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The Quality of Calories: Competing Paradigms of Obesity Pathogenesis, a Historical Perspective

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ByCrossFit November 14, 2019

“What scientists do and what journalists do are similar in that we’re both supposed to be establishing reliable knowledge about the universe,” Gary Taubes told the audience at the annual CrossFit Health Conference on July 31, 2019. Taubes, an award-winning investigative journalist, has spent the last several decades turning a critical eye toward places where received wisdom in the fields of science and medicine has diverged from reliable knowledge. In this presentation, he evaluates what the experts say about why we get fat and explains why he has become a critic of the consensus.

In assessing the scientific evidence related to the question of why we get fat, Taubes uncovers two hypotheses about the relationship between obesity and various metabolic diseases that lead to premature death. Each hypothesis is associated with unique assumptions about the driving cause of obesity. The first hypothesis suggests obesity causes metabolic diseases. The second suggests whatever causes obesity causes these diseases.

The World Health Organization provides an example of the conventional wisdom associated with the first hypothesis: “The fundamental cause of obesity and overweight is an energy imbalance between calories consumed and calories expended.”

In his research, Taubes sought out the origin of this idea about energy balance. He found it dates to the 1860s and the birth of modern nutrition science in Germany, specifically with the invention of the calorimeter, which measures energy expenditure.

“Our ideas are dependent on the technologies we have to observe the universe,” Taubes explains. “So if all you could observe related to obesity is the intake and expenditure of energy, you end up with a theory related to the intake and expenditure of energy.”

Taubes asks several questions that reveal the problems inherent in the energy balance model: Why don’t obese people compensate by eating less or exercising more? Why is it that some people can be thin without starving? We know men and women develop fat tissue differently, so what is determining the specific areas where fat accumulates? If we know puberty is adipogenic (fat-accumulating) for girls but not boys, why don’t we talk about hormonal forces determining fat accumulation when we talk about these caloric imbalance issues?

After pointing to several holes in the energy balance hypothesis, Taubes explains his reasons for supporting the alternative — the hormonal/regulatory hypothesis — which suggests “obesity is a disorder of excess fat accumulation.” Scientists and physicians have construed obesity as a psychological disorder since the 1930s, when L. H. Newburgh claimed it is caused by “various human weaknesses such as overindulgence or ignorance.” The hormonal/regulatory hypothesis, on the other hand, suggests overeating and sedentary behavior are compensatory effects, not causes of obesity.

In his survey of the history of obesity research, Taubes locates two leading proponents of the hormonal/regulatory hypothesis whose work dates back to pre-war Germany and Austria: Gustav von Bergmann and Julius Bauer. Taubes argues the hypothesis Bergmann and Bauer developed fell out of favor after the Second World War, when Bauer fled Austria, the lingua franca of the medical literature shifted, and people no longer read studies in German.

The hormonal/regulatory hypothesis all but disappeared until 1965, when a group of researchers including Rosalyn Yalow and Solomon Berson discovered a method for measuring fatty acids in the blood, thus uncovering a way to study fat metabolism. They discover insulin is the primary regulator. Since then, several scientists have gone against the consensus of their peers and called for new research on the dysregulation of insulin signaling and fat metabolism. Taubes lists a few notable examples and describes the backlash such research often encounters.

Dr. Robert Atkins provides a telling example. Atkins’ research included support for the hormonal/regulatory hypothesis by demonstrating the positive metabolic effects of a low-carbohydrate diet, but physicians and other members of the scientific community who feared fat more than carbohydrates worked to make Atkins’ name synonymous with quackery. “And in order to get rid of Atkins, you had to get rid of the science behind Atkins,” Taubes explains. “So Atkins was the bath water, the endocrinology was the baby, and by the 1980s, there was no discussion anymore of the hormonal, endocrinological regulation of fat metabolism in obesity textbooks or obesity papers, because if you discuss that, you are led de facto to a low-carbohydrate diet.”


To read a complete transcription of the presentation, click here.

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