May 12, 2017 Is International ME/CFS and FM Awareness Day
International ME/CFS and FM Awareness Day is May 12th, 2017. Jody Smith shares some information about upcoming events and ways you can be heard ...
Discuss the article on the Forums.

CDC PCOCA conference call on 2/23/2015 with Dr. Montoya and Dr. Unger

Discussion in 'Upcoming ME/CFS Events' started by Wally, Jan 24, 2015.

  1. Gemini

    Gemini Senior Member

    Messages:
    666
    Likes:
    1,214
    Great transcript @Scarecrow. Thank you!
    Professor Edwards is discussing inflammation and CRP on another thread (hope I copied this link correctly)
    http://forums.phoenixrising.me/inde...ise-in-autoimmune-diseases.35782/#post-563754
     
    Anne, oceiv, Kati and 2 others like this.
  2. Soodie

    Soodie

    Messages:
    1
    Likes:
    0
     
  3. nandixon

    nandixon Senior Member

    Messages:
    844
    Likes:
    2,109
    Anne, Sasha, oceiv and 1 other person like this.
  4. Research 1st

    Research 1st Severe ME, POTS & MCAS.

    Messages:
    697
    Likes:
    2,308
    CDC and homebound patients with CFS, said to be relevant to ME by the IOM (who redefined ME CFS = SEID).

    Lets be realistic and ask ourselves, what does it mean for science (medically speaking) to be home bound CFS or SEID patient? It means little to nothing unfortunately. Sadly, no abnormalities need be present to be classified as severe, other than be someone who lives at home, or lays in a bed with a diagnosis of CFS. Lots of mentally ill people lay in bed. They too can meet the criteria for severe CFS. We know the CDC have used people on the phone for CFS 'research'. Diagnosed 'CFS' over the phone!

    ''the CDC first screened 56,000 people in Wichita, Kansas for CFS via telephone''
    Source: http://phoenixrising.me/research-2/...onic-fatigue-syndrome-mecfs-i-an-introduction

    Should the severe CFS be studied? Yes of course.

    Yet lets make sure when someone is 'severe' we know what that means in comparison to non severe.
    1st problem, no one knows. The CDC don't know either, because the CDC will have to use 'fatigue' as the basis of severe, clearly, as they blueprinted the chronic fatigue syndrome and ignored the whole plethora of organ system dysfunctions in its CFS.

    Since the IOM published their fantasy about SEID replacing 'ME/CFS' after the media blitz settled down, diagnostically we see that SEID is no different to Fukuda CFS (and the same as British CFS/ME), and just adds Post Exertional Malaise (PEM) to CFS diagnostically. Unfortunately for biomedical researchers, PEM can be a form of emotional upset after undertaking an activity in people with fears of activity.This means psychologists and psychiatrists simply need to find people with this form of PEM (somatization over activity), and hey presto. SEID is not an inflammatory disorder. Knowing this, a fool can see the SEID remove inflammation as a required diagnostic signature of SEID. This was probably done by preventing the release of the Montoya paper in May 2014. Where did that 'game changer' go? The one announced in March 2014? How curious the IOM rushed their SEID to market....


    What does this means for researching severe CFS patients? It means a bad deal.
    Post Exertional Relapse (PER) is what the CDC and SEID refuse to categorize, but is a feature of organic
    CFS and ME
    . A relapse, of course, is not a malaise! A person with diabetes may relapse into a state of hyperglycemia by failing to stick to a given insulin regimine. The same happens to someone with ME with their organic disease if their disease state is worsened from activity, infection, etc.

    Example of a relapse below, not malaise: These are classic signs of ME.


    An individual who is short of breath just speaking, eating, drinking (who wasn't before exertion and remains so).
    An individual who cannot sit up or speak (but was able to talk at length most days for house before).
    An individual who's heart rate is 130 standing (and wasn't the week before exertion).
    An individual who's lymph glands are enlarged (and weren't the week before exertion).
    An individual with a flair in endometreosis/prostatis/bronchospasm (that wasn't there the week before exertion).
    An individual with repeat URT infections (that wasn't there the week before exertion) and now plagues them.
    An individual with postural hypertension with narrowed pulse pressure (that wasn't there the week before exertion).
    An individual who cannot dress themselves, wash, or eat (who could the week before exertion).
    And individual with crippling vertigo caused by walking or standing (which wasn't there before).

    And on and on... This is what ME does to people. Something the CDC are in complete denial of:
    (See their website: http://www/cdc.gov/cfs).

