Ladies and gentlemen, a magic trick*.

I am going to take two pieces of data, from two independent experiments, establishing ‘proof’ of two different concepts, presented in to different formats and to different events…

… And turn them into the same figure.

*waits for the astonished mummers to simmer down*

In my left hand I hold ‘Detection of an Infectious Retrovirus, XMRV, in Blood Cells of Patients with Chronic Fatigue Syndrome’, a Science paper from 2009.

Detection of an Infectious Retrovirus, XMRV, in Blood Cells of Patients with Chronic Fatigue Syndrome

We can ignore parts of this paper– they have been retracted, as it seems some samples were contaminated in a rather curious (strategic?) manner. Which is fine, because what I want you, the audience, to focus on is Figure 2:

i-2b43758e27bf90730176b0c81aa5fb68-Science Figure 2.png

Specifically, Part C:

i-cb8eb8e265b6b88d61ef774a574e2e46-Science Figure 2, zoom.png

Lets zoom in on it, to get a nice, clear image. Actually, lets zoom in on the bottom part of that figure:

i-c5e626b967ed434d7c79d3980fe7156c-Science Figure 2, zoom 2.png

Its quite clear, there are 8 lanes.

1– Normal
2– Normal
3– 1235
4– Normal
5– Normal
6– 1236
7– Normal
8– SFFV-infected HCD-57

Here is the figure legend:

(C) Lysates of activated PBMCs from healthy donors (lanes 1, 2, 4, 5, and 7) or from CFS patients (lanes 3 and 6) were analyzed by Western blots using rat mAb to SFFV Env (top panel) or goat antiserum to MLV p30 Gag (bottom panel). Lane 8, SFFV-infected HCD-57 cells. Molecular weight (MW) markers in kilodaltons are at left.

Not hard to interpret, right? Some cells from healthy donors do not express XMRV Gag protein, a couple CFS patients do express Gag protein, and a positive control does express Gag. It provides evidence to support the claim that CFS patients PBMC are infected with XMRV, and are capable of producing viral proteins.

Nothing out of the ordinary. *wink*

Now, in my right hand I hold Slide #13 from a presentation a Miz Judy Mikovits recently gave in Ottawa at the IACFS/ME 2011 conference, graciously provided to us by Miz Jamie Deckoff-Jones. A round of applause for Miz DJ, everyone!

*waits for the applause to die down*

i-62022694ec7582de8dc72d025444770d-IACFS13.png

Another fairly straight forward figure. Again, 8 lanes:

1– Normal
2– 2905 PBMC
3– 2905 PBMC + 5-AZA
4– Normal
5– 1674
6– 1674 + 5-AZA
7– Normal
8– SFFV-infected HCD-57

Again, PBMC from normal individuals do not express XMRV Gag proteins… but this time, though the CFS patients did not initially express viral Gag proteins, when treated with an epigenetic modifier, they could induce Gag expression. Fairly straightforward explanation for why some patients might *appear* to be negative, but with a bit of lab trickery (we do this stuff all the time in labs), we can make a hiding virus come out and play.

How nice for us all, right? *wink*

Lets zoom in a bit:

i-12e861b44c0be2b96d7ad55f5bc59a2d-IACFS13, zoom

And fiddle a bit with the brightness/contrast:

i-79b669f0e379e44949dd75183a5b9b20-IACFS13, zoom, edit 1

Science is all well and good– Two figures, one providing support of the claim that two patients, 1235 and 1236 are infected with XMRV, the other figure showing two patients, 2905 and 1674 might appear negative, but become positive after treatment with an epigenetic modifier. Neat, but so what?

Well, heres the *really* good part!

Now, watch carefully or you will miss the trick, ladies and gentlemen!

i-a1721540aae8cdd36fda3c6f399e2ba1-Comparison1.png
i-47c7973822ab40942fd40618b2cd9179-Comparison6.png
i-ccc51a5d1fbc3dec63233e07349c8292-Comparison7.png

Thats some mighty fine purple.

But how about an alternative view!!! I think Ive made my point, I just like how the far-right blob looks like a rubber ducky:

i-fa3b2ddc701b2403bd15c5a745534d20-Comparison5.png

*BOOMANDHUGEPLUMEOFGREYSMOKE*

TAH DAH!

Two bits of data describing and explaining to two entirely different things… and yet I can make the two images look identical!

I AM MAGIC!!!

Am I magic…?

…or is this a case of arrogant, bold-faced, lazy-ass scientific fraud perpetrated by an apparent pathological liar?

You be the judges, ladies and gentlemen.

I know what my opinions are, but I would very much like to hear your thoughts.

* Though much of this magic trick is my own creation, the original idea was not mine. That individual/Those individuals do not wish to step forward at this time (and rightly so), but should they ever want to take credit for this observation, I will *happily* give it to them. Its wonderful, something I myself missed.

But to all you frauds out there– remember this: Dont. Fuck. With. Scientists. Individually, scientists are smart folks. And even smart folks get screwed over now and then. But together, we are always smarter than you.

Always.

Comments

  1. #1 daedalus2u
    October 12, 2011

    If you send me an email, to the address at nitroceutic dot com, I will send you a write-up that goes into how NO is involved in the fatigue compensatory pathways in great detail.

    Mitochondria biogenesis is regulated by NO. ATP level is regulated by NO. Mitochondria turn-off is regulated by NO. Glycolysis is regulated by NO. Hematocrit is regulated by NO. Blood pressure and blood flow is regulated by NO. Ischemic preconditioning is turned on by low NO, and ischemic precondition is a low ATP state. Synthesis of steroids is regulated by NO.

    NO really is involved in a lot of things. I am pretty sure it is involved in CFS, and I have a pretty good, natural and non-invasive way of raising it that is under complete physiological control.

    I have a good anecdote where a man of ~30 had ARDS, was in the hospital for a few days and lost ~30 pounds and came out a shadow of his former self. Using my bacteria, in 2 months he had gained 9 pounds, had gone hiking, had resumed his PhD program at Yale and by every measure he was better than average for his age. His doctors had never seen such a recovery, they called it a miracle and had no explanation and didn’t want to listen to mine. I appreciate it is a n=1 anecdote. I would like to do real trials with IRBs and stuff. I don’t have the ability to do those, but am willing to work with essentially any non-quack that does.

  2. #2 David
    October 12, 2011

    993 WTF, well thats all fairly accepted stuff you reference, my only problem is the occasional mission creep. Once you accept infection as a stressor, then other forms of stress are looked at, and eventually via analogy psychologists start speculating on ‘life style stress’ and start to include all kinds of dubious stuff like sexual abuse, and personality types that ‘cant handle stress’. Thats why for now I’m happy to consider only infection as stress up to a point. It is a personal position really to keep psychobabble at bay for now – I dont think its necessary yet – I think some secondary opportunist – an HHV-6 like thing eg is more likely, though objectively I have to concede that crashed immune system is as likely.

    996 daedalus2u – Ha – I know one of the guys on that paper just lives round the corner- small world! I agree with your assesment of it though. There is another metabolic theory knocking about isnt there, cant remember his name, and also Dr Bell – you heard of him?, I think he writes a blog called the Lyndonville News….

    I find them all a bit speculative to be honest. Why I seam happier with some of the HPA axis theories, I dont know – possibly educational bias!

  3. #3 daedalus2u
    October 12, 2011

    David,, are you David Bell?

    The other metabolic theory is that of Martin Pall. His idea is 180 degrees from mine. He thinks the problem is too much NO and the resulting formation of peroxynitrite; I think the problem is not enough NO and the resulting formation of peroxynitrite.

    Peroxynitrite only forms when there are near equimolar quantities of superoxide and NO. Usually this never happens. NO and superoxide react at near diffusion limited kinetics so you can’t have both at the same time. Either physiology is in a NO dominated state (the normal at rest state) or a superoxide dominated state (the fight or flight state). The transition from normal to fight or flight is very rapid. Superoxide is made, the NO level is pulled down and there is a very fast transition.

    In the high superoxide state, healing is turned off. To turn healing back on, there needs to be a transition back to the high NO state. The problem is that there is hysteresis and it takes a certain NO level to overcome that hysteresis. If you don’t have that little bit of extra NO to get over that hysteresis, you linger in the transition from high superoxide to high NO. It is lingering in that transition that causes the peroxynitrite formation and the peroxynitrite damage which is not repaired (because healing is still turned off).

    I explain this in my blog post on CFS.

  4. #4 herr doktor bimler
    October 12, 2011

    It’s quite reassuring to watch an outbreak of sanity over at treatingxmrv… people are admitting to one another that Yes, they were lashing out… there seems to be a general attempt among the commenters to learn from one another.

    Apart from Anonymous who has gone all Cathago Delenda Est and is thundering “Paprotka et al. should be retracted!!” at the end of every comment, perhaps in an attempt to be mistaken for Cato the Censor.

  5. #5 EvilYeti
    October 12, 2011

    spit,
    I would cut you some slack as you are obviously a head case, but what the hell. Given the amount of spew you’ve produced today for a supposedly chronically “fatigued” individual you are probably one of those ‘Munchausen’s by Internet’ fakers anyway.

    I’m not interested in an obese patient’s theories about metabolism or genetics.

    I’m not interested a druggie’s theories about addiction.

    And finally and most apropos per this discussion, I’m not interested in an individual with a somatoform disorder lecture on stress management or the science of psychosomatic illness. Or viruses for that matter.

    We might as well ask Charles Manson for his opinion on schizophrenia.

    The very definition of these afflictions is that the patients are simply not competent at managing some external aspect of their own lives. Not only are they the absolutely worst people in the *world* to hypothesize on the nature and treatment of their specific issues, they are also the most likely to be misled and abused by charlatans.

    The only thing we can do is be objective and trust the scientific method. If CBT + GET or psychiatric medication helps, then this is a psychiatric condition and its in the patients best interest to treat it as such. We simply can’t do any better at this point.

