Choline on the Brain? A Guide to Choline in Chronic Fatigue Syndrome
http://phoenixrising.me/research-2/the-brain-in-chronic-fatigue-syndrome-mecfs/choline-on-the-brain-a-guide-to-choline-in-chronic-fatigue-syndrome-by-cort-johnson-aug-2005
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What is your personal theory or understanding of ME/CFS?

Discussion in 'General ME/CFS Discussion' started by Jesse2233, Dec 9, 2017.

  1. Learner1

    Learner1 Professional Patient

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    It is not always acute viral onset, although can be. The US Institute of Medicine's expert committee looked at all the available information and came up with a much broader definition which can be found here:

    http://www.nationalacademies.org/hmd/Reports/2015/ME-CFS.aspx

    It is no longer seen as a diagnosis of exclusion. Many patients have abnormal biochemistry, comorbidities, etc.that contribute to symptoms and the disease process.
     
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  2. JES

    JES Senior Member

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    Welcome to the forums. Most people here use the label CFS/ME to avoid confusion. You are correct that CFS is not the best possible name to describe this disease, and while I tend to agree that ME is a better label, ME stands for Myalgic Encephalomyelitis, where Encephalomyelitis means inflammation in the brain, and currently evidence is lacking for whether there is inflammation and what type of inflammation exists in CFS/ME. So the term ME is not perfect either.

    At the end of the day, it's just a label, and while I agree that the disease should be named better, there are more important issues. The more important thing is that people understand the implications of CFS and that it's a real disease - a term is just a term.
     
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  3. sorin

    sorin Senior Member

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    What specifc tests are used to diagnose this disease and what is the treatment?
     
  4. xak53

    xak53

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    There is an appalling lack of funding into M.E. research, and the many claims of cures based on 'CFS' patient groups are not relevant whatsoever to those with M.E. But intelligent nutritional and other interventions can make a significant difference to a patient's life and can also reduce the severity of the disease to some entent.

    Appropriate biomedical diagnostic testing should be done as a matter of course (and repeated regularly) to ensure that the aspects of the illness which are able to be treated can be diagnosed, monitored and then treated as appropriate. Testing is also important so that dangerous deficiencies and dysfunctions (which may place the patient at significant risk) are not overlooked.

    The foundation of any treatment program for M.E. MUST involve appropriate rest and avoiding overexertion however, if it is to have any chance at success. M.E. patients who are given advice to rest in the early stages of the illness (and who avoid overexertion thereafter) have repeatedly been shown to have the most positive long-term prognosis.

    M.E. expert Dr Elizabeth Dowsett explains that prompt recognition and advice to avoid overexertion is mandatory in M.E. and that:

    After a variable interval, a multi-system syndrome may develop, involving permanent damage to skeletal or cardiac muscle and to other "end organs" such as the liver, pancreas, endocrine glands and lymphoid tissues, signifying the further development of a lengthy chronic, mainly neurological condition with evidence of metabolic dysfunction in the brain stem. Yet, stabilisation, albeit at a low level, can still be achieved by appropriate management and support. The death rate of 10% occurs almost entirely from end-organ damage within this group (mainly from cardiac or pancreatic failure.

    Many people with M.E. are significantly or severely disabled. But what is so tragic about this high level of suffering is that so much of it is needless. The correct type of support (financial, medical and practical) can do much to prevent the physical, occupational and other deterioration in the quality of life for M.E. patients and can stabilise the illness. Many deaths from M.E. could also have been prevented if only those patients had been given a basic level of support and care made available to patients with illnesses with comparable care needs such as multiple sclerosis and motor neurone disease.
     
  5. xak53

    xak53

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    M.E TESTING.

    M.E. is a distinct, recognisable disease entity that is not difficult to diagnose and can in fact be diagnosed relatively early in the course of the disease, within just a few weeks, providing that the physician has some experience with the disease. There is just no other disease that has all the major features of M.E.


    Objective evidence of quantifiable organic abnormalities in M.E. patients has existed since the 1950s. As with a wide variety of illnesses – lupus, multiple sclerosis, and ovarian cancer for example – there is as yet no single test which can diagnose M.E. in all patients. Therefore, like these other illnesses, M.E. must be diagnosed by taking a detailed medical history, noting the type and severity of symptomatology and other characteristics of the illness and the type of onset of the symptoms. (An acute or sudden onset of symptoms is always seen in M.E. and this onset type rules out a wide variety of other illnesses associated with gradual onset). A series of tests may also then be necessary to rule out or confirm a suspected M.E. diagnosis.


