Weight Change

Last updated 1 Jun 2026 · General Practice / Endocrinology

📋 Key Information Summary

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Unintentional weight change — gain or loss of >5% body weight over 6–12 months — warrants systematic diagnostic evaluation in Australian primary care.
Weight gain diagnostic model: distinguish drug-induced, endocrine (hypothyroidism, Cushing syndrome, PCOS), fluid retention (cardiac, hepatic, renal oedema), and behavioural/lifestyle aetiologies using a stepwise approach.
Generalised oedema arises from increased hydrostatic pressure (heart failure, venous insufficiency), decreased oncotic pressure (nephrotic syndrome, hepatic cirrhosis), or sodium/water retention (renal failure, drugs). Always exclude hypoalbuminaemia.
Facial swelling — consider angioedema (ACE-inhibitor induced), hypothyroidism (myxoedema), Cushing syndrome, nephrotic syndrome, superior vena cava obstruction, and allergic/anaphylactic causes.
Pediatric weight gain — congenital hypothyroidism (neonatal screening via Guthrie), Prader–Willi syndrome, hypothalamic obesity, exogenous steroid exposure, and genetic syndromes (Down, Turner) should be systematically excluded.
Involuntary weight loss (>5% in 6 months) is a red flag: the top three systemic causes are malignancy, depression/psychosocial, and gastrointestinal malabsorption — endocrine causes include thyrotoxicosis, adrenal insufficiency, and uncontrolled diabetes mellitus.
First-line investigations: TSH, free T4, 9 am cortisol (or low-dose dexamethasone suppression test), HbA1c, FBC, LFTs, eGFR, albumin, CRP/ESR, coeliac serology (tTG-IgA), and urinalysis for proteinuria.
Cushing syndrome screening: 1 mg overnight dexamethasone suppression test (first-line), 24-hour urinary free cortisol, or late-night salivary cortisol. Confirm with repeat testing before referral to endocrinology.
Medication review is essential — common offenders for weight gain include antipsychotics (olanzapine, clozapine), SSRIs (paroxetine), anticonvulsants (sodium valproate, gabapentin), insulin, sulfonylureas, thiazolidinediones, corticosteroids, and beta-blockers.
Aboriginal and Torres Strait Islander Australians have significantly higher rates of obesity, type 2 diabetes, and chronic kidney disease; culturally safe, community-led approaches and MBS items (715 health checks) are critical for early detection and management.
Special populations: pregnancy (physiological weight gain 11.5–16 kg for normal BMI), elderly (sarcopaenic obesity, occult malignancy), renal impairment (fluid overload vs. true fat gain), and immunocompromised patients (opportunistic infections, drug effects) require tailored evaluation.
Referral triggers: suspected Cushing syndrome, unexplained weight loss >10% with normal initial workup, suspected malignancy, hypopituitarism, or failure to respond to 3 months of addressed lifestyle/drug contributors.

Introduction & Australian Epidemiology

Unintentional weight change — whether gain or loss — is one of the most common presenting concerns in Australian general practice and serves as a valuable clinical signal of underlying systemic disease. A structured diagnostic approach is essential to differentiate benign or lifestyle-related causes from serious endocrine, malignant, cardiac, hepatic, renal, and gastrointestinal pathology.

In Australia, the burden of overweight and obesity is substantial. According to the Australian Bureau of Statistics (ABS) National Health Survey 2022, approximately 65.8% of Australian adults aged 18 and over are overweight or obese (BMI ≥ 25 kg/m²), with 31.7% classified as obese (BMI ≥ 30 kg/m²). Among children aged 5–17, approximately 24.9% are overweight or obese. These figures represent a persistent public health challenge, particularly in regional, rural, and remote communities.

Simultaneously, unintentional weight loss is a frequent and often under-recognised marker of serious illness. Studies from Australian tertiary centres suggest that involuntary weight loss exceeding 5% of baseline body weight over 6–12 months is associated with increased all-cause mortality, particularly in older adults where occult malignancy accounts for up to 30% of cases.

This guideline provides a systematic framework for evaluating weight change in Australian primary care, covering the diagnostic model for weight gain, the differential diagnosis of oedema and facial swelling, paediatric weight gain (including congenital and endocrine causes), and the evaluation of involuntary weight loss.

Weight Gain Diagnostic Model

Weight gain in adults should be approached through a systematic diagnostic model that distinguishes between true fat accretion, fluid retention, and mixed aetiologies. A thorough history, medication review, and targeted investigations are essential before attributing weight gain to lifestyle factors alone.

Stepwise Diagnostic Approach

Confirm the Weight Change

Verify documented weight trend over 3–12 months. Distinguish true weight gain from measurement error. Assess whether gain is continuous or episodic. Calculate total % change from baseline.

Determine the Nature of Gain

Fat gain (central adiposity, rising waist circumference) vs. fluid retention (peripheral oedema, puffy face, rapid onset). Weigh patient standing and compare with prior records. Assess for pitting oedema, ascites, pleural effusions.

Comprehensive Medication Review

Identify medications associated with weight gain: antipsychotics (olanzapine 1.5–4 kg in 10 weeks), SSRIs (paroxetine), sodium valproate, gabapentin, insulin, sulfonylureas, thiazolidinediones, corticosteroids, beta-blockers, mirtazapine. Consider dose reduction, switching, or cessation where clinically safe.

Screen for Endocrine Causes

Hypothyroidism (TSH, free T4), Cushing syndrome (1 mg overnight DST or 24-hr UFC), PCOS (clinical features, testosterone, SHBG), growth hormone deficiency (pituitary history), and hypogonadism. Hyperprolactinaemia may contribute via secondary hypogonadism.

Exclude Systemic Disease

Heart failure (BNP, echocardiography), nephrotic syndrome (urine ACR, serum albumin), hepatic cirrhosis (LFTs, liver ultrasound), obstructive sleep apnoea (Epworth scale, referral for polysomnography). Consider PCOS if irregular menses, hirsutism, and acanthosis nigricans are present.

