Steven Blair is, in his own words, a “short, fat, bald guy”. But at 165cm and 91kg, he may very well be healthier than men much taller and leaner. He runs 40km a week, eats six to eight servings of fruit and vegetables a day and avoids processed and fatty foods. A professor of exercise science and epidemiology at the University of South Carolina, Blair is a living example of how fat doesn’t play fair. And thanks to advances in his field, he is beginning to understand why.
Genes, hormonal imbalances and even viruses are now acknowledged to play a role in obesity. Eating less and working out more, in fact, don’t have nearly as much to do with weight loss as you might assume. “This is all counter to what people think they know,” says Blair. “You can see obesity, so it’s easy to say, ‘Well, that person must not be trying. He must be lazy.’ But that’s often not the case.”
The RD team pored over the latest studies, interviewed the top clinicians in obesity science and listened to the real-life experiences of people struggling to maintain their weight. Here are the results: the latest (and often unexpected) thinking behind size and thighs, fatness and fitness.
1. Honestly, it really is genetic
When scientists first discovered it in certain chubby mice, they called it simply the “fatso gene”. Years later, when they scoured the human genome for markers that signalled increased vulnerability to type 2 diabetes, the fatso gene (now more politely called FTO) showed up there too. It turns out that people with two copies of the gene were 40% more likely to have diabetes and 60% more likely to be obese than those without it. Those with only one copy of the gene also weighed more.
Scientists now suspect that there are lots of “fat genes”. “There could be as many as 100 of them,” says Dr Claude Bouchard, executive director of Pennington Biomedical Research Centre at Louisiana State University System, “each adding a couple of pounds here and a pound or two there. That’s a noticeable difference when it comes to how much more fat we need to burn off.”
As much as 16% of the population have two copies of the FTO gene, and half of us have one copy. So far, scientists suspect that the other possible obesity-promoting genes have a small effect compared with FTO. The good news? “A genetic predisposition isn’t necessarily a life sentence,” says Bouchard. Exercising regularly can offset the risk.
2. Some people just have more fat cells
And the range is enormous, with some people having twice as many fat cells as others, says Dr Kirsty Spalding, of the Karolinska Institute in Stockholm. Even if you’ve lost a few kilos (or gained some), your fat-cell count remains, holding tight to the fat already inside and forever thirsting to be filled up with more. (To add insult to injury, the fat cells of overweight and obese people hold more fat, too.)
New fat cells emerge during childhood but seem to stop by adolescence. Those of us destined to have a lot of these cells probably start producing them as young as age two. The cells’ rate of growth may be faster, too – even if kids cut way back on kilojoules.
Strangers have written to Spalding, telling her how depressed they are by her research. But she says her news isn’t all bleak. You’re better off with more fat cells, she says, than with fewer fat cells that become overstuffed and enlarged. (New research suggests that the overstuffed group are more vulnerable to obesity-related health complications.) So while you can’t reduce your total number of fat cells, there are things you can do to keep them small. (See next point.)