Post Exertion Infection

[Jonathan Edwards]

I am afraid that I think you can construct a story linking just about anything with just about anything in those sorts of terms Hip. Building biological mechanisms for diseases in real life does not work on the basis of what fits with what. Everything fits with everything if you trawl through the literature. Building a useful model is much more to do with trawling through for what DOES NOT fit for a given theory. And often that has to do with broader system dynamics issues, or with quirky details shown up by exceptions to rules. If there was any specific conclusion about mechanism from the IiME workshop I think it was probably that we may be looking for a mechanism that leaves IL-6 well alone. Sickness behaviour is a buzz word that does not quite fit here I think.

 

[msf]

Wouldn't things fitting be a necessary, but insufficient, requirement for a theory? I think this is interesting, because I feel I can account for most of my symptoms using the findings of published medical articles and my test results, but I think Prof. Edwards would argue this, and even if he accepted it was a possible explanation for my symptoms he would insist that the evidence was inconclusive and treatments based on this theory would not be justified. I think this is the right stance for a researcher to take, but as a patient my take on it is quite different - the way I see it, I could be wrong, but no one has offered me an alternative theory that accounts for most of my symptoms (unless you count the NHS ID doc who told me my symptoms were probably caused by the flattening of my vili!), and so I have choice: either to wait until there is no argument about patients like me (i.e. until one theory has seen off the others), which might take several years, if not decades, to come about, or I can decide to take a chance on a theory that has not been proven to everyone's satisfaction yet.

 

[Hip]

Building a useful model is much more to do with trawling through for what DOES NOT fit for a given theory.

I appreciate that, and am always ready to throw out a hypothesis when it no longer can accommodate the known facts. Unfortunately though, with the very limited knowledge of physiology I have, I don't have much of a mental biochemical database to trawl through!

If there was any specific conclusion about mechanism from the IiME workshop I think it was probably that we may be looking for a mechanism that leaves IL-6 well alone.

Wouldn't the simplest way to test whether IL-6 is the cause of PEM be to inject some recombinant IL-6 into willing ME/CFS patients? That should put the matter to rest one way or another. Even a small scale study of 5 or 10 patients would be useful here.

In studies when IL-6 as injected into healthy people, this caused some fatigue and some mild loss of concentration. But if injected IL-6 caused a full PEM episode in ME/CFS patients, that would indicate IL-6 is the driver of PEM.

Sickness behaviour is a buzz word that does not quite fit here I think.

The mechanism I was considering in this instance was whether the down-regulation of the interferon response caused by IL-6 might be what precipitates the viral flu-like symptoms of PEM, as a result of viral reactivation.

 

[JayBO]

Does anyone know if there is research about using steroid medications after exertion to decrease possible immuno-inflammatory effects and disrupt PEM process (such as dexamethasone which, as per Wikipedia, has anti-inflammatory and immunosuppressant effects)?