Random thoughts

It is difficult to imagine how XMRV is being dismissed as a lab contaminant by some supposedly intelligent people despite the publication of the following three papers in The Journal of Urology:

The recent paper Distinct Cerebrospinal Fluid Proteomes Differentiate Post-Treatment Lyme Disease from Chronic Fatigue Syndrome. Schutzer/Natelson contributes to the literature supporting a biological basis for both CFS and chronic Lyme Disease. The authors believe that treatment resistant Lyme Disease is a distinct entity from CFS, and in my opinion, that is not likely. The Lyme group probably met inclusion criteria for the CFS group, but it isn’t clear from the paper. There was much overlap of “proteomes” between the groups, which makes sense, as there are probably some CFS patients without Lyme and possibly some treatment resistant Lyme patients without CFS, whatever “CFS” is. A better explanation than two distinct diseases is that the immune deficit from the underlying retroviral infection causes Lyme to be a bigger problem than it otherwise would be. As I’ve said before, the very few clinicians who care for both groups of patients find them clinically indistinguishable. My impression is that the patients who wind up in the Lyme group are sicker and have more pain, either from neuroborreliosis or excessive treatment, very hard to say.

I love the meeting place feeling that is developing here. There are now well over a thousand comments on this blog. I haven’t moderated it at all. There has been no spam (knock on wood). The comments have been insightful, compassionate, funny, sad. They often stimulate me to write more. They demonstrate that the patients get it, even if most of the scientists and doctors don’t. I’ve removed only two comments, directed at someone else, that were over the top. The invisible counter shows it’ll hit 150,000 pageviews, at a year next month, from six continents. Parts of it have been translated into German and Spanish. It has been discussed and linked to in many languages, some of which I don’t recognize. Every post is read by thousands of people in a few days. It doesn’t cost a dime. The internet is an amazing thing. We would all be alone and powerless and we’re not. Personally I think FaceBook and Twitter are really creepy, but they are powerful enough to bring down dictators, so should be used to our advantage.

I continue to communicate with many patients by email and phone. My impression is firmer than ever that the people who have done very little are doing better than the people who have pursued aggressive or experimental treatments. Radical avoidance has worked to control symptoms for some and the stories of our mold warriors are intriguing. It’s not hard to figure into the model I’ve proposed how biotoxins causing inflammation would activate virus and keep it activated while the exposure continues. My impression is that men are more likely to recover an adequate level of function and more likely to be able to exercise. My husband is an extreme mountain biker at almost 50, seven years after onset of cardiac symptoms and severe dysautonomia; he has thrived with the disease and he mostly refused treatment. Although PEM is probably pathognomonic, there are people who can exercise. I had a year of episodic neurological and vascular symptoms, followed by a full crash and period of disability, then near recovery, without treatment, for most of ten years during which I could exercise, but had symptoms. In addition to the common viral onset and immediate PEM which never goes away, histories like mine are not uncommon. A crash with a very slow recovery over a period of many years is a variation, and lots of others. My general impression is that the second generation is sicker. I have even heard from families with three generations of clinically apparent illness. There is lots and lots of subclinical disease in family members.

It is a relapsing, remitting illness. Whatever someone was taking (or prescribing) at the time the improvement happened is thought to be causative. Lately I’ve had particular difficulty with people who believe they know how to cure me with their favorite therapy. Some people who have recovered have a lot of ego about having gotten well and that makes it even more difficult for those who haven’t. IV hydrogen peroxide comes up a fair bit. Please folks, if you want to try some oxygen, use oxygen. If you want to try a higher dose of oxygen, try HBOT. Don’t let anyone inject peroxide into your veins. Or endanger you in other ways. There is no cure, though some people get better spontaneously. If anybody had the answer, so many people wouldn’t still be sick.

What do I think about Ampligen? I have no personal experience with it. From my mail and the impressions of friends in practice, like everything that has been tried over the years, there seem to be a very few successes, some modest results and some harm. It’s been around forever, so it’s hard for me to believe that it works that well, or we’d know by now. It’s IV, is needed indefinitely, so requires permanent access, and is financially out of reach for most. It’s making some doctors wealthy though. The patients are even paying for their own clinical trials.

IVIG has helped quite a few people, incompletely and the improvement doesn’t always last. It’s intravenous, you have to take it forever, it’s expensive and difficult to get covered. Also it’s a pooled blood product. 

Rituximab? It sounds really scary to me. To take or prescribe. The initial infusion can kill you. Complications include life threatening infections. From the drug monograph:

Serious adverse effects, sometimes fatal, have occurred in patients receiving rituximab. Severe or fatal infusion-related reactions; tumor lysis syndrome associated with fatal renal failure; severe or fatal mucocutaneous reactions; progressive multifocal leukoencephalopathy causing death; hepatitis B reactivation with fulminant hepatitis, hepatic failure, and death; other severe or fatal, bacterial, fungal, and viral infections; serious or life-threatening cardiac arrhythmias; severe or fatal renal toxicity; and fatal bowel obstruction and perforation have occurred in patients receiving rituximab.

Adverse effects, including serious adverse effects, commonly occur with rituximab therapy. In clinical studies of rituximab in patients with relapsed or refractory low-grade or follicular non-Hodgkin’s lymphoma (NHL), adverse effects were reported in 99% of patients, and grade 3 or 4 adverse effects were reported in 57% of patients. The most common adverse effects reported in 25% or more of patients in clinical studies are infusion-related reactions, fever, lymphopenia, chills, infection, and asthenia.

