Scientists affiliated with Montreal's University Hospital Research Centre (CR-CHUM) and the university's Faculty of Medicine are undertaking an advanced neuro-scientific study which may be able to shed light on the line in the Austin Powers' film "I eat because I'm depressed and I'm depressed because I eat".

In the April 17 issue of the International Journal of Obesity, Stephanie Fulton and Sandeep Sharma published a study entitled 'Diet-induced obesity promoted depressive-like behavior that is associated with neural adaptations in brain reward circuitry', which explains the relationship between high-fat diets and depressive symptoms.

Dr. Fulton explains: "In addition to causing obesity, rich foods can actually cause chemical reactions in the brain in a similar way to illicit drugs, ultimately leading to depression as the 'come-downs' take their toll."

It is the start of a vicious circle when 'food-highs' are used as a means to tackle depression. The process is comparable to that of drug addicts.

Fulton declares:

"Data shows that obesity is associated with increased risk of developing depression, but we have very little understanding of the neural mechanisms and brain reward patterns that link the two. We are demonstrating for the first time that the chronic consumption of palatable, high-fat diets has pro-depressive effects."

Dopamine is a chemical molecule in the brain of animals and humans that controls the brain's reward and pleasure centers. It enables people to not only see rewards but also to take action to move towards them by encouraging individuals to learn certain kinds of behavior.

The researchers fed different kinds of food to mice and monitored the food's impact on the animals' behavior. They used various scientifically proven techniques whilst contributing to improve them in order to assess the link between food rewards in mice and the animals' subsequent behavior and emotions. Their experiment is demonstrated in a video. They also examine the mice' brains in order to note any changes.

They observed that mice that received a higher-fat diet showed signs of being anxious by avoiding open areas, as well as signs of depression, given that they made less effort in trying to escape when trapped. They also observed that the experiences physically altered the animals' brains.

For instance, CREB, a molecule that controls the activation of genes involved in brain function is much more activated in the brains of mice that had a higher-fat diet. CREB is also widely recognized for contributing to memory function. The team also noted that mice on a higher fat diet exhibit higher corticosterone levels, which is a hormone linked to stress.



Fulton and her team are collaborating closely with other research networks in order to shed more light on the biological reasons for obesity and obesity related diseases, including type 2 diabetes, cardiovascular diseases, some types of cancer as well as depression.

Fulton declares:

"Although popular culture jokes about these illnesses and even mocks the people who are suffering, obesity is a serious and major public health issue that already affects hundreds of millions of people. As a society, we must avoid creating stigma and discriminating against obese and depressed people. With regards to research, it is urgent that we identify the molecules and neural pathways involved in obesity and obesity-related illnesses. My colleagues and I are committed to identifying the brain circuitry involved in these diseases and to improving the tools available to researchers working in the same field."

Written By Petra Rattue