I am seeing a functional medicine practitioner. Had all sorts of tests done to include stool, urine, blood, saliva, etc… Tested for gut dysbiosis. I am sure there is something going on with the gut. Will report results back in a couple of months or less. Here is an interesting article that just came out recently:
Fecal metagenomic profiles in subgroups of patients with myalgic encephalomyelitis/ chronic fatigue syndrome
Dorottya Nagy-Szakal1†, Brent L. Williams1†, Nischay Mishra1, Xiaoyu Che1, Bohyun Lee1, Lucinda Bateman2, Nancy G. Klimas3,9, Anthony L. Komaroff4, Susan Levine5, Jose G. Montoya6, Daniel L. Peterson7, Devi Ramanan8, Komal Jain1, Meredith L. Eddy1, Mady Hornig1 and W. Ian Lipkin1*
Abstract
Background: Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is characterized by unexplained persistent fatigue, commonly accompanied by cognitive dysfunction, sleeping disturbances, orthostatic intolerance, fever, lymphadenopathy, and irritable bowel syndrome (IBS). The extent to which the gastrointestinal microbiome and peripheral inflammation are associated with ME/CFS remains unclear. We pursued rigorous clinical characterization, fecal bacterial metagenomics, and plasma immune molecule analyses in 50 ME/CFS patients and 50 healthy controls frequency-matched for age, sex, race/ethnicity, geographic site, and season of sampling.
Results: Topological analysis revealed associations between IBS co-morbidity, body mass index, fecal bacterial composition, and bacterial metabolic pathways but not plasma immune molecules. IBS co-morbidity was the strongest driving factor in the separation of topological networks based on bacterial profiles and metabolic pathways. Predictive selection models based on bacterial profiles supported findings from topological analyses indicating that ME/CFS subgroups, defined by IBS status, could be distinguished from control subjects with high predictive accuracy. Bacterial taxa predictive of ME/CFS patients with IBS were distinct from taxa associated with ME/CFS patients without IBS. Increased abundance of unclassified Alistipes and decreased Faecalibacterium emerged as the top biomarkers of ME/ CFS with IBS; while increased unclassified Bacteroides abundance and decreased Bacteroides vulgatus were the top biomarkers of ME/CFS without IBS. Despite findings of differences in bacterial taxa and metabolic pathways defining ME/CFS subgroups, decreased metabolic pathways associated with unsaturated fatty acid biosynthesis and increased atrazine degradation pathways were independent of IBS co-morbidity. Increased vitamin B6 biosynthesis/salvage and pyrimidine ribonucleoside degradation were the top metabolic pathways in ME/CFS without IBS as well as in the total ME/CFS cohort. In ME/CFS subgroups, symptom severity measures including pain, fatigue, and reduced motivation were correlated with the abundance of distinct bacterial taxa and metabolic pathways.
Conclusions: Independent of IBS, ME/CFS is associated with dysbiosis and distinct bacterial metabolic disturbances that may influence disease severity. However, our findings indicate that dysbiotic features that are uniquely ME/CFS- associated may be masked by disturbances arising from the high prevalence of IBS co-morbidity in ME/CFS. These insights may enable more accurate diagnosis and lead to insights that inform the development of specific therapeutic strategies in ME/CFS subgroups.
Keywords: Myalgic encephalomyelitis, Chronic fatigue syndrome, Microbiota-gut-brain axis, Metagenomic, Topological data analysis, Irritable bowel syndrome, Metabolic pathway
- Correspondence: wil2001@cumc.columbia.edu
†Equal contributors
1Center for Infection and Immunity, Columbia University Mailman School of Public Health, 722 W 168th Street 17th Floor, New York, NY 10032, USA Full list of author information is available at the end of the article
© The Author(s). 2017 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
Nagy-Szakal et al. Microbiome (2017) 5:44
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victim"]Clearly digestive issues are a symptom that most of us get. Some think that the gut is the key to recovery. Here is a well written article about a gut inflammation theory.
http://www.pfshealing.com/post-finasteride-syndrome-recovery-how-to-reduce-gut-inflammation/
Its saying that gut inflammatory cytokines produced by systematic inflamation in our bodies (specifically in our gut) are preventing our bodies from stabilizing our hormones and neurosteroids resulting in us not being able to recover. It’s not suggesting that inflammatory cytokines caused PFS but that it’s the main reason why we can’t recover from it.
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5 alpha victim & others,
Thank you for your post. On Feb 16th, I went on pfshealing.com and had the opportunity to read the article on inflammation. Then I wanted to go back to the website on the next day to read more articles, but since then, the website is gone. The web address is for sale…
From the article I read (inflammation) the guy seemed quite scientific, and I would have liked to read more about what he says about supplementation… By any chance, would any one of you have saved the articles written by Josh Abrhams and could share them?
Thank you,
Charles
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I remember reading this as well. It sounded logical but after six normal colonoscopys finding no evidence of gut inflammation Its sounds unlikely.
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