Hoping that everyone can relax a little, here’s yesterday’s song that I couldn’t figure out how to post from my iPhone. We could use a little levity, I think.
When I started writing this blog, it was with a sense of astonishment that the physicians treating the patients, Lyme and CFS, didn’t seem to recognize that they had a new quiver for their arrows. The few that did were quickly censured, or swore a few patients to secrecy. I had been housebound, sometimes bedbound, for years and never expected to return to work, so I didn’t care who I pissed off. Anything was better than the isolation. The good thing about not caring was that I learned to write authentically.
During my 25 years in practice, I didn’t interface at all with the scientific community. Doctors only. I had no idea about the realities of this parallel universe that so impacts what clinical choices are open to us. I thought that the Science paper would be hailed as a great breakthough; scientists and doctors would come together, bringing different things to the table. The pace of progress would accelerate. If only that had happened!
The scientists that I’ve criticized by name were Coffin, Stoye and Racaniello. The first two put themselves out there very early on in a way that appeared designed to stop progress. They also have a long history of publishing things together that minimized the risk, so aren’t clean on the issue and their opinions shouldn’t carry much weight. Dr. Coffin also took it upon himself to try to limit treatment options, my pet peeve.
Professor Racaniello is a media figure, so fair game. I admit to being influenced by hurt feelings in his case, because I wrote to him when I started arv’s, in the midst of the first blush of excitement, wanting to have a discussion with him about the science and he shut me down, much the way Jason did. And to me, the tee-shirt still seems over the top thoughtless, though I think now that he probably didn’t understand what he was doing. There are signs that he is growing, e.g. publishing Dave Tuller’s important piece on his blog.
I was angry at Dr. Singh when she published her negative paper, for the reasons I expressed back then, but essentially the same thing again; scientists trying to call the clinical shots, though in this case I understand that she felt that her former paper was too strongly in favor. I sent her testimonials from patients improving on arv’s at that time. My understanding from Dr. Enlander is that she is back on the case. I thought her a lovely person when I met her and I am glad she is again working on our behalf. The Mt. Sinai initiative is very exciting. It is difficult not to fantasize about Dr.’s Shadt and Lipkin putting their heads together.
And Jason. Sorry Jason, I didn’t mean to hurt your feelings. I hope you learned something from our scuffle. No hard feelings on my end.
I hope I haven’t forgotten anyone. A virtual olive branch offered to all, even those most aghast at my choices…
Believe it or not, there are scientists that share with me, and I protect their privacy. I swear I’ll disavow knowledge of our friendship to my dying day if that’s what any scientist willing to share wants. At risk of scaring off the people we want to be here, there is a tracker on the blog, that allows me to see the IP address, location and the name of the server that loads each blog page, as well as how many prior visits from that address. Institutional servers give the name of the institution. There are at least a dozen readers at the NCI and another dozen who connect from NIH servers in a few different cities. A couple at the CDC in Atlanta. Readers at many universities and teaching hospitals, including a few at Columbia and Harvard. Cancer institutes around the country. Only a few of these people participate in the discussion. This is a potentially powerful thing. When I worked for the WPI, one of things I most wanted to do was establish lines of communication between physicians and scientists with all kinds of points of view. There is little to be learned from consensus when the truth isn’t even on the table. If there is a way to salvage some part of that dream, I’d like to.
Many of the scientists came to read about Dr. Mikovits’ travails, but I am asking them to think about the science with us. In particular, I’d like to know your reactions to Dr. Snyderman’s data. Please adopt a handle and share with us. Your secret is safe with me. I ask you for the sake of the patients that you are now beginning to know, be bold. I realize that you are constrained by the knowledge that a patient community can do what we did, but there are 17 million patients worldwide in the ME/CFS cohort alone, who need creative thinking from you. There is every indication that our disease is reversible until it is very advanced. The unclaimed talent in the patient community is staggering, if only the disease could be calmed, not even cured. Look at me. I am productive after years of being almost unable to care for myself, let alone anyone else.
I would like to put an end to the discussion about the lab science in the Science paper, the WPI, VIP Dx. Nobody knows the answers, including the protagonists. I certainly have no basis for evaluating any of it. I defer to the scientific community to figure it out; discussing it here is not productive. At this point, it is non-contributory and boring. Take it someplace else. This is also not the place to argue about whether Dr. Mikovits should be canonized or not, though she is my friend, and I am very sorry for what is happening to her. But from a clinical point of view it is irrelevant. This blog is about developing a model for treatment and how to best live with the disease.
Thank you to our mold warriors for giving it another shot here, and for keeping it appropriate this time. I for one, think that your experiences of improvement without medication are significant. I also understand why you feel the need to tell others in the hope of reducing their suffering, as well as your frustration when you feel you aren’t being heard. I have been interested in Ritchie Shoemaker’s pioneering work, since 2002 when we shared a couple of patients with Ciguatera poisoning.
And a big thank you to In Vitro Infidelium for the considered comment this morning. No invective or politics at all. Just a reply about the scientific discussion at hand. It was a breath of fresh air. Thank you for the excellent paper by Voisset et al. The quote you lifted in your comment is precisely the point. Although it clearly isn’t a simple, straight forward infection, there is epidemiological evidence that it is an emerging disease of very great proportions, not a stable situation. AIDS isn’t simple and straightforward either, without a test, in that infected people can remain apparently healthy for a long time, or even indefinitely. Only a small percentage of people with HTLV ever become clinically ill from it. Inbred sick mice don’t get sick from their MLV’s, but wild mice and some other rodents can. All I am asking for is that it be studied, not shut down if this attempt fails. Also, that our therapeutic options not be limited by how slow the science will be to unfold, even in a best case scenario in which Dr. Lipkin finds something.
