Fundamentals of Human Nutrition/Manganese Trace
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Manganese is considered a trace mineral and is found in small amounts throughout different parts of the body. It can be found mostly within the bones, liver, pancreas and kidneys. Even though it is rather scarce in the body, manganese helps the body in many different ways. Manganese can be used to form connective tissue, bones, sex hormones and even blood clots. It can also play a role in fat and carbohydrate metabolism, calcium absorption and blood sugar regulation (University of Maryland Medical Center, 2013).
Many manganese-activated enzymes play important roles in the metabolism of these fats and carbohydrates. For example, pyruvate carboxylase is a manganese-activated enzyme and is essential in the process of gluconeogenesis, which produces glucose from non-carbohydrate precursors (Oregon State University, 2015). Arginase is another manganese-containing enzyme, and is required by the liver to help with the urea cycle, a process that makes ammonia produced during amino acid metabolism less toxic to the body (Oregon State University, 2015).
As one may see, manganese is important in regulating the metabolism of different things within the body. Manganese is also necessary in order to maintain normal brain and nerve function. It is a component of the antioxidant enzyme superoxide dismutase (SOD). The purpose of SOD is to fight against free radicals, which occur naturally throughout the body, but can damage the cell membrane and can even harm DNA (University of Maryland Medical Center, 2013). SOD acts as a catalyst of the conversion of the free radicals to hydrogen peroxide, which is further reduced to water by other antioxidant enzymes.
As stated previously, even though manganese is only found in small amounts in the body, it is an essential nutrient. This is because it is involved in many chemical processes such as processing cholesterol, carbohydrates and proteins. Manganese is also involved in the formation of bone, with a manganese deficiency resulting in abnormal skeletal system development. Manganese is a preferred cofactor of enzymes known as glycosyltransferases (Oregon State University, 2015). These enzymes allow for the synthesis of proteoglycans. Proteoglycans are what allow for the healthy production of cartilage and bone (Oregon State University, 2015). When the body is wounded, recovery requires an increase in the production of collagen. Prolidase, which is an enzyme that is used to form this collagen in human skin cells, requires manganese in order to be activated (PubMed, 2013). Thus, manganese is essential in the process of blood clotting and wound healing. Though many of the functions of manganese can be generalized in its use as an activator for enzymes, it still plays an extremely important role within the body.
References University of Maryland Medical Center. (05/31/2013). “Complementary and Alternative Medicine Guide: Manganese”. Retrieved on 11/17/15 at https://umm.edu/health/medical/altmed/supplement/manganese Oregon State University. (03/2015). “Micronutrient Information Center: Manganese”. Retrieved on 11/17/15 at http://lpi.oregonstate.edu/mic/minerals/manganese PubMed. (01/2013). “Manganese Action in Brain Function”. Retrieved on 11/17/15 at http://www.ncbi.nlm.nih.gov/pubmed/12505649
Manganese is not readily available in the body as there are only 20 milligrams, which equates to one fiftieth of a gram, scattered throughout the bones, liver, kidneys, and pancreas. In fact, this mineral was not focused on until the 1930s when a group of researchers uncovered that human bodies require small amounts every day. There is not enough information in order to establish a proper recommended daily allowance (RDA), however, average intakes taken from a yearly survey of the overall mineral content in American diets were incorporated to determine adequate intake levels (AL) and tolerable upper intake level (UL) values. These values were established by the Food and Nutrition Board (FNB) of the Institute of Medicine. No manganese deficiency has ever been documented in humans that are consistently consuming natural diets on a daily basis. The current AL values are 2.3 milligrams per day for men and 1.8 milligrams a day for women. The UL value for adults is 11 milligrams per day.
Freeland-Graves, Bales, and Behmardi (1987) have come to the agreement that a suggested range of 3.5 to 7 milligrams per day of manganese is sufficient in both adults and adolescents. Their reasoning comes from the basis that current diets consist of a substantial amount of meats and refined grains that leads to an imbalance in the intake of manganese. Freeland-Graves (1988) discovered that manganese may have an even more crucial impact on women who are more prone to osteoporosis since the mineral’s role involves bone formation and stability. Freeland-Graves et al. (1987) found that five out of seven of the males in the study who were fed a depleted diet of manganese developed a heat rash identified as Miliaria crystallina.
Maintaining a healthy level of manganese in the body is important because there are health problems associated with having too much as well as too little of the mineral in the body. A daily consumption of less than 2.3 milligrams of manganese may lead to health complications such as bone malformation, seizures, and overall weakness. Levels of manganese that are in excess place individuals at risk for neurological disorders resembling Parkinson’s disease. Despite the given statements, the good news is that American diets usually gravitate towards being well above the required daily intake value. In conclusion, one sure fact is that manganese is a mineral that is most definitely critical to developing and maintaining a healthy lifestyle.
