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ISSN: 2637-6679

Research and Reviews on Healthcare: Open Access Journal

Review Article(ISSN: 2637-6679)

Role of The Gut Microbiota in Mental Health Volume 6 - Issue 1

Sánchez Enríquez Sergio1*, Ortega Morfín Fernanda2, Orozco Barajas Maribel2, Rivera León Edgar Alfonso3, Llamas Covarrubias Iris Monserrat3, and Briseño Ramírez Jaime1

  • 1Department of Clinics, Los Altos University Center, University of Guadalajara, Tepatitlán de Morelos, Jalisco, Mexico.
  • 2Department of Health Sciences , Los Altos University Center, University of Guadalajara, Tepatitlán de Morelos, Jalisco, Mexico.
  • 3Department of Molecular Biology and Genomics, Health Sciences University Center, University of Guadalajara, Guadalajara, Jalisco, Mexico.

Received: December 08, 2020   Published: January 07, 2021

Corresponding author: Sánchez Enríquez S MD, PhD and Briseño Ramírez J MD, specialist in internal medicine and infectology, Department of Clinics, Los Altos University Center, University of Guadalajara, Jalisco, Mexico.

DOI: 10.32474/RRHOAJ.2021.06.000229

Abstract PDF


The human gastrointestinal tract contains distinct microbial communities that differ in composition and function depending on several factors such as age, body location, ethnicity, geography, etc. There is evidence of the bidirectional interaction of the gut microbiota-brain axis and its role in mental health. In this mini review we attempt to summarize and comment on some relevant studies evaluating the role of the gut microbiota in mental health in humans.

Keywords: Gut Microbiota; Stress; Depression; Anxiety; Bipolar Disorder


It is estimated that more than 100 trillion microbes, both eukaryotic and prokaryotic, live in symbiosis with humans. It is known that the human body contains approximately 1000 different bacterial species, in such a way that the intestinal microbiota is considered as an organ [1,2] that contains 150 times more genes than those of the human genome [3]. Factors such as age, sex, race, diet, and body location influence the type of symbiotic microbes and their function [4]. Commensal bacteria settle in the host shortly after birth and progressively develop in a complex and variable ecosystem as the host grows [5]. Association studies have shown that the gut microbiota is related to some chronic degenerative diseases [6,7], including mental illnesses [8,9]. This review focuses on the relationship between the microbiota and mental and psychological illnesses.

Main Text

There is evidence that brain function can be influenced by the gut microbiota through nervous, endocrine and immune pathways [8,10,11]. The mechanisms that relate the microbiota to human health and disease situations are the following:

a) The microbiota has the potential to increase the energy efficiency of food [12], increase nutrient harvesting [13-15] and modify appetite signaling [16,17]. The microbiota contains genes with greater metabolic diversity than human genes and confers unique enzymes and specific biochemical pathways to humans [14]. Some examples of the metabolic processes of the microbiota, which benefit the host, are those that participate in the acquisition of nutrients or in the metabolism of xenobiotics, the metabolism of undigested carbohydrates and the biosynthesis of vitamins [15, 18].
b) The human gut microbiota provides a physical barrier that confers host protection against foreign pathogens through competitive exclusion and the production of antimicrobial substances [19-21].
c) The development of the intestinal mucosa and the host’s immune system is directly influenced by the microbiota [22- 24]. The intestinal epithelium strongly participates in innate immunity. Endocrine cells and stem cells at the base of the intestinal crypts give rise to enterocytes, goblet cells, Paneth cells and enteroendocrine cells. Enterocytes and Paneth cells (PC) produce different molecules such as: antimicrobial peptides, alpha-defensins, lysozyme C, phospholipases, type C lectin, and islet-derived regenerating 3-gamma [25] , which are important in keeping pathogens under control. In addition, goblet cells secrete mucins that lubricate and protect the intestinal epithelial surface, in addition to participating as antigen presenting cells (APC) delivering luminal antigens to CD103+ dendritic cells (DC), which promote the development of regulatory T cells (Tregs ) [26]. Other data supporting the effect of the microbiota on the immune system is that germfree animals have abnormalities in the count of different types of immune cells, deficits in local and systemic lymphoid structures, malformed spleen and lymph nodes, and altered levels. of cytokines [24]. The microbiota appears to modulate immunity by promoting the maturation of immune cells and thus the normal development of immune functions [23].

