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FOR DECADES, OUR response to obesity has been remarkably simple.
Eat less. Move more. Try harder.
It’s advice that sounds logical and sensible. It is also overly simplistic and one of the reasons so many people living with obesity blame themselves when it doesn’t work long term.
Today, science tells a very different story. Obesity is not due to a lack of willpower or simply the consequence of poor choices. It is a complex, chronic medical condition involving the brain, hormones, genetics and metabolism, further shaped by the modern environment and our lived experiences.
Obesity develops through changes in the biological systems that regulate appetite and body weight within the subconscious brain. We don’t expect someone to decide not to feel thirsty. Hunger is similarly generated by biological systems outside conscious control. We still choose whether and what to drink, but we don’t choose whether we feel thirsty in the first place.
Like asthma or high blood pressure, it has biological and environmental drivers, health consequences and evidence-based treatments.
Understanding that doesn’t reduce the importance of good health behaviours, nutrition or physical activity. But it helps us understand why those measures alone may not be enough for many people.
It also helps explain why a new generation of obesity medications has generated so much attention.
Most of us assume that body weight is largely under conscious control. If we simply wanted it enough, we could eat less indefinitely.
Our biology disagrees.
Humans evolved during a time when food was scarce. Our biology prioritises survival, not fitting into modern clothing sizes or sociocultural ideals. Deep within the brain, specialised regions constantly monitor our energy stores and regulate hunger, fullness, food reward and energy expenditure. Like the thermostat in our home maintains temperature, this complex system works continuously to defend body weight.
When we lose weight, the brain interprets it as a potential threat to survival. Hunger hormones rise. Signals that normally tell us we are full become weaker. Food becomes more rewarding. Cravings increase. The body burns fewer calories than expected, making it progressively harder to maintain weight loss.
These changes are not imagined. They have been measured repeatedly in scientific studies and persist long after weight has been lost and regained. For many people, they result in repeated cycles of losing weight and regaining it despite continued effort. It is biology, not a lack of determination.
Research tells us that genetics account for a substantial proportion of a person’s susceptibility to obesity. Some people inherit a more powerful drive or biological systems that defend a higher body weight.
Many other factors, such as sleep deprivation, chronic stress, certain medications, mental health conditions, pain, socioeconomic circumstances and our modern food environment, all interact with our biology to alter our risk.
We now live in a world where highly processed, calorie-dense food is cheap, heavily marketed and available almost everywhere. For someone whose biology is predisposed to obesity, that environment becomes especially difficult to navigate.
None of this means personal choices don’t matter. They absolutely do. But choices are made within a biological system that is not the same for everyone.
Simply understanding the biology of obesity will not treat it. But it can replace shame with understanding – and that is often where effective treatment begins.
One reason the debate around obesity has become so confused is that two very different conversations have become tangled together.
One is about obesity, a chronic disease that affects health and quality of life and is associated with more than 200 health conditions.
The other is society’s long-standing cultural pursuit of thinness.
These are not the same thing.
For decades, “diet culture” promised happiness, health and social acceptance through weight loss. Today, some describe the social media obsession with GLP-1 medications as “Diet Culture 2.0” – the same cultural pressure to become thinner, but now using prescription medicines instead of meal replacements or celebrity diets.
When prescription medicines are promoted primarily for short-term cosmetic weight loss, it reinforces the misconception that obesity is about appearance rather than health and risks obscuring what these medicines were developed to do.
They were not designed to help already healthy people become slimmer. They were developed to treat a chronic disease that impairs health, reduces quality of life and shortens lives. The goal of obesity care is not thinness. It is better health.
The arrival of medications such as Semaglutide (Ozempic & Wegovy) and Tirzepatide (Mounjaro) has changed obesity treatment more than any development has in decades.
The medications are often described as “weight-loss injections” or “skinny jabs”, but that description misses the point. That is like calling insulin a “blood sugar injection”. It focuses on one visible effect while ignoring the underlying disease they were designed to treat.
These are obesity medications – the initial response may be weight loss, but the long-term benefit is maintenance of the lower weight and reducing the impact of excess body fat on current and future health.
Most work by mimicking naturally occurring gut hormones that communicate with the brain after eating. They reduce hunger, increase feelings of fullness and dampen the constant drive to think about food that many people describe as “food noise”. They help manage some of the disrupted biological signals that make weight regulation so difficult.
For many patients, the impact is moving away from calorie counting, restriction and deprivation towards eating well, enjoying food without guilt and engaging more fully with life now that appetite is no longer in charge.
Large clinical trials involving thousands of participants have shown average weight reductions of around 15% with semaglutide and around 20% with tirzepatide when combined with ongoing lifestyle support. Response varies considerably from person to person. Like many medical treatments, this reflects biology rather than intelligence, motivation or moral character.
Perhaps the greatest misconception is that obesity treatment is about making people thinner. It isn’t. It is about helping people become healthier. The benefits extend beyond the number on the scales.
Studies have demonstrated improvements in blood pressure, arthritis, blood sugar, liver disease, obstructive sleep apnoea and quality of life. Semaglutide has also been shown to reduce major cardiovascular events, including heart attack and stroke, in people living with obesity and established cardiovascular disease. The goal is better health, not simply lower weight.