    And if patients insist that anyone that has been successfully treated wasn’t sick in the first place, they are probably hopeless. Sorry.

    And re: you ‘limp’ limbs, that would be a conversion disorder:

    http://en.wikipedia.org/wiki/Conversion_disorder

    Maybe you just have brain damage? You wouldn’t happen to have a history of drug abuse, alcoholism or head injuries, would you?

    daedalus2u,
    You say “If CBT worked every time to cure CFS, that would be one thing…”

    Sorry to break this to you buddy, but we don’t know how to cure *any* mental illness yet. CBT doesn’t work that well for other psychiatric issues, either. But its the best we got.

    For example, a diagnosis of schizophrenia will follow the rule of thirds. Statistically, one third of all diagnosed will recover completely, one third will improve over time and one third will not improve. Sucks to be sure, but that’s where we are for treating mental illness.

    @Justwondering
    You say “You mean treating stress is equivalent with treating an infection?”

    I mean putting out a fire is different than treating a burn. So in other words, no.

    The problem with chronic stress is that its often cyclical in nature. For example, stress can cause acne, which in turn causes more stress. There is your positive feedback loop.

    The point of CBT, GET and medication is simply to give you to the tools to help break that cycle.

  6. #6 David
    October 12, 2011

    daedalus2u @1000 – No, I’m not David Bell.

    Evilyeti @1002 – I think most of us are being quite civil on here, despite disparate opinions. You should certainly quit with the ‘Munchausen’s by Internet’ accusations.

    You had a go at me with that one, despite me being candid about the fact that I care for someone with CFS. You should be aware then that an accusation of Munchausens by Proxy is one of the most dangerous and offensive insults to bandy about. Accusations of this this rare, and dubious condition has resulted in children and people being sectioned – and removed from carers. If you knew anything about why people involved with CFS get a bit tetchy – you would know about this, and not be so blithley offensive.

    Maybe your playing this hard psychiatric card for laughs, or have another agenda, but who cares, I thought we were discussing science.

  7. #7 EvilYeti
    October 13, 2011

    Before anyone attacks me again re: my personal opinion re: autoimmune disorders, allow me explain my hypothesis in full.

    I’m from New Jersey.

    New Jersey is one of the most polluted state in the country (as per number of superfund sites). And it’s not even a particularly ‘big’ state geographically speaking. It’s also in the top five in terms of cancer rates.

    Totally anecdotal, but I know a few people that died in their 20′s from ‘exotic’ cancers. Not the kind of thing you would expect otherwise healthy kids to get.

    So, consider me suspicious that environmental pollutants may be the culprit here. Especially given that cancer was almost unheard of in antiquity:

    http://www.dailymail.co.uk/sciencetech/article-1320507/Cancer-purely-man-say-scientists-finding-trace-disease-Egyptian-mummies.html

    Anyways, autoimmunity. The general consensus is that autoimmunity is a symptom of an over-active immune system targeting its hosts own cells.

    My hypothesis is that in some cases the opposite may be happening.

    What if instead some pathogen or toxin is simply subtly changing our cells to the point that our immune system simply doesn’t recognize them anymore.

    Despite Mr.Spits claims to the contrary, we already know this is possible:

    http://en.wikipedia.org/wiki/Autoimmunity#Environmental_Factors

    I’m just suggesting it may be more common than we think. And may be exacerbated by some other medical or genetic condition that inhibits our bodies natural ability to detoxify itself.

  8. #8 EvilYeti
    October 13, 2011

    David,
    People say and do all sorts of crazy things for all sorts of reasons. Not only would I not at all be surprised if people presenting themselves as CFS patients online (or caregivers) were fakers; I would actually be *more* surprised if this didn’t happen. See:

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1305082/?tool=pmcentrez

    On the Internet, nobody knows you’re a dog (see ERV’s avatar for example).

    I’m not hard selling psychiatric issues, either. I live down the street from our outpatient psych. clinic and occasionally share a bus with the schizos. Psychosomatic fatigue is absolutely pedestrian compared to some of the bizarre behavior I’ve witnessed. You all should consider yourself lucky.

  9. #9 Levi
    October 13, 2011

    Yeti,

    Its funny that you mention Arnie, ERV’s dog. Yesterday, when I read in the news about all those free tickets to Japan:
    http://abcnews.go.com/blogs/lifestyle/2011/10/10000-free-round-trip-tickets-to-japan/

    It triggered a serendipitous daydream about 2 of those tickets being awarded to ERV and Arnie so they could travel to St. Sugar Cancer Sniffing Dog Training Centre located at Chiba, Japan.

    There, Arnie would be given training that would catapult him to fame as the world’s very first CFS SNIFFING DOG.
    http://www.ecancermedicalscience.com/news-insider-news.asp?itemId=1540

    Arnie’s uncanny ability to accurately sniff out CFS patient’s samples under rigorous double blind conditions would ultimately get written up in none other than the prestigious Journal Science.

  10. #10 Sigmund
    October 13, 2011

    About a year ago Mikovits published a paper in the journal ‘Virulence’ in which she compared the different techniques her group had used to detect the virus. Her conclusion was that the best method was: “performing nested PCR for gag sequences from LNCaP cells that have been co-cultured with subject’s plasma or activated PBMCs”.
    I can see a rather obvious questionmark with this method regarding the co-cultured cell line used, LNCaP. There are several variants of this human prostate cancer cell line around that have been produced following the growth of the cell line in immunocompromised nude mice and selection of the surviving cells. The cell line has the property that it is a good host for murine gamma retroviruses (that is why it is used as a co-host!) – and so it is it raises the probability that there are LNCaP variants in use in numerous laboratories that have already picked up mouse viruses during the nude mouse growth and selection procedure.
    Co-culture with such cell lines will inevitably lead to false positives – especially if nested PCR for gag sequences is used.
    Good controls need to be used to rule out this possibility.

  11. #11 Jack
    October 13, 2011

    @ 972 DM

    Yes it is all ‘crazy’ now I agree. Contacting the WPI they referred my query about the ownership rights to their legal team.

    Personally, it seems stupid that Mikovits can effectively be telling patients ‘Don’t let them keep your samples…. Dey is MINE! Or else no research!’ and on the other WPI are telling people ‘Yeah ok then we’ll send yer blood samples back in the mail’!!

    What sort of bloody system are you chaps running over in the states?! How the NIH will continue with the grant in light of all the flipping nonsense and now this – I do not know.

    Crazy! Crazy! Crazy! And what about the patients and avid fans?! What about them Judy and Annette?! Where’s your damn caring attitude gone now?!

    Is it airborne Judy? Is it safe to breastfeed Annette? Can I make babies? Are my children safe or do I have guilt for the rest of my life?

    FFS! SORT OUT YOUR BLOODY MESS! RETRACTION IS THE LEAST OF YOUR CONCERNS!!

  12. #12 Jack
    October 13, 2011

    Further to the latest round of ‘tug-o-war’ over the NIH Grant referred to above. This is an example of one errr… believers thoughts on the subject:

    ‘Judy, the scientists that discovered HIV and its links to Aids went through this fight.
    We stand by your side and believe in your work and will not abandon you in this battle for answers.
    What acts like a virus, infects like a virus, to any rational human being is a Virus.
    I am far away in Australia. Hoping endlessly that you can continue your work to its own end. I have never liked the Mass Mentality of Medical Practices that makes a pact that leaves millions of people sick as dogs and lets them suffer without regard.
    I ask loudly that all people who are enrolled in your Research into Gamma Retroviruses to add their voices together and state clearly … ” that they will withdraw from the research unless it is done under your direction.”
    I admire your integrity to stand and fight for us, the way you have. ‘

    CRAZY! CRAZY! CRAZY! And it won’t ever stop will it? How bloody sad!

  13. #13 Camaro
    October 13, 2011

    ehhm, just back to XMRV+CFS and/or XMRV+PCA:

    The only thing I am still trying to figure out what it means for the whole story are the results of monkey experiment (Onlamoon et al.).

    My guess is you would see the same for any given MLV or even for a single-round XMRV/MLV – there won’t be any replication even in the prostate tissues and no development of any kind of disease.

  14. #14 OWE
    October 13, 2011

    @Camaro 1008

    There is a new paper out by Silverman referring to these artificially infected rhesus macaques.

    http://www.sciencedirect.com/science/article/pii/S0042682211004375

    They find that XMRV is badly hypermytated by several rhesus APOBEC3 proteins and conclude
    “It is unlikely that a virus that is potently inhibited by A3 could circulate in the human population.”
    However, I guess this does not bother Judy as we have already progressed from XMRV to HGRV (I wonder what will come after that)!

    OWE

  15. #15 M.E.
    October 13, 2011

    Daedalus- i’ve noted some really good and informatative posts from you, and will have a look at your blog, what role do you think the MTHFR gene plays in the NO process?

    WTF- you haven’t really added much in the way of discussion to convince me that CBT improves M.E. directly as yet there is no credible data as the recent pace trial excluded those those with M.E. It isn’t a credible study as per previous posts

  16. #16 RRM
    October 13, 2011

    Always wondered what happened with the Blomberg study, as the results of it were already presented at the first XMRV workshop (09/2010). Finally, it’s been published:

    http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0024602

    Despite the fact that this study used “known positive” provided by Mikovits, and the fact that Blomberg obtained positive signals from these “known positive”, the forums are already dismissing it because it ‘also used VP62′. :-/

    Perhaps a stupid suggestion, but since Blomberg is now in possession of these “Mikovits positives”, would it be possible/appropriate to test these samples for VP62 plasmid contamination (either by Blomberg or through sending them to Silverman)? He only tested them for mouse DNA contamination….

