Consensus

A consensus means that everyone agrees to say collectively what no one believes individually.
~ Abba Eban

At the end of the comments from the last blog, the conversation turned to the new International Consensus Criteria for ME: Myalgic Encephalomyelitis: International Consensus Criteria. Carruthers et al. I’m glad that this is becoming a place where we can consider the issues together. My personal reaction to the paper was mixed. While I found it immediately useful for sending to uninformed doctors who might recognize their patient in it, it excludes a lot of patients who will therefore be hurt by it, if anyone pays any attention to it, which they probably won’t. In particular, it excludes a large subset of patients who had gradual onset or recovered to a great extent following a first crash. I didn’t meet criteria for the first decade of my illness. I certainly do now, but if this had been the case definition, the same things would still have happened to me with respect to disability coverage, disbelief and misinformed treatment by physicians.

For the first ten years of my illness, I had no PEM. I could bench press over a hundred pounds, rode on the back of a tandem for an hour or more a couple of times a week, played tennis, could scuba dive and ski. But if I worked a full, normally intense day, I’d get a headache and a hypertensive crisis (up to 220/140). So I was forced to circumscribe my life in ways that didn’t trigger it. I worked in a clinic attached to my home to keep the day short and reduce stress. Ken Wilber’s functional bubble: link to letter and check out his very cool website www.kenwilber.com. I had episodes of severe anxiety, autonomic dysfunction (cyclic vomiting, not OI or POTS) and bizarre sensory symptoms (dysgeusia, globus hystericus, hyperesthesia, hypoesthesia in a dermatomal distribution). Also flu-like malaise. I didn’t meet the new ICC criteria during any of that time. I now have or have had literally everything on the list, except, for some peculiar reason, I’m still sharp, never “foggy”, and my memory is pretty good, as good as it ever was anyway. I wonder why I’m different in that respect, when otherwise I’m classic, and the only thing I can come up with is lots and lots of exposure to high dose oxygen.

The problem with this newest case definition is that it allows minimization of the huge number of affected people by looking only at the tip of the iceberg. In the past, I haven’t been too interested in what they call it; it seemed like little more than semantics to me. I thought that case definitions would surely take a backseat to viral load measures. But it hasn’t happened yet. When I read the Science paper, one of my first thoughts was, thank God, my daughter will be able to walk into any doctor’s office and say, I have XMRV, without being subjected to ridicule, but that hasn’t happened yet either. We are forced back to case definitions, the search for markers to prove a biological basis and fiddling around the edges with respect to treatment. Now in practice again, I can’t bring myself to use CFS as a diagnosis, because it’s a perjorative and will be used to deny my patients treatment. There is no code for ME, but all the components of the illness can be coded separately.

Ali went out with us for lunch yesterday for the first time since the fall, and still feels well after. She seems ready to cross that line again. She said that the things we’ve done with her have been real quality of life improvements, especially if you use hours of suffering as a meter. Glycemic control, hormone balancing, recently high dose oxygen and Meyer’s cocktail plus glutathione infusions, are the things she listed. There is no way to know how much antiretrovirals may be contributing at this point. We’ve considered going off, especially in light of the money involved, but have decided not to rock the boat. In my case, I think it’s worth taking for prophylaxis now that I’m exposed to patients, and they to me.  The trend in HIV is moving towards the use of antiretrovirals for prophylaxis and earlier treatment of infected individuals to prevent spread. The findings of Zhang et al that XMLV’s are highly infectious in a laboratory setting, as well as the isolation of XMRV from tracheal secretions, Xenotropic Murine Leukemia Virus–related Gammaretrovirus in Respiratory Tract. Fischer, suggest that HGRV’s may be spread by casual contact. The cluster outbreaks support this as well. Since many spouses and children are clinically well, host susceptibility is a bigger factor than presence of virus. Like HTLV, most infected people don’t become ill. 

