Current Drug Therapy

Update on antiobesity pharmacotherapy in adults: Current and emerging options

Farah Ziyadeh, MD, Sara Saliba, MD, RD, Dania Salih Bacha, MD, Yael Mauer, MD, MPH, Marcio L. Griebeler, MD, DABOM and Bartolome Burguera, MD, PhD
Cleveland Clinic Journal of Medicine January 2026, 93 (1) 36-46; DOI: https://doi.org/10.3949/ccjm.93a.24112

ABSTRACT

Obesity is a chronic disease that increases the risk of developing other serious health conditions. Pharmacotherapy can help patients effectively manage obesity by achieving a healthier weight, but each antiobesity medication has its own benefits and risks that must be evaluated for each patient. This article reviews the available antiobesity medications, including the incretin mimetics, and emerging antiobesity medications currently under investigation.

KEY POINTS

  • Obesity is a chronic disease and should be managed as such.

  • Antiobesity pharmacotherapy offers other benefits beyond weight loss, including improvements in obesity-associated complications.

  • Antiobesity pharmacotherapy needs to be continued long term, even after weight loss has been achieved, because discontinuation leads to weight regain.

  • Each antiobesity medication class has specific benefits and potential side effects that necessitate careful consideration and should be combined with lifestyle modifications, such as healthy nutrition, adequate physical activity, sufficient quality sleep, and stress management.

Obesity is a chronic relapsing disease characterized by excess adiposity that can negatively impact health. Almost 42% of US adults have obesity, defined as a body mass index (BMI) of 30 kg/m2 or higher, a significant increase since 1999.1 Obesity can lead to other health problems, including cardiometabolic disease, sleep disorders, and cancer,2 resulting in high healthcare costs estimated at $174 billion annually,3 along with absenteeism and presenteeism (working while dealing with an illness or health issue and being less productive than usual) costs of $1,755 per person.4

Because obesity increases the risk of developing multiple diseases and adverse cardiometabolic outcomes, the concept of “healthy” obesity is misleading. Clinical obesity can be classified as complicated when it is associated with comorbidities such as hypertension or type 2 diabetes, or uncomplicated when these comorbidities are absent. Even in uncomplicated obesity, excess adiposity increases metabolic and cardiovascular risk through mechanisms that include chronic inflammation, hormonal and metabolic dysregulation, and structural changes in organs and vasculature.2 Accordingly, obesity itself should be considered a disease similar to type 2 diabetes that is diagnosed based on metabolic dysfunction and not on end-organ complications.

This updated review of antiobesity pharmacotherapy focuses on how to personalize obesity treatment and discusses new data on available medications and emerging options.

LIMITATIONS OF USING BMI TO DIAGNOSE OBESITY

There is no universally accepted gold standard method for diagnosing obesity. BMI is a commonly used tool for assessing obesity, but it does not account for body composition, age, sex, ethnicity, or fitness levels.5 As a result, BMI may misclassify individuals with high muscle mass as having overweight or obesity and overlook health risks in those with “healthy” weight but high body fat.6

Body composition analysis with dual-energy x-ray absorptiometry and bioelectrical impedance offers a more accurate approach by evaluating fat and fat-free components, but these modalities are not widely available in the outpatient setting.6 More accessible tools, such as waist circumference, can estimate abdominal adiposity, which correlates with visceral adiposity and significantly increases the risk of metabolic complications.5 While current obesity treatment guidelines are based on BMI thresholds, clinicians should apply them in the context of each individual patient. These additional assessments, along with clinical judgment, can improve diagnostic accuracy.

SET POINT AND METABOLIC ADAPTATION

Body weight is regulated by complex interactions between the brain, gastrointestinal system, adipose tissue, and pancreas that modulate food intake and energy expenditure.7,8 When an individual loses adipose tissue beyond their body’s set point, a series of compensatory physiologic and hormonal mechanisms ensue to promote weight regain by increasing energy intake and decreasing energy expenditure.

