Obesity and weight management

• Obesity is a chronic, relapsing disease of excess and dysfunctional body fat. It is not simply a failure of willpower, and it raises the risk of type 2 diabetes, hypertension, dyslipidaemia, sleep apnoea, fatty liver disease, osteoarthritis and some cancers.
• Diagnosis and staging use body mass index (BMI) and, in most adults, waist-to-height ratio, read against ethnicity and age. Central adiposity matters as much as overall weight.
• Treatment is multimodal and lifelong: behavioural support and an energy deficit first; medicines such as orlistat, liraglutide, semaglutide and tirzepatide for eligible adults; bariatric surgery for those with severe obesity; and structured follow-up to prevent regain.
• Even a modest, sustained loss of about 5% of body weight improves blood pressure, lipids and glycaemia. The goal is health, not a single target weight.
• Obesity is a population-level problem too. Prevention, non-stigmatising communication and access to care matter as much as prescriptions.

By the end of this page you should be able to:

1. Define obesity, distinguish it from overweight, and classify an adult by BMI and by waist-to-height ratio, including ethnic adjustment and high muscle mass.
2. Describe how an obesogenic environment and disordered appetite regulation drive weight gain, and how excess adiposity produces complications.
3. Take a weight history and identify comorbidities, medications and secondary causes that need different management.
4. Distinguish generalised obesity from oedema, lipedema and endocrine or drug-induced weight gain.
5. Plan first-line investigations and set a realistic weight-loss target.
6. Choose between lifestyle care, pharmacotherapy and bariatric surgery using current eligibility criteria, and monitor each safely.
7. Adapt the approach for children, older adults, pregnancy and resource-limited settings.

BMI is weight divided by height squared (kg/m2). It is a practical screening measure, not a measurement of body fat. It should be read with caution in people with high muscle mass (who may be heavy but not overfat), in older adults (a slightly higher BMI can be protective) and in children (where age- and sex-adjusted centiles are used).^[1]

The World Health Organization recognises obesity as a chronic disease driven by obesogenic environments that limit access to healthy, affordable food and safe physical activity, compounded by inadequate health-system capacity for early identification and long-term care.^[2] It is characterised by dysregulation of neurobiological and metabolic pathways that govern appetite, energy balance and adipose-tissue function, with genetic variation influencing susceptibility.^[2]

This page covers overweight where it flows into obesity, but it concentrates on obesity and its management. It does not cover the surgical techniques of individual bariatric operations in detail.

Classify adults by BMI first, then add central adiposity and complications. That three-step staging is what turns a number into a management plan.^[1]

For adults with a BMI under 35 kg/m2, also measure waist-to-height ratio, because central (visceral) fat carries much of the risk.^[1]

A practical rule to give patients: keep the waist to less than half the height, so the ratio stays below 0.5. Waist is measured midway between the bottom of the ribs and the top of the hips, with the tape snug and the person breathing out.^[1]

In children and young people BMI must be read against age- and sex-adjusted charts.^[1][2]

Obesity is one of the great public-health problems of this century. According to the World Health Organization, in 2024 about 2.6 billion adults aged 18 or over were overweight, of whom 940 million (16% of all adults) lived with obesity; 45% of all adults were overweight. Worldwide adult obesity has more than doubled since 1990, adolescent obesity has quadrupled, and the prevalence of overweight in people aged 5 to 19 rose from 8% in 1990 to 20% in 2024.^[2] An estimated 35 million children under 5 were overweight in 2024.^[2] Overall, 1 in 7 people worldwide, 1.1 billion, now live with obesity.^[2]

The burden is not evenly spread. Higher-than-optimal BMI caused an estimated 3.7 million deaths in 2023 through cardiovascular disease, diabetes and cancer.^[2] NICE notes that lower BMI thresholds are needed for people from some ethnic minority backgrounds, because central adiposity and cardiometabolic risk occur at lower BMI in these groups.^[1] Prevalence varies by region, from about 32% of adults overweight in the WHO South-East Asia and African regions to about 68% in the Americas.^[2]

