Years ago, after a plane trip spent reading Fyodor Dostoyevsky’s Notes from the Underground and Weight Watchers magazine, Woody Allen melded the two experiences into a single essay. ‘I am fat,’ it began. ‘I am disgustingly fat. I am the fattest human I know. I have nothing but excess poundage all over my body. My fingers are fat. My wrists are fat. My eyes are fat. (Can you imagine fat eyes?).’ It was 1968, when most of the world’s people were more or less ‘height-weight proportional’ and millions of the rest were starving. Weight Watchers was a new organisation for an exotic new problem. The notion that being fat could spur Russian-novel anguish was good for a laugh.
That, as we used to say during my Californian adolescence, was then. Now, 1968’s joke has become 2013’s truism. For the first time in human history, overweight people outnumber the underfed, and obesity is widespread in wealthy and poor nations alike. The diseases that obesity makes more likely — diabetes, heart ailments, strokes, kidney failure — are rising fast across the world, and the World Health Organisation predicts that they will be the leading causes of death in all countries, even the poorest, within a couple of years. What's more, the long-term illnesses of the overweight are far more expensive to treat than the infections and accidents for which modern health systems were designed. Obesity threatens individuals with long twilight years of sickness, and health-care systems with bankruptcy.
And so the authorities tell us, ever more loudly, that we are fat — disgustingly, world-threateningly fat. We must take ourselves in hand and address our weakness. After all, it’s obvious who is to blame for this frightening global blanket of lipids: it’s us, choosing over and over again, billions of times a day, to eat too much and exercise too little. What else could it be? If you’re overweight, it must be because you are not saying no to sweets and fast food and fried potatoes. It’s because you take elevators and cars and golf carts where your forebears nobly strained their thighs and calves. How could you do this to yourself, and to society?
Moral panic about the depravity of the heavy has seeped into many aspects of life, confusing even the erudite. Earlier this month, for example, the American evolutionary psychologist Geoffrey Miller expressed the zeitgeist in this tweet: ‘Dear obese PhD applicants: if you don’t have the willpower to stop eating carbs, you won’t have the willpower to do a dissertation. #truth.’ Businesses are moving to profit on the supposed weaknesses of their customers. Meanwhile, governments no longer presume that their citizens know what they are doing when they take up a menu or a shopping cart. Yesterday’s fringe notions are becoming today’s rules for living — such as New York City’s recent attempt to ban large-size cups for sugary soft drinks, or Denmark’s short-lived tax surcharge on foods that contain more than 2.3 per cent saturated fat, or Samoa Air’s 2013 ticket policy, in which a passenger’s fare is based on his weight because: ‘You are the master of your air ‘fair’, you decide how much (or how little) your ticket will cost.’
Several governments now sponsor jauntily named pro-exercise programmes such as Let’s Move! (US), Change4Life (UK) and actionsanté (Switzerland). Less chummy approaches are spreading, too. Since 2008, Japanese law requires companies to measure and report the waist circumference of all employees between the ages of 40 and 74 so that, among other things, anyone over the recommended girth can receive an email of admonition and advice.
Hand-in-glove with the authorities that promote self-scrutiny are the businesses that sell it, in the form of weight-loss foods, medicines, services, surgeries and new technologies. A Hong Kong company named Hapilabs offers an electronic fork that tracks how many bites you take per minute in order to prevent hasty eating: shovel food in too fast and it vibrates to alert you. A report by the consulting firm McKinsey & Co predicted in May 2012 that ‘health and wellness’ would soon become a trillion-dollar global industry. ‘Obesity is expensive in terms of health-care costs,’ it said before adding, with a consultantly chuckle, ‘dealing with it is also a big, fat market.’
And so we appear to have a public consensus that excess body weight (defined as a Body Mass Index of 25 or above) and obesity (BMI of 30 or above) are consequences of individual choice. It is undoubtedly true that societies are spending vast amounts of time and money on this idea. It is also true that the masters of the universe in business and government seem attracted to it, perhaps because stern self-discipline is how many of them attained their status. What we don’t know is whether the theory is actually correct.
Of course, that’s not the impression you will get from the admonishments of public-health agencies and wellness businesses. They are quick to assure us that ‘science says’ obesity is caused by individual choices about food and exercise. As the Mayor of New York, Michael Bloomberg, recently put it, defending his proposed ban on large cups for sugary drinks: ‘If you want to lose weight, don’t eat. This is not medicine, it’s thermodynamics. If you take in more than you use, you store it.’ (Got that? It’s not complicated medicine, it’s simple physics, the most sciencey science of all.)
