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Article: UK Govt Turns New Leaf ? (Why the UK Loves ME/CFS More (!) )

It's a cumbersome analogy, but looking at Sjogrens' syndrome in this way is akin to using an AIDs budget to research candida. Just because some people with ME might have Sjorgens' syndrome (can we even quantify how many given the absurd use of criteria used in most quarters?) it doesn't compute to study that illness and pretend we can extrapolate the data to ME. Ludicrous.

The MRC are no nearer accepting what real ME entails than they ever were. This is a sop...I'm surprised anyone is fooled by it.
 
Any link between Sjogrens and CFS is difficult to tease our, due to all the normal problems with studying CFS, and also because some see Sjogrens as exclusionary. If there is an autoimmune component to CFS, then there will probably be an association with other autoimmune problems... but this could also be interpreted as patients with autoimmune problems being misdiagnosed with CFS.
 
I think I will wait to discover more about the project relating to Sojorn's before making any all-embracing conclusions that it should or should not have been granted funding in the way that it has. Same goes with the previous comment about the 'Hep C' project being included.

Cort - the MRC actually provided a further 150,000 to the total allocated by the way: http://www.mrc.ac.uk/Newspublications/News/MRC008410 that link is the full press release.

I've requested that they update their research page with more detail about all of these projects.
 
I think I will wait to discover more about the project relating to Sojorn's before making any all-embracing conclusions that it should or should not have been granted funding in the way that it has. Same goes with the previous comment about the 'Hep C' project being included.

Cort - the MRC actually provided a further 150,000 to the total allocated by the way: http://www.mrc.ac.uk/Newspublications/News/MRC008410 that link is the full press release.

I've requested that they update their research page with more detail about all of these projects.

The money was supposed to be going to biomedical research into me/cfs how can it be justified to take money from this budget to do a study on an entirely different illness ?

Just because there may be some similarities with some of the symptoms does not justify this at all . Many illness share similar symptoms to ME/CFS Lupus being one MS being another .

can you imagine the outrage if for example research money that had been allocated to those illnesses was suddenley syphoned off for research into ME/CFS instead . Lupus and MS patients would be up in arms and rightly so they deserve their research money just as much as we deserve ours .
 
I am simply saying Polly that we do not know the reasons behind the studies being granted this funding. Details are rather sketchy and we don't know what the premise was for the grants being allocated in this way. I have asked and am waiting for a reply.

Sjoren's does have similarities with CFS/ME beyond the 'fatigue' for example. But you could be right. Maybe I should be negative or more 'realistic' I guess you might say; but I just don't believe I should - this does represent a change from what has gone before.

I will wait to learn more before drawing a conclusion about this project and that other one mentioned is all I am saying. Also the fact that some of the researchers are 'psychiatrists/psychologists' does not raise concerns with me at this point.

If the research is sound - and we can't judge that until more details are forthcoming and/or the studies are complete - then [shrug] what difference does it make? There will always be concern expressed at the projects that didn't get funding - but we also don't know who applied either. By that I mean we don't know what projects were not granted funding.

If nobody else applied for example - that would lead us perhaps to draw other conclusions. Perhaps the Sjoren's study was the only study or the best that met that particular category. I don't know.
 
It would be a good idea to find out what applications were made for funding and how the decision to award funding was made and who made it.
Well done for trying to find out firestormm.

Difficult in Britain though, with our culture of governmental secrecy.


And I do not like sounding negative about this research. I sincerely wish I could be excited and stimulated by it. (!) People deserve some good news.
 
Thanks for this article. I recall someone from the British charity, Me Association, saying that this funding has come about due to a change in the person who heads the MRC. This new guy is supposed to be more sympathetic to M.e.

I echo what others have said that the Pace trial results are still being presented as more favourable than they are which is a worry. Again someone from the m.e association fears when the NICE guidelines ( our NHS treatment recommendations for various conditions) for m.e are due for renewal in 2013, he fears they wil use PACE to continue suggesting GET and CBT as first line treatments. I know people wrote detailed criticisms to Lancet who published the pace results, all of which were ignored apparently

Anyway, for all this, the recent announced research is a small step in the right direction which is encouraging....

