“We are losing this war.”
The sentence sounds dramatic, but it might also be one of the most honest judgments in modern public health. Over the past half-century, human beings have gained unprecedented medical technology, nutritional knowledge, fitness industries, food labels, health guidelines and public campaigns. We know how to measure body weight, how to count calories, how to track steps, how to break down a lunch into protein, fat, carbohydrate and fibre. We have more health advice than any generation before us, and yet we also have larger populations suffering from obesity, diabetes and metabolic disease than any generation before us.
This is the bewildering part. If a problem has been properly explained, and if its solution has been repeatedly advertised, then the failure should not be so complete. We can say that modern people are too busy, too sedentary, too dependent on takeout food, too stressed, too sleep-deprived. None of these explanations is entirely wrong. But when a phenomenon expands across countries, income groups and age categories, and when it expands faster than any plausible change in individual willpower, we have to ask whether the problem is not simply that people lack discipline. Perhaps we misidentified the enemy from the beginning.
Public health authorities usually describe obesity as a problem of energy imbalance: too much energy consumed, too little energy expended. The explanation is simple, intuitive and almost impossible to refute. If a person grows fatter, of course the body has stored more energy. If the mass of a system increases, of course more has entered than left. But describing an outcome is not the same as explaining a cause. To say that a bucket overflows because more water flows in than out does not explain why the tap was opened, why the drain was blocked, or why the valve failed. In obesity, the real question is not merely why the body contains more fat, but why fat tissue becomes so eager to store energy, and why the body’s regulatory system allows, or even encourages, this to happen.
Sugar has long occupied a strange position in this debate. It is acknowledged as something we consume too much of in the modern diet, yet it is often excluded from the category of true cause. Official recommendations tell us to eat less sugar, but usually on the grounds that sugar supplies extra calories. Soda taxes and nutrition labels warn us about added sugars, but the underlying logic remains the same: sugar causes harm because it makes people consume too much energy. In other words, sugar is not treated as a substance with distinctive physiological effects. It is treated as an easily overconsumed carrier of calories.
That distinction matters. If sugar is merely calories, then its difference from bread, rice, nuts, steak or olive oil is only a matter of quantity. Eat less of it, move more, and sugar ceases to be special. But if sugar disrupts metabolism in a distinctive way, affecting insulin, liver fat accumulation, appetite signals and fuel partitioning, then sugar is not merely “empty calories.” It may be a chronic metabolic stressor. The first interpretation places responsibility on behaviour. The second brings the question back to physiology.
For decades, we have mostly lived inside the first interpretation. It appears scientific because it borrows the language of thermodynamics. It appears neutral because it does not demonise any single food. It appears fair because it tells every individual that body weight can be controlled by reducing intake and increasing expenditure. But precisely because it is so simple, it conceals more difficult questions. Why are some people hungrier than others? Why do some people gain weight without eating in any obviously excessive way? Why do obesity, diabetes, hypertension and fatty liver so often appear together? Why does the body, after weight loss, often defend the lost weight as though defending against famine?
When a theory fails to explain such observations, we should not merely blame patients for poor compliance. One of the most dangerous moments in the history of science is not when we know nothing. It is when we believe we already know enough.
To call obesity merely a calorie problem is like calling bankruptcy merely a bookkeeping problem.
Of course bankruptcy appears on paper as spending exceeding income. But that is not a sufficient explanation. The real cause might involve stagnant wages, debt structure, interest rates, medical bills, unemployment, fraud or an entire economic system gone wrong. Likewise, obesity appears at the level of calories as storage exceeding expenditure. But that does not tell us what makes the body more likely to store rather than burn, what increases hunger rather than reduces it, or what makes fat cells behave as though they had an agenda of their own, drawing fuel out of circulation and locking it away.
Early European medicine once took this question seriously. In the first half of the twentieth century, a number of German and Austrian clinical investigators did not regard obesity simply as overeating. They understood it as a disorder of regulation. To them, obesity was not a moral failure or a weakness of will, but the result of an internal defect in the way the body distributed fuel. Fat tissue was not a passive warehouse. It was an active organ governed by hormones and neural signals. Whether it stored, released or allowed the body to burn fat depended on complex biological regulation.
Today this idea should not seem strange. Modern endocrinology has taught us that the human body is not a simple furnace. After we eat, the body does not place all calories into a single account and then spend them at will. Different nutrients trigger different hormonal responses. Different tissues compete for or surrender energy. The liver, muscles, fat cells, brain and pancreas exchange signals continuously. “Intake” and “expenditure” are only the two final numbers on the ledger. They are not the system behind the ledger.