An increase in preprandial and postprandial ghrelin, and a decrease in leptin, amylin, peptide YY, and cholecystokinin, work to increase energy intake by stimulating hunger, cravings, and preference for calorically dense foods.8 Meanwhile, reductions in resting energy expenditure driven by hormonal changes, decreased sympathetic nervous system activity, and increased mitochondrial efficiency (ie, the ability of mitochondria to extract energy from the same fuel load) lead to energy conservation and reduced fat oxidation.9

These physiologic changes, meant to bring an individual back to their set point, are known as metabolic adaptation.9 The degree of metabolic adaptation varies from person to person, but all antiobesity medications mitigate metabolic adaptation by sustaining an energy deficit and reducing compensatory appetite signals. These benefits persist only while patients are actively taking antiobesity medications, and weight regain is common once they are stopped.10

CURRENTLY AVAILABLE ANTIOBESITY MEDICATIONS

The causes of obesity are complex. Genetics and epigenetics are major factors.11 In the past few decades, however, endocrine disruptors (chemicals that interfere with hormonal function), increasingly sedentary lifestyles, obesogenic medications, and the availability of highly processed foods have contributed to the epidemic.2,11,12 Also, obesity is a relapsing and progressive disease and should be managed much like other chronic diseases. Multiple pharmacotherapy options are now approved by the US Food and Drug Administration (FDA) for treating obesity, and several others are used off-label.

First generation

Phentermine and diethylpropion are sympathomimetics that suppress appetite by stimulating norepinephrine release and thus reducing hunger. They are FDA approved for short-term use (3 months), but phentermine is often prescribed off-label for long-term use to manage the chronic nature of obesity.13

Topiramate extended release, an antiepileptic used off-label for weight loss, exerts an anorexigenic effect through modulation of gamma-aminobutyric acid receptors in the brain.

The combination of phentermine and topiramate extended release results in more weight loss than when either medication is used alone, and is FDA approved for this indication.

Bupropion, a dopamine and norepinephrine reuptake inhibitor, promotes weight loss by increasing the activity of pro-opiomelanocortin neurons in the hypothalamus, which reduces appetite. It is frequently used off-label as an antiobesity medication.

Naltrexone is an opioid receptor antagonist that blocks inhibitory feedback on pro-opiomelanocortin neurons.

The combination of naltrexone extended release and bupropion extended release is FDA approved for chronic obesity treatment.

Orlistat is a lipase inhibitor that reduces the absorption of fat from food.

Metformin, a biguanide used to treat type 2 diabetes, reduces appetite and is often used off-label to treat obesity.

Second generation

Newer antiobesity medications are incretin mimetics that act on glucagon-like peptide (GLP) 1 and glucose-dependent insulinotropic polypeptide (GIP) receptors in the brain to reduce appetite and increase satiety. They also delay gastric emptying, which helps promote fullness during and after eating. The following are FDA approved for long-term obesity treatment:

  • Liraglutide and semaglutide (GLP-1 receptor agonists)

  • Tirzepatide (dual GLP-1 and GIP receptor agonist).

Each medication class has specific benefits and potential side effects (Table 1),13,14 necessitating careful consideration, and pharmacotherapy should be combined with lifestyle modifications that support healthy nutrition, adequate physical activity, sufficient quality sleep, and stress management for optimal results.

View this table:
TABLE 1

Current medications approved by the US Food and Drug Administration for treating obesity

EMERGING ANTIOBESITY MEDICATIONS

Several new antiobesity medications are currently under investigation and have encouraging preliminary data. A few are highlighted below.

Oral GLP-1 agonists

Oral semaglutide 50 mg (a dose higher than what is currently approved to treat diabetes, and not available in the United States for purposes other than research) showed a 15.1% decrease in total body weight vs a 2.4% decrease with placebo (an estimated treatment difference of −12.7%) in patients with overweight or obesity and without diabetes.15 Gastrointestinal side effects were more common in the treatment group.

Orforglipron is a novel once-daily oral nonpeptide GLP-1 receptor agonist currently in clinical development for treating type 2 diabetes and obesity.16 Its safety and efficacy profile are consistent with other agents in the GLP-1 receptor agonist class. The main advantage of orforglipron over oral semaglutide is its ease of administration, as orforglipron does not require strict fasting or water intake restrictions, and can be taken without regard to meals, which may improve adherence and convenience for patients. Orforglipron may also allow for cheaper manufacturing compared with oral semaglutide because it is a synthetic nonpeptide small molecule, whereas oral semaglutide is a peptide-based drug that requires complex synthesis, formulation, and stabilization processes.

