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EBV, Candida, Dorsal Root Ganglionitis and Dorsal Defects - putting pieces of the puzzle in place

Discussion in 'General Treatment' started by John H Wolfe, Sep 10, 2012.

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Do you think there may be something to this analysis?

  1. Yes

    4 vote(s)
    57.1%
  2. Didn't read it

    0 vote(s)
    0.0%
  3. No

    3 vote(s)
    42.9%
  1. John H Wolfe

    John H Wolfe Senior Member

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    If you can get your head around the title of this post then you may even be able to get your head around my rambling rhetoric on these topics!

    First, allow me to introduce myself - I am a young man from London, UK who has had CFS/M.E. for the past decade

    Following encouraging email exchanges with members of my local M.E. support group, last week I finally decided to formalise some of my thoughts, in the light of my personal experience/things I have heard/read over the years, in the form of a blog

    Besides sharing my thoughts on how to maximise wellness, in the light of the recent research and theory concerning inflammation of the dorsal root and linked ganglia, including an article on this very website, I decided to try to put some of the pieces of the jigsaw together and came up with the following blog-post-come-article

    I thought I would post here in order to invite consideration of, and discussion and constructive feedback concerning, the composite research and my interpretation from the wider community:

    M.E. & My Analysis [link]

    Many thanks,

    John H Wolfe
     
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  2. mellster

    mellster Marco

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    Nice analysis (I think most if not all has merit)! And keep those lymphs moving.. :)
     
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  3. In Vitro Infidelium

    In Vitro Infidelium Guest

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    It’s never fun to have others rain on your parade – but you did ask:

    Creating hypotheses for M.E/CFS (or M.E, or CFS, or PVFS etc) can become a full time occupation, and while we all need some kind of explanation for ourselves, it’s important not to confuse hypothesis with something which can be tested by science. No one could say your conclusions aren’t true, however mixing and matching science with sources of highly dubious validity isn’t going to produce anything other than a personal narrative. I’m sure there will be people reading here who will appreciate your concept – however relying on Myhill, Shapiro and Perrin would as far as I’m concerned produce more a work of fiction than of science.

    Personally I doubt that there is a single disease process that underlies the illness experienced by the group patients circumscribed by even a restrictive criteria set such as the Canadian Criteria. My guess is that multiple aetiologies will eventuall be demonstrated across the patient population. In that circumstance almost any scientifically based hypothesis could have merit, but no single hypothesis would tell us something useful about the process of disease in the majority of patients. I understand why that perspective is very unattractive because conceptually it pushes discovery of a ‘cure’ into a distant future – but that is where I think we are, others will disagree.

    IVI
     
  4. Marco

    Marco Old blackguard

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    I would tend to agree that there is unlikely to be a single disease etiology even within the more narrowly defined Canadian Criteria hence why I tend not to subscribe to the single pathogen theories. On the other hand this doesn't preclude the potential for a common physiological pathology underlying a wide range of symptom complexes that is not necessarily circumscribed by even the most lax criteria for 'CFS'.

    I don't find this scenario at all unattractive or a cause for pessimism.
     
  5. In Vitro Infidelium

    In Vitro Infidelium Guest

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    Yes, to suggest that there could be no commonalities of pathology between differing aetiologies would be an extreme position, and commonality of gross symptoms very likely does indicate that there is just a limited number of disease processes to be found across the global patient population. The point I think though, is that when we are discussing hypotheses of M.E/CFS, this can only reasonably be done where each and every hypothesis is explicitly couched in terms of the limitation of likely application to a subset of patients, rather than any one hypothesis being a 'single unified theory'.

    I agree. My comment above was an attempt at acknowledging why the idea of multiple aetiologies seems generally unwelcome, rather than specifying my own position. I think one of the problems with the 'single answer' position is that it sets up a distisfaction with the scientific process because science has failed in finding the 'one answer', which ought (axiomatically) to be a simple task. Yet (and yes the level of investment has been woeful) all the research there has been has yielded one vital characteristic - nothing about M.E/CFS is consistent across patient groups. We can't escape that fact, nor that such inconsistency makes the task of establishing aetiologies extremely challenging. Accepting that M.E/CFS is likely more than one 'disease' presenting with common symptomolgy is in my view the only way to make progress, both scientifically and in terms of advocacy. Even at the level of dealing with inappropriate treatments, challenging the one prescription fits all, has significant power.

