Obesity
Exam Tips
- In UK OSCEs, combine BMI with waist-to-height ratio when BMI is <35 kg/m²; this improves central adiposity risk stratification.
- Remember ethnicity-adjusted BMI thresholds for South Asian, Chinese, other Asian, Middle Eastern, Black African, and African-Caribbean adults (risk occurs at lower BMI).
- State that a 5-10% weight loss is clinically meaningful and realistic; examiners reward risk-reduction framing rather than ideal-weight targets.
- When prescribing anti-obesity drugs, always mention contraindications (especially pregnancy) and adverse-effect counselling.
- Use respectful, non-judgemental language and shared decision-making; communication style is a frequent assessed domain.
- For examination technique, review a standard anthropometry diagram showing correct waist measurement midpoint (between lower rib and iliac crest) in your clinical skills textbook figures.
Definition
Obesity is a chronic, relapsing disease of excess adiposity (not just excess weight) that increases morbidity, mortality, and healthcare burden. In UK practice it is usually identified using BMI, with central adiposity (for example by waist-to-height ratio) used to refine cardiometabolic risk, especially when BMI is below 35 kg/m². Ethnicity-specific BMI thresholds are important because some groups develop metabolic complications at lower BMI values.
Pathophysiology
Obesity develops when long-term energy intake exceeds expenditure in a permissive biological and environmental context. Adipocyte hypertrophy and hyperplasia drive ectopic fat deposition (liver, muscle, visceral depots), adipose inflammation, altered adipokines (including leptin resistance and reduced effective satiety signalling), insulin resistance, and neurohormonal changes in hypothalamic appetite pathways. These mechanisms promote a self-reinforcing cycle of weight regain after weight loss, explaining why obesity behaves as a chronic disease requiring long-term management rather than a short-term willpower problem.
Risk Factors
- Energy-dense, ultra-processed diet; frequent fast food and sugar-sweetened drink intake
- Physical inactivity and high sedentary time
- Excess alcohol intake (especially binge-pattern drinking)
- Social deprivation, lower educational attainment, and obesogenic environment
- Psychological factors (for example depression, low self-esteem, emotional eating)
- Sleep deprivation
- Increasing age (particularly mid-late adulthood), perimenopause/menopause, and post-pregnancy weight retention
- Genetic susceptibility/family history (high heritability; appetite and energy-regulation genes)
- Secondary endocrine or hypothalamic causes (for example Cushing syndrome, hypothyroidism, hypothalamic injury)
- Weight-promoting medicines (for example corticosteroids, insulin, sulfonylureas, thiazolidinediones, some antipsychotics, some antidepressants, valproate, pregabalin, gabapentin, carbamazepine, beta-blockers, lithium)
Clinical Features
Symptoms
- Often asymptomatic initially
- Progressive weight gain and reduced exercise tolerance
- Breathlessness, snoring, unrefreshing sleep/daytime somnolence (possible OSA)
- Mechanical pain (knee/hip/back), reduced mobility
- Reflux symptoms
- Psychological distress, low mood, weight stigma-related impact on quality of life
- Menstrual irregularity/subfertility where PCOS coexists
Signs
- BMI in overweight/obesity range (use ethnicity-adjusted thresholds where appropriate)
- Increased waist-to-height ratio (>= 0.5 suggests increased central adiposity risk)
- Raised blood pressure
- Acanthosis nigricans (marker of insulin resistance)
- Features of complications: hepatomegaly/NAFLD signs, osteoarthritis gait limitation
- Features suggesting secondary cause: proximal myopathy/violaceous striae (Cushing), goitre/bradycardia (hypothyroidism)
Investigations
Management
Lifestyle Modifications
- Use person-centred, non-stigmatising discussion; agree realistic goals and readiness to change
- Target clinically meaningful loss (typically 5-10% initial body weight) to improve metabolic risk
- Create a calorie deficit with improved dietary quality (reduce ultra-processed foods, sugary drinks, and excess alcohol)
- Increase physical activity toward UK guidance (about 150 minutes/week moderate or 75 minutes vigorous, plus strength work)
- Reduce sedentary time, improve sleep, and include behavioural strategies (self-monitoring, relapse planning, social support)
- Treat comorbidities in parallel (diabetes, hypertension, OSA, mental health)
Pharmacological Treatment
Gastrointestinal lipase inhibitor
- Orlistat 120 mg orally three times daily with meals containing fat (omit dose if meal missed or fat-free)
Use with a nutritionally balanced, mildly hypocaloric diet; advise reduced-fat intake to limit GI adverse effects (steatorrhoea, urgency). Give multivitamin supplementation at bedtime (separate from dose). Contraindicated in chronic malabsorption syndrome and cholestasis; caution with ciclosporin, levothyroxine, and warfarin (monitor INR).