Part of the reason appears to be that the MHC has an advisory committee with a wide range of researchers/advocates on it. There are behavorists and people with a pathophysiological focus. I think that person is Stephen Holgate - perhaps it was he who put the committee together.
 
Thanks for this article. I recall someone from the British charity, Me Association, saying that this funding has come about due to a change in the person who heads the MRC. This new guy is supposed to be more sympathetic to M.e.

I echo what others have said that the Pace trial results are still being presented as more favourable than they are which is a worry. Again someone from the m.e association fears when the NICE guidelines ( our NHS treatment recommendations for various conditions) for m.e are due for renewal in 2013, he fears they wil use PACE to continue suggesting GET and CBT as first line treatments. I know people wrote detailed criticisms to Lancet who published the pace results, all of which were ignored apparently

Anyway, for all this, the recent announced research is a small step in the right direction which is encouraging....

White, of course, will fight for his study - which Dolphin pointed out ended up being over 7 million dollars - and I'm positive that NICE will continue to recommend GET and CBT - but any researcher who looks closely at the data has to be disappointed at the results. It was a very expensive program and it got mediocre results.

If the UK govt is interested in bang for the buck - and given their financial situation they certainly should be - they pretty have to come to conclusion that they're not getting much from these therapies.
 
The UK government despises people with ME/CFS . People are denied benefits , denied care that they need and portrayed in the press as either lunatics brandishing knives and sending death threats to scientists or lazy bone idle gits who all they need is a kick up the backside to get them back to work .

This money was supposed to be ringfenced for biomedical research into ME so why is some of it going to Sjgren syndrome ? thats not chronic fatigue syndrome and it certainly isnt ME .

why is some of the money going to psychologists ? I thought this was for biomedical research ?

The only study to be honest which I have any faith in is Julia Newton .

There is nothing here that is going to find a cause for ME . This money was supposed to be for that reason I really do feel we have been well and truly ripped off yet again .

We need to be looking at causation not single symptoms like sleep which to be honest someone with genuine ME would probably list way down on their symptom list . with pain , cognitive disfuntion , infections , muscle problems and control ranging far higher . We need to step away from 'fATIGUE ' this illness is far more complicated than mereley being a bit tired . Having a good nights sleep makes bugger all difference to my other symptoms .

Do you realise the 1.6 million actually equates to 6.50 per head per person in the UK with ME/CFS . that equates to a meal at KFC or a ticket to the cinema for fit and healthy people . or you might get 3 loaves of bread and a bit of change left over or perhaps be able to buy a piece of meat for sunday dinner though way prices are going up the piece of meat may be out of price range now .

Thats what this money eqautes to . yet how much was wasted on the pace and fine trials . millions . The pace trial is seriously flawed and should be retracted . will it be will it hell . the fine trial was a flop . All that money millions wasted and were supposed to be grateful for 1.6 million that theyve managed to share out to include psychologists and an illness that isnt ME or CFS .

How can anyone seriously think this government is turning over a new leaf . We are at the bottom of the crap pile as per usual and will remain there until the NICE guidelines are changed , theres research looking at the whole disease and causation , people are awarded the help and benefits they so deserve , the press starts reporting on ME fairly without bias and the likes of wessely and chalder are as far away from ME/CFS research as possible .

Its hard to imagine that you will ever get wholesale change from any institution in a government or even any beauracy quicly. It just doesn't happen. The people who put the CBT and GET policies in in the UK are presumably but new figures are now present as well.

These studies are not going to solve ME/CFS and, in truth, they are not that innovative but they could illuminate some important aspects of it. Autonomic nervous system, mitochondrial functioning, sleep drugs, interferon pathways - could all be quite helpful in elucidating ME/CFS is.

You can see this as well its still too little (which it is) or you can see it as a shift in UK priorities - which at least in this point of time, it is as well. The MRC has never funded a slate of pathophysiological studies like this into ME.
 