My hat is off to Dr. Lipkin. His finely worded communication to the patient community brought tears to my eyes. The only thing I would take exception with at all was the use of the word definitive. If by some quirk of fate, this study is completely negative, we beg you, use those specimens to take the next step.
Today’s song: Learning to Fly: by Tom Petty
>I think the next step, if there is a negative outcome to the Lipkin study, would be to do next generation sequencing on tissue samples from ME patients (including severe cases and/or those who became ill during epidemics), looking for any retroviruses or other pathogens. In hindsight, such an approach could have saved us the trouble we've gone through for the last two years of attempting PCR assays on blood, which is obviously not a great viral reservoir, using primers that were mostly specific for what was likely the wrong virus anyway. It could also help answer questions about herpesviruses, for which good blood-based assays are rare. Happily, we have the initiatives by Ian Lipkin's group and at Mt Sinai which may be taking this next step.
And on that note… Happy New Year Jamie! :)
>Amen.
>Thanks Dr Jones.
"CFS" arose from a dispute, a "rift" between four doctors in rural Nevada over what the illness-entity under consideration really was.
Ever since then, each "Bug of the month" has threatened to hijack the paradigm, starting with EBV and moving through HBLV, Lyme, Brucella, Parvo B19, mycoplasmas and assorted others, right up to XMRV.
I remain the only original survivor of the inception of this syndrome to stick with the very first etiological agent that showed its presence.
If for nothing else but the sake of science, it would have been inappropriate for me to remain silent and allow this cofactor to be forgotten.
>I agree with D.Y. I would like to see next generation sequencing on tissue samples from M.E. patients anyway, regardless of the results of the Lipkin study. Whether the study results are positive or negative, NGS on tissue samples from people severely affected with M.E. and patients who became sick during epidemics would reveal much-needed information about the illness.
I am grateful to you, Dr. Deckoff-Jones, for making such an honest and forward-looking post.
Thank you.
Patricia Carter
>Erik, you said this:
"I remain the only original survivor of the inception of this syndrome to stick with the very first etiological agent that showed its presence."
Question 1: does this mean that you think the Incline Village outbreak that you were part of is a pathophysiologically and epidemiologically different disease from the outbreaks in Hyde's list starting from 1934 and extending (many think) through the 1990s?
Question 2: When you say "inception of this syndrome" are you referring to a collection of symptoms and signs or a label?
Thanks.
>MAIDS is the model you probably need to look toward for treatment options. Well at least as a starting point. Diseases such as MS are also so similar that what has been successful there could very well be of benefit to ME patients.
>NGS is needed and should be looked into by many studies. But merely testing for the virus in the tissue compartments indicated should also be pursued as blood is not really something that is highlighted as a problem for ME patients.
According to 21st century Kochs postulates they should be looking for evidence of viral infections in lymph nodes as that is what plenty of patients do complain about. Also problems with lungs and the gut as well as brain are indicated.
The use of these new methods has led to revised versions of Koch’s postulates: Fredricks and Relman[10] have suggested the following set of Koch’s postulates for the 21st century:
1. A nucleic acid sequence belonging to a putative pathogen should be present in most cases of an infectious disease. Microbial nucleic acids should be found preferentially in those organs or gross anatomic sites known to be diseased, and not in those organs that lack pathology.
2. Fewer, or no, copies of pathogen-associated nucleic acid sequences should occur in hosts or tissues without disease.
3. With resolution of disease, the copy number of pathogen-associated nucleic acid sequences should decrease or become undetectable. With clinical relapse, the opposite should occur.
4. When sequence detection predates disease, or sequence copy number correlates with severity of disease or pathology, the sequence-disease association is more likely to be a causal relationship.
5. The nature of the microorganism inferred from the available sequence should be consistent with the known biological characteristics of that group of organisms.
6. Tissue-sequence correlates should be sought at the cellular level: efforts should be made to demonstrate specific in situ hybridization of microbial sequence to areas of tissue pathology and to visible microorganisms or to areas where microorganisms are presumed to be located.
7. These sequence-based forms of evidence for microbial causation should be reproducible.
>Dr. Deckoff-Jones,
I've been reading (but only once commented on) your blog since very early on. This was a nice post and I agree with most of what you've said.
My only continued beef with you and your blog is your unwavering support of Dr. Mikovits in light of some very serious ethical, and ultimately criminal, indiscretions on her part. As someone who spent over 2 years working on XMRV, largely due to her work, I regret the amount of time and money we (the research community) spent following up on an idea that was the result of, at best, sloppy science. I'm grateful that my own work panned out, in that it is applicable to non-XMRV related ideas, but that cannot be said for the majority of others' work. It's hard to make the case that Mikovits' truly believed in the validity of the Science study all that time. All that said, it's of course your prerogative to support whomever you like.
Sincerely,
Andy Vaughan
Formerly of Dusty Miller's lab at the Fred Hutch
Postdoctoral Fellow, UCSF (starting January)
>@Jamie
Andy is already trying to drag people into discussing the Science papers and what has and has not occurred so that others are not mislead into thinking his personal opinions have any substance. If you don't want this to happen you do need to stop it being posted. Deleting the comment would actually achieve that.
>I'm not trying to do anything. Just posting my feelings. No response to my post is necessary at all.