Careful history taking suggests  that HGRV’s can turn on and off, in a minor way, for a very long time without becoming a big problem. My history suggests this, with intermittent symptoms that went back to childhood, yet I considered myself healthy and had no medical record at all, except for pregnancies, until I became ill at 41. My husband has lots of symptoms, but doesn’t have ME or CFS by anyone’s criteria. I was intrigued by this paper about nail changes in CFS: Secondary structural changes of proteins in fingernails of chronic fatigue syndrome patients from Fourier-transform infrared spectra. Sakudo. I had nail changes that started maybe a decade before I knew I was sick, so over 25 years ago. I wore acrylic nails to hide it for a few years. I couldn’t find an explanation, except a little bit in Chinese medicine which is concerned with such things, but knew it meant that something wasn’t quite right. I have no lunulas now. Nail beds are short, not wide like clubbing. Nail plates curl at the end. I have Raynaud’s, subclinical for years, occasionally visible in the last few years. I think that the changes are probably due to cellular hypoxia at the periphery exacerbated by vascular instability.

There is one anecdotal report of a young patient who improved dramatically on AZT/raltegravir, stopped the drugs after 6 months and has maintained the improvement. Our assumption that the drugs would need to be taken forever, because that’s how we treat HIV, may be completely erroneous. After following a small group of patients informally for a year and a half, my impression remains that the drugs move the illness, but we don’t know how to use them. Dr. Snyderman’s data is certainly compelling, posted last April here in Another Perspective. HIV doses may be wrong for us. There is one report of someone who has improved on very low dose AZT alone. CFS doctors have long known, start low, go slow, but because that is a no no for HIV, there is no experience so far. AZT has been used for HTLV:

The last two papers suggest that low dose AZT may be useful. AZT works for Adult T-cell leukemia/lymphoma (ATLL), a lymphoproliferative malignancy that develops in a subset of HTLV–infected individuals after a long period of latency. Mahieux suggests that in this setting, it works not through antiviral effect, but through an anti-proliferative effect, requiring long term treatment to activate tumor suppressor genes. An explanation is offered for why some patients with ATLL respond to AZT and some don’t, response to treatment being dependent upon an intact tumor suppressor gene. AZT shortens telomeres in fresh ATLL cells, eventually inducing senescence and death of infected cells. Patients with mutated tumor suppressor genes don’t respond. The relative contribution of proliferation versus viral replication likely varies between infected people, possibly determining in which direction the disease progresses, ATLL or HAM/TSP, cancer vs neurodegenerative outcome.

In the meantime, Simon Wessley wonders why people are angry with him when he says that we’d rather have an incurable retrovirus than admit that we are mentally ill: BBC news (audio). Dr. Wessely, it’s because a psychiatrist without compassion is a terrifying thing indeed. Meaningful psychiatric care, safe rehab, disability coverage, the simplest supportive interventions have been denied us for decades, but we’re supposed to thank Dr. Wessely for taking an interest in us. Go push your worthless theories in some other arena, or suffer the reaction. We’ve had enough of your “help”. Enough of your blame. When I first became ill, any real doctor could tell that there was nothing wrong with me. And I was a real doctor… The nephrologist who fancied himself an astute diagnostician was sure I had a pheochromocytoma or carcinoid tumor, but after he did all his fancy tests and couldn’t find anything, he concluded, “You’ve lost your nerve.” My hypertensive crises were diagnosed as “white coat hypertension”. How right he was, though my fear of white coats certainly turned out to be justified.

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66 thoughts on “Consensus

  1. >Where does it "excludes a large subset of patients who had gradual onset"?

    In the document it is clearly stated:

    "C. Immune Impairments
    Most patients have an acute infectious onset with flu-like and/or respiratory symptoms."
    Most, not all.

    "2. Optional Considerations
    Classifying patients by subgroups to enable comparison of patients within the diagnosis of ME may be helpful in some studies.
    a. Onset: acute infectious or gradual"

    Isn't good to classify subgroups? Isn't the type of onset a prime candidate for subgrouping?

  2. >If I,m honest I think this document falls far short of what is needed

    we need to tell drs what tests to run to diagnose a neuroinflammatory disease .The IMEA have published a shortlist. We can worry about labels later for now we need to set objective criteria of inclusion.Biomarkers which can identify a neuroinflammatory disease and differentiate sufferers of such a disease from sufferers of depression exist a plenty.models of causation also exist which can be turned into testible hypotheses.Once the cause is found treatments can be developed or existing drugs used for different conditions adapted.