Amylin agonist plus GLP-1 agonist

Amylin, a hormone secreted along with insulin by pancreatic beta cells, slows gastric emptying and promotes satiety.17 Cagrilintide, an amylin analogue administered weekly, showed up to a 10.8% decrease in total body weight vs 3% with placebo in a phase 2 trial.18 A recent phase 3 trial evaluating the combination medication cagrilintide and semaglutide showed it led to greater weight loss in patients with obesity (20.4%) vs semaglutide (14.9%), cagrilintide alone (11.5%), and placebo (3%).19

Glucagon agonist plus GLP-1 agonist

Glucagon, which is released from pancreatic alpha cells in the setting of low blood glucose, elevates serum glucose by increasing hepatic gluconeogenesis.20 It also reduces appetite, boosts energy expenditure, and promotes hepatic fatty acid oxidation. Combining a glucagon agonist with a GLP-1 agonist may enhance weight loss and mitigate glucagon-induced hyperglycemia. Early trials of GLP-1 and glucagon co-agonists have shown varied effectiveness in treating obesity, type 2 diabetes, and liver disease.21

Survodutide, in a phase 2 trial, demonstrated weight loss of up to approximately 15% over 46 weeks vs 2.8% with placebo in participants with overweight or obesity without diabetes.20

Efinopegdutide resulted in a significantly greater reduction in liver fat content at 24 weeks compared with semaglutide 1 mg weekly, and an 8.5% reduction in body weight among patients with metabolic dysfunction–associated liver disease.22 (Weight loss previously seen with the FDA-approved doses to treat diabetes and obesity was 3%–5% for 2 mg weekly and approximately 15% for 2.4 mg weekly.22) The dual-agonist mechanism is thought to reduce liver fat both indirectly via weight loss and directly by stimulating hepatic fatty acid oxidation and reducing lipogenesis through glucagon receptor activation.

A phase 2b study of cotadutide reported significant reductions in body weight (−5.02% with 300-μg dose vs −0.68% with placebo) and hemoglobin A1c levels at 54 weeks in patients with overweight or obesity and type 2 diabetes with metabolic dysfunction–associated steatotic liver disease.23

Pemvidutide showed weight loss of up to 9.7% vs 1% with placebo at 24 weeks in patients with obesity.24

GIP antagonist plus GLP-1 agonist

Combining GIP receptor inhibition with GLP-1 receptor agonists shows promise for treating obesity because it enhances GLP-1 receptor activity and boosts therapeutic effects.21,25 The potential desensitization of GIP receptors by exposure to GIP agonists is a possible reason why both GIP agonism and antagonism have similar effects on weight.26

Maridebart cafraglutide is a novel monthly peptide-antibody conjugate targeting GLP-1 agonism and GIP antagonism. In a phase 2 study, it demonstrated weight loss of up to about 20% in patients with obesity (and up to about 17% in those with obesity and type 2 diabetes) compared with 2.6% for placebo over 52 weeks. Hemoglobin A1c reductions of up to 2.2% and improved metabolic risk markers, with no observed plateau at 1 year, were also seen.27 Gastrointestinal side effects were mitigated by starting at a low dose and then slowly escalating. To improve tolerance and adherence potential, ongoing phase 3 trials are studying a lower starting dose of maridebart cafraglutide with more gradual dose escalation.

GIP agonist plus glucagon agonist plus GLP-1 agonist

Triple agonists of GIP, glucagon, and GLP-1 have also emerged as potential treatments for obesity.28,29 In a phase 2 trial of retatrutide, participants with overweight or obesity achieved weight loss of up to 24.2%, compared with 2.1% in the placebo group, at 48 weeks.28

GLP-1 agonist plus activin type II receptor antagonist

Combination approaches targeting both appetite regulation and body composition are under investigation. The phase 2b BELIEVE (Safety and Efficacy of Bimagrumab and Semaglutide in Adults Who Are Overweight or Obese) trial30 evaluated semaglutide plus bimagrumab, an activin type II receptor antagonist that increases muscle mass while reducing fat mass. At 72 weeks, participants in the combination therapy group achieved greater loss of body weight (22.1%) compared with semaglutide alone (15.7%) and bimagrumab alone (10.8%). Importantly, 92.8% of the total weight lost in the combination group was from fat mass (2.9% loss of lean muscle mass) vs fat mass loss of 71.8% (7.4% loss of lean muscle mass) with semaglutide monotherapy. Nearly 70% of the combination therapy group achieved total weight loss of 20% or more and 94% achieved fat mass reduction of 30% or more. The combination therapy also produced substantial reductions in waist circumference (about 22 cm [8.7 in]), visceral adipose tissue, and inflammatory markers. Glycemia improvements were also reported, with 100% achieving normoglycemia by week 48. These findings support the potential of a “quality plus quantity” approach to obesity treatment, preserving lean muscle mass while maximizing fat loss.

