A deficiency in zinc might result in stunted growth, a concern that affects children's physical development and long-term health outcomes. Zinc is an essential trace element required for over 300 enzymatic processes, including protein synthesis, DNA replication, and cell division—all critical during periods of rapid childhood growth. When zinc levels are inadequate, production of insulin-like growth factor 1 (IGF-1) decreases, potentially compromising linear growth and leading to faltering growth patterns. This article explores how zinc deficiency impairs development, the clinical signs to recognise, diagnostic approaches available in the UK, and evidence-based strategies for treatment and prevention through diet and supplementation.

How Zinc Deficiency Affects Growth and Development

Zinc is an essential trace element that plays a fundamental role in numerous physiological processes critical for normal growth and development. This micronutrient is required for the function of over 300 enzymes involved in protein synthesis, DNA replication, and cell division—all processes that are particularly active during periods of rapid growth in childhood and adolescence.

The mechanism by which zinc deficiency impairs growth is multifactorial. Zinc is integral to the production and function of insulin-like growth factor 1 (IGF-1), a hormone that mediates the effects of growth hormone on skeletal and tissue development. When zinc levels are inadequate, IGF-1 production decreases, potentially compromising linear growth. Additionally, zinc deficiency impairs appetite and can lead to reduced food intake, creating a secondary nutritional deficit that further compounds growth restriction.

Children with chronic zinc deficiency typically present with faltering growth (low height-for-age), which may be accompanied by delayed sexual maturation in adolescents. The World Health Organisation recognises zinc deficiency as a significant contributor to growth faltering in children globally, with the term 'stunting' (height-for-age more than two standard deviations below the median) often used in international contexts. While severe deficiency is relatively uncommon in the UK, marginal or subclinical deficiency may still affect growth velocity in vulnerable populations.

The impact on development extends beyond physical stature. Zinc is crucial for neurodevelopment, immune function, and wound healing. Deficiency during critical developmental windows—particularly in utero, infancy, and early childhood—may have consequences for cognitive function and overall health outcomes. Early identification and correction of zinc deficiency is therefore essential to optimise both physical growth and developmental potential in children.

Recognising the Signs of Zinc Deficiency in Children

Identifying zinc deficiency in children requires awareness of both specific and non-specific clinical features. The presentation can vary considerably depending on the severity and duration of deficiency, making clinical recognition challenging in mild cases.

Growth-related manifestations are often the most prominent indicators. Parents or healthcare professionals may notice that a child's growth has plateaued or that the child is falling away from their established centile lines on growth charts. According to NICE guideline NG75, concerning patterns include crossing two or more weight centile spaces downward, height below the 0.4th centile, or poor growth velocity. Short stature or faltering growth should prompt consideration of nutritional deficiencies including zinc, though it is important to note that growth concerns have multiple potential causes and require comprehensive assessment.

Dermatological signs can provide valuable diagnostic clues. Children with zinc deficiency may develop a characteristic rash, particularly around body orifices (periorificial dermatitis), on the extremities, and in the nappy area. The skin may appear dry, scaly, or eczematous. In more severe cases, acrodermatitis enteropathica—a condition characterised by the triad of dermatitis, diarrhoea, and alopecia—may occur, though this is typically associated with genetic zinc absorption disorders rather than simple dietary deficiency.

Other clinical features include:

• Impaired immune function leading to recurrent infections, particularly respiratory and gastrointestinal

• Poor wound healing and delayed recovery from injuries

• Hair loss or changes in hair texture

• Loss of appetite and altered taste perception

• Behavioural changes including irritability and lethargy

• Delayed sexual maturation in adolescents

Parents should consult their GP if they observe persistent growth concerns, unexplained rashes, or recurrent infections in their child. Urgent referral is warranted if there are signs of systemic illness, severe diarrhoea, dehydration, or failure to thrive in infants. Early medical assessment enables appropriate investigation and timely intervention to prevent long-term developmental consequences.

Causes and Risk Factors for Low Zinc Levels

Zinc deficiency can arise from inadequate dietary intake, impaired absorption, increased losses, or elevated physiological requirements. Understanding these mechanisms helps identify at-risk populations and guides preventive strategies.

Dietary insufficiency is the most common cause globally, though less prevalent in the UK compared to resource-limited settings. Zinc is predominantly found in animal-source foods such as meat, shellfish, and dairy products. Children following vegetarian or vegan diets are at increased risk because plant-based zinc sources have lower bioavailability due to the presence of phytates (found in wholegrains, legumes, and nuts) which bind zinc and inhibit its absorption. Whilst plant-based diets can provide adequate zinc with careful planning, suboptimal intake may occur without appropriate dietary diversity or supplementation.