Older data from the United States, cited in the 2013 AHA/ACC/TOS guideline, found 69% of adults overweight or obese and 35% obese in 2009-2010.^[3] There is no single global template: in many low- and middle-income countries obesity now rises while undernutrition persists, creating a double burden of malnutrition.^[2]

Obesity arises from sustained positive energy balance in a susceptible person living in an obesogenic environment. Biology sets susceptibility; environment and social conditions set the scale of the problem.^[2]

Environmental and behavioural drivers include cheap, energy-dense, heavily marketed foods; larger portion sizes; sugar-sweetened beverages; low fruit, vegetable and fibre intake; sedentary work and leisure; reliance on motorised transport; poor sleep; high screen time; chronic stress; and social norms that favour weight gain. In low- and middle-income settings these changes occur on top of undernutrition, so childhood stunting and adult obesity can coexist in the same family or community.^[2]

Genetic and biological factors include family history, monogenic and polygenic obesity, neurobiological variation in appetite regulation, and differences in adipose-tissue function. There is no single obesity gene in most patients, but genes strongly modify responses to the same environment.^[2]

Medical and iatrogenic contributors should be sought in every patient, because they change management:

• Endocrine and metabolic disorders: hypothyroidism, Cushing syndrome, polycystic ovary syndrome, growth hormone deficiency, and hypothalamic disorders.
• Medications that promote gain: glucocorticoids, some antipsychotics and antidepressants, insulin and sulfonylureas, antiepileptics such as valproate, and some beta-blockers.
• Sleep and mental health: depression, binge-eating disorder and untreated obstructive sleep apnoea can all drive intake and weight gain.
• Life-course factors: excessive gestational weight gain, early adiposity rebound, and menopausal transition.

Not every heavy person has primary (idiopathic) obesity. Taking a full drug and endocrine history is part of the treatment, not an afterthought.

Socioeconomic and commercial factors are powerful. The AHA/ACC/TOS 2013 guideline noted higher obesity prevalence in ethnic minority groups and in people with lower income and less education.^[3] NICE asks services to identify these groups and to communicate risk in a non-stigmatising way.^[1]

Understanding the mechanism explains both the weight regain that frustrates patients and the complications that motivate treatment.

Energy balance is not symmetric. The body defends weight. When weight is lost, resting metabolic rate falls, appetite signals strengthen and reward-driven eating often intensifies. That is why obesity behaves as a chronic, relapsing condition: the physiological drive to regain weight persists long after the behaviour change.

Appetite is hormonal. Short-term satiety is driven by gut peptides (cholecystokinin, peptide YY, GLP-1, gastric inhibitory polypeptide) and gastric distension. Long-term energy stores are signalled mainly by leptin from adipose tissue. In common obesity, leptin resistance develops: levels are high but the brain under-responds, so satiety signalling fails even when energy stores are large. Insulin, cortisol and gut-brain signalling all modulate intake. GLP-1 agonists exploit this physiology by enhancing satiety signals and slowing gastric emptying.

Adipose tissue becomes dysfunctional. As stores expand, adipocytes enlarge and immune cells infiltrate. Adipokine profiles shift (lower adiponectin, higher leptin and inflammatory cytokines), leading to systemic low-grade inflammation and insulin resistance. Visceral (intra-abdominal) fat is more metabolically active than subcutaneous fat, which is why waist circumference and waist-to-height ratio add risk information beyond BMI.

Complications arise downstream. Insulin resistance drives type 2 diabetes and dyslipidaemia. Increased cardiac output and sodium retention raise blood pressure. Fatty infiltration of the liver produces metabolic dysfunction-associated steatotic liver disease. Mechanical loading produces osteoarthritis. Extra tissue around the airway and reduced lung volumes produce obstructive sleep apnoea. Low-grade inflammation and oestrogen production in adipose tissue contribute to some cancers.