  3. >Thanks for a great post again, Jamie, chock full of useful info.

    @ gerwyn, it's my understanding that the next document coming from the authors of the ICC is a testing and treatment recommendation. I think the definition was the first step.

  4. >I am so confused…this PDF seems to suggest we can easily test for this enzyme to do with RNASe and describes symptoms which may fit and the timescales etc, ,my illness has followed a similar symptom path…but how is he curing it? how is he tested for the enzyme?? I really dont understand what he is saying!
    http://www.kenwilber.com/Writings/PDF/hi_folks.pdf

  5. >Tony,

    I wasn't clear. The ICC allows for gradual onset, but many gradual onset patients don't meet criteria for many years. Therefore the document excludes them. Leaves them high and dry. These patients also need care. If treated, they might never meet criteria.

    Jamie

  6. >it will be interesting to see how this criteria is operationalized, how sensitive and specific it is. I am sure Dr Lenny Jason is working on it.

    i agree with Leela that this is a first step. We need to move away from Fukuda, refine CCC, and move forward.

    What I see is these authors moved on without the CDC, great thing to see since they appeared not interested in moving their viewpoint.

    What I wonder, Jamie, is did you have a presentation that was closer to Lyme disease, which eventually "transformed" into ME? (who knows because I am not sure Lyme has much consensus either)

    So much unknown, a bankrupt government, some terrorist psychiatrists…. I bank on our good doctors and researchers to keep digging. The International
    Consensus is moving in the right direction.

  7. >thanks jamie for the chock-full of info post.

    Can u tell us a bit more about what this means:

    Glycemic control, hormone balancing

    thanks.

  8. >Thanks Jamie, for addressing the issue of less severe cases of ME being left "high and dry" by the ICC. That definitely needs attention.

    For many years I was a moderately to just barely functional case myself, with relapses brought on by trying to achieve NORMAL too quickly. Had I known how sick I could potentially become, I would have been much more careful about how I expended my energy. And yes, it would have also helped if every white coat I consulted had noticed I was ill in the first place.

  9. >Biomarkers would likely solve a lot of criteria issues. Then one needs to convince the governments that the psych lobby is abusing their power and ask them to fund much needed research for biomarkers.

    What comes to my mind is, is Gulf War Illness ME? Is Lyme ME? Or is all that XAND?

    it is interesting to note that Dr Mikovits is part ofthe co-authors. Dr Chia, Dr Klimas, Dr De Merleir, etc lots of well seasoned physicians who see patients on a day to day basis.

  10. >>it is interesting to note that Dr Mikovits is part ofthe co-authors. Dr Chia, Dr Klimas, Dr De Merleir, etc lots of well seasoned physicians who see patients on a day to day basis.

    Klimas and De Meirleir covertly work to cover up CFIDS for the government and can't be trusted. Same for many others. Anybody associated with them should be closely scrutinized.

    virtually all patients are just too politically retarded and dysdunctionally to understand what is going on

  11. >> The trend in HIV is moving towards the use of antiretrovirals for prophylaxis and earlier treatment of infected individuals to prevent spread.

    The trend in HIV is to maintain the preposterous lies surrounding AIDS and neglect talking about the thousands of medical researchers and institutions who aid and abet it.

    AIDS = HIV + cofactor

    HIV only people will be generally healthy

    and what about all those HIV negative people who died from AIDS also – they just swept them under the rug.

    >The last two papers suggest that low dose AZT may be useful.

    a drug that helped kill the healthy HIV only people

    yeah, let's treat CFIDS patients with something that destroys their immune system

    The Hepatitis B vaccine was intentionally tainted like so many other vaccines by the world government because they have depopulation agendas.

    the covert world government was behind the AIDS deaths just like they were behind the explosion of chronic diseases and cancers. most of the population is too retarded to connect on this.

    very few people take the time to inform themselves

    most cfids doctors or researchers work for intel agencies and are covertly there to cover up the disease.

    inspite of a long history of genocide by governments – most people hum the idiotic mantra and say – i just can't believe the powers that be would kill or disable me. – i guess it helps them sleep at night.

