It isn’t the sin of sloth that makes people fat

The hysteria about obesity may have calmed down a little in recent years, but there is no doubt that our apparently ever-expanding waistlines are still regarded as a key health issue of our times.

The figures are certainly dramatic. For example, for American women aged 20 to 29, average weight rose from 128 pounds in 1960 to 157 pounds in 2000. For women aged 40 to 49, the change was from 142 pounds in 1960 to 169 pounds in 2000. The number of people who meet the modern definition of ‘obese’ has also shot up. The US Centers for Disease Control and Prevention (CDC) notes:

‘In 1990, among states participating in the Behavioural Risk Factor Surveillance System, 10 states had a prevalence of obesity less than 10 per cent and no states had prevalence equal to or greater than 15 per cent. By 1998, no state had prevalence less than 10 per cent, seven states had a prevalence of obesity between 20-24 per cent, and no state had prevalence equal to or greater than 25 per cent. In 2008, only one state (Colorado) had a prevalence of obesity less than 20 per cent. Thirty-two states had a prevalence equal to or greater than 25 per cent; six of these states (Alabama, Mississippi, Oklahoma, South Carolina, Tennessee, and West Virginia) had a prevalence of obesity equal to or greater than 30 per cent.’

In the UK, the statistics are less dramatic, but there has been, until very recently, a trend towards rising rates of so-called obesity. In 1980, less than 10 per cent of the British population was considered obese. By 2008, 24 per cent of women and 25 per cent of men fell into the obese category. However, recent official statistics suggest that Britain’s weight gain has plateaued, at least for now (see Whatever happened to the obesity timebomb?, by Rob Lyons).

This does not, despite the scaremongering of government and the medical profession, mean that we’re all about to drop like bloated flies. As other figures from the CDC show, there is little difference in rates of illness and mortality for people in the ‘normal’, ‘overweight’ and ‘mildly obese’ categories. Nonetheless, this dramatic change in our body shapes and weights deserves an explanation. Finding out what is going on may go some way to explaining today’s chronic ‘diseases of civilisation’, like heart disease, stroke, cancer and type-2 diabetes, which finish off most people in developed countries.

As leading US science writer Gary Taubes explains in his new book, Why We Get Fat And What To Do About It, doctors and medical researchers have got stuck in a flawed paradigm that suggests that both the cause and cure of obesity are clear: ‘We get fat, our physicians tell us, because we eat too much and/or move too little, and so the cure is to do the opposite.’ This is the ‘calories in/calories out’ approach: we get fat because there is an imbalance between the amount of energy entering our body as food and the amount that is used up by our metabolisms and our physical activity.

Taubes says that the trouble with this appealingly simple explanation is that it is wrong. As he tells me on the phone from his home in Berkeley, California: ‘I’m arguing that calories in/calories out is a nonsensical paradigm and [is also] the reason why there is an obesity epidemic and the reason why obesity researchers have made zero progress in 100 years.’

This is not the first time Taubes has put his ideas into print. Why We Get Fat is a follow-up to his 2007 tome Good Calories, Bad Calories, which aimed to provide chapter and verse on the evidence for a different approach to this topic. The problem was that in being comprehensive in its analysis of the science, the earlier book was a tricky proposition for anyone without a scientific background. In his introduction to his new book, Taubes explains: ‘Many physicians have asked me to write a book that they can give to their patients, or even to their fellow physicians, a book that doesn’t require such an investment of time and effort.’

So what are his central ideas? Taubes takes the story back to basics. Obesity is ‘a disorder of excess fat accumulation’. Once we go back to first principles in this way, rather than starting from eating habits or fitness regimens, then it’s much easier to ask the next question: ‘What controls fat accumulation?’ And the answer to that question is completely uncontroversial, according to Taubes: insulin. ‘When insulin levels are elevated, we accumulate fat in our fat tissue; when these levels fall, we liberate fat from the fat tissue and burn it for fuel’, he writes.

So what controls insulin? On a day-to-day level, it’s carbohydrate. ‘The more carbohydrates we eat, and the easier they are to digest and the sweeter they are, the more insulin we will ultimately secrete, meaning that the level of it in our bloodstream is greater and so is the fat we retain in our fat cells.’ Or as George Cahill, a former professor of medicine at Harvard Medical School, tells Taubes: ‘Carbohydrate is driving insulin is driving fat.’

The logical upshot of this is that to lose the fat, you should eat a low-carbohydrate diet. The trouble is that such diets are seen by many members of the medical community as dangerous, bordering on quackery. Taubes tells me: ‘What I’m saying is that for someone with a serious weight problem, the Atkins diet or something similar is the only way to cure it… but Atkins has been so demonised that people can agree with my analysis and yet cannot agree with the dietary interpretation’. There is, as Taubes shows in this new book, plenty of evidence to suggest that, firstly, low-carbohydrate diets work (or at least, are more likely to succeed than other kinds of diets) and, secondly, that far from being dangerous they are actually beneficial in ways that go well beyond reducing our waistlines.

