CFI Spinal Fluid study from Lipkin and Hornig is out.

[Helen]

It wouldn't surprise me if the research aimed to solve ME/CFS ends up solving chronic Lyme.

Agree .

 

[Jonathan Edwards]

Is the problem (as Sidereal pointed out) that 100% healthy people have little reason get a spinal tap?

That is the basic issue. Nobody volunteers for a spinal tap. It seems likely that the cases they used were ill and had taps because someone thought they might have infection or an immune disorder but in the end they did not. The question then is why were they ill? There is also an issue in that the samples would be taken under different conditions and that is the sort of thing that can give rise to systematic shifts in results that could confound their use as controls. There is no simple answer to this I think.

 

[duncan]

Where Lyme skews the conversation at least a bit, is that there is a fair likelihood that the problem with Lyme is not based in a given patient's genetics, or the result of a compromised immune system.

The problem with Lyme...the thing that keeps some people sick and unable to recover with recommended treatment (or any treatment, far too often), may be that this is the nature of Borrelia Burgdorferi. That Bb in a small amount of acute cases, and a much more significant portion of late stage cases, becomes difficult to treat, even refractory to all known treatments. In that regard, it could be similar to its distant cousin spirochete, syphilis.

This is where politics and legacy positioning - and even liability concerns - potentially come into play. In order to appreciate those dynamics, though, one has to go back and explore the history of Lyme, both in terms of how diagnostics evolved, and how standard treatments came about. For the former, look to studies around 1993, and the latter, go back ten years,and see what was conjured in 1983.

So if what is keeping some people sick with Lyme is the very nature of Lyme, and has nothing to do with epigenetics or immune collapses...well, that possibility perhaps changes how these comparative studies can be used. Perhaps not. It would explain, however, why not a lot of cytokine profiles of either chronic or late stage Lyme are being executed today, or the few that are done, like the one by Shuster/Natelson/Colye, replicated..

 

[Helen]

@Jonathan Edwards I listened to a discussion some years ago about spinal taps from healthy individuals for ME studies, and at that time they considered asking young people who were going to get anesthesia (called epidural in "Swedish") before knee operations if they would volonteer for this.

 

[Jonathan Edwards]

@Jonathan Edwards I listened to a discussion some years ago about spinal taps from healthy individuals for ME studies, and at that time they considered asking young people who were going to get anesthesia (called epidural in "Swedish") before knee operations if they would volonteer for this.

Yes, that sort of thing ought to be possible I guess, although taking a significant amount of fluid out reduces the pressure and can give a bad headache or even very rarely cause serious brain stem problems (vanishingly rare but maybe an issue in a litigation conscious country). There is also the problem that although young people with knee injuries may be healthy they may, because of age profile or exercise pattern or whatever, be different from PWME for reasons nothing to do with the pathology of ME. Dr Hornig did age matching, I believe, but there are all sorts of other potential confounders. What I liked about the blood study was the comparison within the ME group with the disease duration division.

 

[Helen]

What I liked about the blood study was the comparison within the ME group with the disease duration division.

Me too. I just wanted to tell how samples might have been collected in other studies. And who knows if these young people with knee traumas would get ME later, and have spinal fluid that already is affected.

 

[Sidereal]

I wonder if the controls were psychiatric patients presenting with symptoms that might be suggestive of encephalitis which was then ruled out by doing the lumbar puncture. Pure speculation of course.

 

[alex3619]

I think it is an absolute worst nightmare for psychiatrists who promote the psychological view as it challenges them in their own territory where they are used to having full control of the narrative.

 

[Kati]

That is the basic issue. Nobody volunteers for a spinal tap. It seems likely that the cases they used were ill and had taps because someone thought they might have infection or an immune disorder but in the end they did not. The question then is why were they ill? There is also an issue in that the samples would be taken under different conditions and that is the sort of thing that can give rise to systematic shifts in results that could confound their use as controls. There is no simple answer to this I think.

The control spinal fluid in this study was collected from patients who had suspected brain bleeds and it was ruled out. So they were taken from some kind of biobank.

The US will also pay (healthy) subject to undergo clinical trials or medical procedures of all kimds in order to obtain tissus or data from healthy controls.

 

[lansbergen]

The control spinal fluid in this study was collected from patients who had suspected brain bleeds and it was ruled out. So they were taken from some kind of biobank.

