Stephan Guyenet, a neurobiologist who studies the neurobiology of body fat regulation, wrote a long, detailed critique of Gary Taubes’ book, Good Calories, Bad Calories on his terrific blog, Whole Health Source.
A couple of weeks ago on Gweek, I reviewed Taubes’ followup book, Why We Get Fat: And What to Do About It, which is a slimmed down, easier-to-grok version of Good Calories, Bad Calories. I hope Taubes responds to this interesting critique. But he hasn’t posted to his blog since April.
What I want to discuss is a hypothesis. It’s the idea, championed by Gary Taubes, that carbohydrate (particularly refined carbohydrate) causes obesity by elevating insulin, thereby causing increased fat storage in fat cells. To demonstrate that I’m representing this hypothesis accurately, here is a quote from his book Good Calories, Bad Calories:
This alternative hypothesis of obesity constitutes three distinct propositions. First, as I’ve said, is the basic proposition that obesity is caused by a regulatory defect in fat metabolism, and so a defect in the distribution of energy rather than an imbalance of energy intake and expenditure. The second is that insulin plays a primary role in this fattening process, and the compensatory behaviors of hunger and lethargy. The third is that carbohydrates, and particularly refined carbohydrates– and perhaps the fructose content as well, and thus perhaps the amount of sugars consumed– are the prime suspects in the chronic elevation of insulin; hence, they are the ultimate cause of common obesity.
There are three parts to this idea. I’ll discuss them each separately. I know many people are expecting (hoping for?) a bitter takedown of Gary Taubes, but that’s not what’s going to happen. I don’t feel bitter, but I do think some scientific wrongs need to be righted, for the sake of the ancestral health community as a whole. I also acknowledge that there is a lot of useful information in Taubes’s books.
Part I: A Defect of Fat Metabolism?
The first part of this hypothesis states that energy balance is not the ultimate cause of fat gain, it’s the proximal cause. That is, Taubes is not disagreeing with the first law of thermodynamics: he understands that fat accumulation depends on how much energy is entering the body vs. leaving it. However, he feels that the entire industrialized world didn’t just wake up one morning and decide to eat more calories, therefore something must be driving the increased calorie consumption.
He cited the research of Drs. Jules Hirsch and Rudy Leibel, various underfeeding and overfeeding studies, lipectomy studies, and evidence from genetically obese rodents, to demonstrate that body fatness is biologically regulated rather than being the passive result of voluntary food intake and exercise behaviors. He then advances the idea that it’s an alteration in this body fat regulatory system that is behind obesity. This may sound familiar because I’ve written about it several times on this blog. So far, so good.
This is where he should have mentioned leptin signaling, which would have taken the book [in] a scientifically accurate direction. Leptin is the system that Drs. Jules Hirsch and Rudy Leibel have shown in carefully controlled human studies is responsible for the metabolic defect he’s getting at (1). It’s also the system that is mutated in the genetically obese rodents he discusses (2, 3). Yet it receives no mention in the book. This is a fork in the road, where Taubes discards a plausible hypothesis in favor of an indefensible one.
The Carbohydrate Hypothesis of Obesity: a Critical Examination