Sugar-free drinks may make sweet-detecting circuits numb to the real stuff

By Janet Raloff

Web edition: June 13, 2012
Print edition: July 14, 2012; Vol.182 #1 (p. 14)

By baffling the brain, saccharin and other sugar-free sweeteners — key weapons in the war on obesity — may paradoxically foster overeating.

At some level, the brain can sense a difference between sugar and no-calorie sweeteners, several studies have demonstrated. Using brain imaging, San Diego researchers now show that the brain processes sweet flavors differently depending on whether a person regularly consumes diet soft drinks.

“This idea that there could be fundamental differences in how people respond to sweet tastes based on their experience with diet sodas is not something that has gotten much attention,” says Susan Swithers of Purdue University in West Lafayette, Ind. A key finding, she says: Brains of diet soda drinkers “don’t differentiate very well between sucrose and saccharin.”

Erin Green and Claire Murphy of the University of California, San Diego and San Diego State University recruited 24 healthy young adults for a battery of brain imaging tests. Half reported regularly drinking sugar-free beverages, usually at least once a day. The rest seldom if ever consumed such drinks. While the brain scans were underway, the researchers pumped small amounts of saccharin- or sugar-sweetened water in random order into each recruit’s mouth as the volunteer rated the tastes.

Both the diet soda drinkers and the nondrinkers rated each sweetener about equally pleasant and intense, Green and Murphy report in an upcoming Physiology & Behavior. But which brain regions lit up while making those judgments differed sharply based on who regularly consumed diet drinks.

Certain affected brain regions are associated with offering a pleasurable feedback or reward in response to desirable sensations. And compared with those who don't drink diet soda, the diet soda drinkers “demonstrated more widespread activation to both saccharin and sucrose in reward processing brain regions,” the researchers say.

One of the strongest links seen was diminishing activation of an area known as the caudate head as a recruit’s diet soda consumption climbed. This area is associated with the food motivation and reward system. Green and Murphy also point out that decreased activation of this brain region has been linked with elevated risk of obesity.

The new findings may help explain an oft-observed association between diet soda consumption and weight gain, the researchers say. Once fooled, the brain’s sweet sensors can no longer provide a reliable gauge of energy consumption.

It’s something Swithers’ group demonstrated two years ago in rats. Animals that always received a saccharin-sweetened yogurt learned to modulate their food intake to account for the sweetener’s failure to deliver calories. But animals that alternately got saccharin- and sugar-sweetened yogurts blimped out, gaining substantially more body fat.

“The brain normally uses a learned relationship between sweet taste and the delivery of calories to help it regulate food intake,” Swithers explains. But when a sweet food unreliably delivers bonus calories, the brain “suddenly has no idea what to expect.” Confused, she says, this regulator of food intake learns to ignore sweet tastes in its predictions of a food’s energy content.