There are 10 essential trace minerals for human health, which are obtained from our diets. Here is information on trace minerals, extracted from UpToDate.
CHROMIUM — In 1957, a compound extracted from pork kidney was termed “glucose tolerance factor” because it corrected hyperglycemia in rats. Glucose tolerance factor was ultimately found to be chromium (Cr).
Cr is a transition element and exists in multiple ionic states. Dietary Cr is in the trivalent state. The more oxidized form Cr4+ is a toxic and hazardous substance. Cr occurs as a component of a metalloenzymes and functions as a coenzyme in various metabolic reactions.
COPPER — The variability in the copper content of food reflects the variability in the copper content of soil. Further variability is introduced by variations in manufacturing methods.
In the Western diet, approximately 60 percent of dietary copper comes from vegetable products, with vegetables, grains, and pulses (leguminous seeds such as beans, peas, and lentils) each providing approximately 20 percent. A further 20 percent comes from meat, fish, and poultry. The highest content of copper is found in liver (20 to 180 mg/kg versus 1 to 2.6 mg/kg in white bread and 0.02 to 0.08 mg/kg in cow’s milk). According to the Third National Health and Nutrition Survey, the average daily dietary copper intake for adults in the United States is 1 to 1.6 mg.
Copper is found in high concentrations in liver, brain, and to a lesser degree, in kidney, heart, and pancreas. The total copper content in the adult human body is estimated to be 50 to 120 mg. The newborn term infant contains approximately 12 mg copper. Breast milk contains relatively little copper. Early in lactation breastmilk contains up to 0.7 mg/L copper but this rapidly falls to 0.2 mg/L and may provide less than the recommended copper intake by the WHO. During this period, any shortfall in copper intake can be met by mobilizing liver copper stores.
FLUORIDE — Ground water contains fluoride in amounts between 0 and 40 mg/L. The variability in water content explains much of the variability in total fluoride intake. There is a well described inverse relationship between fluoride intake and dental caries. Many domestic water supplies are fluoridated in order to reduce the incidence of caries.
Other important sources of fluoride are tea, seafood that contains edible bones or shells (eg, canned sardines), medicinal supplements, and fluoridated toothpastes .
Metabolism —In bone and teeth, fluoride can displace hydroxyl ions from hydroxyapatite to produce fluorapatite or fluorohydroxyapatite. About 99 percent of total body fluoride is contained in bones and teeth, and the amount steadily increases during life.
Biological role — It remains unclear whether fluoride is truly essential, although fluoride may have some beneficial effects. Animal models, such as rodents fed fluoride-deficient diets, have failed to show consistent findings of deficiency. However, once taken up into bone, fluoride appears to increase osteoblast activity and bone density, especially in the lumbar spine. Fluoride has been suggested as a therapy for osteoporosis since the 1960s, but despite producing denser bone, fracture risk is not reduced. Indeed, there is some evidence that nonvertebral fractures may be increased.
IODINE — The dietary importance of iodine lies in the metabolism and homeostasis of the thyroid gland
Goiter, described as the enlargement of thyroid gland, was first associated with iodine deficiency in the early 1920s. At that time, goiter was endemic in certain parts of the world and the Midwestern United States. In one study, administration of iodine treated and prevented goiter in children in goiter-endemic areas of Ohio . Iodized salt was then introduced and led to reduction of hypothyroidism-related growth retardation and successful prevention of goiter.
In the United States and other industrialized nations, iodine deficiency is rarely seen due to iodized water, salt, and bread. However, iodine deficiency still remains a major public health issue in parts of the world where its incorporation into diet has been unsuccessful, and iodine deficiency remains among the most common micronutrient deficiencies globally
Dietary sources — Iodine is heterogeneously distributed in the environment, with soil and water varying greatly in their iodine content. Iodine is found naturally in fish and seafood, as well as in drinking water and vegetables. Dairy products contain iodine because of iodine absorption from iodine-containing disinfectants. Some breads contain iodine from the dough oxidizers used in their manufacture.
In many countries, food staples such as table salt are fortified with iodine. Up to 70 percent of the world’s population has access to iodized table salt.
IRON — Heme iron is found in meat, poultry, and fish. Its absorption is good and is relatively unaffected by underlying iron status. Non-heme iron is found in vegetables and fruit, as well as iron-fortified food products. Absorption of non-heme iron increases as iron status declines. American children now consume more iron from cereal or breads than from beef or chicken.
In developing countries, heme iron intake is very low and most dietary iron intake is from non-heme food sources. These foods, however, often have poor bioavailability of the non-heme iron because of the presence of phytate, which chelates iron and prevents its absorption.
