The epidemic no country has managed to reverse

Obesity has become one of the defining health challenges of the modern era. Despite public‑health efforts over the past half-century, rates continue to rise and no country has yet found a way to reverse the trend.

Few puzzles in public health have proved more stubborn.

For decades, researchers have debated the causes. Some point to changes in diet. Others emphasise declining physical activity, genetics, economics or social conditions.

Yet none of these explanations fully accounts for a striking observation: obesity has increased almost everywhere.

Boyd Swinburn, Professor of Population Nutrition and Global Health at the University of Auckland in New Zealand, has spent much of his career trying to understand why – and to move obesity research away from individual blame and towards the environments and systems that make weight gain more likely.

As he points out, obesity has increased in roughly 200 of 200 countries during the past 50 years – even though “none of them wanted this to happen”.

He believes that obesity emerges from multiple self-reinforcing systems.

The idea grew out of two seemingly unrelated questions – one on the global expansion of ultra-processed foods and the other about how the human body regulates energy balance.

For years, Swinburn studied the two questions separately.

A revelation at 3am

Then, during a research trip to France, something clicked.

“At three in the morning they just came together. I was like a little kid who had seen the Virgin Mary,” says Swinburn. “I thought: this is the cause of the obesity pandemic.”

Out of that moment came a framework centred on three interacting systems: a food system designed for growth, an energy-regulation system that can be tricked into passive overconsumption and biological mechanisms that push weight back up after it has been lost.

Individually, none of these systems is enough to explain the obesity pandemic.

Together, they may explain why obesity continues to rise despite decades of effort to stop it.

Why obesity keeps winning

For most of his career, Swinburn has watched two major health trends move in opposite directions. One has become a public-health success story. The other has become a global failure.

Across much of the industrialised world, deaths from cardiovascular disease have fallen dramatically during the past half-century. Better treatments, lower smoking rates and improved prevention have saved millions of lives.

Obesity has followed the opposite trajectory.

Despite decades of nutritional guidelines, school programmes, public-health campaigns and weight-loss interventions, prevalence has continued to rise.

That contrast led Swinburn to a conclusion that increasingly shapes his research.

“Cardiovascular disease is a tame problem. Obesity is a wicked problem,” he says.

A problem that pushes back

A tame problem may be complicated, but its causes are relatively well understood. Interventions tend to produce predictable effects.

Reduce smoking and lung cancer falls.

Lower blood pressure and cardiovascular disease declines.

Obesity behaves differently.

“It is not just a multifactorial problem,” says Swinburn.

Its causes interact with one another. Solutions often produce only modest effects because changing one part of the system can trigger responses elsewhere that weaken the intervention.

“When you have complex adaptive systems and you push against them, they push back,” says Swinburn.

The wrong question

Virtually nobody intends to become obese. Yet the trend has appeared in country after country, across cultures, political systems and food traditions.

For Swinburn, this makes explanations centred solely on individual choices increasingly difficult to sustain.

For Swinburn, the question is no longer why some people gain weight.

The bigger question is why entire populations do.

After all, 200 countries do not independently make the same mistake.

Answering this question required looking beyond individuals and examining the systems that surround them. That search led Swinburn towards two seemingly unrelated lines of research – one on ultra-processed foods and one on energy balance – which he gradually came to see as different parts of the same phenomenon.

Looking underneath the table

One of the two studies that contributed to Swinburn’s thinking did not focus on obesity directly.

Instead, it focused on the system producing an ever-growing share of the world’s food.

Researchers often debate which aspect of ultra-processed foods is most harmful – sugar, fat, salt, additives or the processing itself.

Swinburn believes that these questions can sometimes distract from a larger issue.

“We should take the foods off the table and look underneath the table,” he says.

Rather than asking what ultra-processed foods contain, researchers asked why ultra-processed foods continue expanding across the globe.

Built for growth

The answer lies in the structure of the system itself.

“When we looked underneath the hood at the ultra-processed food system, we saw a whole lot of positive feedback loops,” says Swinburn. “This thing is in growth mode.”

Successful products generate profits, which fund marketing, increase sales, attract investment and expand production. The result is a self-reinforcing cycle.

“It is built, it is refined, it is honed and it is funded for growth everywhere you look,” says Swinburn.

From a business perspective, this growth is a success story.

From a public-health perspective, it creates a challenge.

The more successful the system becomes, the more people are exposed to foods designed to be convenient, attractive and easy to consume.

Nobody designed an obesity pandemic

Importantly, the study does not claim that companies deliberately set out to create an obesity pandemic.

As Swinburn sees it, the issue is not any single ingredient or product but the entire system surrounding it. Nor does it suggest that every ultra-processed food should be viewed in the same way.

Instead, it highlights a structural reality.

A system built around continuous expansion will tend to produce more products, reach more consumers and occupy a larger share of the food environment over time.

The system does not stand still while public-health initiatives attempt to change behaviour. Because it evolves, it often proves remarkably resistant to change.

What happens when this rapidly expanding food system collides with a biological system that evolved under very different conditions?

A system that usually works

The second study started with a deceptively simple question: how does the body maintain such a stable weight?