    most consensus is covertly orchestrated by the powers that be. find a consensus and you'll usually find a grand lie

    most people with cfids are no different than the general population. at the end of the day, their indifferent to most human life and truth around them or maintain a low awareness of the world around them

  12. >http://www.integralworld.net/redd.html

    Ken Wilber's statement about his health

    hi folks,
    several people have asked about my health, so let me give a brief rundown on the situation.
    —–

    in REDD, the mechanism that produces RNase is damaged by any number of causes, the most notable being environmental toxins. in 1985, in incline village, north lake tahoe, there was what has now become a very famous outbreak of REDD, where over 200 people came down with it
    (I was one of the lucky 200. treya and i were in tahoe recovering from her latest round of intensive chemotherapy). a widely circulated hypothesis is that this outbreak was triggered by a local toluene spill, but nobody really knows. the disease itself, however, is not human-to-human transmissible.

    ————————————

    Nobody knows, mainly because nobody looked.

    I guess Ken didn't see what happened in Dr Petersons office to his staff.
    That was sufficent to convince Dr Peterson that it WAS acting person to person infectious.
    Why sometimes and not others?
    That is the mystery.
    -EriKMW
    (One of the unlucky 160, and yes, Ken DOES have a very cool website)

  13. >Hi Jamie!

    All the symptoms you describe for the early years of your illness sound exactly like migraine to me: the onset after a hard day, the headache, vomiting, high blood pressure, flu-like feeling, weird sensory experiences and anxiety. All of those are common migraine symptoms. Is it possible that your (ME) illness had a later onset than you believe, and that your earlier illness was some version of migraine (which can follow many different patterns)?

    In my early 40s, I went through a terrible months-long spell of daily migraine which just about ruined my life. I was lucky, because hormones were a magical "cure" for me. A few years later, I developed sudden-onset ME, with PEM being the most debilitating issue (and I have been largely disabled ever since). I don't really believe my two experiences are connected, mainly because migraine is so common. A quite high percentage of women have migraine at some point in their lives. Unless I had strong evidence for a connection between the two, I would have to assume they were separate illnesses.

    You are a doctor, so no doubt you have a good reason for your conclusion that you had M.E. all along. I'm just curious what your reasoning is.

    All the best,

    Agatha

  14. >Jamie, I think you are right to consider the fact that HGRV'S could be transmissable via respiratory tract secretions etc. I find this topic very overlooked sometimes and yet it ties in well with the cluster outbreaks of this illness. Also, most sexual partners of people with ME do not have ME themselves and I think that the evidence speaks for itself there – that HGRV'S are infact quite a different ball game to HIV in some respects and we would be foolish to assume that transmission and treatments for HIV would be the same for HGRV'S.
    I think that HGRV'S came about in the lab and that people became infected via vaccination originally and then the HGRV'S spread throughout the population including VIA RESPIRATORY TRACT SECRETIONS (less so via sexual intercourse). More research is needed in this particular area. Although I am sure there are many parallels between HIV and HGRV'S, I am sure that there are many differences and I for one, will not be taking antiretrovirals designed to treat HIV because quite simply, I don't have HIV – I have an HGRV.

  15. >Dr J, could I ask your opinion on an aspect of onset that also doesn't fit with the new criteria?

    My own onset occurred 11 years after a major viral episode which was diagnosed at the time as vestibular neuronitis. It took over a year to get well, and for about 5 years 'well' was relative. But, eventually, I did get back to normal, which included a lot of backpacking and a big career.

    Hain in this article cites two references suggesting that the virus responsible for vestibular neuronitis, or neuritis is likely to be a human herpes virus: http://www.dizziness-and-balance.com/disorders/unilat/vneurit.html

    When I then got ME (diagnosed as CFS – all we get in the UK) following relatively light cancer treatment, it felt as though the vestibular virus was attacking me all over again, only this time balance was not the main symptom: flu like symptoms predominated and more symptoms (debilitating headaches, brain fog) were added. But, I always wondered whether that vestibular virus was the root cause.

    Meanwhile, my friend who runs the fibroduck.com and fibroduck Facebook sites, which support people with FMS and ME/CFS, asked a question on their FB page: what do you think triggered your ME? Over 60 people responded. What struck me was how many of them said something along the lines of: 'I had this big virus that went away, but when I had a trauma some years later (sickness, injury, accident, bad childbirth etc) it was as though the virus started all over again, and that's when I got ME'.

