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Zinc Deficiency

Author: Sujatha Baddam Author: Luke Maxfield Author: Samarth Shukla Editor: Jonathan S. Crane Updated: 8/2/2025 11:13:50 PM

Introduction

Zinc is an essential micronutrient that plays a crucial role in the metabolism of proteins, lipids, and nucleic acids, as well as in gene transcription.[1] This micronutrient is critical for numerous physiological processes, including reproduction, immune function, and wound healing. At the cellular level, zinc is indispensable for the normal function of macrophages, neutrophils, natural killer cells, and the complement system.[2][3] 

Despite being one of the most abundant trace elements in the human body, zinc cannot be stored in significant amounts and therefore requires regular dietary intake or supplementation to maintain adequate levels. Dietary sources include meat, fish, legumes, nuts, and other plant-based sources, although absorption efficiency varies depending on the food matrix.

Zinc deficiency is a major global health concern, particularly in developing countries. The World Health Organization recognizes zinc deficiency as a significant contributor to global disease burden.[4][5] Clinically, manifestations include growth retardation, delayed sexual maturation, impaired immune response, inflammation, gastrointestinal disturbances, and cutaneous lesions.[6]

Etiology

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Etiology

Zinc is a divalent cation that is not synthesized within the human body and must be obtained through dietary sources to maintain adequate zinc levels. Daily requirements range from 3 mg/d in children to 8 mg/d in adult females and 11 mg/d in adult males. The need for ninc increases further during pregnancy and lactation due to higher metabolic demand.

Zinc deficiency affects nearly 2 billion people worldwide, particularly in developing countries, and is recognized by the World Health Organization as a major contributor to the global disease burden.[7] Deficiency may be acquired or inherited.

Acquired Zinc Deficiency 

Acquired deficiency results from decreased intake, impaired absorption, increased metabolic demand, or excessive loss. Common contributing factors include the following:

  • Nutritional causes
    • Malnutrition, especially in children and older populations in developing regions.[8]
    • Poor intake of zinc-rich foods, such as low meat consumption
    • Excess phytates (found in legumes, seeds, soy products, and whole grains), oxalates (present in spinach, okra, nuts, and tea), and casein or calcium, which reduce bioavailability.[9]
  • Chronic illnesses
    • Chronic gastrointestinal diseases, diabetes mellitus, liver disease, sickle cell disease, kidney disease, HIV infection, excess alcohol consumption, and chronic infections.[10][11][12][13][14][15][16][17][18]
    • Heart failure, due to hyperzincuria from diuretics, angiotensin receptor blockers, and activation of the renin-angiotensin-aldosterone system.[19]
  • Malabsorption syndromes
    • Crohn disease, short bowel syndrome, pancreatic insufficiency, celiac disease, and hookworm infestation.[20]
  • Medication-related causes
    • Penicillamine, certain diuretics, sodium valproate, angiotensin receptor blockers, and some antibiotics impair absorption or increase losses.[9]
  • Increased demand
    • Pregnancy and lactation (up to 2-fold increased requirement; losses of up to 2 mg/d may persist for 2 months post partum).[4]
    • Preterm infants have low stores, immature absorption, and higher metabolic rates.[21]
  • Excessive losses
    • Burns, hemodialysis, hemolysis, diarrhea, urinary loss from alcohol use or diuretics.[5]

In response to deficiency, the body attempts to increase gastrointestinal absorption and mobilize small zinc reserves in skeletal muscle, bone, hair, liver, brain, and skin.[22] Zinc homeostasis is regulated by a complex network of transporters, primarily the ZIP (Zrt-/Irt-like protein) and ZnT (zinc transporter) protein families.[23]

Inherited Zinc Deficiency

  • Acrodermatitis enteropathica 
    • A rare autosomal recessive disorder caused by mutations in the SLC39A4 gene on chromosome 8q24.3, which encodes the Zip4 transporter, leading to impaired intestinal zinc absorption. The estimated incidence is approximately 1 per 500,000 live births.[24]

Epidemiology

Zinc deficiency is a widespread global health issue, particularly prevalent in low- and middle-income countries.[25] An estimated 17.3% of the global population is at risk of inadequate zinc intake, with regional prevalence ranging from 7.5% in high-income countries to 30% in South Asia.[26][3] Endemic zinc deficiency affects up to one-third of the population in Southeast Asia, sub-Saharan Africa, and parts of the Middle East, including Iran, Egypt, and Turkey, where diets high in phytates limit zinc absorption.[3][27]

In Latin America and the Caribbean, the rates of zinc deficiency in children and women range from 19.1% to 56.3%.[28] In South Asia, prevalence remains elevated across various population groups. Children and older individuals are particularly vulnerable.[29][30][31] 

Globally, trends in zinc deficiency have remained relatively stable; however, some countries have noticed improvements. For instance, China reported a reduction in prevalence from 17% to 8% by 2005.[32][33] In certain regions, pica—particularly clay eating—further exacerbates deficiency by binding dietary zinc and reducing its bioavailability.

