CFI Spinal Fluid study from Lipkin and Hornig is out.

[lansbergen]

The psyche is supposedly in our heads too.

 

[cigana]

I would like to see replication and more research of this study:
Steven E Schutzer, Thomas E Angel, Tao Liu, Athena A Schepmoes, Therese R Clauss, Joshua N Adkins, David G Camp, Bart K Holland, Jonas Bergquist, Patricia K Coyle, Richard D Smith, Brian A Fallon, Benjamin H Natelson.
Distinct Cerebrospinal Fluid Proteomes Differentiate Post-Treatment Lyme Disease from Chronic Fatigue Syndrome. PLoS ONE, 23 Feb 2011

But there will be no replication at all.

For me, replicating the Schutzer study is an absolute priority.

 

[Kati]

View attachment 10512 View attachment 10513 View attachment 10514 View attachment 10515

It is very interesting to me that they compared patients with MS and it looks like the cytokine pattern is fairly similar to MS.

If pooled together, ME and MS compared to control, we can certainly visualize that there is something wrong and different.

I wonder how blood cytokine compares between ME and MS patients.

 

[Bob]

Network analysis revealed an inverse relationship between interleukin 1 receptor antagonist and colony-stimulating factor 1, colony-stimulating factor 2 and interleukin 17F, without effects on interleukin 1α or interleukin 1β, suggesting a disturbance in interleukin 1 signaling.

It's difficult to interpret the exact meaning of this from the abstract, but it seems very similar to what Nancy Klimas and her team have determined from Gordon Broderick's computational models...

Watch Nancy Klimas' presentation @41.55, re IL-1:

These are some notes that I wrote about Nancy Klimas' presentation on another thread:

@ 45 mins.
Drug Trials:
Dr Klimas wants to trial FDA approved drug (biological response modifier) that blocks IL-1 (cytokine). Computational data points towards blocking IL-1. Not able to get it past review boards, because drug is toxic, and review boards don't appreciate the severity of ME. Lost 5 years due to not getting grant proposals past review boards. Requires phase I funding from private donors. Will, instead look at other less optimal drugs (used for rheumatoid arthritis?) which she expects to get through review boards, but frustrated that she can't test the drug she wants to.

​

 

[Antares in NYC]

"Abstract
Myalgic encephalomyelitis/chronic fatigue syndrome is an unexplained debilitating disorder that is frequently associated with cognitive and motor dysfunction. We analyzed cerebrospinal fluid from 32 cases, 40 subjects with multiple sclerosis and 19 normal subjects frequency-matched for age and sex using a 51-plex cytokine assay. Group-specific differences were found for the majority of analytes with an increase in cases of CCL11 (eotaxin), a chemokine involved in eosinophil recruitment. Network analysis revealed an inverse relationship between interleukin 1 receptor antagonist and colony-stimulating factor 1, colony-stimulating factor 2 and interleukin 17F, without effects on interleukin 1α or interleukin 1β, suggesting a disturbance in interleukin 1 signaling. Our results indicate a markedly disturbed immune signature in the cerebrospinal fluid of cases that is consistent with immune activation in the central nervous system, and a shift toward an allergic or T helper type-2 pattern associated with autoimmunity."

Now I understand why my doctor tested me for eosinophils (EOS) a couple of months ago and mentioned that this may be an important cytokine to consider. My numbers for eosinophils were quite elevated, and she mentioned that when they started to test for EOS in ME/CFS patients, they noticed these numbers often came very high.

Kudos to the Hornig/Lipkin team at Columbia. These guys are killing it! Please more funding!

 

[halcyon]

My brain isn't working so great today so I'm having trouble processing all of this. Did they separate out new versus old cases of ME like the other study, or is the finding that both new and old cases have the same cytokine abnormalities?

Would the elevated eotaxin be expected to result in greater numbers of eosinophils? Like many others here I've had elevated eosinophils since becoming ill.

 

[lansbergen]

My problem with Peterson is that the samples are from outbreaks, a very heterogene specific subgroup.

You think samples from outbeaks are less homogene than samples from sporatic cases?

 

[Legendrew]

Very interesting stuff: I haven't been around much here and therefore am not fully abreast of ongoing studies what with university commitments nowadays, indeed i'm currently procrastinating when I should be writing a 3000 word essay, but this has attracted quite a bit of attention! As many other have said the name of the game now is replication but even this study in itself has found some very interesting results in and of itself.

 

[SOC]

My problem with Peterson is that the samples are from outbreaks, a very heterogene specific subgroup.

