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Marazziti, D. Microbiota/Microbiome and the Gut–Brain Axis. Encyclopedia. Available online: (accessed on 22 June 2024).
Marazziti D. Microbiota/Microbiome and the Gut–Brain Axis. Encyclopedia. Available at: Accessed June 22, 2024.
Marazziti, Donatella. "Microbiota/Microbiome and the Gut–Brain Axis" Encyclopedia, (accessed June 22, 2024).
Marazziti, D. (2021, August 05). Microbiota/Microbiome and the Gut–Brain Axis. In Encyclopedia.
Marazziti, Donatella. "Microbiota/Microbiome and the Gut–Brain Axis." Encyclopedia. Web. 05 August, 2021.
Microbiota/Microbiome and the Gut–Brain Axis

The human gut microbiota, mainly consisting of Proteobacterias, Firmicutes, Actinobacteria and Bacteroidetes, changes during the course of life, as it is constantly influenced by several individual factors, such as the type of birth, infections, therapies, diet, smoking, physical activity, stressful events, environmental factors and medical diseases. It is also worth highlighting that the brain’s development, depending on pre- and post-natal genetic and environmental factors, occurs in parallel with the constitution of the microbiota. A newborn’s microbiota has a low density but, as the individual grows, it is enriched with certain microorganisms, becoming increasingly capable of activating signals and metabolic pathways that modulate neuronal function.

microbiota gut–brain axis central nervous system immune system autism spectrum disorders mood disorders obsessive-compulsive disorder schizophrenia novel psychotropic drugs neuropsychiatric disorders

1. Introduction

The terms “microbiota” and microbiome refer, respectively, to the collection of bacteria, viruses and fungi colonising different parts of the body, and to the complete genetic material encoded by the microbiota [1][2][3]. The gut microbiota, i.e., the commensal microorganisms within the gut, performs essential tasks for the normal functioning of the organism, such as the fermentation and digestion of carbohydrates, development of lymphoid tissues associated with the mucous membranes, production of vitamins, prevention of colonisation by pathogenic microorganisms and stimulation of the immune system [2][4][5][6]. The bacterial cells forming intestinal microbiota outnumber human cells by 10 times and encode for a gene set that is 150 times larger than the human one [1]. The human gut microbiota, mainly consisting of Proteobacterias, Firmicutes, Actinobacteria and Bacteroidetes, changes during the course of life, as it is constantly influenced by several individual factors, such as the type of birth, infections, therapies, diet, smoking, physical activity, stressful events, environmental factors and medical diseases [7][8][9]. It is also worth highlighting that the brain’s development, depending on pre- and post-natal genetic and environmental factors, occurs in parallel with the constitution of the microbiota. A newborn’s microbiota has a low density but, as the individual grows, it is enriched with certain microorganisms, becoming increasingly capable of activating signals and metabolic pathways that modulate neuronal function [10][11][12][13].

The immune system appears to be at the heart of the gut–microbiota–brain relationship. Indeed, an altered composition of the gut microbiota might compromise the epithelial intestinal integrity and lead to a defective defence against pathogenic microorganisms, with consequent inflammatory reactions and, ultimately, neuro-inflammation [14]. Moreover, dysbiosis causes an increase in the amount of short-chain fatty acids (SCFAs), such as acetate, propionate and butyrate, that might activate microglia cells, i.e., the immune cells of the CNS, leading to an increase in cytokines that may eventually alter brain connections and the blood–brain barrier (BBB) [15][16]. Interestingly, microbial-induced BBB dysfunction is hypothesised to play a causative role in mood and anxiety disorders, SZ, autism spectrum disorders (ASDs) and neurodegenerative diseases [17]. A role of the gut–brain axis in the development of CNS tumours was also proposed [18]. Finally, a growing number of findings suggest that the microbiota might modulate neuronal maturation and myelination processes in brain areas that are responsible for the control of emotions, executive functions and working memory, which are impaired in SZ, MDs and ASDs [19][20][21].

Given the available evidence, it is plausible that a better understanding of the influence exerted by intestinal flora on the CNS and the role of the gut microbiota in the onset and maintenance of psychiatric disorders might lead to producing novel treatments, including probiotics, personalised lifestyles, faecal microbiota transplantation (FMT) and specific diets [22].

