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Maes & Twisk: Inflammatory Markers are Higher in ME/CFS than in Depression

Discussion in 'Latest ME/CFS Research' started by Firestormm, Jul 23, 2012.

  1. Firestormm

    Firestormm Guest

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    Received: July 27, 2011
    Accepted after revision: January 20, 2012
    Published online: July 20, 2012

    Published in: Karger: Psychotherapy and Psychosomatics: http://content.karger.com/produktedb/produkte.asp?doi=336803

    Inflammatory and Cell-Mediated Immune Biomarkers in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and Depression: Inflammatory Markers Are Higher in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome than in Depression

    Michael Maes, Frank N.M. Twisk, Karl Ringel

    Background:

    Depression is an inflammatory disorder while many authors declare myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) to be a functional disorder. The aim of the present study is to compare inflammatory and cell-mediated immune (CMI) responses between depression and ME/CFS.

    Methods:

    We measured two proinflammatory cytokines (PICs) in plasma, interleukin-1 (IL-1) and tumor necrosis factor-α (TNF-α), with enzyme-linked immunosorbent assays, and serum neopterin with a radioimmunoassay in controls, ME/CFS and depressive patients.

    Results:

    Plasma PICs were significantly higher in ME/CFS than in depression and higher in both patient groups than in controls.

    Increased PIC levels in depression were attributable to the presence of fatigue and physio-somatic symptoms.

    Serum neopterin did not differ significantly between depression and ME/CFS but was higher in both patient groups than in controls.

    The significant positive correlations between neopterin and either IL-1 or TNF-α were significantly greater in depression than in ME/CFS.

    Conclusions:

    Since PICs cause depression-like behaviors and fatigue/malaise, we suggest that inflammation may play a role in the pathophysiology of ME/CFS and depression.

    Increased neopterin also seems to contribute to the pathophysiology of both disorders.

    This study has detected a shared ‘pathway phenotype’, i.e. disorders in inflammatory and CMI pathways, which underpins both ME/CFS and depression and, therefore, may explain the co-occurrence of both disorders.

    ME/CFS and depression are discriminated from each other by increased PICs in ME/CFS and differences in the immune cell communication networks.

    Copyright © 2012 S. Karger AG, Basel
     
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  2. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    Now how do we get rid of this inflammation? Not that i think it would be a cure but the inflammation is a symptom stemming from the cause, infectious?? reducing inflammation is going to make us feel alot better and potentially reduce ongoing damage. I think also that is why antioxidants are of help as well.
     
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  3. Enid

    Enid Senior Member

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    Interesting - thanks Firestorm - I always knew it very different from common parlance (and psyches mumbo jumbo) in ME. A system crash so to speak.
     
  4. Firestormm

    Firestormm Guest

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    I shall reserve comment until reading the whole paper ;) Would hate to think this was entirely a hypothesis based on very little evidence...
     
  5. Marco

    Marco Old blackguard

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    Raised inflammatory markers e.g. CRP; TNF-alpha are common findings in ME/CFS, as are sympathetic nervous system predominance and reduced heart rate variability.

    This is an interesting discussion although, of course, it would be a good idea to check the source references :

    Nervous system regulation of inflammation, cytokines, and heart rate variability


    http://www.lapislight.com/wp/2010/0...mmation-cytokines-and-heart-rate-variability/
     
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  6. Firestormm

    Firestormm Guest

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    Hmmm... I wonder what effect anti-depressants have on this aforementioned source of inflammation? Or indeed if said inflammation is a result of 'depression' or 'depression' leads to inflammation or, indeed, if once again our terminology is proving inadequate in today's world of physical explanations...? Must read the paper.
     
  7. LisaGoddard

    LisaGoddard Senior Member

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    How do we get rid of inflammation? I have tried various immune modulators but now anything with even the slightest immune stimulant activity causes terrible inflammation symptoms. Tried aspirin but it now causes pain in my spleen area. Any suggestions please!!!!
     
