Addressing Obesity and Excess Weight: A Matter of Treatment, Not Willpower
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For years, a person with excess weight was told the same three words: “Eat less.” This was followed by “move more” and, often without being stated openly, “control yourself.” People were praised when they lost weight and considered lacking in willpower when they regained it.
Today, science does not support this narrative. Obesity, shaped jointly by genetic susceptibility, the brain's appetite and reward circuits, hormones, sleep, stress, medications, access to food and the environment in which a person lives, is recognized as a chronic disease with a tendency to recur . Treatment still includes diet and physical activity; however, it transforms them from a test of character into a long-term health plan aligned with biology.
Energy balance is real; however, the system that determines hunger, satiety, energy expenditure and biological defenses against weight loss is extremely complex.
THE QUIETLY GROWING BURDEN IN THE WORLD AND TÜRKİYE
According to the World Health Organization, in 2022, 2,5 billion adults were overweight; 890 million of them were living with obesity. The proportion of adults who were overweight rose from 25% in 1990 to 43% in 2022. Adult obesity more than doubled during the same period.
The 2023 national household survey in Türkiye, involving more than 6.000 people, found an obesity rate of 25,4%. Although this rate decreased from 28,8% in 2017, it still means that approximately one in four people lives with obesity. Moreover, population-level rates alone do not describe waist circumference, organ function or lifetime weight history.
THE BIOLOGY OVERLOOKED BY THE “WILLPOWER” EXPLANATION
When weight loss begins, the body does not always interpret it as a health gain. The brain may activate systems that protected against starvation in the past: hunger increases, satiety lasts less time, high-energy foods become more appealing and energy expenditure at rest may fall more than expected. While a person believes they are following the same plan, weight loss slows or stops.
Eating behavior does not begin solely because the stomach is empty. Sights, smells, stress, habits and anticipation of reward can create a desire to eat even without hunger. “Food noise” describes this constant mental preoccupation.
When body weight falls, signals that increase hunger and support energy conservation may persist for a long time. This explains why weight regain is common.
Genetic susceptibility, childhood, pregnancies, menopause, sleep disorders and some diseases influence why two people living in the same environment have different weight trajectories.
Cheap, calorie-dense food, large portions, relentless marketing, long working hours, stress and a shortage of safe places for physical activity shape the setting in which personal choices are made.
Explaining the biological origins of obesity does not take away a person's capacity for change. On the contrary, it helps people understand why some strategies cannot be sustained, replace guilt with treatment options and gain clinical information from attempts that appear unsuccessful.
FROM THE NUMBER ON THE SCALE TO CLINICAL OBESITY
Body mass index (BMI) is calculated by dividing weight in kilograms by the square of height in meters. It is useful in population screening; however, it does not directly show fat mass, muscle quantity, abdominal fat distribution or whether organs are affected.
The 2025 Lancet Commission recommended that the diagnosis of obesity should not rely solely on BMI. It argued that excess adipose tissue should be confirmed with additional measurements such as waist circumference, waist-to-height or waist-to-hip ratios, or with direct body composition methods; organ function and effects on daily life should then be assessed. This approach has not yet become standard across all healthcare systems; however, it represents an important change in direction that moves obesity beyond a “single number.”
Excess adipose tissue is present; however, no current organ dysfunction or substantial restriction of daily life directly attributable to it can be demonstrated. Prevention and close monitoring are needed because future disease risk is increased.
Excess or abnormally distributed adipose tissue has caused organ dysfunction, symptoms or limitations in daily activities. It is a chronic disease state requiring active, evidence-based medical treatment.
Not everyone with a high BMI has the same risk, and not every person with excess weight needs medication. Conversely, someone with a BMI below 30 may have substantial intra-abdominal fat and metabolic disease. Treatment decisions should be based not solely on “How much do you weigh?” but on “How is adipose tissue affecting health?”
TREATMENT IS NOT A PYRAMID, BUT FOUR COMPLEMENTARY PILLARS
Obesity treatment is not a system of punitive steps that waits for someone to “fail” at lifestyle changes before allowing medication or surgery. Depending on need, some approaches may be used together from the outset.
