Facts, Articles, Research

What the science says (1990–2026): Manganese

These citations support correction of deficiency, specified forms, and elemental amounts — the same logic used in MD's Choice formulas. They are not claims that a supplement treats disease.

Keen 1990s; 2017–2024 trace reviews; cartilage-enzyme literature. Manganese is a cofactor for enzymes in cartilage and antioxidant defense (MnSOD). Amino-acid chelates are used so the elemental amount can be published.

These products are not intended to diagnose, treat, cure, or prevent disease. Historic monograph text below is kept for the original library.

Manganese

I. Physiological Role (see Hurley, 1984. Present Knowledge in Nutrition)

Mn functions biochemically as a cofactor activating a large number of enzymes
1. Many different enzymes can be stimulated by Mn, but the effects are not specific for Mn and the enzymes are not affected by Mn deficiency
2. A pathway specific for Mn is activation of the glycosyl transferases (See J. Nutr. 115:352. 1985)
  1. Required for synthesis of glucosaminoglycans (mucopolysaccharides)
  2. Mn is thus required for normal formation of skeletal cartilage
B. Mn is an integral part of certain metalloenzymes
1. Pyruvate carboxylase which catalyzes the first step of carbohydrate synthesis from pyruvate Mn may not be specifically required since Mg can replace Mn without changing enzyme properties
2. Mn superoxide dismutase belongs to a group of enzymes which catalyze dismutation of superoxide free radical to hydrogen peroxide and water
  1. Mn SOD is present in cellular and subcellular membranes
  2. Cu-Zn SOD functions primarilyy in the aqueous phase of the cytosol and plasma
  3. Mn deficiency reduces Mn SOD activity with a concomitant increase in Cu-Zn SOD
  4. These enzymes work in concert with glutathione peroxidase, chain-breaking antioxidants such as vitamin E and various other radical scavengers to minimize accumulation of reactive forms of oxygen which could damage cells
  5. Reduced Mn SOD activity due to dietary Mn deficiency is associated with higher than normal levels of lipid peroxidation in liver mitochondria (J. NUtr. 113:2498. 1983)
Adequate Mn during development in utero may be required for normal insulin secretion in later life (J. Nutr. 114:1438. 1984)
Mn may also play a complex role in postweaning of the exocrine pancreas and regulation of pancreatic amylase (J. Nutr. 117:305. 1987)
Mn may participate in the regulation of pancreatic amylase content and in the adaptive response of pancreatic lipase to dietary fat (J. Nutr. 117:2079-2085. 1987)

II. Distribution in Tissues

Mn is present in small amounts in most tissues, averaging only 2.5 ppm (DM) in the total body

III. Absorption and Metabolism

Absorption of Mn is low
1. 1.7- 14.5% by humans (Fed. Proc. 46, abstr. 1478, 1987)
  1. Mn absorption was measured using diets intrinsicly labeled with ⁵⁴Mn monitoring whole body retention for 20d
  2. ⁵¹Cr was used as a marker of intestinal transit of the nonabsorbed fraction of the label
  3. Range in absorption for different individuals was 1.7-14.5% from the same diet
  4. Results for repeated occasions in the same subject were highly reproducible
2. Absorption of ⁵⁴Mn introduced into the chicks crop was 2.4% (Fed. Proc. 45:474. 1986)
3. Comparison of amounts of ⁵⁴Mn in the feed, entering the duodenum, leaving the ileum, and appearing in feces reveal relatively little absorption or excretion of Mn in any section of the ruminant GI tract
  1. This procedure measures only net absorption and does not differentiate between absorption and excretion occurring simultaneously in the same location
  2. Work with ⁵⁴Mn allows unidirectional measurement of Mn passage
    1. ⁵⁴Mn is absorbed rapidly following administration via duodenal catheters to calves
    2. Its release back into intestinal contents is also rapid
    3. More ⁵⁴Mn is absorbed in the cranial end of the small intestine than in more caudal sections of the Gl tract.
    4. The percentage of ⁵⁴Mn excreted by feces is high, whether administered orally or IV
    5. Urinary Mn is negligible
4. Mechanism of Mn absorption (Fed. Proc. 46, abstr 3466. 1987)
  1. Mn uptake by brush border membrane vessicles from rats small intestine is characterized by a low affinity, high capacity uptake that is non saturable and may be dependent on Mn valency
  2. Transport of Mn does occur in the presence of a Na gradient
  3. Upon absorption some of the ingested Mn may become bound to a₂-macroglobulin and possibly albumin
  4. Most is removed by the liver and presumably excreted
  5. A small portion is bound to transmargin and released into the systemic circulation for transport to tissues

