Lucan · Conditions

Adult obesity management

Australian guidance: ADS Australian Obesity Management Algorithm 2025

1. Definition and epidemiology

Obesity is a complex, multifactorial chronic disease with genetic, environmental, physiological and behavioural determinants requiring long-term management. In 2022, 65.8% of Australians aged 18 years and over were above a healthy weight, with 31.7% having obesity. The estimated direct and indirect costs of obesity in Australia reached $11.8 billion in 2018.

2. Pathophysiology

Obesity arises from chronic positive energy balance that leads to adipocyte hypertrophy and hyperplasia, with visceral fat accumulation driving the greatest metabolic risk (Robbins Ch 24). Adipose tissue is metabolically active, secreting pro-inflammatory adipokines including tumour necrosis factor alpha and interleukin-6, while leptin resistance develops centrally, impairing satiety signalling. Insulin resistance follows ectopic lipid deposition in skeletal muscle and liver, creating a substrate for type 2 diabetes and dyslipidaemia. Genetic susceptibility accounts for a substantial proportion of variance in body mass, mediated through classical single-gene mutations and epigenetic mechanisms; this underpins why weight bias attributing obesity entirely to behavioural choice is both clinically inaccurate and a barrier to care.

3. Clinical presentation and diagnostic criteria

Patients typically present with weight gain over months to years, fatigue, dyspnoea on exertion, and symptoms attributable to comorbidities such as obstructive sleep apnoea, osteoarthritis or gastro-oesophageal reflux. Examination should document body mass index (BMI) and waist circumference (WC). In Australia the standard diagnostic thresholds remain BMI 25.0 to 29.9 kg/m2 for overweight and BMI 30 kg/m2 or above for obesity. Abdominal obesity is defined as WC greater than 88 cm in females or greater than 102 cm in males. For people of Asian background lower thresholds (BMI 23 kg/m2 for overweight, 27.5 kg/m2 for obesity) are clinically relevant given elevated metabolic risk at lower BMI. Psychological assessment for binge eating, food addiction and depression should be incorporated routinely, as these influence treatment selection and response.

4. Investigations and AU-specific cutoffs

Initial workup targets identification of secondary causes and obesity-related complications. Investigations include fasting glucose or HbA1c, fasting lipid profile, liver function tests, thyroid-stimulating hormone, full blood count, urine albumin-to-creatinine ratio, and estimated glomerular filtration rate (eGFR). Blood pressure measurement and resting electrocardiograph are standard. Polysomnography or an overnight oximetry study is indicated when obstructive sleep apnoea is suspected clinically. AU-specific thresholds: eGFR below 60 mL/min/1.73 m2 warrants closer supervision during dietary interventions, and eGFR below 30 mL/min/1.73 m2 requires specialist input before initiating a very low energy diet (VLED). Liver ultrasound is appropriate when metabolic dysfunction-associated fatty liver disease is suspected on biochemistry.

5. Management

Treatment intensity is stratified by BMI category, waist circumference and the presence of obesity-related complications, following the ADS Australian Obesity Management Algorithm.

For BMI 30 to 40 kg/m2 or abdominal obesity without complications, supervised lifestyle intervention is the initial approach, targeting 5 to 10% weight loss. A reduced energy diet (RED) aims to create a deficit of 2000 to 4000 kJ per day; a low energy diet (LED) restricts total intake to 4200 to 5000 kJ per day. If these approaches are insufficient, a VLED restricting intake to below 3300 kJ per day via formulated meal replacements is appropriate. VLEDs are recommended for up to 12 weeks but can be supervised for 6 to 12 months. Partial VLED regimens use two meal replacements daily plus one lean-protein meal; complete regimens use three daily replacements plus vegetables. A teaspoon of olive oil should be co-prescribed to stimulate gall bladder contraction and reduce gallstone risk. In patients taking sulphonylureas or insulin, doses should be halved on commencing a VLED and adjusted by self-monitored blood glucose. Patients on SGLT2 inhibitors should have ketones monitored or the agent suspended to prevent euglycaemic ketoacidosis.

For BMI 30 to 40 kg/m2 with complications, or BMI above 40 kg/m2, intensive interventions combining VLED with pharmacotherapy or bariatric surgery are recommended, with a target of 10 to 15% weight loss. For BMI above 40 kg/m2 with complications, referral to specialist care is indicated with a target of greater than 15% loss.

