The Gut-Brain Connection: What Counselors Should Know
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The idea that our gut can influence our thoughts and behavior is hardly new. We often say things like, “I had a gut reaction to that,” or “I felt it in my gut.” However, we might not have fully appreciated how closely connected the gut and brain are.
The digestive system, or the gut, is the home of an extensive neural network known as the enteric nervous system. The enteric nervous system contains about the same number of neurons as are found in the spinal cord, earning it the nickname “the second brain.”
The enteric nervous system forms a two-way line of communication with the brain, known as the gut-brain axis or GBA. In particular, the GBA influences and is influenced by the endocrine system, the immune system, and other autonomic nervous system components. This puts the GBA directly in the middle of functions involving hormones, immune responses, and levels of arousal.
An important part of the GBA is played by cranial nerve X, otherwise known as the vagus nerve. The term vagus comes from the same Latin root as the word “vagabond,” or wanderer. The vagus nerve lives up to its name. It exits the lower brainstem and travels to the heart, lungs, and digestive tract. It both issues commands to these structures and obtains feedback from them. The vagus nerve comprises the bulk of the parasympathetic division of the autonomic nervous system, which is responsible for managing glands and organs during times of rest, digestion, and repair.
The system regulates heart rate, breathing, and digestion without your having to think about it. We can override the system temporarily, like holding one’s breath while swimming underwater. The parasympathetic nervous system usually alternates with another autonomic component, the sympathetic nervous system, which is active during times of arousal.
The gut is home to as many as 100 trillion microorganisms, weighing about two pounds in the adult, that make up the gut microbiome. The vagus nerve can sense metabolites produced during microbiome activity, and this information is transmitted to the brain. These bacteria release neurochemicals, including GABA, serotonin, acetylcholine, and dopamine. Although most of this neurochemical activity influences the gut itself, these chemical messengers make it back to the brain through the vagus nerve or through the bloodstream, from which they exit in parts of the brain where the otherwise vigilant blood-brain barrier is relatively porous.
Certain brain states, including stress, can influence the microbiome’s composition. Research using rats has demonstrated that chemical stimulation of the cranial nerve nuclei serving the vagus nerve can shift the balance of pro- and anti-inflammatory bacteria in the gut.
What is Neuroinflammation?
Inflammation generally results from the immune system’s response to an invasion of bacteria or viruses or an injury. We can tell inflammation is present in most body parts when we observe redness, swelling, heat, pain, and impaired function.
In the brain, neuroinflammation is primarily managed by support cells known as microglia and astrocytes. Microglia are mobile cells that can digest debris, such as bacteria or dead cells. Astrocytes protect the brain by cooperating with capillaries to form the blood-brain barrier, which prevents many toxins from exiting the blood supply into the brain.
The normally helpful microglia and astrocytes can go rogue and start causing damage under certain circumstances. T cells, white blood cells that are important components of the immune system, can enter the brain and shift the microglia and astrocytes from their housekeeping roles to their assassin roles. The result is cell death and neuroinflammation above and beyond what is needed to rein in any infection or effects of local damage.
Cytokines, chemicals released by immune system cells, can reduce the levels of monoamines (e.g., serotonin, dopamine, and norepinephrine) in the brain while raising levels of glutamate activity. The excess excitation caused by increased glutamate activity is often toxic to neurons. Cytokines can also inhibit brain plasticity, limiting the brain’s ability to compensate for neural loss or network disruption.
Causes of the neuroinflammatory response are not restricted to infection and damage. Pollutants can also stimulate a response. The GBA enters the process because the microbiome can play helpful and hurtful roles, either reducing or enhancing the brain’s inflammatory response. Because the relationship between the brain and the gut is reciprocal, brain processes also can influence the microbiome and the health of the enteric nervous system.
Why is Inflammation Important?
Researchers were initially puzzled when people known to be mentally sharp showed signs typical of cognitive decline during an autopsy. If their brains looked similar to people with dementia, why didn’t they experience cognitive decline?
One of the big differences is that the brains of people who maintain cognitive function show no evidence of neuroinflammation. In contrast, brains of patients with Alzheimer’s disease, Parkinson’s disease, and other neurodegenerative disorders definitely do.
Many researchers suspect that Parkinson’s disease begins in the gut, when inflammation promotes the development of a toxic alpha-synuclein protein. The vagus nerve transfers the alpha-synuclein to the brain, and degeneration ensues. In support of this view of Parkinson’s disease is the finding that the risk for the disease is higher among people with inflammatory bowel disease.
Neurocognitive conditions are not the only disorders believed to arise from neuroinflammation. Evidence is accumulating that shows that many psychological disorders might have their roots in similar processes, including major depressive disorder, schizophrenia, bipolar disorder, and anxiety. People diagnosed with many psychological disorders have biomarkers of inflammation, such as circulating chemicals known to induce inflammatory responses. When fecal material from people diagnosed with major depressive disorder is transferred to animals, the animals show signs of depression.
For years, people have observed that restricted dietary habits and gastrointestinal distress often accompany autism spectrum disorder. The connection, however, remained a mystery. Now researchers are investigating the possibility that maternal infections during pregnancy produce high levels of an inflammatory signaling molecule that not only affects the fetus’s brain development but also sets the child up for continuing inflammation. Maternal infections during pregnancy also influence the offspring’s risk for schizophrenia and depression.
We still have quite a bit of work to figure out how these many diverse outcomes of inflammation originate. How might inflammation interact with genetic vulnerabilities and experience to produce schizophrenia in one person and bipolar disorder in another? Why are some types of neuroinflammation age-related?
Are Probiotics the Answer?
Although the study of neuroinflammation in psychological disorders is still in its infancy, that has not prevented massive marketing efforts on behalf of probiotics. In 2021, the global probiotic market was approximately $58 billion.
Probiotics contain live microorganisms and are intended to improve health. You might enjoy a tasty yogurt, but many people consume yogurt for its probiotic effects. Prebiotics are substances that stimulate the growth of healthful organisms, and synbiotics are combinations of both prebiotics and probiotics.
Most probiotics are sold as dietary supplements, so government regulation is limited at best. Probiotics sold to treat a specific condition must adhere to higher safety standards and proven efficacy.
While most probiotics are unlikely to cause any harm, much like other dietary supplements, what is actually contained in a product can be very different from what is on the label. People should not self-medicate with probiotics as an alternative to getting professional care.
Until we know more, it’s probably fine to enjoy your yogurt or sourdough bread, as long as you don’t expect it to do more than provide a positive dining experience.