Invest in ME Conference 12: First Class in Every Way
OverTheHills wraps up our series of articles on this year's 12th Invest in ME International Conference (IIMEC12) in London with some reflections on her experience as a patient attending the conference for the first time.
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Fecal metagenomic profiles in subgroups of patients with ME/CFS

Discussion in 'Latest ME/CFS Research' started by Kati, Apr 26, 2017.

  1. Kati

    Kati Patient in training

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    This is a press release from eureka Alert regarding a new publication from the Lipkin team at Columbia University:

    Chronic fatigue syndrome linked to imbalanced microbiome
    Scientists identify abnormal levels of specific gut bacteria in individuals with chronic fatigue syndrome, including those with and without co-morbid IBS

    https://eurekalert.org/pub_releases/2017-04/cums-cfs042117.php

    Exerpt:


    More at the link above. I do not have a link to the paper as of yet.

    Edit: for the purpose of clarity, here is the full abstract and the link to open access paper:

    Fecal metagenomic profiles in subgroups of patients with myalgic encephalomyelitis/chronic fatigue syndrome
    • Dorottya Nagy-Szakal†, Brent L. Williams†, Nischay Mishra, Xiaoyu Che, Bohyun Lee, Lucinda Bateman, Nancy G. Klimas, Anthony L. Komaroff, Susan Levine, Jose G. Montoya, Daniel L. Peterson, Devi Ramanan, Komal Jain, Meredith L. Eddy, Mady Hornig and W. Ian Lipkin
    †Contributed equally
    Microbiome20175:44
    DOI: 10.1186/s40168-017-0261-y

    Received: 11 January 2017, Accepted: 4 April 2017, Published: 26 April 2017

    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 Bacteroidesabundance 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 MetagenomicTopological data analysis Irritable bowel syndrome Metabolic pathway

    https://microbiomejournal.biomedcentral.com/articles/10.1186/s40168-017-0261-y
     
    Last edited: Apr 27, 2017
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  2. Cheshire

    Cheshire Senior Member

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    Article in The Times: https://www.thetimes.co.uk/article/gut-bacteria-linked-to-chronic-fatigue-30wkq5fjp (behind Paywall)

    Couldn't prevent themselves from refering to "Yuppie flu":

    And link to the paper: http://download.springer.com/static...41fb5e8044a6194276c6f84b19b58b950f092764bb353
     
  3. Cheesus

    Cheesus Senior Member

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    I really wish Lipkin's fundraising effort was doing better. His Monster Study would surely add heaps of useful data to existing literature. However the target amount is so high that it is simply daunting, and he is in direct competition with the likes of Ron Davis who has managed to capture the community's imagination more effectively.

    Here's hoping he can get some money via the RFAs due in at the start of next month. Here is a link to make a donation:

    https://giving.columbia.edu/giveonline/?schoolstyle=5881&alloc=21677
     
    Last edited: Apr 26, 2017
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  4. AndyPR

    AndyPR RIP PR :'(

  5. AndyPR

    AndyPR RIP PR :'(

    Couldn't agree more about wanting more funds to go towards the work at CII (Centre for Infection and Immunity). Having said that, I haven't ever seen a total given for OMF, while the Microbe Discovery Project, who fundraise in support of CII, give occasional updates, and didn't Ron recently say that ideally he needs $5 million, which is the same target that MDP has? Of course, the ideal situation would be if both teams were properly funded.

    From a recent MDP blog, http://microbediscovery.org/2017/02...l-this-mean-for-columbia-ciis-mecfs-research/
     
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  6. Manganus

    Manganus Senior Member

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    Canary islands
    The conclusions are comprehensive:

     
  7. Marco

    Marco Grrrrrrr!

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    All very interesting but apart from obvious examples (dysentery) is there any evidence that the gut microbiota directly and unamiguously cause any disease?

    This seems a more reasonable assessment (bold added) :

    "The role of the microbiota in specific diseases and conditions

    The above sections have described some of the many ways that the microbiota can influence human physiology, and it is no surprise that there is great interest in studying microbiota changes associated with diseased states, often referred to as dysbiosis (Table 1). However, the relationship between dysbiosis and disease pathogenesis is uncertain in the majority of examples at this time. It is often not clear what microbiota changes associated with disease are meaningful and distinguishing between cause and effect is inherently challenging. While it is intriguing to speculate that dysbiosis may cause disease as we learn more about how the microbiota can influence the host, it is also noted that the diseased state can lead to changes to the microbiota through various mechanisms, including changes in eating habits and bowel function as well as through the addition of medications such as antibiotics. In this section, we highlight a few of the recent findings on the role of the microbiota in particular diseases or conditions, but we cannot touch on all of the emerging findings in a multitude of other diseases both inside and outside the gut, including but not limited to rheumatoid arthritis (25), colorectal cancer (26), obesity (27), and diabetes (28)."

