Good Calories, Bad Calories

From the 1920s through the 1960s, a series of discoveries in the basic science of fat metabolism led to a revolution in the understanding of the role of insulin and the regulation of fat tissue in the human body. This era began with a handful of naïve assumptions: that fat tissue is relatively inert (a “garbage can,” in the words of the Swiss physiologist Bernard Jeanrenaud); that carbohydrates are the primary fuel for muscular activity (which is still commonly believed today); and that fat is used for fuel only after being converted in the liver into supposedly toxic ketone bodies. The forty years of research that followed would overturn them all—but it would have effectively no influence on the mainstream thinking about human obesity.

Those who paid attention to this research either had no influence themselves—Alfred Pennington comes to mind—or were so convinced that obesity is caused by overeating that they couldn’t imagine why the research would be relevant. From the 1950s onward, clinical investigators studying and treating obese patients, as Hilde Bruch commented, seemed singularly uninterested in this research. “Until recently, knowledge of the synthesis and oxidation of fat was quite rudimentary,” Bruch wrote in 1957. “As long as it was not known how the body builds up and breaks down its fat deposit, the ignorance was glossed over by simply stating that food taken in excess of body needs was stored and deposited in the fat cells, the way potatoes are put into a bag. Obviously, this is not so.” By 1973, after details of the regulation of fat metabolism and storage had been worked out in fine detail, Bruch found it “amazing how little of this increasing awareness…is reflected in the clinical literature on obesity.”

There are three distinct phases of the revolution that converged by the mid-1960s to overturn what Bruch called the “the time-honored assumption that fat tissue is metabolically inert,” and the accompanying conviction that fat only enters the fat tissue after a meal and only leaves it when the body is in negative energy balance.

The first phase began in the 1920s, when biochemists realized that the cells of adipose tissue have distinct structures and are not, as was previously believed, simply connective tissue stuffed with a droplet of oily fat. Researchers then demonstrated that the adipose tissue is interlaced with blood vessels such that “no marked quantity of fat cells escapes close contact with at least one capillary,” and that the fat cells and these blood vessels are regulated by “abundant” nerves running from the central nervous system.

This led to the revelation that the fat in the cells of the adipose tissue is in a continual state of flux. This was initially the work of a German biochemist, Rudolf Schoenheimer. In the early 1930s, while working at the University of Freiburg, Schoenheimer demonstrated that animals continually synthesize and degrade their own cholesterol, independent of the amount of cholesterol in the diet. After Hitler came to power in January 1933, Schoenheimer moved to New York, where he went to work at Columbia University. It was in New York that Schoenheimer collaborated on the development of a technique for measuring serum cholesterol and, by doing so, launched the medical profession’s obsession with cholesterol levels. Then, with David Rittenberg, he developed the technique to label or tag molecules with a heavy form of hydrogen known as deuterium^*111 so that their movement through the metabolic processes of the body could be followed. Schoenheimer and Rittenberg put this technique to work studying the metabolism of fat, protein, and carbohydrates in the body.