As those of you who voted guessed, our genes most definitely play a part in our weight, but not for the reason most people think. Our genes don’t affect how many calories we burn. Like in the mini experiment in Part 1, the amount of calories our bodies burn at rest is dictated by sex, weight, height, and age. Our genes work in a much more interesting and kind of scary way; they change the way we look at food.
If you’ve ever scanned the websites about the secrets of “naturally” skinny people, you’ve probably noticed that a lot of the secrets have to do with the way these skinny minis behave around food. They eat small portions; they don’t treat hunger as an emergency; they fill up on fruits and vegetables. Yes, naturally skinny people all have those things in common. They also look pretty similar genetically, especially on a gene called Fat Mass and Obesity-Related Gene (FTO). (Nope, I’m not even kidding about the name of this gene.)
Researchers at the Bute School of Medicine in the United Kingdom screened for FTO on a group of over 2,700 4- to 10- year-old children. If a child inherits FTO from both parents, the child is described as homozygous, meaning she has two copies of the same gene. Scientists use the shorthand AA for people with two copies of the FTO gene. People who only inherent one copy of the gene are heterozygous; and are labeled with the shorthand AT. Those without the gene are labeled TT. In this study, the scientists also measured the children’s height and weight, waist and hip circumference, and body fat.
Of the children in the study, 14% inherited two copies of FTO from their parents (AA). Nearly half (49%) inherited one copy of the gene (AT). The remaining 37% did not inherent any copies of the gene (TT). Those with one (AT) or two copies (AA) of the gene were more likely to be overweight and had an average of four pounds more body fat than their counterparts. Those who carried two copies of the gene (AA) were heavier than those with just one copy (AT).
Here’s the kicker. The carriers of the gene (AA or AT) burned an average of 84 more calories per day than those who didn’t carry the gene (TT). Both those who carried the FTO gene (AA or AT) and non-carriers (TT) burned about the same amount of calories as the researchers predicted based on their basal metabolic rate; that is, the bigger kids burned more calories than the smaller kids and boys burned more calories than girls.
It all came back to food. During the second part of the study, the researchers measured the children’s food intake. The children were fed a buffet lunch with ham, cheese, carrots, cucumber, potato chips, rolls, crackers, raisins, chocolate candy, grapes, orange juice, and water. Interestingly, all of the children ate about the same amount of food; however, the gene carriers (AA and AT) consumed 16% more calories and 30% more fat than the noncarriers (TT). The carriers of the gene chose the more fattening and higher-calorie foods, like the candy and chips, while the noncarriers gravitated towards the foods with lower calories like the fruit and vegetables (Cecil, 2008).
I absolutely love Nutella and its chocolaty, hazelnutty deliciousness. At a previous job, I kept a jar of it at my desk. I was towards the bottom of the jar and alone in my shared office. I don’t know what came over me, but a few minutes later, I had my hand jammed into the jar so I could get every last morsel of goodness into my mouth. That is until a coworker walked in and said, “What the hell are you doing?” It wasn’t until then that I realized that Nutella was on my chin, shirt, and forearm up to my elbow. Researchers call this phenomenon loss of control eating. It happens to all of us, but it happens more often to FTO carriers. On a research trip to the Chinese buffet, 37% of carriers, both AA and AT, lost control with all the moo su pork in sight. Only 18% of noncarriers (TT) got to the point where they lost control (Tanofsky-Kraff, 2009).
Since FTO was first discovered in the early 2000s, data from over 80,000 people have been analyzed. The probability that FTO’s affect is due to chance is 1.2 in 1,000,000,000,000,000,000,000,000,000,000 (Frayling, 2007). Repeatedly, studies have found the same thing—those with one or two copies of the FTO gene weigh more and eat more than those who do not carry the gene and this trend has nothing to do with metabolism (Speakman, 2008). Of course, FTO isn’t the only gene that has an effect on obesity—it’s just shown the biggest effect to date (Li, 2010).
So, why are we seeing this obesity epidemic now? Has our DNA changed? Stay tuned for Part 3 for more riveting genetic information.
Cecil, J.E., Tavendale ,R., Watt, P., Hetherington, M.M., Palmer, C.N. (2008). An obesity-associated FTO gene variant and increased energy intake in children. New England Journal of Medicine. 359(24), 2558-2566.
Tanofsky-Kraff, M., Han, J.C., Anandalingam, K., Shomaker, L.B., Columbo, K.M., Wolkoff, L.E., Kozlosky, M., Elliott, C., Ranzenhofer, L.M., Roza, C.A., Yanovski, S.Z., Yanovski, J.A. (2009). The FTO gene rs9939609 obesity-risk allele and loss of control over eating. American Journal of Clinical Nutrition. 90(6), 1483-8.
Frayling TM, Timpson NJ, Weedon MN, et al. (2007). A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity. Science. 316, 889-94.
Speakman, J.R., Rance, K.A., Johnstone, A.M. Obesity (Silver Spring). (2008). Polymorphisms of the FTO gene are associated with variation in energy intake, but not energy expenditure. 16(8), 1961-5.
Li, S., Zhao, J.H., Luan, J., Luben, R.N., Rodwell, S.A., Khaw, K.T., Ong, K.K., Wareham, N.J., & Loos, R.J. (2010). Cumulative effects and predictive value of common obesity-susceptibility variants identified by genome-wide association studies. American Journal of Clinical Nutrition. 91(1):184-90.
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