– Andy
>Dear Andy,
Thank you for commenting. And thank you for the work you did. I hope you will continue to work on our behalf.
Warmly,
Jamie
>@Andy
"I'm not trying to do anything. Just posting my feelings."
Except that you claim there was sloppy science when there is no proof of any in the labs of Mikovits or Ruscetti. Or in your comment that Mikovits may not believe in the results when she has stated time and again the opposite.
If only you would go back to the lab and really search for polytropic MRVs.
>Amen to what D.Y.said. Tissue investigations please!
>Help me here……"arv's" what is this? I would try most anything to feel better. Thanks, Leslie
Had some good years, months, really, but it has all come to an end. When I say "good" what I mean is that I could do a few things and enjoy life, now basically housebound…..
Leslie
>" your unwavering support of Dr. Mikovits in light of some very serious ethical, and ultimately criminal, indiscretions on her part"
I forgot your other comment. Amazingly you won't have been anywhere near Dr Mikovits or the WPI, so why so quick to declare that someone is guilty when in possession of virtually no facts at all. It comes off as if mediaeval.
>@Leslie
ARVs are antiretrovirals. Drugs that target retroviruses or the affects of retroviruses.
>I am glad your blog is a meeting place for people from so many different backgrounds, Jamie.
I worked in a patient support group for twenty years. We had to help each other, there was very little help else. In that time I saw ME move from affecting people in their twenties and thirties to become an illness that was common in children.
We had several deaths among our members, all young people, none of which were recorded as being due to ME although ME was a contributing factor in all of them.
Because of the imbalance of power between patients and the medical profession, patients and what they can tell about this illness, are not listened to.
To those with power who come here – research this disease. It is a serious public health threat. It will not go away.
>"wanting to have a discussion with him about the science and he shut me down, much the way Jason did."
Just want to clear one thing up here. You shut me down. Don't try and change the fact that I offered you an olive branch first, which was to comment on a viral etiology for CFS/ME. I was ready to do some serious research and think objectively. You pulled the plug.
"And Jason. Sorry Jason, I didn't mean to hurt your feelings. I hope you learned something from our scuffle. No hard feelings on my end."
No need to apologize, you never hurt my feelings. I'm a grown man and can handle myself.
And yes I did learn a few things from our scuffle. 1) I went after you the wrong way and was too aggressive, I can admit that. 2) Having said #1, it is quite clear that you are only want to hear something that supports your retroviral hypothesis and nothing else. This is contrary to how science and research is done and any effort on my part to understand your disease objectively, and sending it to you, would have been a waste of time.
Jason
>Hi Jason,
Glad you're back. It really is classic, isn't it? A microcosm of how human communication so often goes wrong. We each thought we were being objective and the other was closed. Well that wasn't the case on my part. I'm sure you feel the same. But, it's my blog and you wanted to co-opt it to prove me wrong, not contribute to an honest discussion, or at least that's the way it came across. Why should I have wanted to do that? I tested the waters and you weren't open to learning, only lecturing. So yes, I pulled the plug. I was really bummed. You were a bull in a china shop. There you have it. With the best of intentions on both sides, entirely unproductive. I'd like to change it.
I offer you an olive branch and hope that you will again join the discussion.
Happy New Year,
Jamie
>If I recall correctly, at one point Jason was going to share on this blog some thoughts about an alternative etiology for CFS to the retroviral one. For some reason, that guest blog post never happened.
I personally would still like to hear what Jason has to say. Since most of the "leading CFS doctors" (e.g. Peterson and Levy in this L.A. Times article) seem to be almost proudly stating that they have no good ideas about the etiology at this point, some thoughts from "outsiders" seem like they could be a real breath of fresh air.
http://www.latimes.com/news/opinion/commentary/la-oe-levy-chronic-fatigue-syndrome-20110930,0,4021674.story
Happy holidays, everyone.
Best,
Lisa Petrison, Ph.D.
lisapetrison at yahoo
>Dr. Bell from the Lyndonville, NY outbreak sent Lymph node biopsies to the CDC. I mentioned this while at the meeting where the CDC was apologizing for not using funds for CFS on CFS research. I was told, almost as a joke, that those biopsy samples were around still in a refrigerator somewhere. IF that is true, not just dark humor, it would be good to test them for retroviruses.
I have to raise a lurking concern though. In all of these searches whatis the possibility that samples must be tested within a certain timeframe or with the sample stored a certain way?
Um, on another topic…JASON, just start writing your ideas. Enquiring minds ,like my brain, what to know. What might have caused this new disease in the past 35 years or so?
>Clusters of MS are interesting because they are rare, and suggest a commonality to the cause. Here's one… just down the road from Lyndonville, and just a few years before Dr Bell's outbreak.
_________________________________
Rochester, N.Y.
Zinc also was identified as a possible exposure factor in an earlier report by Drs. E.C. Stein, Schiffer and colleagues, published in the October 1987 issue of Neurology, describing an MS cluster among employees at a manufacturing plant in Rochester, N.Y. When the investigators checked workers’ records, they found that 11 had developed MS during a 10-year period, 1970-79, when two to four cases would have been expected. Even though the investigators concluded that there was a significant excess of cases of MS, they could find no differences in exposure to zinc between the workers who had developed MS and those who had not. However, genetic susceptibility to MS was not taken into account in the investigation.
>I agree with the sentiments of this post and hope things go smoothly from now on, with a new year coming.
