The Harvard Gazette recently published a story about new research out of Harvard Medical School that “raises new questions about weight gain and energy use in the general obese population.” This study represents just one of many that seek to find the a gene that determines a complex human trait, a pursuit that I think is not only fruitless but also short-sighted.
Researchers at Boston Children’s Hospital focused on a gene called Mrap2, which produces melanocortin reception accessory protein, which they thought might have something to do with energy homeostatis. They genetically modified mice which did not have Mrap2, and found that the mice without this gene gained weight while eating the same amount of food as normal mice, suggesting that this gene can somehow trigger weight gain. In a screening of nearly 500 obese humans, the researchers found four people with mutant Mrap2 genes. They suggest that this gene may be one of possibly many that can lead to obesity in humans. The study was published this month in Science, a prestigious scientific journal.
Research on the genetic origins of obesity seems to be motivated in part by a sympathetic attempt to prove that the American “obesity epidemic” isn’t only the fault of working-class Americans eating bad food and not knowing how to exercise—“look, it’s in their genes!” This is a perhaps noble, although certainly misguided, exercise. (See Taonga Leslie’s HPR piece for more on this issue.) Certainly, American discussions about obesity should move away from rhetoric that stigmatizes and blames fat people for not fitting a white upper-middle-class standard of beauty and lifestyle. But “don’t blame them, they were born that way” is not an adequate response.
Research on the genetic cause of obesity is also motivated by a general compulsion among scientists to search for the “gene for” various human characteristics. Since Darwin, scientists have been interested in the hereditary nature of human morphological and behavioral traits. This interest sparked the research that fed into eugenics, a field that purported to show the hereditary nature of such unsavory social characteristics as alcoholism, “imbecility,” unemployment, mental illness, and even ugliness. As history demonstrates, the field of eugenics motivated the mass sterilization of Native Americans in the US and the mass extermination of Jews, Roma people, and homosexuals in the Holocaust.
Biology textbooks now dismiss eugenics as a flawed experiment in Social Darwinism. Modern biology assumes that almost all human characteristics—whether physical traits or behaviors—are influenced by many different genes as well as the interaction of those genes with environmental factors. Yet scientists are still fascinated by the possibility of finding genes that cause, or are highly correlated with, interesting human traits. Dozens upon dozens of labs spending their time searching for the “gene for depression,” the “gay gene,” the “gene for baldness,” or the “gene for intelligence.” Some of these traits are more clearly hereditary than others. It’s much more likely that groups of kids who score well on IQ tests do so because of the education system they’ve been raised in, not because of genetic commonalities. Nonetheless, billions of dollars of NIH grant money goes into searching for the genetic origins of this and other societally important human characteristics.
I am sure that this Harvard Medical School study was well peer-reviewed and demonstrated statistically significant data. If the researchers want to continue looking at this gene, they should compare the rate of Mrap2 mutations among their obese population sample with a random sample of non-obese humans to see if genetic mutation at that site is actually correlated with obesity. They should also investigate the pathway by which a decrease in melanocortin reception accessory protein might lead to obesity.
And what if the researchers at HMS have found a genetic mutation for fatness? Will doctors screen embryos with that gene out from the human population using pre-implantation genetic diagnosis, as we have for Tay-Sachs Disease, allowing parents to select for skinny kids? Will American stop stigmatizing fat people with this gene, forgiving them because they were “born that way”? In the end, none of this would have any effect whatsoever on the lives of most people counted as obese by US medical standards. And if the NIH and HMS really care about discerning the causes of obesity today, they should stop funding a search for the “gene for” fatness and start looking at the structural issues that contribute to obesity in this country and around the world.