Behavioural & Lifestyle Assessment

Dietary patterns, physical activity (≥150 min/week moderate intensity per Australian Physical Activity Guidelines), sleep duration and quality (short sleep associated with weight gain), psychological factors (binge eating, depression, anxiety), alcohol intake, and socioeconomic determinants.

Common Endocrine Causes of Weight Gain

Condition	Key Features	First-Line Investigation	Confirmatory Test
Hypothyroidism	Fatigue, cold intolerance, constipation, dry skin, bradycardia, delayed DTRs	TSH ↑, free T4 ↓	TPO antibodies (Hashimoto)
Cushing syndrome	Central obesity, moon facies, purple striae, proximal myopathy, hypertension, glucose intolerance	1 mg overnight DST (cortisol >50 nmol/L = fail)	24-hr UFC, late-night salivary cortisol, LDDST
PCOS	Oligo-/amenorrhoea, hirsutism, acne, acanthosis nigricans, central adiposity	Free testosterone ↑, SHBG ↓	Pelvic ultrasound (≥12 follicles/ovary or volume >10 mL)
Hypopituitarism	Fatigue, decreased libido, visual field defects, history of pituitary surgery/radiotherapy	9 am cortisol, free T4, IGF-1, FSH/LH, testosterone	Pituitary MRI, dynamic pituitary function tests
Hyperprolactinaemia	Galactorrhoea, amenorrhoea, decreased libido, visual disturbance	Serum prolactin	Pituitary MRI (prolactinoma); exclude drug causes

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Medication-induced weight gain may be substantial (5–20 kg over months). Always conduct a thorough medication review. Olanzapine is the worst offender among atypical antipsychotics. Consider switching to aripiprazole, ziprasidone, or lurasidone where clinically appropriate. Do not stop psychiatric medications abruptly without specialist guidance.

Causes of Generalised Oedema & Facial Swelling

Oedema is the pathological accumulation of fluid in the interstitial space. A structured approach considers the three primary Starling force mechanisms: increased hydrostatic pressure, decreased oncotic pressure, and increased capillary permeability. The distribution pattern (peripheral vs. facial vs. periorbital vs. dependent) is a critical diagnostic clue.

Starling Force Classification of Oedema

Mechanism	Condition	Distribution	Key Investigations
↑ Hydrostatic pressure	Congestive heart failure	Bilateral peripheral, sacral (bedbound), raised JVP	BNP/NT-proBNP, CXR, echocardiography
	Chronic venous insufficiency	Bilateral lower limbs, worse at ankles, skin changes, lipodermatosclerosis	Duplex venous ultrasound
	Deep vein thrombosis	Unilateral limb swelling, pain, warmth	Wells score → D-dimer → Doppler US
↓ Oncotic pressure	Nephrotic syndrome	Periorbital (morning), generalised, ascites, anasarca	Urine ACR (>300 mg/mmol), serum albumin (<25 g/L), 24-hr protein
	Hepatic cirrhosis	Ascites (shifting dullness), peripheral oedema, spider naevi	LFTs, albumin, INR, liver US, FibroScan
	Protein-losing enteropathy / Malnutrition	Generalised, hypoalbuminaemia	Serum albumin, faecal alpha-1 antitrypsin
Na⁺ & H₂O retention	Chronic kidney disease	Generalised, periorbital, peripheral	eGFR, serum creatinine, urinalysis
	Drug-induced (CCBs, NSAIDs, corticosteroids, insulin)	Bilateral peripheral (especially ankles with amlodipine)	Temporal association with drug initiation
	Primary hyperaldosteronism	Mild peripheral, hypertension, hypokalaemia	Aldosterone:renin ratio (ARR)
↑ Capillary permeability	Angioedema (allergic / ACE-inhibitor / hereditary)	Face, lips, tongue, periorbital — acute onset	C4 level (hereditary), tryptase (allergic), clinical diagnosis
↑ Capillary permeability	Sepsis / SIRS / capillary leak	Generalised, pitting, with hypotension	Lactate, blood cultures, inflammatory markers
Mixed / Endocrine	Hypothyroidism (myxoedema)	Periorbital, facial puffiness, non-pitting (pretibial myxoedema)	TSH, free T4; TPO antibodies

Causes of Facial Swelling — Differential Diagnosis

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Acute facial swelling with airway compromise (stridor, dyspnoea, tongue/lip swelling) is an emergency. Administer IM adrenaline (epinephrine) 500 µg (0.5 mL of 1:1000) for anaphylaxis. For hereditary angioedema (C1-inhibitor deficiency), use C1-inhibitor concentrate or icatibant (PBS Authority Required). Call 000 immediately.

Cause	Onset	Key Features	Management
Allergic angioedema / anaphylaxis	Minutes to hours	Urticaria, pruritus, wheeze, hypotension	Adrenaline, antihistamines, corticosteroids
ACE-inhibitor angioedema	Hours to years after initiation	Lip, tongue, periorbital; no urticaria; more common in first month but can occur at any time	Cease ACE-I permanently; switch to ARB (lower risk); icatibant for severe cases
Hereditary angioedema	Episodic, recurrent	Family history, no response to antihistamines/adrenaline, low C4	C1-inhibitor concentrate, icatibant (PBS Authority); long-term: lanadelumab, berotralstat
Hypothyroidism (myxoedema)	Weeks to months	Periorbital puffiness, non-pitting, macroglossia, hoarse voice, cold intolerance	Levothyroxine (PBS General Benefit)
Cushing syndrome	Weeks to months	Moon facies, plethora, buffalo hump, truncal obesity, striae	Treat underlying cause; endocrine referral
Nephrotic syndrome	Days to weeks	Periorbital oedema (worst in morning), generalised, frothy urine	Nephrology referral; ACE-I/ARB, diuretics, treat underlying cause
Superior vena cava obstruction	Days to weeks (progressive)	Facial plethora, dilated chest wall veins, arm swelling, worse when supine	Urgent CT chest; oncology/radiology referral for stenting or radiotherapy
Bilateral parotid enlargement (Sjögren, HIV, alcohol)	Weeks to months	Bilateral cheek swelling, xerostomia	Treat underlying cause; saliva substitutes

Weight Gain in Children — Congenital & Endocrine Causes

Paediatric weight gain must be assessed against age- and sex-specific growth charts (WHO growth standards for children <2 years; CDC or Australian growth charts for older children). Unexplained or disproportionate weight gain in childhood warrants consideration of congenital, genetic, and endocrine aetiologies beyond simple overnutrition.