Obesity medications treat a chronic disease rather than cure it. When treatment stops, the biological drivers of obesity return, resulting in weight regain and loss of health benefits. Like medication for high blood pressure or high cholesterol, these treatments should be viewed as long-term therapies rather than a short-term “kick start.”
Obesity prevention and obesity treatment are often presented as competing priorities. They are not.
We should continue tackling the societal drivers of obesity – education, the food environment, socioeconomic disadvantage, chronic stress, the marketing of ultra-processed foods access to green spaces – while also ensuring that people already living with obesity have access to effective, evidence-based treatment. They are not mutually exclusive.
Medication is only one potential part of modern obesity care.
Nutritional therapy remains the foundation of treatment, helping people optimise quality of food, preserve muscle and support long-term health in a sustainable way. Physical activity, sleep and psychological support all remain important.
For people living with more severe obesity, bariatric surgery remains the most effective treatment we have, producing the greatest and most durable improvements in weight and health.
Like with other chronic conditions, the most appropriate treatment depends on the individual – what is acceptable, sustainable, affordable and enjoyable to them long term.
One thing we now know for certain, stigma, blame and shame do not motivate healthier behaviour.
Research suggests it often has the opposite effect. People who experience weight stigma are more likely to avoid healthcare, delay screening, experience depression and anxiety, and disengage from treatment. Blame has never been an effective therapy.
“People should just eat less.”
If obesity were simply a matter of knowledge, it would be rare. Most people living with obesity already know what constitutes a healthy diet.
The challenge is not knowing what to do. It is sustaining healthy behaviours in the face of powerful biological, environmental and life pressures.
Lifestyle changes remain essential, but may not be sufficient alone for many people living with the chronic disease of obesity.
“Medication is the easy way out.”
Taking a long-term medication for a chronic disease is no more “easy” than using inhalers for asthma or tablets for high blood pressure.
These treatments work alongside nutrition, physical activity, sleep and psychological support rather than replacing them.
“These drugs are too new.”
While public awareness has exploded recently, the underlying science has been developing for more than 20 years.
Earlier GLP-1 medicines have been used in diabetes care for many years, and the newer obesity-specific trials have involved tens of thousands of participants with extensive safety monitoring.
Like every medical treatment, they have side effects and are not suitable for everyone, but they are among the most rigorously studied medications introduced into obesity medicine.
These medications are not perfect. Common side effects include mild to moderate gastrointestinal issues such as nausea, heartburn, diarrhoea and constipation. These are mostly seen when treatment begins and with dose changes but usually improve over time.
Patterns of eating, food choices and gradual dose changes are vital to reduce adverse effects. Medication use and weight loss increase the risk of developing gallstones and in a small number of people this could be associated with a rare complication called pancreatitis.
Muscle loss is often raised as a concern with obesity medications. However, some loss of lean tissue occurs with any significant weight loss and is no greater with these medications than with diet or bariatric surgery. A nutritious diet and resistance exercise help preserve strength and muscle.
Many of the concerns surrounding these treatments are not caused by the medications directly, but by rapid weight loss, unrealistic expectations or using them outside appropriate medical care.
These medications are not recommended during pregnancy or while trying to conceive, and some require consideration of contraception or hormone replacement therapy.
Adherence is also an issue with around half of people stopping obesity medications within the first year of treatment. Cost, side effects, supply shortages and unrealistic expectations all potentially play a role. Good follow-up, personalised dosing and ongoing support can make a substantial difference.
Demand for medications has created another challenge. More people are obtaining obesity medications online, sometimes without speaking to a healthcare professional.
These medicines are generally safe when prescribed and supported appropriately, but they are not suitable for everyone. We would never expect someone to start treatment for heart disease or arthritis after completing a five-step online questionnaire. Obesity should be no different. People deserve expert medical care – not simply access to medication.
The rapid commercialisation of obesity medications has fuelled understandable public scepticism. Commercial interests should always be scrutinised. But we should not allow concerns about marketing or misuse to overshadow the substantial evidence supporting these medicines when prescribed appropriately for people living with obesity.
The greatest challenge may not be scientific but practical.
In many countries, including Ireland, cost remains the biggest barrier in accessing obesity medications and the support needed to use them safely. People who would benefit most are often unable to afford treatment, while others with greater financial means can access it more easily.
Obesity is more common in areas of social disadvantage, creating a paradox whereby those with the greatest medical need often face the greatest barriers to care.
Improving access is about more than funding medication. Effective obesity care requires resources and time in general practice as well as access to multidisciplinary support, including dietitians, psychologists, physical activity and specialist hospital services.
This raises difficult questions for healthcare systems. If obesity is accepted as a chronic disease, should access to treatment depend largely on personal income?
Without greater investment in evidence-based obesity services, there is a risk that more people will turn to poorly regulated online providers or unlicensed products, receiving medication without the comprehensive assessment, education, follow-up and ongoing support that should accompany treatment.
Perhaps the greatest impact of these medications is not the weight people lose. It is the myths they force us to abandon.
If treating the brain can reduce hunger, quieten constant thoughts about food and improve long-term weight regulation, then obesity was never simply a failure of willpower.
Obesity care is not about everyone becoming thinner. It is about helping people whose health is impaired by obesity live longer, healthier lives.
The science has changed. It is time our language, our healthcare systems and our attitudes changed with it.
Dr Michael Crotty is a GP and Obesity Medicine Specialist. He is co-founder and clinical lead at the My Best Weight clinic.
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