I reacted the same way to Dr. Lipkin's letter about continuing the studies, which involve, as he said, 11 investigators. He was principled and determined and appears to want to help those of us with CFS. He gets it. I've posted that letter all around including at websites which seemed to condone the Science editor's retraction of the 2009 article.
It's great to see Dr. Lipkin standing up for objectivity and scientific study.
I'm fine with not discussing Dr. Mikovits or WPI. I am for fair treatment for her and oppose the public attacks on her. I understand her attachment to her work.
However, my main concern is that she is knowledgeable and experienced, and that we, those of us with CFS, need all researchers' brains, work and creative thinking to figure out the mysteries of this darned disease and treatments that work.
So, in that vein, I'd say "We need all hands on deck," those who can contribute to figuring this out. That is my major concern.
I am glad that Dr. Lipkin found a place for her to finish this particular study. I await the conclusions and also am eager to hear the results of his further studies.
And I am also glad that Dr. Enlander set up a center at Mount Sinai to study this disease.
But there are also many other researchers to acknowledge, such as Dr. Komaroff, a long-time upstanding supporter of those with CFS; the Lights in Utah, Dr. Klimas and many more.
It gives me, who just hit the 26-year mark with this illness, some hope for 2012. I really appreciate the hard work and determination of all of these scientists who seem committed to helping those of us with this horrific disease.
>With all due respect Dr. Jones, do you really believe that other's who are just reading and might have a different viewpoint would dare respond on this blog? They would be shot down, not with science but with snide remarks and attacks on the messenger.
I would add one other person and that would be RRM, who like IVI, responds with facts instead of vitriol.
That being said, this is your blog. and it is your prerogative as far as deleting posts.
Barb C. :>)
>Kathy D, Did you get a diagnosis of CFS in 1985 ? Were you in an outbreak? What, if anything, has helped you? Have you been diagnosed with any infections?
>Another post from the classic ME patient and mold avoider CityChanger.
>I can still hardly believe what I’m typing. PEM, the hallmark symptom of ME/CFS. Gone. I increased my hike from a leisurely pace intent on keeping my HR below 105 at all times to a brisk pace with my HR constantly at or exceeding my anaerobic threshold (according to Pacific Fatigue Lab calculations of [220-age]*0.6.) Not only that but I increased my hiking distance to 50 minutes. My HR was at 120-130 nearly the whole time I was hiking today. (That number freaks me out because clearly I still have POTS and I’m acting as if I don’t. )
>By the end of the hike, my muscles were actually in quite a bit of pain (I don’t have fibro, for the record). It’s an almost alien sensation to feel my muscles aching like that, clearly due to my body’s reliance on anaerobic metabolism leading to lactic acidosis, while actually feeling totally clearheaded and, well, “good” overall. Still I keep waiting for the PEM hammer to fall. It’s usually when I discover I feel better at the end of the hike versus at the beginning, that I sheepishly allow in the option that I won’t get PEM. Feeling better after any degree of exercise, mild or moderate, is something which has never happened before in all my 6 years of ME/CFS.
http://ampligen4me.wordpress.com/2011/12/30/another-day-without-pem/
>A HITCH HIKER'S GUIDE TO THE HISTORY OF MYALGIC ENCEPHALOMYELITIS & CHRONIC FATIGUE SYNDROME
(This section may be seen in full by visiting the Nightingale Foundation’s site at http://www.nightingale.ca)
– – – – – – – – – – – – – – – – – – – – – –
THE CENTRE FOR DISEASE CONTROL DEFINITION OF CHRONIC FATIGUE SYNDROME (CFS)
Do not for one minute believe that CFS is simply another name for Myalgic Encephalomyelitis (M.E.). It is not. Though CFS is based upon a typical M.E. epidemic, in my opinion it has always been a confused and distorted view of reality.
The invention of Chronic Fatigue Syndrome has to be one of the most curious cases of inventive American scientific imperialism that one could imagine.
Children and Students
Many of the M.E. epidemics started out among children or students. This occurred in 1936 Fond du Lac epidemic, the 1946 to 1949 Akureyri epidemics, the 1950 St Joseph Infirmary epidemic, the 1952 Middlesex epidemic, the 1955 Cumbria epidemic, the 1955 Addington and Durban epidemics, the 1970-1971 Great Ormond Street Children's Hospital. It was not then surprising that the Incline Village epidemic should also start among students.
The Lake Tahoe Epidemic
The Lake Tahoe epidemic that started in August 1984 also started amongst students. In this case the epidemic began in a high school girls' basketball team that was travelling in a bus to play various other teams. The epidemic spread rapidly with an incubation period of approximately a week. As in many of the other epidemics, it then spread to the general community. After the epidemic started it then involved three high schools, both students and teachers and ultimately spread to the community. For some reason it was considered to be an epidemic of infectious mononucleosis. This is an illness caused by a virus Epstein Barr Syndrome. Associating the Lake Tahoe epidemic with Epstein Barr Syndrome was frankly ridiculous and you will see why almost immediately.
Dr Paul Cheney and Dr Daniel Peterson were inundated by the number of rapidly developing cases of seriously ill patients and called the Centre for Disease Control (CDC) in Atlanta for back up.
First International Symposium on Immunology and Pathogenesis of Persistent Virus Infections
Fast-forward to April 1987 and the First International Symposium on Immunology and Pathogenesis of Persistent Virus Infections held in Atlanta Georgia. This was a symposium hosted by the CDC and Dr Carlos Lopez. At this meeting Dr Gary Holmes gave out his new paper, "A cluster of patients with a chronic mononucleosis-like syndrome," that had just been published in JAMA. (See Holmes, Kaplan, Stewart et al: JAMA 1987:287:2297-2302)
_____________
Paula, until Carlos Lopez emerged from this 1987 meeting and announced that collation of the definition-elements for a new syndrome to be called "Chronic Fatigue Syndrome" was underway, there was not yet any "CFS" to be diagnosed with.
