Humans are animals built for survival. Our brains are designed to meet our basic needs – water, food, shelter, clothing, and sex – and we are driven instinctually to fill them. Most of the body’s survival mechanisms operate constantly without conscious thought.
The stomach digests food after it’s consumed without having to receive conscious instructions from the brain to do so. Such involuntary functions are called autonomic.
The brain is composed of billions of neurons that transmit non-stop electrical signals back and forth to tell you what to do, what to think, and how to feel. The central nervous system’s vagus nerve, which runs from the base of the brain to the bottom of the spinal cord, is the conduit for cerebral messages to travel to the vocal cords, heart, lungs, and the gastrointestinal (GI) tract.
New research is demonstrating that the brain-gut communication goes the other way, too. The enteric nervous system (or intrinsic nervous system) is one of the main parts of the body’s autonomic nervous system (ANS) composed of a mesh-like system of neurons that regulates the function of the GI tract. “Enteric” refers to anything relating to or affecting the intestines.
A whopping 80-90 percent of the nerve fibers in the enteric nervous system (ENS) links the gut to the brain. The ENS can operate on its own even if the vagus nerve is severed.
Because the ENS can go about its business without orders from Brain Control, scientists now consider it the body’s “second brain.”
Gut microbes produce proteins called ClpB 20 minutes after eating and drinking that signal the brain when they are full, as French researcher Sergueï Fetissov of Rouen University and INSERM (the French Institut national de la santé or National Institute of Health and Medical Research) discovered in 2015:
“Our study shows that bacterial proteins from E. coli can be involved in the same molecular pathways that are used by the body to signal satiety, and now we need to know how an altered gut microbiome can affect this physiology.”
Normally, E. coli intestinal populations are self-regulating: they divide and multiply to replace their numbers excreted as stool.
This natural digestive mechanism suppresses food intake in animals. Injected into mice and rats, the bacterially-induced proteins act on the brain to reduce appetite. This finding suggests that intestinal bacteria play a part in governing when and how much we eat.
Fetissov summed up his team’s thinking based on this new information:
“We now think bacteria physiologically participate in appetite regulation immediately after nutrient provision by multiplying and stimulating the release of satiety hormones from the gut. In addition, we believe gut microbiota produce proteins that can be present in the blood longer term and modulate pathways in the brain.”
In reality, we don’t feel full because the brain senses that the stomach and intestines are at full capacity and might literally rupture if you ate that one small after-dinner thin mint (as lampooned in a hilarious Monty Python sketch of yore). Rather, gut bacteria are telegraphing “all-good-down-here” messages to the brain.
So who’s really giving the dietary orders around here?
Fetissov has a pretty good idea about this little matter of the alimentary chain of command:
“It looks like it’s not the host animal that regulates that number [of microbes], but that once bacteria multiply to a certain number, they will stop growing. We provide the nutrients to these bacteria, and they will produce, more or less, a billion more bacteria and then they will stop growing.”
The French scientist continued:
“Why they stop after producing about 1 billion, I have no idea. But in only 20 minutes they produce this new 1 billion bacteria and then they start producing new proteins that have some inhibiting effect on appetite.”
The body’s second brain may provide a way to treat obesity by giving patients supplemental doses of the gut protein ClpB.
But wait, there’s more. British researchers led by Philip Burnet from the University of Oxford’s Department of Psychiatry tested a prebiotic supplement on 45 heathy people aged between 18 and 45 and found that changing the gut microbiome (environment) could relieve anxiety and depression.
A 2011 study linked gut health to emotions and cognition:
“Emerging evidence of a role for gut microbiota on central nervous system functions therefore suggests that oral intake of probiotics may have beneficial consequences on mood and psychological distress.”
It looks like people with healthy and diverse gut microbiomes are less depressed and anxious than those with a GI bacterial imbalance.
One final bit of “gut brain” news is that scientists have demonstrated that lab mice raised in a sterile environment, where no bacteria colonize their guts, “display social traits similar to those in humans on the autism spectrum. When these mice were fed probiotics, their symptoms were alleviated.”
The same results were found in human trials, suggesting that the condition of a person’s gut bacteria influences social behaviors.
Realizing that the gut speaks to the brain independently and regardless of the vagus nerve connection is a game-changer. But before you start worrying that your stomach rules your mind, remember this old saying:
Two heads are better than one.