    IVI
     
  6. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    What about a natural killer cell defiency/dysfunction as the cause, that would explain the different infections found in people and also why herpes viruses seem to be so common as they are normally only reactivating in patients with compromised immune systems like HIV, cancer etc
     
  7. John H Wolfe

    John H Wolfe Senior Member

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    Haha, thanks, will do :)


    Indeed it is


    Hmm, there's constructive feedback and “raining on someone's parade”, and then there's belligerence and pissing on someone's parade. This comment crosses that line, and is, for me, a little too hyperbolic/exclusive to be reasonable - particularly in the context of the discussion of the investigation of an illness(/group of illnesses) with an as yet unknown aetiology, the identification of which will likely call for some degree of imagination, thanks to the intrinsic nature (complex, multi-system) of the condition(s)


    Granted the end product of an ideas based exploration is never going to be (a) hypothesis/es with a particularly meritorious cast iron scientific basis and hence irrevocable validity in the eyes of informed, objective observers. Does that make it futile or worthy of such condescension?

    This is more reasonable, however where is it that you think science sprung from originally?- inherited ethereal wisdom or observation, theorisation (in part a function of
    intuition/imagination), hypothesis and testing?..

    I’d be inclined to agree, although it would be foolhardy to omit the possibility that there could be a root disorder, followed by differing consequential manifest dysfunctions


    Unless it/they helped to unlock the effects of the above-noted possible root process, or indeed one of a number of possible co-dependent processes


    Precisely, and likewise :)

    NK cells do get a mention in my post, in conjunction with candidasis, although I haven’t read up on specific deficiencies – do you know of any relevant papers?
     
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  8. In Vitro Infidelium

    In Vitro Infidelium Guest

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    That would support a model where M.E/CFS is functionally a single condition, but one capable of initiation by one or more pathogens. A criticism of this model would come from the fact that active infection is inconsistently identified, so an hypothesis then has to invoke either an 'on/off' switch for the defiency/dysfunction as a general feature of the illness, or accept multiple aetiologies that don't all rely either on infection or upon killer cell defiency/dysfunction. Multiple aetiologies is in many respects (given what evidence there currently is) the most parsimonious, and therefore scientifically preferable, position; although in itself this wouldn't exclude an on/off switch playing a role in some/all aetiologies.

    Pathogen reactivation is a poorly researched aspect of human health. Immune compromise is seen generally in terms of exceptional challenge - immunosuppressive treatments, HIV etc , but the role of aging (e.g Shingles) or other non exceptional biological (weight gain/loss, reduced/increased activity etc) changes may also be significant. However, the evidence for a reactivation effect would require measures of consistent pathogen activity - or otherwise an on/off switch explantion would be required to support any hypothesis that is reliant upon a reactivation effect. These are all areas worthy of consideration but without consistent evidence, including where necessary evidence that explains otherwise inconsistent evidence, then consideration can only be in terms of tentative speculation.

    IVI
     
  9. snowathlete

    snowathlete

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    I think the herpes virus being involved is certainly a possibilty and i agree that the Rituximab studies would seem to lend support to that hypothesis. I dont like EBV, its the only serious illness (mono) I have ever had apart from ME. and i cant help but suspect a link as there also seems to be some symptom overlap. I find myself resisting to use the word likely - but that is quite deliberate. One of the problems with research into ME is that researchers seem quite stuborn in their believe in a particular hypothesis and people with ME are just the same. We all have our own experience and beliefs. Its just as likely, perhaps, to be something else entirely. Certainly they cant all be right...(well, probably not). Many are logical and have promise and may be the answer. Some (Perin's for example, in my own opinion) dont look likely to me.