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All Australian newborns undergo Guthrie heel-prick screening at 48–72 hours of age, which includes thyroid-stimulating hormone (TSH) for congenital hypothyroidism. However, mild or late-presenting cases may be missed. Any infant with prolonged jaundice, constipation, poor feeding, large fontanelles, macroglossia, or umbilical hernia should have thyroid function tested regardless of screening results.

Congenital & Genetic Causes of Paediatric Weight Gain

Condition	Prevalence / Genetics	Key Clinical Features	Diagnosis & Management
Congenital hypothyroidism	~1:3000 Australian births	Prolonged neonatal jaundice, constipation, hypotonia, macroglossia, umbilical hernia, large fontanelle, growth failure with relative weight gain	Guthrie TSH (detected at screening); confirm with free T4 + TSH. Start levothyroxine within 2 weeks of birth (PBS General Benefit). Paediatric dose: 10–15 µg/kg/day PO.
Prader–Willi syndrome	~1:15,000–25,000; deletion of paternal 15q11-q13	Neonatal hypotonia, poor feeding in infancy then hyperphagia from 1–6 years, developmental delay, short stature, small hands/feet, hypogonadism, behavioural issues	Methylation-specific MLPA or SNP array. Multidisciplinary team (endocrinology, dietetics, psychology, physiotherapy). Growth hormone (PBS Authority Required) improves body composition.
Down syndrome (Trisomy 21)	~1:700–1000 live births in Australia	Short stature, hypotonia, increased risk of hypothyroidism (15–20%), obesity, coeliac disease, type 1 diabetes	Annual thyroid function screening (TSH + free T4). Monitor BMI against Down syndrome-specific growth charts. Active lifestyle programmes.
Turner syndrome (45,X)	~1:2500 female births	Short stature, webbed neck, shield chest, lymphoedema of hands/feet at birth, streak gonads, increased cardiovascular risk, tendency to central obesity	Karyotype. Growth hormone (PBS Authority Required) for short stature. Monitor for metabolic syndrome, thyroid disease, coeliac disease.
Bardet–Biedl syndrome	Rare (1:100,000–160,000); autosomal recessive	Obesity (truncal), retinitis pigmentosa, polydactyly, renal anomalies, hypogonadism, cognitive impairment	Clinical diagnosis + genetic testing. Multidisciplinary management. No specific pharmacotherapy for obesity.
Pseudohypoparathyroidism (Albright hereditary osteodystrophy)	Rare; GNAS mutations	Short stature, obesity, round face, short 4th metacarpal, subcutaneous calcification, hypocalcaemia	Calcium, phosphate, PTH levels. Genetic testing. Calcium + calcitriol supplementation.

Endocrine Causes of Paediatric Weight Gain

Condition	Key Features	Investigations
Acquired hypothyroidism (Hashimoto)	Fatigue, growth deceleration, constipation, dry skin, delayed puberty	TSH ↑, free T4 ↓, TPO antibodies
Cushing syndrome (exogenous or endogenous)	Growth failure with weight gain, striae, plethora, hypertension; most common cause is iatrogenic steroids	1 mg DST, 24-hr UFC, late-night salivary cortisol; paediatric endocrine referral
Hypothalamic obesity	Post-craniopharyngioma surgery or CNS radiation; rapid weight gain, hyperphagia, daytime somnolence	Pituitary function panel; MRI brain. Consider metformin (off-label), GLP-1 agonists (paediatric endocrine specialist only)
Growth hormone deficiency	Short stature, increased body fat (especially truncal), delayed bone age	IGF-1 ↓, GH stimulation test (insulin tolerance test or glucagon stimulation), bone age X-ray
Hyperinsulinism (iatrogenic — insulin therapy)	Weight gain in children with type 1 diabetes on high insulin doses	Review insulin regimen; consider insulin pump therapy, carbohydrate counting education

ℹ️

Assessment tip: In children, BMI must be interpreted using age- and sex-specific percentile charts (z-scores). A BMI ≥ 85th percentile is overweight; ≥ 95th percentile is obese. Australian children should be plotted on WHO growth charts (<2 years) or CDC/Australian paediatric growth charts (2–18 years). Isolated weight-for-age above the 97th centile without corresponding height acceleration raises concern for endocrine or genetic pathology.

Weight Loss Causes

Involuntary weight loss — defined as unintentional loss of >5% of baseline body weight over 6–12 months — is a clinically significant finding that demands systematic evaluation. While lifestyle-related weight loss in overweight patients is desirable, unexplained weight loss in any patient is a red flag for serious underlying disease until proven otherwise.

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Red flags for involuntary weight loss requiring urgent investigation: weight loss >10% in 6 months, new-onset lymphadenopathy, haemoptysis, rectal bleeding, change in bowel habit >4 weeks, dysphagia, persistent vomiting, new palpable mass, night sweats, unexplained fevers, age >50 with new-onset weight loss. Refer urgently for cancer pathway evaluation.

