L16 Metabolism Intro to bariatric surgery

Overview

This lecture covers the medical and surgical treatment of obesity beyond diet and exercise. It moves from the scale of the obesity problem and its associated medical complications, through the physiological reasons weight loss is hard to sustain, into the mechanisms, outcomes, and comparative risks of bariatric surgery procedures (Roux-en-Y gastric bypass, one anastomosis gastric bypass, sleeve gastrectomy), and the mechanisms, drug options, and trial evidence for incretin-based pharmacotherapy (GLP-1 receptor agonists). It closes by comparing the two treatment routes and introducing the Edmonton Obesity Staging System as a tool for deciding who benefits most from surgical versus medical treatment.

Scale and Impact of Obesity

NZ adult population by BMI category:

• BMI 40+ (Class III): 252,000 adults, 5.8%
• BMI 35–40 (Class II): 382,000 adults, 8.8%
• BMI 30–35 (Class I): 843,000 adults, 19.5%
• BMI 25–30 (overweight): 1,434,000 adults, 33.2%

Important

Only a minority of the overweight/obese population (BMI ≥35, or ≥30 with complications) actually meets bariatric surgery indication criteria — the lecture explicitly contrasts the size of the total affected population against the much smaller group eligible for surgery (“But…”).

Medical problems associated with obesity, as listed on slide 4:

• Pulmonary: obstructive sleep apnoea, hypoventilation syndrome, pulmonary hypertension, asthma, abnormal function
• Hepatic: nonalcoholic fatty liver disease — steatosis, steatohepatitis, cirrhosis
• Cardiometabolic: high cholesterol, high blood pressure, coronary heart disease (diabetes, dyslipidaemia, hypertension), stroke, blood clots (phlebitis/venous stasis, immobility)
• Gastrointestinal: gall bladder disease, gastroesophageal reflux, severe pancreatitis
• Gynaecological: abnormal menses, infertility, polycystic ovarian syndrome, obstetric complications
• Musculoskeletal: joint pain/osteoarthritis, degenerative joint disease, low back pain, leg swelling/gout
• Neurological/psychological: idiopathic intracranial hypertension, depression, cataracts
• Other: skin problems, urinary incontinence, cancer (breast, uterus, cervix, colon, oesophagus, pancreas, kidney, prostate)

Warning

Slide 4 highlights a subset of these items in red/bold (e.g. obstructive sleep apnoea, high cholesterol, high blood pressure, infertility, joint pain, depression, reflux, diabetes, low back pain, urinary incontinence, degenerative joint disease) but does not state what the highlighting signifies; interpreted as emphasis only, not confirmed by the slide.

Why Weight Gain Occurs and Why Loss Is Hard to Sustain

• Human bodies, genes, brains and physiology evolved for a hunter-gatherer environment: food was scarce, hard to obtain, and the ability to store fat/food was advantageous.
• The modern environment mismatches this physiology: food is abundant and engineered for taste, and fossil fuels have replaced physical work.

Energy balance model of weight change:

• Weight stable state: energy consumed = energy burned (~2000 kcal/day each side, illustrated as a balanced see-saw). Energy consumed depends on food eaten (amount, energy density); energy burned depends on metabolic rate (~1400–1800 kcal/day) and physical activity (~500 kcal/day).
• Weight loss requires burning more energy than is consumed.
• 1 kg of fat stores 7000 calories.
• Losing 0.5 kg/week requires a 500 calorie/day energy deficit.
• In a weight-loss (deficit) state, the see-saw tips: energy consumed drops (~1500 kcal/day) below energy burned (~2000 kcal/day), but the body resists this via:
  • increased hunger
  • decreased metabolic rate
  • difficulty increasing physical activity
• Weight-loss surgery (WLS) reduces the amount eaten without increasing hunger to the same degree as dieting, which is why it is more effective at sustaining a deficit.

Bariatric Surgery: Procedures and Mechanisms

Three main procedures (slide 9):

1. Roux-en-Y Gastric Bypass — a small stomach pouch is connected to a rerouted section of small intestine in a Y-shaped configuration, bypassing part of the stomach and the duodenum.
2. One Anastomosis Gastric Bypass — a long narrow gastric pouch with a single loop connection to the small intestine (a simpler, single-anastomosis reconstruction than Roux-en-Y).
3. Sleeve Gastrectomy — most of the stomach is removed/stapled off into a narrow tube shape; the intestinal connection is left intact with no rerouting.