The recommended biochemical indicator for assessing population zinc status is serum zinc concentration. A prevalence greater than 20% indicates a need for public health intervention.[34] 

Pathophysiology

Zinc is a vital trace element that plays multiple indispensable roles in human physiology, particularly in growth, tissue repair, and immune defense. This element is essential for molecular synthesis, including the formation of DNA, RNA, and proteins, and is necessary for stabilizing ribosomes and cell membranes. Zinc protects against cellular damage by reducing lipid peroxidation and the generation of free radicals. Zinc is also crucial for spermatogenesis, embryogenesis, and fetal growth.[2][3]

Zinc is primarily absorbed in the distal duodenum and proximal jejunum, whereas its excretion is predominantly through the gastrointestinal tract, with minor losses via urine and sweat. Intracellular zinc homeostasis is tightly regulated by transporters encoded by the SLC30A (ZnT) and SLC39A (ZIP) gene families.

Zinc plays a critical role in maintaining skin integrity. This element is more concentrated in the epidermis than in the dermis, with the highest levels found in the stratum spinosum. Within keratinocytes, zinc suppresses tumor necrosis factor-alpha activation, reduces inducible nitric oxide synthase activity, and limits nitric oxide production, all of which help control inflammation. Zinc deficiency can trigger intracellular chelation, leading to the activation of caspase-3, DNA fragmentation, and the subsequent apoptosis of keratinocytes. As a result, zinc is essential for normal keratinocyte proliferation and differentiation, as well as the suppression of skin inflammation. Specific zinc transporters, including Zip2 and Zip4, are expressed in keratinocytes and are crucial for skin health, whereas Zip10 is present in the outer root sheath of hair follicles and contributes to hair growth and preservation.[35][36]

Zinc plays a crucial role in regulating the immune system. Zinc supports the skin as a physical barrier to pathogens and modulates innate immunity through the activity of natural killer cells, neutrophils, and macrophages. In adaptive immunity, zinc is necessary for T-lymphocyte activation, Th1 cytokine production, B-lymphocyte function, and immunoglobulin G production. Zinc enhances macrophage phagocytosis, intracellular killing, and cytokine secretion, while also potentiating apoptosis as part of the immune response.[3][37][38]

Histopathology

Zinc deficiency induces characteristic histopathological changes in multiple tissues, most notably the skin, but also the eyes, reproductive organs, digestive tract, pancreas, and lymphoid tissues. These changes often reflect impaired epithelial integrity, inflammation, and compromised immune function, underscoring the essential role of zinc in tissue maintenance and repair.

In zinc deficiency, the skin exhibits hyperplastic psoriasiform dermatitis, characterized by parakeratosis and hyperkeratosis. The granular layer is often diminished or absent, and the epidermis may display psoriasiform hyperplasia and replacement by clear cells. Cytoplasmic pallor in the upper epidermis may be among the earliest changes observed; however, this is a nonspecific finding and may be absent in chronic lesions.[39] The papillary dermis may exhibit dilated, tortuous vessels with a mild perivascular mononuclear infiltrate, a finding also observed in other nutritional deficiencies, such as niacin (vitamin B3) deficiency.

In the ocular system, zinc deficiency has been associated with corneal thinning, cataract formation, and retinal degeneration.[40] These changes reflect zinc's essential role in maintaining ocular surface integrity and retinal function.

In the testes, zinc deficiency can cause degeneration of the seminiferous tubules and interstitial tissue, resulting in impaired and reduced reproductive function.[41]

In the digestive system, epithelial changes are observed in the crop and esophagus, characterized by reduced mucosubstance coating prickle cells. Additionally, pancreatic exocrine cells may exhibit enlarged and irregular nuclei, indicating a disruption in cellular function.[42]

In lymphoid tissues, such as the thymus, lymph nodes, and spleen, zinc deficiency results in a significant reduction in lymphocytes, underscoring zinc's crucial role in lymphopoiesis and immune regulation.[43] Importantly, these histopathological changes are largely reversible with appropriate zinc supplementation. Early recognition and correction of deficiency can restore normal tissue architecture and function.