    Those with symptoms of organic ME are not undergoing a post exertional SEID 'malaise', but an inflammatory immuno reaction which the CDC and IOM say they can find no evidence for so took inflammation out as a requirement to have SEID or CFS. :whistle:. As I said, they WOULD have had proof had Montoya's paper not been blocked. The one he said was ready in about 8 weeks, 12 months ago. :cry:

    All ME CFS research is never going to study severe ME sufferers more accurately, unless the CRITERIA are more stringent. (The IOM are proud over creating an equal criteria to British CFS/ME! An inadequate state invented condition, that has utterly failed since it's conception by the British health service, the Department of Health, to help those with ME).

    Statistically, researching ME is impossible if using Fukuda or SEID diagnostic criteria.
    The ME International Consensus Criteria were developed (ME-ICC) to overcome this hurdle. BUT American government health agencies rejected ME-ICC and even rejected CCC CFS (SEID is diluted CCC CFS), and wanted a fatigue based criteria identical to the British (CFS/ME) set up in their National Health Service (NHS) socialized health care system, just with a new bleached teeth smile for the media. SEID has achieved that. CFS achieved that too. This is problematic when considering severe patients for research!

    With CFS or SEID one's house bound illness could be a figment of their imagination. It doesn't mean it is, it just leaves room for it to confuse biomedical research findings. This prevents quality biomedical research, prevents effective treatments and prevents the severely ill with ME recovering as they are never studied fairly.

    After 46 years of being neglected with a 'recognized neurological disease' (ME), we know the drill.
    The drill is American leadership in ME denial, with the British close in line ready to offer their 'exercise' experts to take up an 'advisory role', which is why the CDC and others, have literally, copied and pasted British CFS psychobabble onto their American websites about CBT and GE for American health agencies.

    Does anyone seriously think a CDC who says the following, is going to select people with neuroinflammatory ME CFS who are homebound? :rofl:

    CDC CFS website....

    No scientific evidence exists for this CDC statement.

    No scientific evidence exists again. No studies have been done on patients with evidence of organic inflammatory disease who have CFS diagnosis who have adjusted and coped, to see if they are healthier, because: What does ''feel healthier'' mean. How do you quantify it? Again, no science needed if we have engaged in a form of medicine where subjective 'feelings' is evidence for a therapy being touted as beneficial.

    Where is the proof, that 'spreading out' activities prevents a crash? Define a crash medically or scientifically? What are the CDC criteria for a crash? None are given, it's entirely subjective without biomarkers. The Push Crash theory is a direct copy of the British psychobabblers who believe in the self delusional myth that patients behavior (doing too much) leads to set backs. The science, says the immune system leads to set backs, not 'doing to much' in a push crash cycle!



    I would love to swallow humble pie, but don't wait up for it. (Cytokines are also elevated in stress and depression, and Dr Hornig is a psychiatrist so may be looking to 'prove' that CFS is a neuro-psychiatric disorder in response to to 'X' - X being anything, including an infection and genes). I'm sure certain criteria CFS are a neuropsychiatric condition, but CFS/SEID isn't ME if the diagnosis shuns muscle pain, cardiac, autonomic, endocrine and CNS inflammation as a requirement for having it.

    If the IOM say SEID is ME, then it needs to be ME.
    If the CDC severe CFS research claims to be relevant to ME, then it needs to be relevant to ME historically and diagnostically.

    So any CDC research on 'severe' should mean displaying the signs of severe ME, not having a CFS SEID diagnosis and being home bound. We know this won't happen, as it can't happen. They'd break their own diagnostic criteria of ''unexplained''. And there's the catch 22 of 'severe' research from here onwards.
     
    Last edited: Feb 28, 2015
  5. MeSci

    MeSci ME/CFS since 1995; activity level 6?

    Messages:
    7,985
    Likes:
    12,847
    Cornwall, UK
    Don't worry if you have answered this later in the thread - I hope to finish reading the thread today - but what was the mRNA for? Cytokines? If so, this article I just found may be completely irrelevant but is interesting, as it indicates how dietary components could be used to modulate levels of different cytokines via effects on mRNA.
     
    Anne likes this.
  6. Scarecrow

    Scarecrow Revolting Peasant

    Messages:
    1,903
    Likes:
    5,385
    Scotland
    @MeSci, sorry I didn't hear him saying. The emphasis was very much on the match to SIRS and not what the genes were for. Yet to be revealed?
     
  7. Anne

    Anne Senior Member

    Messages:
    295
    Likes:
    723
    I've listened to the entire PCOCA call now and wow, is Dr Montoya an inspiring force in the ME/CFS field. We need to somehow get him the millions of dollars he needs... Let's keep pushing for an RFA from the NIH.

