Review: 'Through the Shadowlands’ describes Julie Rehmeyer's ME/CFS Odyssey
I should note at the outset that this review is based on an audio version of the galleys and the epilogue from the finished work. Julie Rehmeyer sent me the final version as a PDF, but for some reason my text to voice software (Kurzweil) had issues with it. I understand that it is...
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Article: Light on ME/CFS I: Bad Reception: A Key to ME Uncovered? The Light Gene Expression Studies

Discussion in 'Phoenix Rising Articles' started by Phoenix Rising Team, Jul 15, 2011.

  1. aruschima

    aruschima I know nothing


    What can I say.....just one more of this studies by Big Pharma which will help them sell their product......

    Cort, do you have any conflict of interest to declare ? Maybe like a little ghost writing fees ??? ;)

    And just one more thing, Lucinda Bateman is sitting on the advisory board of Pfizer ....:D

  2. oceanblue

    oceanblue Guest

    Latest paper from Lights doesn't really clarify things

    I think that, along with XMRV and Rituximab, the 2011 report of increased gene expression in response to exercise (that Cort's written about here) is amongst the most interesting findings to emerge about CFS. However, as with XMRV and Rituximab, replication is crucial.

    The biggest concern over the study covered in Cort's article relates to the higher exertion levels of CFS patients than controls, as has been discussed elsewhere in the comments. The authors had indicated that submitted research would demonstrate that in response to exercise MS patients showed no change in the expression of the genes that increased post-exercise in CFS patients. This would go some way to demonstrate the changes were unique to CFS and not related to deconditioning, particularly if the MS patients were well-matched with the CFS ones in terms of activity levels.

    This submitted paper on MS patients has now been published and while it shows that metabolite receptor gene expression is not increased in response to gene expression, it also shows that the adrenergic recepotor genes are similarly increased in MS and CFS patients. Which makes it far less conclusive. It's not clear how well matched the MS patients were to the CFS patients.

    This further study (from a comment from Alan posted by Cort) looks interesting re deconditioning, but like the MS study, we won't know for sure until it's published.
    What I found of most concern was that the moderate-to-strong link found between gene expression and fatgiue and pain scores across all the genes implicated in this (2011) paper was not replicated in the new MS/CFS paper. The only correlation found was for a single adrenergic gene, P2X4, and then only for pain and not for fatigue. It was this correlation between gene expression and fatigue and pain that made the findings of this 2011 paper so compelling.

    Replication studies have not been kind to the XMRV findings to date, though the largest and most rigorous (Lipkin) study has yet to report. Replication of the Rituximab findings are planned by its authors and at least one other group. The authors of these gene expression findings have made it clear they believe their work to date is sufficient:
    As the CAA, who funded this study say "As with any research, these findings will need to be replicated by another research group in another group of CFS (and FM) patients", to establish that these gene expression are a real and important link to fatigue and pain in CFS. Hopefully other groups will do exactly this.

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