Tunnel Vision

If it looks like a duck, and quacks like a duck, we have at least to consider the possibility that we have a small aquatic bird of the family anatidae on our hands.
~ Douglas Adams

I have to hand it to Dr.’s Switzer et al for responding to the vaccine question. Even if it was a very literal response, the findings were imparted clearly and believably. They looked for mouse viruses in 8 vaccines currently on the market. None of the vaccines were grown in mouse cells and, not surprisingly, they didn’t find any mouse viruses. No MLV’s at all in vaccines produced from chick, macaque, guinea pig or hamster cells. However, they did find human, avian and porcine endogenous retroviruses that they already knew were there, plus a new hamster virus in the vaccine grown in hamster cells… but it was DNA only, not a speck of RNA, so no worries… No Evidence of Murine Leukemia Virus-Related Viruses in Live Attenuated Human Vaccines. Switzer. Their conclusion: “We found no evidence of XMRV and MLV in eight live attenuated human vaccines further supporting the safety of these vaccines…”

If it wasn’t so sad, it’d be funny. Here is a paper from almost 30 years ago that says that a replication defective ERV can be rescued by mixing it up in culture with primate cells: Maturation of murine leukemia virus env proteins in the absence of other viral proteins. Schultz, derived from this work: Molecular properties of a gag- pol- env+ murine leukemia virus from cultured AKR lymphoma cells. Rein.

What a concept! Rescuable incompetent ERV’s. They knew about it in the early 80’s, and knew that there were infectious animal retroviruses in vaccines, but decided not to worry about it. And why can’t these parenterally administered xenotropic and polytropic viruses infect humans? “Because they can’t”. “They are inactivated by human serum.” Now that certainly is sound scientific reasoning. And they accuse patients of poor scientific discourse? Scientists please, take your blinders off. There is a whole generation in which 1 in 100 is autistic.

This is where the science is, if anyone cared enough to apply it to us: Endogenous retroviruses and neighboring genes are coordinately repressed by LSD1/KDM1A. Macfarlan

Here are a few good ones:

Dr. Anon, PhD thinks I should do nothing for the next 10 years while I, my daughter and my patients deteriorate. We should all just wait while a bunch of jokers at the CDC try to figure out what the questions are. I know what the questions are. Anyone with critical thinking skills that has actually read what I have written on this blog (including the references) should know what the questions are. Whether or not one particular xenotropic MLV exists in humans or not is now quite besides the point. Not finding MLV’s in 8 vaccines that never came near a mouse cell doesn’t support the safety of anything. Even Switzer et al suggest that maybe they should look at batches of old vaccines, though my understanding is that they were mostly used up in the search for the origin of HIV. They also seem to think that maybe the monoclonal antibody folks should take a closer look into their products, e.g. rituximab, produced via an intentional fusion of mouse and human. They’ve been doing this since the ’70’s. Fooling Mother Nature. Would one of the scientists reading like to explain to us exactly how this is done? The literature is confusing.

But Dr. Anon, PhD, reading my blog, wants to “puke” because I am taking properly prescribed drugs for an off label indication? What a world! Tenofovir is prescribed for chronic Hepatitis B. Does that make you want to puke? We have non-HIV, non-HTLV AIDS, exactly analogous to non-A, non-B hepatitis before C was isolated. Wikipedia article: Off-label Use. The off-label prescribing of existing arv’s is completely legal. The only reason to prohibit it is because of the enormous financial implications if it works. Only a very few people have tried it. No disasters yet attributable to it, unlike most of the pharmaceutical alternatives; and to the scientists reading, you wouldn’t believe the dangerous crap my patients come to me taking, in combinations that have no research at all behind them to tell us about possible interactions. In my case, the only adverse effect of my experiment with arv’s that I can point to is that my straight hair became curly; this happens occasionally with chemotherapy and other drugs.

Tenofovir treats Hepatitis B. Raltegravir inhibits Herpesviruses. AZT has been noted to impact Sjogren’s, which seems to be overrepresented in our patient group. Protease inhibitors kill some parasites. I referenced a paper in the last blog in which it was reported that HAART brought about an impressive remission in a patient with advanced MS (and some of us, myself included, have MS light). Those “confounders” are good things about the drugs in clinical practice; all drugs have good things and bad things about them for a given individual. As a clinician, I love it when a drug hits two things in a patient, making it more likely that the cost/benefit ratio for that drug will be favorable for that person. However, the idea that my response to arv’s is because they controlled my Herpesviruses is almost as ludicrous as the idea that Dr. Snyderman’s cancer cells went down because of a placebo effect. Twice.

This seems like a good time to note that I have never had mono and am serologically negative for EBV. Since I was an ER doctor for 16 years and exposed to lots of mono, my body must be pretty good at keeping invaders out. Ali’s EBV tests are consistent with prior infection, and we both have low titer IgG for HHV-6, like almost everybody. There is really nothing to suggest that we have activated Herpesviruses as part of our picture, opportunistically or otherwise. Ali falls squarely into the Lyme group, not the activated virus group, and opportunistic infectious are not really a part of my clinical picture at all. I catch almost nothing. It’s the inflammatory effect of the physiological changes caused by the persistent immune shift to fight viruses so effectively that creates the subjective illness. Patients, and doctors, often confuse the symptoms of persistent inflammation with an active infection that needs to be killed or treated. There is also a subset of patients that catches everything and has ongoing problems with activated viruses. I have heard from people who have had mono and shingles numerous times.

Most novel uses of existing drugs are figured out serendipitously. Somebody with two things takes a drug for one thing and the other thing gets better. Occasionally, somebody actually connects some dots and tries something on purpose. If it gets reported, it is called a case study. In a sane world it would be followed with an open label trial and then a double blind placebo controlled study.

In response to the criticism that I’ve lead thousands of innocent patients down the garden path, please read what I’ve written, before jumping to conclusions. I have never said anyone should take arv’s. My point is that it should not be prohibited, and most definitely, the decision should not be in the hands of a bunch of lab scientists that have never treated a patient. A retrovirologist has no basis for an opinion about treatment at all. That they would presume to comment is a sign of disordered thinking right there.

