Iodide Deficiency

Introduction

Iodine is an essential micronutrient present in minute quantities in the human body (15–20 mg), primarily in the thyroid gland. It is a critical substrate for the synthesis of thyroid hormones, thyroxine (T4) and triiodothyronine (T3), which are the main determinants of basal metabolic rate. These hormones play a pivotal role in somatic growth and brain development, particularly in the fetus and during the first three years of postnatal life.

• Physiological Role: Iodine is essential for the synthesis of thyroid hormones (T3 and T4),.
• Sources: Sea foods, plants grown in iodine-rich soil, drinking water, and iodized salt,,. The Himalayan belt and Ganges valley are areas of severe deficiency in India due to soil leaching.

Iodine Deficiency Disorders (IDD)

The term "Iodine Deficiency Disorders" (IDD) refers to the spectrum of health consequences resulting from inadequate iodine intake. It affects all stages of life, from the fetus to the adult.

1. Epidemiology and Impact

• Global Burden: Nearly 1.5 billion people in 130 countries live in areas of iodine deficiency.
• Cognitive Impact: IDD is the most common cause of preventable mental retardation globally. It is responsible for an average lowering of IQ scores by 13.5 points in populations living in iodine-deficient areas compared to iodine-sufficient areas.
• Prevalence in India: IDD is a major public health problem across India, including coastal districts (previously thought safe). The prevalence of goiter is reported to be around 16% among preadolescent children.

2. Spectrum of Clinical Features (by Life Stage)

The clinical manifestations of iodine deficiency vary depending on the age of onset.

A. Fetus

Iodine deficiency in the mother leads to inadequate availability of T4 to the fetus.

• Abortion and Stillbirth: Increased risk of fetal loss,.
• Congenital Anomalies: Increased risk of birth defects.
• Neurological Damage: Maternal hypothyroidism adversely affects early brain development, leading to permanent damage.
• Perinatal Mortality: Increased rates of perinatal death.

B. Neonate

• Neonatal Goiter: Enlargement of the thyroid gland at birth.
• Neonatal Hypothyroidism: Transient or permanent hypothyroidism due to inadequate substrate for hormone synthesis.
• Increased Susceptibility: The neonatal thyroid has low iodine content and high turnover, making it very sensitive to deficiency.

C. Child and Adolescent

• Goiter: The earliest and most visible manifestation. It is an adaptive response (hypertrophy and hyperplasia) to increase thyroid hormone production under TSH stimulation,.
  • Endemic Goiter: Defined when the prevalence of goiter in a population is >5%.
  • Simple Colloid Goiter: Often due to subclinical deficiency.
• Hypothyroidism: Clinical features include growth retardation, fatigue, cold intolerance, and dry skin,.
• Impaired Mental Function: Even in clinically euthyroid children, deficiency is associated with abnormalities in psychoneuromotor and intellectual development, poor school performance, and fine motor skill deficits.
• Cretinism: The most severe manifestation of severe iodine deficiency during fetal and early life. It presents in two types:
  • Neurological Cretinism: Characterized by mental retardation, deaf-mutism, spastic diplegia, and squint,.
  • Myxedematous Cretinism: Characterized by severe hypothyroidism, short stature, and coarse features. This form is often seen in areas with combined selenium and iodine deficiency.

D. Adult

• Goiter and Hypothyroidism: Continued enlargement of the thyroid and metabolic slowing.
• Impaired Mental Function: Reduced work capacity and apathy.
• Iodine-Induced Hyperthyroidism (Jod-Basedow phenomenon): Can occur in older adults with longstanding nodular goiters following sudden iodine supplementation.

Diagnosis and Assessment

Assessment is performed at the individual level for diagnosis and at the population level for public health monitoring.

