The infamous case of obesity suggests that to address complex epidemics, we need a better-informed, less overconfident public with a much broader array of scientific evidence.

I’ve had science-related occupations for most of my adult life. I’ve spent countless hours learning about biology, the gut-brain axis, nutrition, brain and behavioural science. In that time, I’ve learned that science creates both curiosity and uncertainty, as the more we discover, the more questions emerge. I thought the countless hours of studying while running experiments would give me the confidence to say, “No, we have proof; I am right, and you are wrong.” Little did I know that science is not about proof, which is final, but about evidence, which evolves and can change as knowledge grows.

Like many, I was drawn to confident arguments full of certainty, declaring hypotheses “proven” to silence doubt. However, my scientific journey was not about selfishly feeding my ego, but about gathering evidence to see if my hypotheses are wrong, changing my mind when the evidence suggests so, and carefully, thoughtfully, and analytically decreasing uncertainty rather than increasing certainty. Like anyone reading this, I understand the temptation to eliminate all doubt, but we cannot simplify complex problems to give ourselves a sense of empowerment.

In my early teens, I remember the local TV news channel reporting the story of a person with obesity. In that short report, they showed video clips of her eating enormous amounts of food and tackled the weight-related issues she experienced during her pregnancy. The most surprising moment came when she was asked if she would change her behaviour after all the complications she had experienced during pregnancy. “Food brings immense joy to my life and I live for it!” she exclaimed. I was appalled that someone would have such an attitude, ignoring her health to such an extent. For years after, this episode shaped my anecdotal opinion, associating certain physical appearances with particular behaviours.

Over the years, I’ve given this opinion some thought; here are some snippets. Weight management – be it loss or gain – can be traced back to energy balance, the rules of which are based on a simple thermodynamic principle. When we take in more energy than we use, our bodies store that extra fuel mainly as fat. Given the global rise in obesity rates, with 890 million people currently affected, and the decline in energy expenditure from physical activity, you could simply argue that we should eat less and exercise more. But is this the whole story? If it’s so simple, why is losing weight and keeping it off so rare? Could our biology be playing a role?

Genes and Environment

What stands out regarding the obesity epidemic is not just the sheer numbers, but how quickly rates of obesity have increased globally. Genes do not change this quickly. Evolution takes centuries to influence single genes, and these genes, alongside environmental pressures, reshape our brain and behaviour. For example, modern humans underwent several million years of evolutionary development before they could walk on two legs. In the case of obesity, however, researchers have observed a worldwide shift toward diets high in processed foods, loaded with fat, refined carbohydrates like sugar, and excess sodium. Some may think this just proves that people are lazy or unable to resist the temptation in our obesogenic environment, but research into obesity genetics over the past two decades has shown that it’s not just our environment – it’s also our genetic diversity. A blessing, but also a curse in today’s environment.

When obesity rates go up, it’s not just that more people have obesity. The entire population grows heavier, with more individuals moving into the overweight range. This shows that broad environmental changes affect everyone, though not to the same degree. Studies of identical twins – like those separated at birth in the Minnesota Twin Study – show that genetics set the starting point, but the environment and our behaviour shape the endpoint. For example, our sense of taste is shaped by our genes as much as our height or hair colour. A single gene called TAS2R38 determines if you find certain foods – like broccoli or kale – extremely bitter or not, which helps explain why we each respond so differently to flavours. Remarkably, one study showed that even babies in the womb can react aversively to bitter tastes before they’re ever exposed to the outside world.

Similarly, genetics also influence body weight in complex ways. While rare cases of obesity stem from a single gene, most involve multiple genes with minor, cumulative effects, combined with environmental factors. Studies of twins and families suggest that genetics can explain between 40 and 70% of a person’s obesity risk. This shows that people face very different biological challenges when making choices about what and how they eat. But how does that happen?

Is overeating an addiction?

