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Did you know DNA makes it harder to feel full?

The FTO gene and your insatiable appetite

Your son has always been a voracious eater. As a toddler, his food intake was more than twice that of the recommended daily amount. By five, he could match his 10-year-old cousin bite for bite. He’s active and thriving, so you just shrug off your mom when she asks you to “watch what he’s eating”. But as his weight shoots past 80 lb before his 8th birthday, you feel something’s amiss. A trip to the doctor confirms your suspicions. You are left wondering how a child that eats relatively healthy, and gets enough exercise, can be so over-weight.

Barring the usual culprits of childhood obesity – poor diet and lack of exercise – genetics is likely the explanation. Genes account for 40-90% of the differences in body mass indices (BMI). Perhaps your son could be having a tough time controlling his appetite because he carries the ‘defective’ version of the FTO gene that keeps him from “feeling full”.

FTO was one of the first “obesity” genes to be identified, and the encoded protein was subsequently named the fat mass and obesity-associated protein. This protein appears to affect appetite, rather than the metabolism of food, altering the balance between hunger and satiety. Children with the rs9930609 risk variant are more likely to consume more food and not feel as full after a meal, compared to children with the normal FTO gene. Furthermore, studies have shown that children with the risk variant are more likely to choose high fat foods.

This inability to feel full may be due to changes in the way food is perceived. When people with the rs9930609 risk variant look at food, the areas of the brain that control appetite, impulse and reward processing respond differently compared to people with the normal FTO gene.

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Studies also show that FTO may influence the levels of two hormones – ghrelin (the “hunger hormone”) and leptin (the “satiety hormone”). Each of these hormones are involved in appetite control, but exactly how these changes explain the link between FTO and obesity remains to be seen. Multiple studies (1, 2, 3, 4) have also identified an association between the rs9939609 risk variant and an increased risk of type 2 diabetes, which is not surprising considering the strong link between obesity and type diabetes.

Weight gain as a child and weight gain as an adult have vastly differing impacts. This is because the final number of adipocytes (fat cells) in the body is set by the end of adolescence. Our fat cell number increases from birth to the age of 20. After that it remains relatively stable, regardless of whether we lose or gain weight. Children are capable of expanding their fat mass by both increasing the number of fat cells in their body, and by increasing the size of existing fat cells. In adults, irrespective of how much weight they gain, they can only increase the volume of their existing fat cells.

Our potential for obesity in adulthood can be thought of as a pre-existing condition. People who are obese have acquired an increased capacity to store fats (or more fat cells) than someone that’s lean. Studies show that overweight children are much more prone to becoming overweight adults, and 62% of children with higher BMIs carry their weight into adulthood. This illustrates why childhood obesity is such a threat to our overall health and life expectancy. It not only establishes our potential for weight gain in adulthood, but also enhances our risk of diseases like cardiovascular disease and type 2 diabetes, even if we manage to maintain a healthy weight as an adult.

So what are your options if you yourself have that insatiable appetite? Or you have a child that carries the rs9939609 risk variant? Eating healthy high fibre foods can definitely make a difference to how full you feel. And it is especially important to control the food intake of your child to save them from a lifelong body weight battle. The good news is, fat cells don’t live forever. About 10% of our fat cells get replaced every year, whether you are lean or obese. This high turnover rate offers a potential therapeutic avenue that could be used to manage obesity, as well as type 2 diabetes. There is still hope!

 

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