Its hard to imagine that you will ever get wholesale change from any institution in a government or even any beauracy quicly. It just doesn't happen. The people who put the CBT and GET policies in in the UK are presumably but new figures are now present as well.

These studies are not going to solve ME/CFS and, in truth, they are not that innovative but they could illuminate some important aspects of it. Autonomic nervous system, mitochondrial functioning, sleep drugs, interferon pathways - could all be quite helpful in elucidating ME/CFS is.

You can see this as well its still too little (which it is) or you can see it as a shift in UK priorities - which at least in this point of time, it is as well. The MRC has never funded a slate of pathophysiological studies like this into ME.

Sleep drugs in King College diagnosed mentally ill patients, Mitochondrial function with grape seed extract, interferon pathways in Hepatitis C patients - Give me a break, Cort! If you correctly detail the studies you would see the truth, non of this could possibly help ME patients. Now if all the above studies - mitochondrial functioning, sleep drugs, interferon pathways - were going to be done on Canandian Criteria ME Patients, then yes it would be of some value, but that is not the case. As some one else wrote, if money for cancer research was being syphoned away to study depressed patients claiming it was valid because both conditions caused "fatigue", cancer patients would be up in arms.
 
I have to completely disagree with everything that Cort has written. Nothing has changed in the UK. The latest round of funding is an absolute sop to patients with ME. All of the proposed studies, except the one by Dr Julia Newton, will use the Oxford criteria. For anyone that doesn't understand, the Oxford Criteria means that depressed, anorexic, and mentally ill patients with no post exertional malaise will be selected. And worse still is that two of the studies are not even on ME patients but so called "related fatigue states".

Although the evidence that ME is physical is now overwhelming, no one knows what causes it, therefore to study other conditions because of a claimed similarity to ME is absolute balderdash, how are they similar if no one knows what ME is? This money was suppose to go towards finding out more about ME, not spending on vague fatigue like mechanisms in other conditions. This is similar to the theft of ME research funds at the CDC for pet projects, except the British like to take dishonesty to a higher level - by even being dishonest about their dishonesty. Would Lupus, MS, HIV patients get wishy washy sleep studies, grape seed extract studies (polyphenols) and the like. No they would get serious research with Rituximab and other immune therapies, and immunoglobulins, things that have been proven to work. Also if ME is so much like Sjgren syndrome that it warrants spending precious little funding designated specifically for ME, and since we know that IV immunoglobulin and Rituximab are effective treatments for severe Sjgren syndrome, why aren't ME patients allowed IV immunoglobulins and Rituximab?

Someone wrote an exceptional review of the projects which I will repost below - has anything changed... I think not, we are just getting lip service.

---------

Upon reading the proposed MRC research projects for ME, I was dismayed to see that only one could really be described as fitting the description of biomedical research into ME.

Given Professor Holgate's insistence that the money would be u...sed for this use only, and his apparent concern that ME research be moved forward, I cannot understand how this has happened. Below I have outlined concerns over each individual study.

1. Identifying the biological fingerprints of fatigue - This is in actual fact a study on Sjgren syndrome which has nothing in common with ME other than that both conditions have "fatigue" in the most general sense of the word. This is the same as studying migraine and claiming to study brain tumours because both cause headaches. Fatigue is a symptom of almost every medical condition and therefore using this as an excuse to study other illnesses is not justifiable. Why not study the immune parameters (as they are going to do in this study) of ME patients? It just makes no sense.

2. Modulation of aberrant mitochondrial function and cytokine production in skeletal muscle of patients with CFS by supplementary polyphenols. - The same point can be made again that mitochondrial dysfunction is a symptom of many chronic illnesses and not unique to people with ME. This study is going to try and treat people using supplements such as grape seed extract. If this kind of intervention worked, all ME patients would be well by now as we have all tried grape seed extract (and wasted money on hundreds of other supplements).