>Paula, interesting questions. I can see you have some thoughts on this. Is there a way I can email you?
I was diagnosed with CFS in late 1985, after I had an unrelenting flu for weeks that would not end. I was very sick for months and months. It was not part of an outbreak. No. (I had flus for about four years before that would start on Jan. 1, I'd be very sick for 2 weeks and then I would drag around until May 1).
I had EBV at the start of the CFS, other infections.
>"If by some quirk of fate, this study is completely negative, we beg you, use those specimens to take the next step."
These are not the words of someone with a scientific bone in their body. You are saying that the results do not matter, unless they are the results that you want to see. That is insane anti-science. If the Lipkin study is negative, which seems likely, I'm sure all the participants, including Dr Mikovits will accept the outcome. She has made a public statement to that effect. I just hope you and those few other blinkered patients can do the same, because the sort of lunacy encapsulated in your above quoted sentence, only serves to damage our cause and the public and scientific community perception of ME/CFS patients.
Science is self correcting, let it do it's job.
Ed
>@Ed
Science is not self correcting because humans interfere in it. Science means never setting up a study as definitive. As these are gamma retroviruses it is time to look in tissue. Gamma, Delta and beta retroviruses are hardly ever found in blood and looking in the blood of ME patients would also not fulfil Koch postulates as patients don't complain about the blood.
@Barb C.
RRM/Mark hasn't been using facts.
>IMHO there are 2 distinct communities here – the scientists and the patients, and in many ways they each need to have their own separate debate. I say that because I see too many patients getting caught up in the drama of the science / politics, whilst doing nothing to treat themselves or understand what is going on in their own body. This is not a homogeneous disease. I look on the forums, and whilst I acknowledge many people have ME, a lot of people don't (they have "CFS"), and even the ones with ME have vastly different symptoms to my own. The idea that we can all be cured with a single treatment which can be tested in some large-scale randomized trial, well frankly I don't think it will ever happen.
Science proceeds at an extraordinarily pedestrian pace. As they say "one funeral at a time". I for one don't have 20 years of my life to wait for scientists to catch-up with what those of us living with the illness already know.
I wish we would let the scientists (and doctors etc.) get on with the science (one funeral at a time if necessary). The vast majority of patients lack the specialized expertise to make a meaningful contribution, but let themselves get caught up in the drama, because they see everyone else doing it.
There are whole forums set up for patients to engage in this type of activity, all the while not talking about the elephant in the room, i.e. treatment.
By contrast take a look at the autism or lyme communities. The Autism parents care only about one thing, getting their child better. They have whole conferences devoted to treatment. We have nothing by comparison. Some so-called ME forums don't even have a treatment section!
Right now the only people in a position to make major strides into this disease are the patients. I wish we had more people like citychanger for example. If the scientists come up with a major breakthrough, great. I for one am not willing to bet my life on them doing so.
I wish this patient community would stop "waiting for godot" and actually realize that it is us who hold the key to this disease.
If we were a community of proactive people treating & researching, we would have a much better understanding of how to treat. This disease is simply too complex for 99.9999% of doctors to treat. Its just not cost effective for them to provide the individualized medicine we need. Just look at the current state-of-art offered by ME/CFS specialists. It's pretty dire. The patients know more than the doctors. Not just slightly more, but way way more. Why aren't we leveraging that knowledge??
Oh and message to scientists: There is at least one nobel to be had by looking at this disease. That should be plenty of incentive for anyone to get involved.
Just my 2 cents.
>Erik, I did not get the answer to my questions from your post.
Are you denying that there were earlier epidemics of the same disease that you got?
>If you think you have toxic mold why not design some studies with people like yourself in them so that progress can be made and you can find a cure for that.
Ann Allergy Asthma Immunol. 2005 Feb;94(2):234-9.
Allergy and "toxic mold syndrome".
Edmondson DA, Nordness ME, Zacharisen MC, Kurup VP, Fink JN.
Source
Division of Allergy/Immunology, Department of Pediatrics, Medical College of Wisconsin, Milwaukee, Wisconsin 53201, USA. dedmonds@mcw.edu
Abstract
BACKGROUND:
"Toxic mold syndrome" is a controversial diagnosis associated with exposure to mold-contaminated environments. Molds are known to induce asthma and allergic rhinitis through IgE-mediated mechanisms, to cause hypersensitivity pneumonitis through other immune mechanisms, and to cause life-threatening primary and secondary infections in immunocompromised patients. Mold metabolites may be irritants and may be involved in "sick building syndrome." Patients with environmental mold exposure have presented with atypical constitutional and systemic symptoms, associating those symptoms with the contaminated environment.
OBJECTIVE:
To characterize the clinical features and possible etiology of symptoms in patients with chief complaints related to mold exposure.
METHODS:
Review of patients presenting to an allergy and asthma center with the chief complaint of toxic mold exposure. Symptoms were recorded, and physical examinations, skin prick/puncture tests, and intracutaneous tests were performed.