TAILORING PHARMACOTHERAPY TO EACH PATIENT

Antiobesity pharmacotherapy is a tool to achieve weight goals, and choosing the right medication involves an individualized, shared decision-making process that accounts for contributing factors, patient preferences, comorbidities, severity of obesity, and out-of-pocket costs.

The FDA has approved antiobesity medications for patients with a BMI of 30 kg/m2 or greater or 27 kg/m2 or greater in the presence of obesity-associated complications; however, personalized cutoffs should be considered (eg, a BMI ≥ 23 kg/m2 is considered overweight in Asian people).2 Antiobesity medications may be prescribed off-label for patients with excess adiposity at high risk of metabolic complications who do not meet the BMI criteria after careful consideration of risks and benefits.13

Which medications are the most effective?

Randomized controlled trials have shown that second-generation antiobesity medications offer significantly greater efficacy. Tirzepatide is the most effective agent, followed by semaglutide and liraglutide. First-generation antiobesity medications are associated with moderate (phentermine-topiramate) and lower (naltrexone-bupropion, topiramate, metformin) amounts of weight loss. Most studies included counseling on lifestyle modification. Total body weight loss percentages from these trials are listed in Table 2.31–36

View this table:
TABLE 2

Mean weight loss with antiobesity medications in randomized, double-blind, placebo-controlled trials

Health benefits other than weight loss

Each antiobesity medication has its own benefits and potential side effects, so the appropriate one should be selected based on the potential adverse effects and an individual patient’s comorbidities. Antiobesity pharmacotherapy can help improve a patient’s blood pressure, waist circumference, insulin sensitivity, lipid profile, and inflammatory markers.14 These medications include liraglutide, semaglutide, tirzepatide, naltrexone-bupropion, phentermine-topiramate, metformin, and orlistat.

Cardiovascular disease. The SELECT (Semaglutide Effects on Heart Disease and Stroke in Patients With Overweight or Obesity) trial37 showed that weekly subcutaneous semaglutide reduced the incidence of major adverse cardiac events by 20% in patients with established cardiovascular disease and no diabetes (hazard ratio 0.80, 95% confidence interval 0.72–0.90). Secondary end points were also met, including significant weight loss, decrease in waist circumference, improvements in inflammatory markers, and reduced low-density lipoprotein and triglyceride levels.

Type 2 diabetes. Weight loss can help patients improve glycemic control, and certain antiobesity medications are particularly beneficial. Metformin is a good choice due to its ability to improve insulin sensitivity and lower blood glucose.33 Incretin mimetics reduce adiposity, improve insulin sensitivity, increase post-prandial insulin release, and lower hemoglobin A1c.38 The cardiovascular benefits provided by tirzepatide, liraglutide, and semaglutide are particularly pertinent in these high-risk patients.

Liver disease. Both semaglutide and tirzepatide have shown promising results in patients with metabolic dysfunction–associated liver disease. Semaglutide has been shown to significantly improve liver steatosis, hepatitis, and fibrosis,39,40 and recently received FDA approval for the treatment of at-risk metabolic dysfunction–associated steatohepatitis. Tirzepatide has also been shown to improve steatosis, hepatitis, and fibrosis.41

In patients with obstructive sleep apnea, tirzepatide significantly improves the apnea–hypopnea index.42 In December 2024, the FDA approved tirzepatide for treating obstructive sleep apnea.

Topiramate is an excellent choice for patients with obesity and migraines because it is an effective preventive treatment.31

Naltrexone-bupropion is particularly beneficial for patients who are trying to quit smoking or those with concomitant depression.13

Contraindications

Antiobesity pharmacotherapy is contraindicated during pregnancy and should be discontinued before conception due to potential risks to the fetus. All women of reproductive age should be counseled to use reliable contraception while on antiobesity medications and to avoid these agents if planning to become pregnant.13 Patients may require a pregnancy test before starting topiramate, which is a known teratogen.

Sympathomimetic antiobesity medications like phentermine should be avoided in patients with cardiovascular disease (eg, arrhythmias, coronary artery disease, valvular heart disease), untreated hyperthyroidism, or uncontrolled hypertension.13,43 A thorough evaluation is advised before prescribing stimulants to high-risk patients.

Bupropion should also be avoided in patients with uncontrolled hypertension.13 Antiobesity medications and weight loss can lower blood pressure,44 necessitating possible dose adjustments to antihypertensive medications.

Risks

Incretin mimetics can increase hypoglycemia risk in patients who are being treated with insulin or secretagogues like sulfonylureas for type 2 diabetes. Adjusting the dose of the diabetes medication is required.13 GLP-1 receptor agonists also increase pulse rate.