3. Can enhancing slow wave sleep SWS improve daytime function in patients with CFS? - Whilst at first glance this project may seem to be of value, again all chronic illnesses cause dysfunction of slow wave sleep, including epilepsy. Pharmaceutical measures to correct this have almost never been successful because the drugs are just too dangerous to be used long term as a symptomatic treatment.

4. Persistent fatigue induced by interferon-alpha: a new immunological model for chronic fatigue syndrome. - This is possibly the most objectionable study in that again it is not looking at ME patients. The study will "follow patients undergoing IFN-alpha treatment for Hepatitis C over a number of months to define the biological changes that occur in relation to the development of fatigue". In actual fact ME patients have in the past have been treated with IFN-alpha and found their fatigue improved, showing that the biological changes induced by IFN-alpha have nothing to do with the "fatigue" of ME (research by John Chia - Alpha 2a interferon significantly increased quality of life scores and natural killer cell functioning in ME/CFS patients with reduced NK cell functioning in a 1994 study. Dr. Chia reported another small early interferon study by Brook et. al. was successful as well. )

It is simply not acceptable for the money that was supposed to go towards ME research to go to a hotch potch group of vague studies that merely look at "fatigue" in a variety of conditions. What Professor Holgate and his team do not seem to appreciate is that ME is not fatigue. Until this basic point is understood, there will be no progress. The unique symptom of ME is an increase in symptoms after exercise (where "exercise" can be as little as getting dressed or drying ones hair for some people). Symptoms can range from flu like (swollen glands, sore throats, general weakness) to cardiovascular (missed heart beats, racing heart) and neurological (dizziness, blurred vision, heightened sensitivities to sound and light, and even seizures). Patients have these symptoms ALL the time, often even at rest, but will experience an increase after any activity. The specific increase of symptoms in patients with ME is measurable with the repeat two day VO2 Max stress testing. This is unique to ME, and therefore as repeated above, studies on Hepatitis C patients and Sjgren syndrome will yield no useful information. Reserach on VO2 max stress testing is now accepted in the USA as the best objective repeatable measure of incapacity - please see the following research.

http://niceguidelines.files.wordpre...ndings-with-repeat-exercise-testing-in-me.pdf

Only the Canadian Consensus Criteria and International Criteria accurately describe these symptoms of ME and therefore should be the only ones used. Not one single study in the UK has ever used this criteria. Psychiatrists who purport to study ME use the Oxford Criteria which simply describes fatigue. An illness cannot be studied unless it is accurately defined.

I cannot even get close to describing my frustration over this most recent funding announcement. The initial press release detailing this 1.6 million funding was a source of hope for many, which has now been dashed. There was hope that somebody might follow up the Norwegian findings which pointed to ME being an autoimmune condition, but this has not happened.

I'll have to disagree. Again - if you expect the UK medical est. to launch a major program to find the pathophysiological problems behind CFS or to treat it like well-defined diseases like lupus, rheumatoid arthritis, etc. I think you're going to be disappointed. Researchers know where to put those diseases but they don't know where to put ME/CFS. Is it an autoimmune disorder? A mitochondrial disorder? A NEID disorder? Metabolic disorder? Behavioral disorder --- talk to any number of researchers and you'll get differing opinions.

CFS isn't even allied with an Health Institute in the US - it was kicked out of the Immune Institute and now its in the Office of the Director.

We're in the same situation with the NIH and CDC as you are with the MRC in the UK. Expecting the CDC to start looking for viruses, for instance, is a recipe for disappointment. Its just unrealistic. The UK is not going to fund a major study into Rituximab on the basis of one double-blinded CFS study. However they will fund research that could apply to it should that finding work out. If you're looking for a complete turnaround at the UK you're not going to get it. If you're looking for signs of change they are there in both programs.

Sjogrens - In light of the Rituximab findings suggesting that ME/CFS may be an autoimmune disorder the Sjogren's study is actually now very interesting even if it is indirect. Finding a biomarker for fatigue in an allied disorder, if that's what Sjogren's is - would be a step forward - so while I agree that the study is indirect - its possibility for making a difference is actually pretty high.

