Minerals and Trace Elements
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Direct answer
Deficiency of even a microgram-level element can undo macro-level metabolism: iodine, needed only in about 90-150 micrograms daily, is indispensable to thyroxine; selenium is built into glutathione peroxidase and deiodinases as the twenty-first amino acid selenocysteine; zinc sits in hundreds of metalloenzymes from carbonic anhydrase to the zinc-finger transcription factors. The macro-minerals run structure and signalling — calcium (99 percent skeletal, serum 8.5-10.5 milligrams per decilitre under PTH-vitamin D-calcitonin control), phosphorus, magnesium (over 300 enzymes) and the electrolytes. Iron is handled by a strictly recycled system governed by hepcidin, copper by ceruloplasmin and the ATP7A/B transporters whose failures give Menkes and Wilson disease. In India the exam-relevant deficiencies are iron, iodine and zinc, and the excess is fluoride.
What you must remember
- Iron economy: no regulated excretion, only regulated absorption; body iron about 3-4 grams, two-thirds in haemoglobin; hepcidin binds ferroportin and blocks enterocyte and macrophage export — the anaemia of chronic disease is hepcidin-mediated iron lockout, which is why oral iron fails in inflammation.
- Iodine and the national programme: requirement about 90-150 micrograms daily (250 in pregnancy); under the National Iodine Deficiency Disorders Control Programme, iodised salt must contain at least 15 parts per million at the household level — a recurring objective question; deficiency ranges from goitre through cretinism.
- Zinc roles: cofactor in carbonic anhydrase, carboxypeptidase, Cu-Zn superoxide dismutase and zinc fingers; WHO and UNICEF recommend 14 days of zinc (10 milligrams under six months, 20 milligrams above) with oral rehydration in childhood diarrhoea; acrodermatitis enteropathica is the inherited malabsorption.
- Copper pair: ATP7A failure causes Menkes disease (kinky hair, neurodegeneration, low serum copper) and ATP7B failure Wilson disease (hepatolenticular degeneration, Kayser-Fleischer rings, low ceruloplasmin) — transporter direction decides the phenotype.
- Selenium: selenocysteine in glutathione peroxidase, thioredoxin reductase and the deiodinases; deficiency causes Keshan cardiomyopathy (China) and worsens iodine-deficiency states.
- Fluoride and other excesses: chronic high fluoride causes dental fluorosis (mottled enamel) and crippling skeletal fluorosis across endemic Indian belts, with arsenic in the Ganga delta — the exam-ready mirror of deficiency questions.
- One-mark minerals: chromium as glucose tolerance factor, cobalt only as cobalamin, molybdenum in xanthine and sulphite oxidases, manganese in mitochondrial superoxide dismutase.
How to work through an iron-refractory-anaemia case
A woman with rheumatoid arthritis has a haemoglobin of 9 grams per decilitre, low serum iron, low total iron-binding capacity and high ferritin, and oral iron produces no reticulocyte response. Reason through hepcidin: interleukin-6 from chronic inflammation drives hepatic hepcidin, which internalises ferroportin, so iron in stores and macrophages cannot reach the marrow. This is the anaemia of chronic disease, and the signature (low iron, low TIBC, high ferritin) mirrors iron deficiency (low iron, high TIBC, low ferritin) — the TIBC line decides the viva.
Contrast a child with acrodermatitis enteropathica: periorificial vesiculopustular dermatitis, alopecia and diarrhoea from ZIP4 transporter failure, responding within days to therapeutic zinc — a single-trace-element deficiency with a pathognomonic rash. The teaching sequence is identical: name the unique chemistry and its transporter, and the syndrome follows.
Where students slip
Students prescribe iron for every microcytic anaemia; thalassaemia trait and the anaemia of chronic disease are the two traps, and a high ferritin with low TIBC argues forcefully against iron deficiency. Second, in Wilson disease serum copper is low — total copper, because ceruloplasmin is low — yet the disease is one of copper overload; quoting a "high serum copper" without specifying free copper loses the mark. Third, zinc and copper compete for absorption, so chronic zinc supplementation can produce copper deficiency and myeloneuropathy. Finally, fluoride strengthens enamel only at around 1 part per million in water; beyond roughly 1.5 parts per million, fluorosis begins — the therapeutic-to-toxic window examiners like to quote.
Frequently asked questions
How does hepcidin regulate iron absorption?
It binds ferroportin on enterocytes and macrophages, triggering its internalisation, so iron export into plasma falls — high in inflammation, low when iron stores are depleted.
What is the household iodine level mandated in iodised salt in India?
At least 15 parts per million at the consumer level under the National Iodine Deficiency Disorders Control Programme, ensuring the roughly 100-150 microgram daily requirement.
Why is zinc given with oral rehydration in childhood diarrhoea?
Fourteen days of zinc shortens the episode and reduces recurrence in the next two to three months, which is why WHO and UNICEF include it in Indian diarrhoea-treatment guidelines.
Which transporters distinguish Menkes from Wilson disease?
ATP7A (copper export across gut-blood barrier) fails in Menkes causing deficiency, while hepatic ATP7B fails in Wilson disease causing copper accumulation in liver and brain.
What is the biochemical role of selenium?
It is incorporated as selenocysteine into glutathione peroxidase, thioredoxin reductase and the iodothyronine deiodinases, supporting antioxidant defence and thyroid hormone activation.