GcMAF? I’ve heard from a few people in Europe who are trying it and so far, the reports I’ve heard haven’t been exciting. Let’s hope it’s better than that. I haven’t heard any first, or even second hand, reports of dramatic response, but nothing negative either. Early days.

I’ve gotten a lot of mail about how awful Trine Tsouderos is, since last week’s Chicago Tribune article. Trine Tsouderos is not my enemy. We actually have a cordial relationship, having agreed to disagree about some things. I thought her chronic Lyme story was pretty good. I do not believe that she is part of a conspiracy. Nor, apparently, is she Paul Offit’s sister-in-law or connected to the CDC in some way. It’s all silliness. She is trying to do her job, which is to report the news. She has always dealt with me in a professional manner. I think it’s great that she’s keeping our plight in the public’s face. She is reporting that ME/CFS is a real disease, even if she thinks that XMRV is a contaminant or that the vaccination program is flawless. It’s a good thing that it’s news. She is raising awareness, even if we disagree on the details.

For the record, I am not “anti-vax”. I vaccinated my kids selectively (no Hep B or chicken pox), other shots a little late and not all at once. Seemed common sense at the time. It had nothing to do with being part of any kind of movement. My concern about vaccinations now is two fold. It seems obvious to me that vaccination injured people are over-represented in the ME/CFS patient group. And the hypothesis outlined in my last few posts explains too much of the mystery to be dismissed. I am completely comfortable urging caution until we know more. Not such a radical concept. We routinely withhold vaccines from other immune compromised people.

Here is the question that I submitted to the chat with Paul Offit hosted by Trine Tsouderos on the Chicago Tribune website a couple of days ago:

Are you concerned that the current epidemics of ME/CFS, ASD and GWI are related to vaccines? These neuroimmune disease cohorts are all of mysterious etiology and share many clinical similarities: sensory and cognitive processing deficits, susceptibility to and inability to clear certain infections, an unusual susceptibility to stress, increased  oxidative stress, glutathione depletion, methylation blocks, mitochondrial defects, high levels of heavy metals, inflammatory bowel issues, hormone abnormalities and a suspicion that vaccines are implicated in pathogenesis. The pathology in humans is extremely similar to what is known of simple retroviral infections in animals. We have evidence that xenotropic and polytropic MuLVs are infecting humans (Lombardi et al Science Oct 2009, Lo et al PNAS Sept 2010). Given the history of the use of mouse and chick embryo cells for vaccine production coinciding with the history of Epidemic Neuromyasthenia (as documented by Henderson and Shelokov, NEJM 1959), the known presence of animal retroviruses in those cells, and the documented ability of these viruses to infect human cells, aren’t you the least bit concerned?

His reply:

The xenotropic murine retrovirus story as a cause of neurologic disease, including chronic fatigue syndrome has clearly fallen apart. And for those of us old enough to remember, many careers have fallen off a cliff claiming retroviruses as a cause of a variety of illnesses: most noteworthy, MS and Kawasaki’s disease. Retroviruses are so ubiquitous and such a frequent lab contaminant that they’re the Sirens of the lab.

Completely non-responsive. How can he sleep at night?

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51 thoughts on “Random thoughts

  1. >I cannot tell you how good it is to read such a measured and rational evaluation of the situation we find ourselves in as this is. I have been living and following this story for 31 years… since before Incline Village… before it was possible to know I was not living it alone. Thank you very much for the role you are playing in moving the dialogue forward.

  2. >It's interesting that you point out how difficult it is to separate correlation from causation regarding improvement in a relapsing/remitting illness, citing hydrogen peroxide therapy as dubious, but go on to find 'radical avoidance' intriguing? Why? Because it fits your personal hypothesis?

    The problem with radical avoidance is the same as any other modality – many people have improved or even recovered while breathing and consuming what supposedly should be avoided: mold spores, gluten, sugar, etc. It is just as anecdotal and often more expensive and energy consuming than the average "treatment".

    That is my small bone to pick. ;)

    Otherwise, nice blog and thank you.

  3. >To the above poster re: radical avoidance. For me, moderate avoidance has helped me dramatically whereas radical did not add much. This is relatively cheap and not very taxing treatment. Moreover, it can only help. There is little chance of it making your health worse. I'd only add that avoidance should also include chemicals and other nasty thing in addition to mold.

    I would guess that hydrogen peroxide and other therapies are dubious because there is risk with little understanding of benefit. With sensible avoidance, there is almost no downside and a potential for a decent upside. I don't think anyone is claiming miracle cures; only moderation of symptoms which is probably the best anyone can expect at the moment.

    To Jamie's point, people who don't take drugs and unproven therapies are better off. Try it you might like it. If not, go back to injecting yourself with dubious things that John Mellors might not approve of.

  4. >Don't you love the confounded use of the word "clearly"?
    "The xenotropic murine retrovirus story as a cause of neurologic disease, including chronic fatigue syndrome has clearly fallen apart. And for those of us old enough to remember, many careers have fallen off a cliff claiming retroviruses as a cause of a variety of illnesses: most noteworthy, MS and Kawasaki's disease."

    And we so clearly understand the causes of MS and Kawasaki's disease…well, at least it isn't a retrovirus that came from a mouse back in the day…

    Would it help if we used cooked mouse brain or scrambled eggs when we make vaccines?