Caution is needed when prescribing phentermine, bupropion, topiramate, and incretin mimetics to patients with severe or uncontrolled mental health disorders, particularly those with active suicidal ideation. Current evidence does not support a causal association between incretin mimetics and suicidal ideation, though postmarketing reports and pharmacovigilance data have identified signals that warrant ongoing monitoring. Consultation with psychiatry is recommended when a patient’s mental health status is uncertain. Caution and guidance from psychiatry are also recommended in patients with complex psychiatric histories, such as bipolar disorder.

All weight loss can result in sarcopenia, but rapid and significant weight loss increases the risk, especially in the elderly and frail (those with low muscle mass and muscle dysfunction).6 Strength training and adequate protein intake can mitigate risks; therefore, lifestyle counseling is paramount. The risk of sarcopenia is associated more with the magnitude and speed of weight loss, exercise, age, sex, protein consumption, and chronic disease and inflammation than antiobesity pharmacotherapy.

Gastrointestinal side effects

Incretin mimetics and metformin are commonly associated with gastrointestinal side effects such as nausea, abdominal cramping, diarrhea (most common with metformin), and constipation (most common with incretin mimetics).14 Most weight loss results from reduced oral intake driven by appetite suppression45 rather than the gastrointestinal side effects. The severity of gastrointestinal symptoms does not reliably correlate with amount of weight loss. Weight loss continues even after gastrointestinal symptoms are better controlled.

Gastrointestinal side effects may be ameliorated by stopping eating when full; avoiding fatty meals and carbonated drinks; increasing fiber consumption (through diet or supplements); and taking antidiarrheal medications as needed. Incretin mimetics decrease thirst, so patients need to be reminded to stay well hydrated. Hydration is important for those experiencing diarrhea, vomiting, or both.

If patients experience gastrointestinal side effects, the typical dose escalations for incretin mimetics (a 4-week titration schedule for semaglutide and tirzepatide, weekly for liraglutide) may be delayed. Maintaining the current dose for additional weeks or even months can enhance tolerability. Once gastrointestinal symptoms have resolved, upward titration may be resumed as clinically indicated to achieve therapeutic goals.

Metformin’s gastrointestinal side effects are generally reduced by using the extended-release formulation, taking the medication with meals, and slowing the upward titration schedule (usually 500 mg per week) as needed.

Orlistat is also associated with gastrointestinal side effects such as nausea, abdominal discomfort, flatulence with discharge, fecal urgency and frequency, incontinence, and oily stool.13 Given its low effectiveness and the fact that patients rarely tolerate long-term use, it is not recommended by the authors.

Other adverse effects

Topiramate’s adverse effects include drowsiness, irritability, neuropathy, memory and cognitive impairment, changes in taste, and kidney stones.13 Cognitive impairment can be improved by taking the medication before bedtime and gradually titrating the dose.

Adverse effects associated with phentermine include insomnia and irritability. Taking it early in the day lessens the impact on sleep. Because phentermine is a stimulant, it has theoretic potential for abuse and addiction, but this concern is not supported by the literature or our clinical experience.46 It can also increase blood pressure and pulse rate.

The combination of phentermine and topiramate can achieve greater weight loss at lower doses of each medication, thus decreasing dose-dependent adverse effects. The increased blood pressure seen with phentermine alone is usually mitigated somewhat when taken with topiramate, but pulse rate still remains increased. However, if patients experience side effects from either topiramate or phentermine (described above), clinicians can consider prescribing the well-tolerated medication by itself, off-label (phentermine alone is only considered off-label if used long term).14

The main side effects of naltrexone-bupropion include headaches, irritability, anxiety, insomnia, and nausea.14 These can be managed by taking lower doses or skipping the afternoon dose to reduce sleep disturbance. If nausea is a prominent side effect, bupropion can be prescribed off-label by itself. Bupropion lowers the seizure threshold, so it is best avoided in high-risk patients with a history of seizures or certain eating disorders predisposing them to electrolyte abnormalities, or who are already using other medications that may lower the seizure threshold.13

Topiramate and bupropion significantly increase the risk of angle-closure glaucoma.47 Phentermine is contraindicated in patients with glaucoma.14 However, many ophthalmologists will allow patients to use bupropion, topiramate, and phentermine when their glaucoma is well controlled, so working with them is key.

Metformin decreases B12 absorption, and topiramate can cause metabolic acidosis; both should be monitored.