Mechanisms contributing to improved glycaemia after RYGB and sleeve gastrectomy (VSG), reproduced from Batterham and Cummings (slide 10), shown as a three-stage causal chain:

A. Immediate anatomical effects of surgery

• Caloric restriction (RYGB, sleeve)
• Rapid emptying of nutrients into the small intestine (RYGB, sleeve)
• Removal of the stomach fundus (sleeve only)
• Exclusion of the duodenum and proximal jejunum from nutrients (RYGB only)
• Enhanced nutrient/bile delivery to the mid/distal jejunum and ileum (RYGB, sleeve)

B. Potential mediators/mechanisms (cross-talk occurs among these)

• Altered bile acid / FGF-19 signalling
• Altered microbiome
• Altered gut hormones
• Altered neural signalling
• Intestinal adaptation / reprogramming of intestinal glucose handling
• Reduced hepatic and pancreatic triglycerides
• Reduced glucotoxicity
• Weight loss
• Altered GI nutrient-sensing

C. Effects on glucose homeostasis

• Improved β-cell function / functional β-cell mass
• Improved insulin sensitivity
• Reduced hepatic glucose production
• Increased glucose utilisation
• Increased glucose effectiveness

Incretins as a surgical mechanism

• GLP-1 (and GIP) are incretin hormones.
• GLP-1 is a 30- or 31-amino acid peptide hormone.
• Produced by L cells from proglucagon, mainly in the distal ileum and colon, but also the duodenum and jejunum.
• Secreted into the portal circulation.
• Degraded by DPP-4; DPP-4 inhibitor drugs block this enzyme, prolonging incretin action.
• Has high first-pass metabolism.

Core incretin action: incretins (GLP-1, GIP) stimulate insulin release and inhibit glucagon release, lowering blood glucose.

Broader GLP-1 effects by organ/tissue (slide 11, also reused on slide 16):

• Brain: neuroprotection, increased satiety, decreased appetite
• Tongue: increased taste sensitivity
• Heart: increased glucose uptake, cardioprotection, increased cardiac function
• Lungs: increased pulmonary protection
• Liver: decreased hepatic glucose production
• Stomach: decreased gastric emptying, gastric acid secretion, and gastric motility
• Adipose tissue: increased lipogenesis, adipogenesis, glucose uptake
• Kidneys: increased renoprotection
• Bones: increased bone formation, decreased bone resorption
• Muscles: increased glucose uptake, increased muscle microvasculature
• Pancreas: increased insulin secretion, insulin gene expression, somatostatin secretion, β-cell neogenesis and proliferation; decreased glucagon secretion

Warning

On slide 11, “β-cell glucose sensitivity” appears listed twice in the pancreas panel — once with an increase arrow and once with a decrease arrow. This is transcribed as it appears in the source figure; it likely represents two distinct sub-points that were not fully legible, not a contradiction to resolve.

Comparing the Three Surgical Procedures

	Roux-en-Y Gastric Bypass	One Anastomosis Gastric Bypass	Sleeve Gastrectomy
Average weight loss	25–35% of starting body weight	25–35%+	20–30%
Effect on diabetes	+++	+++/+	++
Effect on reflux	Improves symptoms	Variable	Worsens symptoms
Risk of vitamin deficiency	++	+++	+
Other long-term consequences	Ulcers, bowel obstruction	Ulcers, bowel obstruction, bile reflux	Reflux
Aspirin/NSAID use	Prohibited lifelong	Prohibited lifelong	Usually OK with caution

Shared across all three procedures:

• Hospital stay and recovery: one night in hospital; two to four weeks off work; two weeks liquid diet then two weeks puréed diet.
• Risk at time of surgery: 1% risk of serious complications; 0.2% risk of leakage from joins or staple lines; 0.1% risk of mortality.

Indications for Bariatric Surgery

• Like any medical intervention, it is a balance of risks versus benefits (benefits: weight loss, improved health; trade-offs: short-term risks, long-term consequences).
• Bariatric surgery is indicated where benefits are likely to outweigh short-term risks and long-term consequences:
  • BMI > 40 kg/m², or
  • BMI > 35 kg/m² with weight-related medical complications, or
  • BMI > 30 kg/m² with type 2 diabetes

Incretin-Based Pharmacotherapy (GLP-1 Receptor Agonists)

• GLP-1 receptor agonists are synthetic molecules that activate the GLP-1 receptor with longer half-lives than native GLP-1.
• Exenatide was the first approved by the US FDA, in 2005.