    Paula on an offit day

  5. >I just don't get how Paul Offit can be so sure, when the evidence is still so mixed. I'm o.k. with him continuing to defend vaccines (which is his big cause), as long as there's no SOLID EVIDENCE (as opposed to anecdotes and informed speculation) that they are causing disease (which, despite the chat on this blog, I continue to believe). But how can he be so convinced that XMRV is not causing disease? I think it is easy enough to separate the XMRV story from the vaccine story. Vaccines are one possible vector of this retrovirus, but given the ubiquity of mice in our world, it is only one among many. So I don't see why Paul Offit has taken an interest in this story, or why he is so keen to dismiss it. If anything, his interest makes me start to wonder if there is scientific concern about a vaccine connection after all….

  6. >Jamie –

    I got sick while living in Lake Tahoe after a tick bite in the groin when traveling to other states.

    Treatment for chronic Lyme has made me much more functional, and I am not having thousands of dollars in MRIs, CTs, ER, and hospital visits anymore (knock on wood). Antibiotics were extremely difficult for me to start that I quit and declined for a year after only a few days of doxycycline. I did test equivocal for RMSF as well, but only IgG antibodies.

    Believe it or not, I made the most progress with colloidal silver (and unfortunately herxed the hardest). Those in that practice mainstream medicine would probably scoff at me (as they hold a belief that it is not effective in vivo and bla bla bla), but I don't care, because it was one of the most important things I took, and lab work reflected it.

    That being said, I also see a CFS doctor that doesn't seem to believe in prescribing antibiotics, and that is fine since he is not telling me what I should or shouldn't be doing. My lab results (including VO2 exercise test, etc) look just like CFS. I didn't have a cortisol response to exercise. I wasn't producing my own HGH. It was 0 before and after exertion. I had disseminated intravascular coagualtion which is now better. My natural killer cells are low. However, my DHEA-S is now the best he has ever seen in a patient like me.

    That being said while Trine Tsouderos' article on Lyme did reflect mainstream opinion, I did not agree with it at all. Believe me, I wish I could stop this damn doxycycline without a relapse after 3 weeks or so. I don't want to be on antibiotics (they screw up your flora amongst other things), and I was literally never on them for anything before becoming ill. I'd rather take be an non-toxic herb, but I haven't found one that really works like doxy for Lyme yet. Well, colloidal silver is very effective for my Lyme, but it didn't seem to go completely systemic, and it's not something I would want to be on forever either. I was very skeptical when I started it (since it is a metal after all) and I honestly never thought it would have worked.

    Take care.

  7. >Hi Kyle,

    I have heard from a number of people who attribute remissions to colloidal silver.

    I hope I have made it clear that there are people who must be maintained on an oral antibiotic to avoid total crash. It is the indiscriminate use of antibiotics despite evidence that it is helping that I object to. A herx may be unavoidable, but should not go on indefinitely.


  8. >I like your "random thoughts". They touch on issues I'm quite familiar with.

    Yet to many readers they will be new, and your audience is vast and varied. So thank you for not only validating the experiences of people like me but for educating people who are unfamiliar with the issues you've raised.

  9. >Hi Jamie, sobering blog! As you have pointed out the treatment situation for ME/CFS patients right now is dire.

    I'm hoping that the translational medicine model that the WPI is pioneering will soon change that.

    I fully agree with you about herxes. They should not go on indefinitely. IMHO the Achilles-heel of ME/CFS treatment is the ability to tolerate detox/herx.

    There are 100 treatments out there which can and do kill pathogens. The problem is how to tolerate them when you have a non-existent stress response, and when you barely produce enough cellular energy to make it through the day. This is the $64,000 question IMHO.

  10. >I am involved in research looking at endogenous retroviruses in my child and I. The researcher involved in our case agrees XMRV is a contaminate, especially after finding tentative evidence of Herv expression in our family I suspect. I am waiting for validation work on research I am involved in and Canadian studies on XMRV to make a firm decision myslef one way, or the other. I have to tell you though, as a patient the evidence is mounting against XMRV and I am considering more dynamic explanations for ME/CFS. I am just saying, I am begining to have real doubts. I wonder if other patients are as well?

  11. >Jamie, I would like to comment on your thoughts about Rituximab. I am well placed to speak about it because before I got ill, I was a chemo nurse. I gave Rituximab hundreds of time, and seen people come back from the dead due to this drug. literally.
    The infusion reactions encountered happen mostly the first time a patient get it. patients I have treated all acetaminophen and benadryl prior to and during the infusion. Some will need a bit more, but most patients manage to get the medicine despite these reactions. it may take up to 8 hours the first time, but the subsequent times are much faster, and usually without reactions, and infused over 90 minutes. Certainly you need someone experienced to administer this drug.
    I am really excited with the idea it may help ME patients because I know it's a very good drug and it is also used in RA and SLE. while expensive, I believe that access to clinical trials and access for this drug by insurance coverage or through socialized medicine, in my case, should be covered as compassionate access. The complication happens because ME is an orphan illness and rheumys would most likely not agree to give it to me, even if I provide evidence from the Norway studies.

    Again, I have never seen someone dying from Rituximab infusion, but I have seen someone coming back from the dead, incidentally an HIV + person with aggressive lymphoma.

  12. >Paul Offit's vaccine, Rotateq, was found to be contaminated with pig virus, so if animal virus-contaminated vaccines are a problem then it's in his best interest to deny it.

  13. >>There are 100 treatments out there which can and do kill pathogens. The problem is how to tolerate them when you have a non-existent stress response, and when you barely produce enough cellular energy to make it through the day. This is the $64,000 question IMHO.

