Many years ago, during a flight, Woody Allen read two things: Fyodor Dostoyevsky’s Notes from Underground and Weight Watchers magazine. Later, he fused these two entirely unrelated reading experiences into a short essay. It began like this: “I am fat. I am disgustingly fat. I am the fattest person I know. My whole body is covered with excess weight. My fingers are fat. My wrists are fat. My eyes are fat. Can you imagine fat eyes?”
That was 1968. At the time, most people in the world were still more or less what might be called height-weight proportional, while millions of others were struggling with hunger. Weight Watchers was still a young organisation, dealing with a problem that seemed new, peculiar, almost exotic. The idea that someone could fall into Russian-novel anguish over being fat was, back then, still something one could laugh at.
But that was another age. Today, the joke of 1968 looks almost like a prophecy. By the 21st century, obesity was no longer a comic anxiety of a few affluent people. It had become one of the most serious issues on the global public-health agenda. For the first time in human history, the number of overweight people surpassed the number of undernourished people. Obesity appeared not only in wealthy countries but also in poor ones, not only in cities but also in rural areas, not only in highly industrialised societies but also in places newly entering consumer culture.
Along with it came the rapid expansion of a long list of chronic diseases: diabetes, heart disease, stroke, kidney failure and various long-term conditions linked to metabolic disorder. The World Health Organization has warned that such diseases are becoming leading causes of death in more and more countries, including those that once struggled more urgently with infection, famine and injury.
The seriousness of the problem lies not only in the diseases themselves. Modern medical systems were originally better suited to acute infections, trauma and conditions that could be treated quickly. Obesity-related illnesses, by contrast, tend to be long, recurring and expensive. They do not always kill swiftly. Instead, they may usher people into years of gradual decline, requiring continuous medication, testing, hospitalisation and care. For the individual, obesity can mean pain in a long twilight of life. For the medical system, it means mounting financial pressure.
And so official agencies, public-health experts, commercial advertising and news reports began telling us, in ever louder voices: we are too fat. Not merely fat, but fat enough to endanger ourselves, burden society and threaten national health budgets. We must control ourselves. We must admit our indulgence. We must take responsibility for our mouths and our legs.
After all, in the most popular explanation, the culprit appears obvious: we eat too much and move too little. Countless times each day, we choose sweets, fried potatoes, sugary drinks, elevators instead of stairs, cars instead of walking. Our ancestors once crossed mud, hills and fields on their legs, while we sit in cars, office chairs and sofas, allowing the body to become a soft storage unit for fat. The conclusion sounds plain, direct, even morally satisfying: you are fat because you lack discipline.
This moral panic around fatness has seeped into ordinary life. It is no longer merely a doctor’s recommendation or a gym advertisement’s motivational slogan. It has become a way of judging people. The American evolutionary psychologist Geoffrey Miller once posted an infamous tweet suggesting that obese PhD applicants who lacked the willpower to stop eating carbohydrates would also lack the willpower to complete a dissertation. What made the remark so sharp was not only its rudeness. It was that it compressed a complicated biological, social and economic problem into a defect of character.
The business world, of course, would not miss such a mood. If obesity is understood as personal weakness, then the market for correcting personal weakness can expand without limit. Weight-loss foods, meal replacements, exercise programmes, surgery, drugs, tracking devices, health-management apps, smart utensils and all manner of self-monitoring technologies have appeared. One company even introduced an electronic fork that records how many bites you take per minute. If you eat too quickly, it vibrates, like a tiny moral instructor reminding you to slow down. Consulting firms, too, have seen the opportunity, predicting that “health and wellness” will become a vast global industry. Obesity is certainly expensive, but managing obesity can also become an enormous market.
Governments have joined in as well. Ideas that once belonged to fringe debates soon became public policy. New York City tried to restrict large sugary soft drinks. Denmark briefly taxed foods high in saturated fat. Samoa Air once priced tickets according to passengers’ weight, as if body mass were not only a health indicator but also a bill. The United States had Let’s Move!, Britain had Change4Life, Switzerland had actionsanté — names so bright and friendly they sounded as if they had wandered out of a children’s programme or toothpaste commercial. Japan took a more serious approach: companies were required to measure and report the waistlines of middle-aged employees, and those who exceeded the recommended size could receive health advice with a distinctly admonishing tone.
