Obesity now affects more than 600 million people worldwide and is increasingly becoming a serious public health problem. But despite this, we still don’t completely understand what causes people to become obese. Scientists know it’s an interaction between our genes and our environment, including the unique environment of microbes that live in our guts, but they are still unsure of how exactly these factors come together to cause someone to become overweight and eventually obese.
A new study out in the journal Cell Metabolism suggests that a popular, yet controversial theory on why our genes make us more susceptible to being obese--known as the thrifty-gene hypothesis--might not hold water, which may cause many researchers to continue to rethink obesity’s root causes and subsequently how they will go about treating it.
The idea behind the thrifty-gene hypothesis is this: back in the day, when we routinely went through periods of famine, those individuals who had genes that made them more likely to store fat were at an advantage compared to others. But now, because we don’t experience these famines anymore, those fat storing genes are actually putting people at a disadvantage by having them store fat for fasting periods that don’t end up happening.
Despite the popularity and simplicity of the idea, researchers have continually poked holes in its thesis for years. If these genes were so advantageous, why did only some people and not others inherit them? Shouldn’t they have, by now, spread to the entire population? To figure it out, researchers in this study looked at 115 genes known to be associated with obesity and tried to identify evidence that showed the genes to be under positive selection, also called Darwinian selection, where a gene that provides an advantage to the individual sweeps through the entire population. Typically, if a gene has very little variation, then it is more likely to be under positive selection.
What they found, though, was that only nine out of those 115 gene variants showed signs of positive selection. And of those nine, only four showed positive selection for fat storage; the other five actually showed positive selection for leanness.
“This is probably the hardest evidence so far against the thrifty gene hypothesis,” John Speakman, a coauthor of the paper wrote in the release. Speakman says their goal now is for researchers to think beyond the thrifty gene hypothesis as the reason for the genetic cause of obesity.
While overall, the results do lean away from the popular hypothesis, the study did have its limitations. As a metric for obesity, the study used BMI (body mass index) which only takes into account body weight and height and isn’t often considered the best measurement for determining if a person is obese. Further, the method they used for determining if a gene variant was positively selective works best if the variant in question is focused on a single mutation where natural selection is quick to eliminate other variants. In the future, the researchers plan to test their results using other toolsets. For now, though, the results of this study could still be enough to cause scientists studying the genetic factors of obesity to focus on other reasons for obesity to arise in an individual.