European Commission logo
polski polski
CORDIS - Wyniki badań wspieranych przez UE
CORDIS

Reshaping cortical circuits to decrease binge eating

Periodic Reporting for period 3 - ReCoDE (Reshaping cortical circuits to decrease binge eating)

Okres sprawozdawczy: 2022-07-01 do 2023-12-31

Stress can drive an increase in appetite for high caloric foods, rich in fat and sugar. Though stress can alter food intake and food choices in the majority of people, it is particularly problematic in those individuals vulnerable to develop obesity or eating disorders characterized by binge eating (voracious intake of a large amount of food in a short period of time). The way in which stress affects food choices and food intake is via its action on the brain. However, the precise pathways (i.e. connections between brain regions) that are specifically affected by stress, the mechanisms through which this occurs, and the specific consequences of such changes for feeding beahavior, remain unclear.

This project aims to understand how stress affects pathways in the brain to promote strong intake of tasty food in a short period of time (binge eating). The project has 3 aims:
1. Determine the longer-term changes in brain pathways caused by stress.
2. Unravel the immediate changes in these pathways in response to stress and during binge eating.
3. Assess whether the stress changes in these pathway are responsible for stress eating.

Overall, this project seeks to find ways to address how stress eating is orchestrated by dysfunction brain pathways. This can have relevance for people suffering from weight problems and eating disorders.
The brain comprises multiple brain regions each harboring many brain cells (neurons). Connections between brain cells within and across distinct brain regions are called neural pathways or neural circuits and serve specific functions.
Among those are pathways that promote food intake and others that brake food intake. We have found that a brain region that exerts cognitive control (cortex) is in direct connection with various cell types in another brain region (hypothalamus) with an important role in food intake.

We have found that the connection between those regions is strong, and that within it there are actual multiple parallel connections, some to neurons that are known to promote food intake and others to neurons known to reduce food intake.
We have found that stimulating this overall connection, depending on the exact stimulation parameters chosen, can increase food intake.
Moreover, we have found that stress (known to increase appetite for food, particularly palatable subtypes) alters the strength of connections in these pathways.
In particular stress weakens connection strength in the pathway linked to 'reducing food intake'. Further investigations into this process are ongoing.
Our work has so far revealed characteristics of a neural pathway that was barely known and understood. We have also found that stress has very specific effects on this pathway that we hypothesize play an important role in driving effects of stress on food choices (more towards fat and sugar-rich food). We expect to further unravel the exact effects of stress on the neural pathways linked to promoting and inhibiting food intake. We also expect to find ways to normalize the effects of stress on these neural pathways to thereby limit stress eating behaviors. Finally we expect to find ways to understand how changes in this pathway may affect other critical nodes in the brain to drive their effects.
figure-for-continousreporting-recode-01.jpg