Over a third of American adults suffer from obesity, a condition characterized by an excess of body fat. Often, this is the result of uncontrolled eating. Anyone who has tried dieting knows that eating less is easier said than done, but new research in PLoS Biology suggests people who are obese have a unique disadvantage when it comes to losing weight. Obesity, they report, kills the tongue’s ability to taste.
The effect of decreased taste sensitivity, as the researchers describe in the study published Tuesday, is that people are compelled to eat more because they’re unsatisfied with what they’ve already tasted. In the past, scientists had already observed that people with obesity suffered from taste deficiency and that their ability to taste could be rescued if those people lost weight, but until now nobody had been able to explain why that happened. In the new study, the team, led by Andrew Kaufman, Ph.D., of Cornell University’s Department of Food Science, shows that it all comes down to changing taste buds.
Everyone has stuck out their tongue in the mirror and looked at their taste buds — pinprick clusters of little red cells dotting the skin like strawberry seeds. The cells in our taste buds register molecules from our food and signal to the brain one of five tastes: sweet, salty, bitter, sour, and umami. Like all cells, those that make up taste buds get old and die about every 10 days, and then new cells grow back to take their place.
Kaufman had a theory, based on his previous work, that obese individuals can’t taste their food as well as healthy counterparts because they have fewer taste buds. To test this, his team took a bunch of healthy mice and made some of them obese by feeding them a 58-percent fat, “obesogenic” diet. After eight weeks of chowing down, the mice were examined for changes in their taste buds.
Just as Kaufman thought, the obese mice had 25 percent fewer taste buds than their lean counterparts. In these mice, apoptosis — that is, programmed cell death — happened more rapidly than usual, offsetting the balance between cell death and regeneration. In addition, they had fewer taste bud progenitor cells — the cells that eventually grow into new taste buds. The net result was fewer functional taste buds, implying a decreased ability to taste (though, of course, the mice couldn’t tell them that).
At this point, it still wasn’t clear what mechanism was shifting the balance of taste bud regeneration, though here, too, Kaufman had a hunch. Obesity is associated with widespread, damaging inflammation in the body, which is mediated by an uptick in levels of the molecule TNF-alpha. It would make sense if TNF-alpha was also involved with the decreased number of taste buds on the obese mice.
As the team looked more closely at the taste buds, they did find high levels of TNF-alpha, suggesting their hunch was correct. The control group of mice that were physically incapable of making TNF-alpha had normal numbers of taste buds, even though they too were obese.
Given the new findings, it seems that controlling inflammation, in theory, could in turn control the untimely death of taste buds, which might help curtail obesity altogether. Often, people have difficulties dieting, not because they feel hungry after eating but because they feel unsatisfied. By giving these people a way to hack their taste buds rather than their food intake, they may have a better chance at beating obesity than people relying on diets alone.