  17. #17 Sigmund
    October 13, 2011

    There’s a report in the news section of this week’s British Medical Journal, entitled “Scientist who linked chronic fatigue syndrome to XMRV is sacked”, written by Claire Dyer.
    “On 22 September the authors of the Science paper retracted part of the paper after two of them learnt that samples were
    contaminated in their laboratory (BMJ 2011;343:d6097, doi:10.1136/bmj.d6097). The same day, Science published a nine laboratory study, including Mikovits’s laboratory, which failed to reliably find XMRV in blinded samples from patients who had previously tested positive (doi:10.1126/science.1213841).
    Now Science is investigating the images published with the
    paper after a graduate student from the University of Oklahoma, Abbie Smith, in her “ERV” (endogenous retrovirus) blog, compared one of them with a slide shown by Dr Mikovits during a presentation at an international conference on chronic fatigue syndrome in Ottawa last month. They appear to be the same image but carry different labels and were said to illustrate two different things in the paper and at the conference.
    Bloggers allege a range of concerns about the slides, but in
    interviews with Science and with Nature Dr Mikovits denies
    deliberate manipulation.
    Science said in a statement: “As is our policy in cases of alleged figure manipulation, we will follow up with the research authors as soon as our own review of the allegation is complete.”
    Mrs Whittemore said, “The Whittemore Peterson Institute has
    recently been made aware of these allegations about Dr
    Mikovits’s presentation. It is our understanding that some patient ID numbers may have been changed to a new set of coded numbers during the research to protect their privacy before publication. We will work with Science in hopes of addressing their concerns and to gain a full understanding of the cause of any potential discrepancies.””

  18. #18 DM
    October 13, 2011

    @ EvilYeti

    “So, consider me suspicious that environmental pollutants may be the culprit here. Especially given that cancer was almost unheard of in antiquity”

    What age were the mummies at death? Consider cancer prevalence rates across age groups and life expectancy.

  19. #19 OWE
    October 13, 2011

    @ RRM, 1013

    Nice idea. And maybe van Kuppeveld should look into his samples too, as he also received some “positives” by the WPI?

    OWE

  20. #20 daedalus2u
    October 13, 2011

    ME, there is a lot of cross-talk between folate and NO. Folate rescues neural tube defects from nitric oxide synthase inhibitors.

    Homocysteine inhibits the enzyme that degrades asymmetric dimethylarginine which is an endogenous nitric oxide synthase inhibitor. Many disorders that are associated with high homocysteine are also associated with low nitric oxide. Which is cause and which is effect is unclear. There is feedback, so low NO will likely cause high homocysteine and high homocysteine will likely cause low NO levels. Many of the adverse effects associated with high homocysteine are likely mediated by the low NO that accompanies it.

    If I were the NIH, I would see this as an opportunity to cancel the R01. Any researcher who is unwilling to share samples and methods and collaborate with other researchers is not a researcher who deserves public funding. Similarly any researcher who tries to thwart the research of any researcher by advocating patients withdraw consent for sample use is not a researcher that deserves public funding.

    The samples are useless now. If they do show contamination, SWMNBN will claim WPI contaminated them, if they show absence of XMRV then there will also be the claim that they were doctored.

    It isn’t like the NIH can’t find a good home for that funding. There is absolutely no reason to send it to the PI that was unable to find true positives and exclude true negatives in the Blood Working Group tests.

  21. #21 WTF
    October 13, 2011

    @M.E.: the PACE trail certainly did not exclude people with ME. That is just Hooper’s insane logic. He says that it excludes people from ME because ME is a ‘proven organic brain disease’, which is patently false.

    @David: why would you only want to consider infectious stress but not other types of stress? That is the position that Leonard Jason takes, and it seems very odd to me. We know that all types of stressors have the same effect on the HPA axis, so why would you not want to consider lifestyle/mental stressors? The research shows that the majority of patients list life stressors as possible precipitating factors (a higher percentage than even infection), and my own anecdotal research seems to show that lifestyle factors are one of the major causes. I don’t believe that infection alone can cause the stress system to ‘crash’, but that’s just my personal opinion. It seems plausible that if people are suppressing emotional/stress issues then that could be a perpetuating factor and CBT/GET could help.

  22. #22 EvilYeti
    October 13, 2011

    @DM,
    Read the full study if you can:

    http://www.nature.com/nrc/journal/v10/n10/full/nrc2914.html

    (subscription required)

  23. #23 gf1
    October 13, 2011

    It seems inevitable to me that all fatigue is affected by psychological factors – even if someone were the epitome of good mental health and had no particular problems with fatigue, it is likely that they could alter their cognitions, values, desires and behaviours in ways that lowered their fatigue levels further.

    There is a danger that this, along with vague points about the way in which mental factors can interact with somatic sensations and processes are then used as a blanket justification for any and all psychological approaches to CFS. As if because viruses often cause fatigue and we all get exposed to viruses, it’s fine to assume CFS is caused by a virus.

    re CFS vs MS: It actually seems that CBT may be much more effective for fatigue in MS than CFS… although in this study the control group receiving just ‘relaxation therapy’ (only intended to account for therapist time and attention) seemed to do nearly as well, with both leading to MS patients reporting no more fatigue than healthy controls – so this could be an indication that fatigue questionnaire scores are easily altered, while disability related to fatigue may not be, as the authors note:

    “However, self-reports are amenable to response bias and social desirability effects. Future studies could also assess more objective measures of change such as increases in activity levels and sleep/wake patterns using actigraphs or mental fatigue using reaction time tasks.”

    http://www.psychosomaticmedicine.org/content/70/2/205/F2.expansion.html

    WTF has said that even placebos seem more effective for CFS than CBT; and that the dubious theories which underpin CBT and GET are unlikely to be correct and tend to put patients off; but still, seems supportive of those who have treated patients in a way that sounds no more respectable than homoeopathy. While this may not be the place to discuss it, surely there should be no less outrage at dishonest psychiatry than dishonest virology or CAM?

    The shamelessness with which transparently misleading claims about the efficacy of CBT/GET for CFS are made by those trying to gain funding for providing these treatments (I’d encourage everyone to look at the claims made by John above – I linked to most of the papers that were needed to check them out), and the use of unrepresentative anecdotes in the media, are exactly the sorts of tactics being used by other scammers. Concerns about stigmatising mental health issues should not mean that psychiatric woo escapes condemnation.

    I’d be very surprised if CFS was all the result of abnormal anxiety responses – but if it were, the thing that CFS patients seem most angry and anxious about is the dubious theories and misleading claims made by some psychiatric researchers – particularly when they end up feeding in to beliefs about CFS patients of others, like with EvilYeti. Removing those responsible and emphasising the need treat all patients honestly, and only according to the available evidence seems like the best way to move forward from here.

  24. #24 daedalus2u
    October 13, 2011

    gf1, feeling fatigued and having a physiology that can support physical activity are two different things, and to some extent they are independent. I don’t care how fatigued you feel, if you got a shot of the right dosage of cocaine, amphetamine, heroin and PCP, you would feel less fatigued. Those stimulants don’t increase your physiological capacity to support physical activity (very much), they do change how fatigued you feel.

    The problems of CFS are not the feelings of fatigue, they are the physiology that is incapable of supporting physical activity. You want your feelings of fatigue to accurately report your immediate physiological capacity to support physical activity. That is why those feelings of fatigue are there. They are there so you don’t try to do a physical activity when you don’t have the physiological resources to do it.

    Changing how how fatigued someone feels does not necessarily change the underlying physiological capacity to do physical activity. If someone’s feelings of fatigue are out of whack with their physiological capacity to do physical activity, that is a problem, and is a problem in both directions. Falsely feeling that you can do something you don’t have the physiological capacity to do is what causes overuse injury. Falsely feeling that you can’t do something without injury is also a problem, but that is not the problem that people with CFS have. When they push themselves they get overuse injury. That is what “crashing” is, overuse injury because they don’t have the physiological capacity to support the physical activity they pushed themselves to do.

    Your body will let you push beyond legitimate and accurate feelings of fatigue to where you cause overuse injury. That is a “feature”. If a bear is chasing you, it is better to escape with overuse injury than to be caught without it. But that overuse injury takes time to heal and doesn’t always. There can be cumulative loss with each overuse injury and in the limit, you can run yourself to death, that is you can injure yourself through overuse injury such that you have fatal damage.

  25. #25 daedalus2u
    October 13, 2011

    sorry, I appear to be getting mouse bounce.

  26. #26 David
    October 13, 2011

    WTF @1019

    Well I think the literature shows that most CFS patients can remember an illnesss as a trigger, either a ‘flu like illness’ or something known, like Eptstein-Barr. Figures for this range from 70 to 80 % ish, including surveys by psychiatrists. Stress is commonly reported as well, up to a third maybe – bit it is not as conspicuous as infection.

    As I stated earlier, to keep it simple, I think it is interesting to consider stress, but not to place to much emphasis on it so that by generalisation, we start to move to far from the original illness.

    Since it is such a catch all definition at the minute, it is highly likely that some people have been diagnosed with CFS that actually only caught a bad cold, but suffered stress at work and had difficulty getting it all back together. Some time off and therapy might help them get it sorted.

    These kind of patients may just be burn out cases, and may or may or not share pathologies with more severe cases.

    I’m interested in what is sometimes called the 25% group, those severley affected, often bedbound, for whome CBT etc is out of the question.

    I suppose its like depression. This includes people who are hospitalised and suicidal, and people shocked by the loss of a girlfriend, and are a bit flat. For me severe clinical depression is most interesting since its study is more likely to elucidate the biochemistry and homestatic mechanisms involved in mood.

    I’m not making value judgements, whatever works for people, but the study of classic infection triggered M.E is for now more important –

    Lifestyle, stress, all kinds of things are important in diabetes, but its insulin we really need to understand.

  27. #27 WTF
    October 13, 2011

    @daedalus: I’m pretty sure that cocaine also increases your metabolism and heart rate. As for your feeling fatigued vs not having the physiological energy: your argument is flawed because psychological factors do influence how much energy you actually have, through the HPA axis and other pathways.