Current GLP-1 receptor agonists available in NZ:

• Dulaglutide (Trulicity) — once-weekly injection; indicated for T2DM, Special Authority (SA) funded
• Liraglutide (Saxenda) — once-daily injection; indicated for T2DM and weight loss
• Semaglutide (Ozempic/Wegovy) — once-weekly injection; indicated for T2DM and weight loss
• Tirzepatide (Monjuro) — once-weekly injection; dual GLP-1/GIP agonist; indicated for T2DM and weight loss

Warning

Slide 15 includes a PubMed search screenshot with a results-by-year bar chart; the exact per-year result counts are not legible from the image.

Indications, cost, and side effects (slide 16):

• Indications: BMI > 30 kg/m², or BMI > 27 kg/m² with weight-related complications
• Cost: approximately $500/month
• Maintenance/withdrawal noted as a consideration [slide does not elaborate further]
• Common side effects: nausea, vomiting, diarrhoea, gallstones, lean body mass (LBM) loss
• Rare but serious side effects: pancreatitis, medullary thyroid cancer

Clinical Trial Evidence

Semaglutide — STEP trials

• STEP 1: 1961 adults with obesity (BMI >30, or >27 with complications); randomised 2:1, 68 weeks once-weekly semaglutide vs placebo; T2DM excluded. Mean weight decrease −14.9% (semaglutide) vs −2.4% (placebo). Also improved waist circumference, blood pressure, lipids, HbA1c, and CRP. GI side effects more common with semaglutide (74.2% vs 47.9%).
• STEP 4: 803 adults, 20-week run-in on semaglutide, then randomised 2:1 to 48 weeks continuation (2.4 mg) vs placebo. ΔWt −17.4% vs −5.0%.
• STEP 5: 304 adults; randomised 1:1; 104 weeks 2.4 mg vs placebo. ΔWt −15.2% vs −2.6%.

Tirzepatide — SURMOUNT trials

• SURMOUNT 1: 2539 adults, 72 weeks; randomised 1:1:1:1 placebo, 5 mg, 10 mg, 15 mg once weekly; T2DM excluded. ΔWt −20.9% vs −3.1% (placebo); discontinuation 6.2% vs 2.6%.
• SURMOUNT 4: withdrawal-and-regain design. 783 adults, 36-week lead-in (10 or 15 mg once weekly), then 670 randomised 1:1 to 52 weeks continuation vs placebo. ΔWt −25.8% vs −9.5%.
• SURMOUNT 5: 751 adults with obesity (BMI >30 or >27); T2DM excluded; randomised 1:1, 72 weeks, semaglutide (1.7 or 2.4 mg) vs tirzepatide (10 or 15 mg). Semaglutide weight change −15.4% vs tirzepatide −21.6%; waist circumference change −14.7 cm vs −20.0 cm. Side effects common and similar between drugs: overall 77.9%, serious 4.1%, discontinuation of treatment 7.1%.

Real-world data

• Retrospective cohort, 7881 patients, semaglutide and tirzepatide.
• High discontinuation rates.
• Low real-world weight loss at 1 year: 8.7% overall, rising to 11.9% if treatment continued at 1 year.
• Mean weight change at 12 months roughly −8% (semaglutide) vs −12% (tirzepatide) in one graph; a further breakdown by discontinuation status showed the largest decline in those who never discontinued (−12%), a smaller decline with late discontinuation, and the smallest decline with early discontinuation (−4%).

Important

Real-world weight loss with incretin therapy is substantially lower than in clinical trials, driven largely by discontinuation — a key limitation compared with the trial-reported 15–26% weight loss figures.

Surgery vs Incretin Therapy: Summary Comparison

Bariatric surgery

• Proven long-term outcomes, especially for BMI >35
• Higher average weight loss, ~25–30%
• Weight loss maintained
• Higher up-front risk of serious side effects (~1%)
• Higher up-front cost, ~$20,000–30,000

Incretin therapy

• Effective short-term weight loss, ~15–22%, but less than surgery (as of 2026)
• Less effective in the real world due to discontinuation, ~7–12% weight loss
• Open question of how to manage weight-loss maintenance
• Lower up-front risk of serious side effects
• Lower up-front cost, but ~$500/month for potentially life-long treatment (9–10 year break-even versus surgery cost)
• Rapidly developing field — improvements expected

Edmonton Obesity Staging System (EOSS)

Warning

Slide 24 is flagged: the Stage 1 case example gives a BMI of 59.2 kg/m² for a presentation described as mild/subclinical, which appears inconsistent with the severity implied by that BMI. This is transcribed exactly as printed on the slide, not corrected.