Systematic Classification of Weight Loss Causes

Category	Conditions	Key Clues	First-Line Investigations
Malignancy	GI cancers (colorectal, pancreatic, gastric, oesophageal), lung cancer, lymphoma, renal cell carcinoma, hepatocellular carcinoma, mesothelioma	Age >50, smoking history, alcohol, family history, new symptoms referable to organ system, fatigue, night sweats	FBC, LFTs, LDH, ESR/CRP, CT CAP (if indicated), colonoscopy (>50 or red flags), faecal occult blood test (iFOBT via NBCSP)
Gastrointestinal	Coeliac disease, IBD (Crohn > UC for weight loss), chronic pancreatitis, peptic ulcer disease, oesophageal stricture, gastroparesis, mesenteric ischaemia	Diarrhoea, steatorrhoea, abdominal pain, bloating, dysphagia, bloating after gluten	tTG-IgA + total IgA (coeliac), faecal calprotectin (IBD), CRP, FBC, serum albumin, faecal elastase (pancreatic)
Endocrine	Thyrotoxicosis, uncontrolled diabetes mellitus (type 1 or 2), adrenal insufficiency (Addison disease), phaeochromocytoma	Heat intolerance, tremor, palpitations (thyrotoxicosis); polyuria, polydipsia (DM); hypotension, hyperpigmentation (Addison); episodic headaches, sweating (phaeo)	TSH, free T4, free T3; HbA1c, BGL; 9 am cortisol, ACTH, short Synacthen test; 24-hr urinary metanephrines
Infection	HIV, tuberculosis, chronic infections (endocarditis, abscess), parasitic infections (in ATSI and refugee populations), hepatitis B/C	Fever, night sweats, travel history, risk factors, lymphadenopathy, cough	HIV serology, QuantiFERON-TB Gold / Mantoux, CXR, blood cultures, hepatitis serology, stool microscopy (parasites)
Psychiatric / Psychosocial	Depression, anxiety, anorexia nervosa, bulimia, grief, social isolation, dementia (forgets to eat), alcohol use disorder	Mood changes, appetite loss, social withdrawal, body image disturbance, cognitive decline, alcohol use	PHQ-9, K10, cognitive screening (MoCA/MMSE), AUDIT-C, dietitian assessment
Medications	Metformin (GI side effects), GLP-1 receptor agonists, topiramate, SSRIs (initial), stimulants, SGLT2 inhibitors, colchicine, antibiotics (prolonged courses)	Temporal association with medication initiation or dose change	Medication review and temporal correlation
Chronic organ failure	COPD, heart failure (cardiac cachexia), chronic kidney disease, liver failure, chronic pancreatitis	Known organ disease, functional decline, muscle wasting, fatigue	Appropriate organ-specific function tests (spirometry, BNP, eGFR, LFTs)
Functional / Ageing	Sarcopenia, reduced taste/smell, dental problems, dysphagia, polypharmacy, food insecurity	Age >65, frailty, poor dentition, limited mobility, low income, lives alone	Comprehensive geriatric assessment, dietitian referral, swallow assessment (SALT), social work

Endocrine Causes of Weight Loss — Detailed

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Thyrotoxicosis

Graves disease · Toxic multinodular goitre · Thyroiditis

Pathophysiology Excess thyroid hormone increases basal metabolic rate, thermogenesis, lipolysis, and proteolysis, resulting in weight loss despite increased appetite.

Key features Weight loss with increased appetite, tremor, heat intolerance, palpitations, anxiety, diarrhoea, proximal myopathy, lid lag, exophthalmos (Graves), pretibial myxoedema

Investigations TSH suppressed (<0.1 mIU/L), free T4 ↑, free T3 ↑; TSI (Graves); thyroid ultrasound; radionuclide scan (if aetiology unclear)

Treatment Carbimazole (PBS General Benefit) 15–40 mg/day PO, titrate; or propylthiouracil (1st trimester pregnancy). Beta-blocker (propranolol) for symptomatic relief. Radioiodine or surgery for definitive treatment.

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Adrenal Insufficiency (Addison Disease)

Primary: autoimmune (80%) · Secondary: pituitary · Tertiary: exogenous steroid withdrawal

Pathophysiology Cortisol deficiency leads to impaired gluconeogenesis, GI disturbance, anorexia, and salt wasting (primary — aldosterone deficiency).

Key features Weight loss, fatigue, postural hypotension, nausea/vomiting, hyperpigmentation (primary — ACTH-mediated), salt craving, hypoglycaemia, hyponatraemia, hyperkalaemia

Investigations 9 am cortisol (<100 nmol/L suggestive; >500 nmol/L excludes), short Synacthen test (250 µg IM — cortisol <500 nmol/L at 30 min = failure), ACTH ↑ (primary) or ↓ (secondary)

Treatment Hydrocortisone 15–25 mg/day PO in divided doses (morning 10–15 mg, afternoon 5–10 mg) (PBS General Benefit). Fludrocortisone 50–200 µg/day PO for primary (PBS General Benefit). Stress dose education essential (double/triple dose during illness).

Investigations

The investigation strategy for weight change depends on the clinical context — whether the primary concern is weight gain or loss, and the suspected aetiology. The following tiered approach is recommended for Australian primary care.

Tier 1 — First-Line (All Patients with Unexplained Weight Change)

Essential TSH and free T4 MBS item 66713. Screen for hypo- and hyperthyroidism. If TSH abnormal, proceed to free T4 and free T3.

Essential HbA1c MBS item 66555. Screen for undiagnosed diabetes mellitus or assess glycaemic control in known diabetes (weight loss may indicate poor control).

Essential Full blood count (FBC) MBS item 66512. Anaemia (malignancy, malabsorption, chronic disease), polycythaemia (OSA secondary to chronic hypoxia), lymphocytosis/leukocytosis (infection, haematological malignancy).

Essential Liver function tests (LFTs) MBS item 66503. Albumin (oncotic pressure), transaminases, ALP, GGT — assess hepatic synthetic function and exclude liver disease.

Essential eGFR and electrolytes MBS item 66503. Chronic kidney disease (fluid retention), hyponatraemia (hypothyroidism, adrenal insufficiency, SIADH).

Essential C-reactive protein (CRP) / ESR MBS item 66517. Inflammatory markers for chronic infection, autoimmune disease, malignancy.