Bariatric surgery is indicated per NHMRC criteria: BMI above 40 kg/m2; BMI 35.0 to 39.9 kg/m2 with weight-responsive comorbidities; or BMI 30.0 to 34.9 kg/m2 with poorly controlled type 2 diabetes and elevated cardiovascular risk. For people with type 2 diabetes, the ADS-endorsed metabolic surgery thresholds allow surgery at BMI 35.0 to 39.9 kg/m2 with inadequate glycaemic control despite optimal medical therapy.

Contraindications to VLED include pregnancy, lactation, severe or unstable psychiatric conditions, recent myocardial infarction or cerebrovascular event, unstable angina, porphyria, and age above 65 years (use with caution given limited safety data).

6. Pharmacology and AU PBS notes

Six agents are TGA-approved in Australia for obesity management. None currently hold PBS subsidy for obesity as a primary indication; all require private prescription.

Phentermine (Duromine, Metermine, Phentermine Juno): Centrally acting adrenergic agonist; TGA-registered for short-term use up to 3 months as a lifestyle adjunct. Achieves 5 to 10% weight loss at 12 weeks. Contraindicated with antidepressants, in coronary artery disease, arrhythmias or uncontrolled hypertension. Side effects include tachycardia, hypertension, insomnia and dry mouth.

Orlistat (Xenical): Inhibits pancreatic and gastric lipase, reducing fat absorption by 30%. Gastrointestinal side effects (steatorrhoea, oily spotting, flatulence) limit adherence when dietary fat intake exceeds 30 g per day. Risk of fat-soluble vitamin deficiency (vitamins A, D, E and K) and oxalate kidney stones with long-term use.

Liraglutide 3 mg (Saxenda): Once-daily subcutaneous GLP-1 receptor agonist. Starting dose 0.6 mg daily, titrated weekly in 0.6 mg increments to a maximum of 3.0 mg. Mean weight loss of 8% versus 2.6% with placebo in the SCALE trial. Increased risk of gallstones and cholecystitis independent of weight loss. Not PBS-listed for obesity.

Naltrexone and bupropion (Contrave): Extended-release combination; naltrexone 8 mg and bupropion 90 mg per tablet. Dose escalated from one tablet daily to two tablets twice daily over four weeks. Mean weight loss of approximately 6% versus 1.3% with placebo. Acts on hypothalamic hunger circuitry and mesolimbic reward pathways.

Semaglutide 2.4 mg (Wegovy): Once-weekly subcutaneous GLP-1 receptor agonist. Starting dose 0.25 mg weekly, escalated monthly to 2.4 mg. Mean weight loss of 16.9% body weight in the STEP-1 trial. Also reduces cardiovascular events by 20% in people with obesity and established cardiovascular disease. Monitor for worsening diabetic retinopathy in those with a prior history.

Tirzepatide (Mounjaro): Dual GLP-1 and glucose-dependent insulinotropic peptide (GIP) co-agonist. TGA-approved for type 2 diabetes, chronic weight management and obstructive sleep apnoea. Starting dose 2.5 mg weekly, titrated monthly to 5, 10 or 15 mg. At the 15 mg dose, mean weight loss of 20.9% was achieved, with 90.9% of participants achieving at least 5% weight reduction. GI side effects and acute pancreatitis risk are class effects.

Off-label options in experienced hands include topiramate (25 to 100 mg daily, additional 5.3 kg loss over placebo in meta-analysis; side effects include paraesthesia, depression and closed-angle glaucoma) and combined low-dose phentermine with topiramate.

7. Complications and monitoring

Key complications of obesity include type 2 diabetes, cardiovascular disease, dyslipidaemia, metabolic dysfunction-associated steatohepatitis (MASH), obstructive sleep apnoea, osteoarthritis, reproductive hormonal abnormalities and certain cancers (colorectal, endometrial, breast). Depression and disordered eating are prevalent and bidirectional.

Monitoring schedule: weight and waist circumference at every visit; HbA1c and fasting lipids at 3 to 6 monthly intervals until targets are met, then annually; blood pressure and liver function tests 6 monthly; renal function annually or more frequently if eGFR is reduced. For patients on orlistat, fat-soluble vitamin levels should be checked annually. INR must be monitored one week after commencing a VLED in patients taking warfarin, as increased vegetable intake may alter vitamin K intake and anticoagulation effect. Patients on semaglutide or tirzepatide with a history of diabetic retinopathy require ophthalmological review following initiation. Weight regain is common after pharmacotherapy cessation, supporting the need for long-term treatment planning in shared-care arrangements.

Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.