    @gf1: I don’t believe that CBT is dishonest. A placebo is a psychological intervention, so CBT and placebos are essentially the same thing in terms of the effect they have on the patient. The problem, I believe, is that a lot of patients don’t think that CBT will help them, whereas they do believe that a pill will help. homeopathy is dishonest because the effects are purely psychological and not from the homeopathy itself. CBT is doing what it says on the tin. Certainly there is an issue with the theory behind CBT in treating CFS, but given the antics of many patients you can see the logic behind the theory of abnormal illness beliefs (and I can see how that could be a factor for some patients).

    If you look at CBT you’ll see that it’s really more of an art than a science. Have a look at the wikipedia page and you’ll probably be shocked at the sheer number of variations (I certainly was). CBT just seems to be a generic term for any type of talking therapy, as far as I can see.

  28. #28 WTF
    October 13, 2011

    @david: have a look at PMID 9201648 (if I post the link, my message will likely have to be moderated). 85% of patients reported stressful events in the year prior to onset, and 72% had infectious onset (although a definite infection was only found in 7%). This seems to be confirmed by other studies.

    One possibility is that there is no actual infectious onset – the apparent ‘infection’ could actually be the body’s immune system going into overdrive as a consequence of low cortisol due to the stress. This is David Smith’s theory (he is the former medical advisor to the ME association).

  29. #29 David
    October 13, 2011

    1027 Well thats quite an extreme, but possible idea I guess, but difficult for me to accept on balance.

    Such extreme immune dysfunction in the absence of any pathogen seams to me an exaggeration by ‘Stress scientists’ obviously wanting to ‘big up’ thier cause, but I find that going to far personally.

    B.T.W – If there was no actual infection, primary or secondary – then WTF are we doing here then !?!

  30. #30 daedalus2u
    October 13, 2011

    WTF, the HPA is not magic. It can’t produce aerobic capacity that wasn’t there a few minutes before. It can turn off things that are consuming ATP, it can’t make mitochondria appear out of nothing. If you have X mitochondria capable of producing 2X ATP of which you are already using 1.5X just to stay alive, your HPA can turn that down to 1X so now you have 1X available to run from the bear (instead of 0.5X), but you still actually need 1.5X to keep your body in repair. If the HPA doesn’t turn that 1X back to 1.5X, you are going to be screwed in the long term. In the short term you might feel great because now you have 1X ATP to use voluntarily instead of the 0.5X that you normally have.

    The HPA can change the allocation of ATP, it can’t increase the ATP production capacity because that takes mitochondria and mitochondria biogenesis and there isn’t time to do that in a fight-or-flight situation.

    People with CFS do not have their exercise limited by heart capacity (usually). Exercise capacity is limited peripherally, by the muscles not having enough ATP generating capacity. Over time, people with CFS do see their hearts shrink, but that is compensatory remodeling (my hypothesis) to match heart size with blood flow demand. If you can’t utilize extra blood flow, it is useless to have a heart that can supply it.

    If you had just run a marathon, and were really fatigued, a shot of stimulants in the right dose would make you feel less fatigued. Those stimulants don’t don’t actually restore what running the marathon depleted. The feeling that you are not tired is a feeling (actually a delusion). Being able to have the delusion that you are not tired when you need to run from a bear is a really important “feature” of physiology. That is what the runner’s high is, the delusion that you are not tired and can run forever. You can’t run forever, you can only run until the bear catches you or until you drop dead of exhaustion, but as far as evolution is concerned, both of those alternatives are the same as forever. Organisms that felt they could run forever survived from more bears than organisms that did not, so extant organisms are able to feel that they can run forever when being chased by a bear.

    Stimulants don’t increase ATP production capacity. People who use stimulants a lot experience lots of degeneration. They are diverting ATP away from body repair into immediate consumption. Your body will let you do that even without drugs, but it hurts and you have these pesky feelings of fatigue. Stimulants suppress the feelings of fatigue and pain, they don’t increase the actual ATP production capacity.

  31. #31 WTF
    October 13, 2011

    @david: stress causing severe physical illness and even death in the absence of any other factor (such as infection) is a pretty well accepted scientific concept. Have a look at Selye’s experiments on rats over 50 years ago, plus there is a lot more recent research backing this up as well. I don’t believe it is in any doubt. Whether or not this explains CFS in some or all patients is another matter, and will need more research.

  32. #32 Levi
    October 13, 2011

    WTF @1026

    Some CBT practices are dishonest, particularly the ones in the UK that are used to treat ME/CFS patients. If a therapist is trained to avoid telling patients that they actually have a mental illness, not an organic illness, and obfuscate by using the term “real disease” in order to gain rapport, how is that not dishonest? They do this with the goal to gain rapport and eventually get the patient to ramp up exercise in order for the patient to ameliorate deconditioning. Its done in the name of the “patients own good”, but it is patronizing and dishonest.

    I would rather see a therapy that lays it all out honestly: “Look, we don’t know what cause CFS, but we have a theory about false illness beliefs and deconditioning. Some patients have been helped. Lets try it.

    Not all CBT relies on this dishonest methodology. Some CBT, including Affective-Cognitive Therapy variants, empathize relaxation techniques and are more like traditional psychotherapy. ACBT seems to be significantly more effective for at least fibromyalgia patients:

    “The very use of relaxation training throughout treatment and the strong emphasis given to it as a valuable stress management skill that should be regularly applied in one’s life and be a permanent part of one’s coping repertory may give our patients a tool that is effective in reducing the discomfort associated with FM.”
    http://www.hindawi.com/journals/prt/2012/937873/

    Personally, I would rather see the limited and precious treatment and research dollars go into more strongly evidence-based work, such as “free surfer” based imaging tools, or looking into the possibility of a micro-deletion association with CFS.

  33. #33 David
    October 13, 2011

    1031 Levi – Spot on. It is the patronising attitude that gets peoples backs up. If it was offered in the spirit of possible help it would make a huge difference. All this ‘but you didn’t fill in your time sheet / stick to your play schedule’ stuff is just awful. I mean physiotherapists never talk down to patients – ‘do you actually want to walk again?!!?’ Or maybe they do, hospitals are full of people like that. Anyhow, that coupled with the effort needed to get to the sessions etc is just to much for some people, when they can be better off pottering in the garden, or getting proper fresh air.

  34. #34 gf1
    October 13, 2011

    I don’t think that anyone was saying that all CBT is necessarily dishonest. It is possible to use placebos in an honest way too. But if claims about the cause of disability in CFS are being made despite a lack of good supporting evidence, then that is a bad thing, and likely to lead to the sort of distrust, resentment, anger and anxiety that many CFS patients feel about their treatment.

    It also seems that some of those involved in the promotion of CBT for CFS in the UK are making deeply misleading claims about its efficacy as part of their drive for more funding.

  35. #35 spit
    October 13, 2011

    That’s Ms. Spit, to you, Yeti. And deciding that “limp = conversion disorder” is just another example of brilliance. Maybe you should actually try using the google — try starting with “cataplexy.”

    Lucky for me, there are doctors who are smarter than you, and some of them occasionally specialize in sleep medicine.

    By the by, yes, I do probably have brain damage. Because my immune cells are eating really specialized sets of neurons, which I suppose under your hypothesis would have to have been magically toxified or something despite the blood-brain barrier and despite the fact that the damage is extremely specific to hypocretin/orexin producing neurons but doesn’t hit the thousands of _other_ neurons right next to them or downstream. Nobody really argues at this point that there aren’t serious connections between environmental pollution and human health, especially things like cancer that involve damage to the genome –> funky mitosis and loss of intentional cell death. That’s _true_. But what you’re talking about is stupid. “Hypothesis” does not, in fact, mean “whatever random guess somebody with clearly little knowledge of this biology can pull out of his ass.”

    Also by the by, an MRI doesn’t have enough fine resolution to tell me whether I have brain damage or not. When I’m dead, they can look at a few slices of my brain under a scope and let me know, I guess.

  36. #36 spit
    October 13, 2011

    PS Yeti, I hate to burst your bubble, but I’ve known several schizophrenics personally, along with several folks who have other extreme mental health disorders. That you have to share a bus with a couple occasionally is, um, not particularly noteworthy, and doesn’t really add much to your cred.

    No, CBT would not work worth diddly on the symptoms specific to schizophrenia — though I’m unaware of any studies on schizophrenics reporting their fatigue levels etc. while trying out CBT for other psychological issues or general support (they do sometimes successfully treat and manage their schizophrenia, you know, and have other challenges just like the rest of humanity).

    Seems to do about as well for most forms of depression as basically any other intervention, though.

  37. #37 spit
    October 13, 2011

    @WTF — “85% of patients reported stressful events in the year prior to onset, and 72% had infectious onset (although a definite infection was only found in 7%). This seems to be confirmed by other studies.”

    If you are sitting there thinking to yourself whether you’ve had any stressful events in the last year, you’re likely to be able to come up with some. Especially if you’re already feeling stressed out by the whole “being sick” thing, since — one of those things that psychology actually does tell us — you’re more likely to recall negative events while feeling negative.

    I can only think of a couple of times in my entire life that I’ve had an infection confirmed. Most people just try to take some nyquil and get over it, they only go to the doctor if it seems like it’s not going away for weeks (by which time the actual infection may be over) or when it’s obvious from the symptoms that it could be something like strep.

    Salye was injuring his rats or subjecting them to hormone injections or leaving them in extreme temperatures — of course that elicits a biological response. Everything elicits a biological response, and the HPA axis is very active in stressful situations. That’s not the same thing as “my job sucks and my spouse divorced me” leading to major, debilitating, and long term physiological dysfunction.

    It’s possible — I’m not arguing that it isn’t. I just don’t think there’s a lot of real evidence, at least that I’ve seen, to suggest that people at stress levels that aren’t incredibly extreme are actually seen to have absolutely debilitating and long-term physiological disorders as a result. And I want good, solid, positive evidence that it actually happens that way for some significant subset of people before I take it any farther than “well, maybe.” I know it’s conventional wisdom in psychology, but that doesn’t make it solidly backed by a lot of data.

