Inflammation in the brain region due to sugar and saturated fat intake leads to depressive behavior.
Highlights
- A diet rich in saturated fat and sugar not only leads to obesity, it creates inflammation in the brain.
- Nucleus accumbens, a part of the brain that controls mood and reward is affected due to high fat and sugar in the diet.
- The inflammation in the brain is found to be the reason behind depressive, anxious and compulsive behaviors associated with metabolic dysfunction and obesity.
The metabolic impairments observed with the saturated high-fat diet, including hyperinsulinemia and glucose intolerance, are associated with the development of type 2 diabetes.
Fulton and her team of researchers worked with two groups of mice fed a diet containing the same number of calories every day, 50% of which were from fat. One of the groups was fed the saturated fat diet, while the other received monounsaturated fat. The third group of mice was fed a low-fat diet.
After 12 weeks, obesity, anxiodepressive behaviors and the metabolic changes associated with prediabetes were found in the group which had the diet rich in saturated fat. The depressive, anxiety and compulsive behaviors and the metabolic changes observed with the diet rich in saturated fat were not observed with a diet rich in monounsaturated fat, the type of fat found in olive oil.
"The animals with the diet rich in saturated fat voluntarily consumed more calories," said Léa Décarie-Spain, the study's first author and a PhD student in the laboratories of Fulton and colleague Thierry Alquier.
Many studies conducted on humans have shown that a Mediterranean diet, low in saturated fat, protects against depression. In this study, the researchers were able to identify neuronal mechanisms that give rise to depressive behavior elicited by the diet-induced obesity.
"This manipulation succeeded in protecting the mice eating the diet rich in saturated fat from brain inflammation; consequently, the signs of depression and anxiety and the compulsive sugar seeking disappeared," explained Décarie-Spain. These findings encourage further research into anti-inflammatory interventions that could inhibit depression caused by immune activity in the nucleus accumbens.
This discovery is also a good illustration of the vicious circle that can be experienced by obese individuals. "Poor diet quality along with metabolic disturbances can lead to negative emotional states, which can stimulate the quest for comfort through food, and thereby lead to compulsive behavior," noted Décarie-Spain.
Saturated fat is found mainly in palm oil, widely used in the processed food industry, as well as in products of animal origin. This study was conducted with animals, but it is believed that the mechanism that occurs in the nucleus accumbens of humans is similar.
"We hope that this study will help educate people about the importance of diet, not only because of the link with cardiovascular diseases and certain cancers but also because of the neurological and psychiatric problems that are increasingly associated with obesity," said Fulton. "We also hope that our results will put pressure on the food industry to reduce the saturated fat content in foods."
A few cookies or a hamburger from time to time won't bring on a case of depression, the researchers cautioned. "We should simply avoid eating such foods in excess in order to keep a healthy metabolism and inflammation at a minimum," said Décarie-Spain. "It's a question of moderation."
This study follows on an earlier study published by Fulton in 2013 which showed that Foods rich in saturated fat and sugar causes anxiodepressive behaviors which have an impact on brain reward signaling and vulnerability to stress.
Reference
- Léa Décarie-Spain, Sandeep Sharma, Cécile Hryhorczuk, Victor Issa Garcia, Philip A. Barker, Nathalie Arbour, Thierry Alquier, Stephanie Fulton. 'Nucleus accumbens inflammation mediates anxiodepressive behavior and compulsive sucrose seeking elicited by saturated dietary fat.' Molecular Metabolism (2018). https://doi.org/10.1016/j.molmet.2018.01.018.
Source-Medindia