Yeah maybe the dopamine system in ME/CFS is less responsive so that those natural stimuli that reduce it centrally have less impact and thus we see a blunted prolactin response.
But when you don't impact the dopamine system itself but simply block the dopamine that's already there, we see an...
There are a couple of studies that tried to block the serotonin route of buspirone and measure what effect it had on its prolactin effect. This 2001 study found that approximately 50% of its effect on prolactin disappeared when participants are first given the 5-HT1A antagonist pindolol.
So...
Thanks, updated. There may be other errors because I didn't double-check.
The 'effect size' are based on simply eyeballing the graphs and dividing the peak by the baseline value regardless at which hour the peak was. If the plan is to publish in a journal, one could perhaps use software to...
Some thoughts about the cause and mechanism
The normal prolactin response after mCPP (and some dl-fenfluramine studies), and attenuated response after exercise and the insulin stress test suggests that there isn't some mechanism at play that simply shows increased prolactin responses in ME/CFS...
Limitations
After reading the studies, one big limitation is that they were all quite small: almost all studies have less than 30 ME/CFS patients.
The prolactine results also show a lot of variability in the results and there are multiple factors that might influence it (sex, menstruation...
Am re-reading the studies anyway, so here's an example of the table I had in mind:
StudyPatients - controlsStimulantEffect on prolactinNotes
Bakheit 1992
(Behan group)15 post-viral fatigue syndrome patients
40% female
13 healthy controls
13 depressed controls60 mg
buspironeSimilar...
Thanks for highlighting this.
ECP = eosinophil cationic protein
EDN = eosinophil-derived neurotoxin
So these are eosinophil proteins that they assume would also be increased in case of chronic mast cell activation.
Impressive work @forestglip, thanks for digging into this!
Small suggestion for your summary: it would be useful to have a table of the ME/CFS studies with the number of participants they used (male/female), the type stimulant and dosage used and possibly info about the effect size.
I checked if the DecodeME signal around BTN2A1 colocalizes with that in this GWAS on anxiety
Genome-wide association study of major anxiety disorders in 122,341 European-ancestry cases identifies 58 loci and highlights GABAergic signaling - PMC
My (amateur) analysis suggests there's a real...
I'm not entirely sure that she takes this position. She seems to criticize both psychosomatic and biomedical approaches, although I only skimmed the article.
Some sections from the discussion section:
....
The article discusses the origin of ME and CFS and subsequent discussions about it...
One idea to study this further is to use PET scans with tracers such as [11C]-UCB-J or [18F]SynVesT-1 that measure synaptic density. It would be interesting to see whether, e.g., this is increased or reduced in various brain areas such as the striatum and hypothalamus.
These are tracers that...
This looks like an interesting study and design, but from what I can tell, the hypoxia didn't really make a clear difference in the results. The main finding was increased lactate, which was also present before the hypoxia and is consistent with previous findings. As the authors write:
This was available from BigaGWAS, a big database of traits that automatically checks correlations with lots of traits from UK biobank and other sources.
I also checked the latest migraine GWAS, which I think is Hautakangas et al. 2022. The 23andMe data isn't available, but those from the UK...
Thanks!
My guess is that genomic control (GC corrected) refers to dividing by the genomic inflation factor: the ratio of your median chi square value by 0.4549 (what the median chi square value would be under the null with no bias). This was an (older) approach intended to control for...
Was wondering if there's an explanation for why the LDSC intercept for DecodeME is below 1.
Higher than 1 is usually seen as a sign of bias such as population stratification but below 1 is less clear. Could it mean that part of the true signal was taken away by the principal components?
The DecodeME team could test this, would be an analysis worth doing. I'm not an expert but think an rg of 0.75 is quite big and probably not fully explained by the 30% of ME/CFS cases that also had fibromyalgia.
Perhaps others can double-check but I calculated the genetic correlation with DecodeME and the European-only GWAS of fibromyalgia from this study using LDSC and I got a value of rg = 0.757. That's quite high and similar to the rg = 0.751 between DecodeME and self-reported irritable bowel...
I think the relationship between viral reactivation and Long Covid was mostly negative.
It's only during the convalescent period that they found an association between Anelloviridae transcripts and one of four subgroup of Long Covid, those with a high score on the "Measurement Information...
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