Meanwhile, I also saw their webinar. They recommend Fluvoxamine for the same reason SSRIs sometimes are recommended for CFS/ME, namely for its anti-inflammatory purposes. They link it with acute COVID-19, not realizing that COVID-19 is a serotonin syndrome and not just organizing pneumonia. I assume this is the reason why they have so much faith in Fluvoxamine. If you assume its anti-inflammatory mechanism is the only mechanism that helps against COVID-19, it should also work later on. Because, obviously, it works against COVID-19. Why shouldn't it work against LHS then? Dr. Mobeen knows the role of serotonin by the way.
What is the problem? All the cytokines, inflammatory molecules that mast cells release along with histamine?
At least, there is more than histamine signaling. It's unclear what cytokines or possibly viral mediators are released once a trigger occurs.
While I agree and that you may be right, significant symptom relief is seen when controlling for only histamine. It does have many downstream effects. So, to many of those patients, that's all they need. So, what is all the other inflammatory molecules and cytokines causing and doing?
My concern isn't really that they address histamine as a solution, but that they imply that MCAS is kind of the causality. I think it plays a predisposing role that affects the manifestation of symptoms. If it was the causality, why doesn't mast cell stabilization cure CFS/ME? Why does it only help with the symptoms? Why does it occur after an infection and never disappear again? There must be some signaling towards the mast cells as well. I'm not satisfied with the explanation of the FLCCC that it's all about rogue macrophages. I think what they will observe is that the repolarization therapy will have to maintain for related symptoms not to reoccur.
I hadn't heard of Rupatadine used for MCAS, but quickly searching it has been studied for that. But I see it's not approved for use in the USA, which must be why it's not more widely seen or mentioned with MCAS.
I wasn't aware of that. I used it against my allergies before. It didn't really do much to MCAS issues. For example, when I still was on a low-histamine diet, I tried to break protocol with Rupatadin. It still triggered severe headache and all the other typical symptoms.
@nerd, I wish you could contact the FLCCC doctors and tell them all this.
They seemed to start out on the right foot but seem to have defaulted back to the same old, same old, unfortunately.
I don't think they would listen since it comes from someone with conflicts of interest. My conflict is that I hope LHS and CFS/ME is finally recognized as the same disease.
They have been asked many many times to come up with a guideline for long haulers, despite the lack of data. And this is the best that was available if you only look at long haulers, leaving out CFS/ME as a whole. There is so much to learn from CFS/ME.
I don't believe equivalent data exist for treating Long Covid with it, just theories as far as I know.
When the serotonin syndrome hypothesis was still in its early shoes and the data on SSRIs' supportive function already existed, their first theory was the sigma-1 receptor. This theory seems to have sustained.
Actually it’s associated with antibodies:
What I meant were SARS-CoV-2 antibodies, indicating that the same viral pathology triggers LHS just as it triggers COVID-19. In this case, it seems to be different. Some of the antibodies that this study determined are quite familiar to the CFS/ME world.