As I have said all along, ours was never a good experiment. What I have reported here is strictly clinical medicine. We were on an uphill course for about six months before starting arv’s, after quitting Lyme treatment. I do think that antibiotics were making us worse and when we stopped them, we went uphill, though an LLMD might say our treatment had worked:). I believe that arv’s helped us, though incompletely, not surprising for patients that have been sick for many years, who most likely have a high proviral load that continues to replicate mitotically. We still seem to be doing better than might be expected, but I have no way of knowing how we would be at this moment had we never taken them. The only marker we had to follow, TGF beta-1, initially very high has normalized for both of us over a year and a half (see numbers posted here; the pending results from 11/30 were normal TGF beta-1 and elevated C4a, for both of us). It is a very bad disease and we both feel lucky that our suffering is reduced. I wish that the science was keeping up so that we might have a better way of monitoring our therapy. We need a viral load measure or RT assay to follow, understanding full well that we might have more than one virus each and replication incompetent contributors. My biggest concern is the possibility of viral resistance, not toxicity of the drugs.

As far as the arv elist is concerned, I try to create a safe place for patients taking arv’s to discuss their experiences. Occasionally, I answer a question, but mostly, it is patients talking to patients. Everyone on the list, thirty or so of them, decided to take arv’s on their own, and all have their own prescribing doctors, except for a few that live outside of the US. In my practice, since I am willing to prescribe arv’s for an extremely informed patient, I must not be pushing it very hard, since none of my private patients have yet swallowed an arv.

Unfortunately, it is still the patients least likely to respond who are trying it, people who have been sick for a very long time with advanced disease that feel like they have nothing to lose. Much scarier to contemplate, but with a much greater possible upside, is the question of what would happen if newly crashed ME/CFS or ASD patients were treated quickly after onset of symptoms. This obviously needs to be investigated, but in a controlled setting. It will be very expensive to do safely, so is unlikely to happen for either of these conditions (cancer more likely). People don’t like to be wrong and there are lots of wrong, powerful people in this story.

My husband has been acting CFSy lately. When his symptoms flare, I am always impressed that it must be an infectious disease. All four members of my nuclear family have certain common symptoms, e.g. painless ocular migraine, which was a rare condition when I was an ER doctor 17 years ago, and orthostatic intolerance, of a form that nobody had ever heard of a few decades ago. Vascular instability and autonomic neuropathy in four members of a nuclear family, two sick, two not. Husband and wife not even distantly related. I thank God every day that my son isn’t autistic. I vaccinated him selectively, for the wrong reasons, but I have heard from that woman out there who, like me, has CFS and a CFS daughter, plus an autistic son. Is it because I didn’t give him the Hep B vaccine (which is not a live vaccine, but causes persistent immune activation over a long period of time)?

I get letters now and then suggesting that I do not know how horrible polio and other infectious diseases were before vaccines. That isn’t true, I do know. But just because the vaccine program saved many people doesn’t mean that we shouldn’t look at problems that may have been caused by it, and modify our recommendations now for people at high risk, e.g. people with CFS and new offspring of ME/CFS women. We desperately need extensive epidemiological studies to find out what happened when. If you want to look at the bigger evolutionary picture, we have changed nature’s culling process. If you take the starfish parable from a few blogs back to it’s natural conclusion, throwing the starfish back is a mistake, because they are vicious predators that overbreed and damage the reef.

In the meantime, the backlash from the flash of illumination has started. The Mayo Clinic says SSRI’s (which many ME/CFS patients don’t tolerate), sleep meds, GET and ‘therapy’ are what we can have as far as treatment goes. That’s the best they can do for a million sick people? On their website: “More than 3,300 physicians, scientists and researchers from Mayo Clinic share their expertise to empower you to manage your health.” Shame on them. May the doctors that came up with this page never have to get sick, or have their child get sick, with a horrible debilitating disease and be faced with such options. May they find some shred of compassion in their hearts of stone before that fate can befall them.

I am writing to you today from the Louisiana bayou. My husband’s 50th birthday present a couple of months ago was our first RV, and this is our first trip. We have always wanted to try the RV lifestyle, but now even more so, since we love to be in nature and it is the only way that I can still travel comfortably. Our son was just accepted to Tulane with a big scholarship, so we decided to take him to New Orleans to help him decide what he wants to do. Ali didn’t come on this trip, but will come on the next one, shorter and closer to home. The trip has been exciting, to say the least. We survived the worst blizzard in 40 years in north Texas and a tornado warning in southern Louisiana.

I love the spontaneity and limitless possibility of seeing the world this way. Change is usually so difficult with this illness, but everything I need is close at hand and comes with us when we move. The pendulum of my disease continues to swing, as always, while I practice the art of transcending symptoms, living as many full moments as I can. Right now, my husband and son are fishing in the rain. We’ve had the worst luck with weather. Adversity is giving us all the opportunity to practice acceptance and work on our interactions in a close space. Like life, the difficulties have been punctuated by amazing moments; yesterday we watched from our canoe as a small otter caught and fought a huge fish, then defended it from a Great Blue Heron. This part of the country is very wild and alive. When I couldn’t sleep for a while last night, I listened to wonderful, unfamiliar night noises.

And the breaking news? Lo et al just retracted, saying the work was perfect, but the conclusion must be wrong, since nobody has replicated it yet, except for one other lab. Therefore, enough money wasted. Now there’s some ironclad logic for you.

Tonight’s song: The Wild Goose
by Kate Rusby

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174 thoughts on “Tunnel Vision

  1. >Personal experiences can provide clues as to what should be researched and they shouldn't be ignored, but this is precisely what the Wessely school relies on to keep the disease in its place for political reasons. They can make up any explanation they please with that approach as it is subjective and easily manipulated. If we are to rid ourselves of them we have to start collecting objective data and use objective criteria to select patients.


    What are they measuring in the Rituximab trials apart from b cell levels that makes you think it will tell us anything about ME biology?

  2. >"@kathy D I completely agree with you, which is why I think those hypotheses made earlier (i.e. natural progression of illness) must sound ludicrous to any ME/CFS patients, even if there's room for such a hypothesis in reality."

    It wasn't a hypothesis. There is always a natural progression for every disease. It may change depending on the person but it is the natural progression without intervention.

