Trace elements in nutrition are defined as ‘biologically important minerals, present in very small amounts (<250 mg/gm of matrix) in human body’. Minerals present in still smaller amounts (<100 ng/gm) are termed as ultra- trace elements.

The role of trace elements in health and disease is being increasingly recognized in recent years. Based on current knowledge, trace elements in human body may be broadly divided into three categories —

1) Essential trace elements with known biological functions e.g. Iron, Iodine, Zinc, Fluorine, Selenium, Copper, Molybdenum and Chromium.

2) Essential trace elements with hitherto ill-identified functions e.g. Manganese, Silicon, Nickel, Boron, Cobalt and Vanadium.

3) Potentially toxic trace elements with unknown biological functions e.g. Lead, Aluminum, Tin, Cadmium, Arsenic, Mercury etc.

Zinc: Zinc is a component of many enzymes e.g. carbonic anhydrase, Carboxypeptidadase, alkaline phosphatase etc. Although widely distributed in tissues, the average adult body contains <2-3 gm of zinc with normal plasma levels of 80-90 g/dl.

Trace elements in Nutrition

Physiology: Zinc is essential trace elements for — a) normal growth, b) normal chemotaxis and T-cell immunity, c) normal wound healing, and d) synthesis of some hormones e.g. insulin & nucleic acids.

RDA for zinc varies from 5 mg/day in infancy to 15 mg/ day in children >12 years.

Important sources of zinc include animal foods e.g. meat, milk and fish, as well as plant foods e.g. grains, legumes and nuts, though the bioavailability of zinc in plant sources in relatively poor.

Etiologically, zinc deficiency is rarely dietary, usually caused by —

i) Increased requirements in early infancy, adolescents and pregnancy

ii) Decreased intake e.g. in maternal zinc deficiency, total parenteral nutrition etc.

iii) Decreased absorption in —

Acrodermatitis enteropathica

• Chronic diarrhea and malabsorptive states iv) Increased urinary excretion in —

• Chronic renal or liver disease

• Hypoalbuminic states e.g. kwashiorkor

• Massive tissue injury e.g. bums

• Iron chelation therapy e.g. in hemolytic anemia

Clinical features of zinc deficiency include Failure to thrive, IUGR & hypogonadism; Chronic diarrhea and anorexia; Eczematous skin lesions and alopecia; Increased infections and delayed wound healing

Acroderinatitis enteropathica is an autosomal recessive defect in zinc absorption, which usually manifests during or after weaning with growth failure, chronic diarrhea, eczematous skin lesions, mainly on acral (hands/feet), inguinal and/or flexural parts of body, and alopecia.

Diagnosis is confirmed on serum zinc estimation (Normal: 6.6-19.4 and response to therapy.


Oral or parenteral supplementation with 5 mg/kg/day (20-40 mg/kg/d in acrodermatitis enteropathica) usually leads to dramatic clinical response within few days, which should be followed by adequate dietary modification to prevent recurrence. Long-term c supplementation is indicated in children with severe growth failure and acrodermatitis enteropathica.

Fluorine: Fluorine is the most abundant trace elements in nature, though never found in free elemental gaseous form. About 96% of body fluorine is present in bones and teeth. Biologically, fluorine is required for formation of apatite – a mineral complex essential for bone mineralization, and dental enamel. Drinking water is the principle source of fluorine to man, though seafood and cheese are other rich sources. Fluorine deficiency is relatively unconmon, considered to be associated with higher incidence of dental caries and can be prevented by use of fluorinated toothpastes. Fluorine excess (Fluorosis) is more important public health problem in India, endemic in areas with high fluoride content in drinking water (> 0.5 – 0.8 mg/L or >2 ppm).

Prolonged ingestion of high-fluoride water presents with mottling of teeth, brittle bones with osteosclerosis, calcification of muscles/tendons, and failure to thrive, anemia and asthenia. As excess fluorine interferes with calcium metabolism, co-existing calcium deficiency is common in these cases and contributes to skeletal changes with osteoporosis/osteomalacia.

Controlling the fluoride content of drinking water is the only method to prevent fluorosis in children.

Copper: Nearly 60% of copper is present within erythrocytes, rest being in plasma (bound to ceruloplasmin) or tissues (bound to metallothionein). Copper is a constituent of many metabolic enzymes, involved in connective tissue formation, iron metabolism, neuronal myelination, melanin synthesis and cellular energy/oxygen utilization. Copper deficiency is rarely dietary, presenting as neutropenia, anemia, hypopigmented hair, osteoporosis and defective immune function. Copper toxicity, usually due to use of copper cooking- utensils has been implicated in Indian childhood cirrhosis and hematological malignancies.

Inborn errors of copper metabolism are most important cause of altered copper status in body and include —

a) Wilson disease – an autosomal recessive defect in mobilization of hepatic copper, presenting with a triad of chronic liver disease, extra-pyramidal signs and Kayser-Fleischer ring over comea.

b) Menkes-kinky-hair syndrome- a rare X-linked recessive disorder, characterized by fine, brittle and light colored hair, progressive psychomotor retardation and hypopigmented skin.

Selenium is mainly required for synthesis of glutathione peroxidase, an important anti-oxidant enzyme, and conversion of ‘l’4 into T3. Selenium deficiency is definitely associated in two endemic diseases in china – Keshan cardiomyopathy and Kashin-Beck osteoarthritis. It has been also implicated in higher risk for malignancies and atherosclerosis. Selenium deficiency may also affect growth and development due to poor conversion of T4 into T3. Selenium excess (selenosis) is associated with alopecia and nail deformities.

Molybdenum is a constituent of many enzymes, specially xanthine oxidase/dehydrogenase – essential for xanthine metabolism. Molybdenum deficiency is mainly seen in children on prolonged total parenteral nutrition, presenting with renal calculi (due to xanthinuria) and myopathy. It has been also implicated in higher risk of dental caries and esophageal cancers.

Chromium: Major biological role of chromium is to potentiate the action of insulin in carbohydrate, lipid and protein metabolism, by probably acting as a glucose tolerance factor.

Chromium deficiency has been reported only in children on prolonged total parenteral nutrition, leading to impaired glucose tolerance and hyperglycemia. Dietary chromium supplementation may improve glucose tolerance in PEM.