If you’ve ever felt like your stomach is controlling your mind, then you could be on to something, as researchers have now revealed what appears to be a direct connection between the gut and brain inflammation. According to a new study in the journal Nature Medicine, the food we eat is broken down by the bacteria in our digestive tracts to produce small molecules that then affect our brain cells, particularly those involved in staving off mental degradation.
The results of this study should provide some serious food for thought – literally – to scientists looking for new ways to treat cognitive diseases. For instance, the research provides evidence that the ability to utilize certain molecules to promote healthy brain function is reduced in people who suffer from multiple sclerosis (MS), illuminating a potential new pathway for treatment.
MS is caused by a malfunction in a type of brain cell called astrocytes. The most abundant cell type in the central nervous system (CNS), astrocytes play a major role in regulating a range of key brain functions. However, in MS, astrocytes actually turn against the brain, attacking and destroying a substance called myelin, which insulates and protects neurons, ensuring the efficient transmission of impulses around the CNS.
Previous studies have shown that astrocytes are stimulated to perform certain key functions by a signaling protein called aryl hydrocarbon receptor (AHR). In particular, AHR causes the cells to reduce inflammation in the brain. As such, the researchers decided to investigate how manipulating AHR levels affects the severity of cognitive diseases.
Knowing that an amino acid called tryptophan – which is contained in foods such as poultry and eggs – is broken down by certain gut bacteria to produce molecules that are capable of binding to AHR, the study authors began by altering levels of tryptophan in the diets of mice that had been bred to suffer from an MS-like condition.
After receiving a tryptophan-depleted diet, the mice suffered an escalation of their cognitive decline, which was then reversed by re-introducing tryptophan to their diet. To confirm that this key amino acid produced this effect by interacting with AHR, the researchers repeated the experiment with mice that had been genetically engineered to lack AHR, finding that tryptophan was powerless to improve the condition of these mice.
Commenting on these results, study co-author Francisco Quintana stated that “for the first time, we've been able to identify that food has some sort of remote control over central nervous system inflammation.”
Furthermore, after conducting a genetic analysis of people suffering from MS and comparing this to non-sufferers, the study authors discovered that those who carry the condition lack certain genetic traits necessary for AHR to stimulate astrocytes to do their job. Understanding how this vital mechanism is disrupted could provide a basis for the development of new therapies for the disorder.