ME/CFS Science
@mecfsskeptic.bsky.social
In-depth analysis of research on myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). Formerly known as ME/CFS Skeptic.
https://mecfsscience.org/
https://mecfsscience.org/
7) Link to the 2005 paper (thanks to Utsikt at the S4ME for highlighting this study).
Severeijns et al. 2005. The causal status of pain catastrophizing: an experimental test with healthy participants.
onlinelibrary.wiley....
Discussion on S4ME:
www.s4me.info/thread...
Severeijns et al. 2005. The causal status of pain catastrophizing: an experimental test with healthy participants.
onlinelibrary.wiley....
Discussion on S4ME:
www.s4me.info/thread...
February 9, 2026 at 1:31 PM
7) Link to the 2005 paper (thanks to Utsikt at the S4ME for highlighting this study).
Severeijns et al. 2005. The causal status of pain catastrophizing: an experimental test with healthy participants.
onlinelibrary.wiley....
Discussion on S4ME:
www.s4me.info/thread...
Severeijns et al. 2005. The causal status of pain catastrophizing: an experimental test with healthy participants.
onlinelibrary.wiley....
Discussion on S4ME:
www.s4me.info/thread...
6) There is a whole literature critical of the concept of catastrophizing because it's difficult to estimate when threats and experiences are exaggerated, especially in poorly understood conditions.
We wrote a detailed article about catastrophizing here:
We wrote a detailed article about catastrophizing here:
Catastrophizing, time to ditch the term? - ME/CFS Science
Catastrophizing, a cognitive distortion that amplifies the perceived threat of symptoms, has been at theContinue readingCatastrophizing, time to ditch the term?
mecfsscience.org
February 9, 2026 at 1:31 PM
6) There is a whole literature critical of the concept of catastrophizing because it's difficult to estimate when threats and experiences are exaggerated, especially in poorly understood conditions.
We wrote a detailed article about catastrophizing here:
We wrote a detailed article about catastrophizing here:
5) The authors caution that the artificially induced catastrophizing at one paricular moment may be quite different from catastrophizing as trait-like quality. But it raises questions about this psychological concept and if it actually causally influences pain.
February 9, 2026 at 1:30 PM
5) The authors caution that the artificially induced catastrophizing at one paricular moment may be quite different from catastrophizing as trait-like quality. But it raises questions about this psychological concept and if it actually causally influences pain.
4) But this did not lead to higher pain scores compared to the control group. In fact, those in the catastrophizing were able to keep their hand longer in the ice water.
In other words, catastrophizing didn't have an effect on pain experience and behavior.
In other words, catastrophizing didn't have an effect on pain experience and behavior.
February 9, 2026 at 1:30 PM
4) But this did not lead to higher pain scores compared to the control group. In fact, those in the catastrophizing were able to keep their hand longer in the ice water.
In other words, catastrophizing didn't have an effect on pain experience and behavior.
In other words, catastrophizing didn't have an effect on pain experience and behavior.
3) Catastrophizing thoughts (negative thinking that interprets things as worse, more threatening and less controllable) were measured with the pain catastrophizing scale (PCS).
The experiment successfully increase the PCS score in the catastrophizing group.
The experiment successfully increase the PCS score in the catastrophizing group.
February 9, 2026 at 1:30 PM
3) Catastrophizing thoughts (negative thinking that interprets things as worse, more threatening and less controllable) were measured with the pain catastrophizing scale (PCS).
The experiment successfully increase the PCS score in the catastrophizing group.
The experiment successfully increase the PCS score in the catastrophizing group.
2) The researchers split the participants into two groups and told one of them (the catastrophizing group) that a few people who did the experiment fainted during the ice-water immersion. And the people who fainted had similar responses to the questionnaire as you.
February 9, 2026 at 1:30 PM
2) The researchers split the participants into two groups and told one of them (the catastrophizing group) that a few people who did the experiment fainted during the ice-water immersion. And the people who fainted had similar responses to the questionnaire as you.
1) In this old study from 2005, researchers induced catastrophic thinking in their participants and then recorded their pain intensity after immersing their hand in ice water.
Catastrophizing didn't have any influence on pain.
Catastrophizing didn't have any influence on pain.
February 9, 2026 at 1:30 PM
1) In this old study from 2005, researchers induced catastrophic thinking in their participants and then recorded their pain intensity after immersing their hand in ice water.
Catastrophizing didn't have any influence on pain.
Catastrophizing didn't have any influence on pain.
Perhaps not the dizziness and fainting part but needing to lie down seems quite common in people and animals that get a severe infection?
February 8, 2026 at 8:03 PM
Perhaps not the dizziness and fainting part but needing to lie down seems quite common in people and animals that get a severe infection?
6) Link to the paper:
Strom et al. 2026. Genome-wide association study of major anxiety disorders in 122,341 European-ancestry cases identifies 58 loci and highlights GABAergic signaling.
www.nature.com/artic...
Discussion on S4ME:
www.s4me.info/thread...
