The gut-brain axis is a bidirectional communication network that links the enteric and central nervous systems. According to an article published in Integrated Medicine: A Clinicians Journal, this network is not only anatomical, but it extends to include endocrine, humoral, metabolic, and immune routes of communication as well. The autonomic nervous system, hypothalamic-pituitary-adrenal (HPA) axis, and nerves within the gastrointestinal tract, all link the gut and the brain, allowing the brain to influence intestinal activities, including activity of functional immune effector cells; and the gut to influence mood, cognition, and mental health.
Gut microbiota are well known to support tight junction integrity between enterocytes. It should therefore come as no surprise that dysbiosis and associated increases in intestinal permeability are now recognized features of rheumatoid arthritis, Alzheimer’s disease, asthma, autism spectrum disorders, and other systemic conditions both inflammatory and otherwise. In recent years, there has been a tremendous amount research validating the mechanisms and role of the microbiome and probiotics in managing inflammatory conditions, particularly IBD. Depression is increasingly recognized as having an inflammatory component; indeed, anti-inflammatory drugs, such as COX-2 inhibitors, have previously demonstrated efficacy in major depression
A new class of probiotics, known as psychobiotics or psychomicrobiotics, has emerged in the last decade and is being fervently embraced by many health care practitioners as a nontoxic intervention for various psychiatric conditions. Several clinical trials have now documented effects, or lack thereof, of certain probiotics for depression and anxiety.
In a 2017 systematic review by Wallace and Milev of 10 clinical trials, most of the studies found positive results on measures of depressive symptoms. Because clinical trials on probiotics for depression and anxiety have been heterogeneous in terms of dosing, probiotic strain selection, and length of treatment, further randomized controlled clinical trials are warranted to validate the efficacy of this promising intervention.
Studies from animal models conducted by independent research groups have corroborated findings of gut dysbiosis and its relation to monoamine disruptions seen in clinical depression, connecting gut microbiota with mood.44-48 In addition, intestinal permeability defects are thought to underlie the chronic low-grade inflammation observed in stress-related psychiatric disorders.49 Those with symptoms of depression frequently exhibit increased expression of proinflammatory cytokines, such as IL-1β, IL-6, tumor necrosis factor-α, as well as interferon gamma, and C-reactive protein.50-51,52 Gut microbiota influence transcription of these same cytokines, with dysbiosis triggering the so-called inflammasome pathway, whereas beneficial metabolites (SCFAs in particular) reduce production of proinflammatory cytokines, such as NF-κB.53
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