    People were consciously linking long-gone viral attacks with the onset of their ME/CFS.

    Do you think there is – or are you seeing in clinic – a significant subset of patients for whom the onset of ME/CFS occurs many years after a viral attack that they had got completely well from?

    I'd be interested in your view as to whether this is a pattern the criteria panel could or should have recognised, or whether it's relatively rare in the ME world.

  16. >you could describe HGRVs as slow transforming retroviruses.An initial infection could take many years to produce symptoms and to produce multisystemic disease.The precise early symptoms are probably related to the early sites of replication and may well be momosystemic or involve a few systems before reaching titres needed to engender multisystemic disease. The speed of onset is rather a silly and entirely arbirary parameter.A major trigger of HGRV replication for example would be mono as the immune system is dysregulated for such a long time.That does not mean that mono is a cause.Other virus infections could also trigger HGRV replication .Equally a HGRV infection could reactivate hhv6 or EBV and mke it look as though those viruses are a cause

  17. >"The perfect is the enemy of the good." ~Voltaire
    I think this represents a great effort, and I think that these people absolutely believe in what they put forth. It was a bold and crucial step.
    It is hard to see people worrying about who may be left out? ALL ME patients have been left out in the meaningful sense with a CFS diagnosis.

  18. >"I wasn't clear. The ICC allows for gradual onset, but many gradual onset patients don't meet criteria for many years. Therefore the document excludes them. Leaves them high and dry. These patients also need care. If treated, they might never meet criteria."

    Are you saying that treatment can prevent the illness from progressing? What is your theory about what will keep that from happening?

  19. >" The ICC allows for gradual onset, but many gradual onset patients don't meet criteria for many years. Therefore the document excludes them. Leaves them high and dry. These patients also need care. If treated, they might never meet criteria."

    Yeah, I know that problem, as I'm gradual onset myself. For years I thought I had "motivational" problems – haha. But how can you put a hotchpotch of "subclinical" problems into a definition? Well, maybe the severity should be more considered. Until there is an definitive test available (preferably with a known cause), there isn't much that can be changed, I'm afraid. Until we know the cause, any grouping can and will be wrong.

    The definition for ME comes from the Royal Free outbreak (and all the others that Ramsay desribed). Maybe it is a fiction that this is a distinct different disease than CFS. Maybe it is wrong not to consider the "fringe" cases. I guess we need a clinical definition that doesn't misses cases (yet dosn't include classical major depression, e.g., or other diseases) and we need a "stricter" research definition that makes sure that all researchers research the same disease (if it is actually only one disease).

    (And I don't want to open this pandoras box in this post – and while I think it is wonderful work the WPI does with regards to ME/CFS – but I don't think XMRV is this definitve test. I hold out my verdict till the Lipkin results are there. Untill then we still need to define this disease(s) by its symptoms).

  20. >One more thing: Doctors are reluctant to make the CFS diagnosis even in clear cases, how is that going to change when the criteria is being "watered down"? Yes, even the "fringe" cases have seriously impaired quality of life and we need to find them and help them. But if the doctors think the definition is a joke, we all suffer.

    My definition of the disease would be presence of the symptoms PLUS (clear/considerable) impairment of life. Maybe the definition should offer a tentative diagnosis if the symptoms are present but cause only a slight impairment.

    The biggest problem is that people with "early" ME/CFS are told to do sports by their doctors, and if they do it and go back to their doctors and tell them it doesn't work, their doctors don't believe them.

  21. >@ Anon July 31, 7:34 PM

    Unfortunately, I believe much of what you are saying. When I stopped reading/watching corporate media (propaganda), which is most of what's offered in the US, I discovered how ignorant I was as to what was going on in the world, esp. what's being perpetrated by the US government so that corporations can make record profits.

    However, I believe the authors of the ICC
    are beyond reproach. They have bent over backwards to provide patients and advocates with a useful tool to take to their physicians. This document is a work in progress, but they didn't wait until it was a final draft. Thanks to them, it's going to be used now and will begin to help so many. Bravo!

