Zinc Deficiency

Description

• Nutritional condition whose manifestations may involve growth retardation, decreased bone mineralization, hypogonadism, cell-mediated immune dysfunction, poor wound healing, poor appetite, hair loss, lethargy, increased infections, anorexia, diarrhea, and eye and skin lesions
• Zinc is a mineral and integral component of >300 enzymes and 3,000 transcription factors and plays structural role in cell membranes and proteins. Zinc is essential for wound healing and anabolic processes (1,2,3).
• System(s) affected: endocrine/metabolic, nervous, skin/exocrine, hematologic/oncologic, gastroenterologic, musculoskeletal

Geriatric Considerations

• 30–40% of ambulatory elderly may have zinc-deficient diets; elderly may also have decreased absorption (1,2).
• Zinc deficiency may cause delayed wound healing, chronic ulcers, and impaired recovery from infections. Poor night vision may contribute to increased falls/accidents; loss of taste, which may contribute to worsening nutrition (4)
• Reactive oxygen species leading to inflammation are involved in many chronic diseases attributed to aging: atherosclerosis, Alzheimer disease, neurodegenerative disorders, diabetes mellitus type 2, and cancer (1).
• Increased depression and poor cognitive function in the elderly are associated with low zinc levels.
• Supplementation in one study with elderly subjects decreased the incidence of infection (1)[B].

Pediatric Considerations

• Zinc deficiency may cause failure to thrive and may impair growth and development of secondary sexual characteristics (1).
• Peak requirement during pubertal growth spurt (ages 10 to 15 years old) (2)
• Supplementing deficient children decreases mortality from diarrhea (5)[A] and pneumonia in certain populations (2,5)[B].

Pregnancy Considerations

• Requirements increase; deficiency may cause spontaneous abortion, preterm labor.
• Supplementation in deficient individuals reduces preterm labor but does not improve birth weight (6)[A].
• Severe deficiency is associated with congenital malformations and increased maternal morbidity.

Epidemiology

Prevalence

• Uncommon in the United States; estimated prevalence is 1–3% (3,7).
• Globally: Estimated prevalence is 20%; worse in developing countries (4,7)
• Predominant age: all ages
• Predominant sex: male = female

Etiology and Pathophysiology

• Insufficient dietary intake
  • Diet lacking in animal proteins (dairy, eggs, meat, seafood)
  • Parenteral nutrition without zinc supplementation
  • Breastfeeding (infants)
  • Alcoholism
  • Restricted eating/eating disorder
• Increased requirements
  • Pregnancy
  • Lactation
  • Preterm infants
  • Rapid growth phases in childhood
  • Burns
  • Major trauma
  • Systemic illness resulting in oxidative stress
• Increased losses
  • Diabetes
  • Cirrhosis, alcoholism
  • Renal disease, dialysis
  • Steatorrhea, enterostomy, fistula
  • Sickle cell disease
  • Diuretics: thiazides, chlorthalidone, ACEI, ARB
• Decreased absorption
  • Diet high in: phytates (plant fiber), cadmium, copper, iron
  • Acrodermatitis enteropathica: autosomal recessive deficiency in the enzyme required for intestinal absorption of zinc
  • Parasitism
  • Liver or pancreas dysfunction
  • Inflammatory bowel disease
  • After bariatric surgery
  • Medications: chelating agents, penicillamine, tetracyclines, quinolones, bisphosphonates, valproate

Genetics

• Usually an acquired deficiency
• Rarely caused by acrodermatitis enteropathica
• Associated with sickle cell anemia

Risk Factors

• Medications: diuretics, penicillamine, valproate, iron chelators, ACEI/ARB, cisplatin
• Low socioeconomic status
• Living in developing nations
• Strict vegetarian diet
• Malabsorption syndromes
• Thermal burns
• Alcoholism
• Chronic renal failure

General Prevention

• Diverse and adequate diet
• Supplementation when indicated (see “Medication”)

Commonly Associated Conditions

• Acrodermatitis enteropathica
• Sickle cell anemia
• Malabsorption
• Advanced age
• Diarrheal illness, especially in children