Obesity itself does not have a single lesion seen under the microscope. Its pathology is the fat organ and its consequences: enlarged adipocytes, crown-like structures of macrophages around dying fat cells, fibrosis in long-standing cases, and ectopic fat in liver, muscle and pancreas. Fatty liver may progress to steatohepatitis, fibrosis and, rarely, cirrhosis. This is why liver enzymes and fibrosis assessment are part of the work-up in selected patients.

Most adults with obesity have no symptoms attributable to fat itself. They present because of complications, because of the weight itself, or because weight is noticed during another consultation.

History. Ask about:

• Weight trajectory: highest and lowest adult weight, timing of gain, rate of gain, previous losses and how regain happened.
• Eating pattern: usual diet, snacking, sugary drinks, alcohol, night eating, binge episodes, restriction, dieting history.
• Physical activity, sedentary time, sleep quality and duration, daytime sleepiness.
• Medications and past medical and psychiatric history; family history of obesity, diabetes and cardiovascular disease.
• Menstrual history and fertility; in women, ask about possible pregnancy and contraception when medicines are considered.
• Perception of weight, readiness to change, barriers (cost, time, access, stigma).

Examination. Measure BMI, waist circumference (and calculate waist-to-height ratio when BMI is under 35 kg/m2), blood pressure, and look for:

• Signs of secondary causes: thyroid changes, Cushingoid features, acanthosis nigricans.
• Oedema, ascites or venous insufficiency that can mimic fat.
• Skin: acanthosis nigricans, intertrigo, striae.
• Joints, gait, feet.
• Airway and neck circumference where sleep apnoea is suspected.
• Anthropometry should be recorded consistently, because trends matter more than single values.

Comorbidities to screen for include type 2 diabetes, hypertension, dyslipidaemia, coronary heart disease, obstructive sleep apnoea, asthma or COPD, metabolic dysfunction-associated steatotic liver disease, osteoarthritis, urinary incontinence, reflux, gallbladder disease, subfertility, depression, anxiety and stigma-related distress. Manage these as they are found; do not wait for weight loss first.^[1]

Not all weight gain is adiposity, and not all adiposity is primary obesity.

Investigations have two jobs: stage the adiposity and find the complications and secondary causes.

Anthropometry: height, weight, BMI, waist circumference when BMI is under 35 kg/m2, and waist-to-height ratio.^[1]

Core blood tests in most adults:

• Fasting glucose or HbA1c, to define glycaemic status. NICE labels non-diabetic hyperglycaemia as HbA1c 42 to 47 mmol/mol (6.0% to 6.4%) or fasting plasma glucose 5.5 to 6.9 mmol/litre.^[1]
• Lipid profile.
• Liver enzymes (alanine aminotransferase and gamma-glutamyl transferase), especially with central adiposity or suspected fatty liver.
• Creatinine and estimated glomerular filtration rate.
• Thyroid-stimulating hormone.
• Urinalysis, and consider microalbuminuria in those with diabetes or hypertension.

Further tests only when indicated: cortisol studies if Cushing syndrome is suspected; polysomnography or validated sleep questionnaires for sleep apnoea; fibrosis assessment (FIB-4 score, elastography) when liver disease is suspected; eating-disorder assessment; and psychological evaluation before surgery.

Avoid over-investigation. Bioimpedance is not a substitute for BMI. Imaging is not routine; reserve it for suspected complications or a genuine differential such as an endocrine tumour.

There is no single laboratory test that diagnoses obesity. The diagnosis rests on anthropometry plus the presence of adiposity-related impairment, and staging combines:

• BMI class and ethnic adjustment.^[1][2]
• Central adiposity by waist-to-height ratio when BMI is under 35 kg/m2.^[1]
• Comorbidity burden: risk-factor metabolic syndrome features, established cardiovascular disease, type 2 diabetes, sleep apnoea, fatty liver disease.
• Functional impact: symptoms, disability, quality of life.
• Readiness and barriers to change.

A useful bedside approach is to state three things in the record: the BMI class, the waist-to-height category if measured, and the principal comorbidities. That single line often carries more information than the word "obesity" alone.

Obesity management is chronic disease management. It should be offered with the same structure as hypertension or diabetes care: agree a goal, start a treatment, review, escalate.