Heme iron is absorbed about twice as well as non-heme iron. Heme-iron absorption is unaffected by iron status Non-heme iron is absorbed throughout the small intestine, especially in the duodenum. Absorption is increased by vitamin C and certain amino acids, and is inhibited by calcium, phytic acid, and tannates.
The body has elaborate mechanisms to prevent “free” iron from being available to invading microorganisms or malignant cells.
Iron losses from the body generally are very low (approximately 1 mg/day). Menstruating women have additional iron losses of approximately 1 to 2 mg/day.
MANGANESE — Manganese (Mn) was first shown to be essential for normal growth and development of rodents. Most studies of manganese deficiency are in experimental animals, where it leads to poor growth, decreased fertility, ataxia, skeletal deformities, and abnormal fat and carbohydrate metabolism. In some animal models, the offspring of manganese-deficient mothers develop irreversible ataxia.
Manganese deficiency in humans is very unusual, but has been reported in individuals on a highly restricted diet. In experimental studies in humans, manganese deprivation was associated with a scaly dermatitis and dyslipidemia
Dietary sources — Meat, fish, poultry, dried fruit, and nuts are good sources of manganese, but absorption is very variable. Tea also contains large amounts of manganese, but its bioavailability appears to be very low.
Approximately one-quarter of total body manganese is found in the bones. Significant amounts also are found in tissues rich in mitochondria (liver, kidney, pancreas) and rich in melanin (retina, pigmented skin).
Biological role — Manganese is found in manganese superoxide dismutase (Mn-SOD), arginase, glutamate synthetase, and pyruvate carboxylase. Particular interest has been paid to Mn-SOD, which is important for detoxifying the superoxide radical to hydrogen peroxide It also is found in other enzymes, where it may replace magnesium.
Toxicity — Manganese toxicity (manganism) is a well recognized hazard in workers exposed to manganese aerosols or dust, as may occur in welding or steel industries; it has also been reported in individuals drinking well water with high concentrations of manganese. High levels of manganese can be neurotoxic, affecting primarily the extrapyramidal parts of the brain. Symptoms are similar to those of Parkinson’s disease, and include dyscoordination, loss of balance, and confusion. Headache, vomiting, and hepatic dysfunction have also been reported.
SELENIUM — Selenium (Se) is a trace mineral with a role in multiple biologic functions.
In free-living animals and humans, selenium is mostly in the form of two selenium-containing amino acids: seleno-cysteine and seleno-methionine. Inorganic forms of selenium are used in supplements.
Seafood, kidney and liver, and meat are good sources of selenium. Drinking water usually contains very little selenium. The selenium content of grains and seeds is variable and depends on the selenium content of the soil and the form in which selenium is present
Biological role — More than 30 selenoproteins have been identified, of which the best known are the four forms of glutathione peroxidase,which are important in antioxidant defense, and iodo-thyronine deiodinase 2 (three forms), which serves as a catalyst for production of thyroid hormone. Other seleno-proteins include seleno-protein P and seleno-protein synthetase. Some have well defined roles, while others are still under investigation.
Severe selenium deficiency is associated with skeletal and heart muscle dysfunction and may also cause mood disorders and impaired immune function, macrocytosis, and whitened nailbeds.
A number of studies have shown a linear relationship between selenium deficiency and a reduction in CD4 cell counts in HIV-infected patients
Impaired cell-mediated immunity has been demonstrated when tissue stores of selenium are depleted. Natural killer cell activity is enhanced when selenium is supplemented in the diet of selenium depleted individuals.
Thyroiditis — Selenium supplementation may decrease inflammatory activity in patients with autoimmune thyroiditis, and may reduce the risk of postpartum thyroiditis in women who are positive for thyroid peroxidase (TPO) antibodies.
Cancer — Epidemiologic studies support a possible relationship between Se and cancer mortality.
Cardiovascular disease — glutathione peroxidase (GPx), a seleno-protein dependent enzyme, reduces hydrogen peroxide and other molecules with oxidative potential. In theory, the antioxidative effect protects lipid membranes, inhibits oxidative modification of low density lipoprotein, and suppresses platelet aggregation.. These effects would predict that Se supplementation should be protective of atherosclerotic disease. However, prospective and epidemiologic studies have shown mixed results.
Glucose metabolism — Animal models suggest that low doses of selenium may improve glucose metabolism, clinical studies in humans suggest that selenium supplementation does not confer benefit and may increase the risk of type 2 diabetes.
