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Yes GRADE recommends downgrading for imprecision if the CI crosses the threshold of interest. Which is the case here.

I noticed that Lillebeth Larun has now responded to a comment: https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD003200.pub9/detailed-comment/en?messageId=446137675

Thanks for all the comments and suggestions. We have just posted the following poll on social media based on 3 options that we like the best thus far. Which name should we choose for our account and blog? 1) ME/CFS Science 2) ME/CFS In Depth 3) Science unravelled 4) None of the above (keep...

https://eprints.whiterose.ac.uk/164981/1/20200428ConversiondisordermisdagnosisGHPaccepted_combined_1_.pdf

Thanks. The data is in .raw filetype and have some trouble converting it to something like CSV or Excel. Anyone who has more experience in this?

This study is listed on MapME/CFS but it doesn't include the raw data from what I can see, only summary statistics of their analyses and modelling.

Just posting the main results here: The Japanese used next-generation sequencing (NGS) and got the following results: They also found that it was related to an infectious-onset and shorter illness duration (perhaps that explains why Ryback only seem to find it in the mild/moderate but not...

Any ideas at what this may point to? If it is not specific antigen driven expansion, what else might be causing this? And why would B-cell abnormalities make sense, as Nath said, if it is likely not related to a specific antigen drive?

Wrote a short section about this in our 2021 review of ME/CFS studies:

Thanks, the two studies these refer to are I believe: 2020 Lipkin study: Plasma proteomic profiling suggests an association between antigen driven clonal B cell expansion and ME/CFS | PLOS ONE 2021 Sato study: Skewing of the B cell receptor repertoire in myalgic encephalomyelitis/chronic...

Looks interesting. The first author is Audrey Ryback who is also trying to replicate the 'something in the blood' theory, as explained by Simon Mcgrath here: Remarkable researchers hunting for ‘something in the blood’ of people with ME | Science for ME

More than a month later and there is still no peer review or reply from the authors to the comments made.

Thanks for the suggestions. It seems that misuse of the term skeptic has become so common (i.e. as in climate skeptics) that a correct use of the term has become confusing to most people. We still plan on changing the name but needed some more time to consider the best options. Will probably...

Later in the text they write: So that suggests that one ME/CFS symptom is enough to meet the ME/CFS-like definition. What they call ME/CFS should have been named ME/CFS-like to be consistent with the literature. And what they named ME/CFS-like shouldn't have been named anything.

Bit sad that they got more than 1 billion in funding and this is the best they could do...

Made a Twitter summary with comments here: https://bsky.app/profile/mecfsskeptic.bsky.social/post/3lfnfst3mev2u 1) The RECOVER study found that adults who got a SARS-CoV-2 infection were approximately 5 times as likely to develop ME/CFS. But there are some important caveats… 2) The main one...

What the paper doesn't really discuss is that the rate of ME/CFS in the acute-infected - 73 of 4,515 (1.6%) - was much lower than in the post-acute infected - 458 of 7,270 (6.3%). The former was enrolled within 30 days of infection.

I think the main reasons are: 1) Many ME/CFS patients are not diagnosed yet. Other have received other diagnoses such as chronic Lyme, POTS, MCAS, CCI, etc that cause confusion and break up the patient community into smaller parts. 2) A lot of ME/CFS patients are disconnected from family and...

Ok thanks, that's useful to know.

I would argue that the causal path is valuable for researchers, and an indication of what treatment to use is useful for doctors, but for patients it can simply be enough to have a description of what you're going through. Even if the pathology or treatment for many us turns out to be very...