Neurotransmitters and the Gut
What are Neurotransmitters?
Neurotransmitters (NTs) are brain chemicals that communicate information throughout our brain and body. They relay signals between neurons. They affect mood, sleep, concentration, weight, carbohydrate cravings, and addictions, and they can contribute to depression, pain, anxiety, and insomnia when they are not in balance.
The Gut-Brain Connection
Research continues to illuminate the ways that foods affect how NTs are made in the gut and how, in turn, this affects the brain and mind. Friendly bacteria play a role in the production of gamma-aminobutyric acid (GABA), the “antianxiety” NT suggesting the complex relationship between the brain and the gut. The gut and the brain regulate eating behavior and appetite by way of NTs.
Dopamine and serotonin are the two primary neurotransmitters associated with the regulation of food intake (Bello & Hajnal, 2010; Capasso, Petrella, & Milano, 2010). For example, when people start selective serotonin reuptake inhibitors (SSRIs), or the serotonergic amino acid 5-HTP, they can become nauseated by the increase in serotonin levels in the gut. Stress impairs digestion, and poor digestion affects the neurochemicals that influence mood and well-being. Like the brain, the second brain uses over 30 NTs, and 95% of the serotonin in the body is located in the gut. High levels of serotonin are also linked with irritable bowel syndrome (Hadhazy, 2010).
Mood, Gut, and Brain
Impaired digestion of protein means the amino acids are not available to the brain to support NTs production, directly affecting mood, sleep, and cravings. The overuse of antibiotics, along with insufficient prebiotics in the diet to prepare the garden of the intestines to grow healthy gut microbiota, impairs the production of NTs and subsequently causes mood problems like depression and anxiety.
Most antidepressants are believed to work by increasing the availability of specific neurotransmitters, but this theory is unproven; they often have side effects, lead to chemical imbalances, have limited efficacy (especially in mild to moderate depression), and become less effective over time. The theory of mood disorders as primarily based in NT imbalance is giving way to a more holistic understanding of multiple influences on mood and cognition of which NT function is only one. Indeed, the groundbreaking work by Kirsch et al. examined the role of the placebo effect on depression and suggested that there is no significant difference between antidepressant effect and placebo effect except in the severely depressed, and for the severely depressed it is “the relationship between initial severity and antidepressant efficacy [that] is attributable to decreased responsiveness to placebo among very severely depressed patients, rather than to increased responsiveness to medication” (2008, p. 266).
In my book Nutrition Essentials for Mental Health, I explore the use of amino acid therapy as an adjunctive or alternative method of influencing NTs, as a natural approach to antidepressant and antianxiety medications. These pharmaceutical-grade amino acids may be compounded according to the specific biochemical needs of the individual to provide the building blocks that support specific NT production.
Read more about the gut-brain connection in my blog post Improve your Health by strengthening your gut brain connection.
Bello, N. T., & Hajnal, A. (2010). Dopamine and binge eating behaviors. Pharmacology Biochemistry and Behavior, 97(1), 25–33.
Capasso, A., Petrella, C., & Milano, W. (2010). Pharmacological profile of SSRIs and SNRIs in the treatment of eating disorders. Current Clinical Pharmacology, 4(1), 78–83.
Hadhazy, A. (2010, February 12). Think twice: How the gut’s “second brain” influences mood and well-being. Scientific American. Retrieved May 2015, from http://www.scientificamerican.com/ article/gut-second-brain/
Kirsch, I., Deacon, B. J., Huedo-Medina, T. B., Scoboria, A., Moore, T. J., & Johnson, B. T. (2008). Initial severity and antidepressant benefits: A meta-analysis of data submitted to the Food and Drug Administration. PLoS Medicine, 5(2), e45.