    One cannot test for ‘CFS’ but M.E. is not the same thing as ‘CFS’ (or ‘ME/CFS.’) The presence or absence of ‘fatigue’ is largely irrelevant in determining an M.E. diagnosis except in that its presence may of course make the diagnosis of a large number of well-known fatigue causing illnesses considerably more likely (depression, vitamin deficiency or malignancy for example) (Hyde & Jain, 1992). M.E. is not a diagnosis of exclusion or an untestable disease. Tests will only all be normal in M.E. patients – as with all illnesses – if the wrong tests are conducted, or if those tested do not in fact have M.E. (Hyde 2007, [Online]) (Hyde 2006, [Online]) (Chabursky et al. 1992, p.22).


    Contrary to common disinformation erroneously linking M.E. with ‘CFS,’ it is not mere ‘fatigue’ that defines M.E. but central nervous system (CNS) dysfunction. M.E. represents a major attack on the CNS by the chronic effects of a viral infection which targets the brain: an enterovirus. As M.E. expert Dr Byron Hyde explains:

    The one essential characteristic of M.E. is acquired CNS dysfunction. A patient with M.E. is a patient whose primary disease is CNS change, and this is measurable. We have excellent tools for measuring these physiological and neuropsychological changes: SPECT, xenon SPECT, PET, and neuropsychological testing (2003, [Online]).


    Tests which together can be used to confirm an M.E. diagnosis include:

    • SPECT and xenon SPECT scans of the brain.
    • MRI scans of the brain.
    • PET scans of the brain.
    • EEG/QEEG brain maps.
    • Neurological examination. Neuropsychological testing.
    • The Romberg test.
    • Immune system tests.
    • Insulin levels and glucose tolerance tests.
    • Erythrocyte Sedimentation Rate (ESR) tests.
    • Circulating blood volume tests.
    • 24 hour Holter monitor testing.
    • Tilt table examination and standing/sitting/reclining blood pressure tests.
    • Exercise testing and chemical stress tests.
    • Physical exam.

    These tests are the most critical in the diagnosis of M.E., although various other types of tests are also useful.
     
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  6. femtosecond99

    femtosecond99 Senior Member

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    CFS isn't defined by "mere fatigue" either. And SPECT scans don't actually show CNS change, they show changes in blood flow. You also see changed in SPECT scans in patients with depression. The consensus is that SPECT scans aren't very useful in diagnosing CFS (or ME).

    The reality is that ME is an invalid etiology because there isn't generally any inflammation, and a lot of the time there isn't even any myalgia. The reason for using the term CFS is that it doesn't imply any etiology, but it definitely isn't "just fatigue".
     
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  7. Hip

    Hip Senior Member

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    What about the Japanese study that found brain inflammation in ME/CFS?
     
  8. ljimbo423

    ljimbo423 Senior Member

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  9. Tammy

    Tammy Senior Member

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    I believe the cause is viral............mainly the EBV...........but other viruses from the herpes family can be involved as well........but I think EBV is the main culprit. Reason for all the varying symptoms between people I think is due to the strain of the virus... (some are mild............some are aggressive)..............and also where the virus ends up in the body. I think the reason the immune system gets F'd up is because of the damage the virus can do............to all systems.
     
  10. femtosecond99

    femtosecond99 Senior Member

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    They didn't actually find inflammation. They found significantly elevated PK-11195. It is found to be elevated in traumatic brain damage, and also in depression, and various other conditions. I suspect in CFS and depression it is more of a symptom than an underlying cause, possibly due to immune activation.
     
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  11. Hip

    Hip Senior Member

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    [11C]PK11195 is a marker for inflammation. It has been superseded by better markers, because it is not very sensitive for detecting lower levels of inflammation; in fact the new ME/CFS brain inflammation study planned in Japan is going to use [18F]DPA-714.



    Yes, well you would expect that, as TBI and depression are linked to neuroinflammation.

    In fact neuroinflammation is increasingly being found in mental health disorders, including major depression, bipolar, OCD and schizophrenia.
     
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  12. femtosecond99

    femtosecond99 Senior Member

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    PK11195 is also involved in stress and anxiety (in fact it is a ligand for benzodiazepine binding sites). So I think it is either both a marker for anxiety and for neuronal damage, or else psychological stress causes neuronal damage. I think both scenarios are equally plausible, but I'm sure someone with more knowledge of the science might be able to shed some more light on this.
     
  13. Stretched

    Stretched Senior Member

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    This thread is entitled ‘...personal theory of CFS,’ but sure has gotten technical and serious! How about...eating M&Ms causes ME?:depressed: ...knee bone connected to the foot bone... .
     