Obesity rarely needs emergency treatment. The acute exceptions are complications: severe sleep apnoea with cor pulmonale, uncontrolled type 2 diabetes or hypertension, or venous thromboembolism. Treat these as their own conditions. Drugs that suppress appetite are not for acute weight loss.

Setting goals. Agree a small, meaningful target, often a 5% reduction in body weight, then maintain. Explain that 5% improves glycaemia, blood pressure and lipids, and that larger losses produce greater metabolic benefits. NICE asks clinicians to agree goals with the person and to review them, noting slower loss in people with type 2 diabetes.^[1]

Diet. The 2013 AHA/ACC/TOS guideline recommends fixing an energy target (usually 1200 to 1500 kcal/day for women and 1500 to 1800 kcal/day for men) or prescribing an energy deficit of 500 kcal/day, 750 kcal/day, or 30% of energy requirements, adjusted for body weight and activity.^[3] NICE adds a flexible approach: keep total energy intake below expenditure, with individualised macronutrient composition (low fat or low carbohydrate) and support from a dietitian.^[1] Low-energy diets of 800 to 1200 kcal/day are used only within specialist services for people living with obesity (with or without diabetes) or with overweight and type 2 diabetes; very-low-energy diets (under 800 kcal/day) only where there is a clinical need for rapid loss (for example, before surgery), and for no more than 12 weeks.^[1] For children, avoid restrictive diets alone; focus on healthy eating within a multicomponent plan.

Physical activity. NICE recommends raising activity even when weight does not change, because of cardiovascular and metabolic benefits. As a guide, 45 to 60 minutes of moderate-intensity activity a day may be needed to prevent obesity, and 60 to 90 minutes a day may be needed to avoid regaining weight after loss.^[1] Build up gradually with agreed goals, starting from everyday activity (brisk walking, cycling, stairs) and structured programmes where available, and reduce sedentary time. Children and young people who already have overweight or obesity may need more than standard recommendations.

Behavioural and psychological care. All dietary plans should be paired with behavioural strategies (goal setting, self-monitoring, stimulus control) and, where needed, psychological therapy. NICE asks services to address weight stigma, provide trained staff and non-stigmatising communication, and to offer support to maintain weight loss when medicines are stopped.^[1] Binge-eating disorder, depression and anxiety should be treated directly; medication alone rarely works in their presence.

Monitoring during lifestyle care. Review at 3 months; if less than about 5% weight loss is achieved, intensify or add pharmacotherapy. Check blood pressure, lipids and HbA1c so that improvement, not just weight, is tracked.

Medicines are an adjunct to, never a replacement for, diet, activity and behavioural support. All licensed obesity medicines should be used alongside a reduced-calorie diet and increased physical activity.^[1]

How to choose. NICE groups eligibility by BMI, comorbidity and setting (see table). In general:

• Orlistat: BMI 30 kg/m2 or more, or BMI 28 kg/m2 or more with risk factors, in all settings.^[1]
• Tirzepatide: BMI at least 35 kg/m2 plus at least one weight-related comorbidity, prescribed in primary care or specialist services; lower thresholds (reduced by 2.5 kg/m2) for some ethnic minority backgrounds.^[1]
• Semaglutide: BMI 35 kg/m2 or more, or BMI 30-34.9 kg/m2 with criteria for referral to specialist services, with at least one comorbidity; prescribed within specialist services.^[1]
• Liraglutide: BMI 35 kg/m2 or more with non-diabetic hyperglycaemia and high cardiovascular risk; prescribed by specialist services.^[1]

Shared decision-making, contraindications, cost and availability should guide the final choice. Effective drug treatment is currently dominated by GLP-1 receptor agonists.