Behind all these policies and products lies a shared assumption: obesity is mainly the result of individual choice. A BMI above 25 means a person has chosen wrongly; a BMI above 30 means the person has kept choosing wrongly. Society is now investing enormous resources to correct these choices. Business leaders and government officials seem especially fond of this explanation, perhaps because they often believe they achieved their own status through discipline and restraint. It is easy for them to see body weight as another test of self-management.
But the real question is: is this explanation actually true?
Where Female Obesity Is Higher, Gender Inequality Often Runs Deeper
If you listen only to public-health campaigns and the wellness industry, the answer seems simple. They will tell you that science has spoken clearly: obesity is what happens when intake exceeds expenditure. Michael Bloomberg, then mayor of New York City, made this argument while defending restrictions on large sugary drinks. If you want to lose weight, he said, then do not eat. This is not medicine. It is thermodynamics. If you take in more energy than you use, your body stores it.
There is something reassuringly neat about this statement. It lifts obesity out of the disorder of real life and places it in a school physics lesson. Intake, expenditure, storage: three steps, problem solved. No class, no gender, no industrial chemicals, no sleeplessness, no stress, no global food trade, no history. Only the law of energy conservation and a person who has failed to control their appetite.
Yet scientists who actually study fat metabolism, and epidemiologists who track changes in population weight, are not all lined up behind this simple model. More and more researchers believe that personal gluttony and laziness cannot explain the global rise in body weight. Richard Atkinson of the University of Wisconsin once stated plainly that the old view of obesity as merely a lack of willpower and an inability to control eating habits could no longer be defended.
Some evidence is downright strange. In 2010, biostatistician David Allison and his colleagues reported that over several decades, as Americans were getting heavier, many American animals were getting heavier too. Marmosets became heavier. Laboratory macaques became heavier. Chimpanzees, vervet monkeys and mice became heavier. Domestic dogs and cats, and domestic or wild rats in both cities and rural areas, also showed rising average body weights. The researchers examined records from multiple species and found that almost every animal population meeting their criteria showed the same upward trend.
Of course, one might say that as humans eat more, they also feed their pets more, and that garbage now contains more sugar and fat, allowing street animals to grow heavier too. But this explanation falters when it reaches laboratory animals. Lab animals have their diets and activity levels carefully controlled. They do not order takeout, drink bubble tea, or collapse onto a sofa to scroll through their phones after work. The records showed that even without obvious changes in diet or activity, their weight rose over many years.
At minimum, this suggests that obesity cannot be only the result of collapsing human willpower. If several species are becoming heavier at the same time, then we have to consider broader, more hidden factors that are harder for individuals to control.
Another difficulty is that human weight usually does not rise suddenly. It creeps upward over many years. If we follow the strict “slightly more intake than expenditure” explanation, a person needs to store only a tiny bit of extra energy each month to become noticeably heavier over decades. One model estimated that eating only 30 calories more than one uses each day would be enough, over time, to cause serious weight gain. What is 30 calories? A few peanut M&Ms. If the problem were truly that simple, then removing a few pieces of candy from the daily diet should prevent obesity, and losing a few pounds should be easy. Reality says otherwise: most people know that long-term weight loss is extremely difficult, and maintaining weight loss is even harder.
The social distribution of obesity also does not support an overly simple personal-choice model. In wealthy nations, obesity is more common among people with lower income, less education and lower social status. In some poor nations, weight gain has likewise been concentrated among those who are less well-off. Nor is obesity evenly distributed between men and women. Jonathan Wells and his colleagues, in a study covering 68 countries, found that women were generally more likely than men to be obese, and that the higher a nation’s female obesity rate, the higher its level of gender inequality tended to be.
If obesity is merely a matter of what an individual decides to eat and how much they decide to move, why should it be so clearly shaped by poverty, status and gender relations? Why does it not fall randomly across populations, but instead gather along the fault lines of social structure?
The thermodynamic model can, of course, keep offering explanations. It can say that poverty creates stress, stress makes people eat, and cheap food is often full of sugar, fat and “empty calories,” which is why poorer people gain more weight. This explanation is not entirely wrong. But it is no longer simple thermodynamics. It is a complicated social and psychological chain. In order to preserve the belief that “a calorie is a calorie,” it must take a long detour through class, stress, food prices and living conditions, only to return everything to individual intake.
The problem is that more and more researchers are beginning to doubt whether all calories are truly the same.
Chemicals Entering the Body on Tuesday May Change How Fat Is Stored on Wednesday
For a long time, the thermodynamic model rested on a simple slogan: a calorie is a calorie. In this model, food matters mainly as a quantity of energy. Cheetos are worse than broccoli because they make it easier to consume more calories. Cola is worse than water because it provides extra energy. The nature of the food itself seems secondary to the amount consumed.