HOW EFFECTIVE ARE THE NEW MEDICATIONS? AN ANSWER FROM 99.791 PEOPLE
In July 2026, BMJ published a network meta-analysis that evaluated 99.791 participants in 262 randomized studies and 19 medications. According to evidence of moderate or high certainty, additional average weight loss over one year compared with lifestyle intervention was 14,9% with tirzepatide, 14,8% with CagriSema, 10,9% with oral semaglutide, 9,9% with orforglipron and 9,8% with subcutaneous semaglutide.
| Approach | What the 2026 evidence says | Clinical interpretation |
|---|---|---|
| Tirzepatide | It was among the medications with the greatest average weight loss in the one-year comparison: an additional 14,9% compared with lifestyle intervention. | It is a dual GIP/GLP-1 agonist. It was found directly superior to semaglutide in SURMOUNT-5; selection depends not only on efficacy but also on safety, accompanying diseases and access. |
| CagriSema | Additional average weight loss of 14,8%; it appeared very close to tirzepatide. | An investigational combination of semaglutide and the amylin analog cagrilintide. Strong results do not automatically mean regulatory approval or evidence of long-term safety. |
| Subcutaneous semaglutide | Additional average weight loss of 9,8%. It stood out in the meta-analysis as the only agent showing benefits for loss of life, heart attack and progression of kidney disease. | Outcome data come particularly from groups at high cardiovascular risk; the same benefit rate cannot be generalized to every person with excess weight. |
| Oral treatments | Oral semaglutide provided additional average weight loss of 10,9%, and orforglipron 9,9%. | Orforglipron received FDA approval in April 2026. Oral administration may facilitate access; however, its discontinuation rate due to adverse effects was noteworthy in the meta-analysis. |
| New candidates | Agents such as retatrutide, ecnoglutide and mazdutide showed signals of substantial weight loss. | The BMJ analysis rated the certainty of evidence for these agents as low or very low. Strong early figures do not replace mature outcome studies. |
In SURMOUNT-5, the first direct comparison study, average weight loss over 72 weeks among 751 adults with obesity and without diabetes was, with tirzepatide, %20,2, and with semaglutide, %13,7 . Waist circumference decreased by 18,4 cm and 13,0 cm, respectively. The most common adverse effects in both groups were mild or moderate gastrointestinal symptoms, mostly occurring during dose escalation.
A ranking of average weight loss should not become a prescription without assessing the person's diabetes, cardiovascular disease, gallbladder problems, gastrointestinal symptoms, kidney function, pregnancy plans, other medications, costs and likelihood of being able to continue treatment.
SUCCESS IS NOT MEASURED ONLY ON THE SCALE
The real goal of obesity treatment is not a particular body appearance but reducing the burden of disease. Blood pressure, glucose, fatty liver, sleep apnea, knee pain, mobility, cardiovascular events and daily function are at least as important as weight.
In SELECT, among 17.604 people with excess weight or obesity who had cardiovascular disease but no diabetes, semaglutide reduced the combined risk of cardiovascular death, nonfatal heart attack or stroke by 20%.
In the three-year SURMOUNT-1 analysis of people with obesity and prediabetes, the incidence of type 2 diabetes in the tirzepatide groups was %1,3, and with placebo, %13,3 .
In the BMJ 2026 analysis, greater weight loss often accompanied more gastrointestinal adverse effects and treatment discontinuation. Weight loss should not be pursued at the expense of muscle and nutritional status.
Not all rapid weight loss comes from adipose tissue. Inadequate protein and a lack of resistance exercise may increase the risk of sarcopenia, particularly in older people, those undergoing cancer treatment or those with low muscle mass at baseline. A good treatment plan reduces the number on the scale without leaving the person weakened; it monitors muscle strength, nutritional adequacy and functional capacity.
WHY DOES WEIGHT RETURN WHEN MEDICATION IS STOPPED?
In January 2026, BMJ published a meta-analysis including 37 studies and 9.341 participants, showing average weight regain of 0,4 kg per month after weight management medications were stopped. In the statistical projection, weight returned to baseline in approximately 1,7 years. Regain was faster after newer, potent incretin medications, at approximately 0,8 kg per month; the time to return to baseline weight was calculated as approximately 1,5 years.
This finding does not mean that “the medications do not work.” Just as blood pressure returning after stopping hypertension medication, or symptoms returning after stopping asthma control treatment, does not demonstrate that the medication was ineffective, biological defenses strengthening again after obesity treatment ends does not invalidate the benefit during treatment.
The real question is: “What plan will preserve weight and health benefits over the long term?” Long-term medication may take priority for some people, a change in dose or agent for others, metabolic surgery for some and intensive behavioral support for others. The decision to stop treatment should be as carefully planned as the decision to start it.
OBESITY AND CANCER: AN ONCOLOGY ISSUE TOO
This group includes endometrial cancer, esophageal adenocarcinoma, gastric cardia, liver, kidney, multiple myeloma, meningioma, pancreatic, colorectal, gallbladder, postmenopausal breast, ovarian and thyroid cancers. Mechanisms include chronic inflammation, insulin and IGF signaling, sex hormones and biological mediators released from adipose tissue.
Effective obesity treatment will therefore become a more visible part of cancer prevention in the future. However, current GLP-1 or other weight management medications are not cancer treatments; anticancer benefits should not be assumed before observational cancer signals are confirmed in prospective, long-term oncology studies.
