The connection between food and memory is one of those fundamentally human experiences with which we can all relate. A compelling new study from the University of Southern California has revealed an intriguing explanation behind this phenomenon and illustrates how strongly the "second brain" in our gut communicates with our brain.
Within our gastrointestinal tract is a massive mesh of neurons often referred to as our "second brain". While this neuronal control system works primarily to independently manage our digestive system, it has also been found to communicate directly with the brain through a long nerve, called a vagus nerve.
It has been discovered that the vagus nerve mediates a large amount of metabolic communication between the intestine and the brain. For example, a recent study revealed how feeding behavior, modulated by activity in the hippocampus, is directly activated by vagus nerve stimulation, mediated by signals from the gastrointestinal tract.
It seems obvious that the signals from the intestine would be communicating with the brain in this way, letting us know when we are full and should stop eating, for example. But what if these bowel-hippocampal communications covered more than just signs of hunger or satiety? Could they also affect other cognitive and memory processes regulated by the hippocampus?
This is the question that USC researchers set out to investigate and the result may have uncovered an ancient trait that we evolved to help us remember where to find the best food. The study used a new rodent model that eliminates about 80 percent of the communication of the vagus nerve with the brain, while retaining the fundamental signaling of the motor from the brain to the intestine.
The study found that when this brain-gut pathway was disconnected, the rats showed impaired episodic and spatial functional memory. This essentially means that the animals could not generate and access effectively the spatial memories triggered by the gastrointestinal system. With this interrupted path, a fascinating connection between our intestine and memory is hypothesized.
"When animals find and eat a meal, for example, the vagus nerve is activated and this global positioning system is activated," says Scott Kanoski, author of the study. "It would be advantageous if an animal remembers its external environment so that it can eat again."
Researchers hypothesize that this mechanism evolved to help us remember where we found particularly good food sources, and helped us navigate back. to those specific places. This is the first time that scientists reveal such a novel and explicit connection between the intestinal signals, the vagus nerve and the memory activity of the hippocampus.
Other studies have revealed that artificial electrical stimulation of the vagus nerve can improve memory function, but this is the first to find an endogenous connection from the intestine to the hippocampus mediating this cognitive pathway. Interestingly, this particular research found that the specific disruption of the vagus nerve studied here did not affect social learning, anxiety or body weight.
The study concludes with a slight concern about the lack of research in this area. It is suggested that common bariatric surgeries, such as a gastric bypass, reduce the effectiveness of vagal nerve signaling in the brain. In addition to that, it has been shown that an obesity treatment recently approved by the FDA, called VLBOC, effectively promotes weight loss by electrically interrupting the vagus nerve.
Could these vagal disruption treatments result in cognitive or memory-related collateral effects not studied? We just do not know at this stage, but the USC team suggests more research.
The new study was published in the journal Nature Communications .