But many researchers increasingly suspect that the issue is not merely the number of calories. Different foods may affect the body’s biochemical systems for storing and burning fat in different ways. Diets high in sugar, fat and ultra-processed foods are not merely energy-dense. They may alter insulin signalling, hormonal responses, appetite regulation and fat-cell activity, nudging the body toward storing more fat.
This may sound like a technical detail, but it changes the entire discussion. If obesity is only a matter of quantity, then the solution is to eat less and move more. But if certain foods or substances directly alter the metabolic system, then what one eats matters as much as how much one eats. The problem with candy is not merely that it contains calories. It may also participate in chemical processes that make the body more willing to create and retain fat.
More broadly, the factors that affect fat metabolism are not limited to food. Lack of sleep disrupts hormonal signals, especially leptin, which is linked to satiety. Stress may not only make people want to eat; it may also directly alter cellular activity and fat storage. Viruses, bacteria, industrial chemicals, light exposure, temperature control and even the pace of modern life have all entered obesity research as possible explanations.
In other words, the issue may not be “stress makes you eat more, so you gain weight.” It may be “stress changes the way your body handles energy, so you gain weight more easily.” These two statements may sound similar, but the difference is enormous. The first keeps the focus on behavioural choice. The second shifts attention to how the body itself is reshaped by its environment.
Industrial chemicals are one major suspect. Bisphenol A, or BPA, was widely used in many plastics and food-packaging materials. Animal studies have suggested that BPA may affect fat regulation. Research on American children and adolescents has also found that those with higher levels of BPA in their urine had a markedly higher risk of obesity. Because BPA has been used in products ranging from children’s cups to the linings of drink cans, traces of it have been found in the bodies of people throughout developed countries.
BPA is not the only suspect. The modern food chain and living environment contain a large number of compounds: heavy metals, ingredients in sunscreens, cleaning agents, detergents, cosmetics, flame retardants and various plastic additives. Some chemicals may promote obesity by disrupting cellular energy use, changing the production of fat cells, influencing appetite hormones or interfering with metabolic signals. A chemical encountered on Tuesday may, in other words, alter the way the body stores fat on Wednesday.
More complicated still, these effects may not begin in adulthood. They may begin before birth. A foetus is not, as we sometimes imagine, peacefully sealed away from the world. It receives important signals about the outside environment through the mother, and one of the most important signals is nutrition.
The epidemiologist David Barker argued that when mothers experience undernutrition during pregnancy, their children face a higher risk of obesity later in life. The logic is this: if the foetus receives the signal that the outside world is scarce, its metabolism may be tuned for famine. It prepares to store energy whenever possible, to seize food when it appears. Such a body might have an advantage in a truly scarce environment. But if the child is born into a world of plenty or excess, this thrifty metabolism may become a risk factor for obesity.
The Dutch Hunger Winter of 1944-45 provided a famous example. Babies gestated during wartime famine later showed higher risks of obesity, diabetes and heart disease. Hunger did not merely damage one generation. It seemed to leave within their bodies a mistaken prediction about the world to come.
Industrial chemicals may further interfere with this prenatal metabolic setting. The researcher Bruce Blumberg found that mice exposed during pregnancy to certain organotin compounds had offspring that were more likely to become heavy. This suggests that chemicals may alter the signals a developing foetus uses to calibrate its metabolism. More disturbingly, such effects may extend beyond a single generation. A person’s birth weight is linked to their mother’s birth weight, hinting that metabolic information may travel along family lines.
If these lines of research are right, then obesity is not simply an adult’s decision at a menu. It may be linked to a mother’s nutrition during pregnancy, hunger experienced by grandparents, chemical exposures in early childhood and the entire industrial and food environment. Individuals still make choices, but those choices are made within bodies and environments that have already been shaped.
Electric Light, Air Conditioning, Viruses and Bacteria May Also Have Joined the Age of Weight Gain
Beyond food and chemicals, there are stranger candidate causes. David Allison and other researchers have called these the “roads less travelled” in obesity research. They may not all turn out to be correct, but they remind us that obesity may be far more complicated than “eat less and move more.”
