Neurotransmitters in the gut: Serotonin, GABA, Norpinephrine, & Dopamine

Neurological diseases and mental disorders are some of the most current research areas in the medical field. According to Liang et al. (2018), only when we take the human self and its microbiota into consideration at the same time is when we can better understand these diseases. Liang et al. (2018) noted that new research has found that the human being carries billions of microorganisms such as archaea, bacteria, fungi, viruses, and protozola living in symbiosis with their human host. These microorganisms contain 300 to 3,000 different species that exceed 1014 the number of human cells representing more than 200 times the number of human genes. These microorganisms have mutated and established a relationship with their host over evolution; therefore, they are called commensal microbiota (Liang et al. 2018).

Strandwitz, (2018) shows that the gut microbiota has trillions of bacteria estimating that humans have about 4 to 6 pounds of bacteria with more than 150 genes working interconnected and reside within the gastrointestinal tract. Strandwitz, (2018) research noted that the microbiota not only has an influence on metabolic health and immune system, but it also interacts with the central nervous system. Moreover, it influences the development of behavioral disorders, such as neurogenerative diseases and neuroimmune disorders. Furthermore, the study reported that by learning with animal models about microbiota and the influence in the brain, they have discovered that one of the mechanisms that influence the "gut-brain-axis" is via the vagus nerve. In brief, the microbiota produces and consumes neurotransmitters along the way, such as dopamine, norepinephrine, serotonin, and gamma-aminobutyric acid (GABA). Suggesting that the manipulation of bacteria in the gut has a direct impact on the physiology and behavior of the host (Strandwitz, 2018). 

Per Galland, (2014) human microbiome does impact the human brain in multiple ways. Galland, (2014), noted that molecular interaction between the host and the gut microbiome is an incredible form of bioactive metabolites that plays a significant role in human health and mental health. The study concluded that the "gut-brain" not only completes its local function, but it also regulates host behavior and cognition (Per Galland, 2014).

Clapp et al. (2017), affirmed that it is, in fact, bidirectional communication between the central nervous system and the gut microbiota. Their study referred to this interaction as the "gut-brain axis". Clapp et al. (2017), shows that the microbiota influences extra-gastrointestinal diseases, induced by dysbiosis and inflammation, and it is linked with several mental illnesses such as anxiety and depression. According to Clapp et al. (2017), new research shows that healthy gut function is also related to adequate central nervous system function. The relation starts on hormones, neurotransmitters, and immunological reactions sending signaling to the brain via autonomic neurons. Moreover, when the microbiome is unbalanced, and the human host had changes in diet, stress, antibiotics that disturb the microbiota, it leads to a dysbiosis state that increased intestinal permeability and allows the bacteria to leak through the intestinal wall into the circulation. We learned that increased intestinal permeability has a direct effect on the host system, including psychiatric disorders such as depression, anxiety, and autism (Clapp et al. 2017).

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Liang et al. 2018).

Liang S, Wu X and Jin F (2018) Gut-Brain Psychology: Rethinking Psychology From 
the Microbiota–Gut–Brain Axis. Front. Integr. Neurosci. 12:33. doi: 10.3389/fnint.2018.00033 

Strandwitz P. (2018). Neurotransmitter modulation by the gut microbiota. Brain research1693(Pt B), 128–133.

Galland L. (2014). The gut microbiome and the brain. Journal of medicinal food17(12), 1261–1272.

Clapp, M., Aurora, N., Herrera, L., Bhatia, M., Wilen, E., & Wakefield, S. (2017). Gut microbiota's effect on mental health: The gut-brain axis. Clinics and practice7(4), 987.


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