    David Bell has described how many of those not so sick at the start tend report improvement later, but when their lifestyle is examined they have reduced what they do to cope and have false wellness beliefs. Later after a time people start to only decline in health for the remainder of their lives.

    As an ME patient with objective signs it does not sound ludicrous. You have misunderstood.

  3. >Two very easy to understand documents on why the negative papers have failed patients.

    "A PMA may be required if the test is for a novel agent, if it is a new method for which clinical relevance and clinical use must be established, or if the analyte poses a health threat (such as Mycobacterium tuberculosis) and a false-positive or false-negative result would be of significant risk to the patient or general public. The manufacturer must provide data that demonstrate a reasonable assurance of safety and effectiveness of the device. FDA review of a PMA application includes an in-depth scientific evaluation of the data and a comprehensive good manufacturing practice inspection at the manufacturing facility."

    "Clinical test validation: This section describes the ability of a test to detect or predict the associated disorder in patients and includes clinical sensitivity and specificity, and/or other performance attributes of testing biological samples."

    "When a new diagnostic is being considered for use in selecting patients to receive or to avoid a particular drug therapy (i.e., drug/test co-developed product) or to stratify patients in some other way, two distinct, but related, issues should be addressed.

    The first is the ability of the test to select (or deselect) patients with the biomarkers (analyte(s)) of interest. This is clinical test validation — use of a test to detect or predict the associated disorder of interest in biological specimens from the target patient groups. This should be considered the domain of clinical test validation."

  4. >Hi all,
    First off I'm grateful for Dr Jamie for providing this place where the big issues / ideas surrounding ME can be discussed.

    I know citychanger (CC), and although I don't believe in everything he believes in, I can vouch that he has most definitely has ME. Having said that there is a vast, vast range of different levels of sickness within the label "ME". Citychanger is young, highly intelligent (as I used to be once), and also has access to resources. He is also without doubt the hardest working ME patient I've come across in my life.

    I'm sorry to say but Eric and Lisa often come across as a pair of loons. Having said that I am open minded enough to differentiate between the messenger and the message. I fully agree with CC that there is a lot to be said for environmental aspects. I also agree that Eric & Lisa shoot themselves in the foot by equating environment purely with "mold".

    There seems to be strong anecdotal evidence that a change of environment can shift this illness, like sadly little else seems to. The scientific approach would be to focus on that (rather than jumping to the conclusion it must be "mold"). Right now we have no way of knowing whether it is mold, biotoxins, or a whole combination of factors helping (climate, sunshine, fresh air, vitamin D etc). We need to keep the hypothesis in the broadest terms possible, and stick to what we know for sure, which is that location seems to matter. Since most of us are immobile, the closest we get to experiencing that is through the change of seasons. I feel much better in summer than I do in winter for example. I have a strong suspicion that I would do better in a hotter climate. Sadly I lack the resources to test that theory.

    Although I believe in the retroviral cause, I have little faith in ARVs to cure someone as sick as me. Like every other treatment out there it seems to help the least sick, and make the really sick people sicker. When I talk about really sick people I'm talking about people who haven't worked for 5-10 years minimum. I'm talking about the people who can barely think straight because their brain is so inflammed. Most of the regulars on the forums aren't *that* sick. If they were they wouldn't be able to post as much as they do.

    One thing I dislike is the use of the word "terrain". It's such a catch-all term that it becomes meaningless (a bit like "chronic fatigue"). Since the terrain means essentially anything and everything other than the pathogen, it is potentially an infinite number of factors. Obviously that large a number of factors is going to matter! The issue Is what *bit* of the terrain are we talking about? Which bit do we need to shift? We need to talk specifics IMHO.

    I would gladly put myself forward as a test subject for the environmental theory. The problem is that I lack the financial resources and health to move. It’s a catch-22. I can't see it being a practical option for those of us who are too sick or too poor.

  5. >@PC December 27, 2011 7:53 PM "But someone,not Abbie Smith made my point, namely that there is a study pointing towars MS being caused by an ERV which seems to be causing disease."

    Abbie wrote two blog posts in 2009:



    each quoting a relevant study



    Abbie Smith noted precisely the implications of these studies – that is that an ERV (part of the human genome, not an infectious agent) is associated with causation of Multiple Sclerosis.

    So just to be absolutely clear – an ERV is part of the genome, and the implication of the quoted research is that MS is a genetic illness. The study that JDJ referred to: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3131726/ does not imply that the "putative multiple sclerosis associated retrovirus" is anything other than an ERV of the HERV-W family.

    There is a family of HERVs – HERV-K for which there is evidence of continued infective replication, but no diseases have been shown to be associated with HERV-K and it feasible HERV-K exists as a 'quiet' RV actively replicating in only very localised human population pools.

    There is no published evidence which suggests that MS is caused by a replicating exogenous pathogen.

  6. >I have a great deal of respect for Harvey Alter, and I don't think that he would have withdrawn the PNAS paper if he thought there was any sort of chance that MLV's are involved in this disease. So I have to say that I have my own doubts about that possibility at this point.

    However, it's hard for me to make sense of what I've seen of the etiology of the disease without a retrovirus being a factor. An ERV, activated by the inflamed toxic terrain of those individuals sequestering a large amount of biotoxin (e.g. Lyme, toxic mold and/or dinoflagellate) in their systems, has made sense to me for a long time.

    This would seem to be a similar dynamic to the situation with ALS. Current thinking is that both an endogenous retrovirus and a biotoxin (BMAA — made by cyanobacteria) may be factors.

    Douville R, Liu J, Rothstein J, & Nath A (2011). Identification of active loci of a human endogenous retrovirus in neurons of patients with amyotrophic lateral sclerosis. Annals of neurology, 69 (1), 141-51 PMID: 21280084



    This could be the dynamic as in MS as well. There appears to be some evidence that an ERV plays a role in it, and Dr. Ritchie Shoemaker has implicated biotoxins as also appearing to be a factor.

    Conceivably some totally unexplored kind of retrovirus could be playing a role in ME/CFS as well, of course. It will be interesting to see what the Lipkin study finds out.