Class effects of GLP-1 agonists (liraglutide, semaglutide, tirzepatide): nausea, vomiting, diarrhoea and constipation are common, especially during dose escalation, and usually settle with slower titration. Serious risks include acute pancreatitis, acute gallbladder disease (cholelithiasis, cholecystitis), acute kidney injury from volume depletion, hypoglycaemia when used with insulin or insulin secretagogues, and severe gastrointestinal reactions (they are not recommended in severe gastroparesis). Tirzepatide severe gastrointestinal adverse reactions occurred in 1.7%, 2.5% and 3.1% at 5, 10 and 15 mg versus 1% with placebo. Semaglutide and liraglutide carry similar cautions.^[5][6][7]

Thyroid C-cell tumour boxed warning. All GLP-1 agonists mentioned carry a boxed warning for thyroid C-cell tumours in rodents; they are contraindicated with a personal or family history of medullary thyroid carcinoma or Multiple Endocrine Neoplasia type 2. Routine calcitonin monitoring is of uncertain value. Counsel patients on symptoms of thyroid masses.^[5][6][7]

Administration points to teach:

• Wegovy injections are given subcutaneously in the abdomen, thigh or upper arm, once weekly, with or without food, escalating every 4 weeks; if 2 or more doses are missed, restart at a lower dose. Wegovy tablets are taken in the morning on an empty stomach, with water, 30 minutes before food or other medicines. ^[5]
• Zepbound is injected once weekly in the abdomen, thigh or upper arm; a missed dose can be taken within 4 days. It delays gastric emptying, so give standard preoperative advice for patients needing anaesthesia. ^[6]
• Saxenda is injected once daily at any time without regard to meals; if more than 3 days are missed, re-titrate from 0.6 mg. ^[7]
• Pregnancy and contraception: GLP-1 medicines are stopped when pregnancy is recognised; tirzepatide requires contraceptive review around initiation and each dose escalation. All three are avoided in pregnancy.
• Regular monitoring should reinforce adherence and include weight, comorbidities and adverse effects.^[1]

Surgery is the most effective treatment for severe obesity and obesity with metabolic disease, offered within a pathway with preoperative assessment, counselling and lifelong follow-up.

Who to refer. NICE offers referral for comprehensive assessment in specialist obesity services to adults with BMI 40 kg/m2 or more, or BMI 35 to 39.9 kg/m2 with a significant health condition that could improve if they lost weight (for example, cardiovascular disease, hypertension, idiopathic intracranial hypertension, fatty liver disease, obstructive sleep apnoea, type 2 diabetes), who agree to long-term follow-up after surgery.^[1] Lower thresholds apply (BMI reduced by 2.5 kg/m2) for South Asian, Chinese, other Asian, Middle Eastern, Black African and African-Caribbean backgrounds.^[1] Expedited assessment is offered for BMI 35 kg/m2 or more with recent-onset (within the last 10 years) type 2 diabetes, and considered for BMI 30 to 34.9 kg/m2 with recent-onset type 2 diabetes.^{[1] [3]}

The ASMBS and IFSO 2022 consensus recommends surgery for BMI more than 35 kg/m2 regardless of comorbidity, and says it should be considered for metabolic disease at BMI 30 to 34.9 kg/m2. It states that BMI more than 25 kg/m2 suggests clinical obesity and that individuals with BMI more than 27.5 kg/m2 should be offered surgery in Asian populations, and that appropriately selected children and adolescents should be considered. It notes that BMI more than 40 kg/m2, or BMI more than 35 kg/m2 with comorbidities, is the historical NIH (1991) threshold still applied by many insurers.^{[4] [1]}

These cut-offs differ between regional guidance and the wider surgical consensus. That is an honest disagreement. Follow local criteria and be transparent with patients.

Preoperative care. A multidisciplinary team (medical, nutritional, psychological and surgical) assesses medical needs, nutritional status, eating behaviour, psychological readiness, previous attempts, factors affecting response such as deprivation, neurodiversity and language, fitness for anaesthesia, and perioperative arrangements.^[1] Discuss benefits, risks including mortality and complications, long-term requirements and family needs. Rare (sometimes treatable) genetic causes should be screened in young people. Medicines may be used to maintain or reduce weight if surgical waiting times are excessive.^[1]

The operation. Common procedures are gastric bypass, sleeve gastrectomy and gastric banding, chosen jointly with the patient according to severity, comorbidities, evidence for long-term effect, facilities and surgeon experience.^[1] All of them reduce stomach capacity or absorption (or both), and all require lifelong nutritional follow-up.

