One-liner#

Obesity management requires treating it as a chronic disease with realistic expectations (5-10% weight loss improves health outcomes), combining lifestyle intervention with pharmacotherapy (GLP-1 RAs most effective) or bariatric surgery referral when BMI criteria met, while addressing metabolic comorbidities and avoiding weight stigma.

Quick nav#

• Definition and epidemiology
• Pathophysiology
• Clinical presentation
• Diagnostic workup
• Treatment
• Patient education
• Prognosis and monitoring
• Special populations
• When to refer
• Smartphrase snippets
• Related pages

Definition and epidemiology#

Diagnostic criteria#

BMI classification (adults):

Ethnic-specific thresholds:

• Asian populations: overweight ≥23, obesity ≥27.5 (increased metabolic risk at lower BMI)
• Use standard thresholds for treatment eligibility but recognize increased risk at lower BMI

Waist circumference (cardiometabolic risk):

• Men: >40 inches (>102 cm) = increased risk
• Women: >35 inches (>88 cm) = increased risk
• Asian populations: Men >35 inches, Women >31 inches

Edmonton Obesity Staging System (functional assessment):

• Stage 0: No obesity-related risk factors or symptoms
• Stage 1: Subclinical risk factors (borderline BP, impaired fasting glucose)
• Stage 2: Established comorbidities (T2DM, HTN, OSA, NAFLD)
• Stage 3: End-organ damage (MI, HF, diabetic complications)
• Stage 4: Severe disability from obesity-related conditions

Epidemiology#

Prevalence is 42% of US adults (2020 data); severe obesity (BMI ≥40) affects 9.2%. Prevalence has tripled since 1980. Higher rates in non-Hispanic Black adults (50%) and Hispanic adults (45%) compared to non-Hispanic White adults (42%). Socioeconomic gradient: higher prevalence with lower income and education. Obesity-related conditions account for $173 billion annually in US healthcare costs. Risk factors include genetic predisposition (40-70% heritability), obesogenic environment (food availability, sedentary lifestyle), medications, sleep deprivation, and psychological factors.

Pathophysiology#

Mechanism (clinical understanding)#

Obesity results from chronic positive energy balance, but the underlying biology is far more complex than “calories in, calories out.” Understanding these mechanisms explains why weight loss is difficult and why medications targeting specific pathways are effective.

Energy homeostasis and set point theory: The hypothalamus regulates body weight around a “set point” through hormonal signals. Leptin (from adipose tissue) signals satiety; ghrelin (from stomach) signals hunger. In obesity, leptin resistance develops—despite high leptin levels, the brain doesn’t receive the satiety signal. This is why weight regain after dieting is so common: the body defends its set point.

Metabolic adaptation: When caloric intake decreases, resting metabolic rate drops disproportionately (beyond what’s expected from weight loss alone). This “metabolic adaptation” can persist for years, making weight maintenance difficult. A person who lost 50 lbs may burn 300-500 fewer calories/day than someone who was never obese at the same weight.

Gut hormones and the incretin effect: GLP-1 and GIP (incretins) are released from the gut after eating, promoting satiety and insulin secretion. In obesity, this incretin effect is blunted. This explains why GLP-1 receptor agonists are so effective—they restore and amplify this satiety signal.

Adipose tissue dysfunction: Adipose tissue is not just storage—it’s an endocrine organ. In obesity, adipocytes become hypertrophied and dysfunctional, releasing pro-inflammatory cytokines (TNF-α, IL-6) and less adiponectin. This creates chronic low-grade inflammation driving insulin resistance, NAFLD, and cardiovascular disease.

Genetic factors: Over 100 genes influence body weight. Monogenic obesity (MC4R mutations, leptin deficiency) is rare but illustrates the biological basis. Common variants (FTO, MC4R polymorphisms) each contribute small effects that aggregate. Genetics explains ~40-70% of BMI variation.

How to explain to patients#

Your body has a built-in system that tries to keep your weight stable, like a thermostat. When you lose weight, your body fights back—it slows down your metabolism and makes you hungrier. This is not a lack of willpower; it is biology.