Yet after the Second World War, as American nutrition science rose to dominance, the energy-balance theory gradually became the governing model. It had immense appeal: it was simple, clear, commonsensical and easy to translate into public advice. Eat less. Move more. Control portions. Reduce laziness. Overcome gluttony. It turned a complex metabolic condition into a behavioural-management problem, and it quietly transferred the burden of failure onto the individual. If a person did not lose weight, the theory itself did not have to be questioned. The person did. Had he really eaten less? Had she really exercised? Had they secretly consumed more calories than they admitted?
That is the power of a paradigm. Once a paradigm occupies the centre, it does not merely explain facts; it filters them. Evidence that fits is amplified. Evidence that does not fit is treated as exception, error or poor adherence. When obese people say they do not eat very much, they are presumed to be underreporting. When dieters regain weight, the explanation is lack of persistence. When diabetes appears in younger and younger populations, the cause is said to be a general deterioration in modern lifestyle. Every observation is absorbed into the same explanatory frame, while the frame itself is rarely put on trial.
Within such a framework, sugar’s suspicious role was long minimised. If all calories are assumed to be equivalent, sugar is merely another calorie source. It might be tempting, cheap and easy to overconsume, but it is not special. The sugar industry and the makers of sugar-rich beverages benefited enormously from this logic. As long as the problem is defined as total caloric excess, any single product can retreat to the edge of responsibility. It is not sugar’s fault; you drank too much. It is not the beverage’s fault; you failed to exercise. It is not sweetness itself; it is your lack of moderation.
This defence sounds reasonable, but it rests on a premise that has never been adequately proved: that the body’s response to all calories is essentially the same. No one who truly understands metabolism believes this. Calories from alcohol are not the same as calories from olive oil. Calories from protein are not the same as calories from glucose. Fructose follows a different metabolic path in the liver than glucose derived from starch. A calorie is a unit of physics, not a physiological destiny. Once food enters the body, what happens first is not arithmetic. It is biochemistry.
If sugar is indeed special, its specialness probably does not lie in the fact that it is “high in calories.” It lies in how it influences the body’s handling of fuel. Sucrose and high-fructose corn syrup both contain fructose. Fructose differs from glucose in that it is processed primarily by the liver. When the frequency and dose of intake chronically exceed the liver’s capacity to handle it, fat may begin to accumulate in the liver, insulin signalling may become progressively impaired, and the body may secrete more insulin to maintain stable blood sugar. Thus an ordinary sweetness, repeated over years, may drive a chain of metabolic changes: fatty liver, insulin resistance, elevated insulin, disordered appetite, increased fat storage, and finally obesity and Type 2 diabetes.
This does not mean sugar is the only cause. No serious theory of complex disease should collapse everything into a single slogan. Sleep, stress, medication, genetics, gut microbiota, socioeconomic environment and overall diet all matter. But “multifactorial” does not mean all factors are equally important, nor does it excuse us from searching for critical triggers. Fires also require many conditions: oxygen, fuel, heat, building materials, wind direction and delayed rescue. But if someone keeps striking matches in the room, we should not refuse to talk about matches merely because fire is complex.
The real question is not why people eat too much, but why fat is retained
We often treat hunger in obesity as a cause: people are hungry, so they eat; they eat too much, so they become fat. But another possibility deserves serious attention: because fat tissue is over-storing energy, other tissues experience a relative shortage of available fuel, and the person becomes hungrier, more tired and less inclined to move. In other words, hunger and inactivity may not be the causes of obesity. They may be consequences of disordered fuel partitioning.
This way of thinking changes the moral judgment. A person gaining weight may not be actively choosing to store excess fat. More likely, the body is being pushed in some way to send energy into fat tissue, leaving other tissues relatively deprived. To tell such a person simply to “eat less” is like telling a freezing person not to shiver. Shivering is not failure. It is a response. Hunger, too, may not be failure. It may be a signal.
Animal experiments have long hinted at this. Some obese animals accumulate more fat even when they do not eat more than their lean controls. Some remain abnormally fat even under food restriction, while sacrificing other bodily functions. Such findings are difficult to explain by gluttony alone. They point more naturally toward a defect in regulation. If fat cells are driven by some signal to keep storing, the rest of the body must pay the price.
In humans, one of the most plausible names for that signal is insulin. Insulin is not merely a hormone involved in diabetes. It is a central dispatcher in the body’s fuel-allocation system. When blood sugar rises, insulin helps cells take up glucose, while inhibiting fat release and promoting fat storage. This mechanism is not itself pathological. It is necessary for life. The question is what happens when insulin remains chronically elevated. Does the body become more inclined to store fat and less able to mobilise it?