WHO classification of weight status by BMI:

• Obese Class I: 30–34.9 kg/m²
• Obese Class II: 35–39.9 kg/m²
• Obese Class III: ≥40 kg/m²

The Edmonton Obesity Staging System stages patients by risk factors, symptoms, and functional/psychological impact, independent of BMI class alone:

• Stage 0: No obesity-related risk factors, no physical symptoms, no psychological symptoms, no functional limitations. Example: physically active female, BMI 32, no risk factors or symptoms — Class I, Stage 0.
• Stage 1: Subclinical risk factors (borderline hypertension, impaired fasting glucose, elevated liver enzymes) OR mild physical symptoms not requiring medical treatment (dyspnoea on moderate exertion, occasional aches, fatigue) OR mild psychological symptoms/mild impairment of well-being with quality of life not impacted. Example: 38-year-old female, BMI 59.2, borderline hypertension, mild back and knee pain, no medical intervention required — Class III, Stage 1.
• Stage 2: Established obesity-related comorbidities requiring medical intervention (hypertension, type 2 diabetes, sleep apnoea, PCOS, osteoarthritis, reflux disease) OR moderate psychological symptoms (depression, eating disorders, anxiety) OR moderate functional limitations, with quality of life beginning to be impacted. Example: 32-year-old male, BMI 36, primary hypertension and obstructive sleep apnoea — Class II, Stage 2.
• Stage 3: Significant obesity-related end-organ damage (myocardial infarction, heart failure, diabetic complications, incapacitating osteoarthritis) OR significant psychological symptoms (major depression, suicidal ideation) OR significant functional limitations (unable to work/complete routine activities, reduced mobility) OR significant impairment of well-being. Example: 49-year-old female, BMI 67, sleep apnoea, cardiovascular disease, GERD, prior stroke, mobility significantly limited by osteoarthritis and gout — Class III, Stage 3.
• Stage 4: Severe, potentially end-stage, obesity-related comorbidities OR severely disabling psychological symptoms OR severe functional limitations. Example: 45-year-old female, BMI 54, wheelchair-bound due to disabling arthritis, severe hyperpnoea, and anxiety disorder — Class III, Stage 4.

EOSS staging predicts mortality in class III obesity (NHANES III cohort, Kaplan-Meier survival by EOSS stage over up to 250 months): Stage 0 and Stage 1 patients stayed close to full survival throughout; Stage 2 patients declined gradually to about 0.78 proportion surviving by 200 months; Stage 3 patients declined fastest, to about 0.63 by 150–200 months.

Conclusion

• Obesity is a serious problem in NZ and worldwide (34.2% of adults have BMI >30).
• Sustained weight loss is very difficult for people with obesity because of normal human physiology (the hunger/metabolic-rate response to a deficit).
• Bariatric surgery is the most effective treatment for obesity and its comorbidities, for BMI >40 kg/m² or BMI >35 kg/m² with comorbidities; it works best in heavier, younger patients with more reversible comorbidities.
• Incretin-based therapies are an effective medical treatment, for BMI >30 kg/m² or BMI >27 kg/m² with comorbidities, but raise questions about maintenance and cost of long-term treatment; suited to lighter, possibly older patients with non-reversible comorbidities.
• Health impacts of obesity and their reversibility should be considered when deciding on surgery, using tools such as the Edmonton Obesity Staging System.

