I have sat with patients who have tried every diet, every exercise programme, every intervention recommended to them - sometimes over twenty years - and who describe their inability to sustain weight loss with a shame and self-blame that I find genuinely painful to witness. They have been told, in clinical rooms and in culture at large, that their weight is a consequence of insufficient willpower.
This narrative is not only unkind. It is also wrong. And the evidence that it is wrong has been accumulating for decades in scientific literature that has simply not made it from journals into the clinical consultation, or from the clinical consultation into public understanding.
The science of obesity has fundamentally changed in the past twenty years. We now understand that body weight is regulated by a complex system of hormones, neural pathways, and genetic factors that actively and powerfully resist weight loss. For most people, sustained significant weight loss through diet and exercise alone is genuinely difficult not because of moral failure but because of how the biology works. And we now have treatments that work with that biology rather than against it.
Why eat less and move more fails most people
When you reduce calorie intake and lose weight, your body responds in multiple documented, measurable ways designed to resist that weight loss and restore your previous weight:
Hormonal changes that persist: The landmark Biggest Loser study followed contestants from a US weight loss television programme for six years after their dramatic weight loss. Despite having maintained some weight loss, they had persistently elevated ghrelin (hunger hormone) and persistently reduced leptin (satiety hormone) compared to people who had never been obese. The hormonal drive to eat more was measurably greater, years after the show ended.
Metabolic downregulation: As weight is lost, resting metabolic rate falls significantly - and falls more than would be predicted from the reduced body mass alone. The body becomes more metabolically efficient. The same calorie intake that maintained your reduced weight six months ago will now cause weight regain.
Neural adaptations: Brain circuits involved in reward and motivation adapt to the reduced food intake, increasing the salience and reward value of food cues. The drive to eat becomes neurologically stronger.
These are not signs of weakness or insufficient commitment. They are physiological mechanisms, documented in controlled trials, that are present to varying degrees in virtually everyone who loses significant weight. The question is no longer why do people regain weight - the biology explains that clearly. The question is what treatments are powerful enough to overcome or work with this biology.
BMI and Black patients - the specific problem
Body Mass Index has known limitations as an individual measure of health risk, and specific limitations in Black patients.
BMI was developed using predominantly European populations. Research consistently shows that people of African origin tend to have greater bone density and muscle mass than white Europeans of comparable size, which increases BMI without reflecting excess body fat. A Black patient with a BMI of 28 may have a comparable fat percentage to a white patient with a BMI of 25.
Conversely, cardiovascular and metabolic risk in Black patients tends to manifest at lower BMI values than in white Europeans - partly through different fat distribution patterns (greater truncal and visceral adiposity at comparable BMI).
Waist circumference (above 88cm in women, above 102cm in men, or the lower ethnic-specific thresholds of 80cm and 90cm respectively) is a better predictor of metabolic risk than BMI alone.
Case study: David's twelve-year struggle
David, 46, an IT manager from Nigeria based in Manchester, came to see me after twelve years of weight management attempts. He had lost significant weight on four separate occasions - 15kg once, 12kg twice, 20kg once. Each time, the weight had returned within 18-24 months, often slightly exceeding his starting weight.
He described the experience with deep shame. He believed he was weak. He had stopped telling people he was trying to lose weight because he was embarrassed in advance about the inevitable failure.
When I explained the hormonal biology - the persistent ghrelin elevation, the metabolic downregulation, the neurological adaptations - I watched his expression change. From shame to something closer to relief.
"You mean this is not just me?" he said.
No. It is not just him. And now there is a medication that specifically targets the hormonal system that makes sustained weight loss so physiologically difficult.
GLP-1 receptor agonists - the treatment that changes the equation
Semaglutide (Ozempic for type 2 diabetes, Wegovy for obesity) and tirzepatide (Mounjaro for both diabetes and obesity) are GLP-1 receptor agonists (or in the case of tirzepatide, dual GIP/GLP-1 agonists) that mimic gut hormones released after eating. They reduce appetite profoundly, slow gastric emptying, and - crucially - appear to reset the hormonal set-point around which weight is regulated.
Clinical trial results are unlike anything previously seen in obesity pharmacotherapy:
The STEP trials of semaglutide 2.4mg weekly: average weight loss of 15% of body weight over 68 weeks. 35% of participants lost more than 20% of body weight.
The SURMOUNT trials of tirzepatide: average weight loss of 20-22% of body weight. 57% of participants lost more than 20%.
The SELECT cardiovascular outcomes trial: semaglutide reduced major adverse cardiovascular events by 20% in people with obesity and cardiovascular disease but without diabetes - a landmark finding that established these drugs as cardiovascular medicines, not just weight loss medicines.
Access in the UK: Wegovy (semaglutide 2.4mg) was approved by NICE for obesity in 2023 with specific criteria (BMI above 35 plus at least one weight-related comorbidity, or BMI 30-34.9 in specified circumstances). Mounjaro (tirzepatide) has been approved in 2024. Access through specialist weight management services and some GP practices is expanding. Ask your GP whether you are eligible.
They are not permanent: These medications must continue to work with the underlying biology to maintain their effect. Weight returns when medications are stopped, because the biological drive to regain weight resumes. This does not make them ineffective - it makes them more like antihypertensives than antibiotics.
Bariatric surgery - the most durable intervention
For severe obesity (BMI above 40, or above 35 with significant comorbidities), bariatric surgery remains the most effective and most durable intervention. Gastric bypass and sleeve gastrectomy produce average weight loss of 25-35% of body weight, with many patients achieving remission of type 2 diabetes, improvement of hypertension, and resolution of sleep apnoea.
Surgery is not a shortcut. It requires lifelong dietary commitment and monitoring. But for people with severe obesity and significant comorbidities, the risk-benefit calculation strongly favours surgery.
Ask your GP for a referral to a specialist weight management service if you have a BMI above 35 with comorbidities.
Sources: Sumithran P et al, NEJM 2011 (persistent hormonal changes after weight loss); Fothergill E et al, Obesity 2016 (Biggest Loser follow-up study); Wilding JPH et al, NEJM 2021 (STEP 1 semaglutide trial); Jastreboff AM et al, NEJM 2022 (SURMOUNT tirzepatide trial); Lincoff AM et al, NEJM 2023 (SELECT cardiovascular trial); NICE NG187 - Obesity in Adults 2023.