Polyphenols/Mitochondria
- this doesn't seem to be the same study as the one I looked at the MHC site (?). That one didn't mention treatment and focused on using new technology to assess mitochondrial functioning in the muscles

Sleep - I don't know what drug they are using but if its sodium oxybate (xyrem) and it is found to be effective and the British Health system starts paying for it on the basis of that study (or those following) that would be a huge win for UK people with ME/CFS. Most people in the US can't afford it and we don't have a federally funded study that will help us afford it.

IFN- a - again this has an indirect link to CFS - as I pointed out in the article - but there are possibilities. A recent study did link the fatigue in IFN-a with CFS and it did follow people getting IFN-a and identified which ones because fatigued, etc. and which did not. The people who got worse on the drug demonstrated an upgregulation of a gene that has been linked to ME/CFS.

Molecular signatures of peripheral blood mononuclear cells during chronic interferon-? treatment: relationship with depression and fatigue. Felger JC, Cole SW, Pace TW, Hu F, Woolwine BJ, Doho GH, Raison CL, Miller AH.

BACKGROUND:
Interferon-alpha (IFN-?) treatment for infectious disease and cancer causes high rates of depression and fatigue, and has been used to investigate the impact of inflammatory cytokines on brain and behavior. However, little is known about the transcriptional impact of chronic IFN-? on immune cells in vivo and its relationship to IFN-?-induced behavioral changes.

RESULTS:
Significance analysis of microarray data identified 252 up-regulated and 116 down-regulated gene transcripts. Of the up-regulated genes, 2'-5'-oligoadenylate synthetase 2 (OAS2), a gene linked to chronic fatigue syndrome (CFS), was the only gene that was differentially expressed in patients with IFN-?-induced depression/fatigue, and correlated with depression and fatigue scores at 12 weeks (r=0.80, p=0.003 and r=0.70, p=0.017 respectively). Promoter-based bioinformatic analyses linked IFN-?-related transcriptional alterations to transcription factors involved in myeloid differentiation, IFN-? signaling, activator protein-1 (AP1) and cAMP responsive element binding protein/activation transcription factor (CREB/ATF) pathways, which were derived primarily from monocytes and plasmacytoid dendritic cells. IFN-?-treated patients with high depression/fatigue scores demonstrated up-regulation of genes bearing promoter motifs for transcription factors involved in myeloid differentiation, IFN-? and AP1 signaling, and reduced prevalence of motifs for CREB/ATF, which has been implicated in major depression.

CONCLUSIONS:

Depression and fatigue during chronic IFN-? administration were associated with alterations in the expression (OAS2) and transcriptional control (CREB/ATF) of genes linked to behavioral disorders including CFS and major depression, further supporting an immune contribution to these diseases.
 
The money was supposed to be going to biomedical research into me/cfs how can it be justified to take money from this budget to do a study on an entirely different illness ?

Just because there may be some similarities with some of the symptoms does not justify this at all . Many illness share similar symptoms to ME/CFS Lupus being one MS being another .

can you imagine the outrage if for example research money that had been allocated to those illnesses was suddenley syphoned off for research into ME/CFS instead . Lupus and MS patients would be up in arms and rightly so they deserve their research money just as much as we deserve ours .

In the US we have dealt with this issue for many years....as the article noted the NIH has frequently labeled research that might have some connection with CFS as 'CFS research". Actually in the US that happens with every disorder...it happens with lupus and MS and heart disease - that appears to be how both federal health institutions attribute funding. I would not assume that that is endemic to CFS. I will look into it, however.

I just looked into this. If you look up diabetes at the MRC you'll get studies on COPD, neuropathic pain, weight loss after obesity surgery, assessing dietary intake, etc., etc. The number of studies that are actually focusing on what is causing diabetes are in the minority. There are alot of studies on managing the symptoms (neuropathic pain), how weight loss works (obesity is a big problem in diabetes), how to optimize diet...all these kind of ancillary projects...
 
as someone living in the UK, i have to agree with most of the comments about this article. I wish it were true Cort, but the RMC and the UK Gov't isnt turning over a new leaf.