Mental Diseases and Microbiota

Here is a brief summary of the evidence that relates the intestinal microbiota with different mental illnesses:

a) Depression: Depression is a mental illness that is considered the main cause of disability and is a major contributor to the burden of disease all over the world. The prevalence of depression throughout life ranges from 20% to 25% in women and 7% to 12% in men. Depression explains approximately 50% of psychiatric consultations and 12% of all hospital admissions [27]. Accumulating evidence suggests that gut microbiota play an important role in the pathogenesis of neuropsychiatric diseases including major depressive disorder (MDD). A study of 36 MDD patients showed that those with MDD had an overrepresentation of phylum Actinobacteria and Firmicutes and the genus Bifidobacterium and Blautia compared to controls [28]. In contrast, another study in China reported that Firmicutes were the most significantly decreased phylum in the MDD samples compared to healthy controls [29]. A metaproteomic study in 10 patients found different bacterial protein signatures in MDD compared with controls, with differences in proteins belonging to glucose and amino acid metabolism. Considering the merits of this profile, the authors concluded that Firmicutes, Actinobacteria and Lachnospiraceae were more abundant in MDD, whereas Bacteroidetes and Proteobacteria were less abundant, in MDD compared to controls [30]. It has been proposed that short chain fatty acids (SCFAs), which are produced during fermentation of nondigestible polysaccharides, are regulatory compounds with the potential to influence inflammatory, as well as emotional state and cognition through the gut–brain axis. In this regard a study reported lower fecal levels of the bacterial metabolites SCFAs acetate and propionic acid, but higher isocaproic acid concentrations in depressed compared to non-depressed Polish women [31]. In a cohort study including 1054 subjects, fecal Dialister and Coprococcus spp. were depleted in depression and using a module-based analytical framework, they also identified the microbial synthesis potential of the dopamine metabolite 3,4-dihydroxyphenylacetic acid as correlating positively with mental quality of life and indicated a potential role of microbial γ-aminobutyric acid production in depression [32]. In another cohort study in the UK, 40 participants from the general population completed self-report questionnaires for depression, self-judgement, over-identification and affective and cognitive empathy. Faecal and blood samples were taken to assay microbiota (Bifidobacterium; Lactobacillus spp.) and pro-inflammatory molecules, they found that the fecal predominance of Lactobacillus spp. was directly related to positive self-judgment but only indirectly to cognitive depression and lower affective empathy [33].

b) Anxiety: Throughout their life 15-20% of people will experience an episode of depression or anxiety and therefore are among the top 10 cases of the global burden of disease. In addition to the relationship between IBS and mental illness, the composition of the gut microbiota in individuals with anxiety or depression is known to differ from that of healthy controls. Studies in mice showed that intestinal infections or chemical-induced colitis caused an increase in anxiety-related behavior patterns. Fecal transplants of anxious-type mice to a more resilient strain increase anxiety-like behaviors in the resilient strain and vice versa. Probiotic supplementation has also shown promise, with a reduction in anxiety and depression reported in many human and animal studies. In the comparisons of microbial changes in humans with generalized anxiety disorder against healthy controls, very few changes have been found, however, a decrease in commensal bacteria is observed, similar to cases of depression [34]. Bacteria of the microbiota produce neurotransmitters similar to those found in the central nervous system of animals such as γ-aminobutyric acid (GABA), acetylcholine, dopamine, serotonin, and norepinephrine [35-39]. GABA, acetylcholine, and norepinephrine are also immunomodulators [40,41]. In addition, short-chain fatty acids (SCFA) such as butyrate decrease the intestinal inflammatory process, [42] improve the integrity of the intestinal epithelial barrier [43], stimulate the secretion of 5-hydroxytryptamine from intestinal enterochromaffin cells and activate to free fatty acid receptors that have a direct anti-inflammatory effect on the activation of microglia [44]. Biotin and niacin produced by the gut microbiota are immunomodulatory, and deficiency could contribute to gut and systemic inflammation [42,45].