Yet the scientists who study the biochemistry of fat and the epidemiologists who track weight trends are not nearly as unanimous as Bloomberg makes out. In fact, many researchers believe that personal gluttony and laziness cannot be the entire explanation for humanity’s global weight gain. Which means, of course, that they think at least some of the official focus on personal conduct is a waste of time and money. As Richard L Atkinson, Emeritus Professor of Medicine and Nutritional Sciences at the University of Wisconsin and editor of the International Journal of Obesity, put it in 2005: ‘The previous belief of many lay people and health professionals that obesity is simply the result of a lack of willpower and an inability to discipline eating habits is no longer defensible.’
Consider, for example, this troublesome fact, reported in 2010 by the biostatistician David B Allison and his co-authors at the University of Alabama in Birmingham: over the past 20 years or more, as the American people were getting fatter, so were America’s marmosets. As were laboratory macaques, chimpanzees, vervet monkeys and mice, as well as domestic dogs, domestic cats, and domestic and feral rats from both rural and urban areas. In fact, the researchers examined records on those eight species and found that average weight for every one had increased. The marmosets gained an average of nine per cent per decade. Lab mice gained about 11 per cent per decade. Chimps, for some reason, are doing especially badly: their average body weight had risen 35 per cent per decade. Allison, who had been hearing about an unexplained rise in the average weight of lab animals, was nonetheless surprised by the consistency across so many species. ‘Virtually in every population of animals we looked at, that met our criteria, there was the same upward trend,’ he told me.
It isn’t hard to imagine that people who are eating more themselves are giving more to their spoiled pets, or leaving sweeter, fattier garbage for street cats and rodents. But such results don’t explain why the weight gain is also occurring in species that human beings don’t pamper, such as animals in labs, whose diets are strictly controlled. In fact, lab animals’ lives are so precisely watched and measured that the researchers can rule out accidental human influence: records show those creatures gained weight over decades without any significant change in their diet or activities. Obviously, if animals are getting heavier along with us, it can’t just be that they’re eating more Snickers bars and driving to work most days. On the contrary, the trend suggests some widely shared cause, beyond the control of individuals, which is contributing to obesity across many species.
Such a global hidden factor (or factors) might help to explain why most people gain weight gradually, over decades, in seeming contradiction of Bloomberg’s thermodynamics. This slow increase in fat stores would suggest that they are eating only a tiny bit more each month than they use in fuel. But if that were so, as Jonathan C K Wells, professor of child nutrition at University College London, has pointed out, it would be easy to lose weight. One recent model estimated that eating a mere 30 calories a day more than you use is enough to lead to serious weight gain. Given what each person consumes in a day (1,500 to 2,000 calories in poorer nations; 2,500 to 4,000 in wealthy ones), 30 calories is a trivial amount: by my calculations, that’s just two or three peanut M&Ms. If eliminating that little from the daily diet were enough to prevent weight gain, then people should have no trouble losing a few pounds. Instead, as we know, they find it extremely hard.
Many other aspects of the worldwide weight gain are also difficult to square with the ‘it’s-just-thermodynamics’ model. In rich nations, obesity is more prevalent in people with less money, education and status. Even in some poor countries, according to a survey published last year in the International Journal of Obesity, increases in weight over time have been concentrated among the least well-off. And the extra weight is unevenly distributed among the sexes, too. In a study published in the Social Science and Medicine journal last year, Wells and his co-authors found that, in a sample that spanned 68 nations, for every two obese men there were three obese women. Moreover, the researchers found that higher levels of female obesity correlated with higher levels of gender inequality in each nation. Why, if body weight is a matter of individual decisions about what to eat, should it be affected by differences in wealth or by relations between the sexes?
To make sense of all this, the purely thermodynamic model must appeal to complicated indirect effects. The story might go like this: being poor is stressful, and stress makes you eat, and the cheapest food available is the stuff with a lot of ‘empty calories’, therefore poorer people are fatter than the better-off. These wheels-within-wheels are required because the mantra of the thermodynamic model is that ‘a calorie is a calorie is a calorie’: who you are and what you eat are irrelevant to whether you will add fat to your frame. The badness of a ‘bad’ food such as a Cheeto is that it makes calorie intake easier than it would be with broccoli or an apple.
