Aibrary Logo
Podcast thumbnail

Why We Get Fat

12 min

And What to Do About It

Introduction

Narrator: Imagine a massive, eight-year-long study involving nearly fifty thousand women. Twenty thousand of them are put on a special low-fat diet, carefully counseled to eat more fruits, vegetables, and fiber. They successfully cut their daily calorie intake by an average of 360 calories. After eight years of this dedicated effort, how much weight do you think they lost? The answer is a shocking two pounds. Even more perplexing, their average waist circumference actually increased, suggesting they lost muscle, not fat. This isn't a fluke; it's a pattern repeated in study after study. We're told the path to leanness is simple: eat less and exercise more. But what if that advice is fundamentally wrong?

In his provocative book, Why We Get Fat: And What to Do About It, science journalist Gary Taubes dismantles this conventional wisdom piece by piece. He argues that we've been asking the wrong questions and that the cause of obesity isn't a failure of willpower, but a flaw in our understanding of human biology.

The Calorie Model is a Failed Hypothesis

Key Insight 1

Narrator: The cornerstone of modern weight-loss advice is the "calories-in, calories-out" model. It treats the human body like a simple machine: if you burn more energy than you consume, you'll lose weight. Yet, as Taubes demonstrates, this idea consistently fails in the real world. The Women's Health Initiative is a prime example, but it's far from the only one.

As far back as 1959, a review by psychologist Albert Stunkard examined all the available studies on dietary treatment for obesity. He found the results to be "remarkably poor." In clinics prescribing diets of just 800-1000 calories a day, only one in four patients managed to lose twenty pounds, and a mere one in twenty lost forty pounds. More recently, a large study from Harvard and the Pennington Biomedical Research Center put over eight hundred people on four different calorie-restricted diets. Despite intensive counseling, they lost an average of only nine pounds, with most of it regained after a year.

Taubes argues that if overeating were the cause of obesity, then undereating should be the cure. The consistent failure of this "cure" suggests the cause lies elsewhere. The calorie model mistakes a symptom—overeating—for the root cause, ignoring the complex biological drivers of fat accumulation.

Exercise is Not a Weight Loss Tool

Key Insight 2

Narrator: The other pillar of conventional wisdom is that we can exercise our way to leanness. Taubes challenges this with a simple paradox: what would you do to work up a massive appetite for a feast? You'd probably eat lightly and get in a vigorous workout—the very same advice given for weight loss. This inherent contradiction highlights a fundamental problem.

Historical accounts support this. In the 1860s, an obese London undertaker named William Banting was advised by his doctor to take up rowing. Banting found that while his muscles grew stronger, he developed a "prodigious appetite" and his weight actually increased. His doctor promptly told him to stop.

Modern science echoes this experience. In 2007, the American Heart Association and the American College of Sports Medicine admitted that data supporting the idea that high energy expenditure prevents weight gain is "not particularly compelling." Studies on habitual runners show they still tend to get fatter over time, even those running over forty miles a week. The body is an adaptive system; when we expend more energy, it compensates by increasing hunger. Exercise has countless health benefits, but reliable, significant fat loss is not one of them.

Obesity is a Disorder of Hormonal Regulation, Not Physics

Key Insight 3

Narrator: If calories and exercise aren't the primary drivers, what is? Taubes proposes a radical shift in perspective: stop thinking about obesity as a problem of physics and start seeing it as a problem of biology. Specifically, it's a disorder of fat regulation.

He uses a powerful analogy to expose the flaw in the calorie model. If you walk into a room and ask why it's chronically overcrowded, and someone answers, "Because more people are entering than leaving," they haven't explained anything. That's just a description of a crowded room. The real question is why more people are entering. Similarly, saying someone is fat because they consume more calories than they expend is a redundant statement, not an explanation. The real question is why their body is driven to store excess energy as fat.

The answer, Taubes argues, lies in our hormones. Just as hormones regulate growth during puberty, they also regulate fat tissue. Conditions like lipodystrophy, where people lose fat in some parts of their body and gain it in others, prove that fat storage is locally regulated and not dependent on a simple, body-wide energy balance.