    Best, Lisa

  7. >Abbie Smith is a student. She has no idea how a gamma retrovirus behaves.

    Mult Scler. 2010 Oct;16(10):1248-51. Epub 2010 Aug 4.

    Multiple sclerosis-associated retrovirus and progressive disability of multiple sclerosis.

    Sotgiu S, Mameli G, Serra C, Zarbo IR, Arru G, Dolei A.
    Section of Neurology, Department of Neurosciences, University of Sassari, Sassari, Italy. stesot@hotmail.com

    Retrovirus-like particles containing the multiple sclerosis-associated retrovirus RNA, significantly found in the cerebrospinal fluid of patients with multiple sclerosis, have been preliminarily associated with a short-term poor clinical and radiological prognosis of the disease. We asked whether these prognostic indications are still measurable after a long-term clinical evaluation (10 years). Our 10-year blind observational study confirms that the presence of multiple sclerosis-associated retrovirus in the cerebrospinal fluid of early multiple sclerosis patients is associated with a significantly greater rate of relapse-unrelated unremitting disability and secondary progression of the disease."

  8. >"I have a great deal of respect for Harvey Alter, and I don't think that he would have withdrawn the PNAS paper if he thought there was any sort of chance that MLV's are involved in this disease. So I have to say that I have my own doubts about that possibility at this point."

    Lisa, Lo and Alter do think HGRVs are involved in ME as he stands by the integrity of the original data. There has been no evidence of contamination or errors in their labs. None of the negative studies even looked for these viruses, including those claiming to look for other MLVs as they still optimised to VP62/XMRV. It is a political retraction.

  9. >Acta Neurol Scand. 1989 Nov;80(5):467-71.
    Retrovirus in multiple sclerosis.
    Kam-Hansen S, Lu CZ, Fredrikson S, Baig S.
    Department of Neurology, Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden.
    Presence of cytopathic effect and enzyme reverse transcriptase in cultures of peripheral blood mononuclear cells is described in 2 of 15 patients with multiple sclerosis and none of healthy controls. These findings might indicate: the presence of a new human retrovirus in these individuals, despite the low detection rate, and the shortcomings inherent in methodology used for detection of known human retroviruses in the study of new groups of diseases, such as those with possible autoimmune background.

    Acta Neurol Scand. 1991 Dec;84(6):507-13.
    Antibody to reverse transcriptase of human retroviruses in multiple sclerosis.
    Perron H, Geny C, Genoulaz O, Pellat J, Perret J, Seigneurin JM.
    Department of Virology, University Hospital, Grenoble, France.
    HTLV-1, HIV-1 and HIV-2 western blot analysis of sera from patients with multiple sclerosis (MS), from patients with other neurological diseases and from blood donors, revealed a rather frequent cross-reactivity with retroviral proteins in the MS group, though no patient was positive with the corresponding specific ELISA serology. Statistical analysis revealed a significant difference between the MS group and the two control groups for HIV-1 and HIV-2 reverse transcriptase fragments and for HTLV-1 p24. The general significance of these observations is discussed in the light of a retroviral hypothesis for the aetiology of MS. It is suggested that, if a retrovirus is present in MS patients, it does not necessarily belong to the HTLV sub-family and could as well be a lentivirus, like Visna virus, the causative agent of a demyelinating disease in sheep which is one–natural–model for MS.

  10. >Gender Issues

    @Anon December 27, 2011 2:37 PM If you want to define an illness in your own terms that’s fine but the gender difference observation goes back as Ramsay, if you consider Ramsay was wrong, then I suggest you stop using M.E as the term for the illness you are concerned with.

    @Flex December 27, 2011 5:42 PM “Why does a "gender imbalance" disprove a RV cause.” I’ve not suggested it does, we have no way of establishing such a proof, and science certainly doesn’t operate on such a basis. The burden of evidence (and where hypothesis is concerned, plausibility) is upon those presenting a proposition or hypothesis, so it’s up those who hypothesise an active retroviral (as opposed to ERV) involvement in M.E/CFS, to provide plausibility for that hypothesis in the face of the ‘fact’ of a diagnostic gender imbalance, or to provide some evidence base that challenges the ‘fact’ of diagnostic gender imbalance.

    Anon December 27, 2011 6:10 PM has provided evidence of why the HIV situation, not only doesn’t support a challenge to the ‘fact’ of a diagnostic gender imbalance in M.E/CFS but actually supports the questioning of the single infection hypothesis. HIV is an emergent disease – it has spread epidemically and unsurprisingly that spread has impacted differentially within and between differing human populations – what HIV has not displayed is any gender preference given an equal opportunity of infection – allow HIV a blood to blood transfer and it has no interest whether a new host is male or female. And there is no known infectious agent that does make such a preference – excepting of course that infection may require specific physiological apparatus.

    Invoking the prostate/XMRV connection is fallacious – if it were relevant then why would any woman be at risk of XMRV infection if a prostate were required to facilitate such infection ? As it is there must be serious doubt about all XMRV positive studies and it would be foolish to seek broad instruction from them.

    I’m making no presumption about M.E/CFS causation, what I do want is all hypotheses of the illness to be subject to a test of plausibility which is matched to what is known about the illness. What we’ve seen on this page is that those who are wedded to the infectious(RV) proposition are willing to alter the acknowledged characteristics of the illness to fit their proposition. And what is quite bizarre about this is that the ‘true M.E/RV causation’ advocates are actually supporting (unless they can find 7 million missing male suffers) a conclusion that would cast(e) some 8 million women M.E/CFS sufferers back into the waiting arms of the psychogenic brigade.

    PC asked “The epidemiology of CFS is simply that more women are sick than men, and that NON BLOOD relatives in the same house are sick. Also doctors, nurses and teachers are sick in higher numbers. What would you speculate on that ?”

    Unfortunately there is no published epidemiology that supports conclusions about non-related building occupants or occupation prevalence. The gender imbalance has been widely recorded and is a likely confounder of any analysis of occupation prevalence – if nursing and teaching do display increased prevalence then account has to be taken of the gender imbalance inherent in those professions. Diagnostic preference also impacts upon occupation prevalence so doctors are more likely to get a diagnosis that is appropriate/accurate than someone outside the profession.