    My primary focus at this point is to encourage researchers to look at the role of toxic mold in our illness in the hopes that this will help them to understand the etiology better — not to exhort patients to try extreme mold avoidance. The latter is, unfortunately, really hard.

    However, one thing that all patients might consider is making an effort to reduce their toxic mold exposures at least somewhat, in the hope that it will allow other treatments to work more effectively as well as prevent further declines. As you say, there are lots of treatments out there that _should_ work for us, theoretically. The problem is tolerating them.

    To this end, reducing the pro-inflammatory stress on our systems in any ways that we can seems like it can only be a good thing. (Based on the interviews I've done of people who have "mostly recovered," avoidance of gluten — another inflammatory substance — also can be helpful for some people, as an addition to being in an environment that's at least "okay.")

    I recently heard from a patient of Dan Peterson's who moved from a really moldy home to a better one, discarded a lot of possessions, washed the rest — and got a "20% improvement" within four months. This individual thinks of moderate avoidance as part of an overall treatment approach (including aggressive antivirals) and is considering further ways to reduce mold exposure in the future.

    I like that story.


    Lisa Petrison

  14. >I have a 10 year niece on biologics for severe juvenile arthritis. She tolerates it well. A bit of nausea, which lessened over time that is all.

  15. >Thank you for sharing your most interesting random thoughts, Dr. Deckoff-Jones.

    Paula on an offit day, you gave me a nice laugh, which I really needed. These statements: "Don't you love the confounded use of the word "clearly"? and "The xenotropic murine retrovirus story as a cause of neurologic disease, including chronic fatigue syndrome has clearly fallen apart." reminds me of of a "tell" (as in poker) I used to see constantly see other lawyers' briefs. They used the word "clearly" so often when the matter was definitely not clear at all that I used to ask my secretary to read briefs and mark wherever they did this. It almost always marked the weakest parts of their arguments.

    Hopefully, it is the same with offit's statement. The xenotropic murine retrovirus story as a cause of neurologic disease, including chronic fatigue syndrome has clearly NOT fallen apart; offit's position is what has fallen apart.

    Patricia Carter

  16. >thanks as always, dr. dj. what i have born, emotionally, through other people's cures could fill a tome. after every, "tried that" (massage, vitamins, minerals, microcurrent, accupuncture, chinese herbs, even cbt, etc…), there's unfailingly that look of "gee you're negative…"

    i had one one-yr remission thanks to dr. jay goldstein and the drug "isoxsuprine" which is an old vassodialator and nmda antagonist. i still had my usual severe fibro pain but no cfs symptoms. then i simply developed tolerance to the max dose. it was horribly depressing to feel myself slipping backward into the void.

    i'm wondering if xmrv tends to hide out in the blood vessels… i have had pretty bad neuropathy and now pots. just my own little theory.

    i'm waiting… as patiently as i can. there is no other choice… xoxoxooxoxox

  17. >"It is difficult to imagine how XMRV is being dismissed as a lab contaminant by some supposedly intelligent people despite the publication of the following three papers in The Journal of Urology"

    Let me count the ways-

    1. XMRV specific antibodies derived from experimentally infected monkeys not being detected in over 1000 blood donors.

    2. Purported gene integration sites of XMRV into human DNA being shown to be exactly the same as occured in an experimentally infected cell line, a finding which has never been reported before yet occured twice in the lab reporting the integration, which just so happened to be the same lab that did the above mentioned cell line experiment.

    3. XMRV gene sequences being more diverse in contaminated cell lines than XMRV purportedly found in human samples which were taken from geographically distinct areas at different time points.

    4. XMRV being pretty much shown to have occured as a result of genetic recombination of two different endogenous mouse retroviruses, with this recombination most likely occuring sometime between 1993-1996 in Case Western labs, if I'm not mistaken.

    5. The Spanish Irsicaixa XMRV study that everyone is so on about actually reporting XMRV positivity in similar amounts between healthy and disease groups, a finding which is more likely to reflect contamination than actual legitimate results.

    6. No other lab finding XMRV in CFS samples other than the ones associated with the WPI.

    7. Dozens upon dozens of other studies not finding jack shit in regards to XMRV despite using numerous and varied approaches, with even the supposedly positive studies not actually replicating anything found in previous studies- One study says it's in this tissue, one says it's in that tissue. One study says it's associated with this genetic polymorphism, one says there's no association with genetic polymorphisms. One study says it's significantly associated with Gleason score, one says there's no association. Even the Alter/Lo findings, which were yet another study to not find XMRV, found two different kinds of MLV's in disease and control groups which is another finding that is more in line with contamination than authentic infection.

    8. The WPI not being able to even come close to replicating their initial results using blinded samples in the XMRV Blood Working Group study, even though they state that they can find XMRV in just about any disease group they look at including autism, Parkinson's, CFS, fibro, Lyme, atypical MS, etc.

    9, 10, 11….99, 100, etc.

    PS- The first study you linked to has nothing to do in regards to XMRV being a contaminant since no one is saying that XMRV can't infect various cell lines.