Although there is not enough information to form a recommended daily intake for manganese, anywhere from 2 - 9 milligrams of dietary manganese per day is considered safe and sufficient for the average adult (Michalke & Fernsebner, 2014). The Average Intake of manganese is 2.3 mg per day for men and 1.8 mg per day for women.
The sufficient amount of manganese required for the average adult is low, and many plant sources (such as wheat germ, rolled oats, parsley, and soybeans) contain significant amounts of manganese. Therefore, manganese deficiency is rare. However, certain factors such as phytate intake and high iron and calcium intake may inhibit manganese absorption, so deficiency is still possible.
According to Blaurock-Busch, several symptoms of manganese deficiency are ataxia (the loss of full control of bodily movements), fainting, hearing loss, and weak tendons and ligaments. According to Watts (1990), manganese deficiencies have been studied in animals, and although the symptoms vary according to species and degree of deficiency, there are many similarities of symptoms between species. These similarities include skeletal abnormalities (which include chondrodystrophy, i.e. retarded bone growth with bowing), postural defects, impaired growth, impaired reproductive function (which is characterized by defective ovulation, increased infant mortality, and ovarian and testicular degeneration), and disturbances in lipid and carbohydrate metabolism. As shown from studies involving rats, a deficiency in manganese may also lead to abnormalities in the integrity of cell membranes and mitochondria.
Watts (1990) also stated that, with one human study in particular, symptoms of manganese deficiency included hypercholesterolemia, decreased triglycerides and phospholipids, weight loss, transient dermatitis, and intermittent nausea. The subject’s hair color also changed from black to red when experiencing manganese deficiency.
The Upper Level for manganese is 11 mg per day and was established based on intakes from food, water, and supplements. Manganese toxicity is more likely to occur as a result of exposure to manganese in the environment (such as with inhalation of manganese by workers in factories and manganese miners) than with excessive dietary manganese.
There are three levels of manganese toxicity, according to Watts (1990). Mild toxicity leads to symptoms that include insomnia, hallucinations, muscular pains, compulsive actions, and impaired memory. Moderate toxicity leads to speech disorders, poor balance, and fine tremors. Severe toxicity leads to symptoms that are similar to those of Parkinson’s disease -- rigidity, spasmodic laughter, and mask-like face.
Several factors that may increase one’s risk for manganese toxicity are alcoholism, decreased excretion, and iron deficiency.
Alcoholism can have a direct effect on how Manganese interacts with the body. Once the liver breaks down alcohol, its toxins are released and the byproducts can often damage the liver cells in the process. Once these liver cells are damaged they are unable to perform their intended task of preventing toxic substances, such as manganese, from traveling to the brain (Tarter et al. 1993). Elements such as Manganese will in turn damage brain cells, potentially leading to the serious and sometimes fatal brain disorder, Hepatic encephalopathy. This disorder ranges from mild, to severe, including symptoms of anxiety, depression, motor disturbances, coma and death (Tarter et al. 1993).
Another condition that can lead to toxicity can be linked to hepatic dysfunction. Manganese homeostasis is largely centered around liver function and the predominant cells in the liver, hepatocytes (Kies, 1994). The balance of this element is controlled by an efficient system of evacuation, where Manganese may be moved across the enterocyte and then returned to the gut lumen or excreted into feces through means of bile. Absorbed Manganese is carried to the liver by the portal blood system, where it is taken up, and therefore anything that damages or interrupts liver function could consequently diminish manganese excretion (Kies, 1994). This could then increase Manganese retention in the body, causing reason for toxicity.
While there are few dietary nutrients that demonstrate a positive or negative interaction with Manganese, studies have revealed that Iron does in fact have a strong interaction with Manganese. (Mills, 1985). When Iron is increased in the diet, manganese absorption is diminished, and alternatively when dietary Manganese is increased, the metabolism of Iron is interrupted. A reason for this phenomenon may be that Manganese might be accepted by the transport mechanism of Iron and therefore absorbed alongside this trace mineral. (Mills, 1985) These findings have led to the conclusion that a deficiency of Iron could lead to high risk for accumulation of Manganese in the brain, which can cause abnormalities and another form of toxicity in regards to this element. Although the chance of Americans consuming too much Manganese in the diet is small, there are still situations where this could occur and cause an imbalance. Individuals should only consume the allowed daily intakes of Manganese, while not exceeding more than the Upper limit. To prevent toxicity, it is also important to limit alcohol use and consume normal amounts of other elements that may have negative impacts on Manganese absorption.