The goal must also be individualized in a patient with cancer. A falling number on the scale may not represent success in someone with involuntary weight loss, poor appetite or muscle wasting during active treatment. Sarcopenia may coexist with obesity. In oncology, body composition, muscle strength, treatment tolerance and adequate nutrition may therefore be more valuable than BMI alone.
WHAT DOES A GOOD OBESITY ASSESSMENT ASK?
- Lifetime weight trajectory and previous cycles of weight loss and regain
- Waist circumference, blood pressure and appropriate body composition measurements
- Prediabetes/diabetes, lipids and risk of fatty liver
- Sleep apnea, snoring and daytime sleepiness
- Binge eating, depression, anxiety and symptoms of eating disorders
- Medications and endocrine diseases that may contribute to weight gain
- Muscle strength, physical capacity, joint pain and risk of falls
- Pregnancy plans, menopause and reproductive health
- Personal health goals, treatment preferences, costs and access conditions
- How success, adverse effects and plans for discontinuation will be monitored during treatment
Nonprescription or counterfeit products, nonstandard injections obtained through social media, rapid dose escalation and very low-calorie plans without protein and muscle monitoring may pose serious risks. WHO specifically warns that rising demand has increased the prevalence of counterfeit and substandard GLP-1 products.
TREATING THE INDIVIDUAL IS NOT ENOUGH; THE ENVIRONMENT MUST ALSO CHANGE
We cannot solve obesity solely in the clinic. Access to healthy food, food advertising aimed at children, school nutrition, sugary drinks, walkable cities, working conditions and the time available for sleep determine a population's weight trajectory. WHO's 2026 acceleration plan therefore addresses individual treatment together with policies for healthy environments and early prevention.
The same equity problem exists with medications. WHO projects that even if production increases rapidly, GLP-1 treatments may reach fewer than 10% of those who could benefit in 2030. Moving obesity beyond a willpower problem only to turn it into a disease that only those with money can have treated is not a solution either.
The “willpower” narrative is clinically harmful as well as scientifically inadequate. It shames people, delays help-seeking and traps a chronic disease in cycles of short-term dieting.
Obesity is a chronic, recurrent disease involving interactions among the brain, hormones, metabolism and environment. Structured lifestyle treatment, medications and metabolic surgery may provide meaningful health benefits in selected people.
Weight-loss data for new medications are impressive; however, major gaps remain regarding long-term safety, when and how to stop treatment, muscle loss, costs and equitable access. An average study result does not guarantee an individual's result.
The treatment goal is not an “ideal weight” but clinically meaningful improvement in organ function, metabolic risk, mobility and quality of life. People should be assessed by their whole health profile rather than the number on the scale.
Obesity treatment will move from a competition among individual molecules toward a precision medicine model combining medication selection based on biological phenotype, muscle preservation, digital monitoring, surgery when necessary and long-term maintenance. The greatest transformation will occur when we stop blaming patients and start treating the system.
Sources:
- World Health Organization. Obesity and Overweight. Updated: 8 December 2025.
- Rubino F, Cummings DE, Eckel RH, et al. Definition and Diagnostic Criteria of Clinical Obesity. Lancet Diabetes Endocrinol. 2025;13:221-262.
- Nong K, et al. Comparative Effects of Drugs for Adults with Overweight or Obesity: Systematic Review and Network Meta-analysis. BMJ. 2026;394:e372161.
- Aronne LJ, Horn DB, le Roux CW, et al. Tirzepatide as Compared with Semaglutide for the Treatment of Obesity. N Engl J Med. 2025;393:26-36.
- West S, Scragg J, Aveyard P, et al. Weight Regain after Cessation of Medication for Weight Management. BMJ. 2026;392:e085304.
- Lincoff AM, Brown-Frandsen K, Colhoun HM, et al. Semaglutide and Cardiovascular Outcomes in Obesity without Diabetes. N Engl J Med. 2023;389:2221-2232.
- Jastreboff AM, le Roux CW, Stefanski A, et al. Tirzepatide for Obesity Treatment and Diabetes Prevention. N Engl J Med. 2025;392:958-971.
- World Health Organization. WHO Issues Global Guideline on the Use of GLP-1 Medicines in Treating Obesity. 1 December 2025.
- WHO Türkiye. Türkiye Household Health Survey on Noncommunicable Disease Risk Factors. 28 May 2025.
- International Agency for Research on Cancer. Excess Adiposity and Cancer: Evaluating a Preclinical–Clinical Obesity Framework. 13 May 2025.
- U.S. Food and Drug Administration. FDA Approves Foundayo (Orforglipron). 1 April 2026.
- DROZDOGAN. An Analysis of 100 Thousand People Examines the Real Effects of Weight-Loss Injections. 2026.
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