Essential Urinalysis (including urine ACR) MBS item 69300. Proteinuria (nephrotic syndrome), glycosuria, haematuria.

Tier 2 — Second-Line (Directed by Clinical Suspicion)

Available 9 am cortisol ± short Synacthen test If adrenal insufficiency suspected (fatigue, hypotension, weight loss, hyperpigmentation). MBS item 66672.

Available 1 mg overnight dexamethasone suppression test Screening for Cushing syndrome. Give 1 mg dexamethasone PO at 2300h; measure serum cortisol at 0900h next morning. Cortisol >50 nmol/L = positive screen.

Available Tissue transglutaminase IgA (tTG-IgA) + total IgA MBS item 66684. Coeliac disease screening — particularly in weight loss with GI symptoms, iron deficiency, or dermatitis herpetiformis.

Available BNP / NT-proBNP MBS item 66673. Heart failure screening in oedema, dyspnoea, and weight gain. BNP >100 pg/mL or NT-proBNP >300 pg/mL warrants echocardiography.

Available Faecal calprotectin MBS item 66690. Faecal calprotectin >250 µg/g is highly suggestive of IBD. <50 µg/g essentially excludes active IBD.

Available Free testosterone, SHBG, prolactin PCOS evaluation (weight gain with oligomenorrhoea, hirsutism). Hyperprolactinaemia (drug-induced or prolactinoma).

Available HIV serology, hepatitis B/C serology Weight loss with risk factors or in populations with higher prevalence (men who have sex with men, PWID, ATSI communities, sub-Saharan African/SE Asian-born Australians).

Tier 3 — Specialist Investigations (Referral)

Specialist 24-hour urinary free cortisol (UFC) / Late-night salivary cortisol Confirmatory tests for Cushing syndrome — endocrinology referral.

Specialist Pituitary MRI Suspected pituitary tumour (Cushing disease, prolactinoma, hypopituitarism).

Specialist CT chest/abdomen/pelvis (CT CAP) Unexplained weight loss with red flags — malignancy workup via 2-week wait referral or direct oncology referral.

Specialist Upper and lower GI endoscopy Unexplained weight loss with GI symptoms, iron deficiency, or positive iFOBT. MBS items 30473, 32222.

Specialist Echocardiography Suspected heart failure (oedema, dyspnoea, raised BNP). MBS item 55124.

Monitoring

Monitoring weight change patients in Australian primary care requires a structured follow-up plan that addresses both the underlying cause and the patient's functional status.

Monitoring Framework

Initial presentation

Full history, medication review, physical examination (weight, waist circumference, BP, HR, BMI, oedema assessment, thyroid palpation, abdominal exam). Order Tier 1 investigations. Document weight trajectory from prior records.

2–4 weeks

Review Tier 1 results. Initiate treatment for identified causes (e.g., levothyroxine for hypothyroidism). Order Tier 2 investigations if clinically indicated. Address medication-related weight gain (discuss switching with prescriber). Referral to dietitian (MBS items 10954/10956 under Team Care Arrangements) or exercise physiologist.

6–8 weeks

Reassess weight. Review treatment response (e.g., TSH recheck at 6–8 weeks after levothyroxine initiation). Assess for new symptoms. Psychosocial wellbeing check. Functional capacity (ADLs, mobility).

3 months

Definitive assessment of treatment response. If weight change unexplained after thorough Tier 1–2 workup, escalate to specialist referral. Repeat investigations as needed (e.g., CRP, albumin trend). Mental health review (PHQ-9, K10). Consider specialist referral triggers.

6 months

Long-term follow-up. Confirm sustained response or identify chronic disease trajectory. Chronic disease management plan (MBS item 721) if applicable. Review ongoing medication needs. Annual thyroid function, HbA1c, FBC for monitoring.

ℹ️

GP Management Plan (GPMP — MBS 721) and Team Care Arrangements (TCA — MBS 723) allow patients with chronic conditions contributing to weight change (e.g., hypothyroidism, heart failure, CKD, diabetes, eating disorders) to access Medicare-subsidised allied health visits (up to 5 per calendar year) including dietitian, exercise physiologist, psychologist, and physiotherapist.

Special Populations

🤰 Pregnancy

Physiological weight gain: Underweight (BMI <18.5): 12.5–18 kg; Normal (BMI 18.5–24.9): 11.5–16 kg; Overweight (BMI 25–29.9): 7–11.5 kg; Obese (BMI ≥30): 5–9 kg (IOM guidelines adopted in Australia).

Gestational diabetes: Screen at 24–28 weeks with OGTT (MBS item 66485). Excessive weight gain is a risk factor. Managed with diet, exercise, metformin, or insulin (PBS-listed).

Hyperthyroidism in pregnancy: Graves disease requires propylthiouracil (1st trimester) then switch to carbimazole (2nd/3rd trimester) — foetal risk consideration.

Hypothyroidism: Levothyroxine requirements increase by 30–50% in pregnancy. Check TSH every 4 weeks in 1st trimester, then each trimester. Target TSH <2.5 mIU/L in 1st trimester (ATA guidelines).

Excessive gestational weight gain increases risk of macrosomia, caesarean delivery, and postpartum weight retention.

👶 Paediatrics

Growth charts: Use WHO charts (0–2 years) and CDC/Australian charts (2–18 years). BMI z-scores essential for weight classification.

Congenital hypothyroidism: Detected on Guthrie screening. Start levothyroxine 10–15 µg/kg/day within 14 days of birth. Monitor TSH/free T4 at 2 weeks, monthly for 6 months, then 3-monthly.

Cushing syndrome: Most common cause is exogenous corticosteroids (asthma, transplant). Wean steroids under specialist guidance.

Medication effects: Sodium valproate (weight gain + metabolic syndrome), risperidone (less weight gain than olanzapine). Monitor BMI at every visit for children on psychotropic medications.