This is where sugar and refined carbohydrates re-enter the story. They enter the bloodstream quickly and stimulate blood sugar and insulin responses. They are cheap, abundant, highly palatable and frequently consumed in the form of beverages, snacks, breakfast cereals, sauces and processed foods. They do not produce the same satiety or chewing cost as whole foods. They may not merely make people “eat a little more.” They may push the body into a metabolic state in which storage becomes easier, release becomes harder, and hunger returns more often.
If this is true, then conventional advice is too crude. We tell people to count calories, but not how different foods alter hunger. We tell them to jog off the energy in a soda, but not what sugary beverages may do over time to the liver and insulin signalling. We tell children to avoid snacks, while supermarkets, schools, social media and household cupboards surround them with cheap sweetness. Then, when obesity rates continue to rise, we say the problem is that people lack restraint.
One of public health’s easiest mistakes is to interpret physiologic impulses created by the environment as defects of personal character. The modern food industry is skilled at combining sugar, refined starch, fat, salt and flavourings into highly rewarding products. These products bypass traditional satiety mechanisms and encourage continued consumption. They are packaged as convenience, pleasure, reward, childhood and sociability. A child is not abstractly choosing “excess calories.” He is being shaped by a food environment designed to target attention and desire. An adult is not freely weighing metabolic risk at every meal. She is often making the fastest decision available amid fatigue, stress and cheap convenience.
For that reason, the problem of sugar is not merely nutritional. It is institutional. As long as sugar is treated as ordinary calories, solutions will tend to take the form of personal education: read labels, control appetite, exercise more. But if sugar is recognised as a substance with distinctive metabolic risks, then we must reconsider food formulation, advertising, school meals, beverage sales, tax policy and medical guidelines. The history of cigarettes has already taught us that when an industry’s profits depend on long-term health damage, what it most wants society to believe is not necessarily that the product is harmless, but that responsibility belongs to the consumer.
Insulin is not a bystander; it is more like the traffic controller of internal fuel
In the calorie model, the body is a simple container. In the hormonal model, it is more like a city. Fuel travels along different roads. Signals determine direction. Warehouses decide what to store. Factories decide what to burn. Administrative systems set priorities. Insulin is one of the most important traffic signals in that city. It does not create energy, but it influences where energy goes. It does not by itself cause obesity, but it may help determine whether the body more readily locks energy into fat tissue.
This can explain many things the calorie model explains poorly. Why do Type 2 diabetes and obesity so often appear together? Perhaps because both are related to insulin resistance and chronically elevated insulin. Why do low-carbohydrate diets work particularly well for some people? Perhaps not only because they reduce calories, but because lower insulin makes fat release easier. Why do many dieters feel unusually hungry, cold, tired and irritable? Perhaps because the body is not passively burning fat, but defending against perceived energy shortage under hormonal instruction.
None of this means the law of energy conservation fails. Thermodynamics remains true, just as the bankrupt person’s ledger remains true. The problem is that physical law tells us fat cannot appear from nowhere. It does not tell us why the body chooses to store it. Thermodynamics is a boundary condition, not a causal explanation. Treating it as a complete explanation is like saying alcoholism is caused by more alcohol entering the body than leaving it: correct, but empty.
Nutrition science has long been trapped by this empty correctness. It is too correct to refute, yet too empty to solve the problem. A useful causal theory must guide intervention. If “eat less, move more” repeatedly fails in the real world, we cannot forever say that the real world is insufficiently obedient. Perhaps the advice itself misses the critical mechanism. Perhaps a person does not first need to become a better accountant in order to repair metabolism. Perhaps he needs to change the kind of fuel entering the body, the hormonal environment, and the physiological basis of hunger and satiety.
This is the core of the case against sugar. It does not claim that every grain of sugar immediately causes disease, nor that everyone who eats sugar is destined to become obese. What it rejects is a careless reassurance: that as long as total calories are controlled, sugar has no special problem. That reassurance has given the food industry a moral escape route and kept public health policy at the level of mild advice. But chronic diseases are not always caused by obvious poisons. Sometimes they arise from a metabolic disturbance repeated a little each day, each meal, each year. The danger of sugar may be precisely that it does not look dangerous. It is sweet, cheap, familiar, pleasant and everywhere.
If a substance can be consumed rapidly in liquid form with little satiety; if it can enter children’s breakfasts, office snacks, sports drinks and supposedly healthy yogurts; if it can quietly raise the sweetness threshold of an entire diet; if it may also affect long-term metabolism through the liver and insulin system, then calling it merely “empty calories” is far too gentle. Empty does not mean harmless. A hollow habit, repeated for enough years, can reshape the body.
To oppose sugar is not to romanticise a pure past. Human beings have never eaten perfectly, and traditional societies were not free of disease. But the scale, frequency and form of modern sugar consumption are different. In the past, sweetness was often tied to seasonality, scarcity and whole foods. Today it is tied to industrial refining, liquid calories and constant availability. The regulatory systems with which the human body evolved may not be well suited to continuous exposure to sweetness. We need not portray sugar as a demon in order to admit that it may be an underestimated modern risk.
