CrossFit - Gary Taubes: Why We Get Fat (Unabridged) Part 1
What this video covers
This is Part 1 of Taubes’s full-length address to the CrossFit HQ seminar staff at the October 2011 Trainer Summit in San Diego — the unabridged version of a talk that became a touchstone in the low-carb fitness world. CrossFit founder Greg Glassman introduces him with a story: when Reason magazine ran a critical review of Good Calories, Bad Calories, Taubes’s rebuttal was so airtight, Glassman says, that scientists with no stake in nutrition judged his the side that had the facts and the logic. Taubes then states his mission plainly: getting the medical-research establishment to rethink obesity, which he calls one of the foremost medical problems of the day.
His own route in was personal. As he tells it, he ate the prescribed low-fat, high-carbohydrate diet — oatmeal and apple juice for breakfast, pasta for lunch, not even olive oil in the pasta water, because fat was fattening — exercised an hour a day, and still gained weight year after year. He also lays out the stakes as he sees them: U.S. obesity rates up some 250% in 50 years, diabetes diagnoses up from under 6 million in 1980 to nearly 17 million. And he states the talk’s subtext up front: his claim that whatever makes people fat is also what drives insulin resistance, type 2 diabetes, fatty liver disease, atherosclerosis, cancer, and Alzheimer’s disease. He concedes that the sweep of that claim is exactly why low-carb advocacy has long been dismissed as quackery — it sounds like quackery, he says, but it might be true.
Part 1 then attacks the reigning explanation: what Taubes calls the positive energy-balance hypothesis — obesity as simply consuming more calories than you expend, gluttony and sloth supercharged by what Yale psychologist Kelly Brownell dubbed the “toxic environment” of cheap, aggressively marketed food. Taubes’s objection is methodological before it is nutritional: a hypothesis has to explain the observations, he argues, and this one cannot explain the observations he spent years digging out of the older literature. Merely asking whether the hypothesis is true is treated as heresy, he says — but this is science, and asking is allowed.
His exhibits are population after population with high obesity rates under conditions the hypothesis says should prevent it. The Pima of Arizona, photographed by Harvard anthropologist Frank Russell in 1902: a people who went from prosperity through some thirty “starvation years,” yet showed striking obesity amid poverty. Sioux families on South Dakota’s Crow Creek reservation in the 1920s, living largely on bread and coffee in one- and two-room cabins, where 40% of the women were markedly overweight alongside frank vitamin-deficiency disease. Black families in Charleston, South Carolina, in 1959, living on $9 to $53 a week, with 30% of the women obese. Women in Trinidad during a malnutrition crisis, eating under 2,000 calories a day on a diet that was 21% fat, a third of the women over 25 obese. Chilean factory women doing heavy assembly-line labor — 30% obese, 10% outright malnourished. Mexican Americans in Starr County, Texas, farm and oil-field workers, half the women in their fifties obese, in a county that in 1981 had exactly one restaurant. And Jamaica, where diabetes specialist Richards reported in 1973 that two-thirds of adult women in Kingston were obese, while childhood undernutrition was rampant — and concluded that obesity was itself best understood as a form of malnutrition. If these populations did not get fat from overeating in a toxic environment, Taubes asks, what made them fat? By Occam’s razor, he argues, whatever it was probably made us fat too.
The description outlines where the talk goes from here: Part 2 continues through the obesity literature and its contradictions, arguing that eating less and exercising more neither reverses nor protects against obesity; Part 3 presents the alternative — “obesity is a disorder of fat accumulation,” regulated by insulin, “the fat-storage hormone,” with the practical conclusion that lowering insulin requires restricting carbohydrates, especially high-glycemic starchy ones. Even as a standalone, Part 1 is a complete statement of the negative case.
Key points
- Taubes tells the CrossFit seminar staff his goal is to change how the medical-research establishment thinks about obesity — a change he says he came to personally, after gaining weight year after year on the low-fat diet he had been prescribed.
- He defines the target: the positive energy-balance hypothesis — obesity as caloric imbalance (gluttony and sloth) amplified by the “toxic environment,” Yale psychologist Kelly Brownell’s term for a world of cheap, marketed, energy-dense food.
- His challenge is methodological: a hypothesis must explain the observations, and this one, he argues, has never been asked to.
- His core evidence is a catalogue of poor, malnourished, physically active populations with modern-level obesity rates: the Pima after their “starvation years,” Sioux families on the Crow Creek reservation living on bread and coffee, women in Trinidad eating under 2,000 calories a day, Chilean factory laborers, and Starr County, Texas — a county with one restaurant.
- In Jamaica, he notes, diabetes specialist Richards concluded in the 1970s that obesity in a poor population was itself a form of malnutrition — the opposite of the overnutrition story.
- Taubes’s larger claim, stated as the talk’s subtext: whatever drives fat accumulation also drives insulin resistance, diabetes, fatty liver disease, atherosclerosis, cancer, and Alzheimer’s — a sweep he concedes sounds like quackery but says might be true.
- The talk previews the positive case developed in later parts: obesity as a disorder of fat accumulation, with insulin as the “fat-storage hormone” — and the practical conclusion that lowering insulin means restricting carbohydrates, particularly high-glycemic, starchy ones.
- Delivered to a sympathetic audience, this is advocacy; the claims about energy balance and insulin remain hotly disputed in obesity science.