Administration method

Incretin mimetics are administered subcutaneously: liraglutide requires daily injections, while semaglutide and tirzepatide require once-weekly injections. In our experience, once started, very few patients discontinue incretin mimetics because of how they are administered.

Coverage and cost

Antiobesity medications frequently are not covered by medical insurance because obesity is still under-recognized as a chronic disease and often perceived as the result of lifestyle choices. However, the FDA has approved semaglutide for preventing cardiovascular events in adults with overweight or obesity and established cardiovascular disease.48 In response, some insurance plans now cover semaglutide for this secondary cardiovascular indication. Semaglutide is also FDA approved for metabolic dysfunction–associated steatohepatitis with liver fibrosis stage 2 or 3 and is covered by some insurance plans. Similarly, tirzepatide has received FDA approval for treating obstructive sleep apnea in adults with obesity,48 and Medicare covers tirzepatide for this indication as of January 2025. Medicare does not cover antiobesity medications for obesity treatment, and Medicaid coverage varies.

The incretin mimetics have the highest out-of-pocket costs, which limit their access.49 Manufacturer discount programs cover some of the costs, and patient assistance programs cover all the costs for patients with type 2 diabetes, but only if their income falls below 200% of the federal poverty level and they are uninsured or insured through Medicare.

Other antiobesity medications have options to reduce costs. For example, naltrexone-bupropion extended release and phentermine-topiramate extended release have no generic options and are often not covered by insurance. As with incretin mimetics, manufacturer discount programs are available. However, the individual components are available as generic formulations and can be prescribed separately, off-label, at a much lower cost.

LONG-TERM USE IS NEEDED

Continued use of antiobesity pharmacotherapy to maintain weight loss and prevent weight regain is necessary because obesity is a chronic and relapsing disease. Discontinuation frequently leads to weight regain and therefore is not recommended.10

If an antiobesity medication needs to be stopped due to side effects, contraindications, patient preference, or affordability, replacing it with a more affordable or better-tolerated alternative is recommended. For example, if a patient can no longer afford an incretin mimetic due to changes in insurance coverage, transition to a first-generation medication, such as phentermine-topiramate, can be offered. No washout period is necessary. If a patient develops headaches with naltrexone-bupropion, semaglutide can be offered instead, and so on.

Selecting an alternative antiobesity medication should be based on preferences, comorbidities, and affordability, as outlined above. This approach is similar to that of managing other chronic conditions, such as hypertension, where effective therapy is continued indefinitely after ideal blood pressure has been achieved, substituting one medication for another in the event of intolerance or new contraindications.

HOLISTIC OBESITY MANAGEMENT

When appropriate, clinicians should aim to replace obesity-inducing medications with alternatives that do not affect body weight (Table 3).14,50

View this table:
TABLE 3

Examples of frequently used obesogenic medications and proposed alternatives (when clinically appropriate)

Comprehensive lifestyle modifications remain a fundamental aspect of obesity treatment and health promotion. Patients should maintain healthy dietary habits, engage in regular physical activity, get adequate sleep, and manage stress. Nutritional counseling is crucial, and clinicians should promote the consumption of nutritionally dense whole foods while reducing processed, calorie-dense, and nutritionally poor foods. Proper hydration and protein consumption (1–1.3 g/kg/day for most adults attempting weight loss is recommended) is important. Regular physical activity not only aids weight loss but also enhances cardiovascular health and preserves muscle mass.51

Behavioral therapy can help patients manage stress and curb emotional eating. Addressing mental health disorders like anxiety and depression is also fundamental.

Sufficient high-quality sleep is important as poor sleep can disrupt metabolism and increase appetite. Patients should also be screened for sleep apnea and other sleep disorders, according to their risk.

Metabolic and bariatric surgeries, such as gastric bypass and sleeve gastrectomy, offer patients significant and sustained weight loss, as well as improvements in obesity-related conditions. Surgery is suitable for individuals with a BMI of 35 kg/m2 or greater, or those with a BMI of 30 kg/m2 or greater with obesity-related complications or those who have not achieved substantial or durable results with nonsurgical therapies.52

Ultimately, effective obesity treatment requires personalized plans that integrate lifestyle modifications and antiobesity pharmacotherapy, along with metabolic and bariatric surgery if indicated, to improve long-term health outcomes.

DISCLOSURES

Dr. Griebeler has disclosed consulting for Aqua Medical and serving as a research principal investigator for Boehringer Ingelheim and Novo Nordisk, Inc. The other authors report no relevant financial relationships which, in the context of their contributions, could be perceived as a potential conflict of interest.

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