The Clinical Effects of Manganese
BY E. BLAUROCK-BUSCH, PH.D.
Biochemistry: The human body contains approximately ten milligrams of manganese, most of which is found in the liver, bones, and kidneys. This trace element is a cofactor for a number of important enzymes, including arginase, cholinesterase, phosphoglucomutase, pyruvate carboxylase, mitochondrial superoxide dismutase and several phosphates, peptidases and glycosyltransferases. In certain instances, Mn2+ may be replaced by Co2+ or Mg2+. Manganese functions with vitamin K in the formation of prothrombin.
Pathophysiology: Inadequate manganese intake has been associated with parenteral nutrition, resulting in dermatitis, changes in hair pigmentation and slowed hair growth. Low cholesterol, triglyceride and phospholipid levels were low. Significant deficiencies have been found in epileptics.
Normal skeletal growth and development
Essential for glucose utilization
Lipid synthesis and lipid metabolism
Pancreatic function and development
Prevention of sterility
Important for protein and nucleic acid metabolism
Activates enzyme functions
Involved in thyroid hormone synthesis
Absorption and excretion: Manganese metabolism is similar to that of iron. It is absorbed in the small intestines and while the absorption process is slow, the total absorption rate is exceptionally high about 40%. Excess manganese is excreted in bile and pancreatic secretion. Only a small amount is excreted in the urine.
Required Daily Amount (mg):
Sources: Liver and kidneys are the primary meat source of manganese. Wheat germ, legumes, nuts, and black tea are good plant sources.
Manganese content of foods (mg/100g):
Deficiency symptoms: Ataxia, fainting, hearing loss, weak tendons and ligaments. Can be a cause of diabetes. Medical studies indicate that manganese deficiency impairs glucose metabolism and reduced insulin production. Deficiency has been linked to myasthenia gravis. Manganese activates several enzyme systems and supports the utilization of vitamin C, E, choline, and other B-vitamins. Inadequate choline utilization reduces the acetylcholine synthesis, causing conditions such as myasthenia gravis (loss of muscle strength). Manganese and zinc therapy can reduce copper levels and therefore manganese and/or zinc may be of therapeutic value in the treatment of symptoms linked to excess copper.
Toxicity: Excess manganese interferes with the absorption of dietary iron. Long-term exposure to excess levels may result in iron-deficiency anemia. Increased manganese intake impairs the activity of copper metallo-enzymes. Manganese overload is generally due to industrial pollution. Workers in the manganese processing industry are most at risk. Well water rich in manganese can be the cause of excessive manganese intake and can increase bacterial growth in water. Manganese poisoning has been found among workers in the battery manufacturing industry. Symptoms of toxicity mimic those of Parkinson’s disease (tremors, stiff muscles) and excessive manganese intake can cause hypertension in patients older than 40. Significant rises in manganese concentrations have been found in patients with severe hepatitis and posthepatic cirrhosis, in dialysis patients and in patients suffering heart attacks.
Laboratory Diagnosis: Manganese influences the copper and iron metabolism and estrogen therapy may raise serum manganese concentration, whereas glucosteroids alter the manganese distribution in the body.
Significance of Blood Levels: Mass spectroscopy levels of whole blood reliably reflect the nutritional intake and acute industrial exposure. Note: In the presence of high levels, dopamine levels are reduced.
Significance of Urinary Levels: 24-hr urine to evaluate excessive industrial exposure.
Significance of Hair Manganese Levels: Dark hair dyes can contain manganese and thus falsely elevate hair levels. In the case of extremely high manganese levels obtained from scalp hair, pubic hair should be tested as a control. Manganese overload is generally due to industrial pollution. Workers in the manganese processing industry are most at risk.
Water: EPA recommends a level of 0.05PPM in drinking water, based upon taste rather than health.
Symptoms of increased manganese levels:
Loss of appetite
Mask-like facial expression and monotonous voice
Impaired thiamin (B1) metabolism
Increased demand for vitamin C and copper
Can cause kidney failure, hallucinations, as well as diseases of the central nervous system. High hair manganese levels indicate problems with calcium and/or iron metabolism.
