Rickets and micronutrient deficiencies in children

• Rickets is a disease of growing bone in which the growth plates fail to mineralise properly, most often because of too little vitamin D, calcium or phosphate. It is preventable, but it still occurs, especially where sunlight exposure, diet or chronic disease are inadequate.
• Nutritional rickets is only one part of the story: vitamin A, iron, zinc and iodine deficiency remain among the commonest serious nutritional problems of childhood worldwide, and each damages growth, immunity, the brain or vision.
• The Global Consensus Recommendations on Prevention and Management of Nutritional Rickets state 400 international units of vitamin D per day for all infants from birth to 12 months, independent of feeding method, and at least 600 IU per day beyond 12 months.
• Treatment of nutritional rickets has an intensive phase followed by a maintenance phase; vitamin D3 (cholecalciferol) is preferred to vitamin D2, and calcium is co-administered whenever calcium intake is low.
• Prevention rests on breastfeeding, timely complementary feeding with calcium-rich foods, sensible sun exposure, routine micronutrient supplementation where programmes exist, and universal salt iodisation.

By the end of this page you should be able to:

1. Explain the difference between calcipenic and phosphopenic rickets and why it determines treatment.
2. Outline the clinical, biochemical and radiological features of vitamin D deficiency rickets and how to monitor recovery.
3. State the doses of vitamin D, calcium, iron, zinc and vitamin A used in children, and the situations in which they are needed.
4. Distinguish iron, zinc, iodine and vitamin A deficiency by their presentations and commonest causes.
5. Describe WHO and NICE guidance on micronutrient supplementation and where it is applied.
6. Plan the management of a child with rickets in both high-resource and low-resource settings.

A useful first division is between two mechanisms:

• Calcipenic rickets is driven by low calcium or by problems with vitamin D availability or action: dietary calcium deficiency, vitamin D deficiency, malabsorption of either, or the rare genetic vitamin D-dependent rickets.
• Phosphopenic rickets is driven by low phosphate: usually renal phosphate wasting (X-linked hypophosphataemia and related genetic disorders), occasionally renal tubular disease, and rarely very poor phosphate intake.

This distinction matters because calcipenic rickets is treated with calcium and vitamin D, whereas phosphopenic rickets needs phosphate and active vitamin D metabolites, and in X-linked hypophosphataemia may now be treated with the monoclonal antibody burosumab.^[1]

Nutritional rickets remains a global problem. Review articles describe it as more prevalent in low- and middle-income countries, particularly the Indian subcontinent, Africa and the Middle East, but it is also seen in high-income settings, especially in dark-skinned or veiled groups, premature infants, and children with chronic disease.^[1]

Micronutrient deficiencies add a population burden beyond rickets. Iron deficiency affects an estimated 2 billion people worldwide, mainly pregnant women, fetuses and children, and is the leading cause of anaemia in children.^[3] Vitamin A deficiency is still a public health problem in many low-income regions and a major cause of preventable childhood blindness.^[5] Iodine deficiency puts roughly 2 billion people at risk and is the leading cause of preventable mental retardation.^[6]

The causes form a cluster that you will meet repeatedly:

• Limited skin synthesis of vitamin D: high latitude, little outdoor time, dark skin, clothing or veiling that covers most of the body, sunscreen use above factor 8.
• Low intake or bioavailability of calcium: lack of dairy or other calcium-rich foods, very high phytate intake, very low fat intake in small children.
• Prematurity and low birth weight: low stores acquired in utero.
• Prolonged breastfeeding without vitamin D supplementation, especially when maternal vitamin D status is poor.
• Malabsorption: coeliac disease, cystic fibrosis, biliary atresia, inflammatory bowel disease.
• Drugs and disease that increase vitamin D catabolism or block its action: anticonvulsants, glucocorticoids, some antiretroviral drugs, chronic liver or kidney disease.
• Obesity, which can make maintaining adequate 25-hydroxyvitamin D harder despite supplementation.

For iron deficiency the risk groups are similar in flavour: premature and low-birth-weight infants, twins, infants of anaemic mothers, infants fed unmodified cow's milk before 12 months, and adolescents—especially girls with heavy or prolonged menstrual bleeding.^[3]

Vitamin D, whether made in skin or taken in food, is 25-hydroxylated in the liver and 1-hydroxylated in the kidney to its active form. Active vitamin D raises intestinal absorption of calcium and phosphate and, with parathyroid hormone, maintains serum calcium. When vitamin D or calcium is too low, serum calcium falls; parathyroid hormone rises; phosphate is lost through the kidney; and growing bone, which needs both calcium and phosphate, mineralises poorly.