Its a step in the right direction, and deserves some attention, but in reality the change is minor. If i can use an analogy to convey this:
its like people with ME/CFS in the UK are represented by a weedy man, and the UK gov't and RMC are wrestlers that have been beating the weedy man with a chair and metal poles for years, and now they have started handing out plasters (band-aids) but only because the international crowd have started to change elsewhere (Norway for example) ...but the important thing is that the UK gov't has not stopped beating the weedy man. They still promote GET and CBT as if it were a cure, and really good for you, and offer no other alternatives, or even evidence of it being safe, let alone beneficial. They still discriminate agaisnt us, and deny us benefits, even if we have irrefutable proof of our illness, and still take children with ME away from their parents, because the parents wont play ball and allow their kids to have the 'treatments' that the UK gov't says they need...

Am i pleased of the change - yes. Is it a hug change - sadly no. Living in the UK with ME/CFS is like living in the stone age, and bronze isnt even on the horrizon.
 
Sleep drugs in King College diagnosed mentally ill patients, Mitochondrial function with grape seed extract, interferon pathways in Hepatitis C patients - Give me a break, Cort! If you correctly detail the studies you would see the truth, non of this could possibly help ME patients. Now if all the above studies - mitochondrial functioning, sleep drugs, interferon pathways - were going to be done on Canandian Criteria ME Patients, then yes it would be of some value, but that is not the case. As some one else wrote, if money for cancer research was being syphoned away to study depressed patients claiming it was valid because both conditions caused "fatigue", cancer patients would be up in arms.

Are you sure they are all using Oxford criteria? I did see that the XMRV study at Kings College used the Fukuda criteria. While the Canadian Criteria would be much better the Fukuda criteria is not worthless; it has been used in studies that demonstrate NK cell dysfunction, exercise intolerance, altered gene expression after exercise, etc. Is the MHC wedded to the Oxford criteria in this set of studies?

Again - the information I got did not indicate that grape seed extract was the focus of the mitochondrial study and if that's true that's quite disappointing.

Even if they are using the Oxford criteria I would still submit that these studies are a distinct change from the MHC's past studies and while the deficiences in them should be pointed out -and there will be deficiencies given where the MHC is coming from - that that the change should be welcomed as well.

Asking a unit that has been almost wholly behaviorally focused for many years to turn around and institute ground breaking pathophysiological studies is a recipe for disappointment.

Dismissing that change could have a negative impact as well. Acknowledging the change and at the same time pressing for more im rovement is the most effective thing to do in my opinion.
 
I have to completely disagree with everything that Cort has written. Nothing has changed in the UK. The latest round of funding is an absolute sop to patients with ME. All of the proposed studies, except the one by Dr Julia Newton, will use the Oxford criteria...

4. Persistent fatigue induced by interferon-alpha: a new immunological model for chronic fatigue syndrome. - This is possibly the most objectionable study in that again it is not looking at ME patients. The study will "follow patients undergoing IFN-alpha treatment for Hepatitis C over a number of months to define the biological changes that occur in relation to the development of fatigue". In actual fact ME patients have in the past have been treated with IFN-alpha and found their fatigue improved, showing that the biological changes induced by IFN-alpha have nothing to do with the "fatigue" of ME (research by John Chia - Alpha 2a interferon significantly increased quality of life scores and natural killer cell functioning in ME/CFS patients with reduced NK cell functioning in a 1994 study. Dr. Chia reported another small early interferon study by Brook et. al. was successful as well. )

Personally I would have liked to see different studies in the mix (eg a Dubbo replication) but I'm still delighted that the MRC are for the first time funding biomedical research. Stephen Holgate deserves our applause for managing to push water uphill at the MRC.

Is there any evidence that thesez studies will use Oxford criteria? I hadn't seen any.

Do you have references for the studies treating CFS patients with interferon? I'd thought they were small and rather inconclusive.