c) Bipolar disorder: Bipolar disorder (BD) is a serious psychological illness characterized by changes in mood and energy [1]. The prevalence of BD, worldwide, is 1% and is independent of nationality, socioeconomic status or ethnicity, it is an important source of disability and is associated with drug abuse and cardiovascular problems [46]. The etiology of BD is not fully understood. There is increasing evidence supporting the presence of a link between gastrointestinal pathologies and psychological illnesses. For example, there is a comorbidity rate of irritable bowel syndrome (IBS) with psychiatric disorders that ranges from 54% to 94% [46]. A meta-analysis consisting of 177,117 IBS patients and 192,092 healthy controls showed that the prevalence of BD was significantly increased in the IBS population compared to healthy volunteers (OR = 2.48, p <0.001) [47]. In one study, the subgroup of IBS patients, who had had traumatic experiences in early life, was associated with a different gut microbiota composition and differences in brain morphology compared to healthy volunteers [48]. It appears that intestinal inflammation causes a “leaky gut” phenotype that generates the escape into circulation of the gram-negative associated lipopolysaccharide that in turn produces both central and systemic inflammatory immune responses while selecting the survival of specific bacterial species that can tolerate the response. host immune [49-51]. BD patients often show lowgrade peripheral inflammation with a further increase in pro-inflammatory cytokine levels during mood episodes [52]. Patients with schizophrenia and BD have been shown to exhibit higher levels of serum antibodies against fungal organisms such as Saccharomyces cerevisiae and Candida albicans, as well as soluble CD14 (sCD14), a protein marker of bacterial translocation [53-57]. Other supporting data are that the use of antipsychotic medications or diet products can attenuate this leaky gut phenotype [53,58]. However, this and other theories that delineate inflammatory mechanisms remain highly nonspecific for psychological illness.

d) Stress: There is evidence that stress affects neuroimmuno- endocrine pathways. Even exposure to acute stress alters the relative proportions of the main phyla of the microbiota, and when researchers deliberately alter the microbiota, the stress response is modified, anxiety-like behavior is generated, and the hypothalamic-pituitary-adrenal axis (HPA) set point changes [59] . In addition, in animal models of stress due to mild and chronic social defeat, they significantly change the intestinal microbiota. These changes are associated with changes in the concentration of some metabolites produced by the intestinal microbiota and in the immune signaling pathways, which suggests that these components may be important in stress-related clinical conditions, including depression [59] . In a rat model, prenatal stress (PNS) induced an exaggerated response of the HPA axis, increased blood pressure, and impaired cognitive function. In addition, an increase in the variability of the baseline respiratory rate and an abnormal response of the rate to hypoxic and hypercapnic insults was observed, which shows that there is an alteration in respiratory control. PNS also affected neurodevelopment and decreased the density of innervation of the distal colon and increased the colonic secretory response to catecholamine stimulation. Finally, the SNP induced lasting alterations in the composition of the intestinal microbiota, which consisted of a decrease in the number of bacteria in the Lactobacillus genus and an increase in the genera of Oscillibacter, Anaerotruncus and Peptococcus generates [60].

e) Suicide: One of the main causes of suicidal ideation is the presence of a pre-existing major depressive disorder (MDD) [61]. There is evidence obtained from animal models that relates MDD and suicidal ideation with the gut microbiota [62]. The most plausible theory that explains this association is that the gut microbiota modulates brain development, function and behavior by recruiting the same neuroimmune, neuroendocrine and neural pathways of the brain-gut axis that are dysfunctional in MDD [63]. Specifically, abnormalities in the serotonergic system have been widely implicated in suicidal behavior and suicide. For example, a strong association between low concentrations of 5-hydroxyindoleacetic acid (a way of measuring serotonin) and increased expression of 5HT2A receptors on platelets has been reported with suicidal behavior [64].

Interest conflict

The authors declare that we have no conflict of interest


We thank the State Council of Science and Technology of Jalisco (COECYTJAL) and the University of Guadalajara for the financial support received (Grant 8097-2019).


There is a growing body of information that establishes the bidirectional relationship between the gut microbiota-brain axis and mental health. In general, the studies reviewed provide support for the relevance of communication between the gut microbiota and the brain and its association with mood disorders in both animals and humans at different stages of life. This generates new research perspectives aimed at discovering interventions that modify the microbiota trying to improve the mental health of patients.