Toxicity — Clinical manifestations of selenium toxicity include nausea, emesis, diarrhea, hair loss, nail changes, mental status changes, and peripheral neuropathy.
Selenium toxicity occurs with excess dietary intake, either through diets naturally high in selenium or “megadose” supplementation. Selenium toxicity occurred in 201 individuals in the United States who took a liquid dietary supplement containing 200 times the labeled content of selenium. The median estimated dose of selenium consumed was over 41,000 micrograms/day, which is almost 800 times the recommended dietary allowance of 55 micrograms/day, and more than 100 times the tolerable upper intake limit of 400 micrograms/day.
ZINC — Subclinical zinc deficiency may significantly increase the incidence of and morbidity and mortality from diarrhea and upper respiratory tract infections. Along with iron, iodine, and vitamin A, zinc deficiency is one of the most important micronutrient deficiencies globally. Several studies have now demonstrated that supplementation of high risk populations can have substantial health benefits, especially for children and adolescents.
According to the Journal of Nutrition, up to 45% of the US population is zinc deficient.
Dietary sources — Meat and chicken are excellent sources of zinc, as are nuts and lentils. In the Western diet, food products such as breakfast cereal are fortified with zinc and these products provide an increasingly important source of zinc. Approximately 45 percent of adults may have inadequate zinc intakes.
Biological role — Zinc owes its biological role to the ability to form tight bonds with certain amino acids, especially histidine and cysteine. When zinc binds four amino acids (tetradentate configuration), it serves a structural role maintaining protein structure (such as the beta-pleated sheet), and maintains nuclear stability and histone structure. It is in this form that zinc contributes to zinc finger proteins that interact with DNA. When zinc binds three amino acids, the fourth site is temporarily taken by a water molecule; in this form, zinc can play a role in the metabolic activity of many proteins.
Approximately 250 proteins contain zinc. These include enzymes such as angiotensin converting enzyme, alkaline phosphatase, carbonic anhydrase, DNA and RNA polymerases, copper-zinc superoxide dismutase, and metallothionein, as well as a large family of zinc proteins involved in gene transcription (such as the zinc finger proteins). Zinc has important roles both in cell division as well as apoptosis (programmed cell death).
Deficiency — Mild dietary zinc deficiency impairs growth velocity while severe depletion of zinc leads to growth retardation. Other clinical manifestations of zinc deficiency include delayed sexual maturation, impotence, hypogonadism, oligospermia, alopecia, dysgeusia (impaired taste), immune dysfunction, night blindness, impaired wound healing, and various skin lesions. The dermatologic changes occur primarily in the extremities or around body orifices and are often characterized by erythematous, vesiculobullous, and pustular lesions. Other signs and symptoms of zinc deficiency include loss of taste, change in hair color, and easy pluckability of hair. Also seen but not specific are night blindness, impaired appetite, delayed wound healing, decubitus ulcers, and decreased sperm counts.
Findings suggesting zinc deficiency, have been described in chronic malnutrition, malabsorption syndromes (such as chronic inflammatory bowel disease), prolonged breastfeeding. Reduced zinc absorption and stores have been demonstrated in patients who have undergone gastric bypass for obesity. Pregnancy also increases the risk for zinc deficiency. Alcoholic cirrhotic patients often have low hepatic concentrations of zinc. Cases of zinc deficiency have been reported among elderly individuals with poor diet qualit. In these cases, the dietary zinc deficiency may have been exacerbated by medications that increase urinary losses of zinc, including thiazides, loop diuretics, and angiotensin receptor blockers.
Zinc deficiency can be seen in chronic TPN use and with an underlying condition causing zinc losses, such as diarrhea, inflammatory bowel disease, or other conditions.
Diabetics also have some alterations of zinc metabolism. Both type 1 and type 2 diabetics can exhibit hyperzincuria, which may have a role in the immune dysfunction associated with diabetes mellitus. Zinc supplementation in diabetic patients may improve immune function, but also increases the HbA1c levels and leads to worsening glucose intolerance.
Mild zinc deficiency appears to be common, especially in developing countries. Individuals in developing countries are at risk of zinc deficiency because the diet is relatively low in zinc and contain significant amounts of phytates (which reduce zinc absorption). There is some evidence supporting the role of zinc supplementation to increase growth velocity in children, and several studies have suggested a benefit of zinc supplementation in children with acute diarrhea in developing countries.
Zinc supplementation during pregnancy for women with mild zinc deficiency appears to promote fetal growth and reduce the risk of premature birth and infant diarrhea. Zinc has also been used to treat the common cold, but probably has little clinical value.
Source: Information has been extracted from UpToDate