Malabsorption disorders significantly increase the risk of zinc deficiency. Conditions such as coeliac disease, inflammatory bowel disease (Crohn's disease and ulcerative colitis), and chronic diarrhoeal illnesses impair zinc absorption in the small intestine. Children with these conditions require monitoring of zinc status as part of their ongoing management. Additionally, genetic disorders affecting zinc transporters, such as acrodermatitis enteropathica, cause severe deficiency despite adequate dietary intake.

Prematurity and low birth weight are important risk factors, as zinc stores are primarily accumulated during the third trimester of pregnancy. Premature infants may have inadequate reserves and increased requirements for catch-up growth. Similarly, exclusively breastfed infants beyond six months may be at risk if complementary foods rich in zinc are not introduced appropriately, as breast milk zinc content decreases over time.

Adolescence is another period of increased zinc requirements due to rapid growth and development, particularly during puberty.

Other risk factors include:

• Nephrotic syndrome with increased urinary zinc losses

• Dialysis treatment which can remove zinc

• Diuretic therapy, particularly thiazides

• Liver disease affecting zinc metabolism

• Prolonged parenteral nutrition without adequate zinc supplementation

• Certain medications including penicillamine and some diuretics

• Poverty and food insecurity limiting access to zinc-rich foods

Healthcare professionals should maintain heightened awareness of zinc deficiency in children with these risk factors and consider screening where clinically indicated.

Diagnosing Zinc Deficiency in the UK

Diagnosing zinc deficiency presents significant challenges due to the lack of a universally accepted gold-standard test and the limitations of available biomarkers. In the UK, diagnosis typically relies on a combination of clinical assessment, dietary evaluation, and laboratory investigations.

Serum or plasma zinc concentration is the most commonly used biochemical marker, despite recognised limitations. Normal reference ranges typically fall between 10.7–22.9 μmol/L (70–150 μg/dL), though these vary between laboratories and local reference ranges should always be used. Levels below 10.7 μmol/L suggest deficiency, whilst values between 10.7–13.8 μmol/L may indicate marginal status. However, serum zinc represents only a small fraction of total body zinc and does not always correlate with tissue stores. Additionally, zinc is an acute-phase reactant, meaning levels can be temporarily reduced during infection or inflammation, potentially leading to false-positive results.

Important pre-analytical considerations include:

• Collecting samples in the morning after an overnight fast

• Using trace element-free collection tubes

• Avoiding sampling during acute illness

• Measuring C-reactive protein (CRP) alongside zinc to aid interpretation

Given these limitations, clinical context is essential when interpreting zinc levels, as emphasised in NICE guideline NG75 on faltering growth. A comprehensive assessment should include:

• Detailed growth measurements plotted on appropriate UK-WHO growth charts

• Dietary history assessing zinc intake and dietary patterns

• Medical history identifying malabsorption disorders or other risk factors

• Physical examination for characteristic signs of deficiency

• Exclusion of other causes of growth faltering

In specialist settings, additional investigations may include red blood cell zinc concentration, which may better reflect tissue stores, though this is not widely available in the UK. Hair zinc analysis lacks standardisation and is not routinely recommended in UK practice. Alkaline phosphatase levels may be reduced in zinc deficiency, as this enzyme is zinc-dependent, providing supportive evidence.

When zinc deficiency is suspected but biochemical confirmation is equivocal, a therapeutic trial of zinc supplementation may be considered. Clinical improvement in growth velocity, appetite, or dermatological manifestations following supplementation can provide retrospective diagnostic support. However, this approach should be undertaken under medical supervision with appropriate monitoring.

Referral to paediatric services or specialist dietitians is appropriate for children with confirmed deficiency, complex medical conditions, or when growth faltering persists despite initial interventions.

Treatment Options and Zinc Supplementation

The management of zinc deficiency aims to restore adequate zinc status, address underlying causes, and optimise growth and development. Treatment strategies must be individualised based on the severity of deficiency, age of the child, and presence of comorbidities.

Zinc supplementation forms the cornerstone of treatment for confirmed deficiency. In the UK, zinc sulfate is the most commonly prescribed formulation, available in various strengths. The British National Formulary for Children (BNFc) provides age-specific dosing guidance. For therapeutic purposes, typical doses range from 0.5–1 mg/kg/day of elemental zinc for mild-to-moderate deficiency, administered in divided doses to enhance absorption and minimise gastrointestinal side effects. Severe deficiency or malabsorption disorders may require higher doses under specialist supervision. The BNFc should be consulted for current maximum dose limits appropriate for age and weight.