  1. Adak A, Khan MR (2019) An insight into gut microbiota and its functionalities. Cellular and Molecular Life Sciences 76: 473–493.
  2. O’Hara AM, Shanahan F (2006) The gut flora as a forgotten organ. EMBO Rep 7: 688-693.
  3. Ursell LK, Haiser HJ, Van Treuren W, Garg N, Reddivari L, et al. (2014) The intestinal metabolome: an intersection between microbiota and host. Gastroenterology 146: 1470-1476.
  4. Hollister EB, Gao C, Versalovic J (2014) Compositional and functional features of the gastrointestinal microbiome and their effects on human health. Gastroenterology 146: 1449-1458.
  5. Rogier EW, Frantz AL, Bruno ME, Wedlund L, Cohen DA, Stromberg AJ, et al.(2014) Lessons from mother: long-term impact of antibodies in breast milk on the gut microbiota and intestinal immune system of breastfed offspring. Gut Microbes 5: 663-668.
  6. Ley RE, Turnbaugh PJ, Klein S, Gordon JI (2006) Microbial ecology: human gut microbes associated with obesity. Nature 444: 1022-1023.
  7. Wang B, Jiang X, Cao M, Ge J, Bao Q, et al. (2016) Altered fecal microbiota correlates with liver biochemistry in nonobese patients with non-alcoholic fatty liver disease. Sci Rep 6: pp.32002.
  8. Järbrink Sehgal E, Andreasson A (2020) The gut microbiota and mental health in adults. Current Opinion in Neurobiology 62:102–114.
  9. Wang B, Yao M, Lv L, Ling Z, Li L (2017) The Human Microbiota in Health and Disease. Engineering 3: 71–82.
  10. Peirce JM, Alviña K (2019) The role of inflammation and the gut microbiome in depression and anxiety. J Neuro Res 97:1223–1241.
  11. Abdrabou AM, Osman EY, Aboubakr OA (2018) Comparative therapeutic efficacy study of Lactobacilli probiotics and T citalopram in treatment of acute stress-induced depression in lab murine models. Human Microbiome Journal 10: 33–36.
  12. Turnbaugh PJ, Ley RE, Mahowald MA, Magrini V, Mardis ER (2006) An obesity-associated gut microbiome with increased capacity for energy harvest. Nature 444: 1027-1031.
  13. Krajmalnik Brown R, Ilhan ZE, Kang DW, DiBaise JK (2012) Effects of Gut Microbes on Nutrient Absorption and Energy Regulation. Nutr Clin Pract 27: 201–214.
  14. Gill SR, Pop M, Deboy RT, Eckburg PB, Turnbaugh TJ, et al. (2006) Metagenomic analysis of the human distal gut microbiome. Science 312: 1355-1359.
  15. Roberfroid MB, Bornet F, Bouley C, Cummings JH (1995) Colonic microflora: nutrition and health. Summary and conclusions of an International Life Sciences Institute (ILSI) [Europe] workshop held in Barcelona, Spain. Nutr Rev 53: 127-130.
  16. Perry RJ, Peng L, Barry NA, Cline GW, Zhang D, et al. (2016) Acetate mediates a microbiome-brain-β-cell axis to promote metabolic syndrome. Nature 534: 213-217.
  17. Cani PD, Dewever C, Delzenne NM (2004) Inulin-type fructans modulate gastrointestinal peptides involved in appetite regulation (glucagon-like peptide-1 and ghrelin) in rats. Br J Nutr 92: 521-526.
  18. Martin AM , Sun EW, Rogers GB, Keating DJ (2019) The Influence of the Gut Microbiome on Host Metabolism Through the Regulation of Gut Hormone Release. Front. Physiol 10: pp.428.
  19. Cash HL, Whitham CV, Behrendt CL, Hooper LV (2006) Symbiotic bacteria direct expression of an intestinal bactericidal lectin. Science 313: 1126-1130.
  20. Hooper LV, Stappenbeck TS, Hong CV, Gordon JI (2003) Angiogenins: a new class of microbicidal proteins involved in innate immunity. Nat Immunol 4: 269-273.
  21. Schauber J, Svanholm C, Termén S, Iffland K, Menzel T, et al. (2003) Expression of the cathelicidin LL-37 is modulated by short chain fatty acids in colonocytes: relevance of signalling pathways. Gut 52: 735-741.
  22. Takiishi T, Morales Fenero CI, Saraiva Câmara NO (2017) Intestinal barrier and gut microbiota: Shaping our immune responses throughout life. Tissue Barriers 5: e1373208.
  23. Bouskra D, Brézillon C, Bérard M, Werts C, Varona R, et al. (2008) Lymphoid tissue genesis induced by commensals through NOD1 regulates intestinal homeostasis. Nature 456: 507-510.
