Wednesday, March 19, 2014

The Stanford Study

The Cytokine Study was presented today (though some results were held back due to publishing). The study has been accepted by a journal but not published yet.

I have to say that this is the most well-designed and significant study of ME/CFS patients in the history of this disease. It has a large number of patients (200) matched by control patients. They accounted for variables that would make replication of the results easy to do.

We all know the disastrous mark left on ME/CFS research from the WPI XMRV study. This study more than makes up for that.

Dr. Montoya stated that ME/CFS presents the greatest medical and research challenge of our time and that understanding ME will help aid in the understanding of other diseases.

They studied 51 cytokines per patients in 200 patients comparing them to 400 healthy people. Patients and controls were matched according to age as well as other variables.

The current standard markers of inflammation (ESR, C-Reactive Protein) are increased in disease like RA and Lupus but not in ME. The typical inflammatory markers are normal in ME.

Dr. Montoya made the point that there are no inflammatory markers for ME because not enough of the inflammatory markers are measured.

Thus the cytokine study.

Cytokines are small proteins that the immune system uses (and are also produced by the immune system) to communicate between cells and pieces of the immune system.  They can be used to communicate in small areas of the body or across major distances in the body.

Inflammation means fire so at its most basic understanding cytokines can be viewed as one way the body attempts to put out fires.

It's worth noting again that systemic inflammation shares similar symptoms with the flu.

The most immune concentrated areas are the lymph nodes, liver, spleen, bone marrow, thymus as well as other places. These organs produce cytokines that can be exported to other areas of the body.

ME is expressed by multiple disjointed symptoms in the body.

One reason why markers for ME are not picked up in the blood, the Montoya team postualtes, is that the inflammatory markers travel from the blood stream to the organ(s) affected. They shift from the blood to organs because there is inflammation in that particular organ or organs. Dr. Montoya believes the brain has major involvement.

Another interesting finding is that in mild ME cytokines decrease whereas in more moderate and severe disease they increase.

He believes this is the reason for such a discrepancy in findings in previous studies. Because there was no analysis according to disease severity the results of other studies evened out making the results appear deceptively normal. For example, one cytokine called Resistin is increased in moderately affected patients but decreased in the severely affected.

Also interesting is that the fire (inflammation) starts somewhere so the cytokines go there, and then other places.

When there are lower levels of cytokines in the blood it could mean they have shifted to the tissues that are inflamed.

IL-17 in particular is increased in severely affected patients. This is a clue to some sort of autoimmune process occurring.

Dr. Montoya believes there is a genetic factor that predisposes patients to ME.

He stated the the triggering factor could be infections, allergies, the environment--combined with the genetics results in ME.

Dr. Montoya, being an infectious disease specialist. postulates taht ME is the result of a hit and run mechanism. That some sort of insult causes a cascade of events and leaves the body in a damaged state.

He thinks its infection AND other factors,but not purely either, that affect the brain, heart, immune system, and digestive system.

He also believes there are subgroups.

He thinks viral onset patients might have a certain pattern of cytokine whereas other types of onset will show a different pattern.

Although a cure may never be discovered it will be possible to treat this disease thereby allowing us to function better, maybe even near normal and definitely good lives. Similar to lupus and RA patients.

Other inflammatory diseases are treated by anti-inflammatory agents. Dr. Montoya believes that some agents currently in use might be able to be used for treatment but there isn't enough info yet to determine which ones will be effective.

He cautions that the tricky part with ME is that one part of the immune system is overactive but another part is weak thereby leaving the door open to infection. Some of the anti-inflammatory treatments reduce the function of the immune system.

The whole secret will be how to use the anti-inflammatory drugs.

Regardless the stage has now been set for a host of things. Biomarkers for this disease, further research studies, new treatments, validation, and more funding for further studies.

Basically ME is a debilitating chronic systemic inflammatory disease.









7 comments:

  1. What an excellent post and something quite complicated so well explained - thank you!

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  2. shoot, were you at the conference?? I don't know how I missed you :(

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  3. Thanks Emma!

    Rambler-I wasn't at the conference but was in the study. I would have liked to have gone but couldn't make it happen unfortunately.

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  4. Great blog, thanks. Retweeted here https://twitter.com/sjmnotes/status/447455236291301376

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  5. Can you give a list of the cytokines that were elevated in cfs?

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  6. Thank you Simon :-)

    Paula--Unfortunately I'm not able to at this time (much as I would love to).

    Because I was a patient in the study I saw the list of cytokines but until the paper is published we are restricted from talking about them (other than what I presented in the post).

    As soon as I hear when it's published (and which journal) I'll post asap.

    It should be sometime soon.

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  7. Thanks, so much. I will be watching.

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