  14. imitate-past-reign

    imitate-past-reign

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    CFS is due persistent viral infection in vulnerable circuits of fatigue detection leading to avoidance behavior, areas near the blood brain barrier which is defective due to an environmental insult.

    I am just going to repeat it until someone with money listens.

    There's leaky gut, autoimmune, metabolic, mold theories as well for the remaining 50% of cases.
     
  15. Stretched

    Stretched Senior Member

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    Hmmm... I see why it get it might get technical;)
     
    Last edited: Feb 5, 2018
  16. Hip

    Hip Senior Member

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    I could not find anything linking PK11195 to stress and anxiety, where did you see that?

    I found this paper which explains that PK11195 binds to the peripheral benzodiazepine receptor (PBR) which is expressed on activated microglia, and thus is a marker for neuroinflammation.

    As an aside: activated microglia pump out lots of glutamate, a neurotransmitter which has an excitatory stimulating effect on neurons. Thus chronically activated microglia in ME/CFS producing excess extracellular glutamate could explain the "wired but tired" over-stimulated feeling that is common in ME/CFS.
     
  17. imitate-past-reign

    imitate-past-reign

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    If it is anti-muscarinic antibodies at CNS synapses, that's really bad news. It would explain the gender imbalance in CFS, that's monoclonal therapy territory and not even at pre-clinical phase. Scopolamine and amantadine would not help because of their adverse effects. Depression researchers tried to tackle the glutamate problem, which is actually easier than antibodies, and they have failed thus far.

    Re: Younger - Vagus Nerve Stimulation has a much stronger case in depression than CFS, and if you read the new drug application, the device has the same clinical efficacy turned on as it does off.

    It's much easier to re-publish the same peripheral cytokine network study every 3 months, using banked samples. Drug companies do this all the time, and it still is budgeted as R&D, cruising on parameter changes. In contrast, they actually get a payoff with a patent application. You would have to take all US funding on CFS to do a replication. Plus, there's no CFS model in mice, so you can't do this cheaper.

    If it is a viral entity causing this inflammation, then acyclovir derivatives are a bad choice, with 20% bioavailability. Only 20% of that 20% gets into the CSF. If that isn't the infectious agent, something is causing the inflammation. If it is natively inside the brain due to programmed cell death then that's a problem we cannot fix currently well (rTMS does increase hippocampal neurogenesis in vivo). But if it is stabilizing the blood brain barrier and preventing repeated intrusions by a non-commensal virus, that can actually be fixed, now.

    or we are, like, hibernating.
     
  18. femtosecond99

    femtosecond99 Senior Member

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    Actually, you're right. It is the benzodiazepine receptors that PK11195 binds to that are linked to stress and anxiety, not PK11195 itself. However there is quite a lot of research showing that psychological stress causes increased microglial activity and neuroinflammation:

    https://link.springer.com/content/pdf/10.1007/s00213-016-4218-9.pdf

    "A number of studies show an association between greater microglial activity and behavioural outcomes that are proxies for depressive and anxiety-like symptoms in animal models. Studies by Wohleb (2011, 2012) using the social defeat model showed anxiety-like behaviour positively associated with microglial activity. Couch et al. (2013), using a model that combined social defeat, restraint and tail suspension, observed a pro-inflammatory profile and heightened microglial activity associated with the development of stress-induced anhedonia in mice susceptible to depression following exposure to stress. These changes in the microglial profile were not present in ‘resilient’ animals that did not develop depressive symptoms following the stress protocol."
     
  19. duncan

    duncan Senior Member

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    Tail suspension is always a killer. That and blue leisure suits.
     
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  20. duncan

    duncan Senior Member

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    It seems to me that most bps theories have been debunked. Certainly we of all communities should know that PACE has.

    Prevailing ME/CFS theories seem generally to fall into two broad camps:

    First, the immune systems of pwME have been corrupted or broken and are mafuntioning. Whether this is an immune system stuck in overdrive after a viral/bacterial insult, or an autoimmune response to the same, the net add is a disrupted immune system that is responsible for the myriad of symptoms experienced by sufferers;

    Second, pwME are infected with a disease and their bodies fail to eradicate the disease. The disease finds or establishes sanctuaries and somehow survives by either abrogating the immune system, or simply evading it. This infection is responsible for the immune response; the infection could be an enterovirus or of a herpes lineage or bacterial or any number of others.

    The notion that symptom clusters usually associated to ME/CFS are reducible to stress is not sustainable. Worse, it ultimately places blame on the patient.
     
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