Opens profile photo
Follow
analogue
@analoguefade
it only hurts when I laugh
Joined February 2015

analogue’s Tweets

It seems a little like starting the house on fire in order to light the stove. Why not just give people NAD+ instead of l-kyn? CFS people have been messing around with NAD+ for decades without much success.
1
Show this thread
I understand that they are looking at it from a metabolic perspective, rather than the immune perspective, but as far as I understand the metabolites they are trying to increase (NAD+) are those that are produced from the neurotoxic substrates.
Image
1
Show this thread
I've recently been thinking that glutamate must play a central role in generating a lot of ME symptoms. l-kynurenine, in the presence of inflammatory cytokines, gets preferentially turned into 3-HK/QA which agonizes the glutamate receptor NMDA and is generally neurotoxic.
Image
1
Show this thread
Pretty wild how AFM largely just took 2020 off. Not too surprising I guess as EV-D68 is largely a respiratory virus. Ongoing mask use could keep kids from getting crippled/dying from AFM until treatment becomes available, but I guess we all know how well that would go over.
Image
Image
Quote Tweet
Image
I’m glad medicine has been holding it’s collective breath for the last 8 years hoping the problem would go away instead of working on an enterovirus protease inhibitor.
Show this thread
1
4
You know what caused these people's disease, it's SARS-CoV-2. Why rediagnose them with a trashcan diagnosis instead of properly defining the case definition of COVID-19 disease to include a chronic form. This does not help people with pre-COVID ME/CFS or people with COVID-19.
2
Show this thread
Extremely troubling and embarrassing that supposed experts on "ME/CFS" don't even understand the basics of medical coding of these diseases. "ME" research will be tainted for years to come with COVID-19 patients and we have no idea how representative they are of classic ME.
1
Show this thread
This document is dangerous misinformation. Claiming chronic COVID-19 should be diagnosed as "ME/CFS" (they specifically state G93.3 ME/PVFS) based on a study that classic SARS patients met Fukuda CFS criteria. (should be dx'd as R53.82, which EXCLUDES an ME/PVFS dx per ICD-10).
Quote Tweet
Replying to @DonnaPh79122599
(1 of 2) Many/most cases of "long COVID" ARE in fact ME/CFS - it is usually caused by some sort of infectious trigger and SARS-family viruses are a known one. Here is more info to share with your doctor from a group of top ME/CFS experts: drive.google.com/file/d/15Z1pPM
1
Show this thread
Personally I had some good effect with amantadine but it wasn't earth shattering. My prolactin levels are even higher than the responders in the above referenced study, so I expect I might respond to a good dopamine agonist as well, just not sure what to try next.
2
3
Show this thread
I think dopamine agonism is a good idea, I just wonder if there isn't a better agent to do it with. Bromocriptine is also somewhat dirty. Amantadine is somewhat cleaner and I know several doctors have used it on ME with some effect, but it's somewhat weak on dopamine agonism.
2
2
Show this thread
The problem with aripiprazole is it's a relatively dirty drug so it's too difficult to decide exactly how it might be working, but to me there's no doubt that ME disrupts all major neurotransmitter systems in the brain, esp. indolamines, catecholamines, and acetylcholine.
1
2
Show this thread
Could the SPECT findings be replicated using PET with an appropriate analogous tracer? I could be wrong, but I don't think this has ever been done. I believe PET with immune cell binding tracer is the only thing that has been done. Perhaps knows the answer to this.
2
1
Show this thread
Now, I know this evidence is often easily dismissed by joking that SPECT scans can change depending on what side of the bed you got up on, or what you ate for breakfast, and that may be true, but if valid I have to assume this evidence should transfer to another imaging modality.
1
1
Show this thread
In ME, what researchers are looking for as proximate causes (viral/immune/autoimmune/metabolic) happen to often be what are considered possible distal causes in these other diseases. Why is it backwards like this?
1
1
Show this thread
In ME, the distal cause is known, it is undeniably caused by viral infection. But the proximate cause of symptoms is not apparent. No obvious lesion can be found to directly explain any of the symptoms.
1
1
Show this thread
So take MS for example, the proximate cause of symptoms is the very apparent gliosis of different parts of the brain, but the distal cause of the disease is completely unknown (viral? immune/autoimmune? metabolic?).
1
1
Show this thread
Aseptic viral meningitis is a reportable disease in California. This allows clusters to be recognized and the responsible agent to be identified. This is the same virus that is causing my ME, but I get no recognition of this fact.
Image
5
Show this thread
From a new study looking at cytokines in enteroviral induced HFMD. These exact three cytokines/chemokines are found elevated in ME also.
Image
1
2
The published paper had an interesting reference to a paper by Mowbray and Yousef (of ME research fame) where they linked the presence of enterovirus antigen in blood with active Meniere’s symptomotology. The link with ME is mentioned also:
Image
1
8
Show this thread