  8. Enid

    Enid Senior Member

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    Firestormm - depression leads to inflammation not a chance in ME - infection sets the whole thing in motion - even my Neurologist knew that. And yes current terminology is proving inadequate (chiefly due to the "all in your minders" - take a little pill/chat and all your depression we think you have though muscles are not responding to keep one upright are ignored claim it will all disappear). So don't let us get muddled up - "depression" in ME is a functional disregulation. And the word depression (open to the mumbo jumbos so happy to step in) should be removed .

    And this article should have removed it anyway. Way past into the Immune workings now - hey do they know. Immune system crashed - that's the why.
    .
     
  9. Bob

    Bob

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    Inflammation has long been thought to be related to depression. But I don't know if there has been much research into this aspect of depression, or into using anti-inflammatory drugs for depression. There are various different types of depression, so inflammation might not be related to all types of depression. Again, I don't know if there has been any research into associating the various types of depression with inflammation.

    Inflammation has also long been said to be associated with ME. There has been an ongoing discussion, for a long time, about the use of the suffix "itis" in 'myalgic encephalitis, because 'itis' denotes diseases characterized by inflammation. Some people argue that there is no inflammation involved in ME, so that it should be called 'myalygic encephalopathy' because 'pathy' means 'disease', and does not denote inflammation. Inflammation has been found in the spinal cord (and maybe other similar tissue - I can't remember the details) in patients who have died from ME. (I can't remember the exact details here, so the facts need to be checked.)

    In my opinion, inflammation, in both depression and ME, is highly likely to be a symptom of another disease process, rather than a cause.
    Inflammation is part of the body's response to disease, and is part of the body's healing process.
    Chronic inflammation, as opposed to acute inflammation, perhaps causes problems in itself, but I don't know any details about this.

    My limited understanding, about all of this, suggests to me that we would need to have access to more specialised drugs than anti-inflammatory drugs in order to see any benefit. For example, I haven't heard of anyone with depression, or ME, being successfully treated by using paracetamol or ibuprofen or any other stronger anti-inflammatory drugs.

    I'm not aware if any research has been carried out into anti-inflammatories for either ME or depression, but it might be worth doing a google search to see if we can find any.
     
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  10. lansbergen

    lansbergen Senior Member

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    Not response to disease but response to harmfull stimuli.

    http://en.wikipedia.org/wiki/Inflammation

    Inflammation is a protective attempt by the organism to remove the injurious stimuli and to initiate the healing process.

    Inflammation is not a synonym for infection, even in cases where inflammation is caused by infection. Although infection is caused by a microorganism, inflammation is one of the responses of the organism to the pathogen. However, inflammation is a stereotyped response, and therefore it is considered as a mechanism of innate immunity, as compared to adaptive immunity, which is specific for each pathogen.[2]

    Without inflammation, wounds and infections would never heal
     
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  11. Bob

    Bob

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    I don't really know what 'harmful stimuli' means. I think it's the same thing as 'disease'.
    Autoimmune disease involves inflammation, and that might not involve any external pathogenic stimuli.
    So it might not require a pathogen to be involved for inflammation to be present.
    Trauma, such as a bruise or brain injury, also involves inflammation.
     
  12. lansbergen

    lansbergen Senior Member

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    http://www.thefreedictionary.com/stimuli

    1. Physiology Something that can elicit or evoke a physiological response in a cell, a tissue, or an organism. A stimulus can be internal or external.

    http://en.wikipedia.org/wiki/Disease

    A disease is an abnormal condition affecting the body of an organism.

    http://www.merriam-webster.com/medical/disease

    Definition of DISEASE

    an impairment of the normal state of the living animal or plant body or one of its parts that interrupts or modifies the performance of the vital functions, is typically manifested by distinguishing signs and symptoms, and is a response to environmental factors (as malnutrition, industrial hazards, or climate), to specific infective agents (as worms, bacteria, or viruses), to inherent defects of the organism (as genetic anomalies), or to combinations of these factors
     
  13. Bob

    Bob

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    Thanks lansbergen. Pretty much the same then.
     
