Clinical trials & what we need from them

[arewenearlythereyet]

You don't expect actual useful things like funding for ME/CFS antiviral studies do you? Good luck with that.

Dr Chia wanted to do a study on oxymatrine treatment for enterovirus ME/CFS, but could not get funding. He ended up doing a quasi-study, the good results of which are available, put it is not published. In 5 patients he took stomach biopsies before and after oxymatrine, and showed the viral loads in the tissues went down as patients improved. But that sort of thing really needs funding to do properly.

I hear you, but that still doesn’t mean you can quote the research with much confidence...just look at ritixumab ?

 

[Hip]

I hear you, but that still doesn’t mean you can quote the research with much confidence...just look at ritixumab ?

You may be right regarding the concomitant reduction of viral titers, but other aspects of the enterovirus theory are more established:

• The findings of chronic enterovirus in ME/CFS patients' tissues: there are numerous studies that have replicated that, and I think that research is unassailable.

• The fact that enterovirus ME/CFS patients improve on antivirals and immunomodulators like ribavirin, interferon and oxymatrine: that's less well established in terms of published studies, but there are three papers showing interferon improves ME/CFS or puts patients into remission; plus Chia's placebo controlled quasi-study on oxymatrine in 100 ME/CFS patients. (For various reasons, interferon is not a viable long-term treatment; but the fact it works in the short-term provides good evidence that enterovirus plays a causal role in ME/CFS).

• The concomitant reduction of enterovirus titers as patients improve on the treatment: that is not very well established in published studies (although Chia may have his own data from his clinical work), and further studies are required.

 

[Alvin]

We do need to home in on a disease mechanism.

I do like to the general ideas outlined by @Jonathan Edwards, that ME/CFS may be caused by some dysfunctions in immune signaling, which then leads to a chronic aberrant immune response. That immune dysfunction ultimately might become the best target for treating ME/CFS.

An aberrant immune response could also neatly explain the viral data we observe in ME/CFS. In the case of enterovirus for example, we know that there is a chronic intracellular infection in ME/CFS patients' muscles and intestinal tissues. And we know that when viral load is reduced by antiviral or immunomodulatory treatment, ME/CFS symptoms substantially improve.

However, that intracellular infection alone may not explain ME/CFS, because you also find the same intracellular infections in a percentage of healthy people. But if you add an aberrant immune response into the equation, then that intracellular infection plus an aberrant response to it might give rise to the viral subset of ME/CFS.

We have lots of evidence that its immune in some form but no confirmation. Its even possible its related to a part of the immune system we do not yet know, if true ME/CFS would not be the first disease that needed a new discovery to become "legitimate"