The worldwide obesity epidemic is alarming, but this year we’ve had some good news. In a recent study of more than 9000 Americans, Cynthia Ogden and her colleagues found that one age group is getting healthier: The rate of obesity among young children (aged 2-5) is 43% lower than it was in 2003.
That’s encouraging, but we should keep in mind: Fighting excess fat isn’t the same battle for everyone. Some children are born with differences that make staying lean more difficult.
Decades of behavioral genetics research suggests that more than half the variation we see in body mass index can be chalked up to hereditary factors. Genetic differences may explain why kids raised in similar environments — even the same household — often end up with very different body fat profiles.
Consider, for instance, the news in this week’s Nature, where researchers report the results of a study that analyzed the DNA from thousands of people in the United Kingdom, France, Sweden, and Singapore.
When Mario Falchi and his colleagues examined sibling-pairs – in which one sibling was obese and the other sibling was not – they found that one particular gene was especially predictive of obesity.
This gene, AMY1, codes for a starch-digesting enzyme in our saliva called amylase, and people vary in the number of copies of the gene they possess. Those descended from a long line of starch-eating ancestors – like Western Europeans, Japanese, and African Hadza foragers – tend to have twice as many copies as do people from historically “low starch” societies.
But there are also striking differences between individuals, even within the same family. In the samples Falchi’s team studied, people ranged between having fewer than 4 copies to having 10 or more, and the more copies they carried the less likely they were to be obese.
It wasn’t a small effect. The researchers estimate that each additional copy of the AMY1 salivary amylase gene lowered the odds of obesity by about 19 percent. This, they say, translated “into about an eightfold difference in risk of obesity” if you compare a high-copy person (>9) to a low-copy person (<4). One in ten of the people studied fell into the latter category.
Why the link with AMY1? That’s not clear. We might speculate that people with many AMY1 copies produce more salivary amylase and receive more immediate feedback about the starches they eat. Perhaps they are more likely to feel they’ve eaten enough of that bagel within the first few minutes, whereas their low-amylase counterparts take longer to feel the effects, and therefore continue eating. Or perhaps low amylase levels interfere with the enjoyment of plain starch, prompting people to add more fat to their meals (hello, cream cheese).
Or maybe people with fewer copies of the AMY1 gene are more likely to develop insulin resistance when they live on high-starch diets – a possibility that’s consistent with recent research and higher obesity risk. Insulin resistance is known to accelerate weight gain.
But whatever the explanation, we’ve got evidence that all children are not created equal with respect to packing on body fat. The lucky kid with “slim” genetics might be able to handle exposure to high-calorie foods without becoming overweight. The unlucky kid may have a lot more trouble.
Should we be plying children with diets high in starch, sugar, and fat? If there is a practical message in the new AMY1 study, it’s that genetic risk factors for obesity are relatively powerful and widespread. Yes, we need to watch portion sizes and resist the temptation to turn every social event into a meal. But we might also consider the kinds of food we are introducing to our children. To protect kids from a lifetime struggle with obesity, we ought to re-think our dietary status quo.
Coming from a family equally split between underweight and overweight members, this makes a lot of sense. My father and sister are both very thin, my mother and I struggle with being overweight. I can see the same patterns emerging in my children. It’s nice to see the science behind what’s happening at home.