RESULTS:
A total of 65 individuals aged 1 1/2 to 52 years were studied. Symptoms included rhinitis (62%), cough (52%), headache (34%), respiratory symptoms (34%), central nervous system symptoms (25%), and fatigue (23%). Physical examination revealed pale nasal mucosa, pharyngeal "cobblestoning," and rhinorrhea. Fifty-three percent (33/62) of the patients had skin reactions to molds.
CONCLUSIONS:
Mold-exposed patients can present with a variety of IgE- and non-IgE-mediated symptoms. Mycotoxins, irritation by spores, or metabolites may be culprits in non-IgE presentations; environmental assays have not been perfected. Symptoms attributable to the toxic effects of molds and not attributable to IgE or other immune mechanisms need further evaluation as to pathogenesis. Allergic, rather than toxic, responses seemed to be the major cause of symptoms in the studied group.
>Danger Mouse, I agree we should (CFS-sufferers) be proactive, true. I think and have said it many times. Many of us don't have the energy to do very much.
I'm lucky. My doctor keeps up on CFS and knows quite a bit.
What do you propose those of us with CFS do?
I'd like to improve my health so that I can enjoy the rest of my life.
And again to cut down on the stress, can commenters disagree with some level of tact? I mean, really. It's time.
>@danger mouse
"IMHO there are 2 distinct communities here – the scientists and the patients, and in many ways they each need to have their own separate debate"
Scientists also have ME. It doesn't pass them by. So don't think there are two separate groups.
Do you actually know of any disease where one drug suits all?
The ME community is aware that the field of science has been brought and is controlled and so they are looking into treatments themselves. It shouldn't be this way, but the more vocal/power researchers are determined to not let this occur either. Why else is there an outcry in using ARVs when they are used no healthy pregnant women, or a ban on ME patients in the UK taking them. If too many people start reporting improvement on drugs that have very particular affects on other diseases it is evidence of what the disease is. Again it is all leading back to a retrovirus.
Now some people don't do conspiracy theories. The trouble with that is that conspiracies are still proven to have occurred and do occur. What is one anyway but the agreement of two or more people to take a particular course of action. It could be a simple as trying to protect their ability to conduct research. If they cannot detect viruses in people reliably because their methods are not sensitive enough then what else have they missed or created? If they cannot control their work, then would their work be stopped.
>Anon. @ 3:38 AM.
"RRM/Mark is not using facts"
I stand corrected. He states scientific facts. These facts are backed up by the latest scientific knowledge.
Barb C. :>)
>@Barb C
No he has stated what he thought the facts were and what he thought the latest scientific facts were. What he has not done is actually report the true facts. He has been wrong.
>@ Kathy D
"Danger Mouse, I agree we should (CFS-sufferers) be proactive, true. I think and have said it many times. Many of us don't have the energy to do very much."
It's true that many of us don't have much energy, but when you look at the amount certain people post on the forums going round in endless circles arguing the toss about this and that, clearly those people at least are not lacking in energy. What they lack is direction.
"What do you propose those of us with CFS do?"
I think we need a major shift in conciousness where instead of relying on outside help which is forever promised but never materializes, we realize that when it comes to treatment we are our own greatest resource. We need to start taking lessons from e.g. the autism and lyme communities IMHO, and become treatment focussed first and foremost.
@Anon 4:03
"Scientists also have ME."
I hear what you are saying, but I personally don't know of any scientists with ME. Let me put it another way – there are 2 groups with 2 purposes. The patients who want to get better. And the Scientists who want something to investigate. Those are 2 completely different goals.
>Do you actually know of any disease where one drug suits all?
For most diseases there is a set treatment(s) (of vastly varying efficacy). There is almost no individualization in current medical practise. The most that happens is if you don't tolerate drug A, they'll offer you drug B. But medicine is basically mass-market, not tailored to the individual. I don't see how that model can work for a disease like ME. Especially severe ME. For example severe ME patients will forever get screwed over by their more vocal, more numerous, and much easier to treat mild counterparts. Treatments will be deemed successful if they cure the mild majority. The severe minority will just be left to rot. That's one reason why even the label "ME" isn't much better than the label "CFS" IMHO.
> The ME community is aware that the field of science has been brought and is controlled and so they are looking into treatments themselves.
Some are, but not enough. I've been dismayed at how intellectually dependent most ME patients are on other people, especially when it comes to treatment. Previously intelligent people become child-like. I'm still not quite sure why that is.
> Why else is there an outcry in using ARVs
I hear what you are saying, but the bottom line is that pretty much anyone who wants ARVs can get hold of them (the main barrier is cost). So why are only a tiny handful of patients taking ARVs? I'm not saying people should be taking ARVs (or any other drugs), but I do think that there is sense of "waiting for godot" amongst many patients.
We are all waiting for manna from heaven, when we should be foraging for food ourselves IMHO, at least whilst we wait for the manna to come (if it ever does).
>@Kathy D
"I hear what you are saying, but I personally don't know of any scientists with ME. Let me put it another way – there are 2 groups with 2 purposes. The patients who want to get better. And the Scientists who want something to investigate. Those are 2 completely different goals. "
I know at least 10. You say there are two groups and that they are both working toward different goals. This is not actually correct. If we for a moment ignore the myriad of other groups there is no explanation for why scientists would not want to investigate to get patients better. That is the work of a scientist in medicine. HIV scientists are ultimately supposed to be building knowledge to accomplish a cure for the disease. If a harmless cure was ever found what would the need for research be?