  22. >"For the first ten years of my illness, I had no PEM. I could bench press over a hundred pounds, rode on the back of a tandem for an hour or more a couple of times a week, played tennis, could scuba dive and ski. But if I worked a full, normally intense day, I'd get a headache and a hypertensive crisis (up to 220/140)."

    With all due sincere respect Jamie, you're right to be concerned: that "illness" is not even remotely CFS or ME.

  23. >Caroline,
    I had severe symptoms, not malaise, after mental exertion, but no problem with physical exertion. I had clusters of neurological symptoms, all sensory and autonomic. I had hormone abnormalities and symptoms of vascular spasm, not just migraine headaches, but cyclic vomiting without headache, chest pain and palpitations, subclinical Raynaud's (not all at the same time). No obvious immune abnormalities, since I was hyperimmune, never caught anything. My current illness is a clear progression from where I was then. After each relapse, it looked more like ME, and I clearly meet criteria now. I mentioned the nail changes because they started years before I had any symptoms at all. I think this is a very important point. The earlier the illness is recognized, the better chance of impacting it positively.
    Jamie

  24. >"The earlier the illness is recognized, the better chance of impacting it positively."

    Would you please explain this? If you could go back in time, what would you have done differently for yourself and your daughter that would have made it less likely that your illness would have progressed?

  25. >"No obvious immune abnormalities, since I was hyperimmune, never caught anything."

    That's not normal, that's a sign of immune dysfunction, a classic sign of CFS/ME (sorry Jill, but that's what I'm calling it). I would guess that 80-90% of us haven't gotten a decent cold or real fever since we became ill.

  26. >Or as we called it for awhile, CFIDS. A better name would be CIDS, for Chronic Immune Dysfunction Syndrome.

  27. >Anonymous at 9:03: Do you think it is really 80-90%? That is so fascinating! I think one of the most striking features of my illness is that, although I developed ME (love the "new" name) when I had a 3-year-old and a 7-year-old bringing home many colds and flus, I haven't had a proper cold or other illness in the 7 years since my onset. I've been plenty sick with ME, but whenever I "catch cold," I barely sniff for a day and then it's suddenly gone, and I seem to be immune to the stomach bugs, etc., that the rest of my family contracts. Before ME, I had a pretty normal immune system (a few colds and bugs per year), but it's really different (hyperactive?) now. I guess I would see it as a "silver lining," if the disease hadn't been so brutal as a whole. I would probably get excited now if I had an actual cold!

  28. >Anon 7:00,
    Your question deserves more than a comment. But the short answer is yes, I suspect early diagnosis and intervention may impact outcome. Anti-inflammatory strategies may be preventive, methylation to encourage proviral latency, early treatment of opportunistic infections, possibly early use of arv's, high dose oxygen acutely and during convalescence. And yes, I would have done things completely differently knowing what I know now.

    Anon 9:03,
    No immune abnormalities of which I was aware.

    Anon 9:05,
    Many of us have predominantly neurological dysfunction.

    To clarify, I don't disagree with any of the inclusion criteria, but I don't think that patients should be excluded because they don't have PEM yet, or if it has resolved after an initial crash. The criteria should be inclusionary, not exclusionary. It is essential that the medical profession begin to recognize preclinical illness.

    Jamie

  29. >The first 4-5 yrs I had frequent colds and constantly ran a low grade fever. Spleen was swollen a great deal during this time as well.

    The last 20+ yrs I haven't had a cold or stomach flu and run sub-clinical temps. Occassionally get respiratory flu.

  30. >One comment got eaten up (spam filter?), so I repost it.

    " The ICC allows for gradual onset, but many gradual onset patients don't meet criteria for many years. Therefore the document excludes them. Leaves them high and dry. These patients also need care. If treated, they might never meet criteria."

    Yeah, I know that problem, as I'm gradual onset myself. For years I thought I had "motivational" problems – haha. But how can you put a hotchpotch of "subclinical" problems into a definition? Well, maybe the severity should be more considered. Until there is an definitive test available (preferably with a known cause), there isn't much that can be changed, I'm afraid. Until we know the cause, any grouping can and will be wrong.

