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Thats interesting Trouble, I think my Mums IBS has improved since she switched to olive oil - and fish oil capsules. I still dont think she takes enough though,

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Some interesting stuff on the comorbidity and bi-directional dysfunction of IBS with with the brain/mood. In other words, the microbiota-gut-brain axis...

World J Gastroenterol. 2014 Oct 21;20(39):14126-31. doi: 10.3748/wjg.v20.i39.14126.

Impact of psychological stress on irritable bowel syndrome.

Qin HY(1), Cheng CW(1), Tang XD(1), Bian ZX(1).

Author information: (1)Hong-Yan Qin, Department of Pharmacy, First Hospital of Lanzhou University, Lanzhou 730000, China.

Psychological stress is an important factor for the development of irritable bowel syndrome (IBS). More and more clinical and experimental evidence showed that IBS is a combination of irritable bowel and irritable brain. In the present review we discuss the potential role of psychological stress in the pathogenesis of IBS and provide comprehensive approaches in clinical treatment. Evidence from clinical and experimental studies showed that psychological stresses have marked impact on intestinal sensitivity, motility, secretion and permeability, and the underlying mechanism has a close correlation with mucosal immune activation, alterations in central nervous system, peripheral neurons and gastrointestinal microbiota. Stress-induced alterations in neuro-endocrine-immune pathways acts on the gut-brain axis and microbiota-gut-brain axis, and cause symptom flare-ups or exaggeration in IBS. IBS is a stress-sensitive disorder, therefore, the treatment of IBS should focus on managing stress and stress-induced responses. Now, non-pharmacological approaches and pharmacological strategies that target on stress-related alterations, such as antidepressants, antipsychotics, miscellaneous agents, 5-HT synthesis inhibitors, selective 5-HT reuptake inhibitors, and specific 5-HT receptor antagonists or agonists have shown a critical role in IBS management. A integrative approach for IBS management is a necessary.

DOI: 10.3748/wjg.v20.i39.14126 PMCID: PMC4202343 PMID: 25339801 [Indexed for MEDLINE]

World J Gastroenterol. 2014 Jun 28;20(24):7570-86. doi: 10.3748/wjg.v20.i24.7570.

Role of negative affects in pathophysiology and clinical expression of irritable bowel syndrome.

Muscatello MR(1), Bruno A(1), Scimeca G(1), Pandolfo G(1), Zoccali RA(1).

Author information: (1)Maria Rosaria A Muscatello, Antonio Bruno, Giuseppe Scimeca, Gianluca Pandolfo, Rocco A Zoccali, Psychiatry Unit, Department of Neurosciences, University of Messina, 98125 Messina, Italy.

Irritable bowel syndrome (IBS) is regarded as a multifactorial disease in which alterations in the brain-gut axis signaling play a major role. The biopsychosocial model applied to the understanding of IBS pathophysiology assumes that psychosocial factors, interacting with peripheral/central neuroendocrine and immune changes, may induce symptoms of IBS, modulate symptom severity, influence illness experience and quality of life, and affect outcome. The present review focuses on the role of negative affects, including depression, anxiety, and anger, on pathogenesis and clinical expression of IBS. The potential role of the autonomic nervous system, stress-hormone system, and immune system in the pathophysiology of both negative affects and IBS are taken into account. Psychiatric comorbidity and subclinical variations in levels of depression, anxiety, and anger are further discussed in relation to the main pathophysiological and symptomatic correlates of IBS, such as sensorimotor functions, gut microbiota, inflammation/immunity, and symptom reporting.

DOI: 10.3748/wjg.v20.i24.7570 PMCID: PMC4069288 PMID: 24976697 [Indexed for MEDLINE]

Psychother Psychosom. 2017;86(1):31-46. Epub 2016 Nov 25.

Gut Microbiota, Bacterial Translocation, and Interactions with Diet: Pathophysiological Links between Major Depressive Disorder and Non-Communicable Medical Comorbidities.

Slyepchenko A(1), Maes M, Jacka FN, Köhler CA, Barichello T, McIntyre RS, Berk M, Grande I, Foster JA, Vieta E, Carvalho AF.

Author information: (1)McMaster Integrative Neuroscience Discovery and Study (MiNDS), McMaster University, Hamilton, Ont., Canada.

BACKGROUND: Persistent low-grade immune-inflammatory processes, oxidative and nitrosative stress (O&NS), and hypothalamic-pituitary-adrenal axis activation are integral to the pathophysiology of major depressive disorder (MDD). The microbiome, intestinal compositional changes, and resultant bacterial translocation add a new element to the bidirectional interactions of the gut-brain axis; new evidence implicates these pathways in the patho-aetiology of MDD. In addition, abnormalities in the gut-brain axis are associated with several chronic non-communicable disorders, which frequently co-occur in individuals with MDD, including but not limited to irritable bowel syndrome (IBS), chronic fatigue syndrome (CFS), obesity, and type 2 diabetes mellitus (T2DM). METHODS: We searched the PubMed/MEDLINE database up until May 1, 2016 for studies which investigated intestinal dysbiosis and bacterial translocation (the 'leaky gut') in the pathophysiology of MDD and co-occurring somatic comorbidities with an emphasis on IBS, CFS, obesity, and T2DM. RESULTS: The composition of the gut microbiota is influenced by several genetic and environmental factors (e.g. diet). Several lines of evidence indicate that gut-microbiota-diet interactions play a significant pathophysiological role in MDD and related medical comorbidities. Gut dysbiosis and the leaky gut may influence several pathways implicated in the biology of MDD, including but not limited to immune activation, O&NS, and neuroplasticity cascades. However, methodological inconsistencies and limitations limit comparisons across studies. CONCLUSIONS: Intestinal dysbiosis and the leaky gut may constitute a key pathophysiological link between MDD and its medical comorbidities. This emerging literature opens relevant preventative and therapeutic perspectives.

© 2016 S. Karger AG, Basel.

DOI: 10.1159/000448957 PMID: 27884012 [Indexed for MEDLINE]


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