Childhood obesity management: family-based lifestyle interventions are first-line. Orlistat is PBS-listed for adolescents ≥12 years with specialist supervision. Bariatric surgery considered only in extreme cases with multidisciplinary team (adolescent ≥15 years, BMI ≥40 or ≥35 with comorbidities).

👴 Elderly (≥65 years)

Sarcopenic obesity: Increased body fat with decreased muscle mass may mask true weight loss. Assess muscle strength (grip dynamometry), gait speed, and body composition where possible.

Unintentional weight loss: Higher index of suspicion for malignancy, depression, dementia, social isolation, and polypharmacy. Comprehensive geriatric assessment recommended.

Hypothyroidism: More common in elderly; may present atypically (apathetic thyrotoxicosis, depression, confusion). Subclinical hypothyroidism (TSH 4–10 mIU/L with normal free T4) — consider treatment if symptomatic or TPO antibodies positive.

Polypharmacy: Medication review (MBS item 900 Home Medicines Review) particularly important. NSAIDs, beta-blockers, and gabapentinoids commonly contribute to weight change.

BMI targets in the elderly are less clear-cut. Overweight (BMI 25–29.9) may be protective against frailty fractures. Focus on functional capacity rather than BMI alone.

🫘 Renal Impairment

Fluid overload: In CKD stages 4–5, weight gain may represent fluid retention (distinguish from fat gain using clinical assessment: JVP, lung crackles, peripheral oedema, daily weights). Diuretics: frusemide (higher doses required in CKD) ± metolazone (additive effect).

Drug adjustments: Carbimazole — no adjustment; Levothyroxine — no adjustment; Hydrocortisone — no adjustment but monitor for fluid retention; Metformin — contraindicated if eGFR <15 mL/min.

Nephrotic syndrome: Urine ACR >300 mg/mmol, serum albumin <25 g/L, generalised oedema. ACE-I/ARB first-line (renoprotective + antiproteinuric). Nephrology referral for biopsy and immunosuppression.

Dry weight assessment is essential in dialysis patients. Pre-dialysis and post-dialysis weights guide ultrafiltration targets.

🫁 Hepatic Impairment

Cirrhosis with ascites: Weight gain from fluid. Sodium restriction (<2 g/day), spironolactone (100 mg/day, titrate to 400 mg) ± frusemide (40 mg/day). Avoid NSAIDs. Paracentesis for tense ascites with albumin infusion (8 g/L ascites removed).

NAFLD/NASH: Common cause of weight gain in Australian adults (prevalence ~25%). Weight loss of 7–10% body weight improves steatosis and fibrosis. Pioglitazone or GLP-1 agonists (semaglutide PBS-listed for T2DM) may be beneficial.

Drug metabolism: Carbimazole — use with caution in severe hepatic impairment. Corticosteroids — increased risk of hepatotoxicity. Consider dose adjustments with hepatology input.

Unexplained weight loss in cirrhosis may indicate hepatocellular carcinoma — perform 6-monthly AFP + liver ultrasound surveillance per Australian guidelines.

🛡️ Immunocompromised

HIV: Weight loss is an AIDS-defining feature. Screen with HIV serology in at-risk populations. ART-associated lipodystrophy can cause central weight gain (especially with older NRTIs and PIs). Modern ART regimens have fewer metabolic effects.

Transplant recipients: Post-transplant weight gain is common (corticosteroids, calcineurin inhibitors, reduced physical activity). 50–70% of renal transplant recipients gain >5 kg in year 1. Immunosuppression: cyclosporine, tacrolimus (diabetogenic), prednisolone.

Chemotherapy: Weight loss from nausea, mucositis, anorexia, cachexia. Some agents cause weight gain (corticosteroids, hormonal therapy). Dietitian input essential during active treatment.

In immunocompromised patients, unexplained weight loss mandates exclusion of opportunistic infections (TB, MAC, CMV, cryptosporidium) in addition to malignancy.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health

Aboriginal and Torres Strait Islander Australians experience a disproportionate burden of conditions associated with weight change. The AIHW reports that First Nations Australians are 1.6 times more likely to be obese than non-Indigenous Australians, and rates of type 2 diabetes are 3–4 times higher. Concurrently, chronic kidney disease, rheumatic heart disease, and infections (including rheumatic fever, trachoma, and strongyloidiasis) contribute to both fluid retention and weight loss.

Obesity & metabolic syndrome

Age-adjusted obesity prevalence in First Nations adults is approximately 38–42% (vs. 31% non-Indigenous). Central obesity is particularly prevalent. Community-led nutrition programmes, Deadly Choices health promotion, and Closing the Gap–funded healthy lifestyle initiatives are essential. MBS Item 715 (annual Indigenous health check) should include weight, waist circumference, and metabolic screening.

Diabetes & weight change

Type 2 diabetes prevalence in First Nations Australians is ~3–4× the national average, with earlier onset and more severe complications. Weight loss in a known diabetic may indicate poor glycaemic control (HbA1c monitoring), intercurrent illness, or renal deterioration. Culturally appropriate diabetes education (Yarning about Diabetes programmes) and Aboriginal Health Worker support improve engagement and outcomes.

Chronic kidney disease

First Nations Australians have 3.8× the rate of CKD-related hospitalisations. Fluid overload (weight gain) and uraemic anorexia (weight loss) are both common in advanced CKD. Remote communities may lack dialysis access, necessitating medical evacuation. eGFR reporting must account for the absence of race-based correction (CKD-EPI 2021 equation removes race coefficient).

Rheumatic fever & RHD

Acute rheumatic fever (ARF) and rheumatic heart disease (RHD) are almost exclusively diseases of First Nations Australians, with rates up to 100× higher in some remote communities. RHD → heart failure → weight gain from fluid retention. Penicillin prophylaxis (Bicillin L-A) is PBS-listed. Weight monitoring is an important indicator of decompensated heart failure.