    The gut microbiome in health and in disease

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4290017/
     
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  8. AndyPR

    AndyPR RIP PR :'(

    And where does this paper make that claim?

    From the paper, https://microbiomejournal.biomedcentral.com/articles/10.1186/s40168-017-0261-y, my bolding.
    ETA: Associated does not equal caused by. There is a connection but they make no claim as to which way the link goes.
     
    Last edited: Apr 26, 2017
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  9. Forbin

    Forbin Senior Member

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    I agree. However, I suspect that using their resources to publish smaller studies like this may help them to bootstrap their way toward getting more sizable grants and getting the interest of additional donors. Hopefully, it will contribute to a process that will "snowball" in the future.
     
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  10. AdamS

    AdamS Senior Member

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    From a brief scan it seems that some of the intestinal bacterial species that were seen to be increased are associated with the following:

    - Increased fermentation
    - Glucose tolerance/metabolism

    Now i'm no expert but we already know from Davis/Fluge & Mella that there's something wrong with energy production and we seem to be falling back on the less efficient methods. Would it not make sense then to see increases in these bacterial species if we're having to rely on anaerobic respiration/fermentation more? To me it seems like changes in the microbiome could be a consequence rather than a cause of ME. I'm definitely interested to hear logical arguments as to why I could be wrong though! :)

    [​IMG]
     
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  11. deleder2k

    deleder2k Senior Member

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    @AdamS that is very interesting! I see that alcoholic and lactic acid fermentation. The only thing that relieve my ME is alcohol. Lots of alcohol. 12 beers makes me feel almost 100% healthy. Could this have anything to do with that?
     
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  12. Aroa

    Aroa

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    I agree with you @AdamS
     
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  13. AdamS

    AdamS Senior Member

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    @deleder2k Haha that's awesome. In all honestly i'm not entirely sure. There have been some theories thrown around that alcohol can help because of its vasodilatory effect. You would think that beer would be counterproductive though because of it's toxic load on the liver...it does contain a hell of a lot of sugar too. Some seem to be intolerant of alcohol and others get on fine with it which I find interesting.
     
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  14. Marco

    Marco Grrrrrrr!

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  15. AndyPR

    AndyPR RIP PR :'(

    Wow, that's deep. What indeed is the point of this research, or any research for that matter?
     
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  16. starlighter

    starlighter

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    Interesting there are a few cases of patients using lots of probiotics and herbs to change their gut who are now recovered or doing very well.
    Ken Lassesen being one of them https://cfsremission.com/probiotics/
     
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  17. Forbin

    Forbin Senior Member

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    This study would seem to support the June 2016 study by Ludovic Giloteaux and Maureen Hason of Cornel University which found a decrease in the diversity of bacteria in the microbiomes of ME/CFS patients vs. controls.
    https://microbiomejournal.biomedcentral.com/articles/10.1186/s40168-016-0171-4

    Both studies found fewer bacteria of the type Faecalibacterium prausnitzii (F. prausnitzii), which apparently have anti-inflammatory properties.

    Lower numbers of Faecalibacterium prausnitzii are also seen in Chron's disease and chronic ulcerative colitis, two inflammatory bowel diseases thought to be autoimmune in nature.
    [bolding mine]
     
    Last edited: Apr 26, 2017
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  18. Marco

    Marco Grrrrrrr!

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    Lighten up. It's a legitimate question and the first question that any funding panel member would ask. In fact they shouldn't/wouldn't need to as a funding application would state a working hypothesis (that ME/CFS will be found to be 'associated' with changes to the microbiome and that association is theoretically/clinically relevant because ....etc.

    I expect they will state this in the full paper - I was hoping someone had an idea what their working hypothesis was.
     
  19. AdamS

    AdamS Senior Member

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    Hmm interesting. Looks like Faecalibacterium Prausnitzii could be quite relevant to us then. I've done a bit of digging and found this:
    [​IMG]

    Perhaps there is an argument to suggest that the microbiome could be a cause of ME then. If low Faecalibacterium prausnitzii (along with other changes to other bacterial species) can impact serum cytokine levels at such a 'high capacity' then maybe this could impact pyruvate catabolism and thus impact energy production. Again just throwing stuff out there, open to comments/criticism.

    Source: https://www.nature.com/articles/srep18507
     
    Last edited: Apr 26, 2017
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  20. BurnA

    BurnA Senior Member

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    If I remember correctly Maureen Hanson was asked about this in general and she didn't seem to think it was that simple.
     
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