New Atmosphere, New Vision: Gibson and Whittemore Kick Off Invest in ME Conference 2016
Mark Berry reports on Dr. Gibson's introduction and Dr. Whittemore's keynote speech, at the 11th Invest in ME International ME Conference in London.
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IACFS/ME conference abstracts (2014)

Discussion in 'Latest ME/CFS Research' started by Bob, Jul 29, 2014.

  1. Bob

    Bob

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  2. taniaaust1

    taniaaust1

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    Yeah that is way heavy going, Ive got part throu and Ive been going throu it reading only the results and conclusions areas of many of the studies (but reading a little bit more of something if it really got my attention). Im going to finish reading the rest of the study results another another day.

    A couple of things got my attention, the bit in the childrens part mentioned many ME/CFS children had issues with milk protein (Ive been sure for ages my body is having an issue with milk protein at times, my sister who has ME/CFS seems to have an issue with milk protein too). Neither of my healthy sisters have issues with milk or any of my other family (only my nanna who has FM). So I can see a link there.

    One part I think would get the attention thou of most here is the following.


    This gives much food for thought "self-referred patients complaining of PENE (post-exertional neuroimmune exhaustion)" Why did it turn out that 60% of them had other illnesses and not ME/CFS seeing they had PENE or thought they did.

    Can we not trust at all that PENE helps define this illness??? or is it the case of many who have ME/CFS not really understanding what PENE is and saying they have it when they do not at all? I want to know how PENE was defined to these people who said they had it.
     
    Last edited: Jul 30, 2014
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  3. Bob

    Bob

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    It's curious, isn't it Tania. Thanks for highlighting.

    They had probably been reading up on ME/CFS and thought that the symptom of PEM/PENE fitted their health experiences. Perhaps they'd been misdiagnosed with ME/CFS by a primary care practitioner. I think that 'PEM' and 'PENE' might be interchangable here, in that 'PENE' might be the author's favoured term rather than the patients' own description.

    The abstract mentions that 43% were re-diagnosed with rheumatological diseases. I've heard before that people with arthritis have post-exertional flare-ups, and experience fatigue, so perhaps it isn't surprising that they identified with 'PENE' or 'PEM', and not entirely surprising if they'd previously been misdiagnosed with ME/CFS by incompetent general practicioners.

    To keep this thread on-topic, I've posted more about this in another thread, here:
    http://forums.phoenixrising.me/index.php?threads/is-cdc-out-to-bury-pem.31292/page-8#post-487660
     
    Last edited: Jul 30, 2014
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  4. Bob

    Bob

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    Just bumping this because there are some really interesting abstracts. It's worth having a flick through, if you're interested, as it hopefully gives a taste what's to come in terms of future publishing re ME/CFS. It's difficult to analyse many of the abstracts without the full information, but there seems to be some interesting research in the pipeline. I don't think there are any stand-out papers that look like they are going to give us answers in the immediate future but, combined, this seems to be quite a substantial body of work, with plenty of overlapping research looking at the same systems. It includes abstracts by some scientific big-hitters.
     
    Last edited: Jul 31, 2014
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  5. Forbin

    Forbin Senior Member

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    As someone who was once apparently erroneously diagnosed with chronic ulcerative colitis several years following the onset of ME (the "chronic" ulcerative colitis simply vanished after a month of treatment with azulfidine), the study below caught my attention:

    Basically, the research finds that the gut microbiome of ME/CFS patients shows a shift characteristic of inflammatory bowel diseases such as Crohn's disease and acute ulcerative colitis.

    [My personal history makes me wonder if there is something going on in ME that is so close to chronic ulcerative colitis that it can "mimic" it well enough to fool an experienced gastroenterologist.]


     
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  6. Tom Kindlon

    Tom Kindlon Senior Member

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    Thought this was interesting:

     
    Last edited: Aug 9, 2014
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  7. Tom Kindlon

    Tom Kindlon Senior Member

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    Another abstract from the same team


     
    Last edited: Aug 9, 2014
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  8. Tom Kindlon

    Tom Kindlon Senior Member

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    3rd paper from same team

     
    Last edited: Aug 9, 2014
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  9. Esther12

    Esther12 Senior Member

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    Ta Tom.