My research has taught me that our need for food is deeply rooted in the nervous system. Human brains have evolved reward systems that help us survive by seeking energy, systems that create pleasurable sensations, reinforcing certain behaviours. First, food cues like smell and sight don’t just build to that first bite; they spark a surge of anticipation and motivation to eat, based on past experiences of pleasure. Then, when the nutrients your body requires reach the gut, a second signal from the gut to the brain triggers a reward response, this time without us even noticing. These two processes, taste and post-ingestive signalling (i.e., nutrients absorbed in the gut signal to the brain), shape how, what, and when we eat. Thus, our conscious control is only partly responsible for our dietary choices, and modern diets packed with refined carbs and fat influence these reward systems, making it much more difficult to change eating habits.

Many compare our drive for food with substance abuse (i.e., addiction) because of the powerful reward modern, highly processed foods create. Interestingly, the term food addiction first appeared in the 1950s . However, not everybody agrees with this comparison; some essentially argue that food is necessary for life, whereas drugs of abuse like cocaine are not. Moreover, unlike drugs, food does not contain a single specific addictive substance (e.g., nicotine). Despite this, several others argue that highly processed foods containing refined carbohydrates and fats meet the criterion for an addictive substance.

Food addiction might be better understood as a behavioural addiction, similar to gambling, but some argue that the term addiction is an unnecessary medicalization of the excessive consumption of pleasurable foods. Whatever opinion you side with, two things remain certain: food and drugs activate similar neurobiological reward mechanisms, and this debate won’t be resolved anytime soon.

Eating is a complex behaviour

Eating is a behaviour that requires calibrated coordination between multiple motivational, cognitive, and motor brain systems. Simply put, our reward systems have evolved to ensure our survival and reproduction. However, modern foods with highly rewarding properties are simply too delicious and expose the weaknesses of our well-calibrated brain systems. Common behaviours, like the overconsumption of food, can be unhealthy, but are they pathological? The evidence suggests we don’t know yet.

What we do know is that people with obesity do not enjoy food more, but in many cases, suffer multiple alterations in the brain systems that could allow them to make better food decisions. For example, our lab’s work has demonstrated that individuals with obesity, when compared to normal-weight participants, show a greater ability to shift attention, adapt, and learn about the changing value of rewards like food or money. Moreover, they show a stronger tendency to approach unhealthy food and find it harder to resist the urge to eat it. Additionally, studies have shown that individuals with obesity fail to accurately evaluate and learn from negative outcomes. To make matters worse, some evidence indicates that even when food loses its motivational value (e.g., when reaching satiety), these individuals are less sensitive to that internal change, leading to overconsumption. In sum, an extensive amount of research suggests there are no differences in food “liking” but “wanting”, or in other words, a stronger motivation to consume food.

Why there is no universally ideal diet

Our bodies don’t use and store energy like a machine; our metabolism is shaped by evolution. Metabolism is the work our bodies’ cells do to transform molecules (like A to B), recovering nutrients for energy production (catabolism) and consumption (anabolism). This energy, measured in kcal or kJ, along with the speed of these transformations and nutrient use, determines our metabolic rate.

One of our most effective survival strategies is storing fat, which packs more energy per gram than any other nutrient. Whether calories come from carbohydrates or fat, our bodies store the surplus as fat, making us remarkably efficient at conserving energy. One experiment showed that even after losing weight, our bodies could “remember” their previous fat levels, making it easier to regain the weight.

Evolution, it seems, is a very good accountant, but this particular accountant is very stringent when it comes to eating less than the body needs but very indulgent in allowing the body to retain superfluous calories in the form of more body fat.

There was never one universal ‘natural’ diet that was available to everyone. Humans adapted. Early humans ate what was available; some groups, like the Hadza in Tanzania and Tsimane in Bolivia, had diets rich in carbohydrates, while the Inuit in the Arctic and Subarctic regions ate mostly fat. As Professor Herman Pontzer puts it, the diets of the past aren’t necessarily the diets that keep us healthy today. And when it comes to modern weight-loss diets, they all work — if you can stick to them. How’s that possible? Genetics, obesogenic environments, the brain, and metabolism all contribute to why most of us fail to stick to a diet. Even after modern anti-obesity drugs and bariatric surgery, which have much better track records, several people still regain the weight they’ve lost.      