Yet a number of researchers have come to believe, as Wells himself wrote earlier this year in the European Journal of Clinical Nutrition, that ‘all calories are not equal’. The problem with diets that are heavy in meat, fat or sugar is not solely that they pack a lot of calories into food; it is that they alter the biochemistry of fat storage and fat expenditure, tilting the body’s system in favour of fat storage. Wells notes, for example, that sugar, trans-fats and alcohol have all been linked to changes in ‘insulin signalling’, which affects how the body processes carbohydrates. This might sound like a merely technical distinction. In fact, it’s a paradigm shift: if the problem isn’t the number of calories but rather biochemical influences on the body’s fat-making and fat-storage processes, then sheer quantity of food or drink are not the all-controlling determinants of weight gain. If candy’s chemistry tilts you toward fat, then the fact that you eat it at all may be as important as the amount of it you consume.
More importantly, ‘things that alter the body’s fat metabolism’ is a much wider category than food. Sleeplessness and stress, for instance, have been linked to disturbances in the effects of leptin, the hormone that tells the brain that the body has had enough to eat. What other factors might be at work? Viruses, bacteria and industrial chemicals have all entered the sights of obesity research. So have such aspects of modern life as electric light, heat and air conditioning. All of these have been proposed, with some evidence, as direct causes of weight gain: the line of reasoning is not that stress causes you to eat more, but rather that it causes you to gain weight by directly altering the activities of your cells. If some or all of these factors are indeed contributing to the worldwide fattening trend, then the thermodynamic model is wrong.
We are, of course, surrounded by industrial chemicals. According to Frederick vom Saal, professor of biological sciences at the University of Missouri, an organic compound called bisphenol-A (or BPA) that is used in many household plastics has the property of altering fat regulation in lab animals. And a recent study by Leonardo Trasande and colleagues at the New York University School of Medicine with a sample size of 2,838 American children and teens found that, for the majority, those with the highest levels of BPA in their urine were five times more likely to be obese than were those with the lowest levels.
BPA has been used so widely — in everything from children’s sippy cups to the aluminium in fizzy drink cans — that almost all residents of developed nations have traces of it in their pee. This is not to say that BPA is unique. In any developed or developing nation there are many compounds in the food chain that seem, at the very least, to be worth studying as possible ‘obesogens’ helping to tip the body’s metabolism towards obesity. For example, a study by the Environmental Working Group of the umbilical cords of 10 babies born in US hospitals in 2004 found 287 different industrial chemicals in their blood. Beatrice Golomb, professor of medicine at the University of California, San Diego, has proposed a long list of candidates — all chemicals that, she has written, disrupt the normal process of energy storage and use in cells. Her suspects include heavy metals in the food supply, chemicals in sunscreens, cleaning products, detergents, cosmetics and the fire retardants that infuse bedclothes and pyjamas.
Chemicals and metals might promote obesity in the short term by altering the way that energy is made and stored within cells, or by changing the signals in the fat-storage process so that the body makes more fat cells, or larger fat cells. They could also affect the hormones that spur or tamp down the appetite. In other words, chemicals ingested on Tuesday might promote more fat retention on Wednesday.
It’s also possible that chemical disrupters could affect people’s body chemistry on longer timescales — starting, for instance, before their birth. Contrary to its popular image of serene imperturbability, a developing foetus is in fact acutely sensitive to the environment into which it will be born, and a key source of information about that environment is the nutrition it gets via the umbilical cord. As David J P Barker, professor of clinical epidemiology of the University of Southampton, noted some 20 years ago, where mothers have gone hungry, their offspring are at a greater risk of obesity. The prenatal environment, Barker argued, tunes the children’s metabolism for a life of scarcity, preparing them to store fat whenever they can, to get them through periods of want. If those spells of scarcity never materialise, the child’s proneness to fat storage ceases to be an advantage. The 40,000 babies gestated during Holland’s ‘Hunger Winter’ of 1944-1945 grew up to have more obesity, more diabetes and more heart trouble than their compatriots who developed without the influence of war-induced starvation.
Just to double down on the complexity of the question, a number of researchers also think that industrial compounds might be affecting these signals. For example, Bruce Blumberg, professor of developmental and cell biology at the University of California, Irvine, has found that pregnant mice exposed to organotins (tin-based chemical compounds that are used in a wide variety of industries) will have heavier offspring than mice in the same lab who were not so exposed. In other words, the chemicals might be changing the signal that the developing foetus uses to set its metabolism. More disturbingly, there is evidence that this ‘foetal programming’ could last more than one generation. A good predictor of your birth weight, for instance, is your mother’s weight at her birth.