  11. >In Vitro/Wessely school psychiatrist.

    If you were a scientist you would know that gender issues tell us nothing about whether a disease is infectious. There is an enormous difference in the number of men compared to women who have HIV. It doesn't matter if you think anything goes back to Ramsey.

  12. >"The burden of evidence (and where hypothesis is concerned, plausibility) is upon those presenting a proposition or hypothesis, so it’s up those who hypothesise an active retroviral (as opposed to ERV) involvement in M.E/CFS, to provide plausibility for that hypothesis in the face of the ‘fact’ of a diagnostic gender imbalance, or to provide some evidence base that challenges the ‘fact’ of diagnostic gender imbalance. "

    Incorrect, because people are not being diagnosed using objective criteria. The Fukuda CFS criteria is the easiest to understand. It does not describe a single disease entity. Therefore the HGRV hypothesis only need apply to some people. Whereas for CCC it would be expected to be higher, although again the criteria does not require the use of objective measures to diagnose a person with ME.

    There is therefore no "fact" about a gender imbalance in ME, or CFS, or CFS/ME or ME/CFS. It is an opinion.

  13. >@Anon December 28, 2011 5:09 AM “multiple sclerosis-associated retrovirus” – it’s an HERV not a replication competent RV, so what's your point ?

    @Anon December 28, 2011 6:12 AM Read previous posts which detail why your HIV reference does not mean what you think it means.

    @Anon December 28, 2011 7:04 AM “Therefore the HGRV hypothesis only need apply to some people.” Absolutely, but then why call it M.E ? Your postulation is that some people currently diagnosed with M.E/CFS have a unique disease which unlike M.E/CFS is not currently recognised by medical science – so why keep using the M.E designation, call it something else. For your HGRV disease not to have a gender differential, you’ll have to work on a basis that the maximum global population is something less than 6 million. No doubt you’ll be happy for the 11 million plus M.E HGRV negative patients to continue campaigning for research that doesn’t include HGRV causation. Your conclusion that “There is therefore no "fact" about a gender imbalance in ME, or CFS, or CFS/ME or ME/CFS. It is an opinion.” simply reduces all M.E/CFS diagnosis to an irrelevance – is that what you actually intend ? – that there is no diagnostic standard for M.E/CFS and that any and every hypothesis is relevant because nothing is ‘known’ about an undescribed condition ?

  14. >@In Vitro/Wessely school psychiatrist.

    Where does it show it was a HERV? And what about the other papers?

    There is no evidence for a gender difference in ME and gender difference makes no difference to whether a disease is caused by an infectious agent.

    ME has always been a discreet neurological disease that has already been recognised by the scientific establishment, but which people like yourself would now wish to eradicate from history. CFS is a label. ME/CFS is the CCC criteria.

    "you’ll have to work on a basis that the maximum global population is something less than 6 million. No doubt you’ll be happy for the 11 million plus M.E HGRV negative patients to continue campaigning for research that doesn’t include HGRV causation."

    Who are they? If you mean the label CFS and not ME, well then it would help in discovering the cause of their disease if those with HGRV infection are separated out. Science cannot progress whilst no one uses scientific criteria. Many diseases can look the same way you rely on opinion and beliefs.

    It is very simple to add objective measures to ME criteria to prove a person does have neurological signs for this neurological disease. Those without do not have ME, but another disease. You do realise you are preventing any scientific investigation of ME by continue to use your opinions?

  15. >Dear all,
    there is some real debate to be had here (e.g. on the environmental issues citychanger has raised). Please don't waste your time/energy on the Wessely trolls. I'd like to hear some intelligent response from the ME patients on what role environmental aspects might play in ME.

  16. >The Clinical Syndrome Variously Called Benign Myalgic Encephalomyelitis,
    Iceland Disease and Epidemic Neuromyasthenia
    E.D. Acheson, D.M., M.R.C.P.

    The first attempt at a descriptive name was
    made by Fog9 who suggested “neuritis
    vegetativa” in the belief that the autonomic
    nervous system bore the brunt of the damage.
    A further suggestion was made in an editorial
    in the Lancet in 195622. It was hoped that the
    term “benign myalgic encephalomyelitis”
    would emphasize the absent mortality, the
    severe muscular pains, the evidence of
    parenchymal damage to the nervous system,
    and the presumed inflammatory nature of the
    disorder. This term has been adopted by
    Galpine and Brady32 and Deisher17 in
    subsequent articles. It has also been criticized
    by Sigurdsson62 and the staff of the Royal Free
    Hospital12,27. Sigurdsson objects that the
    disease is not always benign, not invariably
    myalgic, and possibly never encephalomyelitis.
    Benignity is relative; it seems that “benign” is
    justified by the fact that there is no other
    recorded infective disease of the central
    nervous system without mortality.

    The 1985 Tahoe Mystery Illness was analyzed by Hyde, Parish and Shelokov, and found to "possess all the primary determinants of ME", but we really don't know it was the same.
    The first thing the flu-like illness did was kill a few people, including a co-worker of mine.

  17. >"I'd like to hear some intelligent response from the ME patients on what role environmental aspects might play in ME."

    That would be great to hear. There have been several reports/articles in the past year showing what looks like a high degree of correlation between autism rates and traffic pollution.

  18. >There are already diseases recognised as being caused by biotoxins. People with ME have not been shown to have a disease caused by biotoxins, but biotoxins could cause MRVs to replicate, which would exacerbate the disease.

  19. >People with ME have not been shown to have a disease caused by biotoxins. But people with ME have also not been shown to have a disease caused by viruses either, despite many claims here to the contrary. That is the whole point. And if a study came out tomorrow showing some kind of link or correlation with a biotoxin, traffic exhaust, power lines, solar flares, etc., some on this board would quickly poo poo it and immediately dismiss it out of hand, because they are intent on protecting the retrovirus theory and a certain now fully retracted study at all costs.

  20. >A hypothesis has been presented that ME is associated with HGRVs. Several lines of evidence that are far from being challenged have been used to support this hypothesis. Don't confuse association with causation Anon 11:54. Some of that evidence however does support causation because of how theses viruses behave in mice and what they have been shown to do in human tissue.