IV. Homeostatic Control

According to "Present Knowledge in Nutrition", a small but constant fraction of the Mn intake is absorbed irrespective of its dietary concentration
1. In contrast, there is some evidence that absorption is also a factor in Mn homeostasis in the bovine (J. Anita. Sci. 42:630-636, 1976; 45:1008, 1977)
The liver with its capacity to remove and presumably excrete Mn through the intestine via bile is considered to be the main homeostatic mechanism (Mn is unique in this respect)
1. Bovine liver is capable of excreting 1.2 mg of Mn/min (Hall and Symonds 1981. Brit. J. Nutr. 45:605)
2. Capacity of bile to excrete additional Mn is not exceeded until a maximum concentration of 20 mg/dl in bile is reached when Mn is infused intravenously at 4 mg/min
Under conditions of Mn overloading, auxilary Gl routes may also come into use (see Am. J. Physiol. 21:203-206; 211-216; 217-224, 1966; J. Anim. Sci. 42:630-636, 1976)
In very young animals, excretion of Mn appears to be absent or limited, and increased dietary Mn intake probably results in higher tissue Mn concentrations (Rats used in J. Nutr. 118:1509, 1988 weighed 48-71g)

V. Interactions with Other Elements

Mn and Mg are similar in chemistry and can replace each other in several biochemical systems
1. It is possible dietary Mg may be utilized to a greater extent by the body if dietary Mn is low
2. Normal levels of Mn can be detrimental if Mg is deficient (Fed. Proc. 46, abstr. 2556, 1987)
  1. Normal dietary levels of Ca and Mn induce detrimental changes in growth and other physiological indices in Mg or methionine deprived rats
  2. Growth is improved by reducing Mn or Ca below the requirement levels when diets deficient in Mg or methionine are fed
Ca is antagonistic to Mn in ruminants; increasing Ca increases fecal Mn loss
Dietary K may increase fecal loss of Mn just as it increases fecal Mg loss
Dietary phytate depresses retention and accumulation of Mn in rats
Fe and Mn (see Ho et al, 1984. J. Dairy Sci. 67:1489)
1. Addition of Fe to the diet depresses Mn retention
2. Omission of Fe enhances Mn retention (Fed. Proc. 46, abstr. 3482, 1987)
Supplementation with Mn may increase organ content of Zn but decrease liver Cu

VI. Requirements

Adult Humans....2-5mg
Sheep.................20-40 ppm (NRC, 1975)
Beef Cattle........20 ppm (NRC, 1976)
Dairy Cattle........40 ppm (NRC, 1978)
Poultry................NRC lists 60 ppm; in practice, 100 ppm may give a response
(Fed. Proc. 46, abstr 3464, 1987) Mn-methionine chelate is more available than MnO for chicks

VII. Mn Deficiency

Slipped tendon in chicks
Impaired reproduction in cattle
1. Anestrus despite normal ovulation
2. More services required for conception
3. Reduced Mn content of ovaries
  1. Mn content of ovarian cortical stroma was lower in cows with cystic ovaries than in cows with noncystic ovaries
Changes in animals born to Mn deficient dams
1. Low birth weight
2. Reduced rate of gain
3. Stiffness, twisted legs, joint pains
4. General physical weakness
5. Deformed bones
  1. Shortened tibias
  2. Enlarged joints
  3. Abnormal bony outgrowths on front tarsal joint
Reduced Mn content of liver and kidney
Fatty degeneration of liver
1. Fatty infiltration
2. Liver abscesses
3. Reduced bile volume
Reduced Mn-superoxide dismutase activity in rats breathing ozone (Fed. Proc. 46, abstr. 3469, 1987)
Reduced arginase activity resulting in lower urea cycle capacity (Fed. Proc. 46, Abstr. 1476, 1987)
The effect of Mn deficiency on urea production in rats may not be due directly to lower arginase activity. Abnormal nitrogen metabolism may also be an important factor (Fed. Proc. 46, Abstr. 3467, 1987)
Mn may play a complex role in post weaning development of the exocrine pancreases and regulation of pancreatic amylase (J. Nutr. 117:305-311, 1987)

VIII. Mn Toxicity

In general, adverse health effects have not occurred in most species with dietary Mn of 1000 ppm or less
Whether metabolic changes due to excess Mn would become threats to health on a long-term basis depends on diet composition, age, physiological status and mechanism of the adverse effect
Swine may be more sensitive than sheep or cattle (maximum tolerable level is 400 ppm)
Poultry are less sensitive (maximum tolerable level is 2000 ppm
At 2000 ppm and above, growth retardation, anemia, GI lesions and sometimes neurological signs have been observed

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Manganese — Mn (atomic number 25)

A trace metal and cofactor for enzymes that build proteoglycans in cartilage. That is why it sits in MD's Choice joint formulas as an amino-acid chelate, not as a pain drug.

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What the science says (1990–2026): Manganese

Manganese

Vitamins, Major Elements, Trace Elements, Toxic Elements

Vitamins

Major Elements

Trace Elements

Toxic Elements

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