Think of it like this: if you were stranded without food, this system would help you survive by conserving energy. But in our modern world with abundant food, this same system makes it very hard to lose weight and keep it off.

This is why obesity is a medical condition, not a character flaw. Just like we use medications for high blood pressure or diabetes, we can use medications that work with your body’s hunger and fullness signals to help you lose weight and keep it off.

The good news is that even modest weight loss—5 to 10 percent of your body weight—can significantly improve your health, even if you don’t reach a “normal” BMI.

Clinical presentation#

Characteristic symptoms#

Often asymptomatic: Many patients with obesity have no symptoms directly from excess weight. Symptoms typically arise from complications or comorbidities.

Weight-related symptoms:

• Dyspnea on exertion (mechanical restriction, deconditioning)
• Joint pain (knees, hips, back—mechanical stress)
• Fatigue (may be from OSA, deconditioning, or depression)
• Skin issues (intertrigo, skin tags, acanthosis nigricans)
• GERD symptoms (increased intra-abdominal pressure)
• Urinary incontinence (stress incontinence from increased abdominal pressure)

Symptoms suggesting comorbidities:

• Snoring, witnessed apneas, daytime sleepiness → obstructive sleep apnea
• Polyuria, polydipsia → diabetes
• Chest pain, dyspnea → cardiovascular disease
• Right upper quadrant discomfort → NAFLD/NASH
• Menstrual irregularities, hirsutism → PCOS
• Depression, anxiety, social isolation → mental health impact

Symptoms suggesting secondary obesity:

• Rapid weight gain with purple striae, easy bruising → Cushing’s syndrome
• Fatigue, cold intolerance, constipation → hypothyroidism
• Weight gain temporally related to medication start → drug-induced

Physical exam findings#

Anthropometrics:

• BMI calculation (weight in kg / height in m²)
• Waist circumference (at iliac crest level)
• Weight trend over time (review chart)

Vital signs:

• Blood pressure (often elevated; use appropriate cuff size)
• Heart rate
• Neck circumference >17 inches (men) or >16 inches (women) suggests OSA risk

General:

• Fat distribution: central (android, “apple”) vs peripheral (gynoid, “pear”)
• Central obesity carries higher cardiometabolic risk
• Assess mobility, functional status

Skin:

• Acanthosis nigricans (velvety hyperpigmentation in neck, axillae—marker of insulin resistance)
• Skin tags (associated with insulin resistance)
• Intertrigo (erythema in skin folds)
• Striae (white/narrow = simple obesity; purple/wide = consider Cushing’s)

Cardiovascular:

• Blood pressure (use large cuff if arm circumference >34 cm)
• Peripheral edema (venous insufficiency, heart failure)
• JVD (if heart failure suspected)

Abdomen:

• Central adiposity
• Hepatomegaly (NAFLD)
• Difficult to assess for organomegaly due to habitus

Musculoskeletal:

• Joint tenderness (knees, hips)
• Gait assessment
• Proximal muscle weakness (if Cushing’s suspected)

Signs of secondary causes:

• Moon facies, buffalo hump, thin skin, easy bruising → Cushing’s
• Goiter, delayed reflexes → hypothyroidism
• Hirsutism, acne → PCOS

Red flags#

Rapid weight gain (>5 lbs/week) with:

• Dyspnea, orthopnea, edema → heart failure decompensation → ED
• Decreased urine output → acute kidney injury → ED
• Abdominal distension → ascites, malignancy → urgent evaluation

Features suggesting Cushing’s syndrome:

• Central obesity with thin extremities
• Purple striae >1 cm wide
• Proximal muscle weakness
• Easy bruising, thin skin
• Hypertension, hypokalemia
• Action: Screen with cortisol testing; refer to endocrinology

Severe obesity with respiratory compromise:

• Obesity hypoventilation syndrome (daytime hypercapnia)
• Severe OSA with hypoxemia
• Action: Urgent pulmonology/sleep medicine referral