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urking behind these prime suspects, there are the fugitive possibilities — what David Allison and another band of co-authors recently called the ‘roads less travelled’ of obesity research. For example, consider the increased control civilisation gives people over the temperature of their surroundings. There is a ‘thermoneutral zone’ in which a human body can maintain its normal internal temperature without expending energy. Outside this zone, when it’s hot enough to make you sweat or cold enough to make you shiver, the body has to expend energy to maintain homeostasis. Temperatures above and below the neutral zone have been shown to cause both humans and animals to burn fat, and hotter conditions also have an indirect effect: they make people eat less. A restaurant on a warm day whose air conditioning breaks down will see a sharp decline in sales (yes, someone did a study). Perhaps we are getting fatter in part because our heaters and air conditioners are keeping us in the thermoneutral zone.
And what about light? A study by Laura Fonken and colleagues at the Ohio State University in Columbus, published in 2010 in the Proceedings of the National Academy of Sciences, reported that mice exposed to extra light (experiencing either no dark at all or a sort of semidarkness instead of total night) put on nearly 50 per cent more weight than mice fed the same diet who lived on a normal night-day cycle of alternating light and dark. This effect might be due to the constant light robbing the rodents of their natural cues about when to eat. Wild mice eat at night, but night-deprived mice might have been eating during the day, at the ‘wrong’ time physiologically. It’s possible that widespread electrification is promoting obesity by making humans eat at night, when our ancestors were asleep.
There is also the possibility that obesity could quite literally be contagious. A virus called Ad-36, known for causing eye and respiratory infections in people, also has the curious property of causing weight gain in chickens, rats, mice and monkeys. Of course, it would be unethical to test for this effect on humans, but it is now known that antibodies to the virus are found in a much higher percentage of obese people than in people of normal weight. A research review by Tomohide Yamada and colleagues at the University of Tokyo in Japan, published last year in the journal PLoS One, found that people who had been infected with Ad-36 had significantly higher BMI than those who hadn’t.
As with viruses, so with bacteria. Experiments by Lee Kaplan and colleagues at Massachusetts General Hospital in Boston earlier this year found that bacteria from mice that have lost weight will, when placed in other mice, apparently cause those mice to lose weight, too. And a study in humans by Ruchi Mathur and colleagues at the Cedars-Sinai Medical Center in Los Angeles, published in the Journal of Clinical Endocrinology and Metabolism earlier this year, found that those who were overweight were more likely than others to have elevated populations of a gut microorganisms called Methanobrevibacter smithii. The researchers speculated that these organisms might in fact be especially good at digesting food, yielding up more nutrients and thus contributing to weight gain.
The researcher who first posited a viral connection in 1992 — he had noticed that the chickens in India that were dead of an adenovirus infection were plump instead of gaunt — was Nikhil Dhurandhar, now a professor at the Pennington Biomedical Research Centre in Louisiana. He has proposed a catchy term for the spread of excess weight via bugs and viruses: ‘infectobesity’.
No one has claimed, or should claim, that any of these ‘roads less taken’ is the one true cause of obesity, to drive out the false idol of individual choice. Neither should we imagine that the existence of alternative theories means that governments can stop trying to forestall a major public-health menace. These theories are important for a different reason. Their very existence — the fact that they are plausible, with some supporting evidence and suggestions for further research — gives the lie to the notion that obesity is a closed question, on which science has pronounced its final word. It might be that every one of the ‘roads less travelled’ contributes to global obesity; it might be that some do in some places and not in others. The openness of the issue makes it clear that obesity isn’t a simple school physics experiment.
This is the theme of perhaps the most epic of the alternative theories of obesity, put forward by Jonathan C K Wells. As I understand his view, obesity is like poverty, or financial booms and busts, or war — a large-scale development that no one deliberately intends, but which emerges out of the millions of separate acts that together make human history. His model suggests that the best Russian novelist to invoke when thinking about obesity isn’t Dostoyevsky, with his self-punishing anguish, but Leo Tolstoy, with his vast perspective on the forces of history.
In Wells’s theory, the claim that individual choice drives worldwide weight gain is an illusion — like the illusion that individuals can captain their fates independent of history. In reality, Tolstoy wrote at the end of War and Peace (1869), we are moved by social forces we do not perceive, just as the Earth moves through space, driven by physical forces we do not feel. Such is the tenor of Wells’s explanation for modern obesity. Its root cause, he proposed last year in the American Journal of Human Biology, is nothing less than the history of capitalism.