Therefore, the aim of this paper was to review and comment on the current literature on the role of the intestinal microbiota and gut–brain axis in some common neuropsychiatric conditions.

2. CNS and Microbiota: The Gut–Brain Axis

The large number of novel studies on the relationships between microbiota and the CNS has led to the recognition of the gut–brain axis, that is to say, the bidirectional connection occurring between the gut microbiota and the brain through hormonal, metabolic, immunological and neural signalling, with the latter involving central, autonomic and enteric nervous systems [6][23][24][25]. This mutual connection seems to reflect a reciprocal influence: the diversity in microbiota composition affects brain development and behaviours, and vice versa [25].

Interestingly, brain changes that are promoted by microbiota might occur through the regulation of gene expression and neuronal transcription [26][27]. A murine model study demonstrated the upregulation of myelin-related genes in GF mice, specifically in the prefrontal cortex (PFC), leading to hypermyelinated axons. Furthermore, the subsequent colonisation of these animals (the so-called exGF) resulted in a reverted modulation [27]. Gene expression regulation that was driven by intestinal microbiota also led to the modulation of neuro-inflammation, production of insulin-like growth factor-1 (IGF-1) and changes in multiple neurotransmitter (serotonin (5-hydroxytryptamine, 5-HT), dopamine, glutamate and gamma-aminobutyric acid (GABA)) pathways, transporters and ion channels [26]. Focusing on neurotransmitters, male GF mice show increased 5-HT and 5-hydroxyindoleacetic acid (5-HIAA, the main 5-HT metabolite) in the hippocampus [28], while Bifidobacterium infantis administration in rats increased tryptophan, the 5-HT precursor [29]. As already mentioned, the effects of gut microbiota on neurotransmission extend beyond 5-HT. Non-pathogenic bacteria, such as Lactobacillus rhamnosus, modulate GABAergic transmission in mice, with beneficial effects on anxiety and depression [30], and GABA production by cultured intestinal strains of Lactobacillus and Bifidobacterium was observed [31]. Nonetheless, regarding the relationship between brain and GI tract, it is worth noting that about 90% of 5-HT is synthesised in the gut, where it modulates GI motility, and then is sequestered by platelets and transported to various body sites, acting as a pleiotropic hormone [32][33]. Indeed, the intestinal synthesis of 5-HT seems to be positively influenced by microbiota, consequently increasing 5-HT in the GI mucosa and lumen, platelets, blood and brain. As such, microbiota influence peripheral and central 5-HT concentrations [33].

Furthermore, the links between the brain and gut also play a role in the immune response. An example of this link is provided by microglia. As the resident macrophages of CNS, microglia are involved in the immune surveillance of the CNS itself [34], and as such, possibly in different brain disorders [35][36]. Microglia maturation, activation and function are affected by microbiota composition. According to some authors, microglia changes are driven by gut eradication, re-colonisation and variations in microbiota complexity. Interestingly, GF mice share defective microglia and impaired innate immunity [35].

It should be noted that the GI tract represents the largest immune organ, as well as the largest surface of contact with external agents [37]; therefore, it was hypothesised that alterations of intestinal flora, through regulatory T cells (Treg) abnormalities, might be involved in the epidemic of allergic, inflammatory and autoimmune diseases and also in psychiatric disorders [38][39][40][41][42][43][44][45].

3. Microbiota and Psychiatric Disorders

Indeed, the interactions between the host and its microbiota seem to be able to produce significant changes in brain networks, thus influencing behaviours and neuropsychiatric disorders [46].

