Most animals, including humans, are populated by rich, highly complex and genetically diverse communities of microorganisms. These microorganisms (also referred to as microbes or flora) inhabit nearly every part of our bodies, from our gut to our skin and may in fact vary in populations on our elbow to our face. There are many studies that show the brain effect on gut bacteria (top-down control). It is known, for example, that psychological and physical stress induce dysfunction of the intestinal barrier. However, recent research may imply that gut bacteria can also influence the brain, creating a “chicken or the egg” scenario for clinicians. Clinical research is critical to justify consideration of patients’ gastrointestinal health while treating psychiatric disorders.
A recent article published by Dr. Serguei O. Fetissov and Dr. Pierre Dechelotte in France, suggests that eating disorders, major depressive disorder, and narcolepsy might not originate in the brain but rather is a dysfunction of the “gutbrain axis involving the humoral immune system” (Curr. Opin. Clin. Nutr. Metab. Care 2011;14:477-82). Some of the strongest evidence of this connection may be found in eating disorders.
Dr. Fetissov and Dr. Dechelotte suggest that the microbial environment of the gastrointestinal (GI) system may represent a “”key causative factor triggering production of certain neuropeptide-reactive autoAbs, which in turn will modulate corresponding peptidergic signaling resulting in modification of eating-related behaviors and eventually eating disorders.”
Another study, by Dr. K.M. Neufeld and colleagues at McMaster University, Hamilton, Ont., indicates that intestinal microbiota plays a role in the development of the central nervous system and behavior. They evaluated the behavioral characteristics of germ-free (think of mice with no normal intestinal flora) mice and specific pathogen-free (healthy) adult mice. The germ-free mice showed lowered levels of anxiety, however, they engaged in risky behavior more frequently and for longer periods of time than did healthy mice (specific pathogen-free mice). Germ-free mice also exhibited an up-regulation of the brain-derived neurotrophic factor in the dentate gyrus of the hippocampus, as well as down-regulation of 5HT1A receptors and NMDA receptor expression, all of which are directly related to the stress response and to emotional behavior. (Neurogastroenterol. Motil. 2011;23:255-64).
Not only is there a link between gut microbiota and behavior/stress, but stress in turn, affects the gut microbial environment- a two-way street. A study published by Dr. Michael T. Bailey and his colleagues indicates that social stress can have a profound impact on the population of various intestinal microbiota. The researchers used a form of social stress known to function as a chronic social stressor. They found that exposure to this stressor decreased the number of bacteria of the genus Bacteroides, but also increased the number of bacteria in the genus Clostridium. Stress also increased levels of interleukin-6, a pro-inflammatory cytokine whose expression is known to increase as a result of stress, and Monocyte chemotactic protein-1, which recruits monocytes to injured sites and whose expression is regulated by stress. However, when mice were treated with antibiotics (to redue the number of microbes) prior to social stress stressors, the mice did not show increased interleukin-6 or MCP-1 level. These results suggest that increases in cytokines because of stressors are dependent on microbiota (Brain Behav. Immun. 2011;25:397-407).
The few examples I have provided here are encouraging. I would like to see further clinical studies on probiotics and mood. I encourage patients to evaluate their gut flora through clinical lab tests when natural remedies for stress, anxiety and depression (5-HTP, GABA) or prescriptive medicines (Prozac, Lexapro, Valium, Wellbutrin, etc.) fail to provide optimal results.