Search results

Yes that might be the more conservative option. The plot does show 15-minute intervals before the administration of buspirone. And as ScoutB says, the growth hormone plot also shows the same intervals up unto 240 so perhaps it's simply a bad description in the methods section.

Thanks, I've updated the plot accordingly.

I've been extracting the data from the graphs in the buspirone studies, it looks something like this. For Bakheit 1992 I took males only, Sharpe 1996 is also males only, the other studies have both sexes combined. EDIT: there might be an error in the Sharpe 1996 original data plot, see the...

I think the Sharpe 1996 (Cowen group) study had a pretty good view on the problem saying it was likely the dopamine instead of serotonin pathway that was abnormal. They wrote: Increased prolactin response to buspirone in chronic fatigue syndrome - PubMed My guess is that buspirone was seen as...

I have the CIBA symposium book from 1993 but it doesn't have much discussion on the buspirone tests. Doesn't work to upload the doc but here are some screenshot of the places where buspirone or prolactin is mentioned, the discussion moves to other topic afterwards. First section: Then a bit...

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...

Your little review was probably the most interesting paper I read on ME/CFS in 2026! Hope you can rest well and recover.

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.

DecodeME top SNP rs9358913 chr6:26239404 (GRCh37) p = 4.11e-09 Anxiety top SNP rs58825580 chr6:26365679 (GRCh37) [ = 1.02e-14

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...