5th Invest in ME/CFS Conference - Programme May 24 2010

[Bob]

Thank you Bob. I think I just need a continuous loop of reassurance right now!:tear::tongue:

Hi lulu... it's all a bit 'brain-meltdown' at the moment isn't it! I think I feel the same as you... :tear::tongue:

 

[fred]

The main flaw in Huber's HERV-K18 study

There appear to be many flaws in Huber's work but the 'master flaw', I believe, from which all erroneous conclusions will arise is the absence of a group with mono but without ME.

As a result of this design, we have no way of knowing whether the activation pattern of the HERV in question in patients with ME is any different from its activation pattern in people with a mono infection who do not have ME.

She should also be aware that HERVs are part of the intrisic immune system and are activated as a result of any viral infection, particularily if that virus is a retrovirus. She, therefore, should have checked the activity level of other HERVS.

It is a shame that she missed two glaring opportunities to test her hypothesis. She has, however, provided the information which will enable that hypothesis to be tested by others.

 

[flex]

Interesting Fred,

I think I remember her saying something about folks who had a virus and now they don't and then shied away from explaining why they are still ill. Which in her fairy Godmother way was obviously meant to mean "there's nothing wrong with you" or "I don't care from here on". We all know what happens at that point with doctors. Also she never once referred to the illness as ME or even CFS, just "chronic fatigue".

You are correct in saying that she is an opportunity misser of the highest order. It seems almost deliberate in order to, shall we say, not find an answer at all. Of course apart from the basic flawed one which she wants.

She is like many MDs "if you aint got my illness, you aint ill".

 

[Bob]

There appear to be many flaws in Huber's work but the 'master flaw', I believe, from which all erroneous conclusions will arise is the absence of a group with mono but without ME.

As a result of this design, we have no way of knowing whether the activation pattern of the HERV in question in patients with ME is any different from its activation pattern in people with a mono infection who do not have ME.

She should also be aware that HERVs are part of the intrisic immune system and are activated as a result of any viral infection, particularily if that virus is a retrovirus. She, therefore, should have checked the activity level of other HERVS.

It is a shame that she missed two glaring opportunities to test her hypothesis. She has, however, provided the information which will enable that hypothesis to be tested by others.

I haven't read up on Huber's work yet... I have only just come across it... don't know why... but it sounds interesting... if i understand correctly, she is suggesting that HERV's, which are an endogenous virus (?), are being reactivated by other viruses, and the level of reactivation may correspond to the level of symptoms in a person with CFS/ME... this sound like quite an interesting theory...

I'm becoming quite interested in endogenous retroviruses and how reactivation may contribute to some diseases such as schizophrenia... I like to think that we might see some progress, and results, in this field over the next few years... if not for ME, then for other neuro-immune diseases.

 

[V99]

Why is it that so many scientists fail to design solid studies into ME? What am I missing here?

How come Huber, like you say Fred, did not test mono without ME? She can not be that bad a researcher, so do I go with Flex's assessment or can someone offer another opinion.

Are studies into any disease always this weak, or is it that they rush through to get any result, and drag out these important questions?

 

[Bob]

Why is it that so many scientists fail to design solid studies into ME? What am I missing here?

How come Huber, like you say Fred, did not test mono without ME? She can not be that bad a researcher, so do I go with Flex's assessment or can someone offer another opinion.

Are studies into any disease always this weak, or is it that they rush through to get any result, and drag out these important questions?

I don't know anything about Huber, but could it be something to do with funding? That doesn't excuse a badly planned research study, but it might explain why she can't do as much research in one study as she'd like to... just a thought... because i know that in the UK it's almost impossible to get any funding for ME, unless you are a psychologist or you want to test the lightning process on vulnerable children... in which case they shower you with millions of pounds/dollars.

 

[V99]

Funding does seem to play a part, so why does anyone only get money for small studies? It seams to only lead to more questions and more funding for small studies.
I know the answer, I just say why? The logic is impossible to fathom. Unless there is an ulterior motive, which I don't doubt.
To me the entire system needs to change, it's a real wonder that any discoveries are ever made.

 

[fred]

I do not believe the omission is to do with funding given that it is a five year programme supported by the NIH.

I remember Huber presenting the chart with the two study groups on it and almost fluffing the words that went with it. She said something like "Well, yes, there's just these two groups". At the time, I remember thinking 'there's something missing' but not being able to define what it was. It wasn't until later in the presentation when she showed some initial results and made the conclusions that she did that the penny dropped with me. I thought: 'if you use a mono only cohort, your conclusions may be totally screwed'.

I was going to raise it as a question but her XMRV bombshell took my eye of the ball.