It’s been recognized for a few years that drinking diet sodas can actually cause weight gain, since the phony sweetness of artificial sweeteners disrupts the “predictive relationship” between a sweet taste and caloric satisfaction. In other words, people drink a diet Coke when they are craving a sweet pick-me-up. However, because the soda doesn’t actually contain any calories, the craving remains unsatisfied. The end result is that rodents (and people) end up consuming more calories later on. The craving returns with a vengeance. Here, for instance, is the abstract for a recent paper in Behavioral Neuroscience:
Animals may use sweet taste to predict the caloric contents of food. Eating sweet noncaloric substances may degrade this predictive relationship, leading to positive energy balance through increased food intake and/or diminished energy expenditure. These experiments were designed to test the hypothesis that experiences that reduce the validity of sweet taste as a predictor of the caloric or nutritive consequences of eating may contribute to deficits in the regulation of energy by reducing the ability of sweet-tasting foods that contain calories to evoke physiological responses that underlie tight regulation. Adult male Sprague-Dawley rats were given differential experience with a sweet taste that either predicted increased caloric content (glucose) or did not predict increased calories (saccharin). We found that reducing the correlation between sweet taste and the caloric content of foods using artificial sweeteners in rats resulted in increased caloric intake, increased body weight, and increased adiposity, as well as diminished caloric compensation and blunted thermic responses to sweet-tasting diets. These results suggest that consumption of products containing artificial sweeteners may lead to increased body weight and obesity by interfering with fundamental homeostatic, physiological processes.
So the sweetness of a food is one way the brain keeps track of its intake. More sugar implies more calories, which is why the hypothalamus gets so annoyed when it’s tricked by Splenda. However, the taste of sugar isn’t the only way the brain monitors calories and cravings. According to a new paper in Neuron, the brain also receives rewarding input from metabolic processes that have nothing to do with the tongue. When you eat a big meal, part of the pleasure of the meal comes from the fact that the food is sustenance, fuel, energy. Even shitty food is a little rewarding.
The Duke scientists came up with a clever paradigm for isolating this more indirect rewarding pathway: they studied mice without a functional TRPM5 channel, which is essential for detecting sweetness. As a result, these mutant mice showed no immediate preference for sugar water.
But here comes the cool part of the experiment. The scientists then allowed the mice to spend some time with the sugar water and normal water. After a few hours, it became clear that the mutant mice greatly preferred the sugar water, even though they couldn’t taste the sugar. (A control experiment with sucralose, an artificial sweetener, demonstrated that the rats were responding to the caloric intake, not the sweet taste.)
Finally, the scientists measured dopamine levels (via in vivo microdialysis) in the nucleus accumbens (a brain area that processes rewards) in the mutant mice and normal mice.* While normal mice exhibited an increase in dopamine in response to both fake sugar and real sugar – the reward was the sweet taste – the mutant mice only demonstrated a dopaminergic spike when consuming genuine sugar water. What they enjoyed were the calories. As the authors conclude:
We showed that dopamine-ventral striatum reward systems, previously associated with the detection and assignment of reward value to palatable compounds, respond to the caloric value of sucros in the absence of taste receptor signaling. Thus, these brain pathways…also perform previously unidentified functions that include the detection of gastro-intestinal and metabolic signals.
Obviously, this research has some implications for the obesity epidemic. If we can somehow disrupt this dopamingeric pathway, it might be possible to erase the subtle pleasure we get from ingesting lots of energy. But I think the data also helps explain why diet sodas so often backfire, at least from a weight loss perspective. When the brain tastes something sweet, it makes a prediction that calories are coming. It waits for that dopamine signal from the stomach. But when no calories arrive – the sweetness is indigestible – that useful and predictive relationship is disrupted. It’s as if the brain can no longer trust the tongue.
Update: Yet another reason to avoid fake sugar:
Splenda is not satisfying–at least according to the brain. A new study found that even when the palate cannot distinguish between the artificial sweetener and sugar, our brain knows the difference.
At the University of California, San Diego, 12 women underwent functional MRI while sipping water sweetened with either real sugar (sucrose) or Splenda (sucralose). Sweeteners, real or artificial, bind to and stimulate receptors on the taste buds, which then signal the brain via the cranial nerve. Although both sugar and Splenda initiate the same taste and pleasure pathways in the brain–and the subjects could not tell the solutions apart–the sugar activated pleasure-related brain regions more extensively than the Splenda did. In particular, “the real thing, the sugar, elicits a much greater response in the insula,” says the study’s lead author, psych ia trist Guido Frank, now at the Univer sity of Colorado at Denver. The insula, involved with taste, also plays a role in enjoyment by connecting regions in the reward system that encode the sens a tion of pleasantness.
Although Splenda elicits less overall activity within the brain, the researchers were surprised to find that the artificial sweetener seems to inspire more communication between these regions. “Looking at the connection between the taste areas, Splenda is stronger,” Frank says. He suggests that when we taste Splenda, the reward system becomes activated but not satiated. “Our hypothesis is that Splenda has less of a feedback mechanism to stop the craving, to get satisfied.”