Obesity in Childhood

Childhood obesity is a complex, multifactorial chronic disease defined by excess body fat (adiposity) sufficient to impair health. It is emerging as a serious public health challenge in developing countries like India, coexisting with undernutrition, a phenomenon termed the "Double Burden of Malnutrition".

1. Definition and Classification

Obesity is defined as an excess of body fat. Since direct measurement of body fat is difficult in clinical settings, Body Mass Index (BMI) is the standard proxy used for assessment.

• Formula: $BMI=\frac{Weight(kg)}{Height(m{)}^2}$
• Adiposity Rebound: BMI is high in infancy, decreases to a nadir around 5–6 years, and then increases through adolescence. This physiological rise is called "adiposity rebound". Early adiposity rebound is a risk factor for adult obesity.

Diagnostic Criteria:

• Children < 2 Years (WHO Standards):
  • Overweight: Weight-for-length > +2 SD (Standard Deviations).
  • Obesity: Weight-for-length > +3 SD.
  • Note: The WHO charts are considered "standards" describing how children should grow under optimal conditions.
• Children 2–19 Years (CDC 2000 / WHO Reference):
  • Overweight: BMI $\ge$ 85th percentile and < 95th percentile for age and sex.
  • Obesity: BMI $\ge$ 95th percentile for age and sex.
  • Severe Obesity: BMI $\ge$ 120% of the 95th percentile OR BMI $\ge$ 35 kg/m² (whichever is lower).
• IOTF Classification: The International Obesity Task Force (IOTF) links child BMI centiles to adult cut-offs.
  • Centile curve passing through BMI 25 kg/m² at age 18 defines Overweight.
  • Centile curve passing through BMI 30 kg/m² at age 18 defines Obesity.

2. Epidemiology

• Global: The prevalence has increased dramatically, often described as an "epidemic". In the US, prevalence increased by 300% over 40 years.
• India: There is a steep rise in urban areas and among affluent families.
  • According to NFHS-5 (2019-21), about 4% of children aged 5–9 years are overweight/obese. In the 10–19 years group, the prevalence is 5%.
  • Tracking: Obesity tracks strongly into adulthood; 50–80% of obese children become obese adults.

3. Etiopathogenesis

Obesity results from a chronic imbalance where energy intake exceeds energy expenditure.

A. Energy Balance and Environmental Factors

• Energy Intake:
  • Obesogenic Diet: Increased consumption of energy-dense, micronutrient-poor foods ("junk food") high in fat, sugar, and salt (e.g., fast foods, sweetened beverages).
  • Portion Sizes: Larger portion sizes contribute to passive overconsumption.
• Energy Expenditure:
  • Sedentary Lifestyle: Reduced physical activity due to academic pressure, lack of open spaces, and mechanized transport.
  • Screen Time: Excessive viewing of TV, mobile, and computers decreases metabolic rate and increases snacking. TV viewing is reported to increase obesity risk by 2% per hour of viewing.

B. Biological and Genetic Factors

• Polygenic Obesity: Common obesity is usually polygenic, resulting from the interaction of multiple susceptible genes with an obesogenic environment.
• Monogenic Obesity: Rare defects in the leptin-melanocortin pathway.
  • Leptin Deficiency: Severe early-onset obesity due to mutations in the LEP gene. Leptin is an adipokine that signals satiety to the hypothalamus.
  • MC4R Deficiency: The most common cause of monogenic obesity, characterized by hyperphagia.
• Syndromic Obesity:
  • Prader-Willi Syndrome: Hypotonia, mental retardation, short stature, and insatiable appetite (hyperphagia) due to deletion of paternal chromosome 15q11-13.
  • Laurence-Moon-Biedl Syndrome: Obesity, retinitis pigmentosa, polydactyly, and hypogonadism.
• Endocrine Causes: Rare (<1% of cases).
  • Hypothyroidism: Short stature with weight gain.
  • Cushing Syndrome: Central obesity, moon face, hypertension, striae, and growth arrest.
  • Growth Hormone Deficiency: Reduced lean body mass and increased adiposity.

C. Fetal Programming (Barker’s Hypothesis)

• FOAD: Fetal Origins of Adult Disease hypothesis suggests that intrauterine malnutrition (leading to Low Birth Weight or IUGR) programs the fetus for survival in a scarce environment ("Thrifty Phenotype").
• Mismatch: When these infants are exposed to nutrient abundance postnatally, they develop rapid "catch-up growth," leading to central adiposity, insulin resistance, and metabolic syndrome later in life.

4. Clinical Assessment

A. History

• Dietary History: 24-hour recall to assess caloric intake, frequency of fast food/sweetened beverages, and family eating patterns.
• Physical Activity: Duration of moderate-to-vigorous activity vs. sedentary screen time.
• Family History: Obesity in parents (strong predictor), type 2 diabetes, early cardiovascular disease.
• Review of Systems: Snoring/sleep apnea, hip/knee pain, polyuria/polydipsia, irregular menses.