History and Physical

Risk factors and age of onset help distinguish acquired from inherited forms of zinc deficiency. Acquired zinc deficiency typically presents later in life and is associated with identifiable risk factors, including inadequate dietary supply, regional or geographic factors, such as high phytate intake; excessive loss; or increased metabolic demand. Inherited forms, such as acrodermatitis enteropathica, typically present early in infancy.

Zinc deficiency was first recognized as a cause of nutritional dwarfism in the Middle East, primarily due to diets high in phytates that inhibit zinc absorption.[44][45] Regardless of whether the deficiency is inherited or acquired, many clinical manifestations overlap, although cutaneous involvement may be milder in acquired forms.

Zinc deficiency affects multiple organ systems, including:

  • Reproductive system: Presents as hypogonadism, oligospermia, and associated complications.[46][47][48]
  • Central nervous system: Symptoms may include emotional lability, mental disturbances, impaired taste (hypogeusia), impaired smell (hyposmia), and photophobia.[49]
  • Immune system: Zinc deficiency leads to immune dysfunction, increasing susceptibility to infections.[50]
  • Gastrointestinal system: Patients may experience significant diarrhea.[22]

Cutaneous findings typically progress over several days and predominantly affect the periorificial areas, presenting as angular cheilitis. Friction-prone regions—such as the elbows, knees, knuckles, malleolar areas, ankles, and sacrum—are often affected. Lesions may appear as eczematous scaly plaques, vesiculobullous or pustular eruptions, with a scald-like appearance that can fissure. Pathergy is a common condition characterized by the development of similar lesions at friction sites.[51] Annular psoriasiform plaques may exhibit an overlying black crust with advancing margins, central scaling, and lichenification. Nail changes include paronychia, cuticle inflammation, Beau lines, and white transverse bands. Scalp involvement can lead to hair thinning, brittle spearhead-shaped hair, transverse striations, longitudinal splits, or pseudomonilethrix.[52][53]

In inherited zinc deficiency, such as acrodermatitis enteropathica, symptoms typically appear 4 to 6 weeks after cessation of breastfeeding. Affected infants may exhibit irritability, withdrawn behavior, growth retardation, anorexia, night blindness, pica, and photophobia. Characteristic skin findings include burn-like psoriasiform lesions affecting the periorificial, gluteal, perineal, and acral regions. Other common features include nail dystrophy, paronychia, alopecia, delayed wound healing, conjunctivitis, and increased susceptibility to infections.[54]

Evaluation

Diagnosis is guided by clinical suspicion based on risk factors, geographic prevalence, and age of onset. An appropriate and detailed history can point towards an inherited or acquired deficiency.[55][27]

Acrodermatitis enteropathica is primarily a clinical diagnosis, supported by laboratory and histopathology findings. Laboratory tests typically demonstrate low serum alkaline phosphatase—a zinc-dependent metalloenzyme—and low plasma zinc concentrations. These markers are useful in severe deficiency but may be unreliable in mild cases due to altered protein binding.[56]

For accurate serum zinc measurement, samples should be collected using zinc-free vacuum tubes and stainless steel needles, avoiding rubber stoppers and hemolysis. Plasma or serum should be separated within 45 minutes, using anticoagulants with low zinc concentrations, and ideally obtained as fasting morning samples. Normal adult zinc levels range from 70 to 250 μg/dL, with mild deficiency commonly observed at levels between 40 and 60 μg/dL. Urinary zinc levels and hair zinc concentrations are highly variable and unreliable for assessing acute deficiency.[57]

Punch biopsy and histopathology of the affected tissue can support the diagnosis of necrolysis, characterized by cytoplasmic pallor, vacuolization, ballooning degeneration, and confluent necrosis of keratinocytes in the upper epidermis. Confluent parakeratosis is often accompanied by loss of the granular layer and dermal edema. An associated neutrophilic crust may be present. Individual keratinocytes typically have pyknotic nuclei. These findings are nonspecific and are typically observed in conjunction with pellagra and necrolytic migratory erythema. Late lesions of zinc deficiency may mimic psoriasis. Clinical improvement to zinc supplementation can also be confirmatory.[58]

Treatment / Management

Effective strategies to address zinc deficiency include supplementation, fortification, biofortification, and dietary diversification. These approaches aim to improve zinc intake and absorption across diverse populations.

