According to a new study published in the brain in the brain Neurobiology of the disease.
Depression is one of the most common mental health problems. Traditional antidepressants can take weeks to take effect and often be accompanied by unwanted side effects. Researchers have explored alternative strategies to improve mental health, and a promising avenue is nutrition. Intermittent fasting – a diet that involves alternating catering and fasting periods – has drew growing attention.
Previous studies have suggested that fasting can influence brain neurotransmitters systems, but precise mechanisms have remained clear. In this new research, scientists have studied if intermittent fasting could reduce the symptoms of depression by acting on dopamine D1 receptors, which are known to play a key role in mood regulation.
To test their hypothesis, a research team led by Jingjing Piao from the second hospital of Jilin in China used a well -established mouse model of depression known as the unpredictable chronic light stress (CUMS).
The mice have been exposed to a series of stress factors arranged at random over several weeks – such as foot shocks, water deprivation and pinching of the tail – to imitate the effects of chronic stress in humans. After this period, some of the mice was placed on an intermittent fasting calendar which alternate food availability periods 24 hours a day with a fast 24 hours a day. For comparison, other mouse groups have received the common antidepressive fluoxetine or have undergone a shorter period of 9 hours.
The results were striking. The mice of the intermittent fasting group have shown marked improvements in depression behaviors. They were more likely to engage in pleasant activities, such as drinking a solution of sugar – a sign of reduced anhedonia or loss of pleasure. These mice also presented a decrease in the immobility of behavioral tests designed to assess symptoms of the despair type, which suggests greater stress resilience.
To understand how intermittent fasting produced these effects, researchers have examined brain activity. They found increased neuronal activation in the Médial Cortex (MPFC), a brain region involved in emotional regulation. More specifically, an intermittent improved fasting activity in the signaling route DRD1-CAMP-PKA-DARPP-32-CREB-BDNF-A cascade of molecular events associated with the function of dopamine D1 receivers.
When the researchers administered a medication that blocked dopamine D1 receptors, the antidepressant effects of intermittent fasting have disappeared. This indicated that the advantages depended directly on this dopamine route.
Other experiments using optogenetics – a technique that uses light to control the activity of specific neurons – has strengthened this conclusion. When researchers artificially activate neurons expressing dopamine D1 receptors in the MPFC, mice presented behavioral improvements similar to those observed with fasting. Conversely, the inhibition of these neurons reversed the effects of fasting.
Although the results provide promising information on biological mechanisms connecting the fast and intermittent depression, researchers recognize key limits. The study was conducted in mice, and more research is necessary to determine whether similar effects occur in humans.
The study, “Intermittent fasting produces antidepressant type effects by modulating dopamine D1 receptors in the Médial Médial Cortex“, Was written by Jingjing Piao, Hongyu Chen, Xinmiao Piao, Ziqian Cheng, Fangyi Zhao, Ranji Cui and Bingjin Li.