Exercise

We’ve all heard countless times that exercise is key to losing weight. Most of us assume that the more we move, the more calories we burn – and that this automatically leads to weight loss. But it turns out, exercise might play a different role than we think. In the traditional view, there is a straight line between how much we exercise and how much energy we expend, with more exercise eventually leading to weight loss. However, some research proposes that exercise changes how we spend calories but doesn’t necessarily increase the total number we burn.

Most of our daily energy is devoted to basic functions, such as digestion and organ function, even when we’re resting. Burning more calories doesn’t mean you lose weight: when you expend more energy on one task, your body adapts by decreasing how much it consumes on a different task, keeping our metabolism around a certain average. Having a ‘fast metabolism’ (i.e., burning more calories at rest) isn’t a guarantee of thinness. In fact, if you don’t account for body size and composition, someone with obesity often burns as much or even more energy per day simply because they have more tissue to carry around. Moreover, our metabolism is high in infancy, stays fairly stable from about ages 20 to 60, then declines in older age. Large-scale studies show that most of the variation in energy use can be explained by factors such as body size, composition, and gender, rather than by activity alone. According to two recent studies, the obesity epidemic of the past three decades can’t be blamed on reduced physical activity, and diet plays a far more critical role here. Even if you consider the traditional exercise model, most of us can’t outrun a bad diet; our evolved biology fights back.

One of the most interesting aspects of metabolism is how it reacts to weight loss. Because humans evolved in times of food scarcity, your brain and body often treat losing weight as a risk to survival. Weight loss triggers biological signals aimed at regaining the lost weight: your resting metabolic rate slows down, and both appetite and unconscious drives to eat increase. This is where exercise plays a vital role. While it may not cause significant weight loss on its own, exercise does help maintain lost weight and overall health (e.g., by improving cardiovascular fitness).  Physical activity boosts energy expenditure, curbs hunger, and helps build muscle mass, which in turn burns more calories at rest, limiting the metabolic slowdown that might come as a result of weight loss. These combined effects make exercise essential for long-term weight management, but overcoming the natural physiology of the body with willpower alone still remains incredibly difficult.

Epilogue: The wins and pitfalls of obesity research

The difficulty of weight loss really stands out in obesity research, where experts still hotly debate what causes it and how to tackle it. Public critics often claim modern obesity science is politically driven, swayed by “soft” ideology from younger scientists and activists forcing veteran researchers to flip views in order to save their careers. That’s misguided. In fact, obesity research began moving away from the laziness narrative long before many present-day scientists entered the field. But like any science, obesity research is shifted forward by weighing diverse evidence amid competing theories.

Earlier, the general understanding was that hurting feelings or tough love might motivate people, but current research shows otherwise – even highly driven Biggest Loser contestants often regain the weight years later.  We now know that weight stigma worsens outcomes, increasing emotional eating, exercise avoidance, and healthcare delays, all of which work against lasting weight loss.

I stress these points because public opinion on obesity really matters. It sways the policies and funding that drive real change.  Obesity brings with it real social and health challenges, and people do not choose it willingly. The size of the wellness and weight-loss industry shows the lengths people are willing to go, not just for health but for acceptance.  Thus, it’s not just about “eating less,” but about bigger forces like our food environment and biology: we need solutions at the community and policy level, not just willpower. Scientists have to explain their findings clearly and honestly to leaders and to the public, so that smart policies can keep up with what we know and enable people with obesity and medical professionals to pick the best health strategies. We can consider other people’s perspectives, but recognizing those perspectives does not mean that we cannot question their validity.

Ultimately, this discussion isn’t about promoting a single ideal body; it’s about recognizing obesity as a complex challenge shaped by decades of research, not just stories or opinions. Even as a scientist, what matters isn’t what I believe, but what the evidence shows.

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