.

Disease is reported with low blood manganese concentrations include epilepsy, Mseleni disease, Down's syndrome, osteoporosis and Perthst disease.

Individuals with increased susceptibility to manganese toxicity include patients with chronic liver disease, newborns and children, iron, deficient populations, patients on parenteral nutrition, and occupational exposure.

Manganese is neurotoxic and excess levels have been associated with Parkinson's like symptoms.

A blood manganese level may provide the best estimate for brain manganese levels when exposure is recent.

Manganese toxicity is generally due to environmental or occupational exposures, including airborne (inhaled) and drinking water.

Periods of occupation exposure of six months to two years may lead to manganism and the motor and neural psychiatric symptoms may remain several years after the exposure. Symptoms include dystonia, bradykinesia, and rigidity (due  to damage to dopaminergic neurons) and gliosis.

Additional symptoms include tremors, muscle spasms, tinnitus, hearing loss, ataxia, mania, insomnia, depression, delusions, anorexia, headaches, irritability, lower extremity weakness, changes in mood or short-term memory, altered reaction times, and reduced hand eye coordination.

References:

Aschner M, Erikson K. Manganese. Adv Nutr. 2017;8(3):520-521.

Avila DS, Puntel RL, Aschner M. Manganese in health and disease. Metal ions in life sciences. 2013;13:199-227.

Erikson KM, Aschner M. Manganese: Its Role in Disease and Health. Metal ions in life sciences. 2019;19.

University OS. Manganese. Linus Pauling Institute - Micronutrient Information Center - Minerals 2020; https://lpi. oregonstate.edu/mic/minerals/manganese, 2020.

NIH. Manganese Fact Sheet for Health Professionals. Dietary Supplement Fact Sheets 2020; https://ods.od.nih.gov/ factsheets/Manganese-HealthProfessional/, 2020.

Manganese
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