    There is no study on biotoxins that presents a hypothesis for ME, but if one were published it to would be analysed by people here and all over the net. Whether the paper would be robust is anyones guess, but currently it doesn't exist.

    Don't try and attribute incorrect motives to those who do understand the details and science presented in HGRV research.

  21. >"There is no study on biotoxins that presents a hypothesis for ME, but if one were published it to would be analysed by people here and all over the net. Whether the paper would be robust is anyones guess, but currently it doesn't exist."

    Spoken like someone that operates exclusively within the conventional research framework. As if the fact that there is no study yet on biotoxins has anything to do with the actual role of biotoxins.

    Where do you even begin looking? What are the potential benefits to studying a biotoxin for a researcher if it's something that will incite chaos? Remember the big hubbub recently about the scientists that created avian flu in a lab and Fauci (among others) saying it's perhaps best that this isn't released to the public, citing the fear that others with deviant purposes (i.e. terrorists) would recreate the finding? Some people know very well that science is never non-political and just as economically driven as any other field, yet when it comes to biotoxins act as if "it's just lacking science."

    People are willing to invest into MLVs because of the potential economic rewards: for the institution, for the researcher (nobel prize etc), for drug companies. The whole supply chain benefits from such an investment.

    What about biotoxins? First of all, we don't know what we're looking for, so investments would have to be made on massive air sampling and assays first before we can even conduct a pilot study. This is a whole new paradigm which requires new investment at every step. This requires a purely top-down investment from govt institutions because the private sector will not benefit economically in any way from a study on biotoxins.

    In this case, what incentive does the govt have to do research on biotoxins? If they do, what incentive do they have to release it to the public? In this case, their incentive for not wanting this disseminated is the same as the political barriers we have been witnessing with HGRV research. Surely you can understand this part.

    Anyway, I don't see biotoxin studies happening in any large scale, but I hope that I'm wrong. I hope that someone will see a potential treatment (something that helps us react to the toxins, something that helps us detoxify them as Lisa has been saying). However, the investment in an assay surely has to come from top down, and hopefully it will come from institutional research hoping to get academic rapport for "finding new ways to measure something novel." Then again, how much academic interest was there in the ciguatera toxin?

    Anyway I'm in the camp that there is something to be said for crowdsourcing and the power of numbers. If enough people do biotoxin avoidance and improve in very concrete ways, then perhaps some grassroots institution like the NCF will take notice and find biotoxins worth investigating. The internet allows our individual experiences and lab data to have a cumulative effect on outside interest. The only problem, as danger mouse attributed to above, is that an exercise like this not only requires sacrifice as I've mentioned, but some amount of resources, criteria that exclude most ME/CFS patients.

  22. >"Spoken like someone that operates exclusively within the conventional research framework. As if the fact that there is no study yet on biotoxins has anything to do with the actual role of biotoxins. "

    Incorrect. There is no study. That is not saying there is nothing wrong with conducting one, but what is the hypothesis that you can test?

    Anecdotally we already know that many patients have avoided biotoxins and report it does not make a difference to the underlying disease.

    There is a problem obtaining money for ME research not because one potential cause over another would make more money but because clearly it is not in the interests of the insurance industry, the CDC, NIH, MRC to find the cause.

  23. >@anonymous on autism and traffic polution

    From what I've gathered from all the biotoxin avoiders, traditional air quality indices have very little to do with where ME/CFS patients get big shifts. True there is a correlation between traffic pollution and feeling a shift, but that's all it is because lack of traffic pollution usually correlates with less of everything else that's associated with civilization.

    That's where the "extreme" in "extreme avoidance" comes from. The fact that we don't know what we're avoiding, so the easiest thing to do is to go to where there's nothing. This is also the biggest marketing barrier we have, since most people have no desire to get uprooted from their lives in big cities and robust communities.

    However, as an example of how little traditional air indices can have to do with this shift, I began feeling good enough to work for almost 40 hours a week from my computer when I was in a city that has some of the worst inversions in the U.S. On inversion days, this city has had days where it's the most polluted city in the nation. On a good inversion day, people with any respiratory issues are advised not to go outside.

    Well sure, when I was driving in the inversion I could feel the smog and particulates that were trapped. I had a little shortness of breath and in general didn't feel that great, which is to be expected. However, it was nothing like how I felt in a house that I was reacting to. It was nothing like how I felt in the Bay Area as a whole.

    Right now, many biotoxin avoiders are in Riverside County (palm springs, yucca valley etc) which has some of the worst pollution in the nation. Yet it is here where they are able to hike and continue improving cognitively.

    So as a whole, I would say traditional AQ indices do not address the biotoxins we're focusing on here.

    So again, this is why any reliance on scientific studies to draw correlation in symptoms with biotoxins is misinformed. We don't know what we're measuring, so correlations between AQ indices and our conditions are (I predict) totally useless. Until we know what we're measuring, we shouldn't pretend that there's any study that can be done now that can possibly give credence to the role of biotoxins.

    It's unfortunate but because there is no study that can be done now to lend credence to this, our only choices are to 1) avoid the topic altogether or 2) talk about our personal experiences, observations, and laboratory data.

    You already know where I stand on this.

  24. >"There is a problem obtaining money for ME research not because one potential cause over another would make more money but because clearly it is not in the interests of the insurance industry, the CDC, NIH, MRC to find the cause."

    Then you have no understanding of the economics driving medical research and medicine in general. You're saying a cause for which there is potentially an off-the-shelf treatment and a cause for which there is no potential off-the-shelf treatment draw the same interest? Please.

  25. >There are treatments for MRVs already out there. They won't fund biomedical research into ME not because they can treat but because of the numbers they would have to treat, the impact on the economy, the panic around vaccines and biologicals, and the enviable charges brought against those asleep at the wheel.

    You are not understanding that this has nothing to do with the normal economics driving research and medicine. It could be said to be all about protecting the norm.

  26. >Of course. We've all read Osler's Web here.

    My point is that if there is any interest in ME research at all, the choice between the two from an incentives standpoint for all interested parties is easy. Therefore, to compare the number of studies behind retroviruses versus biotoxins as etiology of ME/CFS (as apples to apples) is flawed and misinformed.