  38. #38 WTF
    October 13, 2011

    @spit: you are wrong in saying “CBT would not work worth diddly on the symptoms specific to schizophrenia”. Although the evidence for CBT on schizophrenia seems to be mixed, behavioural/psychosocial treatments are useful in schizophrenia. Check out the wikipedia page for a brief overview. I’m not sure why you would think that behavioural treatments couldn’t help with schizophrenia…have you not heard of neuroplasticity? Have you any relatives with schizophrenia? Have you done any research on it? Sorry for getting us even further off topic, but I just had to correct this bullshit.

  39. #39 spit
    October 13, 2011

    @WTF — I do, in fact, have several good friends with schizophrenia. Mild forms of schizophrenia may have something to gain from some form of behavioral therapy, but I haven’t seen this work particularly well, no. Whether it’s helpful in conjunction with medication, I don’t know. I will look at research on it, but find it hard to believe that behavioral therapy can meaningfully address the needs of somebody in a severe enough delusional state that they think the person conduction the therapy has probably been sent by the FBI and has wiretapped their house.

    Lest you think I’m being flippant, that is exactly what the result was with the last schizophrenic I knew who was being treated for some of his secondary issues via a behavioral model, once his meds stopped working well.

    I do know plenty about neuroplasticity, thanks. It’s amazing stuff. But it doesn’t just happen the ways we’d like it to with people who seem to have serious problems in fundamental organizational problems or cognitive downstream effects from major problems in neurotransmitter regulation — those are not really easy things for the brain to rework into a more “typical” set of function, without addressing the underlying dysfunction that builds those networks that way in the first place.

  40. #40 spit
    October 13, 2011

    Yeesh. Speaking of fundamental organizational problems, the narcoleptic apparently needs her nap. Apologies for the typos, etc.

  41. #41 mary
    October 13, 2011

    I believe CBT has got to be helpful..(not a cure all) and when used with other treatment modalities..

    On the forums today someone posted that VR’s involvement in me/cfs was not going to be good because she got angry at one of his posts.. that anger led her into a severe crash..therefor VR is no good..

    there are so many things wrong with that sentiment but the one that stuck out for me was that if her emotional state, led to such a bad relapse, perhaps getting help with that emotinal state..learning to deal with that anger in therapy would be better for her health than the arv’s she is screaming for…

  42. #42 mary (abbie's ilk)
    October 13, 2011

    there is a webinar tom. from the authors of the BWG phase 3 study tom…to register go to VR’s virology blog and follow instructions…

    don’t want to post a link cuz of the comment control!

  43. #43 daedalus2u
    October 13, 2011

    WTF, I am very aware of that paper. That is one of the papers I cite in my write-up on CFS. All of those triggering events are consistent with a low NO etiology.

    A good presentation that discusses post exertion malaise is here.

    http://www.hhs.gov/advcomcfs/meetings/presentations/presentation_10132010_snell-stevens.pdf

    This post exertion reduction in VO2 has to be due to insufficient mitochondria and insufficient replacement of mitochondria following exertion. I have a table in my write-up that discusses exactly how this happens.

    Mitochondria biogenesis is triggered by nitric oxide. If you don’t have enough nitric oxide, you won’t have enough mitochondria and you will have CFS.

  44. #44 RRM
    October 13, 2011

    Oh well, if it gets posted tomorrow, not problem…and it’s still useful:

    https://www1.gotomeeting.com/register/606452768

  45. #45 WTF
    October 13, 2011

    VR has been very patient with the nutters who post ridiculous crap on his blog. It’s funny to see lawyers and the like trying to tell Vincent that he’s wrong about XMRV. Sometimes he comes out and says ‘you don’t know what you’re talking about’ when people are posting obvious crap, but he has never said anything disrespecftul about CFS.

  46. #46 Levi
    October 13, 2011

    @Mary, I forgot to thank you for your kind words @974

    Actually, The forums did in fact finally did get to me when I received a lot of vitriolic backlash after making an impolitic speculation about a possible retraction of the Lombardi et al 2009 paper in Science. I have not posted in the big forums in 5 months or more. I have posted regularly to one small ME/CFS forum however. It is a one man show, and he and I have merely “agreed to disagree” about XMRV/HGRV’s and if that theory still has any legs to travel on. We get on fine, and I appreciate having a place to post relevant links about other types of ME/CFS research. I won’t link there here because I do not want to make any grief for that forum.

    As far as the female CFS forum woman you spoke of crashing due to VR’s involvement with CFS, my understanding runs counter to yours. I believe that traditional psychotherapy is more suited to deal with repressed anger issues and the effect on one’s emotional state.

    In contrast, CBT is mainly used to address behavioral anomalies as defined by different psychological/psychiatric authorities in different ways. It is the treatment of choice for getting mental patients to deny their particular self-identity, personal convictions, and realities in order to change those behaviors that are deemed to be self-damaging.

    For instance, CBT is very popular with Christian-based psychotherapist as a tool to “treat” male homosexuality, which is deemed to be an aberrant and self-destructive behavior:
    http://www.narth.com/docs/byrd.html

  47. #47 mary
    October 13, 2011

    @ 1045 Levi

    I will defer to your knowledge about CBT and it’s effectiveness cuz I openly admit I have not followed the different treatments for me/cfs and am ignorant on the topic, preferring to follow the pathogen instead. I will follow your link and read up on it!

  48. #48 FWD
    October 13, 2011

    When people talk about fatigue with CFS, it is a misnomer. It’s not fatigue but total exhaustion. Use this analogy, if there is no gas in the tank, can the engine still run. Nope. There is no energy. It has nothing to do with tiredness. There is absolutely no energy….capeesh? Explain this one. Take 60mg of amphetamines and immediately fall back to sleep for 3 hours. Hello? OR have chicken pox 3 times? Hello.

    Also,
    1.Post-Exertional Malaise. The is a pathologically slow recovery period–usually 24 hours or longer.

    2.Sleep Dysfunction: There is unrefreshed sleep or sleep quantity or rhythm disturbances such as reversed or chaotic diurnal sleep rhythms

    3.Neurological/Cognitive Manifestations: Two or more of the following difficulties should be present: confusion, impairment of concentration and short-term memory consolidation, disorientation, difficulty with information processing, categorizing and word retrieval, and perceptual and sensory disturbances–e.g., spatial instability and disorientation and inability to focus vision.

    4.Autonomic Manifestations

    5.Neuroendocrine Manifestations

    6.Immune Manifestations”

    http://www.name-us.org/DefintionsPages/DefCCC.htm

  49. #49 EvilYeti
    October 14, 2011

    MS.Spits,
    Let me get this straight; you are “skeptical” that your symptoms may be psychiatric. But you are confident that you have a previously unrecorded autoimmune disorder that is destroying your brain in some undetectable manner.

    I can’t think of a better example why we can’t trust patients to diagnose themselves. Especially ones with mental problems.

    And speaking of mental problems, being ‘mildly’ schizo is like being mildly pregnant.

  50. #50 EvilYeti
    October 14, 2011

    FWD,
    You are describing chronic stress to a “T”:

    http://en.wikipedia.org/wiki/Chronic_stress

    If you ignore the etiology and obsess on the symptoms, no wonder you can’t get better!

  51. #51 Camaro
    October 14, 2011

    @ RRM #1013

    Well, as far as I know there are several groups who received samples from JM, and I know for sure that there were some tests for VP62 done – but what could you have done with a positive plasmid result before the whole story came up and Silverman by himself published the retraction ?

    Of course the response would have been that you are contaminating your PCR by yourself and that accusing “The Princess Who Cannot Be Named” of having false-positive results is just a way to distract from your own disability to do “the real stuff to find XMRV”.

  52. #52 John
    October 14, 2011

    More interesting stuff on 5-AZA?

    From the Mikovits ProHealth presentation on Jan. 22, 2010- “[XMRV is] in 90-some percent of the CFS population. I stuck this slide in here, and Frank keeps taking it out, but you might have heard in the press after the paper came out, we didn’t do all of the tests, all four tests, on all of the people prior to the submission in May. We just looked for evidence of infection and looked to see if we could isolate the virus, looked to make the point, and it wasn’t so much about the CFS.

    What we did, after the paper was published, we went back and we looked with all four assays for evidence of XMRV in those PCR negatives. Because now we know that indeed those negative samples may have evidence of infection, and what we found was that 19 of the 33 had antibodies in the plasma. We found transmissible virus in the plasma of 33 of those people, and then we looked at that latent virus because the company I used to work at here in Santa Barbara was called Epigenics, and it was developing methylation-inhibitors for epigenetic silencing, and that’s what happens to viruses. So we used Decitabine, which is a demethylating agent that opens up the genome and turns on the virus and found that there was latent virus in 10 of those people. And when we summed it all up and tabled it out, 99 of the 101 patients in the Science paper had evidence of XMRV infection.”
    http://www.prohealth.com/library/showarticle.cfm?libid=15173

    Presentation slides- http://www.wpinstitute.org/news/docs/WPI_JAM_012210.pdf

    Earlier in the presentation, Mikovits again uses the 5-AZA slide when simply referring to “Activated PBMC”, following a descrition of IL-2 activation of PBMC’s. She doesn’t mention 5-AZA/Decitabine until talking about what they had done to PCR-negative samples following the Science submission in the first quote above- http://www.prohealth.com/library/showarticle.cfm?libid=15172

  53. #53 RRM
    October 14, 2011

    @anonymous #687

    If you are still reading. You posted this:

    5. From the NCI’s Center for Cancer Research 2009 CCR Scientific Advances-

    Detection of a retrovirus, XMRV, in blood products of patients with neurological diseases and cancer – submission by Francis Ruscetti, PhD
    Reference(s): Science. 2009 Oct 23; 326(5952): 585-9

    source- (webpage no longer online, a saved copy does exist)

    Check this (and note that this conference book apparently was created 29/09/09):

    Late Breaking Abstract:

    Detection and Immune Correlates of an Infectious Retrovirus, XMRV, in Blood Cells of Patients with Chronic Fatigue Syndrome and Cancer

    Judy Mikovits

    Later, the title of this talk was changed to “Detection and Immune Correlates of an Infectious Retrovirus, XMRV, in Blood Cells of Patients with Chronic Fatigue Syndrome”(link). This probably means that XMRV cures cancer…. ;-)

    Although probably not very interesting (Van der Meer et al. already referred to this abstract in their comment on Lombardi et al. in Science), does anyone have acces to this abstract that was published in Cytokine?