Postoperative and longer-term follow-up. Offer a follow-up care package for at least 2 years within the bariatric service, including monitoring of nutritional intake (including protein and vitamins) and mineral deficiencies, monitoring of comorbidities, medications review, individualised dietary and nutritional support, advice on physical activity, psychological support and information on support groups. After discharge, offer at least annual monitoring of nutritional status and appropriate supplementation under shared care with primary care.^[1]

Outcomes. Bariatric surgery produces sustained weight loss, remission of type 2 diabetes in many patients, and improvement of hypertension, dyslipidaemia, sleep apnoea and fatty liver. Long-term results consistently demonstrate safety and efficacy.^[4] Complications include staple-line leaks, bleeding, infection, internal hernia, nutritional deficiencies (iron, B12, folate, calcium, vitamin D, thiamine), dumping syndrome and weight regain; revisional surgery has a higher complication rate. Only experienced surgeons in specialist centres should undertake revision.

The complications of obesity are why we treat it. They are driven by insulin resistance, inflammation, mechanical load and endocrine changes.

• Metabolic: type 2 diabetes, dyslipidaemia, metabolic syndrome, metabolic dysfunction-associated steatotic liver disease, which may progress to steatohepatitis and fibrosis.
• Cardiovascular: hypertension, coronary heart disease, stroke, atrial fibrillation, heart failure.
• Musculoskeletal: osteoarthritis of knees, hips and spine; back pain; reduced mobility.
• Gastrointestinal: gallbladder disease, reflux, fatty liver.
• Renal: chronic kidney disease, particularly with diabetes and hypertension.
• Reproductive: polycystic ovary syndrome, subfertility, gestational diabetes, pre-eclampsia, complications of pregnancy and delivery.
• Neoplastic: increased risk of several cancers including endometrium, post-menopausal breast, colorectum, kidney, oesophagus, liver, pancreas, gallbladder, thyroid and multiple myeloma.
• Mental health and stigma: depression, anxiety, eating disorders, impaired quality of life, discrimination.
• Higher all-cause and cardiovascular mortality, particularly with central adiposity.

A useful clinical habit is to list the complications a patient already has, then treat them directly rather than assuming weight loss alone will fix them. Diabetes medicines, antihypertensives and statins should be started when indicated; NICE is explicit that comorbidities should be managed as soon as they are identified, without waiting for weight loss.^[1]

Obesity is a chronic disease with a variable course. Modest, sustained changes improve outcomes. A loss of 5% of body weight typically lowers triglycerides and blood pressure and improves glycaemia; larger losses produce greater gains. Regain is common, because biology drives it, so maintenance (activity, follow-up, medication or surgery) matters as much as loss. Surgery gives the largest and most durable loss in severe disease but still requires lifelong follow-up.

Mortality rises with BMI, especially with central adiposity and metabolic comorbidity. Treating cardiometabolic risk factors directly reduces that risk independently of weight change.

Obesity should be prevented and identified early, without stigma. WHO positions obesity as a societal rather than individual responsibility: food systems, built environments, marketing, pricing and fiscal policy shape choice. Health practitioners need to routinely assess weight status; provide evidence-based counselling on healthy diet, physical activity and sleep to all; assess obesity-related complications and other non-communicable disease risk factors; and deliver or refer to comprehensive, person-centred multimodal chronic care.^[2]

In practice:

• Measure and record BMI and, in adults with BMI under 35 kg/m2, waist-to-height ratio at routine opportunities (registration, long-term condition reviews), with permission.^[1]
• Use non-stigmatising, person-first language and ask permission before weighing or discussing weight. Avoid diagnostic overshadowing (every symptom is not caused by weight).^[1]
• Build prevention into the life course: healthy weight before pregnancy, appropriate gestational weight gain, exclusive breastfeeding for 6 months, healthy eating and activity, sleep and limited screen time in childhood, and support for older adults.^[2]
• Use community networks to reach ethnic minority and socially disadvantaged groups, who face higher risk at lower BMI.^[1][2]
• Keep services accessible: screening should lead to referral and support, not judgement.