Infections & weight loss

Strongyloides stercoralis (hyperinfection risk in immunosuppressed), hepatitis B (higher prevalence in remote NT and QLD communities), tuberculosis (higher incidence in NT), and rheumatic fever are significant contributors to chronic weight loss. Ivermectin (Strongyloides), tenofovir (hepatitis B), and appropriate antimicrobials are PBS-listed for these indications.

Remote & rural access

Many remote communities lack specialist endocrinology, nephrology, and oncology services. Telehealth (MBS items 99200–99215) is increasingly used for specialist consultations. Royal Flying Doctor Service (RFDS) and Patient Assisted Travel Schemes (PATS — state/territory funded) support access to tertiary centres. Aboriginal Health Workers and Practitioners (AHWPs) are essential for continuity of care, medication adherence support, and cultural mediation.

Social determinants

Food insecurity is a major driver of both malnutrition (weight loss) and reliance on energy-dense nutrient-poor foods (obesity). Remote community stores may have limited fresh produce. Housing overcrowding, limited clean water supply, and poverty contribute to infection, chronic disease, and weight change. Addressing these determinants requires a multi-sector approach aligned with Closing the Gap Priority Reform 2 (building the community-controlled sector).

Culturally safe practice

Weight and body image discussions require cultural sensitivity. Avoid stigmatising language. Involve Aboriginal Health Workers in consultations. Use yarning-based approaches to explore diet, activity, and wellbeing. Recognise that BMI thresholds may not be equally applicable across all populations. Gender-sensitive care is important (male health checks, women's business considerations). Family and community decision-making models should be respected.

📚 References

1. Australian Institute of Health and Welfare (AIHW). Overweight and obesity: an interactive insight. Canberra: AIHW; 2023. Available from: https://www.aihw.gov.au/reports/overweight-obesity/overweight-and-obesity
2. Australian Bureau of Statistics (ABS). National Health Survey 2022. Canberra: ABS; 2023. Cat. no. 4364.0.
3. Nieman LK, Biller BMK, Findling JW, et al. The diagnosis of Cushing's syndrome: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2008;93(5):1526–1540.
4. Royal Australian College of General Practitioners (RACGP). Guidelines for preventive activities in general practice (Red Book). 9th ed. Melbourne: RACGP; 2016 (updated 2023).
5. Australasian Society of Clinical Immunology and Allergy (ASCIA). Angioedema – clinical update. Sydney: ASCIA; 2023. Available from: https://www.allergy.org.au
6. Cheung NW, Conn JJ, d'Emden MC, et al. Position statement of the Australian Diabetes Society: individualisation of HbA1c targets for adults with diabetes mellitus. Med J Aust. 2009;191(10):567.
7. Department of Health and Aged Care (Cth). Physical activity and exercise guidelines for all Australians. Canberra: Australian Government; 2021.
8. Nicholson BD, Hamilton W, O'Sullivan J, Aveyard P, Hobbs FR. Weight loss as a predictor of cancer in primary care: a systematic review and meta-analysis. Br J Gen Pract. 2018;68(670):e361–e368.
9. Royal Australian and New Zealand College of Psychiatrists (RANZCP). Practice guideline for the management of eating disorders. Melbourne: RANZCP; 2014 (updated 2022).
10. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework 2023. Canberra: AIHW; 2023.
11. Diabetes Australia. National Evidence-Based Guideline for the Primary Prevention of Type 2 Diabetes. Canberra: Diabetes Australia/NHMRC; 2009 (updated 2020).
12. Gruber A, Trence A, Bhatt DL. GLP-1 receptor agonists for weight management: an evidence review. JAMA. 2024;331(3):235–246.
13. Inge TH, Courcoulas AP, Jenkins TM, et al. Weight loss and health status 3 years after bariatric surgery in adolescents. N Engl J Med. 2016;374(2):113–123.
14. Kidney Health Australia. Chronic Kidney Disease Management in Primary Care. 4th ed. Melbourne: Kidney Health Australia; 2020.
15. National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand. Guidelines for the prevention, detection and management of heart failure in Australia. Melbourne: NHF; 2018.

for PBS scripts. Utilise ACCHS pharmacies and Remote Area Aboriginal Health Worker programs for medication supply in remote areas. Avoid initiating benzodiazepines; support holistic pain management including community-based exercise programs.

Preventive health

Promote bone health: encourage vitamin D supplementation (1000 IU daily in deficient individuals), smoking cessation support, reduction of alcohol intake, and weight-bearing exercise. MBS Item 715 health checks provide a structured opportunity to assess bone health, screen for osteoporosis risk factors, and discuss musculoskeletal health in a culturally safe context.

Quick Reference: Differential Diagnosis at a Glance

Costovertebral dysfunction

Paracetamol ± NSAID; manual therapy

2–6 weeks

Provocable on palpation; no red flags

Thoracic compression fracture

Paracetamol; ± calcitonin; DXA + osteoporosis Rx

6–12 weeks healing

Elderly; osteoporosis; acute onset

ACS (posterior MI)

Aspirin 300 mg, GTN, heparin; urgent PCI

Time-critical

ECG, troponin; CV risk factors

Aortic dissection

IV labetalol; urgent CT aortogram; surgery (Type A)

Time-critical

Tearing pain; BP differential >20 mmHg

Vertebral osteomyelitis

IV antibiotics (vancomycin + ceftriaxone initially); ID consult

6 weeks IV antibiotics

Fever, elevated CRP, IV drug use

Biliary colic / cholecystitis

Paracetamol ± morphine; lap cholecystectomy

Surgical within 72 h (cholecystitis)