  27. >Again you are misunderstanding. The issue is not the number of studies but the data and the hypothesis offered. Why do you think you don't have a disease that has already been explained in the scientific literature as involving biotoxins? And what hypothesis are you proposing for ME that is explained through biotoxins? ME as explained by HGRVs is a testable model that would explain all observations.

  28. >As the originator of "Extreme Avoidance",
    I'd like to make a clarification on what I mean.
    "Extreme" refers to a concerted and deliberately directed strategy regarding perceptions of exposure.

    In a non-exposure environment, no such concerted strategy is required, and this would simply be "avoidance".

    "Extreme" is laying out a plan to wend your way around plumes whenever possible, through them only when necessary, and conducting decontamination protocols afterwards as a means to continue living semi-comfortably in a less than pristine location.

  29. >"ME as explained by HGRVs is a testable model that would explain all observations. "

    It has been tested extensively, all reputable studies to date have been negative.

  30. >"There is criticism in some quarters that this study is unnecessary given results obtained by other investigators with other samples. However, the participating clinical and laboratory investigators and our team at Columbia do not agree. We are fully committed to completing the work rapidly and rigorously. For those who continue to express concerns that this study is an inappropriate use of resources in a challenging fiscal environment, please be assured that more than 85% of the funding associated with this initiative is invested in patient recruitment and characterization and sample collection, archiving, and distribution. Thus, irrespective of study outcome there will be unprecedented opportunity to explore hypotheses other than that disease is due to XMRV or MLV infection."

  31. >@ Hillary Johnson,

    Thank you for the gift you gave us. You documented our history so it wouldn't be lost and you continue to tell it like it is.

    With deep respect,

  32. >"And what hypothesis are you proposing for ME that is explained through biotoxins?"

    If you are the same anonymous I conferred with above, you have a rather selective and short memory. I hate to sound like a broken record, but neither Lisa, Erik, myself, or any other biotoxin avoiders that I know of have been adamant about biotoxins causing ME/CFS. It has been explored as a theory as both causative of ME/CFS and causative of the inflammatory patterns seen in ME/CFS, but without knowing what we're testing, any hypothesis that we come up with is no more than a shot in the dark.

    The reason why a hypothesis for HGRVs is plausible is because of the mountain of literature that already exists for it. A simple pubmed search can piece together a house of cards linking every symptom to HGRVs. No such luxury is available for something (or an effect) you cannot yet identify.

    If you don't understand what I'm trying to say for the 3rd or 4th time, I really don't know how else to explain this.

    From my own perspective, I never thought that inflammation could cause PEM. Well I never had any better theory for it, but that just seemed impossible. However, after looking closely at the Lights research on PEM and inflammatory signatures not seem in healthy controls, there is now evidence of pronounced inflammation in PEM.

    If you take away this pronounced inflammation (which is part of what biotoxin avoiders are able to accomplish by taking away whatever is revving our immunity into constant overdrive) the PEM can become vastly reduced, at least in my case.

    To be clear, it's not as if deep-seated organ damage and the body's oxygen toxicity (as Cheney would call it) or anaerobic reliance is gone. My muscles are in pain after walking at a snail's pace for 40 minutes, and I do not have fibromyalgia. However, I am able to sleep without any sleeping meds (to which I was on daily for years) in spite of the pain and quell the pain by next morning.

    So lowering inflammation is not a cure and does not treat the cause. If that were the case, ampligen would probably be a cure. So would rituximab. However, doing so removes much of the presentation of ME/CFS for myself and others.

    Lisa and others that aren't sure whether toxins are the cause treat the disease as if it were (mostly by taking large quantities of CSM to get the stuff out). I think this is smart from a patient's perspective. Lisa and others have or are planning on adding antivirals such as Valcyte to their regimen. No one is acting as if we know it's one or the other (perhaps besides Erik, but since he can climb Mt. Whitney, why would he want to be on any toxic drug?) This includes myself: I'm taking large quantities of CSM with zero side effects, and I'm also planning on adding famvir/valcyte/antiretroviral drugs if they help.

    The best hypothesis I could come up with is "if CCC ME/CFS patients in location A move to location B without taking any of their belongings with them, they will feel better." Try getting a scientist to man that trial, and try getting someone to pay for it.

    Since you won't be able to, I'll focus on how I feel and what I've observed, and communicating this to patients that may be interested.

  33. >@anonymous

    In theory, if we wanted to test whether an inflammatory signature is associate with the ability to hike without PEM (which just about everyone agrees is the hallmark presentation of ME/CFS), that's really not that difficult.

    We'd have to take patients' baselines of inflammatory signature (per Lights' study) during an exercise stress test (in certain locations) and then have them commit to this exercise for, say, 6 months. All patients that do this exercise would then get a follow-up inflammatory signature during an exercise stress test.

    But again, this requires people being willing to uproot their lives as they know it and someone to pay them to do it. You can have volunteers, but you won't get much of a sample size due to danger mouse's assertions above about resources. How many people have done biotoxin avoidance all these years, the way that Erik Johnson describes it? 10? 20? 30? I'm sure the number of patients that have tried ARVs is way more than that already.

    So yeah, I have a few hypotheses for you to test, but if there's no practical way to test them what's the point?

  34. >@ Lisa,
    Despite the insistence in the past that I am the one with tunnel vision, it is not so. I have never discounted the environmental piece of the puzzle, only that it is of more importance to some than others, and didn't seem likely to be the decisive factor for us. That said, I do notice a "location effect" in Hawaii that going to sea level in Louisiana didn't reproduce. Of course two days in a truck through incredible weather, while adjusting to a new med, is not a good comparison to flying to the Big Island and being in my own place. 

    I quoted a paper somewhere in the last couple of blogs that talked about chemical/radiation inducers of viral replication in vitro. 

    As it may be unnecessary to sequence all the viruses to draw clinical conclusions, it may be unnecessary to identify all the sources of toxin. Reverse transcriptase inhibitors plus an integrase inhibitor move the illness, but not enough. Possibly with a protease inhibitor or with the addition of immune modulation, which is what radical avoidance is. 