GLP-1 receptor agonist
- Liraglutide (Saxenda) SC once daily: start 0.6 mg daily, increase weekly by 0.6 mg to 3 mg daily maintenance
- Semaglutide (Wegovy) SC once weekly: 0.25 mg for 4 weeks, then 0.5 mg, 1 mg, 1.7 mg, then 2.4 mg weekly maintenance
Use as adjunct to diet and activity in eligible adults under specialist/structured weight-management pathways. Common adverse effects are nausea, vomiting, diarrhoea, and constipation; counsel on dehydration risk and possible gallbladder disease. Avoid in pregnancy and breastfeeding; stop if planning pregnancy. Use caution with pancreatitis history and severe GI disease.
Dual GIP/GLP-1 receptor agonist
- Tirzepatide (Mounjaro) SC once weekly: start 2.5 mg weekly for 4 weeks, then 5 mg weekly; may increase by 2.5 mg at >=4-week intervals to 10-15 mg weekly as needed
Adjunct to lifestyle intervention in eligible adults; monitor GI adverse effects, dehydration risk, and gallbladder events. Not for use in pregnancy; review contraception advice where relevant. In people using insulin or sulfonylurea for diabetes, hypoglycaemia risk may rise and background therapy may need adjustment.
Surgical / Interventional
- Bariatric/metabolic surgery (for example sleeve gastrectomy, Roux-en-Y gastric bypass, one-anastomosis gastric bypass) for eligible patients after specialist MDT assessment
- Requires lifelong nutritional monitoring and supplementation, and follow-up for surgical/metabolic complications
Complications
- Type 2 diabetes and insulin resistance
- Hypertension, coronary heart disease, and stroke
- Obstructive sleep apnoea and obesity hypoventilation risk
- Metabolic dysfunction-associated steatotic liver disease (fatty liver) and gallbladder disease
- Osteoarthritis and chronic musculoskeletal pain
- GORD
- Reproductive complications (subfertility, adverse pregnancy outcomes)
- Mental health conditions (depression, anxiety, stigma-related harm)
- Increased risk of some cancers (including breast, colorectal, and endometrial)
- Reduced life expectancy (greater reduction at higher BMI classes)
Prognosis
Prognosis improves with sustained weight reduction and risk-factor control; even 5-10% loss can produce meaningful metabolic and cardiovascular benefit. Relapse is common because biological adaptation favours weight regain, so long-term follow-up is essential. Bariatric surgery gives the most durable weight loss and comorbidity improvement in appropriately selected patients, while pharmacotherapy is effective during treatment but weight may rebound after discontinuation.
Sources & References
💊BNF Drug References(5)
- Agomelatine[cautions]
- Daptomycin[cautions]
- Enoxaparin sodium[cautions]
- Normal immunoglobulin[cautions]
- Pitolisant[cautions]
✅NICE Guidelines(1)
- Obesity[overview]
📖Textbook References(10)
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1250)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1249, 1250)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1428, 1429)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1820, 1821)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 26, 27)[context]
- Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 1011)[context]
- Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 874)[context]
- Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 873)[context]
- Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 129, 130)[context]
- Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 129, 130)[context]