In a brave new world in which we've all had our whole genomes analyzed and know about our genetic predisposition to certain diseases, here's a helpful finding: Don't eat a lot of fried food if you happen to carry several of the genetic variations linked to obesity.
And here's some more good advice: Don't eat a lot of fried food even if you carry few or none of the single nucleotide polymorphisms (or SNPs) that confer a higher risk of obesity.
Why? Well, because people who eat a lot of fried food -- especially away from home, where fried foods tend to be deep-fried -- are highly likely to pack on weight, a new study finds. The same study finds, however, that people who carry many of the 32 known obesity SNPs in their DNA and frequently eat fried foods tend to pack on more weight than do the big fried-food consumers with less genetic propensity toward obesity.
So avoiding fried foods makes good sense, really. Even in a world in which we have not all had our genomes scanned.
The new research, published Wednesday in the journal BMJ, comes from a collection of researchers from Boston University and Harvard University's schools of medicine and of public health. In October 2012, they published the finding -- in the New England Journal of Medicine -- that frequent consumption of sugar-sweetened beverages results in greater weight gain among those with higher genetic predisposition to obesity than it does among those whose genetic vulnerability is less pronounced.
The studies' findings are not as obvious as they may seem. Both aim to explore how genes and behavior interact to drive obesity in large populations. And both suggest that while obesogenic behaviors (such as eating too much and exercising too little) make people fat, they have a magnified effect on those whose genes program them to burn calories more efficiently, to accumulate and store extra calories as fat, and to consume more food when it's available.
That magnifying effect isn't huge. But spread across vast populations -- all of which are eating more fried foods and drinking more sugar-sweetened beverages -- it can become very huge indeed, and with it come increased rates of Type 2 diabetes, heart attacks and strokes, and certain cancers.
In the more than 37,000 men and women of European ancestry who made up the population of the current study, those who ate fried foods four or more times a week on average weighed more than did those who indulged least frequently -- less often than once a week. (Frequent consumers of fried foods were also more likely to smoke, watched more television, drank more sugar-sweetened beverages and less alcohol and engaged in less physical activity than less-frequent consumers of fried foods. But the researchers adjusted for those behavioral differences, and still saw significant differences.)
But here's the bottom line: The BMI difference between light and heavy fried-food consumers was bigger -- as much as twice as big -- when those consumers were at highest genetic risk for obesity than when they were at low risk.
On a scale of zero to 64, a calculation of genetic obesity risk placed all the study's subjects between 13 and 43. And among those whose genetic predisposition to obesity was on the low end, the difference in body mass index between frequent fried-food consumers and infrequent consumers of fried food was less than half a point. Among those with the highest genetic risk of obesity, a difference of between 0.7 and one full BMI point separated the least frequent fried-food consumers from the most frequent.
In an editorial, two obesity experts from Imperial College London said the findings were unlikely to change the way that physicians counsel patients and treat obesity. That's mainly because having even several of the SNPs that predispose to obesity appears to be far less influential in whether one becomes obese than more obvious factors, such as overeating and a sedentary lifestyle.
But it would be "a great shame," wrote Alexandra I.F. Blakemore and Jessica L. Buxton, "to assume that genetics can be ignored in the management of obesity." For starters, they wrote, there are genetic contributors to obesity that are not nearly as subtle as the 32 SNPs measured in this study, and a mutation in just one of those genes, called MC4R, is thought to cause 1 in 20 cases of severe child obesity.
Beyond that, wrote Blakemore and Buxton, a physician might be guided toward more personalized treatment of an obese patient if armed with the knowledge that the patient carries a heavy genetic vulnerability to the condition. As knowledge of genes' role in obesity advances, some genetic variations may be found to, say, disrupt the brain's appetite control system at the molecular level. In such cases, a physician might conclude that calling for more self-restraint, or a reversible measure such as lap-band surgery, are unlikely to work.
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