Duration of supplementation typically ranges from 3–6 months, with clinical and biochemical reassessment to evaluate response. Improvements in growth velocity may not be immediately apparent and require several months of adequate zinc repletion. Parents should be counselled that catch-up growth is a gradual process.

Common adverse effects of zinc supplementation include:

• Gastrointestinal symptoms: nausea, vomiting, abdominal discomfort, and diarrhoea

• Metallic taste which may affect compliance

• Copper deficiency with prolonged high-dose supplementation, as zinc competes with copper absorption

To minimise side effects, zinc supplements should be taken with food (though not with high-phytate foods which reduce absorption) and doses divided throughout the day. If gastrointestinal symptoms are problematic, dose reduction or alternative formulations such as zinc acetate or zinc gluconate may be considered.

Important interactions: Zinc supplements should be separated from tetracyclines, quinolone antibiotics, and iron supplements by at least 2-3 hours, as these can reduce zinc absorption and vice versa.

Addressing underlying causes is essential for long-term management. Children with malabsorption disorders require optimisation of their primary condition alongside zinc supplementation. Those with dietary insufficiency benefit from dietetic input to improve zinc intake through food sources and ensure nutritional adequacy across all micronutrients.

Monitoring during treatment should include:

• Regular growth measurements (weight monthly if needed; height every 3-6 months)

• Repeat zinc levels after approximately 3 months of supplementation

• Assessment of copper status if prolonged high-dose therapy is required

• Evaluation of clinical symptoms and treatment adherence

Parents should be advised to contact their GP if the child develops persistent vomiting, worsening symptoms, or signs of copper deficiency (anaemia, neutropenia) during supplementation. Suspected adverse reactions should be reported via the MHRA Yellow Card scheme. Specialist paediatric review is warranted if growth does not improve despite adequate zinc repletion, suggesting alternative or additional causes of growth faltering.

Preventing Zinc Deficiency Through Diet

Dietary prevention of zinc deficiency is preferable to treatment and can be achieved through appropriate food choices and meal planning. Public health strategies in the UK emphasise the importance of balanced nutrition during childhood to support optimal growth and development.

Zinc-rich food sources should be incorporated regularly into children's diets. The richest sources include:

• Red meat (beef, lamb): highly bioavailable zinc

• Poultry (chicken, turkey)

• Shellfish (oysters, crab, prawns): oysters contain exceptionally high zinc levels

• Dairy products (cheese, milk, yoghurt)

• Eggs

• Fortified breakfast cereals: many UK cereals are fortified with zinc

• Nuts and seeds (particularly pumpkin seeds, cashews)

• Legumes (chickpeas, lentils, beans)

• Wholegrains (wholemeal bread, oats)

The bioavailability of dietary zinc varies considerably. Animal-source foods provide zinc in forms that are more readily absorbed compared to plant sources. Phytates, present in wholegrains, legumes, and nuts, form insoluble complexes with zinc, reducing absorption. However, food preparation techniques can enhance zinc bioavailability from plant sources: soaking, sprouting, and fermenting reduce phytate content, whilst combining plant-based zinc sources with animal proteins may improve overall nutritional adequacy.

Dietary considerations for children following vegetarian or vegan diets include:

• Including zinc-fortified foods daily

• Using food preparation methods that reduce phytate content

• Ensuring adequate dietary diversity with multiple plant protein sources

• Seeking advice from a registered dietitian for individualised guidance

• Considering zinc supplementation under dietetic or medical supervision if dietary intake is insufficient

The NHS Eatwell Guide provides a framework for balanced nutrition that, when followed appropriately, should meet zinc requirements for most children. Parents should aim to provide varied diets incorporating foods from all food groups, with particular attention to protein sources.

Infant feeding practices are crucial for preventing early zinc deficiency. Whilst breast milk provides adequate zinc for the first six months, timely introduction of complementary foods rich in zinc is essential from six months onwards, as recommended in NHS Start for Life guidance. Suitable first foods include pureed meat, poultry, or iron- and zinc-fortified infant cereals. Formula-fed infants receive zinc through fortified infant formula.

Parents concerned about their child's zinc intake should seek advice from their GP or registered dietitian rather than self-prescribing supplements, as excessive zinc intake can cause toxicity and interfere with absorption of other essential minerals, particularly copper and iron. The European Food Safety Authority (EFSA) has established tolerable upper intake levels for zinc that should not be exceeded. Professional guidance ensures appropriate assessment and individualised dietary recommendations to support healthy growth and development.

Frequently Asked Questions