Obesity

Understanding BMI and weight classification

Note: BMI has limitations. It does not distinguish muscle from fat. A muscular person may have a high BMI without excess fat. For Asian populations, risk thresholds are lower (overweight: BMI ≥23; obese: BMI ≥27.5).

Waist circumference: why it matters more than weight

Central obesity (excess belly fat around organs) is more metabolically dangerous than subcutaneous fat (under the skin). A high waist circumference indicates visceral fat and predicts metabolic risk better than BMI alone.

Blood tests essential in obesity

Health conditions caused or worsened by obesity

• Type 2 diabetes: 80% of people with T2D are overweight or obese
• Cardiovascular disease: heart attack and stroke risk doubled
• Hypertension: 60% of obese people have high blood pressure
• Non-alcoholic fatty liver disease (NAFLD): 75% prevalence in obesity
• Obstructive sleep apnoea: most cases are obesity-related
• Osteoarthritis: each kg of weight lost reduces knee load by 4 kg
• Cancers: breast, colon, uterine, kidney and oesophageal cancer all increased
• PCOS: obesity worsens hormonal imbalance and insulin resistance
• Depression and anxiety: bidirectional relationship with obesity

Questions to ask your doctor

• What is my BMI and waist circumference?
• Do I have pre-diabetes or insulin resistance?
• Should I have a sleep study for sleep apnoea?
• Am I a candidate for weight loss medication (GLP-1 agonists)?
• Would I benefit from bariatric surgery?

References

The clinical information on this page is drawn from peer-reviewed sources indexed by the US National Library of Medicine. Links go to the source so you can read it yourself.

1. Obesity and Comorbid Conditions. In: StatPearls. Treasure Island (FL): StatPearls Publishing. NCBI Bookshelf NBK574535

References

Sources cited on this page. PubMed links open the original abstract.

1. GBD 2015 Obesity Collaborators. Health effects of overweight and obesity in 195 countries over 25 years. N Engl J Med. 2017;377(1):13–27. PMID 28604169 · doi:10.1056/NEJMoa1614362

Obesity as a chronic disease – the hormonal reality

Obesity is not simply a behavioural failure but a complex chronic disease driven by hormonal dysregulation, genetic predisposition, and environmental factors that override the simple "eat less, move more" framework. Key physiological mechanisms:

• Leptin resistance: Leptin – produced by adipose tissue – normally signals fullness to the hypothalamus. In obesity, leptin levels are very high (more fat = more leptin) but the brain becomes resistant to its signal, similar to insulin resistance in type 2 diabetes. The hypothalamus perceives starvation despite abundant energy stores, perpetuating hunger.
• Ghrelin dysregulation: Ghrelin – the hunger hormone – normally falls after eating. In people who have lost weight by caloric restriction, ghrelin fails to suppress normally, driving persistent hunger that can last for years after weight loss – a primary mechanism of weight regain after diet-induced loss.
• The "set point": Metabolic rate adapts downward during caloric restriction, reducing by 15–20% beyond what body composition changes alone would predict. This metabolic adaptation persists for years and is a key reason why long-term dietary weight loss is so difficult to maintain – the body actively fights to return to its previous weight.

Blood tests for obesity-related complications

• HbA1c and fasting glucose: Obesity is the primary driver of type 2 diabetes – 90% of type 2 diabetics are overweight or obese. Annual diabetes screening is recommended for BMI above 30 (or above 27.5 in South Asian individuals). HbA1c 42–47 mmol/mol = pre-diabetes; above 48 = diabetes.
• Fasting lipid panel: Obesity-associated dyslipidaemia typically shows raised triglycerides, low HDL, and elevated small dense LDL particles (more atherogenic than large LDL). Total LDL may appear normal while cardiovascular risk is increased – non-HDL cholesterol is a better risk marker in this context.
• Liver enzymes (ALT, GGT): Non-alcoholic fatty liver disease (NAFLD) affects approximately 70–80% of obese individuals. ALT is often mildly elevated. FIB-4 score stratifies fibrosis risk; FibroScan is recommended if FIB-4 is elevated.
• Blood pressure and urine ACR: Obesity is the most modifiable risk factor for hypertension and proteinuric kidney disease. Urine ACR should be checked annually in obese individuals with hypertension or diabetes – early CKD is often completely asymptomatic.
• Testosterone (men): Obesity causes hypogonadism through aromatase activity in fat tissue – converting testosterone to oestrogen. Low testosterone in obese men contributes to fatigue, low libido, depression, and further weight gain – a vicious cycle.

GLP-1 receptor agonists – a paradigm shift in obesity treatment

Semaglutide 2.4 mg weekly (Wegovy) and tirzepatide (Mounjaro) represent the first pharmaceutical treatments to achieve clinically meaningful sustained weight loss (15–25% of body weight) – approaching bariatric surgery outcomes. GLP-1 agonists work by slowing gastric emptying, increasing satiety, and directly signalling hypothalamic appetite centres. The STEP and SURMOUNT trials demonstrated that this weight loss class effect reduces cardiovascular events (SELECT trial: semaglutide reduced major cardiovascular events by 20% in obese adults without diabetes). NICE approved semaglutide 2.4 mg in 2023 for BMI ≥ 35 with at least one weight-related complication, or BMI 30–34.9 in specific populations.