Symptoms and side-effects of manganese deficiency:
Impaired glucose metabolism
Diseases of the skeletal structure, and impaired growth
Elevated blood pressure
Reduced protein metabolism
Reduced immune function
Depressed activity of mammary glands in nursing mothers
Manganese deficiency has been associated with cancer, rheumatic conditions, rickets, morning sickness, jaundice, and diabetes
Excessive ingestion of iron, combined with hypochlorhydria, can cause an imbalance in the Mn/Fe ratio
Therapeutic considerations: A healthy person excretes approximately four mg/day, which is the minimum daily amount that should be consumed. Elevated calcium and/or phosphorus intake suppress the body’s ability to absorb manganese, while an increase in Vitamin C improves cellular exchange. Drinking water should be analyzed. Manganese poisoning can be treated successfully with chelation therapy.
Trace Minerals International of Colorado examined the mineral metabolism of 19 patients with alopecia (hair loss). The spectrophotometric analysis showed manganese deficiency in all 19. Eighteen patients showed considerable problems with calcium absorption, and twelve patients had problems with their zinc metabolism. Specific nutritional and mineral therapy resulted in improved hair growth after 2-3 months of treatment. Blaurock-Busch, E. Wichtige Nahrstoffe fur Gesunde Haut und Haare, Kosmetik Internat. 3/87.
Manganese and learning disabilities: The concentration of manganese in the hair of normal newborn infants increased significantly from 0.19 µg/g at birth to 0.965 µg/g at 6 weeks of age and 0.685 µg/g at 4 months when they were fed infant formula. There was an insignificant increase to 0.330 µg/g at age 4 months in breast-fed infants. After this age there was a slow decline in hair Mn to 0.268 µg/g in normal children at age 8 years and 0.434 in learning disabled (hyperactive) children. This is the 3rd study reporting elevated hair manganese in learning disabled children. Collipp, P.J., et al. Manganese in infant formulas and learning disability. Ann. Nutr. Metab. 27(6):488-494, 1983.
Long term parenteral nutrition has been associated with high blood concentrations of manganese in children who displayed symptoms of toxicity. Fell JME et al. Manganese toxicity in children receiving long-term parenteral nutrition. Lancet Vol 347, May 4, 1996.
Calcium deficiency increases manganese absorption. Murphy VA et al. Elevation of Brain Manganese in Calcium-Deficient Rats. Neurotoxicology 1991, p 265.
Blaurock-Busch E, Mineral & Trace Element Analysis, Laboratory and Clinical Application. TMI 1997.
Kaplan LA, Pesce AJ. Clinical Chemistry. Theory, analysis, and correlation. 2nd ed. Mosby Co. 1989.
Thomas L. Labor & Diagnose, 4th ed Med. Verlag Marburg 1992.
Required Daily Amount (mg)
Infants (0 - 5 months)
0.5 - 0.7
Infants (5 - 12 months)
0.7 - 1.0
Children (1 - 3 years)
1.0 - 1.5
Children (4 - 6 years)
1.5 - 2.0
Children (7 - 10 years)
2.0 - 3.0
Children (11+ years)
2.5 - 5.0
Adults, both genders (18+)
2.5 - 5.0
Wheat Germ 9
Rolled Oats 5
Liver 0.25 - 0.36
Wheat Bran 4
Cheese 0.017 - 0.19
Cereals 2.4 - 4
Fish 0.012 - 0.12
Kidneys 0.06 - 0.11
Wheat Whole Grain Bread 2.3
Meat 0.02 - 0.08
Cottage Cheese 0.06
Pulses 1.3 - 2
Turkey 0.03 - 0.05
Rye Bread 1
Whole Milk 0.003
Vegetables 0.05 - 0.75
Fruit, Berries 0.03 - 0.6s
White Bread 0.6