Peterson's original patients were all from a single outbreak. Since these samples were all taken 1994 or after, it is unlikely that they were all part of the outbreak in the mid-80's. Dr Peterson's current patients come from all over the US, probably even outside the US, so there is no reason to think that all the patients in his biobank are all from a single outbreak -- far from it.

 

[Antares in NYC]

Peterson's original patients were all from a single outbreak. Since these samples were all taken 1994 or after, it is unlikely that they were all part of the outbreak in the mid-80's. Dr Peterson's current patients come from all over the US, probably even outside the US, so there is no reason to think that all the patients in his biobank are all from a single outbreak -- far from it.

If I understand correctly, the samples come from patients of CFS doctors from all over the map, specially those working with the Columbia University group.

One of the best things about the Columbia Microbe Discovery group is that it has, de facto, coordinated the efforts of a large number of ME/CFS researchers, despite the notorious lack of funding. Hornig, Lipkin, Levine, Montoya, Klimas, Peterson... they are sharing their data, with Columbia University leading the research efforts with Harvard and Stanford. That's only good news for us, folks.

 

[Bob]

All figures and tables from the paper are freely accessible:
http://www.nature.com/mp/journal/vaop/ncurrent/fig_tab/mp201529ft.html

(If these were posted earlier in the thread, I missed them.)

 

[DanME]

Peterson's original patients were all from a single outbreak. Since these samples were all taken 1994 or after, it is unlikely that they were all part of the outbreak in the mid-80's. Dr Peterson's current patients come from all over the US, probably even outside the US, so there is no reason to think that all the patients in his biobank are all from a single outbreak -- far from it.

Very good point. So the patients from Dr. Paterson are more heterogenous than I thought.

 

[Snowdrop]

@cigana

Is this the study you're referring to: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0017287

 

[Denise]

All figures and tables from the paper are freely accessible:
http://www.nature.com/mp/journal/vaop/ncurrent/fig_tab/mp201529ft.html

(If these were posted earlier in the thread, I missed them.)

Thanks very much.


(If they were posted earlier I did not see them.)

 

[SOC]

Very good point. So the patients from Dr. Paterson are more heterogenous than I thought.

Certainly they are not all from the Lake Tahoe outbreak. I remember hearing that he only accepts patients with a viral onset, but my memory should not be relied upon. If all the patients in his biobank are his patients (that's not a certainty), then there may be more homogeneity in the group then there might be in a more broadly-defined group that included non-infectious onset, but they're not all from one outbreak, or even any outbreak at all.

What we can be pretty certain of is that they're not burn-out, or overtraining, or primary MDD, or misdiagnosed primary hypothyroid or OI patients. These are people with the illness most of us are talking about here. That's a damned good start for a research patient cohort.

 

[Helen]

Dr Peterson's current patients come from all over the US, probably even outside the US, so there is no reason to think that all the patients in his biobank are all from a single outbreak -- far from it.

I met Dr. Peterson when he lectured in the city nearby some years ago. We had a chat during the coffee break and I was offered to send a sample of spinal fluid to "his" biobank. It was aimed for an ongoing study he told, and I would have received my own results separately. At that time I was diagnosed with ME, but not with Lyme and the two co-infections that I have, and had at that time too. I wonder how the infections would have affected the results. I never sent any sample as I had another spinal tap for neurological symptoms. I guess that other patients at the clinic participated.

 

[beaker]

In a study like this it must be immensely difficult to get normal controls who would agree to a lumbar puncture so I would question how healthy are the people who were undergoing "CSF sampling to rule out CNS infection or hemorrhage".

I don't know anything about MS but I would imagine RRMS and SPMS could differ quite a bit on these cytokines.

Medical students make good healthy controls : ) I have seen it before.
And /or subjects are paid.
Poor college students.

Not saying this is the case here. But it is not uncommon.

 

[alex3619]

You think samples from outbeaks are less homogene than samples from sporatic cases?

Almost by definition a single cluster outbreak is a highly homogeneous group. There is some question as to whether or not that is the case once you merge cluster outbreak cohorts.

 

[halcyon]

Please do keep in mind that this is not replicated, and is not the same result as another recent spinal fluid study.

I wonder why these findings are so much different than Dr. Peterson's February paper. It looks like the only thing common between the two studies was decreased concentrations of IL-10.

 

[Kati]

Considering the conclusions of this paper, it calls in my opinion for attention to the neurologists out there, who may be caring for patients with MS and other chronic neurodegenerative diseases.

(This may help directing our advocacy through social media. Share, share, share.)