    I think that with several 'good' ideas out there it is tempting to piece together several of them to come up with a hypothesis that seems to make the puzzle complete. But im not sure that this approach is going to result in a better hypothesis. Rather than ending up with the complete picture, you're just as likely to end up with the wrong picture because you used pieces from two different jigsaw puzzles.

    So, yeah, this hypothesis is alright, but i dont think its likely to be correct, but then thats the problem isnt it?
    trying to get to the bottom of ME is like trying to do a jigsaw puzzle but the pieces in the pile come from several different puzzles, and maybe there are pieces missing. What is most certain is that there are pieces in the pile that do not belong. So, i would be enclined to thin the hypothesis down as much as you can so that what you do have, though there may be holes, is solid.
     
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  10. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    heapsreal said:
    What about a natural killer cell defiency/dysfunction as the cause, that would explain the different infections found in people and also why herpes viruses seem to be so common as they are normally only reactivating in patients with compromised immune systems like HIV, cancer etc​
    NK cells do get a mention in my post, in conjunction with candidasis, although I haven’t read up on specific deficiencies – do you know of any relevant papers?
    http://www.translational-medicine.com/content/pdf/1479-5876-9-81.pdfThe above study is mainly of nk bright cell dysfunction as a biomarker for cfs/me.

    Herpes virus reactivation ie ebv/cmv/hhv6 i agree is poorly studied but looking into Dr Lerners work where he treats people above a certain levels of igg viral titres as a reactivation and then antivirals reduce these titres with an improvement in symptoms i think is very relevant and this is also seen by other docs treating patients with antivirals.
    I think to help find answers we need to work backwards from helpful cfs treatments like antivirals, ritux and ampligen treatments. Ampligen is a strong interferon inducer, interferon itself has antiviral properties as well as having the ability to improve nk function. One more thing to tie in herpes viruses and nk cells, herpes viruses have the ability to avoid the immune system by turning down natural interferon, therefore reduced antiviral activity from interferon and reduced nk function. reduced nk function also then leaves us open to other infections that become chronic as nk cells now cant kill or reduce the number of these infections.

    I wish i had more links to what i have said but it is stuff that ihave plucked out of the library in my head after doing alot of my own research.

    Also there is a piece of the puzzle missing because even withthese treatments full remission is hard to obtain, maybe this occurrs due to the damage to our nervous system from these infections. Also an underlying retrovirus fits in well to the cfs/me theory too.

    Personally i think using ritux or ampligen(both for immune system) with antivirals and antibiotics when needed for bacterial co-infections, we are onto something. At a guess i would say the above treatment regeme has been used by few, sperately(mainky antivirals) by alot more producing partial results.

    Symptom treatments show us alot more about where the dysfunctions are, daa in my brain, as this is where manythings are controlled from like sleep, blood pressure, etcetc

    interesting subject guys,
    cheers!!!
     
  11. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    One more thing to tie in herpes viruses and nk cells, herpes viruses have the ability to avoid the immune system by turning down natural interferon, therefore reduced antiviral activity from interferon and reduced nk function. reduced nk function also then leaves us open to other infections that become chronic as nk cells now cant kill or reduce the number of these infections.

