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Nervous System

Part of the Clinical Practicum series on WholisticMatters designed to bring you clinical information for your practice.

 Gut Health

The gut-brain connection is the hard wiring between the body’s central nervous system housed in the brain and the gut’s enteric nervous system, also referred to as the body’s “second brain.” This axis facilitates bi-directional flow of information via neural, hormonal, and immunological communication between the brain, gut, and microbiome. Researchers have known for centuries that there is a link between the brain and the gut when terms like “gut feelings” and “butterflies in my stomach” and “nervous stomach” are used in expression. Emerging science is now placing the gut-brain-microbiota axis at the center of nervous system disorders including depression, anxiety, ADHD, autism, Parkinson’s disease, and multiple sclerosis. It is also this dysfunction that helps to explain the inter-connectivity between irritable bowel syndrome (IBS), elevated stress, poor coping, and lower resilience.

The first connection between the brain and gut is neurally mediated. Delving into the neural connection between the brain and the gut makes it easier to interpret the interrelationship between emotion, hypervigilance, gut function, and chronic abdominal pain. The local enteric nervous system connects to the brain via the intermediary vagus nerve. Within the central nervous system, the region of gut control is the limbic system, which also controls systems that facilitate survival, threat avoidance, social interaction, and learning. From a neuroanatomic perspective, the limbic system is the interface between the mind and body. The limbic system is also responsible for up- or down-regulating visceral pain transmission and perception.

When there is gut-brain dysfunction, the nerve signals from the gastrointestinal (GI) tract can be misinterpreted by the brain’s emotion centers as “pain.” Studies have shown that the brain has the amazing capability of turning down these signals, but patients diagnosed with IBS and gut dysfunction have an impairment in their ability to squash these signals to the brain. The end result is visceral hypersensitivity. Furthermore, recent research in neuro-gastroenterology has shown that strong emotion associated with psychiatric trauma, such as abuse or post-traumatic stress disorder (PTSD), can lead to loss of nerves in the brain that are associated with pain perception, and treatment with medications like antidepressants can play a role in nerve re-growth. This concept is called neuroplasticity, and it has also been applied to patients with severe depression or chronic pain who show reduced brain density in areas of the brain that interface between emotions and pain regulation, particularly the anterior cingulate cortex.

A rationale for the stress-IBS connection is housed in the brain’s hormone center called the hypothalamic-pituitary adrenal (HPA) axis. Corticotropin releasing factor (CRF), a peptide in the HPA axis, is released during periods of acute stress, where the stressor can evoke a “fight or flight” response for survival. This triggers the HPA axis to release stress hormones that further stimulate the adrenal gland to release cortisol, the major stress hormone in the body. Cortisol coordinates a hyper-immune response that promotes inflammation and diverts resources from digestion. The hypothalamic release of corticotropin-releasing hormone (CRH) also charges up the sympathetic nervous system, which kicks in the “adrenaline” response that induces heart rate and blood pressure to increase, leads to more labored breathing, promotes sweating, and disrupts normal bodily functions. After the stress subsides, the adrenaline quickly leaves the body’s circulation, as it returns to a relaxed “rest and digest” state. In subjects with chronic stress, the CRF response is perpetually activated. This leads to long-term effects on intestinal sensitivity, gut motility, secretion and permeability of the gut, immune activation, and alterations in the microbiome.

Finally, there is the emerging role of the microbiome in neuroinflammation. Conditions like depression, autism, and neurodegenerative disorders have been linked to the microbiome. Early studies showed the elevated risk for neurodegenerative disorders very early and late in life, both time points in which the gut microbiome demonstrates low microbial diversity. Other studies have demonstrated associations between antibiotic exposure and depression, leading to the observation that disrupting the microbiome may have downstream implications for development of mood disorders and diseases of the nervous system.

The mechanism of gut microbial interaction with the brain is multi-faceted and complex. Gut microbes can alter the availability of tryptophan, an amino acid required to produce the mood-regulating neurotransmitter serotonin that is produced primarily in the gut. Gut bacteria are capable of sending neural signals via neuropeptides from the gut to the brain, leading to a heightened stress response and visceral hypersensitivity. Microbes synthesize short chain fatty acids from fiber that are implicated in the integrity of the blood-brain barrier. Microbes are implicated in chronic gut inflammation which can extend to an inflammatory response in the brain. Finally, there is an emerging role for gut microbes in manipulating microRNAs to alter DNA expression in nerve cells. The role of probiotics, termed “psychobiotics” in neurosciences, is an area of active research for treatment of “neuroinflammatory disorders.” The gut-brain-microbiota axis is an important area of active research and will provide an important avenue for addressing mental health with treatment strategies that target the gut.

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