Self-test

1. What four BMI-based population bands were used to describe the scale of obesity in NZ, and what percentage of adults fell into the BMI 40+ band?
2. List at least five medical problems of obesity from each of the pulmonary/hepatic and musculoskeletal/gynaecological groupings.
3. Why does modern human physiology, evolved for a hunter-gatherer environment, predispose to weight gain in the current environment?
4. In the weight-stable energy balance model, what two components make up “energy burned,” and what are their approximate daily kcal contributions?
5. How many calories does 1 kg of fat store, and what daily energy deficit is required to lose 0.5 kg per week?
6. Describe the three physiological “problems” that occur during a dieting-induced energy deficit, and explain why weight-loss surgery avoids one of them.
7. Name the three bariatric surgical procedures described and briefly describe the anatomical change each makes.
8. Distinguish Roux-en-Y gastric bypass from sleeve gastrectomy in terms of what happens to the duodenum.
9. Describe the three-stage causal chain (A → B → C) by which RYGB and sleeve gastrectomy are thought to improve glycaemia, giving one example from each stage.
10. Define an incretin hormone. Where is GLP-1 produced, and what enzyme degrades it?
11. What are the two core actions of incretins on insulin and glucagon, and what is the net effect on blood glucose?
12. List three organ-level effects of GLP-1 beyond the pancreas.
13. Compare the three surgical procedures on average weight loss and effect on diabetes.
14. Compare the three surgical procedures on effect on reflux and long-term aspirin/NSAID use.
15. What are the shared risks of bariatric surgery at the time of operation (three risk figures)?
16. What are the three BMI-based indication criteria for bariatric surgery?
17. Name the four GLP-1 receptor agonists available in NZ, their dosing frequency, and their approved uses.
18. What are the common versus rare-but-serious side effects of GLP-1 receptor agonists?
19. In the STEP 1 trial, what was the mean weight change with semaglutide versus placebo, and how did GI side effect rates compare?
20. What did the SURMOUNT 4 and STEP 4 “withdrawal” trial designs show about weight regain after stopping medication?
21. In real-world data (7881 patients), what were the overall and continued-treatment weight loss percentages at 1 year, and why do these differ from the trial results?
22. A 34-year-old patient with BMI 33 kg/m² and no other complications asks about bariatric surgery. Using the BMI-based indication criteria, would they currently qualify, and why?
23. Distinguish bariatric surgery from incretin therapy in terms of average weight loss, up-front risk, and up-front cost.
24. What are the BMI cut-offs for Obese Class I, II, and III as given on slide 24?
25. A 32-year-old male has a BMI of 36 kg/m², primary hypertension, and obstructive sleep apnoea. Using the Edmonton Obesity Staging System, what class and stage would this patient be assigned, and why?
26. According to the EOSS mortality data, how did survival differ between EOSS Stage 0/1 and Stage 2/3 patients with class III obesity over up to 200 months?
27. Integrative: Using the lecture’s summary comparison, explain why a younger, heavier patient with reversible comorbidities might be steered toward bariatric surgery, while an older patient with lighter obesity and non-reversible comorbidities might be steered toward incretin therapy.
28. Integrative: Explain how the EOSS system could be used alongside the BMI-based indication criteria to decide between offering bariatric surgery, incretin therapy, or neither.