1. Biochemical Indicators

• Urinary Iodine Excretion (UIE): Since >90% of dietary iodine is excreted in urine, this is the most useful indicator of recent iodine intake,.
  • Normal: >100 $\mu$g/L.
  • Insufficient: <100 $\mu$g/L.
  • Severe Deficiency: <20 $\mu$g/L,,.
• Thyroid Function Tests:
  • Serum TSH: Elevated in deficiency (especially sensitive in neonates).
  • Serum T3/T4: T4 may be low or low-normal; T3 may be normal or elevated (adaptive mechanism).
• Serum Thyroglobulin: Elevated in iodine deficiency (reflects thyroid cell proliferation).

2. Clinical Assessment

• Goiter Grading: Palpation of the thyroid gland to grade the size (Grade 0, 1, 2) is used in field surveys.
• Cretinism Features: Evaluation for developmental delay, deafness, and spasticity.

3. Epidemiological Criteria (WHO)

Based on Median Urinary Iodine Levels:

• < 20 $\mu$g/L: Severe IDD.
• 20–49 $\mu$g/L: Moderate IDD.
• 50–99 $\mu$g/L: Mild IDD.
• > 100 $\mu$g/L: No deficiency.

Management and Treatment

1. Treatment of Overt Deficiency

• Hypothyroidism: Replacement therapy with Levothyroxine is required.
• Goiter:
  • Small, diffuse goiters in children often regress with iodine supplementation (iodized salt or oil).
  • Levothyroxine may be used to suppress TSH and shrink the gland.
  • Surgery is indicated only for cosmetic reasons or pressure symptoms.
• Cretinism: The neurological damage is permanent; treatment focuses on rehabilitation and managing hypothyroidism.

2. Interactions with Other Micronutrients

• Goitrogens: Substances in food (e.g., cabbage, cauliflower, cassava) interfere with iodine utilization.
• Selenium Deficiency: Selenium is required for the deiodinase enzyme (conversion of T4 to T3). Combined deficiency exacerbates hypothyroidism and causes myxedematous cretinism,.
• Iron Deficiency: Iron is a component of thyroid peroxidase; anemia impairs thyroid metabolism.

Prevention and Control

The goal is virtually virtual elimination of IDD. Prevention relies on increasing iodine intake in the entire population.

1. Recommended Daily Intake (RDA)

• Infants (0–12 months): 90 $\mu$g/day.
• Children (1–5 years): 90 $\mu$g/day.
• Children (6–12 years): 120 $\mu$g/day,.
• Adolescents and Adults: 150 $\mu$g/day,.
• Pregnant and Lactating Women: 200–250 $\mu$g/day (higher demand).

2. Universal Salt Iodization (USI)

• Strategy: This is the most successful global public health intervention. It involves fortification of all salt for human and animal consumption with iodine.
• Formulation: In India, Potassium Iodate ($KI{O}_3$) is used due to its stability in hot and humid climates.
• Targets (National Iodine Deficiency Disorders Control Program):
  • Manufacturing Level: Salt must contain 30 ppm (parts per million) of iodine,.
  • Consumer Level: Salt must contain 15 ppm of iodine to account for losses during transport and storage,,.
• Monitoring: Regular testing of salt samples using spot testing kits and monitoring urinary iodine in the population are essential components of the program.

3. Alternative Supplementation Strategies

• Double Fortified Salt (DFS): Salt fortified with both Iron and Iodine. This is an innovative strategy (e.g., tried in Andhra Pradesh) to tackle the dual burden of anemia and goiter simultaneously,.
• Iodized Oil: In areas of severe endemicity where iodized salt is not yet available or effective, oral or intramuscular administration of iodized oil (e.g., Lipiodol) can provide protection for 6–12 months.
• Water Iodization: Used in some specific small communities.

4. Public Health Education

• Storage of salt in closed containers to prevent iodine loss (iodine is volatile).
• Adding salt at the end of cooking to preserve iodine content.
• Promotion of consumption of sea foods.

Complications of Prophylaxis

• Iodism: Chronic toxicity manifesting as acneiform rash, metallic taste, and increased salivation.
• Jod-Basedow Phenomenon: Iodine-induced thyrotoxicosis, particularly in adults with pre-existing autonomous nodules who receive sudden high loads of iodine.