    Virus resistance to interferons
    Many viruses have evolved mechanisms to resist interferon activity.[11] They circumvent the IFN response by blocking downstream signaling events that occur after the cytokine binds to its receptor, by preventing further IFN production, and by inhibiting the functions of proteins that are induced by IFN.[12] Viruses that inhibit IFN signaling include Japanese Encephalitis Virus (JEV), dengue type 2 virus (DEN-2) and viruses of the herpesvirus family, such as human cytomegalovirus (HCMV) and Kaposi's sarcoma-associated herpesvirus (KSHV or HHV8).[12][13] Viral proteins proven to affect IFN signaling include EBV nuclear antigen 1 (EBNA1) and EBV nuclear antigen 2 (EBNA-2) from Epstein-Barr virus, the large T antigen of Polyomavirus, the E7 protein of Human papillomavirus (HPV), and the B18R protein of vaccinia virus.[13][14] Reducing IFN-α activity may prevent signaling via STAT1, STAT2, or IRF9 (as with JEV infection) or through the JAK-STAT pathway (as with DEN-2 infection).[12] Several poxviruses encode soluble IFN receptor homologs—like the B18R protein of the vaccinia virus—that bind to and prevent IFN interacting with its cellular receptor, impeding communication between this cytokine and its target cells.[14] Some viruses can encode proteins that bind to double-stranded RNA (dsRNA) to prevent the activity of RNA-dependent protein kinases; this is the mechanism reovirus adopts using its sigma 3 (σ3) protein, and vaccinia virus employs using the gene product of its E3L gene, p25.[15][16][17] The ability of interferon to induce protein production from interferon stimulated genes (ISGs) can also be affected. Production of protein kinase R, for example, can be disrupted in cells infected with JEV or flaviviruses.[12] Some viruses escape the anti-viral activities of interferons by gene (and thus protein) mutation. The H5N1 influenza virus, also known as bird flu, has resistance to interferon and other anti-viral cytokines that is attributed to a single amino acid change in its Non-Structural Protein 1 (NS1), although the precise mechanism of how this confers immunity is unclear.[18]
     
  12. mellster

    mellster Marco

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    I agree on the theory that there is much likely not a single cause, I think it's almost a given a this point. However I'd like to make a bet that there is a link to EBV (and/or possibly other HHV viruses that can cause mono-like illnesses such as CMV) in a solid majority of the cases (unless it is proven that it i simply a bystander).
     
  13. In Vitro Infidelium

    In Vitro Infidelium Guest

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    No condescension - but an observation of a practical problem, that translates into a general existentialist difficulty. Either the endeavour of creating a reasoned hypothesis is governed by limitation to points of reference which are themselves of valid reasoning, otherwise the endeavour becomes only a narrative, a story. We all tell these kinds of 'stories' to ourslves all the time, it's essential to mental functioning, but to have reasoned validity and to make an hypothesis something other than just another 'life tale' requires strict limitation on the points of reference. Myhill's 'environmental medicine' and Perrin's osteopathy, do not provide reasoned points of reference for a scientific endeavour - they are fundamentally a-scientific.


    I don't think science sprang from anywhere - it's just a way of doing things that has been developed to maximise objectivity and reason. In practice the ideal may not always be achieved, but that's the nature of ideals. Neverthless science has become very good at avoiding mere story telling and while there's much fantasy about the the grand insights of gifted individuals - science fundamentally proceeds on the basis of accummulative knowledge with imagination and intuition playing only moderate roles. Of course the strorytellers of science (which often includes those whose imaginitive leaps happened to pan out) present the triumph of the mind as the source of progress but in reality scientific progress is 99% process. M.E/CFS has had far more stories than was ever healthy, hypothesising can be fun, but to avoid the seduction of a sexy narrative, hypotheses are best treated as footballs - most interesting when they are kicked around on a muddy field.

    IVI
     
  14. justy

    justy Senior Member

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    Hi John H, welcome aboard. Thanks for sharing your hypotheses and blog posts with the forum. My brain is way too fried today to think abou this properly but i voted that the idea has merit as far as i can ascertain, sorry i'm not able to discuss furhter today. I'm personally not keen on Perrins theory - i know he has helped some and achieved remissions in others (some of whom i believe have relpased again later)

    The main point i wanted to make was about your blog post on ways to manage the illness (sorry cant remember the title) I am concerned about the advice to try 'light' exercise such as yoga, walking swimming etc every other day - i understand the need to keep the lymph moving, but for most people who are more than very mildly affected this level of activity could cause a severe relapse. I have seen this advice given by many patients and doctors and cant understand where it comes from. I have been both mildly and severely ill in the 17 years since i first came down with M.E - currently improving from moderate but i can honestly say that i couldnt swim for more than a couple of minutes once a month - let alone do yoga or Tai chi - just the stretching required to warm up would send me inot a relapse. If there is one thing with this illness that i am absolutely certain of, it is that activity beyond available energy makes a worsening of the condition and all symptoms which can be anyhting from troublesome to catastrophic.