Strom et al. 2026. Genome-wide association study of major anxiety disorders in 122,341 European-ancestry cases identifies 58 loci and highlights GABAergic signaling.
www.nature.com/artic...
Discussion on S4ME:
www.s4me.info/thread...
Genome-wide association study of major anxiety disorders in 122,341 European-ancestry cases identifies 58 loci and highlights GABAergic signaling
Nature Genetics - Genome-wide association meta-analysis identifies 58 independent risk loci for major anxiety disorders among individuals of European ancestry and implicates GABAergic signaling as...
www.nature.com
February 8, 2026 at 3:17 PM
6) Link to the paper:
Strom et al. 2026. Genome-wide association study of major anxiety disorders in 122,341 European-ancestry cases identifies 58 loci and highlights GABAergic signaling.
www.nature.com/artic...
Discussion on S4ME:
www.s4me.info/thread...
Strom et al. 2026. Genome-wide association study of major anxiety disorders in 122,341 European-ancestry cases identifies 58 loci and highlights GABAergic signaling.
www.nature.com/artic...
Discussion on S4ME:
www.s4me.info/thread...
5) Most of the other genetic signals for anxiety differ from these of ME/CFS (see e.g the two Manhattan plots below).
The genetic data for anxiety did correlate strongly with those for depression (rg = 0.9) and was associated with GABAergic neurons.
The genetic data for anxiety did correlate strongly with those for depression (rg = 0.9) and was associated with GABAergic neurons.
February 8, 2026 at 3:17 PM
5) Most of the other genetic signals for anxiety differ from these of ME/CFS (see e.g the two Manhattan plots below).
The genetic data for anxiety did correlate strongly with those for depression (rg = 0.9) and was associated with GABAergic neurons.
The genetic data for anxiety did correlate strongly with those for depression (rg = 0.9) and was associated with GABAergic neurons.
4) But there are also studies that link BTN3A2 to brain diseases such as schizophrenia, suggesting it alters excitatory synaptic activity (how and when neurons fire). This link to anxiety likely also points in that direction.
link.springer.com/ar...
www.nature.com/artic...
link.springer.com/ar...
www.nature.com/artic...
The butyrophilin (BTN) gene family: from milk fat to the regulation of the immune response
Immunogenetics - Butyrophilins (BTN) belong to the immunoglobulin (Ig) superfamily of transmembrane proteins. These molecules are of increasing interest to immunologists, as they share a structural...
link.springer.com
February 8, 2026 at 3:16 PM
4) But there are also studies that link BTN3A2 to brain diseases such as schizophrenia, suggesting it alters excitatory synaptic activity (how and when neurons fire). This link to anxiety likely also points in that direction.
link.springer.com/ar...
www.nature.com/artic...
link.springer.com/ar...
www.nature.com/artic...
3) The BTN family of genes including BTN3A2 are members of the immunoglobulin superfamily (they make proteins that are very similar to antibodies) and have a clear link to the immune system.
February 8, 2026 at 3:16 PM
3) The BTN family of genes including BTN3A2 are members of the immunoglobulin superfamily (they make proteins that are very similar to antibodies) and have a clear link to the immune system.
2) NEGR1 is involved in nervous system development and regulation of synapse assembly. It has been been linked to brain diseases such as schizophrenia, insomnia, and depression.
February 8, 2026 at 3:16 PM
2) NEGR1 is involved in nervous system development and regulation of synapse assembly. It has been been linked to brain diseases such as schizophrenia, insomnia, and depression.
1) A large genetic study of anxiety disorder found 58 independent risk variants. Two of the signals were similar to those of DecodeME in ME/CFS:
- Neuronal growth regulator 1 (NEGR1) on chromosome 1
- BTN3A2 of the butyrophilin family of genes on chromosome 6
- Neuronal growth regulator 1 (NEGR1) on chromosome 1
- BTN3A2 of the butyrophilin family of genes on chromosome 6
February 8, 2026 at 3:16 PM
1) A large genetic study of anxiety disorder found 58 independent risk variants. Two of the signals were similar to those of DecodeME in ME/CFS:
- Neuronal growth regulator 1 (NEGR1) on chromosome 1
- BTN3A2 of the butyrophilin family of genes on chromosome 6
- Neuronal growth regulator 1 (NEGR1) on chromosome 1
- BTN3A2 of the butyrophilin family of genes on chromosome 6
Reposted by ME/CFS Science
This is really interesting, it ties in with my doctor's findings of low cortisol and adrenal dysfunction. I hope this leads somewhere positive for us all x
1) Dr. Felipe Correa da Silva shared more info about the first 10 brain autopsies from the Netherlands.
In this new thread, we made a brief summary of his presentation.
In this new thread, we made a brief summary of his presentation.
February 7, 2026 at 2:24 PM
This is really interesting, it ties in with my doctor's findings of low cortisol and adrenal dysfunction. I hope this leads somewhere positive for us all x
20) The full presentation of Dr. Felipe Correa da Silva at the NMCB meeting can be watched here:
www.youtube.com/watch?v=30Dk...
www.youtube.com/watch?v=30Dk...