Regarding the relationship between microbiota and SZ, research is still in its infancy. As mentioned above, animal studies underlined the role of microbiota in the postnatal development and maturation of neuronal, immune and endocrine systems, which influence processes, such as cognition and social behaviour, that are altered in SZ patients [47]. Studies conducted on schizophrenic patients led to intriguing results. Indeed, both treated and untreated patients with SZ showed altered gut microbiota and decreased microbiome heterogeneity compared with healthy controls. Moreover, some unique bacterial taxa and high Lactobacillus gut levels were related to the severity of the clinical picture in patients with SZ [48][49]. A cross-sectional study that analysed the composition of faecal microbiota in both schizophrenic and healthy subjects through 16S rRNA sequencing showed that the first showed abundances of the Proteobacteria Phylum, Succinivibrio, Megasphaera, Collinsella, Clostridium, Klebsiella and Methanobrevibacter. Therefore, the authors proposed a microbiota-based diagnosis and prognosis of SZ [50]. A study conducted on first-episode schizophrenic patients reported altered microbiota composition that was significantly modulated by risperidone, a first-generation antipsychotic (FGA), an effect possibly related to drug-induced metabolic changes [51]. Further evidence suggests that antipsychotics may indeed affect microbiota levels in patients with SZ, specifically in regard to the taxonomic distribution in the case of chronic treatments [52]. The effects of antipsychotic may also be boosted by some antibiotics, such as minocycline, which are able to modify the gut microbiota [53]. However, evidence on this matter is still controversial, as different studies did not detect similar effects of APs in the modulation of gut microbiota [54][55]. Again, the gut microbiota has been proposed as a factor that is responsible for the lack of response observed in some schizophrenic patients [56]. On the other hand, it was pointed out how probiotics showed no clinical utility in both negative or positive symptoms, albeit only three studies were fully reviewed [57]. Interestingly, in a murine model, inulin, which is a dietary fibre mainly produced by plants [58], was also proposed as a potential treatment in SZ patients due to its anti-inflammatory action and the effects exerted on the gut microbiota [59].

Recently, the relationship between the gut microbiome and brain morphological and functional correlates was investigated in patients with SZ. At the genus level, compared to healthy control subjects, SZ patients displayed a higher abundance of Veillonella, whilst the abundance of Roseburia and Ruminococcus was lower. Moreover, a comparison of MRI images highlighted significant differences in both the volume of gray matter and the regional homogeneity amongst the two groups and higher amplitudes of low-frequency fluctuation in SZ patients. Finally, both changes in gray matter volume and regional homogeneity correlated with the diversity of the gut microbiota [60]. In a similar fashion, significant changes in the volume of the right middle frontal gyrus seem to be related to the specific composition of gut microbiota in SZ [52]. Besides the hypothesis stating that altered gut microbiota might cause the abnormal activation of the immune system, making the gut barrier more susceptible to micro-environmental changes and leading to neuro-inflammation processes involving microglia-mediated neuronal damage, apoptosis, abnormal brain development and altered connectivity between brain regions, even epigenetic modulation might be a mechanism underlying the link between microbiota and SZ [61]. Indeed, gut microbiota might affect gene expression through acetylation and methylation processes in response to environmental cues, possibly constituting a link between environmental risk factors and epigenetic changes [62][63].

Since more specific data on these disorders are lacking, more in-depth studies are warranted to better understand the possible links between gut microbiota and EDs ( Table 1 ).

Table 1. Studies on the relationships between gut microbiota and eating disorders.
Authors and Year Type of Study Findings
Santonicola et al., 2019 [64] Review
Differences in alpha-diversity and composition of microbiota in EDs, possibly contributing to symptomatic manifestations and pathophysiology;
Seitz et al., 2019 [65] Review
Decreased alpha-diversity in AN, which showed an increase during weight restoration and a correlation with depressive and anxious symptoms;
Increased beta-diversity in AN, which decreased after weight rehabilitation;
Specific taxa abundance in AN could influence gut permeability, inflammation and symptomatic manifestations
Seitz et al., 2019 [66] Review
Decreased diversity and taxa abundance in AN;
AN-related changes in microbiome could increase gut permeability, inflammation and autoantibody formation;
Increased microbiome diversity in AN associated with depressive, anxious and EDs symptoms

Legend: AN—anorexia nervosa, ED—eating disorders.