    PPS- Even the co-discoverer of XMRV is concerned about the potential for contamination- "I am concerned about lab contamination, despite our best efforts to avoid it," Silverman wrote in an e-mail, adding that similar cell lines "are in many, many labs around the world. Contamination could come from any one of a number of different sites."(1)

    PPPS- Re: your 'personal correspondance' about none of the XMRV+ labs using the 22rv1 cell line? "22RV1 cells were once previously (more than a year earlier) grown in my lab but were being stored in a liquid nitrogen freezer at the time, and not the same freezer used to store prostate tissues," Silverman wrote in an e-mail. "At the time it was unknown that 22RV1 cells were infected with XMRV."(2)

    1. http://articles.chicagotribune.com/2011-03-17/news/ct-met-chronic-fatigue-xmrv-20110317_1_whittemore-peterson-institute-chronic-fatigue-neuro-immune-disease

    2. http://articles.chicagotribune.com/2011-03-17/news/ct-met-chronic-fatigue-xmrv-20110317_1_whittemore-peterson-institute-chronic-fatigue-neuro-immune-disease/4

  18. >As a CFS/Lyme/XMRV patient for 22 years I have enjoyed and learned from your blogs sent to me by my brother who subscribed to an internet FAX service which allows him to send internet postings to my FAX. Due to eye sensitivity and eye infections from this illness, I cannot process information directly from a computer.

    As someone who has been on Ampligen twice I do disagee with your paragraph on Ampligen and am hopeful some of the more articulate and energetic patients will contact you with the other side of the story.

    The FDA approval process was designed for large companies, not small companies such as Hemispherx Biopharma. As Dr. Lapp, whom I have never met, recently stated in his letter, Hemispherx "have experienced the same kind of humiliation and disdain that all of us involved with CFS have experienced".

    Your statement that "it's making some doctors wealthy" indicates a need to explore this story more thoroughly and carefully. Just a four month round of Ampligen in '97 got me from a bedridden state to walking four tenths of a mile and a little bit of a life. I would love to be on it again.

    I appreciate you and WPI and am hoping politics/research/treatment make a sharp turn for the better soon.

  19. >#101- The epidemiology of classical ME being much more consistant with enteroviral infection than retroviral.

    #102- The widespread belief that CFS is comprised of subgroups, a belief derived from thousands of lab studies not showing consistant abnormalities in all patients, the clinical course of disease in seperate patients with some having sudden acute onset while others have gradual, progressive onsets, as well as treatment response with it being common knowledge that what helps one patient might do nothing for another and make yet another worse, etc. All of these indicate a disease composed of subtypes therefore to find a common pathogen in nearly all cases, as the WPI has claimed it is able to do, doesn't make a whole lot of sense. Plus even the WPI has reported finding distinct cytokine/chemokine profiles which is yet another argument against common causation.

  20. >Dear Susan (and all),

    Thank you for contributing your thoughts and personal experiences. As I've said before, I could be wrong about anything. I have been before.

    Warmest regards,

  21. >Dear John:

    It's wonderfully easy being a critic. You might even be right with some of your points. But how about some solutions rather than more problems? Why don't you do something constructive and lay out your thoughts of what this is disease is all about and how to move research and treatment forward. Rather than just attacking what other's have put out for the world to see?


  22. >It's axiomatic that "if anyone found something that helps, everyone would know about it."
    Word would spread like wildfire, or so it is firmly believed.

    But if you think about it for a second, this means if anyone stumbles over anything,
    there is no possibility for anybody to believe him, because everyone DOESN'T already know about it.

    It can be safely assumed that anything that everyone doesn't already know about is not worth knowing.

    Catch 22.

    Even if I had invented my whole mold story as a test of what would happen if someone "found something", the results are unequivocal, objective, verifiable and reproducibly universal:

    "Your story is anecdotal. YOU can't prove it. Your "theory" must be wrong because everyone doesn't know it."

    Well shucks, I guess "everyone" got me!
    Yup, "everyone" sure taught me a thing or two alright.
    "everyone" wins, I lose.
    Ain't that just an awful darn shame?


  23. >Dear Anonymous who asks John for solutions:

    I actually appreciate having this summary of the negative evidence. If John has been following the evidence of contamination closely, it's helpful to hear from him too. I don't think he seems hostile about the disease itself, and that puts him in our corner, as far as I'm concerned. Anyone who takes CFS seriously and pays attention to the science, whatever conclusions they are drawing right now, is o.k. by me, even if I am drawing different conclusions.

    Although John lays out a lot of negative evidence, there is a long way to go before I am convinced. Today I listened to Alter and Lo's seminar at the NIH from late February, and it is clear that they are standing by their study and that they have answers to many of John's points. I'm pretty confident that whatever Lipkin's multicenter study shows will be fairly conclusive, since Alter, Lo, and Mikovitz are all involved in the study, and then we'll have our answer about association, although the question of causality will still remain to be shown.

    Dr. Deckoff-Jones says she thinks it's a sign of ignorance or ill will if a scientist is ready to dismiss XMRV as a contaminant. John obviously thinks it's a sign of ignorance or self-delusion to believe it isn't a contaminant. I don't agree with either of these positions, but I'm really glad to have both of them thinking hard about this.

    Anonymous, why does John need to put forth a constructive theory about the disease? I'm a six-year CFSer, and I don't have a clear theory. I still think I have a right to be part of this discussion, as does John, even if he is just "being a critic" in this instance. The only thing I don't want to hear is covert or overt disrespect of the disease experience itself.

  24. >Me thinks the anonymous post after Garcia could be a certain BH of Tufts? One of the legions of soon to be sore losers.

  25. >Thanks for this very informative post. The info and opinions on the treatments are VERY useful to me.

    I disagree on Trine T. She distorts the news. She said that XMRV has been proven to be a lab contaminant and unassociated with ME. She should not be reporting if she is going to be misleading. Her sister apparently worked with CDC on autism and/or is a PR person for their vaccine effort. I would appreciate more info on this if anyone has it.

