Prerequisites and Baseline Assessment

  1. General principles

Before initiating obesity treatment, adults should undergo a comprehensive, person-centred assessment. Permission should be obtained before discussing weight or taking anthropometric measurements. Communication should be respectful, non-judgemental and free from weight-related stigma. Clinicians should also avoid automatically attributing unrelated symptoms or medical conditions to obesity.

Body mass index (BMI) is a practical screening measure but does not directly measure body fat, fat distribution, organ dysfunction or functional impairment. It should therefore be interpreted together with waist circumference or waist-to-height ratio, the presence of obesity-related complications, physical functioning and quality of life. (NICE)

2. Medical history

The initial medical history should include:

  • Weight history: age at onset, previous weight trajectory, periods of rapid weight gain, previous weight-management interventions and their outcomes, weight cycling, and possible precipitating factors.
  • Family history: obesity, type 2 diabetes, dyslipidaemia, hypertension, premature cardiovascular disease and relevant endocrine disorders.
  • Eating patterns and dietary history: meal frequency and timing, portion sizes, highly processed foods, sugar-sweetened beverages, alcohol intake, emotional eating, loss-of-control eating, binge-eating episodes and night-eating behaviour.
  • Physical activity and sedentary behaviour: occupational and leisure-time activity, mobility limitations and physical capacity.
  • Sleep: sleep duration and quality, shift work, snoring, witnessed apnoeas and daytime sleepiness.
  • Medication history: drugs that may promote weight gain, including glucocorticoids, some antipsychotics, antidepressants, antiepileptic medicines, insulin and certain other glucose-lowering medicines.
  • Glucocorticoid exposure: oral, injected, inhaled, topical, nasal and rectal glucocorticoids must be considered before investigating endogenous Cushing syndrome.
  • Obesity-related complications: prediabetes or diabetes, hypertension, dyslipidaemia, cardiovascular disease, metabolic dysfunction-associated steatotic liver disease, obstructive sleep apnoea, osteoarthritis, gastro-oesophageal reflux, kidney disease and reproductive or menstrual disorders.
  • Mental health and psychosocial factors: depression, anxiety, eating disorders, chronic stress, quality of life, experiences of stigma, social support, financial constraints and food insecurity.
  • Smoking and alcohol use.
  • Pregnancy, pregnancy plans and contraception, when relevant to the proposed treatment.
  • The patient’s goals, expectations, preferences and previous experiences of treatment.

Eating disorders, clinically relevant psychological distress and obesity-related limitations in everyday functioning should be identified and addressed because they may affect treatment planning and outcomes. (EASO)

Physical examination

The baseline examination should include:

  • Height and body weight, measured using suitable and adequately sized equipment.
  • Calculation of BMI.
  • Waist circumference and, where appropriate, waist-to-height ratio.
  • Blood pressure using a correctly sized cuff; pulse rate should also be documented.
  • Assessment of fat distribution, mobility, muscle strength and functional capacity.
  • Examination for obesity-related complications and signs of secondary causes of weight gain.

Relevant clinical signs may include acanthosis nigricans, oedema, features of hypothyroidism, and features suggestive of hypercortisolism, such as wide reddish-purple striae, easy bruising, thin skin, facial plethora, proximal muscle weakness and otherwise unexplained osteoporosis. BMI should be interpreted cautiously in people with high muscle mass, older adults and some ethnic populations in whom cardiometabolic risk may occur at lower BMI values. (EASO)

4. Baseline laboratory assessment

Laboratory investigations should be adapted to the individual’s medical history, comorbidities and planned treatment. A reasonable baseline assessment includes:

  • Fasting plasma glucose and/or HbA1c.
  • Total cholesterol, LDL cholesterol, HDL cholesterol and triglycerides.
  • Serum creatinine and estimated glomerular filtration rate.
  • Urine albumin-to-creatinine ratio, particularly in people with diabetes, hypertension or kidney disease.
  • Serum uric acid.
  • Thyroid-stimulating hormone (TSH).
  • Free thyroxine (free T4) if the TSH result is abnormal or thyroid disease is clinically suspected.
  • Liver enzymes, such as ALT, AST and GGT, with further liver or fibrosis assessment when indicated.
  • Additional investigations according to symptoms, comorbidities and the intended intervention.

Routine measurement of random serum cortisol is not suitable for excluding Cushing syndrome because cortisol secretion varies substantially throughout the day. Broad endocrine testing is not required in every person with obesity unless the history or examination suggests a specific endocrine disorder.

5. Endocrine causes of weight gain

Endocrine disorders such as overt hypothyroidism and endogenous Cushing syndrome can contribute to weight gain, but they are uncommon primary causes of marked obesity.