Zinc supplementation has been shown to reduce the risk of infection in multiple studies.[59] In children older than 6 months at risk for zinc deficiency, it also shortens the duration of diarrhea.[60] Given the limited sensitivity of plasma zinc levels for detecting mild deficiency, supplementation is reasonable when clinical symptoms are present, even if laboratory values are equivocal or normal. Empirical supplementation should be considered for high-risk populations.(A1)

Oral replacement is the first-line treatment for zinc deficiency. Adults typically require 20 to 40 mg of elemental zinc daily, with symptom resolution expected within 1 to 2 weeks. In acrodermatitis enteropathica, lifelong oral supplementation remains the standard treatment despite underlying malabsorption, at a dose of 1 to 2 mg/kg/d.[61][62]

Recommended daily elemental zinc intake for the prevention of zinc deficiency includes the following: 

  • 3 mg/d for children younger than 4
  • 5 mg/d for children aged 4 to 8 
  • 8 mg/d for children aged 9 to 13
  • 9 mg/d for nonpregnant, nonlactating women
  • 11 mg/d for men
  • 11 to 12 mg/d for pregnant and lactating women

In cases of severe deficiency due to malnutrition or malabsorption, such as Crohn disease, short bowel syndrome, higher doses of more than 50 mg/d may be required acutely. In preterm infants, breastfeeding typically corrects the deficiency within weeks; however, if maternal stores are depleted or if an SLC30A2 mutation impairs zinc secretion in breast milk, supplementation may be necessary.

Precautions with zinc supplementation include the following:

  • Doses more than 50 mg/d may cause gastrointestinal adverse effects, including nausea, abdominal discomfort, and diarrhea.
  • Doses more than 150 mg/d may impair immune function, alter lipid profiles, and interfere with iron and copper absorption, potentially leading to genitourinary complications.
  • Long-term or high-dose supplementation requires monitoring of serum copper levels, as zinc competes with copper for absorption.

Available formulations include zinc sulfate, zinc acetate, zinc aspartate, zinc orotate, and zinc gluconate.

Patients should be monitored for clinical response and serum zinc levels after 3 to 6 months of therapy. If the response is inadequate, the dose may be increased, with careful monitoring for toxicity. In acrodermatitis enteropathica, lifelong supplementation is required, with dosing individualized based on serial zinc levels. Long-term therapy may also necessitate copper monitoring and supplementation to prevent zinc-induced copper deficiency.

Parenteral zinc is rarely necessary, except in cases of intestinal failure or prolonged total parenteral nutrition.[63] In such settings, zinc must be included in the total parenteral nutrition formulation to prevent deficiency, particularly in patients with high gastrointestinal losses or impaired absorption.

Zinc supplementation has been shown to benefit the prevention and treatment of diarrhea, respiratory infections, and promote child growth in developing countries. Fortifying staple foods is a cost-effective strategy when suitable food vehicles are available. Biofortification and dietary diversification—increasing consumption of zinc-rich foods and reducing intake of phytic acid—are sustainable, long-term solutions. For optimal public health impact, these interventions should be integrated into existing health and nutrition programs.[64][65]

Differential Diagnosis

The differential diagnosis for zinc deficiency includes other nutritional deficiencies and systemic conditions with overlapping clinical features. Accurate identification relies on clinical context, associated symptoms, and targeted laboratory testing.

  • Biotin deficiency can present with similar cutaneous findings, including periorificial dermatitis and alopecia. Additional distinguishing features include hypotonia, ataxia, seizures, and hearing loss. Diagnosis is supported by low serum biotin levels and increased urinary excretion of 3-hydroxyisovaleric acid.

  • Vitamin B2 (riboflavin) deficiency may also cause mucocutaneous changes resembling those of zinc deficiency, often accompanied by ocular involvement such as corneal vascularization. Elevated erythrocyte glutathione reductase activity supports the diagnosis. 

  • Essential fatty acid deficiency can mimic zinc deficiency, presenting with features such as scaly dermatitis, but often also features diffuse alopecia and poor wound healing.