Thanks

I spent a lot of time looking at the case for using Interferon-alpha as a model, which you can see summarised in the post below:
When the MRC grants were announced last week there was a lot of scepticism about the Pariente study of fatigue in Interferon-alpha treated Hepatitis C patients. First, it isn't actually studying CFS and second, Carmine Pariente is a psychologist from the Institute of Pschiatry, Kings College London, making him a stablemate of Simon Wessely, which understandably causes some suspicion.

Read the rest of the post here
 
re Action for ME - well, I'd been wondering why they are pushing that dreadful psychological "study" being done on ME, but reading this thread has explained it. I naively rang AfME on Thursday to complain, and they said they'd look into it and ring me back on Friday. Oddly enough, they didn't.
 
When the MRC grants were announced last week there was a lot of scepticism about the Pariente study of fatigue in Interferon-alpha treated Hepatitis C patients. First, it isn't actually studying CFS and second, Carmine Pariente is a psychologist from the Institute of Pschiatry, Kings College London, making him a stablemate of Simon Wessely, which understandably causes some suspicion.

My guess is that most people studying fatigue produced by IFN-a will be psychologists or psychoneuroimmunologists. Andrew Miller, for instance, is a psychiatrist at Emory studying IFN-a who believes the fatigue is caused by cytokines, epigenetics or a virus - based on a talk I had with him. In fact he said - he didn't think it was the stress response - its a virus. He is in the body/mind camp; ie he is interested in how the immune system effects the brain.

Here's from Miller's Emory profile

Dr. Miller currently has several studies funded by the National Institute of Mental Health, the Centers for Disease Control and Prevention and pharmaceutical companies to examine the mechanism and treatment of cytokine-induced depression as represented by the cytokine, interferon alpha, which is used for the treatment of infectious diseases and cancer. His interferon alpha studies provide a model to understand and treat depression, fatigue and cognitive dysfunction in medically ill patients.

I certainly understand the suspicion. These are the studies Pariente has been involved in recently. They apparently picked him at least in part because he's does alot of research into cortisol, childhood stress and inflammation.
Isabelle Ouellet-Morin, Andrea Danese, Lucy Bowes, Sania Shakoor, Antony Ambler, Carmine M Pariante, Andrew S Papadopoulos, Avshalom Caspi, Terrie E Moffitt, Louise Arseneault (2011) 'A Discordant Monozygotic Twin Design Shows Blunted Cortisol Reactivity Among Bullied Children' Journal of the American Academy of Child and Adolescent Psychiatry, 50 (6), pp. 574-582.
[Article in print Journal]

M Aas, P Dazzan, V Mondelli, T Toulopoulou, A Reichenberg, M Di Forti, H L Fisher, R Handley, N Hepgul, T Marques, A Miorelli, H Taylor, M Russo, B Wiffen, A Papadopoulos, K J Aitchison, C Morgan, R M Murray, C M Pariante (2011) 'Abnormal cortisol awakening response predicts worse cognitive function in patients with first-episode psychosis' Psychological Medicine, 41 (3), pp. 463-476.
[Article in print Journal]

Susan Pawlby, Dale Hay, Deborah Sharp, Cerith S Waters, Carmine M Pariante (2011) 'Antenatal depression and offspring psychopathology: the influence of childhood maltreatment' British Journal of Psychiatry, 199 (2), pp. 106-112.
[Article in print Journal]

C Anacker, P A Zunszain, A Cattaneo, L A Carvalho, M J Garabedian, S Thuret, J Price, C M Pariante (2011) 'Antidepressants increase human hippocampal neurogenesis by activating the glucocorticoid receptor' Molecular Psychiatry, 16 (7), pp. 738-750.
[Article in print Journal]

A Danese, A Caspi, B Williams, A Ambler, K Sugden, J Mika, H Werts, J Freeman, C M Pariante, T E Moffitt, L Arseneault (2011) 'Biological embedding of stress through inflammation processes in childhood' Molecular Psychiatry, 16 (3), pp. 244-246.
[Letter (Print)]