  54. #54 RRM
    October 14, 2011

    Linkfail. Here is the link for the conference program book:

    http://www.isicr.org/pdf/Lisbon%20Meeting%20Program%20FINAL%20(9.29.09).pdf

    And here is the link to the published abstract that is behind a paywall:
    http://www.sciencedirect.com/science/article/pii/S1043466609002270

  55. #55 Sigmund
    October 14, 2011

    RRM, there is no abstract for her talk at that link.
    It contains the following:
    “PL3-3 Detection and Immune Correlates of an Infectious Retrovirus, XMRV, in Blood Cells of Patients with Chronic Fatigue Syndrome
    Judy Mikovits, Invited Speaker
    Detection and Immune Correlates of an Infectious Retrovirus, XMRV, in Blood Cells of Patients with Chronic Fatigue Syndrome Judy Mikovits, Whittemore Peterson Institute for Neuro Immune Disease
    doi:10.1016/j.cyto.2009.07.043″

  56. #56 RRM Ilk
    October 14, 2011

    Sorry RRM @ 1053. Nothing but the abstract title on the XMRV talk. Here’s what is behind the paywall under “Mikovits”:

    PP1-083 Aberrant type I IFN pathway response to viral infection in chronic fatigue syndrome (CFS)
    Judy A. Mikovits, Kathryn S. Hagen, Daniel L. Peterson, Michael Dean, Vincent C.Lombardi, Poster Presentation I

    Aberrant type I IFN pathway response to viral infection in chronic fatigue syndrome(CFS)
    Judy A. Mikovits 1, Kathryn S. Hagen 1, Daniel L. Peterson 1, Michael Dean 2, Vincent C. Lombardi 1, 1 Whittemore Peterson Institute, Reno, NV, USA, 2 Laboratory of Experimental Immunology, National Cancer Institute-Frederick, Frederick, MD, USA

    Viral infection of host cells leads to the initiation of antiviral innate immune responses, which include the expression of the type I interferons (IFNs) IFN-a and
    IFN-b, and pro-inflammatory cytokines and inflammatory chemokines such as IL-6 ical residue for mediating viral infection. Confocal studies suggest a physical interaction
    between cellular proteins and the VACV. Using mass spectrometry-based proteomics, glomulin was identified as a host cell protein that interacts with VACV. Knockdown of glomulin expression in human T cells reduces VACV infection. Moreover,inhibition of c-Met phosphorylation reduces the cytosolic availability of activated
    glomulin, and leads to a decrease in VACV infectivity. Since permissive infection of T cells might represent a mechanism for VACV dissemination throughout the lymphatic system, we proposed that the absence of CCR5 may be protective against VACV infection in vivo. We provide evidence for aggressive VACV replication in the lungs and spleens of CCR5+/+ mice, with no evidence of infection in CCR5_/_mice. Furthermore, associated with VACV infection, we provide evidence for CD4+ and CD8+ T as well as CD11c+ and F4/80+ cell infiltration into the lungs of CCR5+/+
    but not CCR5_/_ mice, and show that CCR5-expressing T cells harbor replicating virus. This CCR5-dependence is VACV-specific, since CCR5_/_ mice are equally susceptible
    to intranasal influenza (A/WSN/33) virus infection as CCR5+/+ mice. In adoptive transfer experiments we show that introduction of CCR5+/+ bone marrow into CCR5_/_
    recipient mice restores VACV permissiveness. Taken together, our data show a critical and novel role for CCR5 in VACV infection.

    PL3-3 Detection and Immune Correlates of an Infectious Retrovirus, XMRV, in Blood Cells of Patients with Chronic Fatigue Syndrome
    Judy Mikovits, Invited Speaker
    Detection and Immune Correlates of an Infectious Retrovirus, XMRV, in Blood Cells of Patients with Chronic Fatigue Syndrome
    Judy Mikovits, Whittemore Peterson Institute for Neuro Immune Disease
    doi:10.1016/j.cyto.2009.07.043

  57. #57 windy
    October 14, 2011

    anonymous on x rx opines again:
    “You will have to ask john Coffin as the peer reviewer why the published gels and the gels as sent were described differently.”

  58. #58 Sigmund
    October 14, 2011

    windy said: “”You will have to ask john Coffin as the peer reviewer why the published gels and the gels as sent were described differently.”"
    So they labelled and described the original gels correctly but one of the peer reviewers made them change the text so that the critical additive was entirely absent from the paper?
    Not only that but he made them promise to not talk about this alteration of their paper for the next two years!
    I guess that could explain it…
    However I have a better ‘innocent’ explanation.
    I think that the problem that ERV has uncovered isn’t one of misrepresentation of critical data.
    It’s simply a question of accidental identification of patient names. You see if several of the patients tested on the critical slide 2C had the surnames “5-Azacytidine”, “Normal-Control” and “PBMC” (quite rare, I suspect, but you never know!) then all is explained!

  59. #59 RRM
    October 14, 2011

    @Sigmund.

    Strange. Still, it’s suspect that indeed a cancer connection was mentioned earlier with this cohort (I cannot believe these would be seperate cohorts).

    Other news: Vincent Lombardi had issued the following statement at the VipDx site:

    A number of recent publications and individuals have mischaracterized the nature of certain clinical laboratory results reported by VIP Dx, a CLIA certified clinical laboratory. VIP Dx has met the required CLIA Program standards and is certified to offer and perform only clinically validated laboratory tests. The “XMRV test” offered by VIP Dx is clinically validated and performed under rigorous protocols to ensure the accuracy and reliability of the test results. XMRV testing was offered based upon the existing scientific knowledge at the time. The original assays for XMRV testing were based on the 2009 Science publication. Those assays, as well as all subsequent modifications, were internally validated prior to being used to process patients’ samples. WPI’s Research Director was instrumental in the decision to make such a test available to physicians. The interpretation of the XMRV test results, as with all laboratory tests, is the responsibility of the ordering physician.

    Before offering any test to the public, VIP Dx established comprehensive performance specifications including accuracy, precision, analytical sensitivity, specificity, and others required for test performance.

    Funny how he doesn’t mention Mikovits by name…

  60. #60 Lisa
    October 14, 2011

    The fact that Trine would write a big story about this case makes me really question her agenda with regard to anything she writes.

    I didn’t think that until now.

  61. #62 spit
    October 14, 2011

    Yeti — this is the last time I’ll bother, because all of it is, indeed, way off topic to the post (not that it probably matters at this point).

    We understand some of the underlying physiology of narcolepsy with cataplexy. Less than we’d like, but more than nothing. It is a reasonably defined brain disease involving, at least it appears, cell death or other malfunction in the hypocretin/orexin pathways that we know are involved in regulating sleep/wake, REM, emotional response, olfactory sense, and metabolism, among other things still being studied.

    I have described a little of it to you. It is almost certainly at least partly autoimmune, and many narcoleptics’ brains show extremely targeted regions of cell death that cannot be seen until they are dead enough to have their brains examined under microscopes. I could link you the many, many studies on this topic, but I’m sure you don’t actually care.

    I’m not sure how you got to self-diagnosis. Sleep doctors diagnose narcolepsy based on clinical history and sleep studies, but there is no perfect diagnostic tool for it. We have a lot to learn about the brain.

    Given the choice between some guy on the internet who throws around his university cred (but later admits that his expertise is in compsci, not bio, and continues making statements that anybody who knows much about bio finds totally stupid) and… um… my team of doctors, I’m afraid I’ll just have to rely on the latter.

    PS — yes, there is “mild” schizophrenia, more or less. Some people have occasional episodes of more severe symptoms, but are otherwise pretty much ok. Some people have lower levels of symptoms, which they have learned to handle reasonably well, and that still allow them to be functional. I know people in both situations, and I know people with severe symptoms and for whom no medications are effective anymore. There are patterns, but schizophrenia varies just like any other disease.

  62. #63 Jack
    October 14, 2011

    @RRM

    Maybe it was V99/Gerwyn et al.? You know they do have a long reach…..

    …162 signatures now from the ‘avid fans’ ;)

    Of course Lombardi’s statement will not remove the ‘concern’ that Mikovits expressed that he somehow didn’t do EXACTLY what she and only she was capable of doing to those blood samples.

    You know the ubber secret stuff that no-one else in the world knows how to do because, well, it’s a secret…. :) :)

  63. #64 spit
    October 14, 2011

    Addendum 1, (mostly just added because it’s interesting):

    We also know that if we breed a line of dogs that has a consistent mutation at their hypocretin/orexin receptors, they will have every single symptom of narcolepsy with cataplexy.

    We’ve known that since the late 90′s. Dobermans, in fact, have a pretty strong genetic tendency to have narcolepsy via this mutation. Poor dogs are usually euthanized, since most vets have no knowledge of this and just see “holy crap, dog has some weird seizure thing when you feed it!”

    I would love someday to figure out how to adopt one before some dumbass vet “puts it out of its misery.”

    I will truly stop now, because it is all way off-topic, because I do realize that trying to actually engage is a waste of time on this front, and because I actually do have some shit to do.

