June 2

The Thrifty Gene Theory: Survival of the Fattest


Below is an approximation of this video’s audio content. To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video.

It’s been said that “Nothing in biology makes sense except in the light of evolution.” The known genetic contribution to obesity may be small, but in a certain sense, you could argue, it’s all in our genes. The excess consumption of available calories may be hardwired into our DNA.

We were born to eat. Throughout most of human history and beyond, we existed in survival mode, in a context of unpredictable scarcity. So, we’ve been programmed with a powerful drive to eat as much as we can, while we can, and just store the rest for later. Food availability could never be taken for granted, so those who ate more in the moment and were best able to store more fat for the future might better survive subsequent shortages to pass along their genes. So, generation after generation, millennia after millennia, those with lesser appetites may have died out, and those who gorged may have selectively lived long enough to pass along their genetic predisposition to eat and store more calories. That may be how we evolved into such voracious calorie-conserving machines. Now that we’re no longer living in such lean times, though, we’re no longer so lean.

What I just described is the “thrifty gene” concept proposed in 1962: the proposal that obesity is the result of a “mismatch” between the modern environment and the environment in which we evolved. It’s like we’re now polar bears in a jungle. All that fur and fat may have given them an edge up in the Arctic, but would be decidedly disadvantageous in the Congo. Similarly, a propensity to pack on the pounds may have been a plus in prehistoric times, but can turn into a liability when our scarcity-sculpted biology is plopped down into the land of plenty. So, it’s not gluttony or sloth. Obesity may simply be a normal response to an abnormal environment.

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Much of our physiology is finely tuned to stay within a narrow range of upper and lower limits. If we get too hot, we sweat; if we get too cold, we shiver. Our body has mechanisms to keep us in balance. In contrast, our bodies have had little reason to develop an upper limit to the accumulation of body fat. In the beginning, there may have been evolutionary pressures to keep lithe and nimble in the face of predation. But, thanks to things like weapons and fire, we haven’t had to outrun as many saber-tooth tigers for about two million years or so. This may have just left our genes with the one-sided selection pressures to binge on every morsel in sight, and stockpile as many calories onto our bodies as possible.

What was once adaptive is now a problem––or at least so says the thrifty gene hypothesis that originated more than a half century ago. It provides a simple and elegant explanation for the modern obesity epidemic and was quickly embraced by scientists and lay people alike. Although Neel later distanced himself from the original proposal, despite remaining mostly theoretical, the basic premise remains largely accepted by the scientific community. The implications are profound.

In 2013, the American Medical Association voted to classify obesity as a disease (against the advice of their own Council on Science and Public Health). Not that it necessarily matters what we call it (a rose by any other name would cause just as much diabetes), but disease implies dysfunction. Bariatric drugs and surgery are not correcting some anomaly of human physiology. Our bodies are just doing what they were designed to do in the face of excess calories. Rather than some sort of disorder, weight gain is largely a normal response, by normal people, to an abnormal situation. More than 70 percent of Americans are now overweight—it’s literally normal.

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A body gaining weight when excess calories are available for consumption is behaving normally. Efforts to curtail such weight gain with drugs or surgery are not efforts to correct an anomaly in human physiology, but rather to deconstruct and reconstruct its normal operations at the core.

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