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Gut Microbiome and Mental Health

  • Writer: Sophia Yang
    Sophia Yang
  • Sep 13
  • 5 min read
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Imagine if treating depression started with not a pill, but a gut check. Emerging research suggests that this might soon be more than just an intriguing idea. Rather, it could be something that reshapes the future of mental health care. By influencing neurotransmitters, inflammation, and stress systems, the gut microbiome may prove itself to be as crucial to managing depression and anxiety as the brain itself.


The gut and brain are closely linked through what scientists call the gut-brain axis, a network that involves neural pathways like the vagus nerve, hormonal signals, and immune responses. Surprisingly, more than 90% of the body’s serotonin—a neurotransmitter central to mood regulation—is produced in the gut, rather than in the brain.1 The gut microbiota shapes this communication network in many ways. Aside from serotonin, certain bacterial strains help produce other neurotransmitters like gamma-aminobutyric acid, which also plays an essential role in regulating emotions.2,3 When the composition of gut bacteria becomes imbalanced (or dysbiosis), it can increase intestinal permeability, also called “leaky gut,” allowing inflammatory molecules to enter circulation and affect brain function.4 The gut microbiota also influences the hypothalamic-pituitary-adrenal axis, which manages how the body responds to stress by controlling cortisol levels. Disruptions in this system have been linked to a higher risk of developing anxiety and depression.5 


Studies continue to uncover striking differences in the gut microbiota of people with psychiatric conditions. For instance, a landmark study from 2015 found that patients with major depressive disorder had a reduced diversity in their gut bacteria and, subsequently, different levels of key microbial species compared to healthy controls.6 Other research has observed that people with depression often have fewer bacteria that produce butyrate, a short chain fatty acid that helps maintain the gut lining and reduces inflammation.7 These microbial shifts are not just passive byproducts of mental illness. Animal studies have shown that transferring gut bacteria from humans with depression into germ-free mice can actually trigger depression-like behaviours in the mice.8 This suggests that the microbiome may actively drive emotional and cognitive changes. These discoveries have sparked a surge of interest in whether it might be possible to treat the mind by targeting the gut. Early findings offer cautious optimism. A systematic review published in 2017 concluded that probiotic supplements could significantly reduce depressive symptoms, especially in people with mild to moderate depression.9 Prebiotics, which are dietary fibers that nourish beneficial gut bacteria, have also shown promise by lowering cortisol levels and positively influencing how people process emotional information.10 Additionally, diets rich in fiber, polyphenols, and fermented foods(e.g. Mediterranean diet) have been associated with lower rates of depression, potentially by promoting a healthier gut microbiome.11 Even fecal microbiota transplantation (FMT), an approach that involves transferring gut bacteria from healthy donors into patients, has produced interesting results. Although still experimental for psychiatric uses, small studies suggest it may help improve both digestive issues and mood-related symptoms.12 


Despite these exciting developments, there are still major challenges to overcome. One of the biggest questions is whether changes in the microbiome cause depression or whether depression leads to changes in the microbiome. It is likely that the relationship goes both ways, creating a complex feedback loop. Another significant challenge is personalization. Each person’s microbiome is as unique as a fingerprint, which means that treatments effective for one individual might not work for another.13 This showcases the importance of developing tailored approaches to future microbiome-based therapies. There are also regulatory and ethical concerns, particularly when it comes to interventions like FMT. Ensuring safety, quality control, and informed consent is essential before such treatments can become mainstream. Even with these obstacles, the potential impact of this research is profound. If scientists can learn how to harness the power of the microbiome effectively, it could open the door to safer, more personalized alternatives or complements to traditional psychiatric medications. This is especially important given that many existing treatments for depression and anxiety come with significant side effects and do not work for everyone. Future research will likely focus on various efforts: (1) using microbial profiles to predict how patients will respond to different treatments, (2) developing psychobiotics or specific probiotic strains aimed at improving mental health), and (3) creating dietary recommendations based on an individual’s unique microbiome composition.The gut microbiome is not just a silent passenger. If anything, it could be an active partner in shaping our emotional and cognitive health. This growing understanding brings us back to a question that once seemed far-fetched: what if treating depression did not start with a pill, but with a closer look at the gut? While many questions remain, the evidence so far makes it clear that gut bacteria have the potential to shape how we think, feel, and handle stress. This suggests that truly comprehensive mental health care might one day start by examining, and even treating, the gut as carefully as we do the brain. What began as a surprising idea is rapidly becoming a necessary direction for future research and care.

Written by Noor Oglah


References

  1. Carabotti M, Scirocco A, Maselli MA, Severi C. The gut-brain axis: interactions between enteric microbiota, central and enteric nervous systems. Ann Gastroenterol. 2015;28(2):203-209.

  2. Yano JM, Yu K, Donaldson GP, et al. Indigenous bacteria from the gut microbiota regulate host serotonin biosynthesis [published correction appears in Cell. 2015 Sep 24;163:258]. Cell. 2015;161(2):264-276. doi:10.1016/j.cell.2015.02.047

  3. Silva YP, Bernardi A, Frozza RL. The role of short-chain fatty acids from gut microbiota in gut-brain communication. Front Endocrinol (Lausanne). 2020;11:25. doi:10.3389/fendo.2020.00025

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  7. Lozupone CA, Stombaugh JI, Gordon JI, Jansson JK, Knight R. Diversity, stability and resilience of the human gut microbiota. Nature. 2012;489(7415):220-230.  doi:10.1038/nature11550

  8. Kelly JR, Borre Y, O' Brien C, et al. Transferring the blues: Depression-associated gut microbiota induces neurobehavioural changes in the rat. J Psychiatr Res. 2016;82:109-118. doi:10.1016/j.jpsychires.2016.07.019

  9. Wallace CJK, Milev R. The effects of probiotics on depressive symptoms in humans: a systematic review [published correction appears in Ann Gen Psychiatry. 2017 Mar 7;16:18. doi: 10.1186/s12991-017-0141-7.]. Ann Gen Psychiatry. 2017;16:14. doi:10.1186/s12991-017-0138-2

  10. Schmidt K, Cowen PJ, Harmer CJ, Tzortzis G, Errington S, Burnet PW. Prebiotic intake reduces the waking cortisol response and alters emotional bias in healthy volunteers. Psychopharmacology (Berl). 2015;232(10):1793-1801. doi:10.1007/s00213-014-3810-0

  11. Parletta N, Zarnowiecki D, Cho J, et al. A Mediterranean-style dietary intervention supplemented with fish oil improves diet quality and mental health in people with depression: A randomized controlled trial (HELFIMED). Nutr Neurosci. 2019;22(7):474-487. doi:10.1080/1028415X.2017.1411320

  12. Kurokawa S, Kishimoto T, Mizuno S, et al. The effect of fecal microbiota transplantation on psychiatric symptoms among patients with irritable bowel syndrome, functional diarrhea and functional constipation: An open-label observational study. J Affect Disord. 2018;235:506-512. doi:10.1016/j.jad.2018.04.03

  13. Zmora N, Zilberman-Schapira G, Suez J, et al. Personalized gut mucosal colonization resistance to empiric probiotics is associated with unique host and microbiome features. Cell. 2018;174(6):1388-1405.e21. doi:10.1016/j.cell.2018.08.041

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