Insulin is the Master Regulator of Fat Storage

Key Insight 4

Narrator: The primary hormone controlling fat storage is insulin. When we eat, our body releases insulin to help our cells absorb nutrients. Taubes explains that insulin plays a dual role: it tells our fat cells to pull fat out of the bloodstream and store it, and it simultaneously prevents them from releasing the fat they already hold. In essence, when insulin is elevated, we are in fat-storage mode. We can only burn stored body fat when insulin levels are low.

This process is controlled by key enzymes. Lipoprotein lipase (LPL) sits on the surface of cells and acts like a gatekeeper, pulling fat in. Insulin activates LPL on fat cells. Meanwhile, another enzyme inside the fat cell, hormone-sensitive lipase (HSL), is responsible for breaking fat down so it can be released. Insulin suppresses HSL.

Therefore, any food that significantly raises insulin will promote fat accumulation. This shifts the focus from the amount of calories to the type of calories.

Carbohydrates are the Primary Driver of Insulin

Key Insight 5

Narrator: While all macronutrients affect insulin to some degree, carbohydrates—especially refined grains, starches, and sugars—cause the most dramatic and prolonged spike in insulin levels. This is the core of Taubes's argument. For individuals predisposed to obesity, a diet high in these carbohydrates keeps insulin levels chronically elevated, trapping their bodies in a perpetual state of fat storage.

This isn't a new idea. In 1825, the French gastronome Jean Anthelme Brillat-Savarin observed that the cause of obesity was a diet based on "starchy and floury substances." This was conventional wisdom for over a century. It was only in the latter half of the 20th century, with the rise of the fear of dietary fat, that this knowledge was abandoned in favor of low-fat, high-carbohydrate diets—the very diets that coincided with the explosion of the obesity epidemic.

The story of the "nutrition transition" in populations like the Pima Indians provides stark evidence. When these populations abandoned their traditional, low-carb diets for modern Western foods rich in sugar and refined flour, they experienced catastrophic rates of obesity and diabetes. The fattening agent wasn't just calories; it was the specific hormonal effect of these carbohydrates.

A Healthy Diet Re-evaluates Our Fear of Fat

Key Insight 6

Narrator: The biggest objection to a carbohydrate-restricted diet is that it is necessarily high in fat, which we've been told for decades causes heart disease. Taubes argues this fear is based on surprisingly weak science. He points to the landmark A TO Z Weight Loss Study from Stanford University, which compared the low-carb Atkins diet to low-fat diets like the Ornish diet. The results were stunning: the Atkins group lost more weight and saw better improvements in their heart disease risk factors, including lower triglycerides and higher levels of "good" HDL cholesterol.

Taubes explains that when we restrict carbohydrates, our bodies enter a state of ketosis, where they burn fat for fuel. This metabolic state is not dangerous; it's a natural adaptation. A diet that controls for fattening carbohydrates doesn't have to be unbalanced. It can be rich in meat, fish, eggs, and non-starchy vegetables, providing all essential nutrients. The key is to shift the focus from avoiding fat to avoiding the sugars and starches that drive the hormonal cascade of fat accumulation.

Conclusion

Narrator: The single most important takeaway from Why We Get Fat is that obesity is not a moral failing or a simple accounting error of calories. It is a hormonal disorder. The hormone insulin, primarily stimulated by the carbohydrates we eat, is the principal regulator of fat storage. For those of us prone to weight gain, the refined carbohydrates and sugars of the modern diet are the true culprits, creating a metabolic environment that forces our bodies to accumulate fat.

This reframes the entire conversation around weight. It suggests that the path to a healthy weight isn't about enduring hunger through calorie restriction, but about changing the type of food we eat to change our hormonal signals. The challenge, then, is a profound one: can we unlearn a lifetime of dietary advice and look past the fear of fat to address the real driver of the obesity epidemic?

00:00/00:00