The growth plate therefore widens, frays and becomes cupped. In adolescents, whose growth plates are closing, the picture is closer to osteomalacia: bone pain, proximal weakness and a waddling gait.

Each symptom can be reasoned from this:

• Bone pain and tenderness come from unmineralised bone bending under load.
• Delayed motor milestones and hypotonia come from low serum calcium and, in severe cases, tetany or seizures.
• Enlarged wrists and ankles, rachitic rosary, frontal bossing and Harrison's sulcus are the physical expression of widened, uncalcified costochondral junctions and metaphyses.
• Limb deformity—bow legs in the toddler, knock-knees in the older child—comes from weight on softened long bones.
• Dental enamel hypoplasia follows abnormal mineralisation of developing teeth.
• Height faltering reflects poor bone growth.

Parents usually describe a previously well child who has become reluctant to walk, or who now walks with an unusual gait; bone or joint pain; muscle cramps; and sometimes seizures or breath-holding spells. In children with calcium-deficiency rickets the diet may be low in dairy or high in unfortified cereal. Antenatal, birth and drug histories matter, because prematurity, renal or liver disease, and anticonvulsants all change the diagnosis.

Look for:

• widening of the wrists and ankles (rachitic "bracelets");
• a rachitic rosary along the costochondral junctions;
• frontal bossing and delayed closure of the fontanelle;
• Harrison's sulcus and a pectus carinatum;
• bowing or knock-knee deformity;
• hypotonia, proximal weakness and a waddling gait;
• signs of tetany or laryngospasm in severe hypocalcaemia.

Tests follow from what each measures:

• Serum calcium may be low or low-normal; in severe deficiency it can be frankly hypocalcaemic.
• Serum phosphate is usually low.
• Alkaline phosphatase is raised; this is a useful, cheap marker of rachitic activity.^[1]
• Parathyroid hormone is raised in calcipenic rickets, which is the key biochemical separator from many phosphopenic causes.
• 25-hydroxyvitamin D is the status marker: levels under 30 nmol/L define deficiency, 30 to 50 nmol/L insufficiency, and above 50 nmol/L sufficiency in the Global Consensus guide; other guidelines set the adequate threshold at above 75 nmol/L (30 ng/mL). Levels above 250 nmol/L with hypercalcaemia, hypercalciuria and suppressed parathyroid hormone suggest toxicity.^[1]
• Radiographs of wrists and knees show widening and cupping of the metaphyses, fraying, and sometimes Looser's zones in older children.
• Renal and liver function tests are basic: they exclude renal or hepatic causes.
• Urine phosphate handling (tubular maximum phosphate reabsorption per glomerular filtration rate) helps separate dietary or overall phosphate deficiency from renal phosphate wasting.

There is no single score. The diagnosis is clinical, biochemical and radiological taken together. Things that strengthen the diagnosis are a raised alkaline phosphatase, low 25-hydroxyvitamin D, raised parathyroid hormone, typical radiological changes and response to treatment. Long-bone deformity that persists after biochemistry normalises suggests a genetic or refractory cause.

The standard approach is an intensive replacement phase followed by maintenance.

Vitamin D3 (cholecalciferol) is preferred to vitamin D2 (ergocalciferol) because it has a longer half-life and greater efficacy.^[1] A minimum of 3 months is recommended for the intensive phase.^[1]

Dosage tables differ between guidelines, which is worth being honest about. The review cited here summarises them as follows:^[1]

• The US Endocrine Society recommends 2000 IU of vitamin D per day for all ages during intensive treatment, then 400 to 600 IU per day for maintenance.
• The National Osteoporosis Society of the United Kingdom recommends 3000 IU per day for infants under 6 months, 6000 IU per day for children 6 months to 12 years, and 10,000 IU per day for 12 to 18 years during intensive treatment, then 400 to 600 IU per day for maintenance.
• The Global Consensus states 400 IU per day for all infants in the first year of life and 600 to 2000 IU per day beyond 12 months, with pregnant women taking 600 IU per day throughout pregnancy.