  • Necrolytic migratory erythema is a paraneoplastic dermatosis most commonly associated with glucagon-secreting tumors (glucagonoma). The clinical resemblance of necrolytic migratory erythema can closely mimic that of zinc deficiency. Diagnosis is confirmed by markedly elevated serum glucagon levels (>1000 pg/mL).

Other conditions to consider in the differential diagnosis include the following:

  • Depression
  • Iron deficiency
  • Vitamin B12 deficiency
  • Folate deficiency
  • Vitamin D deficiency
  • Vitamin A deficiency
  • Pellagra (niacin deficiency)
  • Celiac disease or protein-energy malnutrition

These conditions may produce overlapping systemic or cutaneous manifestations and should be evaluated based on clinical presentation and targeted laboratory findings. Early identification and appropriate management of these deficiencies are essential to prevent long-term complications and improve patient outcomes.

Toxicity and Adverse Effect Management

Zinc toxicity from over-supplementation is rare but can lead to significant adverse effects. Excessive intake may cause gastric irritation, presenting with nausea, vomiting, abdominal pain, and, in severe cases, gastric hemorrhage.[3]

A key concern with chronic high-dose zinc supplementation is its potential to interfere with copper absorption. Zinc and copper share similar intestinal transport pathways, and excess zinc can lead to copper deficiency, potentially resulting in anemia, neutropenia, and neurologic complications. As noted, copper levels should be monitored during prolonged or high-dose zinc therapy, with supplementation added if needed to prevent deficiency.

Management of zinc toxicity involves discontinuing excess zinc intake and providing supportive care for gastrointestinal symptoms. In cases of documented copper deficiency secondary to zinc over-supplementation, appropriate copper replacement should be initiated.

Prognosis

Zinc deficiency typically responds well to supplementation and correction of contributing dietary factors. Symptoms often improve rapidly. Diarrhea may resolve within 24 hours, and skin lesions generally heal within 1 to 2 weeks.

In patients with inherited zinc deficiency, zinc levels and serum alkaline phosphatase should be monitored 3 to 6 months after initiating therapy, with dose adjustments as needed.[4][21] Ongoing monitoring is essential to ensure therapeutic efficacy, prevent toxicity, and guide long-term management.

Zinc deficiency is associated with immune function, including weakened cell-mediated immunity due to reduced thymulin activity and decreased expression of the interleukin-2 and interferon-gamma genes. With appropriate zinc supplementation, improvements in immune function, reduced oxidative stress, and decreased production of inflammatory cytokines are typically observed.[66]

Emerging evidence suggests that zinc deficiency may increase susceptibility to and severity of COVID-19 by compromising the pathogen defense and promoting dysregulated immune response.[67] Zinc's antiviral properties and role in modulating inflammatory pathways highlight its potential importance in mitigating disease progression.

Complications

Prolonged and severe zinc deficiency can lead to a wide range of complications affecting growth, immunity, endocrine function, and tissue integrity. These complications are particularly pronounced in vulnerable populations, such as children, older adults, and individuals with chronic illnesses or malabsorption syndromes.

  • Growth failure: Untreated zinc deficiency is strongly associated with permanently stunted growth and developmental delays, particularly in children.[68]
  • Hypogonadism: Zinc is essential for normal reproductive development, and deficiency can impair gonadal function.
  • Recurrent infections: Zinc deficiency weakens immune defenses, contributing to both acute and chronic infections. These infections can, in turn, exacerbate zinc deficiency. Although zinc supplementation is well established in the management of diarrheal illnesses, evidence for its role in other infections such as malaria and pneumonia remains limited.[60][69]
  • Diarrhea: A common symptom and complication of zinc deficiency, persistent diarrhea exacerbates zinc loss and deficiency.
  • Skin manifestations: Chronic zinc deficiency can cause or exacerbate dermatologic conditions such as acrodermatitis enteropathica, cheilitis, and dermatitis.
  • Delayed wound healing: Zinc is crucial for tissue repair, and deficiency impairs the healing process.
  • Low bone mineral density: The impact of zinc deficiency on bone health remains unclear; however, some evidence suggests that zinc combined with calcium may better support bone density than calcium alone.[70]
  • Metabolic risk: Zinc deficiency is a potential risk factor for the development of diabetes mellitus and obesity, although its direct causal role remains under investigation.[38]

Consultations

In the early stages of zinc deficiency, particularly in patients with known risk factors, primary care providers can often effectively manage the condition through dietary counseling and zinc supplementation. However, specialist referral may be warranted when symptoms are severe, persistent, or the underlying cause is unclear. Relevant consultations may include:

  • Gastroenterologist: To evaluate for malabsorptive disorders such as Crohn disease, celiac disease, and short bowel syndrome.
  • Dermatologist: For assessment and management of complex or atypical skin manifestations.
  • Endocrinologist: When zinc deficiency is associated with growth failure, hypogonadism, or suspected endocrine abnormalities.
  • Nutritionist or dietitian: For comprehensive dietary assessment, counseling on zinc-rich foods, and strategies to address inhibitory factors, such as phytate intake.