When policy focuses only on self-control, it misses physiology itself
Public health language prefers moderation. It speaks of balance, healthy lifestyles and reasonable portions. These words are not wrong, but they often become so smooth that they lose force. For a healthy, active, metabolically normal person, an occasional dessert may indeed be no great issue. But for someone already insulin resistant, with fatty liver, abdominal obesity or abnormal blood sugar, what exactly does “moderate sugar” mean? For a child exposed daily to dozens of sweetened foods, who defines moderation? For a low-income family, when the cheapest, most convenient and most shelf-stable foods are often highly processed, how is balance to be achieved?
If we reduce sugar to a matter of personal choice, we ignore how choices are manufactured. Food companies know that sweetness increases repeat purchase. Advertisers know children influence family shopping. Platforms know short videos can bind beverages, snacks and emotional reward together. Stores know the checkout aisle is the perfect place for small sweet products. Individuals still have responsibility, of course. But responsibility does not mean the environment is innocent. A society that manufactures temptation and then condemns those who fail to resist it is not practising science. It is shifting blame.
Medicine, too, must be more honest about its own history. Many guidelines did not emerge only after evidence had become perfectly clear. They were fixed gradually through a mixture of industry influence, research tools, academic authority and the prejudices of the age. Low-fat eating was once given something close to moral authority, while sugar and refined carbohydrates often filled the flavour space that fat had vacated. People bought low-fat yogurts, low-fat cookies and low-fat cereals believing they were making healthy choices, while often consuming more sugar. The danger of a mistaken paradigm is not only that it explains the world badly. It also creates new markets.
Today, there is no reason to pretend that every controversy has been settled. The scale of the obesity and diabetes epidemics is itself a long trial of the existing theory. If one explanation has dominated policy, education and clinical advice for decades, while disease continues to spread, then at the very least another explanation deserves to re-enter the discussion. Does sugar drive insulin resistance through distinctive mechanisms? Should added sugar be treated as a public health risk requiring special regulation, like alcohol or tobacco? Should low-sugar and low-refined-carbohydrate diets have a more central role in treating metabolic disease? These questions should not be dismissed merely because they disturb the old paradigm.
The dignity of science does not lie in defending established consensus forever. It lies in having the courage to reopen basic questions when reality continues to contradict that consensus. Why do we become fat? Why is diabetes so common? Why do so many people follow the advice and still fail to restore long-term health? Why has a public health system built around energy balance had so little effect on this crisis?
Perhaps the answer is not so complicated. Perhaps we have been mistaking the result for the cause, the ledger for the disease, the behaviour for the underlying physiology. Perhaps for too long we have told people how to fight hunger without seriously asking what creates hunger; told them to burn calories without asking why the body refuses to release fat; talked about the choices of obese people without talking about how sugar and refined carbohydrates may alter the bodily state in which choices are made.
Sugar does not explain everything. But in a public health war so vast, so persistent and so unsuccessful, a substance repeatedly forgiven, repeatedly minimised and repeatedly packaged as ordinary calories deserves to be tried again. The real question is not whether we can prove sugar is the only culprit. It is whether we are willing to admit that it may not be innocent.
If obesity and diabetes are merely calorie problems, then the failures of the past decades can only be blamed on hundreds of millions of people simultaneously lacking willpower. But if they are first disorders of metabolic regulation, driven in part by a modern diet that continually stimulates the insulin system and liver metabolism, then the failure is no longer mysterious. We failed because we aimed at the wrong target. We failed because we described chronic physiological dysregulation as poor lifestyle. We failed because we asked individuals to use willpower against a sweetened environment built jointly by industry, policy and mistaken science.
At this point, the least scientific attitude may be to continue pretending that the old answers are sufficient. The curves of obesity and diabetes still remind us that a paradigm can remain popular for a long time. It can be written into textbooks, repeated by policy, sponsored by industry and accepted by the public as common sense. But popularity is not proof, and common sense is not truth.
What we need is not another sermon about restraint, but a renewed trial of causation. Sugar should stand in the dock. Not as a symbol of moral panic, but as a biological suspect long underestimated. Only when we are willing to do that can public health begin to step out of its cycle of failure and return to the most basic, most avoided question of all: if we have never defeated obesity and diabetes, is it because we have never truly understood them?
Adapted from ‘The Case Against Sugar’ by Gary Taubes. Copyright © 2016 by Penguin Random House. Adapted by permission of Alfred A Knopf, a division of Penguin Random House LLC. All rights reserved. No part of this piece may be reproduced or reprinted without permission in writing from the publisher.