    We bought a barely used, gassed off hybrid, with fold out tent beds. Lots of ventilation. Ali will try a night in it soon. As I've noted in the past, her issues are with perfumes, triggering dysautonomia. I view it as a paroxysmal neurological response to sensory input, similar to the way a strobe can trigger seizure activity in some epileptics. It is currently limiting her, as she isn't that limited physically. Will take her to the GFD soon, and probably Hawaii in March. 


  35. >@jamie I disagree that it may be unnecessary to identify the agents just because that may be the case for retrovirii. You cited RT inhibitors and protease inhibitors: both of these tell you you're dealing with a retrovirus. Whereas when biotoxin avoiders say they feel better from radical avoidance, the untrained eyes and ears just interpret that as avoiding the entire environment in Civilization. Hence the burden is on us to provide an identifiable agent to start.

    However, as I mentioned earlier it's much easier run a hypothesis on changes of inflammatory signature of PEM with biotoxin avoidance/location effect and associated symptomatic improvement. I'm just not naive enough to believe anyone with money or clout would want their name associated with the study design.

  36. >"It has been tested extensively, all reputable studies to date have been negative."

    No a synthetic virus called VP62 that is a xenotropic polytropic hybrid has been tested a bit. A polytropic MRV that integrates into human DNA and produces an immune response has not been tested by anyone other than Mikovits, Lo, Alter and Ruscetti. Prostate cancer VP42 has also not been extensively tested, but it is logical that it may exhibit many of the properties identified in it's brother VP62 and those of other gamma retroviruses.

  37. >Different environmental toxins may affect CFS sufferers differently.

    I have respiratory problems which are exacerbated by airborne allergens in nature — pollen, mold, ragweed, cigarette smoke, smoke from barbecue stands, traffic exhaust, perfume, bleach, ammonia and lots of chemicals. They all cause my throat to tighten up and for my chest to tighten up, making it hard to breathe.

    Since I live in a big city where smoke of all kinds and traffic exhaust are rife, and worse in the hot weather, I stay home most of the time. If the air is thick with pollution, including when there are ozone alerts in the summer, I cannot go outside at all.

    I have to walk far from anyone smoking or from outdoor food/cooking stands, and from traffic exhaust, especially from buses and trucks.

    I feel better on crisp, cool or cold days where there is little pollution, where the wind is blowing and smoke or other chemicals are not trapped between buildings. Heat destroys me. That has worsened over the years. I cannot go out on hot days and have no energy whatsoever, even within my residence.

    I think I would feel better living in fresh, cool, nonpolluted air — not in a desert, too hot. Maybe the Canadian wilds. Not likely I'd move there.

  38. >" It has been explored as a theory as both causative of ME/CFS and causative of the inflammatory patterns seen in ME/CFS, but without knowing what we're testing, any hypothesis that we come up with is no more than a shot in the dark. "

    An idea does not become a hypothesis until you do know what you are testing. Where as HGRVs are a hypothesis.

  39. >"Whereas when biotoxin avoiders say they feel better from radical avoidance, the untrained eyes and ears just interpret that as avoiding the entire environment in Civilization. "

    That could still be a HGRV.

  40. >@kathy d's last post is Exhibit A for why we absolutely need identification of agent(s) to legitimize our avoidance efforts in any way. No matter how many ME patients lose their PEM, the chorus will continue to shout "we're all different! we all react to different things!"

    I think what's closer to reality is that we all react to just about everything. I think most long-time ME/CFS patients develop MCS, increased allergies etc. All universal signs of upregulated inflammatory immunity.

    However, the trend we've seen with the biotoxin avoiders is that they lose their chemical sensitivities, EMF sensitivities etc after they do radical avoidance for some time. In the end they are still sensitive to changes in outdoor air, so one would reasonably think that reactivity to stuff we can actually smell (smoke, pollution, grass, perfume).

    One very good comparison is addressing the MCS. Do ME/CFS patients ever lose their PEM from wearing respirators that rule out particulates? I addressed my MCS religiously for years but it never touched my PEM. I just stopped getting more ill from exposure; I didn't actually get better. I've never heard of someone that has, but I would love to hear it if anyone has.

    However, from what I understanding, every ME/CFS patient that has done biotoxin avoidance according to Erik's guidelines has improved measurably.

    This outcome tells me that whatever we're dealing with isn't even remotely in the same category as chemicals, smoke, or other recognizable particulates

  41. >@anonymous's last comment. This is the point where I throw my hands up and wish you the best of health.

  42. >Correction to above:

    "In the end they are still sensitive to changes in outdoor air, so one would reasonably think that reactivity to stuff we can actually smell (smoke, pollution, grass, perfume) is downstream."

  43. >Damn straight!

    citychanger said…
    This outcome tells me that whatever we're dealing with isn't even remotely in the same category as chemicals, smoke, or other recognizable particulates

  44. >"kathy d's last post is Exhibit A for why we absolutely need identification of agent(s) to legitimize our avoidance efforts in any way. "

    Everyone will be different though and living in different places. It's really is very similar to dietary needs.

    If you take the HGRV hypothesis and construct a model of how that causes ME you could start to pinpoint why certain things will be a trigger, however it is still going to come down to the nuances of the individuals biology and the need to use trial and error.

  45. >@anonymous

    Again, based off my experience, I can tell you whatever I'm avoiding is a totally different ballgame from dietary needs. It's really as simple as whether removing something resolves PEM, the hallmark of ME/CFS. Have you heard of a ME/CFS patient changing to a paleo diet and losing PEM? Again, I have not but if you have I would love to hear it.

    And like I said, until we are able to identify what it is we are actually successfully removing from our respiration to lower inflammation so drastically that we can hike without PEM, then of course your analogies to EMFs, diet, chemicals etc are all founded. I can't argue with you because we are lacking the scientific framework with which we could actually defend our experiences.

    Until identification comes, most people will say exactly what you've just said, and we really can't blame them.

  46. >As another "extreme avoider", I'd not characterize what I personally do as avoiding the entire environment at all. I live in a pretty civilized setup, and go to stores, restaurants, and even cigar bars on a regular basis. There is a very specific effect, and ONLY that effect, that I avoid.

    Just my two cents. :)

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