  64. #65 daedalus2u
    October 14, 2011

    Lisa @1060, I thought the article was fair and long overdue. Children with autism have been subjected to some awful quackery. Some have even been killed by it. There are more details on LBRB (one of the best autism blogs around).

    http://leftbrainrightbrain.co.uk/2011/10/defending-alternative-medicine-and-autism-the-charges-against-anju-usman/

  65. #66 spit
    October 14, 2011

    Because I apparently can’t shut up, I’ll add this to make it more relevant to the actual topic:

    My (male) relative with similar symptoms never had the words “chronic fatigue” brought up with him by any doctor. I did. Repeatedly. If I hadn’t already had his knowledge base to work from — at least well enough to say, “I have a (first degree male relative) who has been diagnosed with narcolepsy with cataplexy,” I wouldn’t ever have been sent to a sleep doctor at all, most likely. And I would be diagnosed with CFS. Because they were, many of them, pretty much ready to say it within the second appointment, when my thyroid looked OK. Unlike with my male relative, under the same conditions.

    Something folks should keep in mind when they’re talking about the epidemiology here.

  66. #67 mary (abbie's ilk)
    October 14, 2011

    webinar was great..nothing that we haven’t discussed here..the 10 questions addressed should shut up gerwyn et. al..but we know it won’t!

  67. #68 RRM
    October 14, 2011

    Yes, it was an excellent webinar…but although it was good they addressed those sometimes idiotic ideas and questions, it surely was the toe-curling part….

    I mean, do people really think that Lo/Alter used two assays in their study of which one worked, and that they were somehow forced (or decided for themselves) to use the one non-working assay? Or that Ruscetti was “forced” to cut down his original contamination culture time in half?

  68. #69 mo (one of Abbies's elk)
    October 14, 2011

    what webinar?

  69. #70 RRM
    October 14, 2011

    The CFIDS (CFS patients organization) held a webinar today, with the “authors” of the BWG study (the Simmons et al. study that was published 09/22 in Science). Simmons and Busch were the main apeakers.

    The explained the results and debunked some of the ridiculous claims.

    The webinar will become available through the CFIDS Youtuve channel shortly.

  70. #71 RRM
    October 14, 2011

    Most typos ever in such a short post…sorry… :-/

  71. #72 anonymouse
    October 14, 2011

    RRM — could you post a link to the webinar video when it becomes available. Thanks so much.

  72. #73 David
    October 14, 2011
  73. #74 David
    October 14, 2011

    IGNORE ABOVE – Thats part 2 – Sorry —

  74. #75 John
    October 14, 2011

    Title: Results of the Blood XMRV Scientific Research Working Group Study

    Speakers:
    Graham Simmons, PhD of Blood Systems Research Institute Michael Busch, MD, PhD of Blood Systems Research Institute Steven Kleinman, BSc, MD of University of British Columbia

    Link to video- http://www.youtube.com/watch?v=ayUUIT85KZQ&feature=channel_video_title

    Slides- http://www.cfids.org/xmrv/srwg-webinar-oct2011.pdf

    Webinar summary plus ‘Answers to 10 Common Criticisms of the SRWG study’ by Graham Simmons, PhD
    http://www.research1st.com/2011/10/14/xmrv-updates/

    From the webinar:
    Answers to 10 Common Criticisms of the SRWG study
    by Graham Simmons, PhD

    1. All of the controls were not screened by all of the labs.

    Response: Controls were screened by at least five labs: WPI, National Cancer Insitute/NCI-Ruscetti, Food and Drug Administration/FDA-Lo, Centers for Disease Control & Prevention (CDC) and NCI/Drug Resistance Program (DRP).

    2. Control peripheral blood mononuclear cells (PBMCs) were not screened prior to blinding, so could not have been ruled as negative.

    Response: Three out of the 15 did have their PBMCs extensively screened prior to blinding, yet two of these were still called “positive” in various assays by the WPI and NCI/Ruscetti in the study.

    3. No cryopreservative was used for the storage of the PBMCs, which would prevent the WPI’s assay from working. No Trizol was used.

    Response: Due to the short-term nature of the study it was not felt that preservatives were required for PBMC cryopreservation. The Lo/Alter study detected sequences in PBMCs stored for 15 years in the absence of preservatives. Trizol is for the extraction of nucleic acid and laboratories were given the option of choosing their own extraction methods

    4. The length of time allotted for the serology and culture assays was massively reduced, so that the WPI or NCI/Ruscetti assays were not performed as desired.

    Response: All the laboratories were allowed as much time as required to perform their desired assays. The culture and serological assays were performed by WPI and NCI/Ruscetti to their own specifications.

    5. The WPI was not given the opportunity to complete virus culture assays.

    Response: The WPI encountered mycoplasma contamination of their target cell population, and used the plasma samples without results. This was very unfortunate. There were no further stocks left to perform repeat cultures with. It was deemed by both the WPI and the working group that performing the studies on freeze/thawed material would be invalid.

    6. Samples and collection tubes were handled in the same laboratory as 22Rv1 cells used to spike the analytical controls.

    Response: As stated in the paper, 22Rv1 cells were handled in a separate facility to where all other activities were performed. The fact that only one laboratory detected PCR and virus culture in clinical samples supports the fact that 22Rv1 contamination did not occur at the central laboratory.

    7. Patients were on additional therapies that would produce false negatives.

    Response: Lo/Alter patients were not on any additional treatments. It is unclear what additional treatments patients were on at the time of Lombardi et al. There is no published evidence that additional treatments would have positive or negative effects.

    8. FDA/Lo used the wrong assay from Lo et al. and instead used the one that could not detect positives.


    Response: Lo et al. used their own criteria to decide on which assay(s) to use, but it is clear that both primer sets in their paper are equally capable of amplifying diverse polytropic murine leukemia viruses (MLVs), so it is not obvious that one would be better that the other at detecting “positives.”

    9. The NCI did no PCR and could not use their clinically validated serology and culture assays.

    Response: NCI felt that they were not sufficiently experienced at PCR to participate in the study. They did perform their serology and culture assays – just as performed in Lombardi et al.

    10. All the SRWG labs optimized their assays to VP62. VP62 does not exist in nature and Lombardi et al. is now known to have discovered HGRVs. Does your study include HGRVs? Or how do HGRVs relate to XMRV?

    Response: As demonstrated in an earlier slide, although this study was initiated after Lombardi et al. as a study of XMRV, as soon as Lo et al. was published the mission of the study was broadened to include all MLV-like viruses. Thus, almost all of the assays were designed to perform against MLVs in general and were optimized and tested as such. As our study has demonstrated there is no such thing as an independently validated clinically positive sample against which to test. Currently there is no such thing as human gammaretroviruses (HGRV). No published virus has been isolated, cloned or sequenced from a human.

  75. #76 Tess
    October 15, 2011

    I have been reading this rather fascinating saga of XMRV ..trying to understand the events and the science involved. On Dr. Vincent Racaniello’s blog post “XMRV is a recombinant virus from mice”
    http://tiny.cc/r6fzz , he writes “An important question is whether XMRV was present in the original prostate tumor, or was obtained by passage through nude mice. To answer this question, DNA from various passages of the prostate tumor in nude mice (called xenografts), and the mouse strains used to passage the tumor, were analyzed for the presence of XMRV proviral DNA..”

    Can someone please tell me what “passage(s)” means? Does it mean they implanted the PC xenografts into the mouse’s body and then extract it for analysis? I tried to Goggle this but so far have not found a reference that explains “passage” in more detail. If anyone can explain briefly or provide a link, it would be very much appreciated!

    Thank you!

  76. #77 Sigmund
    October 15, 2011

    Tess, in cancer research the aim is always to test models of malignancy that mirror the sort of conditions that a tumor will normally experience. This means that growing a cancer cell line in a plastic flask (a common procedure) is not ideal since it means the cells will not encounter things like growth factors and support cells that are present in a growing body. Obviously we cannot use the ideal environment – a human body – for such studies so we try to use an approximation of this – a mouse that has an inactivated immune system that allows human cells to grow.
    “Passaging” the cells means growing the cancer cell line in the mouse. This is either done by injecting the cells into the mouses bloodstream where they find their own way to the site that is best for that particular tumor. Human cancer cell lines often undergo selective pressure while growing in this mouse model and it is common to find that the original cell line has mutated in some way and so the mutated cells are often taken from the mouse and regrown in the flask system in order to find out exactly which gene has mutated.
    There are, however, some dangers associated with this sort of passaging that are important for the XMRV story. First the human cell line might pick up mouse viruses and second, the human cell line might pick up mouse genomic DNA (which will contain mouse ervs) that mean you are susceptible to getting false positives by PCR.

  77. #78 Richard Jefferys
    October 15, 2011

    Here is a sickening insight into what an incredibly lovely person “V99″ is:

    http://www.mecfsforums.com/index.php/topic,9946.msg118328.html#msg118328

    “What an imagination! Really where have you been hanging out?

    Anyone would think you had been talking to a bunch of AIDS patients from the 80s using a Ouija board.”

  78. #79 David
    October 15, 2011

    On that point Richard, @1077 what do you think of the paper referenced at the top of the thread?

    http://projectreporter.nih.gov/project_info_description.cfm?aid=8144150&icde=10094017

    I mean is that just crazy talk!?!

    It is a bit confusing at the minute when there seams to be so many projects ready to go with XMRV, assuming it still to be what it might have been, if you know what I mean!

    (B.T. W. – I’m not sure what Mr 99 is getting at there, is he referencing some of the conspiracy theories doing the rounds in the 80′s? I mean they obviously turned out to be wrong, yet all the speculation that went on while science was in the the dark is sometimes used to support the ideas of conspiracy theorists now?)

  79. #80 John
    October 15, 2011

    On the webinar slides, there’s a pretty neat phylogenetic tree of all the various XMRV/MLV’s reported thus far, both in the literature and to genbank. For anyone who’s been keeping up with the situation, the Lithuania ‘XMRV’ is there, the CDC’s ‘XMRV’s’ are there, Lo’s MLV sequences, the WPI’s new ‘XMRV’ sequences, everthing is in there as far as I can tell. The slide is fairly large and can be zoomed in quite well.

    It’s slide 27-
    http://www.cfids.org/xmrv/srwg-webinar-oct2011.pdf

  80. #81 EvilYeti
    October 15, 2011

    MS.spits,
    I’m not surprised you can’t shut up, OCD has a high co-morbidity with anxiety disorders.