    Sorry a bit off topic.
    I also dont see why M.E isnnt one illness and why it has to be many. Lots of diseases have variations within them of symptoms, severeity etc, eg MS or lupus where there are different types. I have so much in common with other PWME i dont see why the insistence that it has to be many diseases/causes under one umbrella.

    All the best, Justy
    Please excuse my ramblings, in a bit of a downward spiral this week and unable to think clearly.
     
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  15. Marco

    Marco Old blackguard

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    I'm afraid I don't have much faith in diagnostic labels or differential diagnosis.

    Let me explain using a little analogy.

    Imagine a young child who has a large collection of Matchbox toy cars (small scale die cast metal cars for those not familiar) which he keeps in a suitably large biscuit tin.

    Having become bored with these toys, one day he goes to his father's tool shed and in a particularly destructive mood (kids do these things) takes a hammer, tips his toy cars all over the floor and sets about bashing them up with the hammer.

    If a conscientious researcher were to come along and try to make sense of the resulting carnage how would they go about it? They may logically decide that they can group a number of the cars together based on the visible damage. Some have lost their wheels, some have smashed windows, some have the roof bashed in and some have the plastic floor cracked.

    Our dilligent researcher decides to name these groups with reference to their most visible 'symptoms' e.g. 'wheels off syndrome', 'smashed window syndrome', 'bashed roof syndrome' etc. Some examples defy easy classification e.g. smashed windows with one or two lost wheels. These are discarded into an 'atypical' pile.

    From now on researchers studying these groups do so only with regard to the primary 'symptoms' and largely in isolation from the other 'syndromes'. For example, they may try to determine why the wheels came off (literally) in one group.

    Unfortunately in his (or her) haste to make sense of this seemingly diverse collection our dilligent researcher has overlooked a small but significant detail that they all share. All will show the marks of the impact of the hammer whether it be chipped paint, dented metal or cracked plastic.

    Perhaps not a perfect analogy but workable for the purposes of discussion. It also begs the question of why a biomarker needs to be specific?
     
  16. In Vitro Infidelium

    In Vitro Infidelium Guest

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    EBV is interesting because it is ubiquitous - most adults will show positive for EBV antibodies. Such ubiquity would mean that if we allow that a range of aetiologies is present within the global M.E/CFS patient population, then in at least some cases, EBV must be a bystander pathogen - unless it's to be argued that EBV were to play a common role within differing aetiologies. Further if it is to be accepted that in some cases EBV is a bystander, then one has to consider that it may not have any general signficance at all, and from that, the role of pathogens in general may need to be seen as non essential to M.E/CFS aetiologies. That of course is wildly counter intuitive as much patient experience links progress of the illness from a point of acute infection.

    Perhaps rather than EBV as an organism, it is the process of Mononucleosis that is of significance in M.E/CFS, with Mono (glandular fever for Brits) being genetically mediated and the consequence of intense infection leading to chronic dysfunction. It might even be the case that Mono is merely a signpost illness, an indicator of a dysfunction that has wider consequences that are expressed as the full symptom load of M.E/CFS.

    IVI
     
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  17. Marco

    Marco Old blackguard

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    NK cell deficiency could also very well be a downstream effect.

    Plus the few consistently demonstrated immune irregularities found in ME/CFS are not necessarily specific to the condition (as per my previous post I don't see this as a problem).

    Reductions in NK cell numbers and/or cytotoxity are found in major depression and bipolar disorder for example :

    http://www.ncbi.nlm.nih.gov/pubmed/17974152

    ... while patients with bipolar disorder are also found to have B cell proliferation :

    http://www.cnsspectrums.com/aspx/articledetail.aspx?articleid=3596

    There is a groundswell of opinion that many 'psychiatric' and neurodegnerative disorders are neuroinflammatory in nature.
     
