Regardless of the genes involved, genetics could never be the full explanation for the obesity epidemic, because sixty years ago almost everyone was slim, despite having broadly the same gene variants as the human population today. What probably matters far more is the impact that a changing environment – our diets and lifestyles, for example – has on the workings of our genes.
Our other favourite explanation is that of a ‘slow metabolism’. ‘I don’t have to watch what I eat, I’ve got a quick metabolism,’ must be one of the most irritating comments a lean person can make, but it has no basis in science. A slow metabolism – or more correctly, a low basal metabolic rate – means that a person burns relatively little energy whilst doing absolutely nothing at all – no moving, no watching TV, no doing mental arithmetic. Metabolic rates do vary from person to person, but it is actually overweight people who have the faster metabolisms, not lean people. It simply takes more energy to run a big body than a small one.
So if genetics and low basal metabolic rates aren’t behind the obesity epidemic, and the amount we eat and move doesn’t fully explain our collective weight gain, what is the explanation? Like many people, Nikhil Dhurandhar wondered if there’s more to it than we assume. The possibility that a virus could be causing or exacerbating obesity in some people played on his mind. He tested fifty-two of his human patients in Mumbai for antibodies to the chicken virus – evidence that they had been infected by it at some stage. To his surprise, the ten most obese of these patients had had the virus at some point. Dhurandhar made up his mind; he would stop trying to treat obesity and start researching its causes instead.
We have reached the point in human history where we are considering, in the United Kingdom at least, that redesigning and re-routing the digestive system that evolution has given us is the best way to prevent us from eating ourselves to death. It seems that gastric bands and bypasses, which reduce the size of the stomach and prevent people from consuming everything that their brains and bodies tell them to, are the most effective and the cheapest way to get a grip on the obesity epidemic and its consequences for our collective health.
If diets and exercise are so futile that gastric bypasses are our only hope for significant weight loss, what does that say for the straightforward application of the laws of physics – energy intake minus energy burned equals energy stored – to us as animals governed by the laws of biochemistry?
As we are just beginning to learn, it’s not that simple. As the warblers and many hibernating mammals show, there’s more to managing weight than counting calories. Subscribing to a simple one-in, one-out system of balancing the body’s energy books utterly undermines the great complexities of nutrition, appetite regulation and energy storage. As George Bray, a doctor who has been researching obesity since the start of the epidemic, once said: ‘Obesity isn’t rocket science. It’s much more complicated.’
Two and a half thousand years ago, Hippocrates – the father of modern medicine – believed that all diseases begin in the gut. He knew little of the gut’s anatomy, let alone of the 100 trillion microbes that live there, but as we are learning two millennia later, Hippocrates was on to something. Back then, obesity was relatively uncommon, as was another twenty-first-century illness that clearly has its origins in the gut: irritable bowel syndrome. It’s with this most unpleasant of maladies that our microbes come into the picture.
In the first week of May 2000, unseasonably heavy rain drenched the rural town of Walkerton, Canada. As the rainstorms passed, Walkerton’s residents began to fall ill in their hundreds. With ever more people developing gastroenteritis and bloody diarrhoea, the authorities tested the water supply. They discovered what the water company had been keeping quiet for days: the town’s drinking water was contaminated with a deadly strain of E. coli.
It transpired that bosses at the water company had known for weeks that the chlorination system on one of the town’s wells was broken. During the rains, their negligence had meant that run-off from farmland had carried residues from manure straight into the water supply. A day after the contamination was revealed, three adults and a baby died from their illnesses. Over the next few weeks, three more people succumbed. In total, half of Walkerton’s 5,000-strong population were infected in just a couple of weeks
Even though the water supply was quickly cleaned and made safe to drink, the story didn’t end there for many of those that had fallen ill. The diarrhoea and cramps just kept coming. A full two years later, one-third of the people affected were still ill. They had developed post-infectious irritable bowel syndrome (IBS), and more than half of them still had it eight years after the outbreak.
As new IBS sufferers, these unfortunate Walkerton residents had joined the growing ranks of people in the West whose bowels rule their lives. For most with the condition, severe abdominal pain and unpredictable bouts of diarrhoea determine the freedom of their days. For others, it’s the opposite – constipation, and the pain that goes with it, lasting days and sometimes weeks at a time. ‘At least,’ says the British gastroenterologist Peter Whorwell of those with constipation-predominant IBS, ‘these patients can get out of the house.’ For a minority, the double difficulty of both diarrhoea and constipation makes daily life particularly unpredictable.
The trouble is, even though nearly one in five people in the West – mostly women – are stuck with this life-changing illness, we don’t actually know what it is. It’s not normal, that much is clear. The word ‘irritable’ belies the impact that IBS has on the lives of its sufferers; the disease is consistently ranked as reducing quality of life even more than for patients on kidney dialysis and diabetics reliant on insulin injections. Perhaps it’s the hopelessness that comes with not knowing what’s wrong, nor how to fix it.
The spread of IBS is an unremarked global pandemic. One in ten visits to the doctor relate to the condition, and gastroenterologists are kept in a job by the steady flow of sufferers who make up half of their patients. In the United States, IBS leads to 3 million visits to the doctor, 2.2 million prescriptions, and 100,000 hospital visits each year. But we keep it quiet. No one wants to talk about diarrhoea.
The cause, however, remains elusive. Whereas the colon of a person suffering from inflammatory bowel disease would be coated with ulcers, the intestines of people with IBS appear as pink and smooth as those of a healthy person. This lack of physical signs has led to IBS becoming tainted by the historical assumption that it is all in the mind. Though for most sufferers their IBS is at its worst when they are stressed, it’s unlikely that stress alone is the sole cause of such a persistent illness. The staggering proportion of people with IBS deserves an explanation – we haven’t been through millions of years of evolution just to need to be within thirty seconds of a loo.
A clue is to be found in the Walkerton tragedy. The people stuck with IBS after the water-contamination incident are not the only IBS sufferers to blame their illness on a gastrointestinal infection of some kind. Around a third of patients pinpoint the moment their gut troubles started on an episode of food poisoning or similar, which never seemed to resolve. Traveller’s diarrhoea is often the beginning – people who pick up a bug abroad are up to seven times more likely to get IBS. But testing for the original bug yields nothing – they are no longer suffering from the gastroenteritis itself. It’s as if the original infection has thrown the gut’s normal residents into disarray.
For others, the onset of their IBS coincides not with an infection, but with a