Those recommendations differ because trials are small and cut-off definitions vary; choose local guidance. Higher replacement doses are needed in obesity or when the child is on anticonvulsants, glucocorticoids or antiretroviral drugs, where doses as high as 6000 IU daily may be used, with monitoring.^[1]

Calcium is not a passive bystander. Calcipenic rickets with hypocalcaemia needs replacement, and calcium alone can heal rickets when calcium rather than vitamin D is the limiting factor.^[1]

Practical calcium regimens:^[1]

• Symptomatic acute hypocalcaemia (tetany, seizures): 10% calcium gluconate 5 to 20 mg per kg (0.5 to 2.0 mL per kg of a 10% solution, which contains about 90 mg elemental calcium per 10 mL), given intravenously slowly over 10 to 15 minutes, diluted in normal saline or 5% dextrose.
• Asymptomatic hypocalcaemia or normocalcaemia in rickets: oral calcium carbonate or citrate, 30 to 75 mg per kg per day, given in 2 to 3 divided doses; about 500 mg per day for a 5-year-old and 1000 mg per day for a 10-year-old. Carbonate contains about 40% elemental calcium and citrate about 21%.
• Combining high calcium with high vitamin D risks nephrocalcinosis, so doses and monitoring are kept sensible.

If a child who looks as if they have nutritional rickets fails to improve with appropriate vitamin D and calcium, step back. Refractory forms include vitamin D-dependent rickets (types 1, 2 and 3) and FGF23-dependent or independent hypophosphataemic rickets, including X-linked hypophosphataemia. These need specialist care: active metabolites such as calcitriol or alfacalcidol, phosphate supplements, or in X-linked hypophosphataemia, burosumab. Drug-induced vitamin D deficiency may need 400 to 4000 IU of vitamin D.^[1]

Use this as a teaching scaffold, and follow local guidance and involve paediatric endocrinology or nephrology when genetic or refractory disease is suspected.

Most children respond quickly and the response confirms the diagnosis:^[1]

• symptoms such as aches and pains settle within about 2 weeks;
• serum calcium and phosphate normalise within 3 weeks, sometimes 6 to 10 days;
• parathyroid hormone falls into the normal range;
• serum 25-hydroxyvitamin D reaches normal after 4 to 6 weeks;
• the zone of provisional calcification appears on X-ray within 3 to 4 weeks;
• alkaline phosphatase falls over 3 to 6 months;
• metaphyseal swelling resolves over about 6 months, but correction of bow legs and knock-knees may take 2 years, with residual deformity in adolescents.

• Tetany, seizures or laryngospasm in severe hypocalcaemia.
• Growth failure and stunting.
• Skeletal deformity, which in older children may need surgical correction.
• Dental enamel defects.
• Cardiomyopathy has been reported in extreme cases.
• Nephrocalcinosis when calcium and vitamin D are combined carelessly, or when phosphate supplements are given unsupervised in some phosphopenic disorders.
• Metaphyseal fractures in severe disease can be mistaken for non-accidental injury; careful interpretation and documentation matter.

With prompt treatment, biochemistry normalises and radiological healing is usually evident within weeks to months. Linear growth recovers. Some deformity persists into adolescence, and in phosphopenic rickets dental and skeletal problems recur and need long-term follow-up.^[1]

Prevention follows directly from the causes:

• Universal vitamin D 400 IU per day for all infants from birth to 12 months, regardless of feeding method, and at least 600 IU per day beyond 12 months where intake or sunlight is limited.^[2]
• Complementary foods introduced no later than 26 weeks should include calcium-rich foods, and intake of at least 500 mg per day of elemental calcium should be ensured during childhood and adolescence.^[2]
• Attention to maternal vitamin D status during pregnancy.
• Sensible sun exposure and outdoor play where available.
• Food fortification and population nutrition programmes.
• Continued supplementation beyond infancy for groups at risk of deficiency.

Context from other guidance: WHO, at the time of the review, placed vitamin D supplementation in a "Category 2 intervention": systematic reviews exist, but no WHO-approved guideline was yet available, and further research was called for before specific recommendations could be made.^[2] NICE offers children's Healthy Start vitamin supplements (vitamins A, C and D) to children 6 months to 4 years in families receiving the Healthy Start benefit.^[2] CDC advice is 400 IU daily for children under 12 months and 600 IU daily for children 12 to 24 months.^[2]

A guideline comparison:

Vitamin A (retinol) maintains epithelial integrity and mucosal barriers, supports immune function, is essential for growth, and is the chromophore of rhodopsin in the retina. Deficiency causes night blindness and conjunctival dryness (xerophthalmia), Bitot's spots, corneal ulceration and keratomalacia (which can destroy vision within days), impaired resistance to infection (measles, diarrhoea), and growth failure.^[5]

WHO recommendations for vitamin A supplementation of children (Malik 2018):^[5]

Additional high-dose vitamin A is used during measles infection and severe malnutrition as part of standard management. Prevention overall pairs supplementation with breastfeeding, dietary diversification and food fortification; high-dose programmes only work if dosing every 4 to 6 months is maintained. VAS is most useful where clinical vitamin A deficiency is a public health problem and where diets cannot meet needs. The evidence behind the WHO table found VAS reduced Bitot's spots and night blindness, and measles-related mortality falls when children with measles receive vitamin A.^[5]

Clinical picture. Iron deficiency may be silent, or may show pallor, tiredness, poor exercise tolerance, irritability, poor concentration, delayed psychomotor development, and mucocutaneous changes such as angular cheilitis, glossitis and koilonychia in longstanding deficiency. Chronic deficiency, even without anaemia, can be associated with impaired neurodevelopment, though evidence remains mixed.^[3]

Causes. Low iron stores from prematurity, twins or small-for-gestational-age infants; inadequate dietary iron; rapid growth; excess cow's milk; malabsorption (coeliac disease, inflammatory bowel disease); chronic blood loss (heavy menstruation, gastrointestinal lesions).^[3]

Investigations. Full blood count (microcytic hypochromic anaemia), ferritin and transferrin saturation. Ferritin is an acute-phase reactant, so inflammation can mask deficiency. Obesity, chronic infection and inflammatory disease raise hepcidin and make iron unavailable.^[3]

Treatment. Oral iron is the most physiological route.^[3]

• Therapeutic dose of elemental iron: 3 to 6 mg per kg per day, in 1 to 3 divided doses, with a maximum of 150 to 200 mg per day. Doses around 3 mg per kg are as effective as higher doses.
• Alternate-day dosing improves absorption in pharmacokinetic studies cited in the review.
• Give with vitamin C; avoid giving simultaneously with tea, coffee, milk or calcium supplements, which reduce absorption.
• Premature and low-birth-weight infants need 2 to 4 mg per kg per day (maximum 15 mg depending on weight band); term infants about 1 mg per kg per day (maximum 15 mg).^[3]
• Prevention-oriented daily needs: 7 mg from 1 to 3 years, 10 mg from 4 to 8 years, 8 mg from 9 to 13 years, 11 mg for boys and 15 mg for girls from 14 to 18 years, and 27 mg for pregnant adolescents.^[3]
• Treat for 3 to 6 months and recheck; if oral iron fails or is not absorbed, intravenous iron is an alternative, with careful weight-based dosing.

Low-resource notes. Limit cow's milk to under 600 mL per day in children 1 to 5 years, introduce meat from 6 months, continue breastfeeding to 6 months and use iron-fortified formulas. Avoid blanket iron supplementation where infection is endemic without local evidence, and consider malaria, helminth infection and HIV as causes of anaemia.^[3]

Zinc is a cofactor for hundreds of enzymes and matters for growth, skin and mucosal integrity, and host defence against infection. Deficiency causes stunting, dermatitis (often acral and perioral), alopecia, diarrhoea, impaired taste and smell, and increased infection susceptibility; severe deficiency is uncommon but dramatic.^[4]

Management and supplementation. Free supplementation for prevention is not as standardised as for vitamin A, but there is a well-established therapeutic use. WHO and UNICEF recommend 10 to 20 mg of oral zinc per day for 14 days for children under 5 years with diarrhoea.^[4] This shortens diarrhoea and reduces progression to persistent diarrhoea; low-dose regimens caused less vomiting than high-dose regimens while still improving recovery in the systematic review.^[4]

Iodine is the essential component of thyroid hormones. Deficiency is the leading cause of preventable intellectual disability and produces the spectrum of iodine deficiency disorders: goitre at any age, hypothyroidism, and in the fetus, impaired neurodevelopment, cretinism, congenital anomalies and perinatal loss. Pregnant and breastfeeding women are the highest-priority group.^[6]

Recommended intakes. Daily iodine intake should be 110 micrograms for infants 0 to 6 months, 130 micrograms for 7 to 12 months, 90 micrograms for children 1 to 8 years, 120 micrograms for 9 to 13 years, 150 micrograms for adolescents and adults, 220 micrograms in pregnancy, and 290 micrograms while breastfeeding.^[6]