    The definition for ME comes from the Royal Free outbreak (and all the others that Ramsay desribed). Maybe it is a fiction that this is a distinct different disease than CFS. Maybe it is wrong not to consider the "fringe" cases. I guess we need a clinical definition that doesn't misses cases (yet dosn't include classical major depression, e.g., or other diseases) and we need a "stricter" research definition that makes sure that all researchers research the same disease (if it is actually only one disease).

  31. >Since developing ME I had never caught a cold or the flu, even though I too have children in the house who are often coming home from school with various bugs etc. However that has changed recently since starting on acyclovir. I have had definite improvement on acyclovir but have also had 2 colds since beginning it about 3 months ago. Wasn't sure at first whether this was a good or bad sign but it was a definite change. I perhaps think that my immune system has 'calmed down' a bit since beginning this treatment and it has allowed me to catch the odd snivel etc – more like a healthy person would because on reflection it wasn't normal to go on never catching anything – it was actually a bit of a worrying sign that my immune system was not functioning as it should be.

  32. >I live in the UK. My doctor's practice wouldn't even put up a poster (very professionally produced) advertising the helpline number of our mildest ME charity, despite there being posters for nail-clipping services, dog walking services and other illness support groups. The reluctant disdain with which the practice manager took my poster (before clearly disposing of it) has stayed with me, sowing a seed of fear and despair in my heart. If I can't get my doctor's to simply put up an innocuous poster, how can I ever get any help from them?

    So when I see the International Consensus Criteria for ME – compiled by an international body of experts, with unimpeachable medical and scientific credentials and extensive experience, who have given their time and knowledge for free and without any sponsorship, I know I have something I can hold in my hand and give to my doctor and say 'You cannot deny the credibility of this. You cannot dismiss it, as much as you have been trained or are inclined to do so. This trumps the lie of the self-serving psychiatrists'. The doctor may ignore me for a while, but now, in my heart, I no longer have despair. I have strength, that I am supported by the work of these people.

    It is good to know that it can be improved, and to cite where the weaknesses may be and who might be affected by that. But as a document and as a statement, I am deeply deeply grateful for those who made it exist.

    Belle

  33. >"Anti-inflammatory strategies may be preventive, methylation to encourage proviral latency, early treatment of opportunistic infections, possibly early use of arv's, high dose oxygen acutely and during convalescence. "

    What sort of anti-inflammatory strategies? Curcumin?

    Thanks for sharing your treatment thoughts. It's nice to have an ME doctor who will share them openly.

  34. >I am in the UK too Belle. Have to go to Dr.Myhill for treatment privately – her testing and my shocking results, made my GP acknowledge my illness and he now believes it is biological. However, my friend with ME had the same testing done and also had results indicating biological illness but her GP didn't take as much notice of them. In any case, check out Dr.Myhill's website if you haven't already – lots of useful info on it for free. Sorry for hijacking this thread to respond but I really feel for you Belle. It is tough here in the UK.

  35. >@ ihave3kinds

    Thank you very much for that information – I will definitely follow it up. And for your kind thoughts too, which are lovely.

    Belle

  36. >Jamie–

    "It is essential that the medical profession begin to recognize preclinical illness." I echo this sentiment as well. There are so many of us who would not have slid down the slippery slope into full blown ME, if someone had noticed we were teetering on the brink of it.

    In regard to intervention, I have a question about the HIGH DOSE OXYGEN use. By this do you mean hyperbaric oxygen? or something else? and how exactly is it used?

    Thanks for your great blog.

  37. >Jaime,

    I, too, am interested in high dose oxygen. Would like to be able to pass along the information to my doc who's never had a patient on oxygen.

    Please forgive my asking if you've covered this prior. Am fairly new to this site.

  38. >Dr. Jamie…Dr. Chia is getting some very interesting results with Epivir/Lamivudine/3TC, combined with an immune modulator such as Equilibrant. That is my protocol…with the addition of high dose Acyclovir. I agree with your statement that we dont entirely know how to use the drugs in questions. Viral break-through can be a problem for some people with Epivir (though the addition of an immune modulator can jump-start the ARV again and suppress the replication). And sustaining the positive results (long term) can also be a challenge. But Epivir is very well tolerated, to my understanding. Even without the addition of Tenofovir to this combination (which HAS been done in the past)…this FEELS like it might be a good prototcol. I'm satisfied with it, as is my newly diagnosed husband – and the improvements to my brain function have been nothing short of remarkable. Once again…a great blog..thanks so much! Best wishes to you and Ali. j & j nance.

