I-5. Prevalence, causes and definition of obesity

肥満の有病率・原因・定義

Prevalence

Rising in all countries, having tripled since 1975 — pandemic proportions.
More than 1.9 billion people are overweight, 650 million obese.
Except sub-Saharan Africa and parts of Asia, obese people outnumber underweight worldwide.
Increasing among children.

Definition & Measurement

Obesity = chronic condition of excess body fat that poses a health risk.
Anthropometric measures:
- BMI (kg/m²): good at population level, cheap, reliable, but weaker for individuals.
- Circumferences: waist-to-hip ratio, waist circumference (men >102 cm, women >88 cm) — add information on body composition.
Body-fat estimation: skinfold thickness, bioelectrical impedance, densitometry.

Classification	BMI (kg/m²)	Comorbidity risk
Underweight	< 18.5	Increased (other)
Normal	18.5–24.9	Average
Overweight	25.0–29.9	Mildly increased
Obesity I	30.0–34.9	Moderate
Obesity II	35.0–39.9	Severe
Obesity III	≥ 40	Very severe

Energy Metabolism

Glucose enters the portal circulation → liver, where it is stored as glycogen or directed to lipogenesis (TAG). Remaining glucose goes to the systemic circulation for ATP/glycogen in other organs, or to adipose tissue (lipid storage is the most efficient energy store).
Insulin (pancreatic β-cells): promotes glucose→glycogen and glucose→lipid conversion (liver, fat), and GLUT4-mediated uptake into muscle/fat — directs post-meal calories into storage.

Appetite regulation (short-term, GI-derived)

Stomach stretch → vagal signal → hypothalamic appetite center.
Incretins (GIP, GLP): cause satiety. Insulin: acts on CNS. Ghrelin: released from empty stomach (hunger). Leptin: from adipose tissue when TAG stores full → ↑energy expenditure (BMR).
Regulation is designed for short-term imbalances. Chronically high leptin/incretin levels lose their appetite-regulating ability.

Causes of Positive Energy Balance

Intake > expenditure (physical activity + BMR) → weight gain.

Genetic: monogenic (few large-effect genes — appetite/receptor mutations: leptin, melanocortin), syndromic (e.g. Prader-Willi, dysregulated ghrelin), polygenic (PPARγ, FTO).
Epigenetic: DNA methylation, histone modification, ncRNA, plus metabolic imprinting (mothers with metabolic hardship, rapid neonatal weight gain).
Age: weight ↑ until ~65 (↓BMR, ↑fat), pregnancies, menopause.
Hormonal: hypothyroidism (half obese), Cushing’s (almost all obese), GH deficiency, insulinoma, hypothalamic disorders.
Psychiatric: depression, bulimia.
Medications: antipsychotics, antidepressants, sedatives/anxiolytics, β-blockers, antidiabetics, steroids.

Socio-economic Background

Westernization: less home cooking, high-calorie fast food, ↓physical activity, sedentary leisure.
Local environment: urbanization, density of fast-food chains, poor walkability.
Food industry: larger portions, processed high-fat/sugar food, sweetened beverages.
Politics: historically overcoming famine — now regulating the food industry, taxing unhealthy food, reducing inequality.
Healthcare: guidelines.

一問一答

▶What are the BMI cutoffs for overweight and the obesity classes?

Overweight 25.0–29.9; Obesity I 30.0–34.9; Obesity II 35.0–39.9; Obesity III ≥40 kg/m² (normal 18.5–24.9).

▶How is obesity defined?

A chronic condition of excess body fat that poses a health risk.

▶What waist circumference thresholds indicate increased risk?

Men >102 cm and women >88 cm; waist-to-hip ratio and waist circumference add information on body composition.

▶What is the fundamental cause of obesity (energy balance)?

A positive energy balance: intake exceeds expenditure (physical activity + BMR) → weight gain.

▶What are the strengths and weaknesses of BMI?

Good at the population level, cheap and reliable, but weaker for assessing individuals (doesn't capture body composition).

▶What is the role of insulin in energy storage?

It promotes glucose→glycogen and glucose→lipid conversion (liver, fat) and GLUT4-mediated uptake into muscle/fat, directing post-meal calories into storage.

▶Why does appetite regulation fail in chronic obesity?

The system is designed for short-term imbalances; chronically high leptin/incretin levels lose their appetite-regulating ability (resistance).

▶Which hormones regulate short-term appetite and what are their effects?

Incretins (GIP, GLP) and insulin cause satiety; ghrelin (from the empty stomach) signals hunger; leptin (from full TAG stores) increases energy expenditure.

▶What are the genetic categories of obesity?

Monogenic (large-effect appetite/receptor mutations — leptin, melanocortin), syndromic (e.g., Prader-Willi — dysregulated ghrelin), and polygenic (PPARγ, FTO).

▶What is metabolic imprinting in obesity?

An epigenetic effect: mothers with metabolic hardship and rapid neonatal weight gain predispose offspring to obesity (via DNA methylation, histone modification, ncRNA).

▶Which hormonal disorders cause secondary obesity?

Hypothyroidism (half are obese), Cushing's syndrome (almost all obese), GH deficiency, insulinoma, and hypothalamic disorders.

▶Which medication classes promote weight gain?

Antipsychotics, antidepressants, sedatives/anxiolytics, β-blockers, some antidiabetics, and steroids.

▶How does age affect body weight?

Weight tends to increase until about age 65 (decreasing BMR, increasing fat), influenced also by pregnancies and menopause.

▶What socio-economic factors drive the obesity pandemic?

Westernization (less home cooking, high-calorie fast food, sedentary lifestyle), obesogenic local environments, and a food industry favoring large portions and processed high-fat/sugar foods.

▶How has obesity prevalence changed globally?

It has tripled since 1975 (pandemic proportions): >1.9 billion overweight and 650 million obese, with obese people now outnumbering underweight in most regions.

▶What methods estimate body fat beyond anthropometry?

Skinfold thickness, bioelectrical impedance, and densitometry.

▶Why is fat the most efficient energy store, and how is dietary glucose routed?

Glucose enters the portal circulation → liver (glycogen or lipogenesis to TAG); the rest goes to other organs for ATP/glycogen or to adipose tissue, where lipid is the most efficient store.

▶How does the stomach signal satiety in the short term?

Stomach stretch sends a vagal signal to the hypothalamic appetite center.

▶What psychiatric conditions are associated with obesity?

Depression and bulimia.

▶What political and healthcare measures address obesity?

Regulating the food industry, taxing unhealthy food, reducing inequality, and providing clinical guidelines.