Overt hypothyroidism is associated with weight gain, although the increase is usually modest and is partly caused by fluid retention. TSH is the recommended initial investigation. If TSH is elevated, it should generally be repeated and supplemented by free T4 and, where appropriate, thyroid peroxidase antibodies. Subclinical hypothyroidism does not necessarily cause weight gain, and thyroid hormone treatment should not be prescribed solely as a weight-loss intervention in euthyroid individuals.

Cushing syndrome

Endogenous Cushing syndrome is very rare. Its incidence is approximately 2–3 cases per million people per year, although recent global estimates range from approximately 1.8 to 4.5 cases per million per year. Exogenous glucocorticoid exposure is the most common cause of Cushing syndrome overall and must be excluded before biochemical testing for an endogenous cause. “Cushing disease” specifically refers to the pituitary ACTH-producing form of endogenous Cushing syndrome.

Routine screening for Cushing syndrome in every person with obesity is not recommended. Testing is appropriate when there are multiple, progressive or relatively specific features of hypercortisolism, unusual findings for the patient’s age, or a relevant adrenal incidentaloma. The German S3 guideline also recommends biochemical exclusion of hypercortisolism in patients being evaluated for bariatric surgery.

  1. The 1-mg Overnight Dexamethasone Suppression Test

When there is a justified clinical suspicion of Cushing syndrome, an overnight 1-mg dexamethasone suppression test may be performed.

Procedure

  1. The patient takes 1 mg of dexamethasone orally at approximately 23:00, or between 23:00 and midnight.
  2. Serum cortisol is measured the following morning, usually between 08:00 and 09:00.
  3. The patient should follow the laboratory’s instructions regarding fasting and the timing of regular medication.

Interpretation

A morning serum cortisol concentration of less than 1.8 µg/dL, equivalent to less than 50 nmol/L, generally represents adequate suppression and makes endogenous Cushing syndrome unlikely. However, the result must be interpreted using the assay-specific reference range and the local laboratory’s validated cut-off.

A cortisol result above the cut-off is an abnormal screening result but does not, by itself, establish the diagnosis of Cushing syndrome. The patient should be referred for endocrinological assessment and usually undergo a second recommended test, such as:

  • Two late-night salivary cortisol measurements.
  • At least two 24-hour urinary free-cortisol measurements.
  • A repeated or alternative dexamethasone suppression test, depending on the clinical circumstances.

A normal test does not completely exclude cyclic Cushing syndrome or disease in a patient with a very high clinical probability. Such patients require specialist assessment.

Factors that may interfere with the test include poor adherence, oestrogen-containing medication, pregnancy, alcohol misuse, severe depression, acute illness and medicines that alter dexamethasone metabolism. These factors should be reviewed before testing and considered when interpreting an unexpected result.

7. Readiness, resources and shared treatment planning

The patient’s readiness for change, confidence, treatment preferences and available resources should be explored in relation to nutritional treatment, physical activity, behavioural support, pharmacotherapy and metabolic or bariatric surgery. Readiness should be assessed collaboratively and should not be used as a simplistic test of whether a patient is “sufficiently motivated” to receive care.

Potential barriers should be identified, including pain, mobility limitations, mental illness, eating disorders, caregiving responsibilities, working hours, financial restrictions, limited access to healthy food, language barriers and previous experiences of stigma.

Treatment goals should be agreed through shared decision-making and should not focus exclusively on body weight. Relevant goals may include:

  • Prevention or improvement of obesity-related complications.
  • Improved physical function, mobility and fitness.
  • Better sleep, pain control and quality of life.
  • Sustainable changes in eating and activity patterns.
  • Clinically meaningful weight reduction and prevention of weight regain.
  • Reduction of medication burden where medically appropriate.

Obesity should be managed as a chronic, frequently relapsing condition. The treatment plan should specify the selected interventions, safety monitoring, follow-up intervals and criteria for modifying or escalating treatment.

References

  1. Deutsche Adipositas-Gesellschaft (DAG) e.V., et al. S3 Guideline: Prevention and Treatment of Obesity. Version 5.0. AWMF Register No. 050-001; October 2024. (AWMF Leitlinienregister)
  2. National Institute for Health and Care Excellence. Overweight and Obesity Management. NICE Guideline NG246. Published January 2025; reviewed January 2026. (NICE)
  3. Rubino F, Cummings DE, Eckel RH, et al. Definition and diagnostic criteria of clinical obesity. Lancet Diabetes Endocrinol. 2025;13(3):221–262. doi:10.1016/S2213-8587(24)00316-4. (PubMed)
  4. 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. (OUP Academic)
  5. Gadelha M, Gatto F, Wildemberg LE, Fleseriu M. Cushing’s syndrome. Lancet. 2023;402(10418):2237–2252. doi:10.1016/S0140-6736(23)01961-X. (ScienceDirect)