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Almost all of these individuals could have gone to a sleep doctor and been prescribed the same treatment. There are surely already many other trials showing that CPAP improves symptoms in individuals with OSA. So I'm not seeing what new information this study provides.

Thanks for the quotes, but they don't really answer the question for me. I didn't know the criteria, but you're saying 15/18 participants had diagnosable OSA? If the goal is to show that CPAP works for non-apnea related flow limitation or for GWI, the trial should exclude those with OSA...

Note the discussion on another thread which includes the following about a Canadian journal: The New Yorker: Did a Celebrated Researcher Obscure a Baby’s Poisoning?

Are they saying that for the entire trial, the CPAP would only turn on after the individual fell asleep, and then turn off after 3 hours? The following sentence is in the section about the in-lab pre-trial tuning of the settings. And I'm not sure if the CPAP device is able to only turn [edit...

I would assume they used the same equipment. I'm encompassing any possible change that could have happened between the two groups being tested separately. Maybe the seasons and weather changed and had some effect on sleep. Maybe a different technician attached the equipment to the second group...

Maybe related to a batch effect of doing the sleep study on all the cases before they had finished recruiting the controls: To me, it seems too good to be true to have that good of separation. Especially as this is a 15 year old study. I would expect a biomarker that perfectly separates groups...

Note that the thread has been split into two threads. The other paper for the CPAP trial is here: The effect of nasal continuous positive airway pressure on the symptoms of Gulf War illness, 2011, Amin et al

Link to thread for an observational study with the same 18 subjects: Inspiratory airflow dynamics during sleep in veterans with Gulf War illness: A controlled study, 2011, Amin et al.

I haven't read the paper, but that's a very striking table. Zero overlap between groups for % flow limited

I'm curious how good the blinding is. It refers to another paper for a description of the sham treatment: That paper cites ref 10: Sham continuous positive airway pressure for placebo-controlled studies in sleep apnoea I may be misunderstanding, but it seems they are saying they validated...

Comment on PubPeer about that figure:

Extracellular Vesicle Protein and MiRNA Signatures as Biomarkers for Post-Infectious ME/CFS Patients [Line breaks added] Abstract Post-infectious Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a chronic disease with unresolved pathophysiology and limited diagnostic options...

Neuroscience News: "Home Drinking Water May Impact Parkinson’s Risk" Link Younger Groundwater Associated with Greater Risk of Parkinson’s Disease in Nationwide Medicare Study: Implications of Aquifer Type Renee Tessman, Michelle Uher PDF | American Academy of Neurology | Abstract Only

I wouldn't say that the above issues necessarily suggest that there is not actually a gene-environment interaction for nerve gas alarms or other exposures. The study may have been underpowered to detect these effects. A previous study that did find an interaction had 508 GWI cases and 508...

Unfortunately, I don't think this study provides strong evidence of a gene-environment interaction in regard to PON1 status and hearing chemical alarms, because the authors didn't report the results of testing the actual interaction. They reported that the odds ratio for RR individuals was...

I think you might be looking at the p-value, which isn't a measure of effect size. The difference between groups looks to be 0.059.

They also tested excluding purely psychiatric post-COVID cases, and the risk ratios were about the same. They also tested with minimum 8 weeks duration:

Retraction Watch: "A medical journal says the case reports it has published for 25 years are, in fact, fiction" Link

I feel represented. So great to hear some cool science knowledge from Dianna again with her characteristic overflowing excitement.

Ah okay. I assumed the non-specific Fukuda could easily hit a prevalence around 4x the prevalence with PEM. I see this one also gives a pretty high figure, but seems to also be based on questionnaires. Chronic fatigue syndrome prevalence is grossly overestimated using Oxford criteria compared...