Prevention. Since 1993 WHO and UNICEF have recommended universal salt iodisation; about 70% of households in more than 120 countries now have access to iodised salt, up from under 10% in 1990.^[6] Where salt intake is reduced for cardiovascular reasons, or where iodised salt is unavailable, other dietary sources (fish, seafood, dairy, eggs) or supplementation become important; pregnant women may need iodine supplements. Both deficiency and excess cause thyroid dysfunction, and population median urinary iodine under 100 micrograms per day defines deficiency.^[6]

Population programmes should combine salt iodisation with periodic surveys; 23 countries still had low intake in the report cited. Households using non-iodised or reduced-sodium salts need education and alternative sources.^[6]

• Vitamin A deficiency can be mistaken for repeated respiratory infection or severe malnutrition; the eye signs (night blindness, Bitot's spots, corneal haze) are the useful clues.
• Iron deficiency overlaps with lead poisoning, thalassaemia, anaemia of chronic disease and B12/folate deficiency, so the blood film and iron stores must be interpreted together with growth and diet.
• Iodine deficiency overlaps with autoimmune thyroiditis; the goitre of iodine deficiency is usually soft and diffuse in childhood, while autoimmune disease is firmer and often appears in adolescence.
• Zinc deficiency dermatitis can look like acrodermatitis enteropathica or severe eczema; a low-risk diet and poor growth support the diagnosis.

A practical reading of the bloods:

• Raised alkaline phosphatase with low phosphate and raised parathyroid hormone points to calcipenic rickets even before vitamin D comes back.
• A low 25-hydroxyvitamin D supports the diagnosis but is not on its own enough; some children have low vitamin D without any bone disease.
• Normal or high 25-hydroxyvitamin D with hypophosphataemia suggests phosphopenic or renal disease, and FGF23 measurement or phosphate handling tests become useful.
• In iron deficiency, ferritin is the most specific test, but it is also an acute-phase reactant; in a child with infection or inflammation, a ferritin at the lower end of the reference range may still represent depleted stores.
• In iodine deficiency, median urinary iodine and thyroid function (TSH, free T4) are the population tests; a single child's result is harder to interpret, so clinicians rely on epidemiology plus goitre and thyroid function.
• Zinc has no convenient, well-validated status marker for routine use; low plasma zinc is suggestive but affected by infection, fasting and inflammation, so diagnosis rests on the clinical picture and, where possible, response to supplementation.

• Pregnancy. Vitamin D, iodine and iron requirements rise. Vitamin D 600 IU daily throughout pregnancy appears in the Consensus table; iodine 220 micrograms and iron 27 mg for pregnant adolescents come from the sources used here. Avoid high-dose retinol (vitamin A) in pregnancy because of teratogenicity.
• Prematurity. Low stores, rapid growth and medical complications make premature infants especially prone to rickets and iron deficiency; they usually need earlier, closer monitoring.
• Chronic disease. Renal, hepatic, intestinal or genetic disease changes both the cause of rickets and the treatment; involve specialists early.
• Adolescence. Growth plate closure changes the skeletal picture towards osteomalacia; deformity tolerance is lower and surgery may be needed.

• Where 25-hydroxyvitamin D testing is unavailable, treat on clinical and radiographic grounds: a raised alkaline phosphatase, typical metaphyseal changes and response to therapy are usually enough.
• Calcium can be the limiting nutrient where dairy is scarce; high-phytate cereal diets provide calcium poorly. Improving complementary foods or supplementing calcium addresses this, not vitamin D alone.
• Universal infant vitamin D supplementation and universal salt iodisation are the highest-yield population interventions; zinc with oral rehydration is cheap and effective for diarrhoea.
• Where surgery or genetic testing is unavailable, refer the non-responder (apparent nutritional rickets that does not heal) rather than escalating doses indefinitely.
• Vitamin A and iron programmes work best when bundled with immunisation and growth monitoring.