  26. >To Agatha:

    The problem with many of these critics is that they are drive-bys. If XMRV is contamination they will forget what ME stands for within a day. If it isn't contamination they will run even faster. Either way they aren't in it to make progress.

    Do you find stating "they couldn't find jack shit" and rather obnoxiously doing a string of PSs as constructive? I do not. Maybe it's just me. Perhaps I don't watch enough Glenn Beck.


  27. >JMO Anonymous,

    Yeah, you are right that the tone wasn't always respectful, but I took that as being a response to Dr. Deckoff-Jones's implied insult ("supposedly intelligent").

    I have the same disgust for the drive-by critics, who are only in it to "debunk" XMRV or CFS or both. I guess I interpreted John differently, because, in his second post, he seemed to know a bit about the illness and its variety and to know that it's a biological entity.

    Anyway, I can see why you felt offended by his post, but I read it differently. I found it useful to have the whole case against XMRV enumerated, even if the case ends up being wrong. And by the way, I've never seen Glenn Beck or any of his ilk.



  28. >John wrote:

    >#102- The widespread belief that CFS is comprised of subgroups, a belief derived from thousands of lab studies not showing consistant abnormalities in all patients, the clinical course of disease in seperate patients with some having sudden acute onset while others have gradual, progressive onsets, as well as treatment response with it being common knowledge that what helps one patient might do nothing for another and make yet another worse, etc. All of these indicate a disease composed of subtypes therefore to find a common pathogen in nearly all cases, as the WPI has claimed it is able to do, doesn't make a whole lot of sense. Plus even the WPI has reported finding distinct cytokine/chemokine profiles which is yet another argument against common causation.

    Whenever anybody mentions this “subgroup” concept, my first thought is, “Great, let’s figure out what those subgroups are in order to learn more about the disease(s).”

    That’s usually not why people bring up “subgroups” though. As seems to be the case here, it usually is more like, “CFS can be anything or everything, so let’s throw the whole disease in the waste paper basket and go look at some other disease that’s more interesting.”

    We’ll never get anywhere that way.

    Let’s presume for the moment that it’s the case that some people who have what the CDC defines as “CFS” have XMRV, and that some other people who have what the CDC defines as “CFS” don’t have XMRV.

    And for the sake of argument, let’s say that in those people who have XMRV, it actually does something.

Wouldn’t we want to know that? Just out of curiosity, if nothing else?

    And if that’s the case, wouldn’t we want to look hard at the subgroups (such as the Incline Village one used in the WPI study) who had it, just to see if there was anything else interesting about them that wasn’t present in other populations?


    Lisa Petrison

  29. >"And if that’s the case, wouldn’t we want to look hard at the subgroups (such as the Incline Village one used in the WPI study) who had it, just to see if there was anything else interesting about them that wasn’t present in other populations?"

    We'll "look". But hard? Nahhhh.

    Have you heard how much snow is in Tahoe right now? Wouldn't you rather go skiiing?!

    So sorry. Couldn't resist.

  30. >Osler's Web: Inside The Labyrinth of the Chronic Fatigue Syndrome Epidemic.
    By Hillary Johnson
    Crown Publishers Inc. NY
    Page 372.

    (Retort to Dr Giovanna Tosato, co-author of Straus's CEBV Syndrome Annals paper and of the 1988 Holmes CFS criteria, who told Dr Peterson that his patients can't possibly have CFS if they have all the other abnormalities he and Dr Cheney identified in the "Raggedy Ann Disease")


    So there you go.
    If one thinks of the "Definition as the disease", then we don't have our own syndrome.

    We aren't any any kind of CFS-subset at all.

    Not unless one thinks of the DISEASE as being CFS.

  31. >There's another reason why I'm returning to my roots.

    Not just to delineate clues from the original 1985 "Raggedy Ann Disease", but because RAD is a
    neat-a-roo acronym for a mechanism that could really lay a whup job on neurovascular mechanisms, and leave a lasting CNS injury which wouldn't leave overt evidence behind.

    ( I am only speculating, but I have my reasons )

    "Repetitive Astrocyte Depolarization"

  32. >"Repetitive Astrocyte Depolarization"

    . . . Dude, what the heck does that mean, in English? O.o

  33. >"a mechanism that could really lay a whup job on neurovascular mechanisms, and leave a lasting CNS injury which wouldn't leave overt evidence behind.(I am only speculating, but I have my reasons)"

    i'll second that, eric. whatever disease you're talking about, that just about describes it for me, in fact it describes me. i can actually think of multiple mechanisms that could have done this to me, including something dr. dj mentioned in another post, psychiatric abuse (bad drugs), and like so many longterm untreated ptsd. i know a woman who got "cfs" after 20 shock treatments. sadly, she died at 70 in a nursing home, never able to leave bed.

    yet, why does it feel so viral?

  34. >after i wrote the last question, i thought, because the autonomic nervous system is dyregulated: temp control, heart rate, digestion, visual acuity, stress response, you name it.

  35. >Look on page 179 of Osler's Web.

    Our community was furious with us for destroying the local economy by scaring away the tourists. It went so far as having the hospital refuse to admit us for any complaints related to the "mystery malady", which they considered to be nothing more than mass-hysteria generated by those two "quack doctors".
    I remember the hostility from the hospital staff as they glared at us.
    The exception was the radiologist at Lakeside Hospital. He reviewed Dr Cheney's (now famous) MRI scans and reached this conclusion.

    McNamara: "It's the changeability that would make one very suspicious that one is dealing with some infectious process or some reversible demyelinating disease which is, to my mind, otherwise unheard of. And (the lesions) struck me, some of them, as being very unusual in their size and their immediate subcortical location… We were quite suspicious that these lesions seen on the MR were directly related to the disease."

