The Gut-Brain Axis: Influence of Microbiota on Mood and Mental Health

From Integrative Medicine • Vol.17, No. 4
By Jeremy Appleton, ND

The gut-brain axis is a bidirectional communication network that links the enteric and central nervous systems. 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 pituitaryadrenal (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 metal health.

The gut-brain axis is a bidirectional communication network that links the enteric and central nervous systems. This network is not only anatomical, but it extends to include endocrine, humoral, metabolic, and immune routes of communication as well. The autonomic nervous adrenal (HPA) axis, and nerves within the gastrointestinal (GI) 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.

Clinical, epidemiological, and immunological evidence suggest that enteric microbiota extensively and profoundly influences the gut-brain relationship (ie, mental state, emotional regulation, neuromuscular function, and regulation of the HPA). Research continues to elucidate mechanisms of action to explain the effects of microbiota, both directly and indirectly, on emotional and cognitive centres of the brain1 and has demonstrated that fluctuations of the microbiota are linked to changes within these systems of communication.

For example, several mood disorders, such as anxiety, depression, and autism spectrum disorders now have well-established links to functional GI disruptions, whereas GI disease (eg, irritable bowel syndrome, irritable bowel disease) often involve psychological comorbidities associated with alteration of the gut microbiome.3-9 In addition, research has demonstrated that the composition of gut bacteria appears to be influential in fetal and neonatal neurologic development.10 And, not surprising, diet has also been shown to influence the gut microbiome’s impact on cognitive function.11
Pathways of the Gut-Brain Axis As early as 1998, oral administration of a single, Unique bacterium (Campylobacter jejuni) to rats in subclinical doses was found to lead to anxiety-like
behavior, without an accompanying immune response.12 Later research confirmed that introduction C jejuni caused anxiety-like behavior in mice, with concomitant activation of neuronal regions in the brain that were dependent on information received from the gut via the vagus nerve.

The seminal first studies establishing mechanisms of the gut-brain axis made use of animals raised in a sterile environment. Sudo et al14 sought to answer the question of whether postnatal microbial colonization could affect the development of brain plasticity and subsequent physiological response. To test the idea that gut microbes might affect the development of neural systems that govern the endocrine response to stress, they studied the HPA axis reaction to stress by comparing germ-free (GF), specific pathogen free (SPF) and gnotobiotic mice. They found that colonizing microbes altered the HPA response to restraint stress, indicating that the interaction of gut bacteria with the brain is also bidirectional, just like the brain-gut axis. This was the first report to show commensal microbes affecting the neural network responsible for controlling stress responsiveness. In this study, the HPA response of the GF mice was more sensitive to restraint stress than that of the SPF mice, whereas both groups of mice failed to show any difference in the sensitivity to
ether stress. In addition, GF mice exhibited reduced brainderived neurotrophic factor (BDNF) expression levels in the cortex and hippocampus relative to SPF mice.

The authors concluded: Because the HPA response to restraint stress is affected by the limbic system, including the prefrontal cortex, hippocampus and amygdala, and requires assembly and processing of signals from multiple sensory modalities before initiation of a stress response, whereas ether stress does not…, these results indicate that cognitive processing in the limbic system may be involved in an exaggerated HPA response by GF mice.

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