Choline on the Brain? A Guide to Choline in Chronic Fatigue Syndrome
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Famous report of 1934 LA outbreak

Discussion in 'General ME/CFS News' started by Persimmon, Jul 22, 2013.

  1. Andrew

    Andrew Senior Member

    Los Angeles, USA
    I cannot read the whole thread, so I don't know if this was mentioned. But my recollection is that the survivors developed antibodies to polio. I think I might have read this in The Clinical and Scientific Basis of Myalgic Encephalomyelitis--Chronic Fatigue Syndrome, Byron M. Hyde and Jay A. Goldstein 1992
  2. SOC

    SOC Senior Member

    Interesting. I wonder if that may be the place where two illnesses were erroneously and catastrophically lumped under the same name. I wonder if there's a subset of us that initiated with herpes viruses and another subset that initiated with ME.

    We could easily share a lot of symptoms in the long run if both resulted in immune dysfunction. It's even possible that over a long period of non-treatment, those of us who started with the ME pathogen (an enterovirus?) developed chronic herpesvirus infections and vice versa.

    I'm looking forward to the day when our history, although a still sad story of medical failure, will be more clear.
    alex3619 likes this.
  3. akrasia

    akrasia Senior Member

    I would describe my onset as Holmes +++. And the first doctor I went to see described the myriad symptoms I presented with, including marked stiff neck and upper arm ache, which continued for a very long time, as atypical mono, basing the laboratory evidence on EBV titers, which we now know are problematic as a diagnostic tool.

    The Holmes definition, in my view, was a sop, a stopgap, an evasion of a developing, widespread health crisis. It was more than anything a rhetorical feint rather than good science and allowed fatigue to be the face of the illness.

    On the other hand, Ramsey and people like Shelokov and Parish probably never thought that their work was definitive. This should have been the beginning of the conversation.

    Whatever intellectual value Ramsey's m.e. had at the time, it provided a conceptual life raft, a place of clarity, a bulwark against the forces of reduction and trivialization. There would have been no significant well defined touchstone for the reality of the illness, something that validated Royal Free and established a lineage, a way of addressing something that grew more and more contested without Ramsey.

    Once there is enough money for research, and the diagnostic challenges framed appropriately, we can probably expect a great deal of revision on just what we're talking about when we talk about m.e. and cfs.

    Samuel, of the estimable Kafka Pandemic, often speaks of m.e. lite, how important it is to include both the sickest, the house bound and bedridden, but also the people who are functioning, to whatever degree, in our discussions. These aspects are important both from the point of view of research but also advocacy. We don't know who is vulnerable and how 'light' a version they might have. With the emergence and triumph of the BPS position, there was no choice but to hunker down in the clearest, most well defined position in order to wage a fight for our lives but that deeply compromised the science. Part of the story of m.e. is a betrayal of intellectual inquiry, the short circuiting of critical thought.

    I expect, one day perhaps soon, the pervasiveness of the vulnerability of great swathes of humanity to m.e. and related illnesses will be alarmingly evident.

    I share your desire for comprehensively knowing how things were made so problematic but wonder if we can expect revelation or will have to demand it?

  4. In surveys, the majority of patients report getting ME after a herpes infection, mostly EBV. Others may have had a herpes infection without noticing it.

    It is possible that other viruses play a similar role, i.e. compromising the same immune functions, but it's not immediately apparent.

    The role of enteroviruses in ME is different. They are the trigger (and therefore determine the incubation period), the attacker that the compromised immune system can't handle properly.
  5. alex3619

    alex3619 Senior Member

    Logan, Queensland, Australia
    Enteroviruses and other viruses that have peristent non-lytic lifecycles are important in understanding ME in my opinion. Incubation periods are irrlevant with these viruses. All an incubation period tells you is how long it takes the current virus to become symptomatic after infection. It tells you nothing about the long-term viral infection of tissue. A person with a deep enterviral infection, such as found in striclty defined CFS (Chia wasn't using ME criteria I think) may have profound immunological weakness ... thats not fully demonstrated yet, but its possible. So when another infection comes along it can trigger consequences that were already there. Its like lighting the fuse on a bomb. The lighter is the new pathogen trigger, the current infection, but the bomb is the pervasive tissue infection with enteroviruses.

    Herpes viruses show similar tissue infection as enteroviruses. Indeed, most ME patients will have both viruses persistent in their tissues. It might even be that ME requires both to trigger.

    As for triggering events, if you have a pervasive enteroviral infection, then a similar strain of virus can reactivate it with who knows what consequences. Maybe ME?

    We need to know much more about the alternate lifecycles of these viruses, and their effects. Tissue infections are very different from blood-borne viremia, and most doctors are simply unaware of this. We also need to know just how different tissue infections interact with each other. In evolutionary terms it is likely that they have evolved to co-exist and maybe even assist each other.

    This is what I have been calling the two hit hypothesis for many years now. Earlier infections set someone up for the current trigger, and that trigger does not even have to be a pathogen. This doesn't mean that the current trigger is unimportant. Some things are more likely to trigger ME than others, and viruses that have persistent lifecycles are highly implicated, as other other immunologically suppressing factors like mycotoxins.
    SOC likes this.
  6. SickOfSickness

    SickOfSickness Senior Member


    Is this it? It was published 1985-1986. The short name was "Journal of the ANZME Society (N.Z.)" and the long name was "Meeting place : the journal of the Australian and New Zealand Myalgic Encephalomyelitis Society Inc."
    This link shows some locations in NZ that have copies.

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