B. Physical Examination

• Anthropometry: Weight, Height, BMI.
  • Constitutional Obesity: Tall stature (height > 50th percentile) and advanced bone age.
  • Pathological/Endocrine Obesity: Short stature or slowing growth velocity suggests an underlying organic cause (e.g., Cushing's, Hypothyroidism).
• General Signs:
  • Acanthosis Nigricans: Dark, velvety thickening of skin on the neck and axilla; a marker of insulin resistance.
  • Blood Pressure: Essential to screen for hypertension using appropriate cuff size.
  • Dysmorphism: Check for features of syndromes (e.g., polydactyly, retinal issues).
• Systemic Exam: Hepatomegaly (fatty liver), tonsillar hypertrophy (OSA), orthopedic abnormalities (Blount disease, slipped capital femoral epiphysis).

C. Laboratory Evaluation

Routine screening is recommended for children with BMI $\ge$ 85th percentile (overweight) who have risk factors, or all children with BMI $\ge$ 95th percentile.

• Metabolic Screen: Fasting lipid profile (Cholesterol, Triglycerides, HDL, LDL), Fasting blood glucose, HbA1c, Liver function tests (ALT/AST for NAFLD).
• Endocrine Workup: TSH, Free T4, Cortisol (only if growth failure/clinical suspicion exists).

5. Comorbidities

Obesity affects nearly every organ system:

• Metabolic:
  • Metabolic Syndrome: A cluster of central obesity, hypertension, dyslipidemia, and glucose intolerance.
  • Type 2 Diabetes: Rising incidence in adolescents; linked to insulin resistance.
• Gastrointestinal:
  • NAFLD (Non-Alcoholic Fatty Liver Disease): Most common chronic liver disease in children; can progress to steatohepatitis (NASH) and cirrhosis.
  • Gallstones.
• Respiratory:
  • Obstructive Sleep Apnea (OSA): Caused by fat deposition in the pharyngeal wall; presents with snoring and daytime somnolence.
  • Pickwickian Syndrome: Obesity hypoventilation syndrome with cyanosis and heart failure (rare).
• Orthopedic: Slipped Capital Femoral Epiphysis (SCFE), Blount disease (tibia vara), flat feet.
• Psychosocial: Poor self-esteem, depression, body image dissatisfaction, and social stigmatization (bullying).
• Cardiovascular: Hypertension, left ventricular hypertrophy, early atherosclerosis.

6. Management

The goal is usually weight maintenance (allowing height to catch up) or slow weight loss, depending on severity and age.

A. Dietary Management

• Balanced Diet: Use the "Traffic Light" approach:
  • Green (Go): Fruits, vegetables, whole grains (consume freely).
  • Yellow (Caution): Dairy, staples, lean meat (consume in moderation).
  • Red (Stop): Fried foods, sweets, sugary drinks (avoid/limit rare treats).
• Modifications:
  • Eliminate sugar-sweetened beverages (sodas, juices).
  • Control portion sizes.
  • Increase fiber intake.
  • Regular meals (breakfast is mandatory) and family meals.
• Caloric Restriction: For older children/adolescents with severe obesity, a deficit of 600 kcal/day or a 1200–1500 kcal diet may be prescribed under supervision.

B. Physical Activity and Lifestyle

• Activity: Minimum of 60 minutes of moderate-to-vigorous physical activity daily.
• Screen Time: Limit non-academic screen time to < 2 hours/day. No screen time for children < 2 years.
• Sleep: Ensure adequate sleep duration, as sleep debt increases ghrelin (hunger) and decreases leptin.

C. Behavioral Modification

• Cognitive Behavioral Therapy (CBT): Focuses on self-monitoring (food diaries), stimulus control (removing junk food from home), and goal setting.
• Family Involvement: Interventions are most successful when the entire family changes habits, not just the child.

D. Pharmacotherapy

Drug therapy is limited in children and usually reserved for adolescents with severe obesity who fail lifestyle interventions.

• Orlistat: Lipase inhibitor that reduces fat absorption. Approved for children > 12 years (FDA) or < 16 years (some guidelines). Side effects: Steatorrhea, gas.
• Metformin: Used off-label for insulin resistance; modest weight reduction.

E. Bariatric Surgery

Considered only for adolescents who have reached skeletal maturity (Tanner stage IV/V) with:

• BMI $\ge$ 40 kg/m², OR
• BMI $\ge$ 35 kg/m² with serious comorbidities (e.g., severe OSA, Type 2 Diabetes).
• Procedures include Roux-en-Y gastric bypass or Sleeve gastrectomy.

7. Prevention

• Primordial Prevention: Preventing the emergence of risk factors.
  • Life Cycle Approach: Ensure optimal maternal nutrition (prevent LBW), encourage exclusive breastfeeding for 6 months (protective effect), and timely complementary feeding.
  • Growth Monitoring: Identifying upward crossing of centiles (e.g., BMI rebound) early.
• Societal/Policy: Regulating junk food marketing, labeling (traffic light system on packs), ensuring playgrounds in schools, and promoting "Malnutrition Free India".