  18. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    That could show that the psychobabblers are probably wrongly diagnosing people with depression/bipolar and that those people have some type of infectious/immune problem that is being missed, im sure if they are trained by Wessely & Co he would be promoting those abnormalites as being the norm in psych conditions. Many docs treating so called cfs/me patients especially in the UK are told to do minimal testing on them, this might be why many of these psych patients are wrongly diagnosed.

    In cfs/me its not numbers of nk cells but function of nk cells, more specifically nk bright cell function. It could be down stream from some type of chronic infections, true.

    Dr John Martin has tested a number of so called Psychiatric patients that have been institutionalised after family members were not convinced of the psych diagnosis and found them to have had viral infections (stealth infections as he calls them) as the cause of their 'psych' problems, probably better to say its a neurological problem caused by possible infection.

    There is know specific tests for psych conditions to verify the diagnosis only questionaires and studying someones behaviour. I think if proper amounts of money were put into cfs/me research then diagnostic markers would be found or the markers found already would be more accurately verified.

    Personally i think psychiatry is 90% crap and an industry inventing new disorders to further feather their nests, thats my opinion and im weary of any psych studies as they know how to twist things in their favour more then other groups with main interests being big pharma with the next prozac.

    sorry for dribbling, just dont trust the psychobabblers.

    cheers!!!
     
  19. user9876

    user9876 Senior Member

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    What you say about classification is interesting. A while ago I heard a programme on the radio where a cancer specialist was talking about how we have the wrong view of cancer. He was saying that currently it is classified according to the part of the body where the growth is but that as we understand more about genes a better classification would be to look at the genetic form of the cancer cells. The point being that this may help determine which drugs will sucessfully treat the tumor.

    Since we are speculating in this thread: I believe that ME is an autoimmune disease. I was wondering if the way we look at auto immune dieseases is also wrong in that currently it is the part of the body affected rather than looking at the immune system mechanism. So in the Rituximab trials I think around 2/3rds of people responded, with Rituximab treatment of RA again not everyone reacts. I was wondering if therefore there are a number of different ways in which autoimmune diseases can attact the body. Currently many of the treatments are immune suppressants or antiimflamatory drugs that help reduce symptoms. Something like Rituximab is interesting since it seems to change the immune system cycle. In one paper
    http://rheumatology.oxfordjournals.org/content/40/2/205.full

    In one paper by Jonathan Edwards (who started using Rituximab for RA) speculates about an immune cycle where the B cells produce antibodies that cause T cells to damage the body. There also seems to be a body of work looking at mouse models of the immune system. As a better understanding of immune system mechanisms emerges then maybe we will see different auto immune effects with better drugs treatments to stop these cycles.

    The big question for me is if ME is an auto immune disease then what is being attacked and how this explain the range of symptoms. I believe that the PHANU group http://phoenixrising.me/archives/13315 have talked a lot about auto immunity. Light and Light talk of infections in the dorsell ganglia but could there be an auto immune imflamation there instead of an infection http://phoenixrising.me/archives/5802 . Or there has been talk of the Basal ganglia and insula cortes http://phoenixrising.me/archives/8707 . Some of these are interesting since they control the autonomic function of the body and I wonder if that could explain the wide range of symptoms.
     
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  20. In Vitro Infidelium

    In Vitro Infidelium Guest

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    M.E/CFS may be explained by a single aetiology, but the challeng to the 'single aetiology' proposition, comes from the limited biological research that there has already been. Of course this research may be misleading because it is incomlete or improperly focussed, but it is all we have to go on, and when aggregated the conclusion it most strongly supports is that all the different disease citeria sets for M.E/CFS, in one way or another, encapsulate an heterogenous medical condition. Biomarker research ( list of: Biomarkers) makes the case pretty starkly - because although a numer of different research teams have identified significant biological differences between patients and controls, there is little commonality between patient groups, so the broad conclusion has to be - "there are things going on in M.E/CFS patients (as distinct from healthy people) but these 'things' vary substantially between M.E/CFS patients". This is not the case in conditions such as a MS and Lupus, where a fairly narrow range of organic testing is consistent across the patient population.

    IVI
     

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