  24. Macpherson AJ, Harris NL (2004) Interactions between commensal intestinal bacteria and the immune system. Nat Rev Immunol 4: 478-485.
  25. Pott J, Hornef M (2012) Innate immune signalling at the intestinal epithelium in homeostasis and disease. EMBO Rep13: 684-698.
  26. McDole JR, Wheeler LW, McDonald KG, Wang B, Konjufca V, et al.(2012) Goblet cells deliver luminal antigen to CD103+ dendritic cells in the small intestine. Nature 483: 345-349.
  27. Wang J, Wu X, Lai W (2017) Prevalence of depression and depressive symptoms among outpatients: a systematic review and meta-analysis. BMJ Open 7: e017173.
  28. Chung YE, Chen HC, Chou HL, Chen IM, Lee MS, et al. (2019) Exploration of microbiota targets for major depressive disorder and mood related traits. J Psychiat Res 111: 74-82.
  29. Huang Y, Shi X, Li Z, Shen Y, Shi X, et al. (2018) Possible association of Firmicutes in the gut microbiota of patients with major depressive disorder. Neuropsychiatr Dis Treat 14: 3329-3337.
  30. Chen Z, Li J, Gui S, Zhou C, Chen J, et al. (2018) Comparative metaproteomics analysis shows altered fecal microbiota signatures in patients with major depressive disorder. Neuroreport 29: 417-425.
  31. Skonieczna Zydecka K, Grochans E, Maciejewska D, Szkup M, Schneider Matyka D, et al. (2018) Faecal short chain fatty acids profile is changed in polish depressive women. Nutrients 10(12): pp.1939.
  32. Valles Colomer M, Falony G, Darzi Y, Tigchelaar EF, Wang J, et al. (2019) The neuroactive potential of the human gut microbiota in quality of life and depression. Nat Microbiol 4: 623-632.
  33. Heym N, Heasman BC, Hunter K, Blanco SR, Wang GY, et al. (2019) The role of microbiota and inflammation in self-judgement and empathy: implications for understanding the brain-gut-microbiome axis in depression. Psychopharmacology (Berl) 236: 1459-1470.
  34. Bear TLK, Dalziel JE, Coad J, Roy NC, Butts CA (2020) The Role of the Gut Microbiota in Dietary Interventions for Depression and Anxiety. Advances in Nutrition 11(4) : 890–907.
  35. Tsavkelova E, Klimova SY, Cherdyntseva T, Netrusov A (2006) Hormones and hormone-like substances of microorganisms: a review. Appl Biochem Microbiol 42: 229–235.
  36. Roshchina VV (2010) Evolutionary considerations of neurotransmitters in microbial, plant, and animal cells. In: Lyte M, Freestone PPE, editors. Microbial endocrinology: interkingdom signaling in infectious disease and health. Cham (Switzerland) Springer :pp. 17–52.
  37. Ross RP, Mills S, Hill C, Fitzgerald GF, Stanton C (2010) Specific metabolite production by gut microbiota as a basis for probiotic function. Int Dairy J 20: 269–726.
  38. Lyte M (2011) Probiotics function mechanistically as delivery vehicles for neuroactive compounds: microbial endocrinology in the design and use of probiotics. Bioessays 33: 574–581.
  39. Holzer P, Farzi A (2014) Neuropeptides and the microbiota-gut-brain axis. In: Lyte M, Cryan JF, editors. Microbial endocrinology: the microbiota-gut-brain axis in health and disease. New York: Springer pp.195–219.
  40. Bjurstöm H, Wang J, Ericsson I, Bengtsson M, Liu Y (2008) GABA, a natural immunomodulator of T lymphocytes. J Neuroimmunology 205: 44–50.
  41. de Jonge WJ (2013) The gut's little brain in control of intestinal immunity. ISRN Gastroenterol pp. 630159.
  42. Singh N, Gurav A, Sivaprakasam S, Brady E, Padia R, et al. (2014) Activation of Gpr109a, receptor for niacin and the commensal metabolite butyrate, suppresses colonic inflammation and carcinogenesis. Immunity 40:128–39.
  43. Stilling RM, van de Wouw M, Clarke G, Stanton C, Dinan TG (2016) The neuropharmacology of butyrate: the bread and butter of the microbiota-gut-brain axis? Neurochem Int 99: 110–132.
