Why Do We Carry Genes That Make Us Fat?
Obesity and diabetes are rising worldwide, yet evolution should have eliminated harmful genes. The thrifty gene hypothesis and the drifty gene hypothesis ry to explain why humans still carry them.
Obesity and type 2 diabetes are among the most pressing health concerns of modern life. What makes it more puzzling is that these conditions have a strong genetic component, yet evolution is expected to weed out genes that harm survival. Why, then, would so many people carry genes that seem to predispose them to these diseases? Two competing evolutionary theories, the Thrifty Gene Hypothesis and the Drifty Gene Hypothesis, attempt to answer this question.
The Thrifty Gene Hypothesis
Proposed in 1962 by geneticist James Neel, the thrifty gene hypothesis suggests that our ancestors evolved genes that helped them survive times of famine. These "thrifty" genes made people highly efficient at storing fat during periods of food abundance, which they could then use during lean times. In an era of unpredictable food supply, this was a survival advantage. So, during the time of the feast, humans stored fat, which can be used during times of famine.
Neel's idea was widely accepted for decades. As famine has been a recurring theme in human history, many researchers found it plausible that natural selection favored individuals who could build up fat quickly. However, in the modern world, where food is abundant and physical activity is limited, the same genes that once helped our ancestors survive now make us vulnerable to obesity and diabetes.
Despite its appeal, recent studies have questioned the validity of the hypothesis. For example, evolutionary biologist John R. Speakman argues that if these thrifty genes were so advantageous, they should have become nearly universal in human populations. Nevertheless, not everyone is obese. Also, detailed historical data show that famines weren’t frequent or deadly enough to create the strong selection pressure required for such genes to spread rapidly.
The Drifty Gene Hypothesis
In response to the flaws in the thrifty gene idea, Speakman proposed an alternative in 2008: the drifty gene hypothesis. According to this theory, obesity-related genes didn't spread because they were helpful. They spread because they were neutral and drifted into the population by chance.
The drifty gene hypothesis is based on the idea that early humans were once at high risk of being eaten by predators, so genes that kept body weight in check (so people could run and escape) were under strong selection. But around 2 million years ago, with the advent of fire, weapons, and group living, humans became top predators. The selective pressure to stay lean disappeared, and the regulation of body fat started to drift without evolutionary checks. Some people ended up with genes that allow them to gain weight easily, and others didn’t.
A Scientific Debate
While the thrifty gene hypothesis offers a purposeful story of survival, it lacks robust genetic and evolutionary evidence. On the other hand, the drifty gene hypothesis doesn't assume fatness was ever useful. It suggests that the variation in body fat regulation is a product of random evolutionary processes.
Modern studies, including genome-wide studies, have found little support for widespread positive selection at obesity-related genes. Instead, the genetic architecture of obesity seems to fit better with the drifty gene view.
In the end, this debate is not just academic. Understanding the roots of obesity can reshape public health approaches. This also reminds us that blaming individuals for their weight may ignore a much deeper evolutionary and genetic reality.
Reference:
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Speakman JR. Thrifty genes for obesity, an attractive but flawed idea, and an alternative perspective: the ‘drifty gene’ hypothesis. Int J Obes (Lond). 2008;32(11):1611–7. doi: 10.1038/ijo.2008.161.
Southam L, Soranzo N, Montgomery SB, Frayling TM, McCarthy MI, Barroso I, et al. Is the thrifty genotype hypothesis supported by evidence based on confirmed type 2 diabetes- and obesity-susceptibility variants? Diabetologia. 2009;52(9):1846–51. doi: 10.1007/s00125-009-1419-3. PMID: 19526209; PMCID: PMC2723682.