Most people experience large fluctuations in how much they eat and how much energy they expend from one day to the next, yet body weight often remains surprisingly stable over long periods.

“It is a bloody miracle,” says Swinburn. “How does it do that?”

His team built a quantitative model of human energy balance and tested it against weight maintenance, weight gain, overfeeding and weight-loss scenarios. The model showed that the body’s energy-regulation system works extraordinarily well most of the time, continuously adjusting food intake, metabolism and energy expenditure to maintain equilibrium.

But the model also suggested a weakness.

It evolved under conditions very different from the modern food environment.

“If your diet is real foods, then it works perfectly fine,” says Swinburn. “But if your diet is high in ultra-processed foods, then it gets fooled.”

A few calories too many

According to the model, common characteristics of ultra-processed foods – including high energy density and rapid consumption – may enable calories to enter the system faster than the body’s regulatory mechanisms evolved to detect and compensate for.

The imbalance may consist of only a few extra calories each day. Over years, these small discrepancies accumulate.

Swinburn calls the phenomenon passive overconsumption.

People do not consciously decide to overeat. In Swinburn’s view, the excess often emerges below the level of conscious decision-making.

“You do not want to overeat calories,” he says. “But you just do.”

The insight helps to explain how obesity can develop gradually without dramatic changes in behaviour and provides the missing link between the two studies.

A system designed for growth can interact with a system designed for stability – and slowly push this stability in the wrong direction.

The body pushes back

Long-term studies consistently show that sustaining substantial weight loss is remarkably difficult. Swinburn’s model suggests that one reason may be that the body actively resists weight loss.

“It has an appetite dial and a metabolic dial,” says Swinburn.

As weight falls, appetite tends to increase and energy expenditure can decrease, pushing in the same direction: restoring the lost weight.

From an evolutionary perspective, that response makes sense. For most of human history, starvation posed a far greater threat than obesity, so the body evolved to defend against weight loss far more aggressively than against weight gain.

People attempting to maintain weight loss are often working against powerful biological signals. This does not make weight loss impossible, but it means that success requires overcoming systems designed to pull weight back towards its previous level.

“You need each of these three conditions,” says Swinburn. “This is why it is a systemic problem. This is why it is so bloody hard to treat.”

The drug that changed his mind

The framework also forced him to rethink obesity medicines.

For years, he doubted whether drugs targeting appetite could have a major impact. Human appetite regulation seemed too important, too deeply embedded and too redundant to be altered through a single intervention.

“I was quite surprised when the GLP-1s came along.”

He compares it to trying to solve city-wide traffic congestion by blocking a single road.

Traffic simply finds another route.

"The obesity drugs we've had until now have been pretty poor," he says. "It was the fact that a single molecule targeting a single pathway could have such a strong effect that surprised me."

The emergence of GLP-1-based medicines suggests that intervening in one of the feedback loops contributing to obesity may be possible.

Swinburn believes that they may act as a kind of circuit breaker.

"The GLP-1s clearly operate within these physiological feedback loops in our model to act like a circuit breaker," he says.

The medicines do not alter the food system itself or many of the environmental forces that contribute to obesity. In Swinburn’s framework, they affect one part of a much larger system and may weaken one of the forces that drives weight regain.

For Swinburn, the drugs are interesting less because they offer a complete solution and more because they demonstrate that one of the system’s feedback loops may be modifiable.

Where can you intervene?

The three-system framework does not provide an immediate solution to the obesity pandemic. Instead, it helps explain why so many interventions have struggled.

Educational campaigns, nutrition labels and weight-loss programmes may help. Yet the broader system continues to operate, helping explain why obesity has proved so difficult to reverse at the population level.

One of the more sobering conclusions of Swinburn’s recent work is that both major systems appear remarkably resilient.

“Both these complex adaptive systems – the ultra-processed food system and the energy-balance system – push back on whatever we try to do.”

“It is not just the ultra-processed food itself,” says Swinburn. “It is the whole system. It is the availability, the pricing, how they have captured the food supply system, the politicians, the storekeepers, the school canteens, us – everybody. We are all semi-willing captives within that system.”

Yet he does not see the situation as hopeless.

Understanding the system, he argues, may reveal new opportunities.

Finding the leverage points

For much of his career, Boyd Swinburn has helped shift obesity research from risk factors to environments, systems and accountability. Today, he is increasingly interested in leverage points – ways in which relatively small changes, whether through policy, food environments or medicines such as GLP-1 receptor agonists, could produce disproportionately large effects.

The common requirement is that they work with the system as it actually operates.

For Swinburn, this has become the central lesson of more than four decades spent studying obesity.

The goal is no longer simply to understand why individuals gain weight.

The goal is to understand why entire populations drift towards positive energy balance.

Many of the most pressing health challenges of the 21st century emerge from multiple systems interacting over time.

Because if Swinburn is right, the obesity pandemic is not primarily the consequence of individual failure.

It is the product of systems that have become extraordinarily effective at producing an outcome that almost nobody wants – not governments, not public-health agencies and not the people gaining the weight.

And unlike human biology, these systems can be redesigned.