  1. Gill, S.R.; Pop, M.; Deboy, R.T.; Eckburg, P.B.; Turnbaugh, P.J.; Samuel, B.S.; Gordon, J.I.; Relman, D.A.; Fraser-Liggett, C.M.; Nelson, K.E. Metagenomic analysis of the human distal gut microbiome. Science 2006, 312, 1355–1359.
  2. Clemente, J.C.; Ursell, L.K.; Parfrey, L.W.; Knight, R. The impact of the gut microbiota on human health: An integrative view. Cell 2012, 148, 1258–1270.
  3. Ma, Q.; Xing, C.; Long, W.; Wang, H.Y.; Liu, Q.; Wang, R.F. Impact of microbiota on central nervous system and neurological diseases: The gut-brain axis. J. Neuroinflamm. 2019, 16, 53.
  4. Stecher, B.; Hardt, W.D. Mechanisms controlling pathogen colonization of the gut. Curr. Opin. Microbiol. 2011, 14, 82–91.
  5. Tilg, H.; Kaser, A. Gut microbiome, obesity, and metabolic dysfunction. J. Clin. Investig. 2011, 121, 2126–2132.
  6. Collins, S.M.; Surette, M.G.; Bercik, P. The interplay between the intestinal microbiota and the brain. Nat. Rev. Microbiol. 2012, 10, 735–742.
  7. Ojeda, J.; Ávila, A.; Vidal, P.M. Gut microbiota interaction with the central nervous system throughout life. J. Clin. Med. 2021, 10, 1299.
  8. Rinninella, E.; Cintoni, M.; Raoul, P.; Lopetuso, L.R.; Scaldaferri, F.; Pulcini, G.; Miggiano, G.; Gasbarrini, A.; Mele, M.C. Food components and dietary habits: Keys for a healthy gut microbiota composition. Nutrients 2019, 11, 2393.
  9. Dinan, T.G.; Cryan, J.F. Regulation of the stress response by the gut microbiota: Implications for psychoneuroendocrinology. Psychoneuroendocrinology 2012, 37, 1369–1378.
  10. Redondo-Useros, N.; Nova, E.; González-Zancada, N.; Díaz, L.E.; Gómez-Martínez, S.; Marcos, A. Microbiota and lifestyle: A special focus on diet. Nutrients 2020, 12, 1776.
  11. Borre, Y.E.; O’Keeffe, G.W.; Clarke, G.; Stanton, C.; Dinan, T.G.; Cryan, J.F. Microbiota and neurodevelopmental windows: Implications for brain disorders. Trends. Mol. Med. 2014, 20, 509–518.
  12. Chu, D.M.; Antony, K.; Ma, J.; Prince, A.L.; Showalter, L.; Moller, M.; Aagaard, K.M. The early infant gut microbiome varies in association with a maternal high-fat diet. Genome Med. 2016, 8, 7.
  13. Chu, D.M.; Ma, J.; Prince, A.L.; Antony, K.M.; Seferovic, M.D.; Aagard, K.M. Maturation of the infant microbiome community structure and function across multiple body sites and in relation to mode of delivery. Nat. Med. 2017, 23, 314–326.
  14. Reyes, R.E.N.; Zhang, Z.; Gao, L.; Asatryan, L. Microbiome meets microglia in neuroinflammation and neurological disorders. Neuroimmunol. Neuroinflamm. 2020, 7, 215–233.
  15. Houser, M.C.; Tansey, M.G. The gut-brain axis: Is intestinal inflammation a silent driver of Parkinson’s disease pathogenesis? NPJ Parkinson’s Dis. 2017, 3, 3.
  16. Warner, B.B. The contribution of the gut microbiome to neurodevelopment and neuropsychiatric disorders. Pediatr. Res. 2019, 85, 216–224.
  17. Zhu, S.; Jiang, Y.; Xu, K.; Cui, M.; Ye, W.; Zhao, G.; Jin, L.; Chen, X. The progress of gut microbiome research related to brain disorders. J. Neuroinflamm. 2020, 17, 25.
  18. Mehrian-Shai, R.; Reichardt, J.K.V.; Harris, C.C.; Toren, A. The gut-brain axis, paving the way to brain cancer. Trends Cancer 2019, 5, 200–207.
