Fork U with Dr. Terry Simpson podcast

Obesity is not about Forks and Willpower

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15 Sekunden vorwärts
15 Sekunden vorwärts

Obesity: Not Just About Forks and Willpower

For years, obesity has been misunderstood, oversimplified, and even stigmatized. It's been framed as a personal failing, a lifestyle choice, or simply a matter of "eating less and moving more." But science tells a different, more nuanced story—one where our brains, biology, and ultra-processed food environment play starring roles. And thanks to groundbreaking medications like GLP-1 drugs, we’re gaining a clearer picture of how obesity works and how to treat it.

Let’s dive into why obesity is a disease, how ultra-processed foods exacerbate it, and why we need to ditch the harmful myth that obesity is a lifestyle choice.

The Myth of "Just Eat Less and Move More"

"Just eat less and move more." It’s the phrase everyone loves to repeat—and no one finds helpful. This simplistic advice ignores the reality that obesity is not merely about calories in and calories out. It’s about a complex interplay between your biology, brain chemistry, and environment.

Obesity isn’t a character flaw or a lack of willpower. If it were, we wouldn’t see an obesity epidemic in societies flooded with cheap, ultra-processed foods engineered to make us eat more. These foods hijack our biology, overpowering the mechanisms our bodies use to regulate hunger and fullness.

The Hungry Brain: Why You Can’t Stop Eating

Our brains evolved to keep us alive in times of scarcity. Back in the caveman days, this was helpful. Today, it’s less so because our brains are still wired to seek out high-calorie foods to avoid starvation—even when we’re surrounded by abundance.

When you eat ultra-processed foods, they light up the reward centers in your brain like a Christmas tree. These foods—laden with sugar, fat, and salt—trigger the release of dopamine, the same neurotransmitter involved in addiction. It’s no wonder we keep going back for more.

Adding to the complexity, hormones like ghrelin (the "hunger hormone") and leptin (the "fullness hormone") can go haywire in people with obesity. Ultra-processed foods amplify ghrelin’s effects, making you feel hungrier while reducing your sensitivity to leptin, so you never feel full. It’s a biological double whammy.

Citation: Studies show that diets high in ultra-processed foods increase calorie consumption by about 500 calories per day compared to diets of unprocessed foods (Hall et al., 2019).

GLP-1: The Game-Changing Hormone

Here’s where things get interesting: GLP-1, or glucagon-like peptide-1, is a hormone that helps regulate appetite. It tells your brain, “You’re full; you can stop eating now.” But for many people with obesity, this system doesn’t work properly. Their brains don’t get the message, leading to overeating.

Enter GLP-1 receptor agonists like semaglutide and liraglutide—medications that mimic the effects of GLP-1. These drugs help regulate appetite, making people feel full sooner and reducing cravings. The results have been extraordinary: clinical trials show average weight loss of 15% or more with these medications, far outpacing what’s possible with lifestyle changes alone.

These drugs have done more than help people lose weight—they’ve also shifted the way we think about obesity. They show that obesity is a medical condition influenced by hormones and brain chemistry, not just a matter of willpower.

Citation: Clinical trials on GLP-1 receptor agonists show significant and sustained weight loss, with participants losing 15% or more of their body weight (Wilding et al., 2021).

Why Obesity Is a Disease, Not a Lifestyle Choice

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