Take temperature, for example. Modern civilisation has given humans unprecedented control over their surroundings. We use heating to avoid cold and air conditioning to avoid heat, keeping the body for long periods within a comfortable temperature range. The human body has what is called a thermoneutral zone, a range in which it does not need to expend extra energy to maintain its internal temperature. When the environment is too cold, we shiver; when it is too hot, we sweat. These processes use energy.
If modern people spend most of their lives in temperature-controlled spaces, the energy once spent regulating temperature naturally declines. Heat also suppresses appetite. Research has even found that when a restaurant’s air conditioning fails on a hot day, sales drop noticeably. Perhaps part of the reason we have become heavier is not that we are greedier than our ancestors, but that we are less often forced to endure cold, heat and environmental fluctuation.
Light is another possible factor. Modern electrification has made night no longer truly dark. We work, eat and look at screens under artificial light, rearranging the body’s circadian rhythms. Experiments with mice have shown that mice exposed to extra light gain more weight than mice living under normal light-dark cycles, even when they eat the same food. One possible reason is that they eat at times that are physiologically “wrong.”
For humans, this is not hard to understand. Our ancestors slept in darkness. Modern people can open the refrigerator at midnight, order food, drink sugary beverages, keep working or keep entertaining themselves. Electric light has lengthened the day, and it has lengthened the hours available for eating. Widespread electrification may be quietly altering metabolism by encouraging humans to eat at night, when our ancestors would have been asleep.
There is an even more startling possibility: obesity may, in some cases, be contagious. A virus called Ad-36, known to cause eye and respiratory infections, also causes weight gain in chickens, rats, mice and monkeys. For ethical reasons, researchers cannot deliberately infect humans to see whether they become fat. But studies have found that antibodies to Ad-36 appear more frequently in obese people than in people of normal weight. Those who have been infected with the virus tend to have higher BMIs.
As with viruses, so with bacteria. The gut microbiome has become a major field in metabolic research. Experiments suggest that transferring certain bacteria from mice that have lost weight to other mice may cause the recipient mice to lose weight too. Human studies have also found that some overweight people have higher levels of particular gut microorganisms. These microbes may be especially good at breaking down food and releasing energy, allowing the body to absorb more nutrition from the same meal.
Nikhil Dhurandhar, who proposed a possible link between viruses and obesity, once noticed that chickens in India that had died of adenovirus infection were not thin, but plump. He later coined the striking term “infectobesity” for the idea that excess weight might, in part, spread through infectious agents. The concept certainly cannot explain all obesity, but it is enough to disturb an overly simple worldview. If certain viruses and microbes can affect body weight, then obesity cannot be entirely a moral failure.
This does not mean we should discard personal choice and search for one new single cause. No serious researcher should claim that BPA, air conditioning, electric light, viruses or gut bacteria alone explain the obesity era. What matters is that these alternative theories exist at all. Their existence proves that obesity is not a question science has already closed. It remains open, complex and in need of explanation at many scales.
Some factors may matter more in certain countries, others in certain classes, still others only at particular historical moments. Obesity is not a simple school physics experiment, with food on one side of the scale, exercise on the other and a moral score at the end. It is more like a historical process woven from biology, economics, industrialisation, urbanisation, gender relations and global trade.
Blaming Obesity on Personal Responsibility Is Too Convenient an Explanation
Among all the alternative theories, Jonathan Wells’s explanation may be the grandest, and the most like a historical novel. He sees obesity as something akin to poverty, war or financial crisis: no single person deliberately creates it, but countless choices, institutions, trade arrangements, technological changes and power relations accumulate until they produce a vast result. If one were to invoke a Russian novelist to think about obesity, perhaps the right figure is not Dostoyevsky, with his self-accusing torment, but Tolstoy, with his sense of historical force.
In Wells’s view, the claim that individual choice drives global obesity is an illusion. It resembles the illusion that individuals can fully escape history and master their own fate. At the end of War and Peace, Tolstoy reminds us that people are moved by social forces they cannot see, just as the Earth is moved through space by physical forces we cannot feel. Wells’s account of modern obesity carries a similar historical sensibility. One root of modern obesity, he argues, lies in the history of capitalism.
The argument can begin with a poor farmer. Imagine, in the late 18th or early 19th century, a farmer in a poor region of Africa or Asia who once grew food crops to feed himself and his family. Then European colonial power and expanding capitalist markets reorganised the local economy. Through taxes, debt, coercive systems and sometimes violence, farmers were forced or strongly “encouraged” to abandon subsistence food production and grow exportable commodities instead — coffee, cotton, sugar.