Diagnostic workup#

Initial evaluation#

For all patients with obesity (BMI ≥30) or overweight (BMI ≥25) with comorbidities:

Interpretation notes:

• Hypothyroidism causes modest weight gain (5-10 lbs); if TSH normal, do not repeat
• Elevated ALT suggests NAFLD; consider hepatology referral if ALT >2x ULN or fibrosis suspected
• Prediabetes/diabetes: initiate appropriate management; weight loss improves glycemic control

Confirmatory testing#

When to screen for Cushing’s syndrome:

• Central obesity with any of: purple striae, easy bruising, proximal weakness, facial plethora, hypertension, hypokalemia
• Do NOT screen for Cushing’s in typical obesity without these features

Cushing’s screening options (choose one):

• 24-hour urine free cortisol (×2 collections)
• Late-night salivary cortisol (×2 samples)
• 1 mg overnight dexamethasone suppression test (cortisol <1.8 mcg/dL = normal)

If Cushing’s screen positive: Refer to endocrinology for confirmation and localization. Do NOT attempt to diagnose or manage in primary care.

When to screen for sleep apnea:

• STOP-BANG score ≥3 (Snoring, Tiredness, Observed apnea, Pressure [HTN], BMI >35, Age >50, Neck >17"/16", Gender male)
• Symptoms: snoring, witnessed apneas, daytime sleepiness, morning headaches
• Order: home sleep apnea test (HSAT) or refer for polysomnography

When to assess for PCOS:

• Premenopausal women with obesity + menstrual irregularity, hirsutism, or infertility
• Order: total testosterone, DHEA-S; consider pelvic ultrasound
• Refer to GYN or endocrinology for comprehensive evaluation

When to refer for specialist workup#

• Suspected Cushing’s syndrome (positive screening test)
• Suspected genetic/syndromic obesity (early-onset severe obesity, developmental delay, dysmorphic features)
• PCOS requiring comprehensive management
• Severe NAFLD/NASH (elevated ALT, fibrosis suspected)
• Obesity hypoventilation syndrome

What NOT to order#

• Extensive endocrine workup for typical obesity without red flags (Cushing’s features, rapid onset)
• Leptin levels: Not clinically useful; leptin resistance, not deficiency, is the issue
• Insulin levels: Do not guide management; insulin resistance is assumed
• Thyroid testing if recently normal: Hypothyroidism causes only modest weight gain
• Genetic testing: Only if syndromic obesity suspected (early-onset, severe, dysmorphic features)
• Resting metabolic rate testing: Rarely changes management; expensive

Treatment#

Goals of therapy#

Weight loss targets:

• Initial goal: 5-10% of body weight over 6-12 months
• This modest loss significantly improves: BP (5-10 mmHg), A1c (0.5-1%), lipids, OSA, NAFLD, joint pain
• Further weight loss (10-15%+) provides additional benefits
• “Normal BMI” is not the goal for most patients—focus on health improvement

Realistic expectations:

• Lifestyle alone: 3-5% weight loss (sustained)
• Lifestyle + medication: 5-15% weight loss (varies by agent)
• Bariatric surgery: 20-35% weight loss (sustained)
• Weight regain is common; obesity is a chronic disease requiring ongoing treatment

Comorbidity targets:

• BP <130/80 mmHg
• A1c <7% (or individualized)
• LDL per cardiovascular risk
• OSA: CPAP adherence, AHI improvement

Non-pharmacologic management#

Dietary intervention:

• Caloric deficit: 500-750 kcal/day below estimated needs (yields ~1 lb/week loss)
• No single “best diet”—adherence matters more than specific approach
• Evidence-based options: Mediterranean, DASH, low-carbohydrate, low-fat, intermittent fasting
• Key principles: reduce ultra-processed foods, sugar-sweetened beverages, large portions
• Emphasize: vegetables, fruits, whole grains, lean protein, healthy fats
• Refer to registered dietitian for medical nutrition therapy

Physical activity:

• 150-300 minutes/week moderate-intensity aerobic activity (brisk walking, cycling)
• Resistance training 2-3 days/week (preserves muscle mass during weight loss)
• Any activity is better than none; start where patient is
• Exercise alone produces modest weight loss (~2-3%) but improves metabolic health independent of weight
• Critical for weight maintenance after loss

Behavioral strategies:

• Self-monitoring: food diary, regular weigh-ins (weekly)
• Stimulus control: remove trigger foods from home, smaller plates
• Stress management: identify emotional eating triggers
• Sleep optimization: 7-9 hours/night (sleep deprivation increases hunger hormones)
• Social support: family involvement, support groups

Structured programs:

• Intensive behavioral therapy (IBT): ≥14 sessions in 6 months; covered by Medicare for BMI ≥30
• Commercial programs with evidence: WW (Weight Watchers), Noom
• Consider referral to obesity medicine specialist or comprehensive weight management program

Pharmacologic management#

Indications for anti-obesity medications:

• BMI ≥30, OR
• BMI ≥27 with weight-related comorbidity (T2DM, HTN, dyslipidemia, OSA)
• After lifestyle intervention alone is insufficient (typically 3-6 months trial)

First-line agents (GLP-1 receptor agonists—most effective):

GLP-1 RA prescribing pearls:

• Start low, titrate slowly to minimize GI side effects (nausea, vomiting, diarrhea)
• GI side effects usually improve over 4-8 weeks
• Counsel: eat smaller portions, stop eating when full, avoid fatty foods
• Weight regain is common if medication stopped—plan for long-term use
• Check insurance coverage before prescribing; prior authorization often required

Second-line/alternative agents:

Choosing anti-obesity medication:

• Most effective: Tirzepatide > semaglutide > liraglutide > phentermine-topiramate
• Comorbid T2DM: Tirzepatide or semaglutide (also treat diabetes; use diabetes-labeled versions)
• Comorbid depression: Consider naltrexone-bupropion (bupropion component)
• Cost-sensitive: Phentermine (short-term), orlistat (OTC available)
• Avoid if: Eating disorder history (most agents); seizure disorder (bupropion); opioid use (naltrexone); pregnancy (all)

Medication access and insurance:

• Many insurers exclude weight loss medications; verify coverage before prescribing
• Prior authorization typically required; document BMI, comorbidities, failed lifestyle intervention
• Manufacturer savings programs available (check manufacturer websites)
• Avoid compounded semaglutide/tirzepatide: FDA warnings about safety, sterility, and efficacy concerns

Assessing medication efficacy:

• Evaluate at 12-16 weeks on maintenance dose
• If <5% weight loss: reassess adherence, consider alternative agent or bariatric surgery
• If ≥5% weight loss: continue; medication is working

Duration of therapy:

• Obesity is a chronic disease; medications are typically long-term
• Weight regain is expected if medication stopped
• If stopping medication, taper and intensify lifestyle support

Patient counseling points#

For GLP-1 receptor agonists:

• “This medication works with your body’s natural fullness signals. It helps you feel satisfied with less food.”
• “We start at a low dose and increase slowly over several months to reduce side effects.”
• “Nausea is common at first. Eat smaller meals, avoid fatty foods, and it usually improves.”
• “Most people lose 15-20% of their body weight. This significantly improves your health.”
• “If you stop the medication, weight regain is common. Plan to take it long-term.”
• “This is not a shortcut—you still need to eat well and stay active. The medication makes it easier.”

For phentermine-topiramate:

• “This combination reduces appetite and helps you feel full. It’s quite effective.”
• “It can cause tingling in hands/feet, taste changes, and difficulty concentrating. These usually improve.”
• “You must use reliable birth control—this medication can cause serious birth defects.”
• “Avoid alcohol—it can worsen side effects.”

For naltrexone-bupropion:

• “This medication reduces food cravings and the reward you get from eating.”
• “It can cause nausea, headache, and constipation initially.”
• “Do not take this if you use opioid pain medications—it will block their effect.”
• “Tell me if you have mood changes or thoughts of self-harm.”