    Now bear in mind, "changeable demyelinating disease".
    If that "change" corresponded to an shift in location, it would suggest that viral factors are not working alone.
    There would be an environmental component too!

    Does anyone want to look to see what it might be?

  36. >Great post as usual.
    One thing though. Trine has shown us on several occasions that she really does not understand the complicated nature of ME/CFS and the Retrovirus family, etc. That's dangerous for a journalist to write about something so complicated and the public reads and believes. I do think Trine needs to stick to Food and just stay away from science. Surely the Trib must have or could hire someone with a REAL background in medicine/science.

    Aside from my irritation with Trine's "reporting", everything else written is great! Thank you so much for taking the time and energy to blog for us sick folks!

  37. >I do agree there are overlapping subtypes and that's what makes it so complicated; teasing out answers for even some subtypes is extremely challenging.

  38. >Once the new syndrome of "CFS" was coined, rather than concentrate on the original evidence and reasons the syndome was created, the loose definition, by itself, BECAME the disease, and left everyone wondering if the prototypes for CFS even had their own syndrome.
    CFS became such a wastebasket for "anything and everything" that this investigative-tool became completely disconnected from its roots.

    It seems pretty silly to have the original group of patients be placed in speculative jeopardy of being sidelined as a remote "subset" or possibly even REMOVED entirely from a syndrome coined to address their very illness, but this is what happened.
    It seems even sillier to try and pluck the original-entity back out of a wastebasket in which it never should have been thrown. Especially when we know right where to find it.

    The best way I see to clarify the situation is to tell you what happened in RAD, "Raggedy Ann Disease", the original illness that I was in a good position to observe, and the one CFS was directly based on.

    Yes, the strange flu-like illness went through and did what it did.
    But this strange flu "did it" the MOST in people who were enduring even seemingly exposure to certain buildings and places which had a peculiar and unfamiliar "mold effect".

    The sum-total of this collision was strongly associated with the "Raggedy Ann Disease"


    Improvement of attention span and reaction time with hyperbaric oxygen treatment in patients with toxic injury due to mold exposure.

    Toxic chemical exposure such as mold and mycotoxins can significantly affect brain function in children and adults. Mycotoxins are secondary metabolites of fungi, usually molds, which can cause injury to animals or humans. It has been shown that these effects may last for years after toxic exposure has ceased.
    Exposure to toxins, including mold, can lead to significant long-lasting impairment of brain function, often inducing temporary to permanent disability. Typical complaints include impairment of short-term memory, intermittent disorientation, disturbed balance and coordination, inability to multi-task, and impairment of attention span and reaction time. Sick building syndrome (SBS) may be caused by exposure to mold and mold toxins. Symptoms of SBS, a widely described but poorly understood constellation of symptoms that has been observed in certain persons in “sick” buildings, include headaches, poor concentration, fatigue, memory loss, dry skin, and itchy eyes. This is seen in adults as well as young people.



  39. >Ground Zero for CFS: the Raggedy Ann Disease.

    Clin Infect Dis. 1994 Jan;18 Suppl 1:S43-8.
    Concurrent sick building syndrome and chronic fatigue syndrome: epidemic neuromyasthenia revisited.
    Chester AC, Levine PH.
    Georgetown University Medical Center, Washington, D.C.
    Sick building syndrome (SBS) is usually characterized by upper respiratory complaints, headache, and mild fatigue. Chronic fatigue syndrome (CFS) is an illness with defined criteria including extreme fatigue, sore throat, headache, and neurological symptoms. We investigated three apparent outbreaks of SBS and observed another more serious illness (or illnesses), characterized predominantly by severe fatigue, that was noted by 9 (90%) of the 10 teachers who frequently used a single conference room at a high school in Truckee, California; 5 (23%) of the 22 responding teachers in the J wing of a high school in Elk Grove, California; and 9 (10%) of the 93 responding workers from an office building in Washington, D.C. In those individuals with severe fatigue, symptoms of mucous membrane irritation that are characteristic of SBS were noted but also noted were neurological complaints not typical of SBS but quite characteristic of CFS. We conclude that CFS is often associated with SBS.
    PMID: 8148452 [PubMed – indexed for MEDLINE]

  40. >Maybe the subgroups or subtypes we find in people diagnosed with ME has to do with progression of the disease and/or coinfections? There are many factors involved with quick vs. slow onset that could also be explained with genetic susceptibility and environmental triggers (hormones, infections, traumatic event, chemical exposure, overtraining, vaccination).

  41. >It's a good thing that some researchers are taking an interest in all these various contributions to illness which may be involved with people diagnosed with ME.
    It does, however, make for a very complicated puzzle, as more people, more theories, and more components keep being added.

    I have a very narrow focus, which makes my particular investigation much easier.
    My interest is only the actual factors I observed to be associated with the Raggedy Ann Disease at North Lake Tahoe in 1985.

  42. >The latest contamination theory that of the derivation of this virus from a single cell line created in 1992 is so preposterous (If it were not so sad it would be hysterically funny) I cannot even imagine how Stoye and Coffin can think anyone can be so naive as to believe this garbage… I wish many, many scientists get serious about investigating XMRV, MRV's and everything that has to do with CFS.


  43. >To ErikMoldWarrior:
    Are you aware of anyone who did not live in the Tahoe area but who is nonetheless a member of the Tahoe cohort? I spent a few days in the area during the outbreak but was unaware of the situation until last year. I've been progressively more ill since that time.

