The Gut-Brain Axis

Note: I originally researched and wrote this post and the following in 2013 for a more clinical audience. After posting these two I will resume posting more accessible blogs posts.

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As I begin this exploration of the innovative edge just outside of the mainstream of the common paradigms of mental health and human psychosocial functioning, I want to introduce a rising idea in science about gut health. Why gut health? Well, there has been more and more information coming to light about the role of the gut in psychological health. This has been termed “the gut-brain axis.”

Because many in the mental health and social work professions lack in depth education in biology, I won’t go in too much depth on complex pathophysiology, but the main idea is that there are communication pathways between the gut and the nervous system.

For example, it has been known for some time that there is a subset of schizophrenic patients who seem to find remission after adopting a gluten free diet. This research goes back to the 1950’s (Kalaydjian et al. 2006). It is interesting to note that if schizophrenia was one disease caused by one genetic abnormality or biological mechanism, then why does a treatment such as this affect only a subset of the population? This lends more credence to the notion that schizophrenia is a collection of disorders.

Possibly dysfunctions in nervous system coming from different angles may easily cause similar presentations of symptoms.

Food sensitivities are one area of research into mental health, the gut microbiome is another. The microbiome is simply a term used to describe the micro-organisms living in our intestines. This is a classic symbiotic relationship where the body and the bacteria require each other to live. On a brief survey of a few articles on my former university’s search engine I discovered several studies pertaining to the status of the gut microbiome and mental health.
For starters, there is a link between a compromised gut and the concentration of serotonin in the central nervous system (Clarke et al. 2013). This study as well as the reference that follows compare animals with a “germ free” or GF gut compared to a “colonized” system. The compromised or GF males appeared to have significantly higher metabolites of serotonin compared to the animals with normal gut health. Another finding was that the animals that had compromised microbiomes early in life had difficulty normalizing their system later in life and may not have been able to reach a fully functioning system even after their intestines were re-colonized.
According to these authors there are mechanisms in the gut microbiome that regulate the autonomic nervous system via the vagus nerve and the neuroendocrine response to stress leading to changes in behavior. Case in point, GF rodents demonstrated an exaggerated response to HPA axis activation leading to heightened corticoid levels (cortisol in humans). When treated with probiotics the pathological behaviors of GF animals appeared to normalize.
In a similar article that reviewed the present literature on the subject, Cryan & O’Mahony (2011) stated that there are multiple pathways by which a compromised gut, either by colonization by parasites or other alterations in gut flora effect behavior. One is direct communication with the nervous system and the other is inflammation.
Inflammation is an interesting player in this story. For those with little background in biology, inflammation is a normal bodily process of healing when there is some insult to a bodily tissue. Think of a small burn or bumping your knee and the subsequent swelling. Consider rubbing your skin with sand paper and think of how red and inflamed it can become. Now think of the lining of your digestive tract as internal skin. What if it is constantly being rubbed by sandpaper? It would become pretty inflamed right? One quality of inflammation is cellular permeability. The gaps between cells widen so more healing materials can move to the tissues that need this healing. What occurs in an inflamed gut, let’s say by gluten sensitivity or severe alcoholism is heightened gut permeability or leaky gut. The gut leaks out what it is supposed to keep in.
When this occurs there are many bugs, chemicals, and materials that can travel all over the body. Our own immune system will also leak out and attack ourselves. For example: chemicals called pro-inflammatory cytokines and lipopolysacharides that are produced from gut bacteria cause an inflammatory response in the nervous system and even cross the blood brain barrier causing some symptoms of major depression (Maes et al. 2008). This seems intuitive to me, the nervous system is in a state of illness, thus the body puts itself in a state of recuperation: depression. Why does the flu come with a subjective experience of depression? Because it knows that it is in a state of illness and needs to conserve energy and the body needs to slow down and rest. Interestingly, the majority of antidepressants have anti-inflammatory properties (Maes 2008). The first article (these are two different papers by the same author) described a high comorbidity between people with IBS and other gut inflammatory conditions and depressive illnesses. If we settle the inflammatory bowl conditions of this population, how much effect is left with the use of antidepressants acting on serotonin and other neuroendicrine pathways? Is this simply a subset of the population of those who suffer from clinical depression that have a compromised gut and benefit from the anti-inflammatory effects of their meds?
It is interesting how the simple hypothesis of a “chemical imbalance” ends up not so simple. I would dare posit that it is but a piece of the puzzle if not simply describing a subset of the population of the mentally ill. More research on this topic to come.

I apologize to those in the service fields who are not innately akin to biology for my beginning this blog venture on a topic that may be complex to some. I plan to cover a variety of topics here. Some deeply biological, others more psychological or sociological and clinical. Stay tuned.
References:
Clarke, G. et al. (2013). The Microbiome-Gut-Brain Axis During Early Life Regulates the Hypocampal Serotonergic System in a Sex-Dependant Manner. Molecular Psychiatry. 18, 666-673.
Cryan, J. F. & O’Mahony, S. M. (2011). The Microbiome Gut-Brain Axis: From bowl to behavior. Neurogastroenterology & Motility. 23, 187-192.
Foster, J. A. & Neufeld, K. M. (2013). Gut-Brain Axis: How the microbiome influences anxiety and depression. Trends in Neurosciences. 36, 305-312.
Kaladjian, E. A.; Easton, W.; Cascella, N.; & Fasano, A. (2006). The Gluten Connection: The association between schizophrenia and celiac disease. Acta Psychiatrica Scandinavica. 113, 82-90.
Maes, M. (2008). The Cytokine Hypothesis of Depression: inflammation, oxidative & nitrosative stress (IO&NS) and leaky gut as new targets for adjunctive treatments in depression. Neuroendocrinology Letters. 29.
Maes, M.; Kubera, M.; & Leunis, J. (2008). The Gut-Brain Barrier in Major Depression: Intestinal mucosal dysfunction with an increased translocation of LPS from gram negative enterobacteria (leaky gut) plays a role in the inflammatory pathophysiology of depression. Neuroendorcrinology Letters. 29, 117-124.

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