    Could you at least explain why you are talking about narcolepsy/catalepsy? If your fatigue is related to that, then you don’t have CFS. Same with pernicious anemia, which can be an auto-immune disorder.

    Or chronic stress, viral meningitis, lyme disease or any of a number of known conditions that may cause symptoms of fatigue. Hence my skepticism and suggestion that classifying a ‘symptom’ as a ‘syndrome’ might lead to an epidemic of misdiagnosed, chronically ill patients. Which does seem to be the case, you will have to admit.

    I’ll post this link again, as I’ll suggest the potential link between viral infection, mental illness and CFS may in fact be real, but much more subtle than anyone has hypothesized to date:

    http://discovermagazine.com/2010/jun/03-the-insanity-virus

  81. #82 Got Ilk?
    October 15, 2011

    @1079 – John, is Grossberg’s “I’m calling it XMRV now” sequence on there? I can’t find it, but I’m prone to error when reading fine print. Like the fine print on the bottom of the VIPDx test results that reads, “For entertainment purposes only.”

  82. #83 David
    October 15, 2011

    @1080

    Yep, that is a nice article, quite well known amongst the CFS community.

    As said…

    “These things “convinced me that this is a brain disease,” Torrey says, “not a psychological problem.”

    Everyone I know who knows these ideas is accepting of them, making nonsense of the idea that people with CFS have some phobia of being classed as having a ‘psychiatric problem’ per se.

  83. #84 Tess
    October 16, 2011

    Sigmund,

    Thank you for answering my question about passaging! Very much appreciated! :)

  84. #85 John
    October 16, 2011

    1081- I could be wrong, but I think it might be DG-75 down near the bottom. Isn’t that what Grossberg did, sequence the DG-75 virus?

  85. #86 mo (one of Abbies's elk)
    October 16, 2011

    re: “the insanity virus”:

    Can you spot the difference to what Mikovits did, kids?

  86. #87 John
    October 16, 2011

    1081- I think I was wrong about Grossberg/DG-75, that’s a different virus than Grossberg’s JHK ‘XMRV’. I’m not sure if I see the JHK/’XMRV’ one on there.

  87. #88 mo (one of Abbies's elk)
    October 16, 2011

    I meant to write:

    re: “the insanity virus”:

    “Perron learned from their failures. “I decided that I should not have an a priori idea of what I would find,” he says.”

    Can you spot the difference to what Mikovits did, kids?

  88. #89 EvilYeti
    October 16, 2011

    Mo– Eggs-actaly.

    I’ve been doing this scientific skepticism thing for ’bout 20 years now and the unifying theory of ‘woo’ is an “a priori” assumption that the faithful then try and warp reality to fit.

    This strikes me as a colossally poor use of resources.

    Its actually much easier just to let reality tell you how it works and pay careful attention when it does.

  89. #90 David
    October 16, 2011

    @ 1087 Well that was the whole problem with the WPI. I remember seeing just a picture of the new premises, and within what seamed no time at all – they were headline news. It was literally incredible. I mean if it had come from anywere else it would have been amazing, but, what – you set up this institute to help your daughter – and then – BAMM – got it!?

    I accepted it initially though as most people did though with ‘one paper’ sized caution, the red flag for me was similarly for many people the initial responses to negative findings, moving in with the autism thing etc etc.

    But yes, all in all a cautionary tale about the ‘collective will’ – well meant, or otherwise.

  90. #91 EvilYeti
    October 16, 2011

    I haven’t followed this “debate” in depth, but is that really what happened?

    If so, its a prime example of what I call “Hollywood Science”. I.e., the scrappy minority goes up against the status quo, overcomes all odds, there is a sick kid involved, a talking pie, etc…

    Does the WPI have a teenage whiz-kid computer hacker on their team as well? Preferably female and of an appropriately indeterminate mixed-race ethnicity.

    Anyways, true scientific breakthroughs never, ever happen this way. Of course there are “Eureka” moments, but after comes the necessary process of publishing and peer-review.

    Science by press-release tends to end badly.

  91. #92 Poodle Stomper
    October 16, 2011

    Apparently a group called IMEA is trying to dispute one of the XMRV papers. Not so surprisingly, the same group is trying to get Gallo’s HIV paper retracted. Once a loon…

    http://www.imeassoc.com/Response__Paprotka_et_al.html

  92. #93 Anonymouse
    October 16, 2011

    @1091 — The IMEA, I believe, was started by Wildaisy (aka Patricia Carter) who coincidentally is the administrator of the me/cfsforums. The IMEA appears to get all their information from Gerwyn (who has rejoined the forum after a huge temperamental flounce aimed at Wildaisy) and V99 (who we all know is Judy Mikovits – (wink,wink).

  93. #94 laurie b
    October 16, 2011

    The IMEA group was started by the same people who run the me/cfs forum. However, there has been so much infighting, I’m not sure who is still connected to the organization.

  94. #95 herr doktor bimler
    October 16, 2011

    I enjoyed the Upcoming positive papers” page at the IMEAssoc site (dated 9th July):

    Thanks to the CFIDS Association of America for announcing the upcoming publication of papers where the researchers have successfully detected XMRV. They also mention some papers where the workers, using different PCR assays, have failed to detect XMRV once more. Perhaps next time they may consider using techniques which have a history of success and not of failure.

    All that is missing are *titles* and *publication details* for these papers.

    For some reason the site’s creators have included a “Disable select-text script” in every page to deter people from quoting their words.

  95. #96 herr doktor bimler
    October 16, 2011

    Not so surprisingly, the same group is trying to get Gallo’s HIV paper retracted.

    Heh. “IMEA requests that the editors of Science magazine retract the Gallo papers of 1984″

    – They rake up an earlier case when a virologist gained headlines and fame and research grants by announcing a breakthrough that later turned out to be a combination of plagiarism and straight dishonesty. They seem to be under the impression that they are thereby doing Mikovits a favour.

  96. #97 Jack
    October 17, 2011

    I noticed the same ‘logic’ with the postings about Wakefield for heaven’s sake!

    Mikovits spouts a ‘connection’ with autism and now Wakefield is trying to rally the troops and those of the ‘faithful’ Mikovits crowd are busy circulating his latest rantings as some sort of ‘defence’.

    The responses to that BWG Webinair are equally astounding.

    Expect more weirdness…

  97. #98 TylerD
    October 17, 2011

    For your entertainment, folks.

    http://www.freetext2speech.com/hear/2048

  98. #99 Smurfette
    October 19, 2011

    @David, re:

    I’m interested in what is sometimes called the 25% group, those severley affected, often bedbound, for whome CBT etc is out of the question.

    It’s only CBT in a therapist’s office that is out of the question. The main part of CBT is the homework. Nowadays computerized CBT is starting to grow. You might also find other forms of coaching that have methods in common with CBT.

    Personally, I found a blog of a behavior change coach who focuses on entrepreneurship and career stuff. This has nothing to do with CFS but I found the same psychology could be applied to help me make the most of my limited functionality and time. The benefit I found there is that I don’t have to deal with any of the irksome stuff (e.g. abnormal illness beliefs), and instead just get the cognitive and behavioral stuff.

    Bedridden CFS patients still have the options of books, blogs, and computerized CBT. I also think they would be more willing to try it that way for the reason I mentioned as well as it being within their physical ability.

    General comment on stress after reading various @WTF and other comments. Yes, stress includes physical and psychological stressors, physical stressors including infection, surgery, physical trauma, pain, sleep deprivation, etc. It has not been determined that the stressors are only a trigger for CFS. And if as @EvilYeti hypothesized, that chronic stress can lead to chronic infection, and we have here that infection is itself a stressor, then it would be possible to have a vicious cycle that is purely physical. To address stress, one needs to address both physical and psychological stress, whatever stress is relevant to the particular patient. In my experience, physical stress gets overlooked. Most of my improvement to date is from me trying what I can to break the physical stress cycle (pain, muscle spasms). The cognitive and behavioral stuff just helps me make the most of the state of things.

    The viral and other stress trigger hypotheses also exist for illnesses such as MS and lupus. CBT also helps with fatigue and depression for those. But perpetuation of those illnesses isn’t attributed to “abnormal illness beliefs”, nor is CBT considered the main or best treatment, nor are patients lambasted for seeking physical treatments for those.

    Also, food for thought regarding retrospective look at life stressors. The sicker I was, the worse I thought prior events were, and the more I wondered if they contributed to my illness. Before I got sick, I didn’t even consider the same events as big stressors. After I improved a little, the same events looked in retrospect pretty normal again.

  99. #100 Levi
    October 19, 2011

    Smurfette @692,

    The CBT that is a defacto mandatory therapy for UK ME/CFS patients that want continuing medical care and at least limited disability benefits is nothing like coaching in my understanding. The behavioral therapy you describe could certainly be of use to ME/CFS patients that almost universally need to come to grips with new energy limitations and acquire time management skills to marshal their energies and survive. That is not what is being offered.

    Instead, patients are subjected to therapy methods that are at best dishonest, and in the worse case coercive and stressful. It can be even physically harmful if combined with GET therapy. The CBT for UK patients has its roots in “reparative therapy”, as I mentioned upstream in this thread.
    http://en.wikipedia.org/wiki/Conversion_therapy

    In reparative therapy, the operant reality construct is that gay patients are mentally ill and need to be repaired by “conditioning” methods. In CBT for CFS patients, the operant reality is that CFS patients are mentally ill and have “deconditioned” themselves. They need to be repaired by “conditioning” methods. If you add coercion in the form of Christian “guilting” of a homosexual patient, or the withholding of care and benefits in the case of CFS, then it is not helpful to the patients in the long view of things.

    Sadly, the powers that be and vested interests in the UK have chosen to devote almost all available funding to CBT and GET therapies in the context of ME/CFS treatment and research efforts. It is the only game in town.