" I don't see how that model can work for a disease like ME. Especially severe ME. For example severe ME patients will forever get screwed over by their more vocal, more numerous, and much easier to treat mild counterparts. "
Governments use what works for those mildly affected by other diseases to cut costs. It isn't unique to ME. They are already trying to fit CBT and GET into MS for instance as it is cheaper. The problem with ME is that researchers are not using or are not permitted to use scientific criteria. Consequently you will get all sorts of claims about this psychosocial treatment and that psychosocial treatment because the cohorts are mixed fatigue illnesses, not ME.
"I hear what you are saying, but the bottom line is that pretty much anyone who wants ARVs can get hold of them (the main barrier is cost). "
Patients in the UK cannot get ARVs. They are also banned from donating blood and deceased tissue. Other patients in other countries cannot afford them. Access to drugs is not related to why people are trying them, if that is what you mean? Patients if they can get access to them and a doctor who can prescribe them should certainly try. The disease is no less severe then HIV/AIDS and the evidence does indicate the involvement of a retrovirus.
"We are all waiting for manna from heaven, when we should be foraging for food ourselves IMHO, at least whilst we wait for the manna to come (if it ever does)."
No people are not. Many are starting to work out exactly what will work.
>@anon 6:43am
>I know at least 10
Are you able to name them? I don't know if you mean people who happen to have scientific qualifications in other fields, or scientists in this field? If it is other fields, then it doesn't really matter if they are scientists or not.
> there is no explanation for why scientists would not want to investigate to get patients better. That is the work of a scientist in medicine
For most scientists it is not in their job description to get patients better. That is the job of clinicians.
> Patients in the UK cannot get ARVs
They can. Maybe not through "official channels". But they can get hold of them. (again I'm not advocating anyone do this).
> The disease is no less severe then HIV/AIDS and the evidence does indicate the involvement of a retrovirus.
I agree 100%.
>With regard to treatments.
A major problem that we seem to have in CFS/ME (aka ME/CFS) is not that we don't have any treatments that work, but that they don't work consistently across patients. Certainly this seems to be the case for antiretrovirals, Ampligen and Valcyte. I would suggest this may be the case for other potential treatments (such as GcMAF, methylation support, oxygen, stem cells or gut repair) as well.
Insofar as treatments only work on a small percentage of patients, it is hard to get the results of clinical studies to the sort of statistical significance that is needed in order to get them into the literature or covered by insurance. Thus, patients are left to rot because "there are no treatments."
Based on the cases that I've seen, I would like to extend the hypothesis that one reason that some patients benefit from these treatments while others do not is because their exposure to the inflammatory toxins/biotoxins that appear to be problematic for us is relatively low.
This would not be a difficult hypothesis to test.
For instance, if we are looking at people considering Ampligen, we could measure either their living environments (e.g. with an ERMI environmental mold test) or their inflammatory response (e.g. with a C4a test). We then could see if those measures had a correlation with positive response to the drug. Or we could look just at people who are in better environments or who have a lower inflammation level, to see if the results for that group alone reached statistical significance.
Insofar as environmental conditions do make a difference with regard to allowing people to benefit from these expensive (and toxic) drugs, we should know about it since it would seem to have the potential benefits of a) moving us toward the point where we can get the drugs approved and covered for at least some people; b) making people who might actually benefit from the drugs more confident about using them; c) preventing people who would not benefit from the drugs (or who might be made more sick from them) from wasting their time and money on them; and d) giving us some insights into the etiology of the disease.
This is not suggesting that patients pursue extreme/scrupulous mold avoidance of the sort that people like Erik Johnson and CityChanger have described here. It's unrealistic to think more than a very tiny group of people ever would do that. That is a clue, not a cure.
This is just looking at total exposure and total inflammatory response, with the hypothesis that (for instance) living in a horrifically moldy environment might keep people with this disease from benefiting from drugs that people in ordinary environments might be able to use effectively.
As research studies go, this one seems to me that this one would be fairly doable. It thus would be interesting to hear some discussion about the concept.
>Anonymous 6:43 a.m.: that wasn't a response to what I wrote. I didn't write about scientists and ME.
I am interested in what we as sufferers can do. I tend to look at political medical and how to change it, not at treatments. I take ARV's which are helping with a particular virus, but not overall CFS…No. And the CFS has been worse in the last six months, with being housebound 95 percent of the time the usual scenario.
>Sorry Kathy, yes it was danger mouse.
"Are you able to name them? I don't know if you mean people who happen to have scientific qualifications in other fields, or scientists in this field? If it is other fields, then it doesn't really matter if they are scientists or not."
Yes, but not without permission and yes some are virologists. You cannot possible believe that out of 17 million people there are not going to be scientists with the disease. There was a time when scientists also didn't need formal qualifications and the world progressed much more quickly when they were allowed to be heard.
"For most scientists it is not in their job description to get patients better. That is the job of clinicians."
It is the job of a scientist to find out what you can treat and how certain drugs will affect humans. They do not work in a vacuum, unless you are suggesting there is no point to any of their work, which I am sure you are not.
"They can. Maybe not through "official channels". But they can get hold of them. (again I'm not advocating anyone do this)."
That's a whole different thing and the cost would still be a problem. Other treatments though that do have a similar affect to ARVs can also be tried.
>@Kathy
"I am interested in what we as sufferers can do. I tend to look at political medical and how to change it, not at treatments."
This is our biggest problem. Too many are trying to prevent good science into the disease. Private funding is the only avenue less likely to be corrupted.
>To understand Chronic Fatigue Syndrome, before doing anything else or making any conclusions, one first has to know the crazy and convoluted story of why this syndrome was created.