Felipe Correa da Silva
YouTube video by NMCB | Nederlandse MECVS Cohort en Biobank
www.youtube.com
February 7, 2026 at 1:54 PM
20) The full presentation of Dr. Felipe Correa da Silva at the NMCB meeting can be watched here:
www.youtube.com/watch?v=30Dk...
www.youtube.com/watch?v=30Dk...
19) So what's next? The researchers plan to also look at mitochondria-related changes and use other tools than histopathology.
They got another grant for single cell transcriptomics (snRNA-seq) of 3 regions: the hypothalamus, frontal cortex and hippocampus.
They got another grant for single cell transcriptomics (snRNA-seq) of 3 regions: the hypothalamus, frontal cortex and hippocampus.
February 7, 2026 at 1:54 PM
19) So what's next? The researchers plan to also look at mitochondria-related changes and use other tools than histopathology.
They got another grant for single cell transcriptomics (snRNA-seq) of 3 regions: the hypothalamus, frontal cortex and hippocampus.
They got another grant for single cell transcriptomics (snRNA-seq) of 3 regions: the hypothalamus, frontal cortex and hippocampus.
18) In other parts of the brain such as the the parietal cortex, they do not see that. So it seems to be triggered by local events, rather than a widespread mechanism.
February 7, 2026 at 1:54 PM
18) In other parts of the brain such as the the parietal cortex, they do not see that. So it seems to be triggered by local events, rather than a widespread mechanism.
17) One extra interesting finding is that in the Hypothalamus (the PVN) they found increased CD68 positive microglia.
CD68 is a protein found on the membrane of lysosomes so this points to increased phagocytosis (clean-up) and possibly micro-enviromental injury.
CD68 is a protein found on the membrane of lysosomes so this points to increased phagocytosis (clean-up) and possibly micro-enviromental injury.
February 7, 2026 at 1:54 PM
17) One extra interesting finding is that in the Hypothalamus (the PVN) they found increased CD68 positive microglia.
CD68 is a protein found on the membrane of lysosomes so this points to increased phagocytosis (clean-up) and possibly micro-enviromental injury.
CD68 is a protein found on the membrane of lysosomes so this points to increased phagocytosis (clean-up) and possibly micro-enviromental injury.
16) "ME/CFS has been thought to be a neuro-inflammatory throughout the whole disorder but this might not be true. It might be that after a certain point the neuro-inflammation stops because the cells are senescent and cannot keep up with their continuous activation."
February 7, 2026 at 1:54 PM
16) "ME/CFS has been thought to be a neuro-inflammatory throughout the whole disorder but this might not be true. It might be that after a certain point the neuro-inflammation stops because the cells are senescent and cannot keep up with their continuous activation."
15) Correa da Silva described the findings as follows:
"So in the patients that donate their brains, possibly endstage patients, we do not see signs of classical neuro-inflammation, but we see dystrophic, rather senescent microglia."
"So in the patients that donate their brains, possibly endstage patients, we do not see signs of classical neuro-inflammation, but we see dystrophic, rather senescent microglia."
February 7, 2026 at 1:54 PM
15) Correa da Silva described the findings as follows:
"So in the patients that donate their brains, possibly endstage patients, we do not see signs of classical neuro-inflammation, but we see dystrophic, rather senescent microglia."
"So in the patients that donate their brains, possibly endstage patients, we do not see signs of classical neuro-inflammation, but we see dystrophic, rather senescent microglia."
14) The authors also looked at HLA which acts as a proxy for microglia activation and this showed no clear effect.
They also found no evidence of abnormal T (CD3) or B (CD79a) cell presence in the central nervous system of ME/CFS patients.
They also found no evidence of abnormal T (CD3) or B (CD79a) cell presence in the central nervous system of ME/CFS patients.
February 7, 2026 at 1:54 PM
14) The authors also looked at HLA which acts as a proxy for microglia activation and this showed no clear effect.
They also found no evidence of abnormal T (CD3) or B (CD79a) cell presence in the central nervous system of ME/CFS patients.
They also found no evidence of abnormal T (CD3) or B (CD79a) cell presence in the central nervous system of ME/CFS patients.
13) This was not only in the hypothalamus, but something that seems to be a widespread effect, in both gray and white matter.
February 7, 2026 at 1:54 PM
13) This was not only in the hypothalamus, but something that seems to be a widespread effect, in both gray and white matter.
12) This is a somewhat new histological feature. Not a lot of people in the world have described it.
There’s no harmonized system to quantify this yet but they certainly see it in the brains of ME/CFS patients.
There’s no harmonized system to quantify this yet but they certainly see it in the brains of ME/CFS patients.
February 7, 2026 at 1:54 PM
12) This is a somewhat new histological feature. Not a lot of people in the world have described it.
There’s no harmonized system to quantify this yet but they certainly see it in the brains of ME/CFS patients.
There’s no harmonized system to quantify this yet but they certainly see it in the brains of ME/CFS patients.