Manganese Healthy Joints

The Benefits of Manganese
By: Dr. Obikoya

Manganese is a mineral element that is nutritionally essential. The derivation of its name from the Greek word for magic remains appropriate because scientists are still working to understand the diverse effects of manganese deficiency.

Manganese is an antioxidant nutrient that is important in the breakdown of amino acids and the production of energy. It is necessary for the metabolism of Vitamin B-1 and Vitamin E and it activates various enzymes which are important for proper digestion & utilization of foods.

Manganese is a catalyst in the breakdown of fats and cholesterol. It helps nourish the nerves and brain, is necessary for normal skeletal development, and helps to maintain sex hormone production and to regulate blood sugar levels.
Manganese plays an important role in a number of physiologic processes as a constituent of some enzymes and an activator of other enzymes.

Manganese superoxide dismutase (MnSOD) is the principal antioxidant enzyme of mitochondria, the power house in our cells. Because mitochondria consume over 90% of the oxygen used by cells, they are especially vulnerable to oxidative stress. The superoxide radical is one of the reactive oxygen species produced in mitochondria during ATP synthesis. MnSOD catalyzes the conversion of superoxide radicals to hydrogen peroxide, which can be reduced to water by other antioxidant enzymes.

A number of manganese-activated enzymes play important roles in the metabolism of carbohydrates, amino acids, and cholesterol. Pyruvate carboxylase, a manganese-containing enzyme, and phosphoenolpyruvate carboxykinase (PEPCK), a manganese-activated enzyme, play critical roles in gluconeogenesis, the production of glucose from non-carbohydrate precursors.

Arginase, another manganese-containing enzyme, is required by the liver for the urea cycle, a process that detoxifies ammonia generated during amino acid metabolism.

Manganese deficiency results in abnormal skeletal development in a number of animal species. Manganese is the preferred cofactor of enzymes called glycosyltransferases, which are required for the synthesis of proteoglycans that are needed for the formation of healthy cartilage and bone.

Wound healing is a complex process that requires increased production of collagen. Manganese is required for the activation of prolidase, an enzyme that functions to provide the amino acid, proline, for collagen formation in human skin cells. A genetic disorder known as prolidase deficiency results in abnormal wound healing among other problems, and is characterized by abnormal manganese metabolism. Glycosaminoglycan synthesis, which requires manganese-activated glycosyltranserases, may also play an important role in wound healing.

Although the specific mechanisms for manganese absorption and transport have not been determined, some evidence suggests that iron and manganese can share common absorption and transport pathways. Absorption of manganese from a meal is reduced as the meal's iron content is increased. Iron supplementation (60 mg/day for 4 months) was associated with decreased blood manganese levels and decreased MnSOD activity in white blood cells, indicating a reduction in manganese nutritional status. An individual's iron status can affect manganese bioavailability.

Intestinal absorption of manganese is increased during iron deficiency, and increased iron stores (ferritin levels) are associated with decreased manganese absorption. The finding that men generally absorb less manganese than women may be related to the fact that men usually have higher iron stores than women. Supplemental magnesium (200 mg/day) decreased manganese bioavailability slightly, either by decreasing manganese absorption or by increasing its loss in healthy adults.

In one set of studies, supplemental calcium (500 mg/day) resulted in slightly lower manganese bioavailability in healthy adults. As a source of calcium, milk had the least effect, while calcium carbonate and calcium phosphate had the greatest effect. Several others studies have found the effect of supplemental calcium on manganese metabolism to be minimal.

Manganese deficiency has been observed in a number of animal species. Signs of manganese deficiency include impaired growth, impaired reproductive function, skeletal abnormalities, impaired glucose tolerance, and altered carbohydrate and lipid metabolism.

In humans, demonstration of a manganese deficiency syndrome has been less clear. A child on long-term total parenteral nutrition (TPN) that lacked manganese developed bone demineralization and impaired growth that were corrected by manganese supplementation.

Young men who were fed a low-manganese diet developed decreased serum cholesterol levels and a transient skin rash. Blood calcium, phosphorus, and alkaline phosphatase levels were also elevated, which may indicate increased bone remodeling as a consequence of insufficient dietary manganese.

Young women fed a manganese-poor diet developed mildly abnormal glucose tolerance in response to an intravenous (IV) infusion of glucose. The adequate intake (AI) for manganese (2.3 mg/day for adult men and 1.8 mg/day for adult women) appears sufficient to prevent deficiency in most individuals.

References
Kies C. Bioavailability of manganese. In: Klimis-Tavantzis DL, ed. Manganese in health and disease. Boca Raton: CRC Press, Inc; 1994:39-58.

Johnson PE, Lykken GI. Manganese and calcium absorption and balance in young women fed diets with varying amounts of manganese and calcium. J Trace Elem Exp Med. 1991;4:19-35.

Norose N, Terai M, Norose K. Manganese deficiency in a child with very short bowel syndrome receiving long-term parenteral nutrition. J Trace Elem Exp Med. 1992;5:100-101 (abstract).

Friedman BJ, Freeland-Graves JH, Bales CW, et al. Manganese balance and clinical observations in young men fed a manganese-deficient diet. J Nutr. 1987;117(1):133-143.

Shetlar MR, Shetlar CL. The role of manganese in wound healing. In: Klimis-Tavantzis DL, ed. Manganese in health and disease. Boca Raton: CRC Press, Inc.; 1994:145-157.