Monica Aas, Paola Dazzan, Helen L Fisher, Craig Morgan, Kevin Morgan, Abraham Reichenberg, Jolanta Zanelli, Paul Fearon, Peter B Jones, Robin M Murray, Carmine M Pariante (2011) 'Childhood trauma and cognitive function in first-episode affective and non-affective psychosis' Schizophrenia Research, 129 (1), pp. 12-19.
[Article in print Journal]

Patricia A Zunszain, Christoph Anacker, Annamaria Cattaneo, Livia A Carvalho, Carmine M Pariante (2011) 'Glucocorticoids, cytokines and brain abnormalities in depression' Progress in Neuro-Psychopharmacology and Biological Psychiatry, 35 (3), pp. 722-729.
[Review (research) (Print)]

C M Pariante, G Seneviratne, L Howard (2011) 'Should we stop using tricyclic antidepressants in pregnancy?' Psychological Medicine, 41 (1), pp. 15-17.
[Editorial Material (Print)]

Isabelle Ouellet-Morin, Andrea Danese, Lucy Bowes, Sania Shakoor, Antony Ambler, Carmine M Pariante, Andrew S Papadopoulos, Avshalom Caspi, Terrie E Moffitt, Louise Arseneault (2011) 'A Discordant Monozygotic Twin Design Shows Blunted Cortisol Reactivity Among Bullied Children' Journal of the American Academy of Child and Adolescent Psychiatry, 50 (6), pp. 574-582.
[Article in print Journal]

Tiago Reis Marques, Francisco Marques-Teixeira, Heather Taylor, Andy Simmons, Valeria Mondelli, Flavio Dell'Acqua, Carmine Pariante, Anthony S David, Robin Murray, Paola Dazzan (2011) 'AUDITORY HALLUCINATIONS IN FIRST EPISODE PSYCHOSIS: A DTI STUDY OF THE ARCUATE FASCICULUS', , pp. 174-174.
[Meeting Abstract in Journal (Print)]

M Aas, P Dazzan, V Mondelli, T Toulopoulou, A Reichenberg, M Di Forti, H L Fisher, R Handley, N Hepgul, T Marques, A Miorelli, H Taylor, M Russo, B Wiffen, A Papadopoulos, K J Aitchison, C Morgan, R M Murray, C M Pariante (2011) 'Abnormal cortisol awakening response predicts worse cognitive function in patients with first-episode psychosis' Psychological Medicine, 41 (3), pp. 463-476.
[Article in print Journal]
 
My guess is that most people studying fatigue produced by IFN-a will be psychologists or psychoneuroimmunologists. Andrew Miller, for instance, is a psychiatrist at Emory studying IFN-a who believes the fatigue is caused by cytokines, epigenetics or a virus - based on a talk I had with him. In fact he said - he didn't think it was the stress response - its a virus. He is in the body/mind camp; ie he is interested in how the immune system effects the brain.

Here's from Miller's Emory profile

I certainly understand the suspicion. These are the studies Pariente has been involved in recently. They apparently picked him at least in part because he's does alot of research into cortisol, childhood stress and inflammation.
Sorry, clumsy writing by me: the para I put within a quote above was just the first part of a much longer post, which i rather more informative. I think some of the Dubbo crowd are also bioloogical psychologists, interested more in how the immune system affects the brain than how the 'mind controls the body'.

I would have been happier if Pariente had some experience of working with IFN-alpha, rather than endless studies on cortisol but lets see what he comes up with.
 
Are you sure they are all using Oxford criteria? I did see that the XMRV study at Kings College used the Fukuda criteria. While the Canadian Criteria would be much better the Fukuda criteria is not worthless; it has been used in studies that demonstrate NK cell dysfunction, exercise intolerance, altered gene expression after exercise, etc. Is the MHC wedded to the Oxford criteria in this set of studies?

No big deal? According to an international panel of experts (ICC), Patient sets that include people who do not have the disease lead to biased research findings, inappropriate treatments and waste scarce research funds.