For bariatric surgery discussion:

• “Surgery is the most effective treatment for severe obesity. Most people lose 25-35% of their weight.”
• “It’s not the ’easy way out’—it requires lifelong dietary changes and follow-up.”
• “Surgery significantly improves or resolves diabetes, sleep apnea, and high blood pressure.”
• “There are risks, but for most people with severe obesity, the benefits outweigh the risks.”

Monitoring and follow-up#

During medication titration:

• Follow-up every 4 weeks during dose escalation
• Assess tolerability, side effects, weight change
• Adjust titration speed based on tolerability

Once on stable dose:

• Follow-up every 3 months
• Monitor: weight, BP, comorbidity status
• Reassess medication efficacy at 12-16 weeks

Annual monitoring:

• Fasting glucose or A1c
• Lipid panel
• ALT (if NAFLD)
• Reassess comorbidities (OSA, HTN, diabetes)

Comorbidity improvement timeline:

• BP: improves within weeks of weight loss
• A1c: improves over 2-3 months
• OSA: reassess after 10% weight loss; may need CPAP adjustment
• NAFLD: ALT improves; fibrosis regression takes longer

Patient education#

What is this condition?#

Obesity is a medical condition where your body stores more energy as fat than is healthy. It is not about willpower or character—it is about biology.

Your body has a system that controls hunger and fullness, like a thermostat. In obesity, this system is set higher than it should be. When you try to lose weight, your body fights back by making you hungrier and slowing your metabolism. This is why losing weight and keeping it off is so hard.

Obesity increases your risk for many health problems including diabetes, high blood pressure, heart disease, sleep apnea, joint pain, and some cancers. The good news is that even losing 5 to 10 percent of your weight can significantly improve your health.

What you can do#

Focus on sustainable changes, not quick fixes. Aim to lose 1 to 2 pounds per week.

Eat more vegetables, fruits, whole grains, and lean proteins. Reduce sugary drinks, processed foods, and large portions. You do not need a special diet—find an eating pattern you can stick with.

Be active for at least 150 minutes per week. Walking counts. Any movement is better than none. Exercise helps you keep weight off and improves your health even without weight loss.

Get enough sleep—7 to 9 hours per night. Poor sleep increases hunger hormones and makes weight loss harder.

Keep a food diary or use an app to track what you eat. This helps you become aware of your eating patterns.

If lifestyle changes are not enough, medications or surgery may help. These are medical treatments, not signs of failure.

When to seek care#

Call your doctor if you gain weight rapidly (more than 5 pounds in a week) with swelling in your legs or shortness of breath.

Call if you have symptoms of diabetes: increased thirst, frequent urination, or blurred vision.

Call if you have symptoms of sleep apnea: loud snoring, gasping at night, or severe daytime sleepiness.

Call if you are having side effects from weight loss medications that are not improving.

Call if you feel depressed, hopeless, or have thoughts of harming yourself.

Questions to ask your doctor#

• What is my BMI, and what does it mean for my health?
• What health problems do I have that are related to my weight?
• What is a realistic weight loss goal for me?
• Would weight loss medication help me? What are the options?
• Am I a candidate for weight loss surgery?
• Can you refer me to a dietitian or weight management program?
• How often should I follow up with you?

Prognosis and monitoring#

Expected course#

With treatment:

• Lifestyle alone: 3-5% sustained weight loss; significant health benefits
• Lifestyle + medication: 5-20% weight loss depending on agent; requires ongoing treatment
• Bariatric surgery: 20-35% sustained weight loss; highest remission rates for comorbidities
• Weight maintenance requires ongoing effort; obesity is a chronic disease

Without treatment:

• Progressive weight gain in most individuals
• Increasing comorbidity burden (diabetes, HTN, OSA, NAFLD, CVD)
• Reduced quality of life and functional status
• Reduced life expectancy (BMI 30-35: 2-4 years; BMI >40: 8-14 years)

Weight regain:

• Common after any weight loss intervention
• ~50% of lost weight regained within 2 years without ongoing treatment
• Metabolic adaptation persists, making maintenance difficult
• This is biology, not failure—emphasize ongoing treatment

Monitoring parameters#

Complications to watch for#

Metabolic:

• Type 2 diabetes: screen annually; weight loss can prevent or reverse
• Dyslipidemia: screen annually; improves with weight loss
• NAFLD/NASH: monitor ALT; consider hepatology referral if fibrosis suspected

Cardiovascular:

• Hypertension: monitor every visit; improves with weight loss
• Coronary artery disease: assess cardiovascular risk; statin therapy per guidelines
• Heart failure: watch for symptoms; obesity is a risk factor

Respiratory:

• Obstructive sleep apnea: screen with STOP-BANG; treat with CPAP; reassess after weight loss
• Obesity hypoventilation syndrome: rare but serious; refer to pulmonology

Musculoskeletal:

• Osteoarthritis: weight loss reduces joint stress; consider orthopedic referral if severe
• Gout: weight loss can trigger flares initially; prophylaxis may be needed

Psychological:

• Depression: screen regularly; weight stigma contributes; treat concurrently
• Eating disorders: screen before starting medications; contraindication to some agents
• Body image concerns: address with supportive counseling

Medication-related:

• GLP-1 RA: GI side effects, rare pancreatitis, gallbladder disease
• Phentermine-topiramate: cognitive effects, teratogenicity, mood changes
• Rapid weight loss: gallstones (consider ursodiol prophylaxis if >1.5 kg/week loss)

Special populations#

Elderly/geriatric#

Considerations:

• Sarcopenic obesity: loss of muscle mass with preserved or increased fat mass
• Weight loss may worsen sarcopenia and frailty
• Focus on functional status, not just BMI
• Intentional weight loss in elderly is controversial; individualize

Approach:

• Emphasize protein intake (1.0-1.2 g/kg/day) to preserve muscle
• Prioritize resistance training
• Modest caloric restriction (avoid severe deficits)
• Consider anti-obesity medications cautiously; less data in elderly
• GLP-1 RA: may cause excessive weight loss; monitor closely
• Avoid phentermine (cardiovascular concerns)

Goals:

• Improve functional status and quality of life
• Manage comorbidities
• Prevent further weight gain
• Avoid unintentional weight loss (may indicate illness)

Chronic kidney disease#

Medication adjustments:

• GLP-1 RA (semaglutide, liraglutide, tirzepatide): no dose adjustment; use cautiously in severe CKD (limited data)
• Orlistat: no adjustment; may impair fat-soluble vitamin absorption
• Phentermine: avoid in severe CKD
• Naltrexone-bupropion: avoid if eGFR <30

Considerations:

• Obesity accelerates CKD progression
• Weight loss may slow CKD progression
• SGLT2 inhibitors provide renal protection independent of weight loss
• Bariatric surgery: can be performed in CKD; improves renal outcomes

Other populations#

Pregnancy:

• Weight loss medications contraindicated in pregnancy
• Phentermine-topiramate: teratogenic (REMS program requires pregnancy testing)
• GLP-1 RA: discontinue 2 months before planned conception
• Focus on healthy weight gain during pregnancy per IOM guidelines
• Postpartum: can resume weight management after breastfeeding (or during, depending on agent)

Type 2 diabetes:

• Prioritize weight loss agents that also improve glycemic control
• Tirzepatide (Mounjaro for diabetes; Zepbound for obesity): most effective for both
• Semaglutide (Ozempic for diabetes; Wegovy for obesity): excellent for both
• Avoid sulfonylureas, TZDs, insulin if possible (cause weight gain)
• SGLT2 inhibitors: modest weight loss + cardiorenal protection
• Weight loss can lead to diabetes remission, especially if early in disease course

Cardiovascular disease:

• GLP-1 RA (semaglutide, liraglutide): cardiovascular benefit demonstrated
• Avoid phentermine and phentermine-topiramate (cardiovascular concerns)
• Weight loss improves cardiovascular risk factors
• Bariatric surgery reduces cardiovascular events

