Search results

Some critical comments by Data Sleuth Sholto David

Here's what I got for tryptase-related genes on chromosome 16 (using GRCh38) And using locuszoom: Looks like my own code doesn't pick up on IGHE (position: chr14:105,597,691-105,601,728) for some reason but here's the data around that position. And here's the location on locuszoom with...

There were no signals at the p < 10^-6 level on chromosome 14 or 16.

Oxaloacetate is also listed with no mention of the conflicts of interest of the people who conducted these trials.

For antihistamines, no mention of this small RCT that trialled an older antihistamine terfenadine and got negative results. https://pubmed.ncbi.nlm.nih.gov/8568124/

For Modafinil, no mention of this negative (but very small) trial: https://pubmed.ncbi.nlm.nih.gov/16272188/

Same issue with IVIG where they mention " In ME/CFS, three studies reported positive outcomes" but this refers to case reports. They don't seem to mention the randomized trials that had negative results. https://pubmed.ncbi.nlm.nih.gov/2239975/ https://pubmed.ncbi.nlm.nih.gov/9236484/

The only randomized trial of Valganciclovir in ME/CFS had null results. https://pubmed.ncbi.nlm.nih.gov/23959519/ Also no mention here of the ME/CFS randomized trial that null results. https://www.nejm.org/doi/10.1056/NEJM198812293192602

The paper gives me the impression that they collected a lot of data but can't seem to make sense out of it themselves.

What were your reasons for thinking about IFN-gamma in ME/CFS, because it's crucial in the cytotoxic T-cell response against intracellular infection?

Made a social media summary about this study: 1) Interesting study showing that a brain infection in mice can lead to loss of synapses and altered excitability of neurons that outlasts the immune response against the virus. Changes are induced by interferon-gamma and involve epigenetic...

In my experience the biggest difference in prevalence estimates is not in the criteria and whether PEM is required but whether it is based on questionnaires or a medical examination by a physician who talks to the patient and checks for other plausible causes for the symptoms. The latter results...

Other studies that used the Fukuda criteria.

The CDC's CFS symptom inventory likely isn't very reliable, diagnostic criteria require a clinical examination to assess symptoms and exclude alternative causes for the symptoms, not just a quesitonnaire. So rather than a large number of people with CFS being undiagnosed, it might just be that...

Perhaps not much as there doesn't seem any immune deficiency or notable susceptibility to cancer in ME/CFS. A risk factor for ME/CFS also doesn't seem likely. So it's presumably some innocuous downstream side-effect of the hidden immune process that is relevant to ME/CFS pathology? When I look...

Looks like low NK cell cytotoxicity has also been reported in systemic sclerosis where increased TGF-beta is a hallmark feature. Abnormal Natural Killer Cell Function in Systemic Sclerosis: Altered Cytokine Production and Defective Killing Activity - ScienceDirect There are lots of things that...

Could lower NK cell cytotoxicity in ME/CFS be due to increased TGF-beta (the cytokine found to be most consistently increased in ME/CFS). Think these are the two immune findings with most consistency across studies (although there is still quite some inconsistency). There are several studies...

Very lage sample size (n = 2068) but hard to extract any new or useful info from the study.

They give an indication of the sampling variance of your estimate if you repeated the experiment multiple times. Suppose you test 20 ME/CFS patients and find that their mean fatigue score is 10 points. But the 20 ME/CFS patients you've chosen might not be representative of the entire ME/CFS...

The biobanks will likely record the most important stratifiers and harmonize their methods. Not sure if it will take everything you mention into account but it will likely be better and more robust than most of the studies we had thus far. And with big enough sample sizes abnormaliities limited...