Why You Just Ate An Entire Bag of Potato Chips, According to Genetics
If you’ve ever housed a family-sized bag of Ruffles at supersonic speeds, you acutely understand why potato chips can so easily make a mockery of the idea of “moderation” — to say nothing of the suggested serving size on the back of the bag. But per a new study, this has very little to do with the Ruffles themselves and everything to do with human genetics.
Like most genetic research, the language used to explain what’s happening here might sound like gibberish from a Boomer trying to reset their internet password — just an endless stream of random letters and numbers strung together inexplicably. But if it’s the key to a collective free pass on devouring an extra-large Domino’s pizza in 30 minutes or less, it should be decoded for all of humanity immediately.
The trouble more or less starts with a specific gene that’s been linked with obesity in humans known as the CREB-Regulated Transcription Coactivator 1, or CRTC1 gene (see what I’m saying about gibberish?). Previous studies show that when the CRTC1 gene is deleted in mice, they become obese, suggesting that if there is an obesity gene, it’s the CRTC1. The only problem is, since CRTC1 is found in all neurons in the brain, narrowing down the exact one responsible for obesity has proven difficult.
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And so, this most recent study focused on neurons that “expressed” the melanocortin-4 receptor, or MC4R (now do you see what I’m talking about?), because mutations in the MC4R gene have been found to cause obesity as well. The researchers behind the study theorized that the CRTC1 gene combined with these MC4R-expressing neurons (GIBBERISH, I TOLD YOU) could be critical for preventing the very, very relatable impulse to want to inhale potato chips in Dirt-Vac-like fashion.
To test their theory, the researchers studied mice who had the CRTC1 gene, but whose MC4R neurons were blocked. When fed a standard diet, the mice showed no change in weight, but when they were fed a high-fat diet, they gained significantly more weight compared to the control group, mostly because they were unable to push away their figurative plate from their figurative table (it probably had a lot more to do with some kind of trans-fat-equivalent mouse pellets in a mouse cage).
“This study has revealed the role that the CRTC1 gene plays in the brain, and part of the mechanism that stops us from overeating high-calorie, fatty and sugary foods,” lead author of the study, Shigenobu Matsumura, an associate professor at Osaka Metropolitan University in Japan, explained in a press release. “We hope this will lead to a better understanding of what causes people to overeat.”
Until there’s a definitive answer, though, there’s nothing left to do but let the chips fall where they may — namely, in our mouths.