    One thing: It's obvious that there are scripts for these presentations, both from Dr Unger and the guest speaker.

    WHY doesn't CDC just publish the scripts afterwards? So much easier than us listening in, scribbling down things and sitting here in this thread trying to figure out what was said....

    (I can understand if the Q&A section is harder to publish, but the scripts of the presentations...!)
     
    mango and Wally like this.
  8. Anne

    Anne Senior Member

    Messages:
    295
    Likes:
    723
    Here's a transcript of some of the most interesting parts. Can anyone help with the text in bold?

    Valgancyclovir – we discovered this drug has immunomodulatory abilities that were not known before our work at Stanford. These include a temporary but significant decrease in circulated monocytes and a shift towards a TH1 profile.

    We believe that immunomodulation not only could partially explain the benefit of Valgancyclovir, but could easily turn out to be crucial in the treatment of ME/CFS. In fact, our cytokine data and that of others support this view.NK cell function: we’ll apply novel technology to the NK cell deficiency in ME/CFS shown by several groups

    We believe suppressing herpes viruses may be an important component in what should be a holistic approach to treat ME/CFS patients

    Mark Davis, Center, Stanford Human Systems Immunology Center (Human Immunome Project)

    Cytokine study – Jarred Younger – leptin – a cytokine with high capacity to trigger inflammation.

    In ME/CFS there is progressive inflammation that worsens as disease severity increases.

    Conventional indicators of inflammation such as ESR/Sed Rate and CRP are often normal. However, Sed Rate and CRP are primitive and very limited indicators of inflammation. Our cytokine data contradicts the erroneous conclusion that ME/CFS is not an inflammatory disease and supports that not only an inflammatory state exists in these patients but also opens the door for the use of anti-inflammatory drugs or biologics, as has been done for other inflammatory diseases whose aetiology is still unknown, including rheumatoid arthritis and systemic lupus erythematosus.

    We are in the process of analyzing messenger RNA gene expression data (– but what was the mRNA for? cytokines? I don't think he says, does anybody know?) from the cohorts of 200 patients and 400 controls. We compared the gene expression data for ME/CFS with other diseases for which data has been published. The disease process with closest resemblance to ME/CFS was Systemic Inflammatory Response Syndrome, SIRS.

    From the Stanford data and the Columbia [Lipkin/Hornig] data the picture that clearly emerges is that ME/CFS is indeed an inflammatory disease.

    The heart is highly unlikely to be affected in ME/CFS. We are still working on endothelial function and cytokine levels before/after exercise; we are in the process of analyzing that data.
     
    Last edited: Mar 18, 2015
    zzz and Blue like this.
  9. Anne

    Anne Senior Member

    Messages:
    295
    Likes:
    723
    I've been thinking about Montoya's statements mean in relation to Lipkin's and Hornig's statements. Montoya seems to say that ME/CFS is an inflammatory disease, period - no mention of the 3 year-limit, while Lipkin and Hornig seem to think ME/CFS is inflammatory during the first 3 years (or so), then the immune system downshifts into some other dysfunction. Right? It would be interesting to hear them discuss this!

    As mentioned in another thread the two studies of cytokines in spinal fluid (the one newly published by Peterson, NCNED + the one coming up by Lipkin/Hornig) seem to show contradictory results.

    Thoughts, anyone?
     
  10. alex3619

    alex3619 Senior Member

    Messages:
    12,637
    Likes:
    35,704
    Logan, Queensland, Australia
    It might still be inflammatory. We need to see the spinal fluid studies to see what brain cytokines are doing. In addition there may be other inflammatory processes. Strictly speaking, inflammation is an over-used word. Its not quite as bad as fatigue, but it can still be about a wide range of factors when it is used.

    Lipkin et. al. showed lower cytokines in long term patients, but not all of the relevant cytokines, in blood. It has been speculated by some of the researchers that this represents immune exhaustion. That is they would be pumping out inflammatory cytokines but no longer have the energy or other capacity to do so. This implies that, potentially, if energy is restored, so are the cytokines.
     
    aimossy, halcyon, MeSci and 3 others like this.
  11. shannah

    shannah Senior Member

    Messages:
    1,390
    Likes:
    1,659
    This has been really bothering me as well. Like everything with ME, more confusion.

    I'm a long termer and my inflammation is scary - through the roof.

    Perhaps genetics plays a role?
     
    Anne likes this.

See more popular forum discussions.

Share This Page