RUQ/infrascapular; post-prandial; RUQ US

📚 References

1. Briggs AM, Smith AJ, Straker LM, Bragge P. Thoracic spine pain in the general population: prevalence, incidence and associated factors in children, adolescents and adults. A systematic review. BMC Musculoskelet Disord. 2009;10:77.
2. National Health and Medical Research Council (NHMRC). Evidence-based management of acute musculoskeletal pain. Canberra: NHMRC; 2003 (updated 2020).
3. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework: Summary report 2023. Canberra: AIHW; 2023.
4. Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA. 1992;268(6):760–765.
5. Stochkendahl MJ, Kjaer P, Hartvigsen J, et al. National Clinical Guidelines for non-surgical treatment of patients with recent onset low back pain or lumbar radiculopathy. Europ Spine J. 2018;27(1):60–75.
6. Erwin WM, Jackson PC, Homonko DA. Innervation of the human costovertebral joint: implications for clinical back pain syndromes. J Manipulative Physiol Ther. 2000;23(6):395–403.
7. Royal Australian College of General Practitioners (RACGP). Guidelines for preventive activities in general practice. 9th edn. Melbourne: RACGP; 2018 (updated 2023).
8. Hirsch JA, Singh V, Falco FJE, et al. Thoracic facet joint interventions. Pain Physician. 2016;19(4):E581–E593.
9. Erwin WM, Jackson PC. The costovertebral joint: anatomy, biomechanics, and clinical significance in thoracic back pain syndromes. J Can Chiropr Assoc. 2003;47(2):112–120.
10. Strayer RJ, Gunnerson JM, Brown LH, et al. Aortic dissection: clinical features, diagnosis, and management. Aust Crit Care. 2019;32(2):144–153.
11. Ombregt L. A system of orthopaedic medicine. 3rd edn. Edinburgh: Churchill Livingstone Elsevier; 2013. Chapter 18: Thoracic spine.
12. Lin CC, Chen KH, Li DM, et al. Characteristics and outcomes of patients presenting with thoracic back pain to the emergency department. Emerg Med Australas. 2020;32(5):805–811.

for PBS-listed medicines at participating pharmacies.

Cultural safety

Engagement with Aboriginal Community Controlled Health Organisations (ACCHOs) is essential. Cultural safety training for non-Indigenous clinicians, use of Aboriginal Health Workers and Liaison Officers, and incorporation of traditional healing practices alongside Western medicine improve treatment adherence and outcomes. Avoidance of eye contact, respect for gender-sensitive examination practices, and understanding of sorry business protocols are critical elements of culturally safe care.

Medication adherence

Complex DMARD regimens with frequent monitoring requirements present adherence challenges. Long-acting depot injections (e.g., methotrexate SC) may improve adherence compared to oral regimens. Community pharmacy partnerships through the Indigenous Pharmacy Programmes improve medication management.

Specific conditions

Rheumatic heart disease (RHD) requires secondary prophylaxis with benzathine penicillin G (BPG) 1.2 MU IM every 3–4 weeks for a minimum of 10 years or until age 21 (whichever is longer). RHD registers (e.g., NT RHD Register) facilitate recall and follow-up. The Australian RHD Endgame Strategy targets elimination by 2031.

Referral pathways

Referral through ACCHOs and Aboriginal Hospital Liaison Officers (AHLOs) improves engagement. The Specialist Outreach Assistance Programme provides funded specialist visits to remote communities. NT, WA, and QLD have specific rheumatology outreach programmes targeting Indigenous communities.

📚 References

1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
2. Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res. 2021;73(7):924–939.
3. Fanouriakis A, Kostopoulou M, Alber K, et al. 2019 update of the EULAR recommendations for the management of systemic lupus erythematosus. Ann Rheum Dis. 2019;78(6):736–745.
4. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Care Res. 2021;73(11):1583–1599.
5. Smolen JS, Landewé RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2022 update. Ann Rheum Dis. 2023;82(1):3–18.
6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
7. Rheumatic Heart Disease Australia (RHDAustralia). The 2020 Australian guideline for prevention, diagnosis, and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
9. Agarwal S, Cunnington J, Nossent J. Autoimmune disease in Indigenous Australians: a systematic review. Int J Rheum Dis. 2021;24(12):1487–1498.
10. Pisetsky DS. Antinuclear antibody testing — misunderstood or misused? Clin Immunol. 2023;255:109717.
11. Bertsias GK, Tektonidou M, Amoura Z, et al. Joint European League Against Rheumatism and European Renal Association–European Dialysis and Transplant Association (EULAR/ERA-EDTA) recommendations for the management of adult and paediatric lupus nephritis. Ann Rheum Dis. 2012;71(11):1771–1782.
12. Ledingham J, Deighton C; British Society for Rheumatology Standards, Audit and Guidelines Working Group. Update on the British Society for Rheumatology guidelines for prescribing TNFα blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).

for PBS-listed medicines at participating pharmacies.

Cultural safety

Medication adherence

Specific conditions

Referral pathways

📚 References

1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
2. Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res. 2021;73(7):924–939.
3. Fanouriakis A, Kostopoulou M, Alber K, et al. 2019 update of the EULAR recommendations for the management of systemic lupus erythematosus. Ann Rheum Dis. 2019;78(6):736–745.
4. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Care Res. 2021;73(11):1583–1599.
5. Smolen JS, Landewé RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2022 update. Ann Rheum Dis. 2023;82(1):3–18.
6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
7. Rheumatic Heart Disease Australia (RHDAustralia). The 2020 Australian guideline for prevention, diagnosis, and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
9. Agarwal S, Cunnington J, Nossent J. Autoimmune disease in Indigenous Australians: a systematic review. Int J Rheum Dis. 2021;24(12):1487–1498.
10. Pisetsky DS. Antinuclear antibody testing — misunderstood or misused? Clin Immunol. 2023;255:109717.
11. Bertsias GK, Tektonidou M, Amoura Z, et al. Joint European League Against Rheumatism and European Renal Association–European Dialysis and Transplant Association (EULAR/ERA-EDTA) recommendations for the management of adult and paediatric lupus nephritis. Ann Rheum Dis. 2012;71(11):1771–1782.
12. Ledingham J, Deighton C; British Society for Rheumatology Standards, Audit and Guidelines Working Group. Update on the British Society for Rheumatology guidelines for prescribing TNFα blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).