  19. Phillips, M.L.; Swartz, H.A. A critical appraisal of neuroimaging studies of bipolar disorder: Toward a new conceptualization of underlying neural circuitry and a road map for future research. Am. J. Psychiatry 2014, 171, 829–843.
  20. Zhou, Y.; Fan, L.; Qiu, C.; Jiang, T. Prefrontal cortex and the dysconnectivity hypothesis of schizophrenia. Neurosci. Bull. 2015, 31, 207–219.
  21. Karim, H.T.; Wang, M.; Andreescu, C.; Tudorascu, D.; Butters, M.A.; Karp, J.F.; Reynolds, C.F., 3rd; Aizenstein, H.J. Acute trajectories of neural activation predict remission to pharmacotherapy in late-life depression. Neuroimage Clin. 2018, 19, 831–839.
  22. Liang, S.; Wu, X.; Jin, F. Gut-brain psychology: Rethinking psychology from the microbiota-gut-brain axis. Front. Integr. Neurosci. 2018, 12, 33.
  23. Cryan, J.F.; Dinan, T.G. Mind-altering microorganisms: The impact of the gut microbiota on brain and behaviour. Nat. Rev. Neurosci. 2012, 13, 701–712.
  24. Foster, J.A.; McVey Neufeld, K.A. Gut-brain axis: How the microbiome influences anxiety and depression. Trends Neurosci. 2013, 36, 305–312.
  25. Turna, J.; Grosman Kaplan, K.; Anglin, R.; Van Ameringen, M. “What’s bugging the gut in ocd?” A review of the gut microbiome in obsessive-compulsive disorder. Depress. Anxiety 2016, 33, 171–178.
  26. Lu, J.; Lu, L.; Yu, Y.; Cluette-Brown, J.; Martin, M.C.; Claud, C.E. Effects of intestinal microbiota on brain development in humanized gnotobiotic mice. Sci. Rep. 2018, 8, 5443.
  27. Hoban, A.E.; Stilling, R.M.; Ryan, F.J.; Shanahan, F.; Dinan, T.G.; Claesson, M.J.; Clarke, G.; Cryan, J.F. Regulation of prefrontal cortex myelination by the microbiota. Transl. Psychiatry 2016, 6, e774.
  28. Clarke, G.; Grenham, S.; Scully, P.; Fitzgerald, P.; Moloney, R.D.; Shanahan, F.; Dinan, T.G.; Cryan, J.F. The microbiome-gut-brain axis during early life regulates the hippocampal serotonergic system in a sex-dependent manner. Mol. Psychiatry 2013, 18, 666–673.
  29. Desbonnet, L.; Garrett, L.; Clarke, G.; Bienenstock, J.; Dinan, T.G. The probiotic Bifidobacteria infantis: An assessment of potential antidepressant properties in the rat. J. Psychiatr. Res. 2008, 43, 164–174.
  30. Bravo, J.A.; Forsythe, P.; Chew, M.V.; Escaravage, E.; Savignac, H.M.; Dinan, T.G.; Bienenstock, J.; Cryan, J.F. Ingestion of Lactobacillus strain regulates emotional behavior and central GABA receptor expression in a mouse via the vagus nerve. Proc. Natl. Acad. Sci. USA 2011, 108, 16050–16065.
  31. Barrett, E.; Ross, R.P.; O’Toole, P.W.; Fitzgerald, G.F.; Stanton, C. γ-Aminobutyric acid production by culturable bacteria from the human intestine. J. Appl. Microbiol. 2012, 113, 411–417.
  32. Amireault, P.; Sibon, D.; Cote, F. Life without peripheral serotonin: Insights from tryptophan hydroxylase 1 knockout mice reveal the existence of paracrine/autocrine serotonergic networks. ACS Chem. Neurosci. 2013, 4, 64–71.
  33. Yano, J.M.; Yu, K.; Donaldson, G.P.; Shastri, G.G.; Ann, P.; Ma, L.; Nagler, C.R.; Ismagilov, R.F.; Mazmanian, S.K.; Hsiao, E.Y. Indigenous bacteria from the gut microbiota regulate host serotonin biosynthesis. Cell 2015, 161, 264–276.
  34. Gehrmann, J.; Banati, R.B.; Kreutzberg, G.W. Microglia in the immune surveillance of the brain: Human microglia constitutively express HLA-DR molecules. J. Neuroimmunol. 1993, 48, 189–198.