Early multidisciplinary involvement can help identify underlying causes and optimize treatment outcomes.

Deterrence and Patient Education

Patient education is essential for preventing zinc deficiency and supporting long-term health. Dietary counseling should focus on regular consumption of zinc-rich foods, alongside counseling on reducing intake of substances that impair zinc absorption, such as phytates found in whole grains and legumes. Good dietary sources of zinc include red meat, poultry, wheat germ, wild rice, seeds, and nuts.

Vegetarians and individuals following plant-based diets may face additional challenges in meeting their zinc requirements due to the lower bioavailability of zinc from plant sources. Vegetarian-friendly zinc sources include baked beans, peas, lentils, cashews, and almonds.

Patients should be educated about food preparation techniques, such as soaking, sprouting, and fermenting legumes and grains, which can help reduce phytate levels and enhance zinc absorption.

For high-risk groups—including pregnant and lactating women, children, individuals with chronic gastrointestinal conditions, and those on restrictive diets—proactive dietary planning and, when appropriate, supplementation should be emphasized as part of routine preventive care.

Pearls and Other Issues

Key facts to keep in mind about zinc deficiency include the following:

  • Zinc is an essential trace element involved in growth, immune function, wound healing, and DNA synthesis.
  • Zinc requires regular dietary intake.
  • Deficiency is common in developing countries and high-risk groups, such as malnourished, alcoholics, and those with malabsorption syndromes.
  • Phytates in grains and legumes inhibit zinc absorption.
  • Clinical features include periorificial dermatitis, alopecia, diarrhea, poor wound healing, growth retardation, and immunodeficiency.
  • Acrodermatitis enteropathica is an inherited condition caused by mutations in the SLC39A4 gene, typically presenting after weaning.
  • Diagnosis is clinical; serum zinc levels may be low but are not always reliable in mild cases.
  • Oral zinc supplementation is the mainstay of treatment; lifelong therapy is often necessary in cases of inherited deficiency.
  • Excess zinc can cause copper deficiency, leading to anemia and neurological symptoms.
  • Zinc plays a crucial role in immune modulation, particularly in regulating T-cell function.
  • Relying solely on plasma zinc levels for diagnosis may miss mild or subclinical deficiency, as levels can be influenced by acute-phase responses or hypoalbuminemia.
  • Failure to address underlying causes, such as malabsorption syndromes, high-phytate diets, and chronic alcohol use, can result in recurrent deficiency despite supplementation.
  • Zinc deficiency may contribute to increased susceptibility and severity of infections, including COVID-19, highlighting the importance of maintaining adequate zinc status for overall immune resilience.

Enhancing Healthcare Team Outcomes

Zinc deficiency is relatively uncommon in developed countries but can occur in individuals with restricted diets, malabsorptive disorders, or chronic illnesses. Prevention is achievable in most cases through public education and interprofessional collaboration.

Clinicians, pharmacists, nurses, and dietitians play essential roles in educating patients and the public about dietary sources of zinc and strategies to prevent deficiency. Public health guidelines emphasize meeting nutritional needs primarily through a balanced diet rather than unnecessary supplementation. Zinc-rich foods include whole grains, low-fat dairy products, seafood, poultry, legumes, soy, and red meat.

Pharmacists play a crucial role in counseling patients about potential medication interactions with zinc supplements. Certain medications—including antibiotics, penicillamine, and diuretics—can impair zinc absorption or alter its excretion. Additionally, pharmacists should educate patients about the risks of excessive zinc intake, which can lead to adverse effects such as copper deficiency and gastrointestinal distress. Coordinated care between pharmacists and clinicians is crucial for monitoring potential drug-nutrient interactions and optimizing supplementation strategies.

An interprofessional, team-based approach involving healthcare providers, pharmacists, nurses, and dietitians can effectively prevent and manage zinc deficiency, ultimately leading to better patient outcomes.[5][71]

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