I’ve never been thin. I was a solid kid without a hint of gangly limbs or scrawiness; even in poverty I had a bit of a pot belly. Once I hit puberty, my body took the cues to go curvy very seriously, and breasts and hips and thighs got thick and rounded quickly.
Later, after trying to diet those curves away, I got fat. I’ve written about my recent struggles with body image and weight loss both here and at my personal blog, so obesity is, to say the least, on my mind as I pursue weight loss with vigor.
So you can imagine that I got quite interested in this article in the New York Times recently, suggesting that there has is proof finally really and truly that obesity has a genetic component.
I mean, this seems obvious. My grandmother was fat, my mom was fat, and I’m fat. The jury is out on my daughter, although she definitely is a solid kid like I was (but far more active than I was as a kid). And my friend Wendy is the kind of naturally thin that makes people accuse her of having anorexia (she doesn’t), and her mother’s body is exactly the same way.
But even so, the medical community and media’s (and, frankly, many people’s) attitude has been, “If you’re fat, it’s your fault. Just eat less and move more and the pounds will magically melt away!” and this is something that those of us that struggle with morbid obesity is, frankly, bullshit.
Here’s the hypothesis this most recent study pursued.
In their paper, Dr. Majzoub and his colleagues describe figuring out how the gene they deleted, known as MRAP2, acts in the brain to control weight. They discovered that it is a helper gene. It normally acts in the brain to signal another gene already known to be involved in controlling appetite. So they developed a hypothesis. If the helper gene was deleted, the brakes should come off the gene that controls appetite. Animals should eat voraciously.
This is pretty interesting, but the part that got me was a bit later in the NYTimes article. Emphasis is mine.
The surprise came when the researchers figured out why. When the mice were young, they had normal appetites. The researchers measured what they and their normal siblings ate and determined they were eating the same amount of food. Yet the mice with the deleted gene still gained weight. The only way the obesity-prone mice could be kept slim was to be fed 10 to 15 percent less than their siblings.
But as adults, the mice with the missing gene developed monstrous appetites. Given a chance, they ate much more than their siblings, exacerbating the effects of their tendency to turn food into fat.
I’m not sure I have a monstrous appetite; I don’t want to saddle myself with the moniker of monster, but I do know that unless I train myself and diligently watch what I eat, I can crave more food than other people. But when I do monitor my food, my husband is constantly stunned at how I eat the same amount he does yet either maintain my body weight or just lose weight very slowly.
I’m not a fat apologist, but I do believe that there are myriad factors that play a role in obesity, and genetics is just one piece of the puzzle. But it’s nice to know that there is a possibility that those of us that struggle so hard with our weight are NOT starting from the same place that thin people are.
I’d love to hear your thoughts. Did the article help you or make you feel any better about your issues with weight?