  35. Erny, D.; Hrabě de Angelis, A.L.; Jaitin, D.; Wieghofer, P.; Staszewski, O.; David, E.; Keren-Shaul, H.; Mahlakoiv, T.; Jakobshagen, K.; Buch, T.; et al. Host microbiota constantly control maturation and function of microglia in the CNS. Nat. Neurosci. 2015, 18, 965–977.
  36. Priller, J.; Prinz, M. Targeting microglia in brain disorders. Science 2019, 365, 32–33.
  37. Rudzki, L.; Szulc, A. “Immune gate” of psychopathology—The role of gut derived immune activation in major psychiatric disorders. Front. Psychiatry 2018, 9, 205.
  38. Fazekas de St Groth, B. Regulatory T-cell abnormalities and the global epidemic of immuno-inflammatory disease. Immunol. Cell. Biol. 2012, 90, 256–259.
  39. Marazziti, D.; Hollander, E.; Lensi, P.; Ravagli, S.; Cassano, G.B. Peripheral markers of serotonin and dopamine function in obsessive-compulsive disorder. Psychiatry Res. 1992, 42, 41–51.
  40. Benros, M.E.; Eaton, W.W.; Mortensen, P.B. The epidemiologic evidence linking autoimmune diseases and psychosis. Biol. Psychiatry 2014, 75, 300–306.
  41. Al-Diwani, A.A.J.; Pollak, T.A.; Irani, S.R.; Lennox, B.R. Psychosis: An autoimmune disease? Immunology 2017, 152, 388–401.
  42. Gerentes, M.; Pelissolo, A.; Rajagopal, K.; Tamouza, R.; Hamdani, N. Obsessive-compulsive disorder: Autoimmunity and neuroinflammation. Curr. Psychiatry Rep. 2019, 21, 78.
  43. Jeppesen, R.; Benros, M.E. Autoimmune diseases and psychotic disorders. Front. Psychiatry 2019, 10, 131.
  44. Marazziti, D.; Mucci, F.; Fontanelle, L.F. Immune system and obsessive-compulsive disorder. Psychoneuroendocrinology 2018, 93, 39–44.
  45. Rogers, J.P.; Pollak, T.A.; Blackman, G.; David, A.S. Catatonia and the immune system: A review. Lancet Psychiatry 2019, 6, 620–630.
  46. Cenit, M.C.; Sanz, Y.; Codoñer-Franch, P. Influence of gut microbiota on neuropsychiatric disorders. World J. Gastroenterol. 2017, 23, 5486–5498.
  47. Golofast, B.; Vales, K. The connection between microbiome and schizophrenia. Neurosci. Biobehav. Rev. 2020, 108, 712–731.
  48. Schwarz, E.; Maukonen, J.; Hyytiäinen, T.; Kieseppä, T.; Orešič, M.; Sabunciyan, S.; Mantere, O.; Saarela, M.; Yolken, R.; Suvisaari, J. Analysis of microbiota in first episode psychosis identifies preliminary associations with symptom severity and treatment response. Schizophr. Res. 2018, 192, 398–403.
  49. Zheng, P.; Zeng, B.; Liu, M.; Chen, J.; Pan, J.; Han, Y.; Liu, Y.; Cheng, K.; Zhou, C.; Wang, H.; et al. The gut microbiome from patients with schizophrenia modulates the glutamate-glutamine-GABA cycle and schizophrenia-relevant behaviors in mice. Sci. Adv. 2019, 5, eaau8317.
  50. Shen, Y.; Xu, J.; Li, Z.; Huang, Y.; Yuan, Y.; Wang, J.; Zhang, M.; Hu, S.; Liang, Y. Analysis of gut microbiota diversity and auxiliary diagnosis as a biomarker in patients with schizophrenia: A cross-sectional study. Schizophr. Res. 2018, 197, 470–477.
  51. Yuan, X.; Zhang, P.; Wang, Y.; Liu, Y.; Li, X.; Kumar, B.U.; Hei, G.; Lv, L.; Huang, X.F.; Fan, X.; et al. Changes in metabolism and microbiota after 24-week risperidone treatment in drug naïve, normal weight patients with first episode schizophrenia. Schizophr. Res. 2018, 201, 299–306.
