Serendip is an independent site partnering with faculty at multiple colleges and universities around the world. Happy exploring!

The Brain in Your Gut

SerendipUpdate's picture

Biology 103
2000 Second Web Report
On Serendip

The Brain in Your Gut

Biology of a Thanksgiving Meal

Promise Partner

Before we travel home to sit down to an enormous feast, I would like to introduce you to a very important participant of your Thanksgiving holiday: the brain in your stomach. Have you noticed that you do not consciously control digestion? Ever had butterflies in your stomach? Been nauseous before an exam? Feel tired after you eat? All these are functions of your enteric nervous system. Considered a "complex, integrated brain in its own right" (4), this system has over one hundred million neurons, more than the number in the spinal cord, located within the lining of the gastrointestinal tract (3).

When animals were first evolving, their main concern was physical sustenance and so the first nerves to develop were those in the digestive track. As life evolved further, animals required a more complex brain, but the gut's nervous system was too important to be marginalized. Nature thus maintained the enteric nervous system independent of the central nervous system in the brain and spinal cord. Both brains originate during fetal development from tissues called the neural crest. This structure divides to form the two brains, loosely connected by a group of only a few thousand nerve fibers called the vagus nerve (1, 2).

The enteric nervous system, the lesser-know of the two brains, manages the gastrointestinal tract without the assistance of the cranial brain (3). It regulates the esophagus, stomach, small intestine, and colon by mixing food with digestive enzymes and pushing food along the tract. It also helps control the absorption of nutrients into the bloodstream and protects the body against harmful bacteria and toxins that may enter with food (2). The autonomy of the ENS has great advantages. Its proximity to the structures it controls provides "second-to-second control" and eliminates the need for a thick cable of nerves linking it to the cranial brain (1).

Structurally the enteric nervous system is quite similar to the central nervous system. They use the same structures of sensory and motor neurons, information processing circuits, and glial cells (1), as well as the same neurotransmitters, including acetylcholine, norepinephrine, dopamine, and seratonin (2). Because the neurotransmitters of the brain are also present in the bowels, drugs designed for one tend to affect the other (4). For example, many patients who take Prozac, designed to increase seratonin levels in the brain, also experience gastrointestinal problems like diarrhea or constipation stimulated by seratonin in the ENS (3).

The brain-gut connection through the vagus nerve creates a complicated relationship between the two nervous systems. A working vagus nerve sends a steady stream of messages between the brain and the gut, with the number of messages going to the brain from the gut outnumbering those from the gut to the brain. For example, the ENS informs the brain of the danger of infected food by inducing nausea or abdominal pain (4).

Through the vagus nerve, the enteric nervous system plays a major role in protecting the body from external threats. In normal circumstances, the ENS moves food down the gastrointestinal tract in an organized fashion, but it reacts differently if it receives a stress signal from the brain. The response varies depending on the individual system, but ENS may shut down the digestive system or empty it through excretion or vomit. The brain in the gut thus intelligently prepares the body for fight or flight, easier on an empty stomach (1, 2).

When the gut receives a signal of danger from the brain, it helps protect the body by triggering the immune system. Mast cells in the lining of the small intestine and colon release histamine, causing an inflammatory response to attract immune cells from the blood stream into the area. In this way, the ENS can protect the body from animal bites, knives, or bullets that threaten it with infectious material from the outside (1, 2).

Now, the question you've all been waiting for: Why do you get sleepy after eating turkey? Turkey meat is a source of the amino acid tryptophan, a natural sedative. Tryptophan is an amino acid needed to create the seratonin in the ENS, which then causes sleepiness and calmness through the CNS, as they share this type of neurotransmitter. However, the drowsiness after a Thanksgiving meal is not attributed to tryptophan, as it is not effective as a sedative unless no other protein is present in the stomach. Because we gorge on high-carbohydrate foods, blood flow increases to the stomach and decreases to the brain, as the ENS prepares to digest the meal (5).

The enteric nervous system is a complex system, controlling many bodily functions independently while also intricately linked to the central nervous system. The brain-gut does not usually receive any attention, as it works diligently and effectively on its own. So as we enjoy family and food over the holiday, remember to thank the brain in your stomach before falling asleep after all that turkey.

 

WWW Sources

1) "Two brains are better than one, especially if you're hungry." A fun and easy-to-understand site from the National Institute for Science Education.

2) "Why Your Brains Love Thanksgiving." John D. MacArthur writes a great commentary on the gut-brain.

3) "Wyoming researcher studies 'second brain' in gut tissues." An article from the University of Washington introducing a specialist of ENS.

4) "The Enteric Nervous System: A Second Brain." Dr. Michael D. Gershon, the most knowledgable and prolific scientist on the enteric nervous system, writes a thorough article including diagrams and scientific terms.

5) "Why does eating turkey make you sleepy?" A message from the National Turkey Federation.

 

 

Comments made prior to 2007

This all leaves me wondering whether a core/chronic problem in one "brain" (stomach/digestion) can lead to CNS/brain problems. Stress knows no boundaries, especially in this relationship. Can a tendency to be tight and even cramped in the stomach or small intestine, particularly during the night, end up causing a brain tumor? This may sound like a stretch, but in my own case I'm very curious to find out. Of course, it is hard to delineate cause and effect here. Any thoughts?!? ... Noel Kaufmann, 7 May 2006

Comments

Serendip Visitor's picture

typo

In the the 5th paragraph I believe theres a typo. It should read the signals from the brain to the gut far outnumber those from the gut to the brain.

John Innes's picture

Enteric brain and addiction

I am a novice at science. But it seems to me that behavior addictions (i.e., gambling, eating, sex, self-cutting etc.) is likely caused by miscues between the ENS and CNS. Each system has the ability to produce and release its own endogenous opiods. These powerful neurotransmitters are closely guarded by the body, only being released during extreme physical or psychological distress.

This article has influenced my hypothesis that distress signals from the CNS can trigger powerful reactions in the ENS. And the ENS can likewise send powerful distress signals to the CNS. In layman’s terms, one nervous system can “fool” the other into releasing endorphins.

I see no indication that nature protects against this false-signaling, nor would I expect it to. Disturbances which are severe enough to release endorphins are typically very unpleasant. I doubt animals would seek out predators merely to trigger recreational endorphin releases.

Yet I suspect that is precisely what behavior addicts do. When viewed from this perspective of false signaling, several baffling aspects of addictive behavior make a certain amount of sense.

Some examples:

• Repetitive behavior – Behavior addicts often repeat their behaviors dozens and even hundreds of times for no apparent reason. Viewed in light of the constant reuptake of endorphins, this makes sense. To compensate for the brevity of the characteristic euphoric and anesthetic effect, the addict must constantly trigger new releases.

• Risky behavior – As addiction progresses, the addict takes greater and often needless risks. The constant contemplation of various close calls (i.e., arrest, bankruptcy, or physical assault) transmits a steady stream of distress signals from the CNS to the ENS.

• Epithelial distress – A surprising number of behavior addictions involve deliberately hurting the layer of epithelial cells which underlie the epidermis. Common examples include addictive hair-pulling, teeth grinding, sun tanning, self-cutting, etc. All of these behaviors are directed at the integumentary system which the ENS safeguards against parasite activity. I view many such behaviors as examples of false-signals being sent to the ENS specifically to trigger a release of endorphins.

I wish I knew more about the science. Many people suffer from behavior addictions. And many of those who suffer it believe it cannot possibly exist. I think time will prove that these serious behavior addictions are simply a repetitive cycle of false signals between the CNS and ENS.