Of mice and stress
The relationship between stress and food can sometimes be rather toxic. “Stress can have a direct impact on food intake, causing people to binge on fatty and sugary foods,” explains Frank Meye(opens in new window), a researcher at UMC Utrecht(opens in new window). But what exactly does stress do to the brain that triggers this binge eating? With the support of the EU-funded ReCoDE project, Meye decided to find out. Using mice models, the European Research Council(opens in new window) supported project looked at which brain circuits are linked to stress eating.
The brain and its role in food intake
The project focused on a region in the front of the brain called the prefrontal cortex (PFC), which is known to play an important role in decision-making, impulse control and formulating behaviour strategies. “It’s also a very stress-sensitive region and one associated in eating disorders and obesity,” adds Meye. Researchers also looked at another brain region called the lateral hypothalamic area (LHA). According to Meye, this region plays a big role in food intake. “Within the LHA you have neurons that are actively involved in driving our appetite for tasty foods and also neurons that are involved in reducing our appetite,” he says. The neurons in the LHA also happen to receive a strong input signal from neurons in the PFC. “Knowing this, we set out to test our hypothesis that stress would change the communication between PFC and LHA in such a way that the LHA’s ‘drive for food’ neurons become more active and the LHA’s ‘brake for food’ neurons become less active, to the point that enhanced appetite for food and even binge eating follows,” notes Meye.
Stress eating starts after the fact
What researchers discovered is that, when a mouse is stressed, there is an immediate reactivity of those PFC neurons that project to the LHA. However, what was particularly interesting is what researchers saw a day after the stress event. On the one hand, they found a strengthening of the communication of PFC neurons and some of the LHA cells that increase food intake when active. On the other hand, they saw that the stress event weakened the communication of PFC neurons and those LHA cells responsible for decreasing food intake. Researchers further noted that these protracted plasticity changes in the PFC-LHA network coincided with the mice exhibiting an increase in appetite and binge-eating behaviour. “That this happened a day after the stress is important as it highlights how it’s not necessarily in the peak of the stress that one thinks about eating but a bit afterwards,” remarks Meye.
Opening the door to new ways of treating eating disorders
Another key outcome was the finding that the PFC’s role in food intake only emerges in the stressed context. “When we inhibited the PFC-LHA pathway in stressed mice, something interesting happened – they ate a normal amount of food, as if they weren’t stressed at all,” says Meye. It’s groundbreaking discoveries such as this that could pave the way towards new ways of treating eating disorders and obesity. “Understanding the neurobiology underlying stress’s effects on eating may, in the longer run, provide targets for intervention strategies, with a biological basis, for treating such conditions,” concludes Meye.