  52. Ma, X.; Asif, H.; Dai, L.; He, Y.; Zheng, W.; Wang, D.; Ren, H.; Tang, J.M.; Li, C.; Jin, K.; et al. Alteration of the gut microbiome in first-episode drug-naïve and chronic medicated schizophrenia correlate with regional brain volumes. J. Psych. Res. 2020, 123, 136–144.
  53. Khodaie-Ardakani, M.R.; Mirshafiee, O.; Farokhnia, M.; Tajdini, M.; Hosseini, S.M.; Modabbernia, A.; Rezaei, F.; Salehi, B.; Yekehtaz, H.; Ashrafi, M.; et al. Minocycline add-on to risperidone for treatment of negative symptoms in patients with stable schizophrenia: Randomized double-blind placebo-controlled study. Psychiatry Res. 2014, 215, 540–546.
  54. Kao, A.C.; Spitzer, S.; Anthony, D.C.; Lennox, B.; Burnet, P. Prebiotic attenuation of olanzapine-induced weight gain in rats: Analysis of central and peripheral biomarkers and gut microbiota. Transl. Psychiatry 2018, 8, 66.
  55. Pełka-Wysiecka, J.; Kaczmarczyk, M.; Bąba-Kubiś, A.; Liśkiewicz, P.; Wroński, M.; Skonieczna-Żydecka, K.; Marlicz, W.; Misiak, B.; Starzyńska, T.; Kucharska-Mazur, J.; et al. Analysis of gut microbiota and their metabolic potential in patients with schizophrenia treated with olanzapine: Results from a six-week observational prospective cohort study. J. Clin. Med. 2019, 8, 1605.
  56. Seeman, M.V. The gut microbiome and treatment-resistance in schizophrenia. Psychiatr Q. 2020, 91, 127–136.
  57. Ng, Q.X.; Soh, A.; Venkatanarayanan, N.; Ho, C.; Lim, D.Y.; Yeo, W.S. A systematic review of the effect of probiotic supplementation on schizophrenia symptoms. Neuropsychobiology 2019, 78, 1–6.
  58. Roberfroid, M.B. Introducing inulin-type fructans. Br. J. Nutr. 2005, 93 (Suppl. 1), S13–S25.
  59. Guo, L.; Xiao, P.; Zhang, X.K.; Yang, Y.; Yang, M.; Wang, T.; Lu, H.; Tian, H.; Wang, H.; Liu, J. Inulin ameliorates schizophrenia via modulation of the gut microbiota and anti-inflammation in mice. Food Funct. 2021, 12, 1156–1175.
  60. Li, S.; Song, J.; Ke, P.; Kong, L.; Lei, B.; Zhou, J.; Huang, Y.; Li, H.; Li, G.; Chen, J.; et al. The gut microbiome is associated with brain structure and function in schizophrenia. Sci. Rep. 2021, 11, 9743.
  61. Yuan, X.; Kang, Y.; Zhuo, C.; Huang, X.F.; Song, X. The gut microbiota promotes the pathogenesis of schizophrenia via multiple pathways. Biochem. Biophys. Res. Commun. 2019, 512, 373–380.
  62. Stilling, R.M.; Dinan, T.G.; Cryan, J.F. Microbial genes, brain & behaviour-epigenetic regulation of the gut-brain axis. Genes Brain Behav. 2014, 13, 69–86.
  63. Zhou, J.; Park, C.Y.; Theesfeld, C.L.; Wong, A.K.; Yuan, Y.; Scheckel, C.; Fak, J.J.; Funk, J.; Yao, K.; Tajima, Y.; et al. Whole-genome deep learning analysis identifies contribution of noncoding mutations to autism risk. Nat. Genet. 2019, 51, 973–980.
  64. Santonicola, A.; Gagliardi, M.; Guarino, M.; Siniscalchi, M.; Ciacci, C.; Iovino, P. Eating disorders and gastrointestinal diseases. Nutrients 2019, 11, 3038.
  65. Seitz, J.; Belheouane, M.; Schulz, N.; Dempfle, A.; Baines, J.F.; Herpertz-Dahlmann, B. The impact of starvation on the microbiome and gut-brain interaction in anorexia nervosa. Front. Endocrinol 2019, 10, 41.
  66. Seitz, J.; Trinh, S.; Herpertz-Dahlmann, B. The microbiome and eating disorders. Psychiatr. Clin. N. Am. 2019, 42, 93–103.
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