2 results
Chapter 2 - Diet and the Microbiome–Gut–Brain Axis
- Edited by Ted Dinan, Emeritus Professor, University College Cork, Ireland
-
- Book:
- Nutritional Psychiatry
- Published online:
- 17 August 2023
- Print publication:
- 31 August 2023, pp 15-38
-
- Chapter
- Export citation
-
Summary
The assortment of trillions of microorganisms resident along the human gastrointestinal tract, our gut microbiota, has co-evolved with us over thousands of years. It can influence a plethora of aspects of human physiology, including host metabolism, immunity and even brain function, cognition and behaviour across the lifespan. The gut microbiota and the brain can communicate with one another, directly and indirectly, through immune system modulation, tryptophan metabolism, vagus nerve activity, the enteric nervous system and bioactive microbial by-products, or metabolites produced by the gut microbiome. Indeed, the gut microbiota are responsible for a rich reservoir of novel metabolites and bioactive substances that can have pleiotropic functionalities for the host. Moreover, diet, an easily accessible and thus powerful interventional tool, can act as a modulator of gut-microbial composition and activity, impacting on host physiology. As such, nutrition is seen as one of the major modulators of the gut microbiota. Intriguingly, although psychiatric conditions often include a dietary aspect, much research investigating this link in clinical populations ignores this relationship, missing a key therapeutic avenue. This has led to the concept of nutritional psychiatry, where we can use food and supplements to support mental health and brain function. As a result, it is critical to consider emerging microbiome-targeted dietary approaches with the greatest potential to improve health outcomes in a psychiatric population.
Evidence of causal effect of major depression on alcohol dependence: findings from the psychiatric genomics consortium
- Renato Polimanti, Roseann E. Peterson, Jue-Sheng Ong, Stuart MacGregor, Alexis C. Edwards, Toni-Kim Clarke, Josef Frank, Zachary Gerring, Nathan A. Gillespie, Penelope A. Lind, Hermine H. Maes, Nicholas G. Martin, Hamdi Mbarek, Sarah E. Medland, Fabian Streit, Major Depressive Disorder Working Group of the Psychiatric Genomics Consortium, Substance Use Disorder Working Group of the Psychiatric Genomics Consortium, 23andMe Research Team, Arpana Agrawal, Howard J. Edenberg, Kenneth S. Kendler, Cathryn M. Lewis, Patrick F. Sullivan, Naomi R. Wray, Joel Gelernter, Eske M. Derks
-
- Journal:
- Psychological Medicine / Volume 49 / Issue 7 / May 2019
- Published online by Cambridge University Press:
- 01 April 2019, pp. 1218-1226
-
- Article
- Export citation
-
Background
Despite established clinical associations among major depression (MD), alcohol dependence (AD), and alcohol consumption (AC), the nature of the causal relationship between them is not completely understood. We leveraged genome-wide data from the Psychiatric Genomics Consortium (PGC) and UK Biobank to test for the presence of shared genetic mechanisms and causal relationships among MD, AD, and AC.
MethodsLinkage disequilibrium score regression and Mendelian randomization (MR) were performed using genome-wide data from the PGC (MD: 135 458 cases and 344 901 controls; AD: 10 206 cases and 28 480 controls) and UK Biobank (AC-frequency: 438 308 individuals; AC-quantity: 307 098 individuals).
ResultsPositive genetic correlation was observed between MD and AD (rgMD−AD = + 0.47, P = 6.6 × 10−10). AC-quantity showed positive genetic correlation with both AD (rgAD−AC quantity = + 0.75, P = 1.8 × 10−14) and MD (rgMD−AC quantity = + 0.14, P = 2.9 × 10−7), while there was negative correlation of AC-frequency with MD (rgMD−AC frequency = −0.17, P = 1.5 × 10−10) and a non-significant result with AD. MR analyses confirmed the presence of pleiotropy among these four traits. However, the MD-AD results reflect a mediated-pleiotropy mechanism (i.e. causal relationship) with an effect of MD on AD (beta = 0.28, P = 1.29 × 10−6). There was no evidence for reverse causation.
ConclusionThis study supports a causal role for genetic liability of MD on AD based on genetic datasets including thousands of individuals. Understanding mechanisms underlying MD-AD comorbidity addresses important public health concerns and has the potential to facilitate prevention and intervention efforts.