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You write "understanding" but for some reason I read "speculate with little to no objective support".

Possible subtitle: How not to find a tissue-tropic pathogen.

Of course, trial variables can be manipulated in such a fashion as to still enable biases to tip the scales. A general rule of thumb, but precisely the rub in some medical communities,i.e. clinicians with apparently good reason can, in some instances, doubt the voracity (integrity?) of the...

A sign of things to come? https://www.lymedisease.org/torrey-v-idsa-kaiser-settles/

Two banner decades for biowarfare. Wonder what "considered" constitutes.

Sickness behavior. :arghh:

Wow. Very cool! I should not have qualified early days. That was poorly worded. I should have said have there ever been indications of MS outbreaks, or the such. For those who think MS is an immune dysfunction of sorts, or auto-immune, how would they explain this, I wonder?

I don't think that's quite accurate. As you say, there may be many paths to ME; some of those paths may not have to lend themselves to outbreaks, e.g., be contageous, or have a shared trigger like mass trial vaccine. Some clearly would. I wonder if in the early days of reporting MS there were...

Some people get ME in outbreaks. Many with ME are not part of any known outbreak. The operative phase here is "we know about". We are learning more about channelopathies all the time. It could be that some are triggered by insults such as infections; maybe not. Ultimately, what is rare relative...

Why? I actually doubt it is genetic as well, but I am curious as to why you make this statement. It seems that almost once a month a new genetic marker is stumbled upon that suggests a form of channelopathy, so, I'm curious as to why you say this? Agreed, except I'm unclear how it works other...

Poor appetite? Neck pain? Who are these people?

Before they did anything, they should have performed the same metrics on HC and late stage Lyme (as opposed to early Lyme) and what they call PTLDS to see if there were any differences between LS Lyme and PTLDS. I suspect there would have been no meaningful differences. If that is the case...

I qualified for both the ME/CFS and Lyme parts of this study, and was in fact recruited to participate. Somewhere along the line it was decided I could not participate since I did in fact have both diseases. In a way, for me at least, that pretty much sums up the results.

Wisconsin is in the thick of things, too, when it comes to tick-borne diseases...

Is this just a case of suggesting the rooster makes the sun rise? Inference is no longer a strength of mine, but that deficit seems endemic in medicine so I don't feel too lonely.

"...ion handling..." A potential channelopathy reference again? Are we talking channelopathies as downstream effects, and abnormal RBC deformability simply further downstream? I know - way too speculative. Also, I always thought of channelopathies as the starting point, ie, genetic, usually...

Our's would be an acquired altered RBC deformability, if applicable - I think (it could be genetic, but adult onset in some and childhood onset in others makes that proposition seem less likely). This paper addresses hereditary hemolytic anemia. What about acquired hemolytic anemia, or...

This paper specifies skeletal muscle. Maybe the Australians were on to something with the calcium channelopathy theory. But the tie to EV escapes me. Are EVs remnants or blebs from skeletal muscle cells?

Not unlike the logic underpinning MS, truth be told.

Well, not obvious to everyone.