Your appetite is governed by many things, from the immediate, physical sensation of a full stomach to hormones that tell the brain how much energy is stored as fat. The chemical I mentioned earlier that was missing in the genetically obese mice – leptin – is one such hormone. It is produced directly by fat tissue, so the more fat cells we have, the more leptin gets released into the blood. It’s a great system – it tells the brain we’re satiated once we have accumulated a healthy amount of stored fat, and our appetites are suppressed.
So why don’t people lose interest in food once they start to put on weight? When leptin was discovered in the 1990s, courtesy of the ob/ob mice who were genetically unable to make leptin of their own, there was a flurry of excitement about using the hormone to treat patients with obesity. Injecting ob/ob mice with it led to very rapid loss – they ate less, they moved around more, and they dropped to nearly half of their body weight in a month. Even giving leptin to normal, lean mice made them lose weight. If mice could be treated this way, could leptin be the cure for human obesity?
The answer, as is obvious from the continuing obesity epidemic, was no. Giving obese people leptin injections had hardly any effect on their weight or their appetites. Though disappointing, this failure shed light on the true nature of obesity. Unlike in the ob/ob mice, it is not too little leptin that allows people to become fat. In fact, overweight people have particularly high levels of leptin, because they have extra fat tissue that produces it. The trouble is, their brains have become resistant to its effects. In a lean person, gaining a bit of weight leads to extra leptin production, and a decrease in appetite. But in an obese person, though plenty of leptin is being produced, the brain can’t detect it and so they never feel full.
This leptin resistance hints at something important. In obesity, normal mechanisms of appetite regulation and energy storage have fundamentally changed. Excess fat is not just a place to pack away unburnt calories, it’s an energy-usage control centre, a bit like a thermostat. When the body’s fat cells are comfortably full, the thermostat clicks off, reducing appetite and preventing further food intake from being stored. Then as fat stores fall low, the thermostat clicks back on again, increasing appetite and storing more food as fat. As in the garden warblers, weight gain is not just about eating more, it’s about biochemical shifts in how the body manages energy. This ‘warbler effect’ undermines the basic assumption that balancing what we eat with how much we move is all that’s necessary to maintain a stable weight. If this belief is wrong, perhaps obesity is not a straightforward ‘lifestyle disease’, born of gluttony and sloth, but an illness with an organic origin beyond our control.
If this seems like too radical a suggestion, consider this: just a few decades ago, stomach ulcers were ‘known’ to be caused by stress and caffeine. Like obesity, they were thought of as a lifestyle disease – change your habits and the problem will go away. The solution was simple: keep calm and drink water. But this treatment didn’t work – patients returned again and again, with acid burning holes in their stomachs. The cause of their failure to recover was deemed obvious; these patients must not be sticking to their treatment plans, allowing stress to prevent them from getting better.
But then, in 1982, two Australian scientists, Robin Warren and Barry Marshall, discovered the truth. A bacterium called Helicobacter pylori that sometimes colonised the stomach was causing ulcers and the related condition gastritis. Stress and caffeine simply made them more painful. Such was the resistance of the scientific community to Warren and Marshall’s idea, that Marshall drank a solution of H. pylori, giving himself gastritis in the process, to prove the connection. It took fifteen years for the medical community to fully embrace this new cause. Now, antibiotics are a cheap and effective way to cure ulcers for good. In 2005, Warren and Marshall won a Nobel Prize in Physiology or Medicine for their discovery that stomach ulcers were not a lifestyle disease, as dogma dictated, but the result of an infection.
Likewise, with his virus, Nikhil Dhurandhar was challenging the dogma that obesity was a lifestyle disease – one of excess. To investigate the possibility that a viral infection could be capable of causing weight gain in humans, he needed to switch from practising medicine to researching the science behind it. Dhurandhar decided to uproot his family and move to the United States, in the hope of getting the research funding he would need to find answers to his questions. It was a leap of faith, in the face of stiff opposition from the scientific establishment. But it would eventually pay off.
Two years after he had moved to America, Dhurandhar had still not managed to convince anyone to support his research into the chicken virus. He was on the brink of giving up and returning to India when the nutritional scientist Professor Richard Atkinson, at the University of Wisconsin, agreed to give him a job. At last, Dhurandhar was ready to begin his experiments. But there was a major obstacle: the American authorities refused them permission to import the chicken virus into the United States – it might cause obesity, after all.
Together, Atkinson and Dhurandhar devised a new plan. They would study another virus – this time one that was common in Americans – in the hope that it too might be responsible for weight gain. Based on a hunch that it was similar to the chicken virus, they selected a different virus that was known to cause respiratory infections from a laboratory catalogue, and ordered it through the post. Its name was Adenovirus 36, or Ad-36.
Once again, Dhurandhar began his experiments with a group of chickens. He infected half the birds with Ad-36 and the other half with a different adenovirus, more normally found in birds. And then he and Atkinson waited. Would Ad-36 make the birds fat, just as the Indian virus had done?
If it did, Dhurandhar would be making a big claim. He would be suggesting that overeating and being under-active were not the sole cause of human obesity; that the obesity epidemic might have another origin; that obesity could be an infectious disease – not just a lack of will-power. And most controversially, Dhurandhar would be implying that obesity was contagious.
Looking at maps charting the spread of the obesity epidemic in the United States over the past thirty-five years certainly gives the impression that it’s an infectious disease sweeping through the population. The epidemic begins in the south-eastern states and quickly begins to spread. As more and more people become overweight at the epicentre of the disease, it pushes outward to the north and west, affecting ever-greater swathes of the country. Hot spots crop up in major cities, setting off new bubbles of obesity that expand over time. Though a handful of scientific studies have commented on this infectious-disease-like pattern, it’s usually put down to the spread of an ‘obesogenic environment’ – more fast-food restaurants, supermarkets with calorie-dense foods, and lifestyles with ever less physical activity.
One study in people has found that obesity spreads in a manner that mimics a contagious disease even on an individual level. By analysing the weights and social connections of over 12,000 people over thirty-two years, researchers found that a person’s chances of becoming obese are closely tied to weight gain in their nearest and dearest. For example, if a person’s spouse became obese, that person’s risk of becoming obese themselves went up by 37 per cent. Fair enough, you might think – they probably have the same diet. But the same is true for adult siblings, most of whom don’t live together. More strikingly, if a person’s close friend became obese, then that person’s risk of following suit shot up by 171 per cent. It didn’t seem to be down to choosing friends of a similar weight – these people were close before the weight gain. Neighbours who were not counted as friends were exempt from the increased risk of obesity, which makes it seem less likely to be the opening of a fast-food restaurant or closure of a gym nearby that pushes the tied weight gain among social groups.
Of course, there are many possible social reasons for this phenomenon – a shared shift in attitude towards obesity, or joint consumption of unhealthy foods, for example – but a thought-provoking addition to the list of explanations is that of microbial cross-over, viral or otherwise. Even if Dhurandhar’s virus is not the main culprit, there are many other microbes to consider.