Skip to content

Unified Comprehensive Notes on Obesity

1. Introduction

Obesity is a complex metabolic condition characterized by excessive body fat accumulation that adversely affects health. Its global prevalence has tripled since 1975, now involving adults and children in alarming numbers. Although rooted in caloric surplus and sedentary lifestyles, genetic factors significantly influence individual susceptibility and severity.

2. Definitions and Measurements

2.1 Obesity

  • General Definition: Excess adipose tissue mass that harms health.
  • Key Consideration: Not simply weight but fat distribution (particularly visceral fat) matters.

2.2 Body Mass Index (BMI)

  • Formula: BMI = weight (kg) / [height (m)]².
  • WHO Classification:
    • Overweight: 25.0–29.9 kg/m²
    • Obesity: ≥30.0 kg/m²
  • Asian Classification (often used cutoffs):
    • Underweight: <18.5
    • Normal: 18.5–22.9
    • Overweight: 23.0–24.9
    • Pre-obese: 25.0–29.9
    • Obese (Class 1): 30.0–39.9
    • Obese (Class 2): 40.0–49.9
    • Obese (Class 3): ≥50.0
  • Limitations:
    • Does not distinguish between lean mass and fat mass.
    • Ethnic and individual differences may alter risk thresholds.

2.3 Waist Circumference (WC) & Waist-Hip Ratio (WHR)

  • WC is a key measure of central (abdominal) obesity.
  • High visceral fat correlates strongly with cardiometabolic risk.
  • Asian Cutoffs:
    • Males: <90 cm
    • Females: <80 cm
  • WHR can provide additional data but often WC alone is sufficient for risk assessment.

2.4 Other Techniques

  • Skinfold thickness, bioelectrical impedance, underwater weighing, CT/MRI, DXA: More precise but less commonly used in routine clinical practice.

3. Epidemiology

  • Obesity prevalence has surged worldwide; over 650 million adults are obese, with millions of children also affected.
  • Rates have tripled since 1975.
  • The problem is evident across all age groups and socioeconomic strata.

4. Pathophysiology

Obesity arises from a chronic positive energy balance (excess intake > expenditure) in the context of complex neurohormonal, genetic, and environmental interactions.

4.1 Energy Balance

  • Energy Intake: Driven by appetite, psychological factors, food availability.
  • Energy Expenditure:
    1. Basal Metabolic Rate (BMR)
    2. Thermic Effect of Feeding
    3. Physical Activity
    4. Adaptive Thermogenesis (brown/beige fat)

4.2 Hypothalamic Regulation & Leptin

  • The hypothalamus integrates signals from:
    • Leptin (from adipose)
    • Ghrelin (stomach)
    • Insulin (pancreas)
    • Gut hormones (GLP-1, PYY, etc.)
  • Leptin normally suppresses appetite (via POMC → α-MSH → MC4R) and enhances energy expenditure. In obesity, leptin resistance often occurs.
  • AGRP/NPY neurons stimulate hunger; POMC neurons promote satiety. The balance of these pathways determines feeding behavior.

4.3 Brown Adipose Tissue & Adaptive Thermogenesis

  • Brown (BAT) and beige adipocytes can dissipate energy as heat (via UCP-1). Humans have limited BAT in adulthood; upregulation is an active research area.

4.4 Adipokines and Chronic Inflammation

  • Adipose tissue is an endocrine organ, secreting:
    • Leptin, Adiponectin (involved in insulin sensitivity, satiety)
    • TNF-α, IL-6, Resistin (pro-inflammatory)
  • Visceral obesity: Tends to have more pro-inflammatory secretions, contributing to insulin resistance, metabolic syndrome, and cardiovascular disease.

4.5 Genetic & Environmental Interactions

  • Monogenic obesity (rare): Leptin or leptin receptor deficiency, MC4R mutations, POMC deficiency, etc.
  • Syndromic obesity: Prader-Willi, Bardet-Biedl, etc.
  • Secondary causes: Hypothyroidism, Cushing’s, hypothalamic damage.
  • Environment: Calorie-dense foods, sedentary routines, stress, and socioeconomic factors.

5. Complications & Consequences

  1. Cardiovascular
    • Hypertension, coronary artery disease, stroke, heart failure
  2. Metabolic
    • Insulin resistance, type 2 diabetes (T2DM), dyslipidemia
    • NAFLD/NASH → cirrhosis
  3. Respiratory
    • Obesity hypoventilation, obstructive sleep apnea
  4. Musculoskeletal
    • Osteoarthritis, joint stress
  5. Cancer
    • Increased risk: colon, breast, endometrium, prostate, etc.
  6. Reproductive/Hormonal
    • PCOS (women), hypogonadism (men)
  7. Neurologic
    • Idiopathic intracranial hypertension
  8. Psychological/Social
    • Depression, anxiety, stigma, reduced quality of life

6. Key Takeaways

  • Obesity is a chronic disease shaped by genetics, environment, and physiology.
  • Visceral (central) fat confers especially high risk due to pro-inflammatory secretions.
  • High leptin often fails to curb appetite in obesity (leptin resistance).
  • Prevalence is rising globally in both adults and children.
  • Long-term management relies on lifestyle intervention, addressing environment, and in some cases pharmacotherapy or bariatric surgery.

7. Conclusion

Obesity is a major global health burden, driving increased morbidity and mortality across numerous organ systems. Its causes include an interplay of excess calories, sedentary lifestyle, genetic predisposition, and hormonal dysregulation. Effective management necessitates multifactorial interventions—addressing diet, physical activity, behavior, and, when indicated, medications or surgical options. Ongoing research aims to clarify mechanisms and improve both prevention and treatment strategies.