A study published recently in the New England Journal of Medicine has rekindled hope among the overweight that their cries of “I have a slow metabolism” just might be true. According to the study, it’s our genes that are determining whether our bodies store food as fat or burn it up.
Turning to an extensive, eight-year collection of DNA data, the researchers from Massachusetts Institute of Technology, Harvard University and Broad Institute of Cambridge were able to show how a previously discovered obesity-related gene called FTO influences the activity of eight additional genes thought to be involved in regulating metabolism.
The study subjects were healthy Europeans whose genes were prompting developing cells to become white fat (storage lockers) or brown fat (heat pumps). Scientists have known for years that brown or beige fat cells are the kind we want more of, while white fat cells are not.
While this research is encouraging and could lead to the discovery of a drug or other treatment to “cure” obesity, it is far too soon to throw away the bathroom scale and the healthy diet and exercise regimens. I suspect that this “fat gene” accounts for only about seven to 10 pounds of fat, a small pinch in the obesity epidemic.
In fact, in another study of the impact of genes on obesity conducted earlier in 2015, scientists found that some 97 gene variants explained only 3% of the variation in the body mass index (BMI) of more than 300,000 participants.
The researchers in this latest undertaking admit that having a faulty FTO gene does not even necessarily mean that someone will become obese. People found to have the gene from both their mother and father weighed a miniscule seven pounds more on average than those without the gene, team member Manolis Kellis said.
While the study is being touted as a big deal in some circles — one exuberant doctor and associate New England Journal of Medicine editor actually called it that, adding, “Our fat cells play a role in how food gets used and you now have a pathway for drugs that can make those fat cells work differently”— I maintain that the bigger issue is the quality and quantity of the foods we’re eating. Of greater concern too is the impact of the food industry’s deliberate efforts to sell more junk food by tinkering with ingredients known to trigger addictive eating.
Even this study’s team members, led by Harvard genetics specialist Melina Claussnitzer, refrain from predicting where their data might lead. In their article summary, they state what they learned, not how they think it will help anyone lose weight.
On the other hand, some independent experts have read about this work and gushed enthusiastically about its (positive) implications.
Cell biologist Shingo Kajimura of UC San Francisco told Science magazine that this new information about how FTO works in fat cells “is of huge clinical relevance” and that the study “suggests that beige fat is playing an important role in human obesity.” In the same article, Kellis went so far as to predict that doctors in the future would be able to turn genes on or off, for “energy storage or energy dissipation.” Kajimura cautions, however, that it is not yet clear how increasing beige fat would prompt weight loss.
For my money, I like the reactions of two laypeople who read a newspaper article about this study by Claussnitzer et al and had some rather telling comments. “Why do we care?” wrote one. “Maybe we could focus on cancer.” Another suggested that simply paying attention to one’s diet and exercise rather than “such research which comes out every week” was a better idea. “People need to stop micro-analyzing such things … It is important to not go into this hereditary stuff,” she wrote.
Although it would be interesting to have a pill that would let people (especially food addicts) eat anything they wanted without gaining weight or experiencing other negative consequences, let’s not get ahead of ourselves here with false hope that this might happen any time soon — or ever.