Could artificial sweeteners make people more hungry?
You may be relying on them to shed those extra kilos, but turns out, artificial sweeteners may actually be making you eat more.
A comprehensive new study co-led by the University of Sydney has revealed for the first time why this response occurs.
The results shed light on the effects of artificial sweeteners on the brain in regulating appetite and in altering taste perceptions.
Researchers identified a new system in the brain that senses and integrates the sweetness and energy content of food.
"After chronic exposure to a diet that contained the artificial sweetener sucralose, we saw that animals began eating a lot more," said lead researcher Greg Neely, adding "Through systematic investigation of this effect, we found that inside the brain's reward centres, sweet sensation is integrated with energy content. When sweetness versus energy is out of balance for a period of time, the brain recalibrates and increases total calories consumed."
In the study, fruit flies that were exposed to a diet laced with artificial sweetener for prolonged periods (more than five days) were found to consume 30 percent more calories when they were then given naturally sweetened food.
"When we investigated why animals were eating more even though they had enough calories, we found that chronic consumption of this artificial sweetener actually increases the sweet intensity of real nutritive sugar, and this then increases the animal's overall motivation to eat more food," said Neely.
The researchers also found artificial sweeteners promoted hyperactivity, insomnia and decreased sleep quality - behaviours consistent with a mild starvation or fasting state - with similar effects on sleep also previously reported in human studies.
To discover whether artificial sweeteners also increased food intake in mammals, Herbert Herzog's lab from Garvan then replicated the study using mice. Again the mice that consumed a sucralose-sweetened diet for seven days displayed a significant increase in food consumption, and the neuronal pathway involved was the same as in the fruit flies.