Micronutrient deficiencies are rarely solved one child at a time. The interventions with the best evidence-to-cost ratio are:

• Universal infant vitamin D supplementation in the first year of life, delivered alongside vaccination programmes.
• Universal salt iodisation with quality assurance of iodine content, and periodic urinary iodine surveys.
• Iron and folic acid supplementation in pregnancy, and delayed cord clamping at birth to improve iron stores.
• Iron fortification of staple flours where iron deficiency is prevalent, with programme monitoring.
• Home fortification with multiple micronutrient powders in areas of high deficiency, as recommended by WHO for children 6 to 23 months.
• Zinc and oral rehydration for diarrhoea distributed through community health workers and primary care.
• Vitamin A supplementation linked to immunisation contacts every 4 to 6 months in deficient populations.
• Dietary counselling that keeps breastfeeding to 6 months, introduces iron-rich foods, and limits excess unmodified cow's milk.
• Sunlight and outdoor play as part of child health advice where culturally and practically possible.
• Screening and fortification programmes for women of reproductive age to protect fetal stores.

These measures are not glamorous, but they prevent the bulk of the rickets, anaemia, eye disease and cognitive loss described above. When they are working, clinicians in those populations see fewer cases; when they lapse, the old diseases reappear even in wealthy countries.

• Rickets is failure of mineralisation of growing bone, usually calcipenic (vitamin D or calcium) and less commonly phosphopenic (phosphate wasting).
• Never separate vitamin D and calcium: calcium provision determines whether vitamin D can heal bone.
• The Global Consensus figures of 400 IU per day for infants to 12 months and 600 IU or more per day thereafter are the most widely cited international standard, but national guidelines give different intensive-treatment doses; use local guidance.
• Vitamin D3 is preferred; a minimum of 3 months in the intensive phase; aim for at least 500 mg per day of elemental calcium in older children.
• 25-hydroxyvitamin D should be 30 nmol/L or above in the consensus scheme and 75 nmol/L or above in others; toxicity above 250 nmol/L.
• Clinical, biochemical and radiological improvement happens in weeks; alkaline phosphatase can stay high for months.
• Vitamin A: 100,000 IU for 6 to 11 months and 200,000 IU for 12 to 59 months every 4 to 6 months where deficiency is a public health problem.^[5]
• Iron: treat 3 to 6 mg per kg per day elemental for 3 to 6 months; prevent with breast milk to 6 months, iron-fortified formula, meat from 6 months, limited cow's milk.
• Zinc: 10 to 20 mg daily for 14 days with acute diarrhoea; low dose reduces vomiting.^[4]
• Iodine: keep to recommended intakes; universal salt iodisation is the backbone.
• WHO, NICE and the CDC converge on roughly 400 IU of vitamin D in infancy; beyond that, local and risk-group guidance applies.
• The child who does not heal on correct treatment probably does not have nutritional rickets.

A few points that commonly catch students out:

• Rickets is not just vitamin D. Persistent low-calcium rickets in regions with poor dairy intake can heal with calcium alone, and calling every case "vitamin D deficiency" misses the dietary cause.
• Alkaline phosphatase is the working marker. It rises in active rickets and falls quietly over months, even when biochemistry has already normalised.
• The first week can look worse. Parathyroid hormone may surge and calcium may still be unstable early in treatment; this is expected and is not a reason to stop replacement.
• A normal 25-hydroxyvitamin D does not exclude rickets in a phosphate-wasting disorder. Phosphopenic disease can look bone-weak with normal or near-normal vitamin D.
• Maternal history matters as much as the child's diet. A mother with poor vitamin D status, dark skin or limited sun exposure produces a baby with low stores at birth.
• Delayed fontanelle closure, tall on X-ray metaphyses and swollen wrists appear before deformity, so an occassional 9-month review of at-risk infants is justified in high-prevalence settings.
• Iron and zinc interact with infection. In malaria-endemic or HIV-prevalent settings, blanket iron may be harmful; decisions should be local and based on stores, not colour alone.
• Iodine is a pregnancy issue first. The damage is mostly antenatal; waiting for a goitre in a child means the window has passed.
• Vitamin A dosing is by public-health programme. Routine high-dose vitamin A is reserved for populations with defined deficiency; in a well-nourished population it adds risk without benefit.
• Zinc during diarrhoea is short-course. Fourteen days at 10 to 20 mg daily is the evidence-based adjunct to oral rehydration; beyond that it becomes an unsupported supplement.

Rickets and micronutrient deficiencies connect to faltering growth; short stature and growth hormone disorders; anaemia approach and iron deficiency; childhood asthma and wheeze; dehydration and paediatric fluids; acute gastroenteritis in children; osteoporosis; bone and mineral metabolism; and malnutrition.