  44. Fukumoto S, Tatewaki M, Yamada T, Fujimiya M, Mantyh C, Voss M, et al.(2003) Short-chain fatty acids stimulate colonic transit via intraluminal 5-HT release in rats. Am J Physiol Regul Integr Comp Physiol 284: R1269–1276.
  45. Agrawal S, Agrawal A, Said HM (2016) Biotin deficiency enhances the inflammatory response of human dendritic cells. Am J Physiol Cell Physiol 311: C386–391.
  46. Flowers SA, Ward KM, Clark CT (2020) The Gut Microbiome in Bipolar Disorder and Pharmacotherapy Management. Neuropsychobiology 79: 43–49.
  47. Tseng PT, Zeng BS, Chen YW, Wu MK, Wu CK, et al. (2016) A meta-analysis and systematic review of the comorbidity between irritable bowel syndrome and bipolar disorder. Medicine (Baltimore) 95: e4617.
  48. Labus JS, Hollister EB, Jacobs J, Kirbach K, Oezguen N, et al. (2017) Differences in gut microbial composition correlate with regional brain volumes in irritable bowel syndrome. Microbiome 5: p.49.
  49. Zhao Y, Cong L, Jaber V, Lukiw WJ (2017) Microbiome-derived lipopolysaccharide enriched in the perinuclear region of Alzheimer’s disease brain. Front Immunol 8:1064.
  50. Abraham C, Medzhitov R (2011) Interactions between the host innate immune system and microbes in inflammatory bowel disease. Gastroenterology 140:1729–1737.
  51. Schirmer M, Smeekens SP, Vlamakis H, Jaeger M, Oosting M, et al. (2016) Linking the human gut microbiome to inflammatory cytokine production capacity. Cell 167: 1125–1136.
  52. Bai YM, Su TP, Tsai SJ, Wen Fei C, Li CT, et al. (2014) Comparison of inflammatory cytokine levels among type I/type II and manic/hypomanic/euthymic/depressive states of bipolar disorder. J Affect Disord 166: 187–92.
  53. Severance EG, Alaedini A, Yang S, Halling M, Gressitt KL, et al. (2012) Gastrointestinal inflammation and associated immune activation in schizophrenia. Schizophr Res.138: 48–53.
  54. Severance EG, Gressitt KL, Stallings CR, Katsafanas E, Schweinfurth LA, et al. (2016) Candida albicans exposures, sex specificity and cognitive deficits in schizophrenia and bipolar disorder. NPJ Schizophr. 2: 16018.
  55. Severance EG, Gressitt KL, Stallings CR, Origoni AE, Khushalani S, et al. (2013) Discordant patterns of bacterial translocation markers and implications for innate immune imbalances in schizophrenia. Schizophr Res. 148: 130–137.
  56. Kim YK, Jung HG, Myint AM, Kim H, Park SH (2007) Imbalance between pro-inflammatory and anti-inflammatory cytokines in bipolar disorder. J Affect Disord 104: 91–95.
  57. Debnath M, Berk M (2014) Th17 pathway-mediated immunopathogenesis of schizophrenia: mechanisms and implications. Schizophr Bull 40: 1412–1421.
  58. Severance EG, Gressitt KL, Stallings CR, Katsafanas E, Schweinfurth LA, et al. (2017) Probiotic normalization of Candida albicans in schizophrenia: a randomized, placebo-controlled, longitudinal pilot study. Brain Behav Immun 62: 41–45.
  59. Foster JA, Rinaman L, Cryan JF (2017) Stress & the gut-brain axis: Regulation by the microbiome. Neurobiology of Stress 7: 124-136.
  60. Golubeva AV, Crampton S, Desbonnet L, Edge D, O'Sullivan O, et al. (2015) Prenatal stress-induced alterations in major physiological systems correlate with gut microbiota composition in adulthood. Psychoneuroendocrinology 60: 58-74.
  61. Gacche RN (2018) Gut Microbiome and Suicidal Ideation: An Inscrutable Link?. EC Gastroenterology and Digestive System 5: 931-933.
  62. Kelly JR, Clarke G, Cryan JF, Dinan TG (2016) Brain-gut-microbiota axis: challenges for translation in psychiatry. Annals of Epidemiology 26: 366-372.
  63. De Vadder F, Grasset E, Holm LM, Karsenty G, Macpherson AJ, et al. (2018) Gut microbiota regulates maturation of the adult enteric nervous system via enteric serotonin networks. Proceedings of the National Academy of Sciences of the United States of America 115: 6458-6463.
  64. Pandey GN (2013) Biological basis of suicide and suicidal behavior. Bipolar Disorders 15: 524-541.

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