Answers

Reveal answers

1. BMI 40+ (5.8%), BMI 35–40 (8.8%), BMI 30–35 (19.5%), BMI 25–30 (33.2%). The BMI 40+ band was 5.8% of adults (252,000 people).
2. Pulmonary/hepatic: obstructive sleep apnoea, hypoventilation syndrome, pulmonary hypertension, asthma, nonalcoholic fatty liver disease (steatosis/steatohepatitis/cirrhosis). Musculoskeletal/gynaecological: joint pain/osteoarthritis, degenerative joint disease, low back pain, abnormal menses, infertility, PCOS.
3. Human physiology evolved when food was scarce and hard to obtain, so the ability to store food/fat was advantageous. The modern environment has abundant food engineered for taste and fossil fuels replacing physical work, so the same physiology now drives excess intake and reduced expenditure.
4. Metabolic rate (~1400–1800 kcal/day) and physical activity (~500 kcal/day), together balancing energy consumed (~2000 kcal/day).
5. 1 kg fat stores 7000 calories; 0.5 kg/week weight loss requires a 500 calorie/day energy deficit.
6. During a deficit: hunger increases, metabolic rate decreases, and physical activity may be difficult to increase. Weight-loss surgery reduces the amount eaten without increasing hunger to the same degree, avoiding the first problem.
7. Roux-en-Y gastric bypass: small stomach pouch connected via rerouted small intestine in a Y-configuration, bypassing part of the stomach and duodenum. One anastomosis gastric bypass: long narrow gastric pouch with a single-loop intestinal connection. Sleeve gastrectomy: most of the stomach removed/stapled into a narrow tube, no intestinal rerouting.
8. RYGB excludes the duodenum and proximal jejunum from nutrient contact (bypass); sleeve gastrectomy leaves the duodenum and intestinal connections intact with no rerouting.
9. A (immediate anatomical effects) e.g. caloric restriction or removal of the stomach fundus → B (mediators) e.g. altered gut hormones or altered bile acid/FGF-19 signalling → C (glucose effects) e.g. improved β-cell function or increased glucose utilisation.
10. An incretin is a gut hormone (e.g. GLP-1, GIP) that stimulates insulin release and inhibits glucagon release in response to nutrients. GLP-1 is produced by L cells from proglucagon, mainly in the distal ileum and colon (also duodenum and jejunum), and is degraded by DPP-4.
11. Incretins stimulate insulin release and inhibit glucagon release, resulting in lowering of blood glucose.
12. Any three of: brain (satiety/appetite/neuroprotection), heart (cardioprotection, glucose uptake), stomach (decreased gastric emptying/motility/acid secretion), adipose tissue (lipogenesis/adipogenesis/glucose uptake), kidneys (renoprotection), bones (increased formation, decreased resorption), muscles (glucose uptake).
13. Average weight loss: RYGB 25–35%, OAGB 25–35%+, sleeve 20–30%. Effect on diabetes: RYGB +++, OAGB +++/+, sleeve ++.
14. Reflux: RYGB improves symptoms, OAGB variable, sleeve worsens symptoms. Aspirin/NSAIDs: prohibited lifelong after RYGB and OAGB, usually OK with caution after sleeve.
15. 1% risk of serious complications; 0.2% risk of leakage from joins or staple lines; 0.1% risk of mortality.
16. BMI >40 kg/m²; BMI >35 kg/m² with weight-related medical complications; BMI >30 kg/m² with type 2 diabetes.
17. Dulaglutide (Trulicity, once weekly, T2DM/SA funded); liraglutide (Saxenda, once daily, T2DM and weight loss); semaglutide (Ozempic/Wegovy, once weekly, T2DM and weight loss); tirzepatide (Monjuro, once weekly, dual GLP-1/GIP agonist, T2DM and weight loss).
18. Common: nausea, vomiting, diarrhoea, gallstones, lean body mass loss. Rare but serious: pancreatitis, medullary thyroid cancer.
19. Mean weight decrease −14.9% (semaglutide) vs −2.4% (placebo). GI side effects were more common with semaglutide (74.2%) than placebo (47.9%).
20. Both showed substantial weight regain after switching from active drug to placebo (STEP 4: continued semaglutide −17.4% vs switched-to-placebo −5.0%; SURMOUNT 4: continued tirzepatide −25.8% vs switched-to-placebo −9.5%), indicating weight loss is not maintained after stopping the medication.
21. Overall weight loss was 8.7% at 1 year, rising to 11.9% among those who continued treatment at 1 year — both well below trial-reported figures (15–26%), reflecting high real-world discontinuation rates.
22. No — BMI 33 kg/m² with no weight-related complications does not meet any of the three criteria (needs BMI >40, or >35 with complications, or >30 with type 2 diabetes), so they would not currently qualify.
23. Bariatric surgery: higher average weight loss (~25–30%), higher up-front risk (1% serious side effects), higher up-front cost ($20–30k).Incretintherapy:lowerweightloss(15–22$500/month.
24. Obese Class I: 30–34.9 kg/m²; Obese Class II: 35–39.9 kg/m²; Obese Class III: ≥40 kg/m² [slide does not give normal/overweight cut-offs].
25. Class II, Stage 2 — BMI 36 falls in Class II (35–39.9), and the patient has established obesity-related comorbidities requiring medical intervention (hypertension, sleep apnoea), matching Stage 2 criteria.
26. Stage 0 and Stage 1 patients stayed close to full survival (near 1.0) throughout up to 250 months, while Stage 2 declined to about 0.78 and Stage 3 declined faster to about 0.63 by 150–200 months — higher EOSS stage predicted worse survival.
27. Per the lecture’s summary: surgery gives higher, better-maintained weight loss and works best in heavier, younger patients with more reversible comorbidities, justifying its higher up-front risk/cost in that group. Incretin therapy gives lower weight loss with lower up-front risk/cost but ongoing expense, and per the conclusion is suited to lighter, possibly older patients with non-reversible comorbidities where major surgery’s added benefit may be lower relative to its risks.
28. BMI-based criteria set the eligibility threshold for surgery (BMI >40, or >35/>30 with complications) or incretin therapy (BMI >30, or >27 with complications); EOSS adds a severity/reversibility layer on top — stage and reversibility of comorbidities (per the conclusion, “consider health impacts of obesity and reversibility when deciding on surgery”) help judge how much benefit a patient at a given BMI is likely to gain, refining the choice beyond BMI alone.