A manganese (Mn) deficiency was found to induce poor growth in mice and abnormal reproduction in rats.
Manganese is an essential trace mineral that is widely distributed in nature, but is only found in trace amounts in animals.
The body of a healthy 70 kg man is estimated to contain a total of 10-20 mg of manganese.
Results from the Total Dietary Study (1982-1989) indicated that estimated intakes of manganese for young children, adolescent boys, young and older adult men and women were all within the Estimated Safe Daily Dietary Intake (ESADDI). However, manganese intake by 14-16 year old girls was approximately 10% below the lower limit of the ESADDI.1
The ESADDI for adults for manganese was 2-5 mg Mn/day.2
Absorption of dietary manganese is low; approximately 6% in humans.
Most enzymes activated by manganese can also be
activated by other metals, such as magnesium.
Manganese is involved in bone formation and in protein, fat, and carbohydrate metabolism.
Manganese functions, like other trace elements, as an enzyme activator and as a constituent of metalloenzymes.
The metalloenzymes that are activated by manganese are:
manganese superoxide dismutase (SOD)
Manganese is the preferred metal cofactor for
glycosyltransferases. These are important in the synthesis of glycoproteins
and glycosaminoglycans (GAGs or mucopolysaccharides). Glycoproteins help in
synthesis of myelin and clotting factors.
Manganese deficiency has been induced in several species of animals by feeding low manganese diets. Signs of deficiency include: impaired growth skeletal defects depressed reproductive functions weight loss possible abnormal glucose tolerance ataxia in the newborn defects in metabolism34
Manganese deficiency in humans has not been clearly
established. However, symptoms of manganese deficiency in adults include:
depressed growth of hair and nails, failure in normal hair pigmentation,
dermatitis and hypocholesterolemia. 4
Manganese has been considered as one of the least toxic of the trace elements for oral consumption.
Several data sources have demonstrated that oral manganese intakes of 10 mg per day, or the no observed adverse effect level (NOAEL), do not cause adverse effects in adults.6
The lowest observed adverse effect level (LOAEL) for manganese was 4.2 mg Mn/day for a 70-kg individual.2
In animals, excess manganese may inhibit absorption of iron and result in iron deficiency anemia. Additional adverse effects of excess manganese can include depressed growth, decreased appetite, and altered neurological function.6
Individuals with cholestatic liver disease are susceptible to manganese overload, since they lack the means to excrete excess metals.1
Individuals receiving total parenteral nutrition are also at risk of manganese toxicity if liver and biliary functions are compromised.1 One paper reported that children receiving the standard dose of manganese in parenteral nutrition formulas saw a high incidence of hypermanganesaemia, that was associated with impaired liver function.7 It has been recommended that manganese be reduced in parenteral formulas, suggesting that manganese toxicity itself can be a factor in causing cholestatic liver disease, particularly in young children.
Excess brain manganese adversely affects motor and cognitive function. In addition, accumulation of manganese over time can lead to severe psychiatric disorders and permanent neurological dysfunction. 48
Neurologic side effects, like those similar to
symptoms caused by Parkinson's disease, were observed in an earlier study
among subjects who consumed 15 mg Mn/day. 9
Minerals such as calcium, copper, iron magnesium, and zinc compete for absorption in the small intestines. An excess of one can interfere with the absorption of other metals. An excess amount of manganese may induce iron-deficiency anemia. Avoiding excessive amounts of any mineral is advised.
Information on the relationship between substances and disease is provided for general information, in order to convey a balanced review of the scientific literature. In many cases the relationship between a substance and a disease is tentative and additional research is needed to confirm such a relationship.
Diabetes: From previous research, it has not been reported whether differences in trace mineral status are a consequence of diabetes, or whether it contributes to expression of the disease.14
One study compared trace element status of 53 patients with type II diabetes with those of 50 healthy controls. Concentrations of seven trace elements were determined in whole blood, plasma, erythrocytes, and lymphocytes. Lower manganese and selenium concentrations were detected in lymphocytes of diabetic patients versus the healthy subjects.15
Oxidative stress is a contributing factor to the development of late complications in diabetic patients, likely due to hyperglycemia. One study compared the oxidative susceptibility and plasma alpha-tocopherol concentration of low-density lipoproteins (LDL) with the concentrations of glycated hemoglobin (HbA1c), copper and manganese in 63 type I and type II diabetics. Results indicated that although plasma copper and manganese concentrations in diabetic patients were not decreased, both copper and manganese concentrations were significantly related and positively correlated to the amount and rate of LDL oxidation.16
One study measured the urinary excretion of chromium,
copper and manganese in 185 diabetic patients and control subjects. There was
no correlation found between urinary excretion of any metals examined with
either age or sex of the two groups. However, diabetic patients with liver
disorders, or those not taking insulin, excreted significantly more manganese
than their diabetic counterparts. 17
Premenstrual symptoms: Research has indicated that nutritional intake, metabolism and status may play a role in regulating normal menstrual cycles.
Currently, there has only been one study reported on
manganese and PMS. In a metabolic ward study, 10 women with normal menstrual
cycles were given either low (587 mg) or high (1,336 mg) calcium, with a low
(1.0 mg) or high (5.6 mg) amount of manganese for 39 days. Results indicated
that low dietary manganese intake significantly increased mood and pain
symptoms during the premenstrual phase. However, this was true only when
calcium intakes were high. It was concluded that low intakes of either
manganese or calcium may increase the occurrence of negative mood states. It
was also found that the relationship between manganese and mood states is also
mediated by the menstrual cycle.18
Parkinson's Disease: A population-based case control study was conducted in a metropolitan area to assess occupational exposure to manganese and other metals as risk factors for Parkinson's disease (PD). Non-demented middle-aged men and women receiving primary care at a metropolitan health system were enrolled and frequency-matched for age, sex, race and smoking status. After adjusting for these factors, it was found that more than 20 years exposure to manganese or copper was associated with risk for PD. 19
Joint/Cartilage Stability: Therapy for the medical management of osteoarthrosis, a progressive age-related degeneration of articular cartilage in joints, has been largely focused on the alleviation of symptoms.
Supplements of glucosamine hydrochloride, low
molecular weight chondroitin sulfate, and manganese ascorbate were tested
separately and in combination for their ability to retard progression of
cartilage degeneration. An in vitro combination of glucosamine hydrochloride
and chondroitin sulfate synergistically stimulated glycosaminoglycan synthesis
better than taken alone. Chondroitin sulfate and manganese ascorbate (but not
glucosamine) were both effective in decreasing degradative enzyme activity.
This suggested that the reduction in the progression of cartilage degeneration
from a mixture of glucosamine, chondroitin and manganese ascorbate was more
efficacious than either agent alone. 20
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