So, in a nutshell, Taubes is arguing that our expanding waistlines are caused by (in most people) a very small hormonal overreaction to carbohydrates. That’s it. It’s not greed, sloth or some psychological disorder that has befallen the fat – just the interaction of insulin and carbohydrate.

Just how small this overreaction would need to be can be illustrated like this: if someone gained an excess amount of fat of just one ounce per week, then over 20 years that would amount to 65 pounds (about 30 kilos). For most people, that accumulation of excess weight, often put down to ‘middle-age spread’, is considerably slower.

Nor is Taubes simply concerned with obesity; he argues there are other consequences to eating an excess of carbohydrate. When we have excess glucose (the simple sugar that most carbohydrates break down into) in our blood, insulin can deal with it by storing it in our fat cells or in muscle cells. Over time, these cells – particularly muscle cells – become ‘resistant’ to the effect of insulin. To compensate, the pancreas produces more and more insulin, leading to even greater fat storage and increasing insulin resistance. The result is that we get fatter. Eventually, when our bodies become so resistant to insulin that glucose remains in our blood for too long, we develop type-2 diabetes.

So, Taubes is arguing that are bodies are reacting to carbohydrates in two different ways, both driven by insulin: we are getting fat, and we are developing type-2 diabetes. There is a strong correlation between these two reactions, such that people who are very obese are also much more likely to develop type-2 diabetes. However, this correlation is far from perfect: many very-overweight people will not develop diabetes, while a significant number of people who are not overweight, or only mildly so, will.

‘What I’m saying is that the problem isn’t obesity’, Taubes tells me. ‘The problem is that the sugar and refined carbohydrate that causes the obesity also causes heart disease and diabetes, with different causal pathways. The conventional wisdom is that you get fat and then the condition of being fat increases your risk of all these other disorders.’ While Taubes accepts that there may be some truth to the idea that fatty tissue exacerbates the tendency towards diabetes, the ‘fundamental insult’ to our bodies is the stodge and sugar.

As mentioned earlier, these ideas are not new. The notion that carbohydrate makes you fat was observed as early as 1825 by the French writer Jean Anthelme Brillat-Savarin in his groundbreaking book The Physiology of Taste. Brillat-Savarin memorably wrote: ‘Tell me what you eat and I shall tell you what you are.’ Or, as Gillian McKeith would have it, you are what you eat. Taubes observes that Brillat-Savarin held more than 500 conversations with dinner companions who were ‘threatened or afflicted with obesity’, noting they tended to declare a devotion to bread, rice, pasta or potatoes. Some people, but by no means all, react to eating lots of carbohydrate by piling on the pounds.

In Britain, this observation was popularised in the 1860s by William Banting, an undertaker who had struggled with his weight for years and for whom no diet or exercise regimen worked. Then, a doctor told him of the latest ideas from France and prescribed a diet that almost entirely cut out carbohydrates and sugar. Banting lost 35 pounds in nine months and a total of 50 pounds eventually. His short pamphlet on the matter, A Letter on Corpulence, was a hit in Victorian London, so much so that the verb for dieting became ‘to bant’.

As Taubes describes in Why We Get Fat, an approach to obesity that put hormones – and thus, things like carbohydrates that influence hormone levels – at the centre of the problem of obesity was the leading one in prewar Europe in Germany and Austria, but largely failed to survive the conflict. While individual practitioners and academics – like John Yudkin in London and Robert Atkins in New York – later picked up on these ideas and used them with considerable success to treat overweight patients, the concept of the fattening carbohydrate remained stubbornly outside the mainstream.

The trouble now is that, despite decades of failure from exhorting the overweight to eat less and exercise more – in the vast majority of cases, an utterly useless prescription that works, at best, only for a short time – the medical establishment would rather we believed that we lack willpower, that we are lazy, rather than admit that its ideas were wrong. Taubes suggests to me that it would be a difficult position for governments and health bodies to back away from. ‘What would they say? “Oh, by the way, what we’ve been saying for the past 40 years is wrong. We apologise if we happened to cause anyone any obesity, diabetes, heart disease or cancer. But now this is what you should listen to.” There is no way around it. Once they get into this business of giving advice, they’re trapped.’

I find Taubes’ arguments, both in Why We Get Fat and in Good Calories, Bad Calories, highly persuasive. But I’m not a medical researcher or practitioner. What’s needed is a recognition that after decades of being told to eat less and move more, we’re fatter than ever; we could also use a little humility from the medical establishment in admitting that this advice has utterly failed. Then we could at last have a sensible debate about how we can deal with obesity once and for all, freed from endless moralising about the failings of the fat.

While the notion of an ‘obesity timebomb’ is ludicrous, few overweight people actively want to be fat; most would like to be slimmer, if they could. Why We Get Fat could be an invaluable contribution to that debate and a useful tool for those who want a well-argued explanation of how they gained those excess pounds – and how they might lose them.

Rob Lyons is deputy editor of spiked.