Children and young people. Use age- and sex-adjusted charts. Implement multicomponent, family-based interventions rather than restrictive diets alone. Orlistat is generally reserved for 12 years and older with comorbidities, started in a specialist paediatric setting; other medicines are not generally recommended below 12 years, and surgery only in exceptional circumstances after physiological maturity.^[1] Address bullying, self-esteem and school performance. WHO notes obesity persists into adulthood and should be identified and treated early.^[2]

Pregnancy. Avoid intentional weight loss during pregnancy. Counsel on gestational weight gain, diet and safe activity. All GLP-1 medicines are avoided in pregnancy; women of childbearing potential need contraceptive planning, particularly around tirzepatide dose changes.^[5][6][7] Bariatric surgery requires specific preconception and pregnancy advice.

Older adults. Interpret BMI with caution; a slightly higher BMI can be protective when frail. Focus on function, sarcopenia and comorbidities. Micronutrient supplementation may be needed if intake is poor or after surgery.

Ethnic minority and socially disadvantaged groups. Apply lower BMI thresholds, recognise earlier central adiposity, communicate risk in a non-stigmatising way, and address barriers to engagement. Use community-based delivery where possible.^[1][2]

Mental health conditions. Binge-eating disorder, depression and anxiety reduce treatment response if ignored. Integrate psychological support into pathways.

• BMI and, in lower BMI ranges, waist circumference or waist-to-height ratio are the only assessment tools needed; both can be measured with a tape.
• Base management on dietary advice (reduce energy-dense foods and sugary drinks, increase legumes, vegetables, fruit and whole grains), activity, and behavioural support delivered by trained lay or primary-care staff.
• Orlistat is cheap and widely available, but its benefit is modest; adherence and diet matter.
• GLP-1 medicines and surgery are often unaffordable or unavailable. Use them where access exists, and arrange referral to specialist centres when possible. WHO's 2025 guideline supports including GLP-1 therapy as one component of multimodal chronic obesity care where accessible.^[2]
• Build community and peer support, and avoid stigma in public messaging.
• Refer red flags: severe sleep apnoea, failed medical management in severe obesity, and genetic or syndromic obesity in childhood.

• Obesity is a chronic, relapsing disease of excess adiposity, not a personal failure.
• Classify adults by BMI plus waist-to-height ratio (when BMI is under 35) and ethnic adjustment.
• Central adiposity at a normal BMI still raises cardiometabolic risk.
• Causes are obesogenic environments acting on biological susceptibility; screen for endocrine and iatrogenic contributors.
• Complications cluster around insulin resistance, inflammation, mechanical load and some cancers.
• Lifestyle care is multimodal: energy deficit, activity, behavioural support and non-stigmatising care.
• Standard energy targets are 1200 to 1500 kcal/day for women and 1500 to 1800 kcal/day for men, or a deficit of 500 to 750 kcal/day, with 45 to 90 minutes of daily activity depending on goal.
• Orlistat, liraglutide, semaglutide and tirzepatide differ in route, dose and eligibility, but all are adjuncts to lifestyle change.
• GLP-1 agonists work by satiety biology; watch for pancreatitis, gallbladder disease, renal injury, gastroparesis and the shared thyroid C-cell boxed warning.
• Surgery is the most effective treatment for severe obesity, with criteria around BMI 35 to 40 kg/m2 and ethnic adjustment, and requires lifelong follow-up.
• Treat comorbidities directly, without waiting for weight loss.
• Aim for health: a 5% loss is clinically meaningful.
• Prevention, early identification and equity are part of clinical care.

Obesity sits beside type 2 diabetes, dyslipidaemia, hypertension, metabolic dysfunction-associated steatotic liver disease, obstructive sleep apnoea, cardiovascular disease prevention, polycystic ovary syndrome and bariatric surgery. These topics cover the complications and comorbidities in their own right.