  44. >Bravada, yes I do.
    People who very much appear to have just passed through, and had the same thing happen to them.

    What else could it possibly be, than some kind of bacteria or virus?
    This makes the association purely infectious.
    It has to be!

    Or…. does it?
    Can we be so absolutely certain that we never bother to look at any other possibility?
    Or even to consider that other possibilities might exist?

    I don't think so!

  45. >Categorization is a challenge.

    Groups overlap. Relevant characteristics are not always immediately obvious. Specific cases have anomalies.

    Finding a small group where the members look really similar is the easiest way to start. Once you figure out the core characteristics of that group, you can broaden out and see how other cases relate.

    All the people in the Tahoe cohort got super sick with a bizarre form of this illness at the same time, in the same relatively isolated place, with a disease that looked remarkably consistent across cases.

    Understanding the illness dynamic for these people is a first step. Following that, we can look at other people and figure out why they’re different.

    But we’ve got to start somewhere. Otherwise it’s just a mess.

    It’s not a surprise that everyone in the Tahoe cohort came up positive for the same retrovirus. This was not a “CFS is everything and anything” group. It was an extremely discrete, carefully screened subgroup.

    The studies that showed no association with the retrovirus did use the “everything and anything” definition. Maybe there was no one at all who would inherently fit into the Tahoe subgroup in those studies! We just don’t know.

    So, what I’d like to see a comparison (done by a good lab) of the Tahoe cohort vs. (say) the CDC Wichita CFS cohort vs. truly healthy controls (not just random blood donors).

    If the Tahoe cohort all came up positive (again) and the other groups all came up negative…..then a good question would be:

    What makes the Tahoe group different than the Wichita one? How come the Tahoe group all had XMRV active, whereas nobody in the Wichita sample did?

    Figure out that and maybe we’ll finally be getting somewhere.

    Best, Lisa Petrison

  46. >As related in Dr Shoemakers books Mold-Warriors and Surviving-Mold, after agreeing to participate in the Holmes et al CFS definition study group, I told Dr Cheney,
    "Until you figure out what the cause of CFS is, I'm going to stay away from the mold".
    I wasn't trying to propose that mold causes CFS, just that it was One Helluva Clue.

    Is there any relation between moldy building exposure and chronic fatigue syndrome?

    Journal: Med Hypotheses. 2006 Mar 7; [Authors: Shahriar Gharibzadeh and Sayed Shahabuddin Hoseini

    Affiliations: Neuromuscular Systems Laboratory, Faculty of Biomedical
    Engineering, Amirkabir University of Technology, Somayyeh, Hafez,
    15875-4413, Iran, and Faculty of Medicine, Tehran University of Medical
    Sciences, Enghelab Street, Tehran, Iran

    Available online 9 March 2006.

    It is reported that workers who are employed in moldy buildings, show different symptoms like respiratory difficulties, fatigue, fever and
    headache. Hirvonen et al. have reported elevated cytokines (interleukin-1, interleukin-6 and tumor necrosis factor a) and nitric oxide (NO) levels in nasal lavage of workers in exposure to moldy buildings. Due to laboratory tests, Aspergillus fumigatus, Trichoderma, Actinomycetes, etc. were detected in indoor air [1].

    On the other hand, chronic fatigue syndrome (CFS) is the current name for a disorder characterized by debilitating fatigue and several associated complaints including headache, sleep disorder, low grade fever and concentration difficulties [2]. It is mentioned that post-infectious, immunological, and psychological factors are involved in the syndrome

    Researches in patients with CFS have shown a significant elevation in serum levels of interleukin-1 and tumor necrosis factors a and ß [4]. which
    can result in the appearance of CFS symptoms. Small amounts of circulating cytokines can enter the cerebrospinal fluid and the parenchyma of the brain
    [5]. Cytokines administered systemically or directly into the
    central nervous system have shown to alter the activity of hypothalamus, hippocampus, and prefrontal cortex [6].

    In addition, elevated nitric oxide levels have been documented in CFS patients. It is hypothesized that NO plays a significant role in pain sensitization, which is seen in these patients [7]. Moreover, excessive NO production is an important factor in pulmonary manifestations including vasodilation, edema and cytotoxicity [1].

    It seems from the abovementioned points that, in accordance with the post-infectious theory of CFS, the exposure to moldy conditions may be a trigger for the onset of CFS. Moreover, the working of persons with CFS in moldy conditions may aggravate their symptoms including pulmonary pain and psychoneurological manifestations. Surely, our hypothesis needs to
    be validated by experimental evaluation.

    I corresponded with one of the authors when this abstract was published, and told him it was incredible to see there was a better understanding of the Tahoe situation to be found in Iran, than I could find just across the street.
    Surely this hypothesis needs to be validated by experimental evaluation!

  47. >But only if people want to find out by experimentation and research.

    There's always the other option.

    "Learn it the hard way"

  48. >I don't take vitamins, supplements, painkillers or drugs of any kind.

    Except a draught from a jug of Captain Morgan.

    I regret all the money I spent on supplements that didn't do squat.
    If I had known then what I know now, things would have been so much different.
    What I'm doing, I would have done MORE and SOONER.

  49. >Hey!

    Are researchers looking for clues?
    Or are they looking to not to find any that doesn't confirm their preconcepions?

    (How's that for a double negative?)

    One thing I know for sure.
    Not one of them tried to help me with this "other" phenomenon.

    Why? Because it's not the one they want to play with.

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