  14. lansbergen

    lansbergen Senior Member

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    My mnemonic is: A harmfull stimulus is the starter. A disease is the result.
     
  15. jeffrez

    jeffrez Senior Member

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    Well, obviously - we're just MORE depressed! Lol : P
     
  16. Mula

    Mula Senior Member

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    I feel that these same markers could be present in other similar neurological diseases. Then it would only be necessary to find the immune markers that each disease produces.
     
  17. Snow Leopard

    Snow Leopard Senior Member

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    The problem in general is that these are non-specific markers of inflammation. That is why they are present in many diseases. The key is to not measure these markers once in each patient and do a group-wide analysis, but to measure their regulatory cycles in real time and compare with the cycles of the other markers within the same individual. That way we will see if there are different inflammatory patterns across these diseases.

    Biosensors that will permit this aren't that far off (20 years tops for small/safe biosensors that can record or transmit regular data), the difficulty is the cost and finding patients who are willing to take part. (normally these sorts of biosensors are reserved for 'animal models' of studying disease).
     
  18. Firestormm

    Firestormm Guest

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    My concern I suppose is with the terminology and the way in which it's used. As mentioned above I think we tend to see (even search) for 'inflammation' as a way of perhaps justifying the nomenclature attached to our condition. (I haven't read the paper) But not all 'inflammation' is the same inflammation as can be attached to a disease within the neurological categorisation.

    Bob - were you referring to the autopsies carried out revealing abnormalities on basal ganglia in (I think) two out of four patients with a diagnosis of ME? I too cannot recall the revelence to 'inflammation' but I can always post the report. Of course it wasn't a publication although it is another area that should be funded (about time) but as it involves autopsies there are complications...

    And it is true that inflammation has been attracting research in with regards to understanding more about 'depression', whilst the above extract appears to suggest that from the evidence at which they looked (doesn't appear to have been a blinded study and I can't tell how many were involved, etc. etc.), this form of inflammation was common to both 'depression' and ME, but that in ME it was more dominant or recorded some sort of higher response.

    I am especially cautious about Maes. Sorry but his past papers just haven't 'cut the mustard'. My question about antidepressants is not as naive or searching as it might have appeared - if one of the consequences e.g. of raising/suppressing serotonin levels was to lead to a suppression of inflammation... well maybe putting patients on such drugs might not be as bad a thing as was thought. Just saying. Probably cobblers - lots of ADs out there...

    This too might be of concern to some:

    'Plasma PICs were significantly higher in ME/CFS than in depression and higher in both patient groups than in controls. Increased PIC levels in depression were attributable to the presence of fatigue and physio-somatic symptoms.'

    Are 'PIC levels' a recognised measure of depression or even looked at in such research? I don't know. And is it their contention that this attribution for 'Depression' does not apply similarly to ME or that it does i.e. that as the PIC levels were higher in ME that they too were responsible for 'fatigue and physio-somatic symptoms' and if so in what way?

    And what about severe forms of depression? Do they result in levels 'significantly higher' as in ME?

    Again I am not familiar with this line of reasoning.
     
  19. user9876

    user9876 Senior Member

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    There has been some work on using anti depressants to manage chronic pain. I seem to recall it was due to changing chemicals involved in messaging for main within the insula cortex. I think it was research into FM. I can't remember exactly where I read it but there is a hint in an article on the ottowa conference:

    http://phoenixrising.me/archives/6651
     
  20. Bob

    Bob

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    I'm afraid I haven't got a clue what research I was referring to. :confused: I'm just aware that it has been reported that inflammation has been seen in certain tissues in post-mortem examinations of ME patients. I thought that inflammation had been found in spinal tissue, but I might be wrong, and it might be other similar tissue such as the basal ganglia or other brain tissue.
     

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