Meta-analysis of alcohol induced gut dysbiosis and the resulting behavioral impact.

Abstract:

:About 99% of the unique genes and almost half of the cells found in the human body come from microbes including bacteria, archaea, fungi, and viruses. Collectively these microorganisms contribute to the microbiome and often reside in the gut. The gut microbiome plays an important role in the body and contributes to digestive health, the immune system, and brain function. The gut microbiome interacts with the central nervous system through the vagal pathways as well as the endocrine or immune pathways. Changes in the proportion or diversity of the microbiota can have an impact on normal physiology and has been implicated in inflammation, depression, obesity, and addiction. Several animal studies suggest the involvement of gut microbiome in the regulation of pain, emotion, and cognition. Alcoholism has been linked with gut microbiome dysbiosis and thus can have deleterious effects on the gut-brain axis balance. Gut microbiome produces important metabolites such as gastrointestinal hormones, short chain fatty acids, precursors to the neuroactive compounds and neurotransmitters that impact the physiology and normal functioning of the body. The microbiome imbalance has been correlated with behavioral changes and alcohol dependence in the host. The objective of this study is to elucidate the link between alcohol induced gut microbiota dysbiosis and any behavioral impact that could incur. A thorough literature search of various databases was conducted to gather data for the alcohol prompted gut microbiome dysbiosis. Ingenuity Pathway Analysis (IPA1) software was then utilized to identify links between alcoholism, gut microbiome derived metabolites, and their role in behavior alterations. Overall, this meta-analysis reviews information available on the connection between alcohol induced gut microbiome dysbiosis and the resulting behavioral impact.

journal_name

Behav Brain Res

authors

Qamar N,Castano D,Patt C,Chu T,Cottrell J,Chang SL

doi

10.1016/j.bbr.2019.112196

subject

Has Abstract

pub_date

2019-12-30 00:00:00

pages

112196

eissn

0166-4328

issn

1872-7549

pii

S0166-4328(19)31164-7

journal_volume

376

pub_type

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