———————————————-
http://www.cfids-me.org/holmes1988.html
The 1988 Holmes Definition for CFS
Chronic Fatigue Syndrome: A Working Case Definition
Ann Intern Med. 1988; 108:387-389
The chronic Epstein-Barr virus syndrome is a poorly defined symptom complex characterized primarily by chronic or recurrent debilitating fatigue and various combinations of other symptoms, including sore throat, lymph node pain and tenderness, headache, myalgia, and arthralgias. Although the syndrome has received recent attention, and has been diagnosed in many patients, the chronic Epstein-Barr virus syndrome has not been defined consistently. Despite the name of the syndrome, both the diagnostic value of Epstein-Barr virus serologic tests and the proposed causal relationship between Epstein-Barr virus infection and patients who have been diagnosed with the chronic Epstein-Barr virus syndrome remain doubtful. We propose a new name for the chronic Epstein-Barr virus syndrome – the chronic fatigue syndrome – that more accurately describes this symptom complex as a syndrome of unknown cause characterized primarily by chronic fatigue. We also present a working definition for the chronic fatigue syndrome designed to improve the comparability and reproducibility of clinical research and epidemiologic studies, and to provide a rational basis for evaluating patients who have chronic fatigue of undetermined cause.
>Erik, then how do you fit ME within the category of CFS? Obviously not Oxford CFS.
>I can let Byron Hyde answer that.
"CFS" wasn't originally created as a category, but rather, the ambiguity of the definition was not sufficient to prevent people from thinking of it this way… and the CDC simply never made any objection or effort to clarify the confusion.
————————————–
http://www.imet.ie/imet_documents/BYRON_HYDE_little_red_book.pdf
A Brief History of Myalgic Encephalomyelitis and an Irreverent
History of Chronic Fatigue Syndrome
If we consider the Lake Tahoe epidemic alone we have the primary
definitional determinant of Myalgic Encephalomyelitis.
The Lake Tahoe Epidemic represented an illness
a. With an acute onset.
b. With an incubation period of 4-7 days,
c. Occurring in both students and adults,
d. Involving the central nervous system in a diffuse, non focal
manner,
e. The onset of a Raynaud’s disease along with a peripheral coldness,
blanching and pain syndrome of fingers, hands and feet or
significant
postural hypotension or instability. A non-tramatic, acute onset
of these
two syndromes is consistent with an injury or a significant
diffuse change
in the autonomic physiology of the subcortical brain.
f. Rapidly developing flaccid muscle weakness with minimal effort or
activity, (The Lake Tahoe epidemic was initially called Raggedy
Anne
Syndrome due to this finding.)
g. There were two illnesses, an acute viral like illness and a
secondary
persisting illness that in the more severe cases left permanent
persisting
sequelae.
h. With peripheral pain symptoms that have variable features
resembling in
some cases, a radiculopathy,, in some cases a vasculitis, and
even a
very low grade Guillain-Barre’.
Although the final terminology of conclusion “h” is subject to
debate, are features “a to g” a very difficult set of conclusions to
come to? I don’t think so. There is a consistent similarity of the
Lake Tahoe epidemic patients to all of the previous epidemics
mentioned in this short history and the many others that are
documented in our textbook. The Clinical and Scientific Basis of
Myalgic Encephalomyelitis / Chronic Fatigue Syndrome.
>Major Problems of the 1988 CDC definition
It is my opinion that the CDC 1988 definition of CFS describes a non-
existing chimera based upon inexperience individuals who lack any
historical knowledge this disease process. The CDC definition is not
a disease process. It is (a) partial mix of infectious
mononucleosis / glandular fever, (b) a mix of some of the least
important aspects of M.E. and (c) what amounts to a possibly
unintended psychiatric slant to an epidemic and endemic disease
process of major importance.
>Yet retain these above Lake Tahoe Features in mind when we come to
the first CDC definition that was largely based upon this very same
Lake Tahoe epidemic ilness.
1987: The first CDC definitional meeting
I have mentioned the April 1987, First International Symposium on
Immunology and Pathogenesis of Persistent Virus Infections held in
Atlanta Georgia hosted by the CDC and Dr Carlos Lopez. At the
termination of this meeting to discuss the creation of a definition
for this 1984 Lake Tahoe Raggedy Anne Illness that had appeared
sporadically and in clusters in many areas of the United States and
Canada.
Approximately 25 people showed up for the meeting. Included in the
25 physicians and scientists were Dr Alexis Shelokov, Dr J Gordon
Parish and myself. Other than Dr Gary Holmes and Dr Stephen Straus,
at that time I was not aware of whom the other people present may
have been. Of Shelekov, Parish and myself, I was clearly the least
knowledeable of the three having seen by then some hundred or so
patients with M.E. and read extensively the existing literature.
However my knowledge at that time could not be compared to these two
published giants.
It was obvious that most of the assembly associated this epidemic
disease with Epstein Barr Virus and infectious Mononucleosis, what
the British refer to as glandular fever. It was immediately apparent
that the concensus was going to be highjacked by this majority. Dr
Shelokov and Dr Parish decided that this meeting was going nowhere
and so decided to leave before it terminated. I followed them
knowing full well that if I was going to learn anything credible
about this disease process then I had to understand their incredible
knowledge bse that had been developed for over 20 years.
It was a wise choice for me in terms of acquiring knowledge but it
was a bad choice in that had we stayed, we might have influenced the
decision that was to appear in 1988.
>@Erik
So you agree that CFS as defined in 1988 mixes together ME patients and other diseases that cause fatigue?