    Does seem they're looking at areas most 'biopsychosocial' researchers have turned a blind eye to.

     
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  10. Tom Kindlon

    Tom Kindlon Senior Member

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    From Norway
    This is only one particular vaccine of course.
     
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  11. Tom Kindlon

    Tom Kindlon Senior Member

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    Another from Norway
    I would have been more interested in information on incidence as ME/CFS is a chronic illness.

    The prevalence would likely be an underestimate as many people either never get diagnosed or it takes them years to get diagnosed (but some people also get misdiagnosed with CFS/ME).
     
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  12. Tom Kindlon

    Tom Kindlon Senior Member

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  13. Tom Kindlon

    Tom Kindlon Senior Member

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  14. Tom Kindlon

    Tom Kindlon Senior Member

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  15. Tom Kindlon

    Tom Kindlon Senior Member

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    It would have been more interesting to know their score (TSH, etc.) before or off therapy.
     
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  16. aimossy

    aimossy Senior Member

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    I really like seeing the higher number in cohort from the CFI work.
     
  17. aimossy

    aimossy Senior Member

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    [QUOTEImmune signatures associated with cognitive dysfunction in CFS

    Mady Hornig
    ,1* Xiaoyu Che,1 Andrew F. Schultz,1 Susan Levine,2 W. Ian Lipkin1 and the CFI Study Group 1Columbia University Mailman School of Public Health, NY, NY; 2Private practice, NY, NY

    Objectives: Mental fatigue, memory deficits and perceptual processing problems are major contributors to dysfunction in CFS, but the severity of cognitive disturbance varies both within individuals over the course of illness and across phenotypic subsets. Access to a robust biomarker of cognitive dysfunction in CFS would accelerate identification of patients responsive to select treatment strategies and also provide clues to pathogenesis. Although cytokine disturbances are reported in many CFS investigations, study populations and findings are heterogeneous, limiting their utility as biomarkers. We used feature selection and 51-plex immunoassays in an effort to define immune signatures associated with cognitive deficit in CFS.

    Methods: Data from 298 CFS and 348 control subjects from the NIH CFS and the Chronic Fatigue Initiative studies, frequency-matched on age and gender, were pooled. High/low cognitive impairment subgroups were established using mean scores for 4 mental fatigue items from the Multidimensional Fatigue Inventory (MFI4, cases and controls; cutoff 1 SD > population mean): 142 high/147 low MFI4 cases; 29 high/312 low MFI4 controls. Plasma samples were subjected to immune profiling analysis. Principal components (PCA) and partial least square (PLS) feature selection approaches were applied to the 51-cytokine data set to derive latent variables for application as independent variables in logistic regression. Cytokines with odds ratios (OR) >1.1 or <0.9 (p<0.05) by PCA or PLS for the association with high MFI4 subgroups were included in the final logistic regression model along with age as a covariate.

    Results: Elevated IFNγ levels were strongly associated with cognitive impairment in cases (high MFI4) (OR, 67.42; 95% CI, 5.34, 850.83; p=0.0011). Increased CXCL1 levels were also associated with more impaired case MFI4 (OR, 1.23; p=0.0285), with a trend in the same direction for IL13 (OR, 1.26; p=0.08). The pattern within controls was similar to that within cases for IL13, with elevated levels predicting greater cognitive impairment (OR, 1.71; p=0.0088); however, other cytokines associated with cognitive impairment among cases did not show a similar pattern among controls. Stratified analyses showed no relationship with sex.

    Conclusion: Cognitive dysfunction in CFS is associated with specific patterns of elevated cytokines. Increased circulating levels of IFNγ have a striking relationship with cognitive impairment. Individuals with CFS but without cognitive dysfunction did not demonstrate these disturbances. These results suggest immune homeostasis may be dysregulated in the subset of subjects with CFS with prominent cognitive disturbance. IFNγ elevations among cases with cognitive impairment may point toward a subgroup with higher probability of viral triggers and/or persistent infection.][/QUOTE]

    It didn't do the pink block for me this time, I feel like we are starting to get somewhere when cohorts like this get published with this type of work. These are posters - I just wish they were in Journals already!!
     
    Last edited: Aug 10, 2014
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