  39. >The results of the Lipkin study will be negative

    The cytokine profiles produced when patients enrolled into studies by Dr Bateman and Dr Klimas are not consistent with a retroviral infection.They are consistent with people who have had prolonged experience of elevated stress hormones or epstein barr infection.Thus as they combined with susan Levine are going to be supplying the vast bulk of the patients it is unlikely that many patients in the study will have a neuroimmune illness.Why were Dr Bells and dr Chaneys patients not included?

  40. >Gerwyn,

    I find it improbable that NONE of the patients in the study will have true ME. I have read a lot of what is written by Dr. Bateman and Dr. Klimas, and I feel confident that at least a substantial subset of their patients have ME. Surely plenty of people ill with ME will have sought them out and ended up as their patients. The study, as I understand it, is designed so that it isn't necessary for all or most of the patients to show positive for XMRV in order for there to be "positive" results. One or a few patients could do it. Also, would Dr. Mikovits have agreed to participate if she had the same doubts as you have? I doubt it.

  41. >Ladies and gentlemen we have a prophet within our community… Gerwyn predicts a negative Lipkin study.

    Bashing doctors who care for ME patients is counterproductive and believing that these patient's cohort.is different than his disease is pretentious.

    There, I said it! Now watch this post Being destroyed by the ever pretentious IMEA (who by the way doesn't represent me) and MECFS forums

  42. >Bateman and Klimas have an awfully lot of patients who have something that looks an awfully lot like what the most severe patients ME have, except in some cases it's not as bad. If those patients do not have XMRV, then it seems reasonable to question whether XMRV (assuming for the moment that it is associated with this disease) is actually causal rather than a "progression factor."

    Of course, it could be that only the super-sick patients have XMRV in the blood, and the rest only have it in the viral reservoirs. I wonder why the WPI hasn't pushed for tissue testing.

  43. >I can only judge on the patients that bateman and klimas enrol in studies.Whatever ails them it is not a neuroinflammatory disease because they dont have the cytokine and chemokine signatures which are common to all neuroinflammatory diseases.CFS is just a sociopolitical label,Chronic fatigue could be caused by a myriad of different underlying abnormalities.It would be a simple matter to distinguish between those patients who have a neuroinflammatory disease and people with chronic fatigue of uncertain aetiology. This is a minimum requirement of any study which hopes to study this matter scientifically. To do anything else will make the study completely open to manipulation or impossible to interpret due to a hetereogenious cohort where people with entirely different illnesses are given the same label.This should be simple enough even for our anonymous friends to understand

  44. >"This should be simple enough even for our anonymous friends to understand"

    Did you realize what you just said was insulting?

    Patients, whether they are under the care of Klimas, Peterson, Bateman, Enlander, Lapp, and those who have no care at all, are sick, period. it is not up to you, who does not practice medicine or science to decide whether a particular patient should belong to the ME family or not.

    Insulting physicians who have worked for us relentlessly is not warranted either.

  45. >@ Anon August 3, 9:13 AM

    While I don’t necessarily agree (or disagree) with Gerwyn’s comment, I certainly did not hear any “bashing” of doctors. Gerwyn has presented a belief/theory based on how he is interpreting the facts (cytokine profiles).

    I believe one of the objectives of this blog and comment area is to logically debate the science. If you disagree with what has been proposed by Gerwyn, please provide your thoughts on the use of cytokine profiles for determining illness and debate the results of those tests. I would love to hear your input, as I do not have a good understanding of the implications of cytokine abnormalities.

    Thanks.

  46. >Dear Anonymous, you can find said doctor bashing all over mecfs forums, where insults fly left and right.

  47. >@ Anon August 3, 1:22 PM

    So, you are hijacking this blog to go on your own personal rant about what is getting posted on mecfs forums….?

    I would request that you make those complaints on the forums where you feel they are taking place and that we keep this blob on topic.

    Thanks Again.

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