PCOS:

• Weight loss improves all PCOS features (menstrual regularity, hirsutism, fertility)
• 5-10% weight loss can restore ovulation
• GLP-1 RA effective; metformin provides modest benefit
• Coordinate with GYN/endocrinology

Polypharmacy:

• Review medications for weight-promoting agents
• Common culprits: antipsychotics, some antidepressants, anticonvulsants, insulin, sulfonylureas, corticosteroids
• Substitute weight-neutral or weight-losing alternatives when possible
• Coordinate with prescribing providers before changing psychiatric medications

When to refer#

Specialist referral criteria#

Obesity medicine/bariatric medicine referral:

• BMI ≥40 (or ≥35 with comorbidities) for bariatric surgery evaluation
• Failed multiple weight loss attempts; need comprehensive program
• Complex medication management
• Patient preference for specialist care

Bariatric surgery referral criteria:

• BMI ≥40, OR
• BMI ≥35 with obesity-related comorbidity (T2DM, HTN, OSA, NAFLD, GERD, etc.)
• Failed medical weight loss attempts
• Patient understands lifelong dietary changes and follow-up required
• No active substance abuse or uncontrolled psychiatric illness

Endocrinology referral:

• Suspected Cushing’s syndrome (positive screening test)
• Suspected genetic/syndromic obesity
• Complex diabetes management with obesity
• PCOS requiring comprehensive management

Hepatology/GI referral:

• NAFLD with elevated ALT >2× ULN
• Suspected NASH or fibrosis (FIB-4 >1.3)
• Abnormal liver imaging

Sleep medicine referral:

• Suspected OSA (positive screening, symptoms)
• Obesity hypoventilation syndrome

Psychiatry/psychology referral:

• Eating disorder (binge eating disorder, bulimia)
• Severe depression or anxiety affecting weight management
• Psychological evaluation required for bariatric surgery

Dietitian referral:

• All patients benefit from medical nutrition therapy
• Complex dietary needs (diabetes, CKD, food allergies)
• Bariatric surgery pre- and post-operative nutrition

Urgency levels#

Smartphrase snippets#

Obesity, initial evaluation: Obesity class [I/II/III], BMI [X] with comorbidity screening showing [A1c, lipids, ALT, BP results]. Discussed obesity as chronic disease; plan includes lifestyle intervention with [caloric goal, activity goal] and referral to [dietitian/program]. Will consider anti-obesity medication if insufficient response at follow-up in [4-8 weeks].

Obesity, initiating GLP-1 RA: Obesity BMI [X] with [comorbidities], initiating [semaglutide/tirzepatide] [dose] for weight management after ongoing lifestyle intervention. Counseled on GI side effects, slow titration schedule, and need for long-term use as weight regain is common if stopped. Follow-up in 4 weeks to assess tolerability.

Obesity, stable on medication: Obesity on [medication] [dose] with weight [X] lbs, down [X] lbs ([X]%) from baseline. Tolerating medication well with [comorbidity improvements: BP, A1c, etc.]. Continue current regimen with follow-up in 3 months.

Obesity, bariatric surgery referral: Obesity class [II/III], BMI [X] with [comorbidities] after failed medical weight loss including [lifestyle, medications tried]. Discussed bariatric surgery as most effective treatment; patient interested and understands lifelong commitment. Referring to bariatric surgery for evaluation.

Related pages#

• Weight Gain (complaint) — symptom-based approach to weight gain differential and initial evaluation
• Type 2 Diabetes (problem) — commonly comorbid; weight loss improves glycemic control
• Hypothyroidism (problem) — secondary cause of modest weight gain
• Hypertension (problem) — obesity-related comorbidity; improves with weight loss
• Hyperlipidemia (problem) — metabolic syndrome component
• Obstructive Sleep Apnea (problem) — obesity-related; improves with weight loss
• Heart Failure (problem) — obesity is risk factor; weight loss may help HFpEF