From that point on, they no longer grew their own food directly. They had to buy it with market income. But markets did not care whether they ate well. Buyers of the crop sought the lowest possible prices. Employers sought the lowest possible wages. People who had once relied on traditional forms of production to buffer themselves against hunger were pushed into a new economic position: they participated in global trade, but did not earn enough to secure good nutrition.
Generations later, their descendants may, through globalisation, industrialisation and outsourcing, enter the emerging middle class. They are no longer hungry; they may even have consumer power. Capitalism welcomes them again, this time not primarily as cheap labour, but as consumers. They begin to encounter ultra-processed foods, sugary drinks, air-conditioned offices, elevators, chronic stress, night-time light and all manner of metabolic disruptors. They move from a world of undernutrition into a world of overnutrition, but their bodies and family histories are not reset.
This is the trap Wells describes. A past of undernutrition can make the body more inclined to store energy. A present of overnutrition constantly supplies high-sugar, high-fat food and low-activity ways of living. Past hunger and present excess meet, forming what Wells memorably calls a “metabolic ghetto.” People may imagine that escaping poverty and entering consumer society means improved health. But that very transition may trigger the risk of obesity.
Worse still, metabolic effects may continue across generations. The children of the undernourished may be more likely to store fat; the children of the obese may also inherit metabolic settings that raise the risk of obesity. Undernutrition and overnutrition are therefore not opposite problems, but two forms of malnutrition produced by the same global food system. Wells argues that both are linked to the profit-driven manipulation of food supply and food quality.
Food companies, of course, do not usually set out to “create obesity.” They set out to make profit. And the most profitable foods are often not the most nutritious. Through advertising, pricing, packaging, supply chains and control of availability, companies constantly encourage consumers to choose products that are easier to produce, easier to preserve, more addictive and more profitable. Sugar, fat, salt and refined carbohydrates make food cheap, pleasurable and difficult to stop eating. Choice appears to belong to the individual, but it has already been shaped by price, convenience, marketing and the physiology of reward.
Wells’s point is not that individuals have no responsibility at all. It is that placing most of the blame for obesity on personal responsibility is far too simple. It ignores how bodies are shaped by early nutrition, how food markets design choices, how poverty and stress alter life possibilities, and how the global economy produces undernutrition and overnutrition at the same time.
If this view is right, then solving obesity cannot rely only on electronic forks, waistline emails, diet slogans and restrictions on the size of sugary-drink cups. The real questions are larger. Can people afford nutritious food? Do cities support walking and movement? Do work systems allow sleep and rest? Are food companies allowed to endlessly promote products that are metabolically harmful but highly profitable? Are chemicals adequately regulated? Is public policy willing to touch structural problems, rather than merely scold individuals?
Of course, some will say that because the science is still debated, policy should not act. This sounds cautious, but it is really an easy escape. Science is never completely settled on every question. It is always revising, arguing and updating its evidence. If action had to wait until every uncertainty disappeared, public policy would never begin. Historically, many industries have liked to say that the science is not yet fully settled, because waiting is itself a political choice.
Policy is never made under perfect evidence. It is made by trying to make the best possible decisions with incomplete evidence. Faced with a growing public-health crisis, governments are right to act. The question is whether their actions truly reflect the evidence already available, or merely flatter the most convenient moral story.
If obesity is mainly the result of personal indulgence, then waist measurement, vibrating forks, warning emails and shame-based campaigns may work. But if obesity involves metabolic disruption, poverty, the food industry, gender inequality, sleep, chemical exposure, microbes and the nutritional history of generations, then billions spent on individual-centred policies and products may simply be targeting the easiest people to blame, rather than the most useful points of intervention.
Today’s authorities on obesity prevention often speak with great confidence, as if they already possess the answer. History has seen such confidence before. In the mid-20th century, Bruno Bettelheim confidently blamed autism on “refrigerator mothers,” claiming that emotionally cold mothers caused the condition in their children. After the Lisbon earthquake in the 18th century, clerics blamed the disaster on human sin. In hindsight, such explanations moralised complex problems, turned sufferers into culprits and produced immense suffering and futile effort in the wrong direction.
The history of the obesity era has not yet been fully written. Perhaps future generations will look back and be astonished that we once so easily believed a global change in body weight — crossing species, classes, genders and generations — could be explained simply by billions of people losing willpower at the same time. By then, “eat less and move more” may not be completely dismissed, but it may be returned to a more proper place: not the final truth that explains everything, but one small part of a much more complicated story.
