Fitting Into Those Skinny Genes (Part 3)

We are absolutely not made to
handle the toppings bar at
FroZenYo.

FroZenYo, a self-serve frozen yogurt Mecca of yumminess, opened in my neighborhood last month. You walk in, pick up an oversized cup, fill it with fro yo, add toppings, and then weigh the monstrosity to pay per the ounce. After you pay, “free” hot fudge beckons from beyond the register. With all of those options, it’s pretty hard to limit yogurt flavors and toppings. The sheer quantity of hard-to-resist treats leads me to make some pretty interesting flavor combinations. Coconut and pistachio yogurt with berries, wet nuts, Oreo pieces, and hot fudge, anyone? Oh well, guess I’ll blame my inability to resist all of these sweet, crunchy, gooey delights on my genes.

Since FTO and similar genes make food more attractive and lower a person’s ability to resist yummy, sweet, and fatty foods, these genes definitely make living in our society harder. It wasn’t always so. Hundreds of years ago, this genetic predisposition to eat large quantities of fattening foods would have helped us survive. Throughout history, humans ate when the harvest came in or when someone from the village killed a large animal. There were periods of feast and famine. The drive to chow down kept us alive through the harsh winter. Now we power through the cold weather with venti hot chocolates, big bowls of meaty chili con queso, and non-stop streaming Netflix.

Technology has created the perfect obesity storm by making food-like substances easier and cheaper to produce. Food (or something that closely resembles it) is always around us. (Ever walked past Chipotle at 3:00 in the afternoon? There’s a long line. What meal is that exactly? Linner? Or maybe dunch? Who knows, but I need that 1,100-calorie burrito the size of my head!) Technology also enables us to stay perfectly still for long periods of time, save for pressing buttons on the remote control, smart phone, computer, etc.

These changes in our society have happened really fast, and, as a society, we’ve gained weight really fast…

… and evolution happens slowly. So, on the nature vs. nurture debate, I’m going to have to side with nurture.

Genes don’t directly affect our weight; they affect how we interact with our environment. Simply, our bodies aren’t made to live in our current society and we are going to keep getting fatter unless our environment and culture change. I’m fully aware that I’m not going to solve the obesity epidemic with this blog post, but this is how I think we can set ourselves up for success in this sedentary, food-crazed culture:

Step 1: Boycott buffets and all-you-can-eat situations. FTO and similar genes don’t allow most of us to handle them. Hey, 18% of noncarriers lost control when confronted with a Chinese buffet too. Buffets are bad news. Willpower is a myth and, unless famine is imminent, stay far away.

Step 2: More importantly, cut back on eating out all together. If we’re going to change the obesity epidemic in one generation as Mrs. Obama has promised, there needs to be a return to healthy home cooking.

Step 3: Vote for policies/politicians that work to make healthier foods cheaper and more available than junk food. To make it work, healthier foods, like farmer’s market produce, would have to be subsidized and unhealthy foods, like soda, would have to be taxed. Current government policies are setting us up for fatness.* I’m personally working to create a generation of conspiracy theorists at the college where I teach health. The truth is out there. Trust no one.

Step 4: Don’t keep crappy food in your house. Just skip the chip aisle. You know you can’t avoid it if it’s in the house. Blame it on FTO.

Step 5: Exercise for at least an hour a day. FTO carriers who exercise weigh less than those who don’t exercise (Mitchell, 2010). Duh.

Step 6: Breastfeed. Some new research shows that being breastfed for at least a month may lessen the effect of FTO in childhood (Dedoussis, 2011).

How else could we change our food environment and culture? Comment!

Sources

Dedoussis, G.V., et al. (2011). Does a short breastfeeding period protect from FTO-induced adiposity in children. International Journal of Pediatric Obesity. 6(2-2):e326-335.

Mitchell, J.A., et al. (2010). FTO genotype and the weight loss benefits of moderate intensity exercise. Obesity (Silver Spring). 18(3):641-643.

*To be described in a future post.

Fitting Into Those Skinny Genes (Part 2)

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.