I will paraphrase Wells’s intricate argument (the only one I’ve ever read that references both receptor pathways for leptin and data on the size of the Indian economy in the 18th century). It is a saga spanning many generations. Let's start with a poor farmer growing food crops in a poor country in Africa or Asia. In a capitalistic quest for new markets and cheap materials and labour, Europeans take control of the economy in the late 18th or early 19th century. With taxes, fees and sometimes violent repression, their new system strongly ‘encourages’ the farmer and his neighbours to stop growing their own food and start cultivating some more marketable commodity instead – coffee for export, perhaps. Now that they aren’t growing food, the farmers must buy it. But since everyone is out to maximise profit, those who purchase the coffee crop strive to pay as little as possible, and so the farmers go hungry. Years later, when the farmer’s children go to work in factories, they confront the same logic: they too are paid as little as possible for their labour. By changing the farming system, capitalism first removes traditional protections against starvation, and then pushes many previously self-sufficient people into an economic niche where they aren't paid enough to eat well.
Eighty years later, the farmer’s descendants have risen out of the ranks of the poor and joined the fast-growing ranks of the world’s 21st-century middle-class consumers, thanks to globalisation and outsourcing. Capitalism welcomes them: these descendants are now prime targets to live the obesogenic life (the chemicals, the stress, the air conditioning, the elevators-instead-of-stairs) and to buy the kinds of foods and beverages that are ‘metabolic disturbers’.
But that’s not the worst of it. As I’ve mentioned, the human body’s response to its nutrition can last a lifetime, and even be passed on to the next generation. If you or your parents – or their parents – were undernourished, you’re more likely to become obese in a food-rich environment. Moreover, obese people, when they have children, pass on changes in metabolism that can predispose the next generation to obesity as well. Like the children of underfed people, the children of the overfed have their metabolism set in ways that tend to promote obesity. This means that a past of undernutrition, combined with a present of overnutrition, is an obesity trap.
Wells memorably calls this double-bind the ‘metabolic ghetto’, and you can’t escape it just by turning poor people into middle-class consumers: that turn to prosperity is precisely what triggers the trap. ‘Obesity,’ he writes, ‘like undernutrition, is thus fundamentally a state of malnutrition, in each case promoted by powerful profit-led manipulations of the global supply and quality of food.’
The trap is deeper than that, however. The ‘unifying logic of capitalism’, Wells continues, requires that food companies seek immediate profit and long-term success, and their optimal strategy for that involves encouraging people to choose foods that are most profitable to produce and sell — ‘both at the behavioural level, through advertising, price manipulations and restriction of choice, and at the physiological level through the enhancement of addictive properties of foods’ (by which he means those sugars and fats that make ‘metabolic disturber’ foods so habit-forming). In short, Wells told me via email, ‘We need to understand that we have not yet grasped how to address this situation, but we are increasingly understanding that attributing obesity to personal responsibility is very simplistic.’ Rather than harping on personal responsibility so much, Wells believes, we should be looking at the global economic system, seeking to reform it so that it promotes access to nutritious food for everyone. That is, admittedly, a tall order. But the argument is worth considering, if only as a bracing critique of our individual-responsibility ideology of fatness.
What are we onlookers — non-activists, non-scientists — to make of these scientific debates? One possible response, of course, is to decide that no obesity policy is possible, because ‘science is undecided’. But this is a moron’s answer: science is never completely decided; it is always in a state of change and self-questioning, and it offers no final answers. There is never a moment in science when all doubts are gone and all questions settled, which is why ‘wait for settled science’ is an argument advanced by industries that want no interference with their status quo.
Making policy, as the British politician Wayland Young once said, is ‘the art of taking good decisions on insufficient evidence’. Faced with signs of a massive public-health crisis in the making, governments are right to seek to do something, using the best information that science can render, in the full knowledge that science will have different information to offer in 10 or 20 years.
The issue, rather, is whether the government policies and corporate business plans are in fact doing their best with the evidence they already have. Does the science justify assuming that obesity is a simple matter of individuals letting themselves eat too much? To the extent that it is, policies such as Japan’s mandatory waist-measuring and products like the Hapifork will be effective. If, on the other hand, there is more to obesity than simple thermodynamics, some of the billions spent on individual-centred policies and products may be being wasted. Time, in that case, to try some alternative policies based on alternative theories, and see how they fare.
Today’s priests of obesity prevention proclaim with confidence and authority that they have the answer. So did Bruno Bettelheim in the 1950s, when he blamed autism on mothers with cold personalities. So, for that matter, did the clerics of 18th-century Lisbon, who blamed earthquakes on people’s sinful ways. History is not kind to authorities whose mistaken dogmas cause unnecessary suffering and pointless effort, while ignoring the real causes of trouble. And the history of the obesity era has yet to be written.