It is a mixed cohert.
From the paper

and 19 subjects who had undergone CSF sampling to rule out CNS infection or hemorrhage (ND controls)

 

[Kati]

It is a mixed cohert.
F

It is a mixed cohert.
From the paper

Indeed, I was not totally precised in not mentioning ruling out infection. However the normal control were deemed free of CNS pathology.

 

[Antares in NYC]

So if what is keeping some people sick with Lyme is the very nature of Lyme, and has nothing to do with epigenetics or immune collapses...well, that possibility perhaps changes how these comparative studies can be used. Perhaps not. It would explain, however, why not a lot of cytokine profiles of either chronic or late stage Lyme are being executed today, or the few that are done, like the one by Shuster/Natelson/Colye, replicated..

So basically those of us with Lyme are screwed, and nothing can be done now.
Just wondering if that's the music I should be facing and abandon any hopes that it will get better.

 

[Forbin]

That is assuming that the point of the study was to see if they could differentiate 'CFS patients' (since they used the Fukuda criteria, another problem with the study) en masse from Lyme patients. If however, they were trying to differentiate those CFS patients who don't have Lyme from Lyme patients, then (assuming the screening was sensitive enough) the result itself doesn't really tell us anything, apart from the fact that people with different diseases have different cerebrospinal proteomes. As the paper says, the differences might allow some inferences to be drawn about the pathologies of these diseases, but that assumes that the CFS group you are left with is a heterogeneous group.

The point of the Schutzer study was to look for spinal fluid proteins that were exclusive to the CFS group. 738 proteins were found among the CFS group that were not found in either the Lyme or control group. If there were Lyme cases among the CFS group, they lacked any of the 692 proteins found exclusively among the Lyme group. There were also 305 proteins shared by the Lyme and CFS groups but which were not found in controls.

At any rate, the 738 CFS exclusive proteins represent potential CFS biomarkers. That's what they study was actually looking for. However, because the groups were pooled, there is no way to tell from this study how prevalent any of the proteins were in the CFS group. This phase of the study was never intended to do that. It's purpose was to narrow the field of potential spinal fluid protein biomarkers. Replication of the study could narrow the field further. Once the field is small enough, it becomes practical (by different means) to test individual patients for individual proteins to see which, if any, are consistently - and exclusively - found in CFS patients. A spinal fluid protein(s) found consistently and exclusively in CFS patients would be a biomarker.

This is like looking for a needle in a haystack where the first phase is to rule out 95% of the haystack. That's what the Schutzer study is trying to do. The needle may or may not be in the remaining 5%, but you have just made it a lot easier to look for it.

 

[Kati]

What I would like to know is, if the cytokine results are so similar to relapsing-remitting MS patients, what are the chances that patients respond well to at least some of the drugs offered to MS patients and would it be worthwile to explore that route?
@Jonathan Edwards

 

[alex3619]

What I would like to know is, if the cytokine results are so similar to relapsing-remitting MS patients, what are the chances that patients respond well to at least some of the drugs offered to MS patients and would it be worthwile to explore that route?
@Jonathan Edwards

Actually if you go to MS sites, according to @heapsreal, the treatments they find help are nearly the same as the treatments we find help.

 

[Kati]

Actually if you go to MS sites, according to @heapsreal, the treatments they find help are nearly the same as the treatments we find help.

I disagree Alex, at least according to my source, MS Society Canada.
If you look at this link on the left column, there are at least 10 drugs which I don't know about. They are using a few monoclonal antibodies which are different than Rituximab.

 

[alex3619]

I disagree Alex, at least according to my source, MS Society Canada.
If you look at this link on the left column, there are at least 10 drugs which I don't know about. They are using a few monoclonal antibodies which are different than Rituximab.

We lack approved drug treatments, but there are lots of other things, including vitamins and natural therapies, in which we find similar responses. Also the off-label use of drugs, apparently, is similar. I have not looked into this, and I am getting my information second hand from a variety of sources.

One thing that is markedly different appears to be how we respond to exercise though.

PS I had a look at one of those drugs, lemtrada, and like rituximab its used to treat cll. In other words, it has the same target cell (but is cd52, so its actually less specific). Another attacks T cells. Most of the rest are beta interferon variants, in other words, different versions of the same drug. There are a couple of others I am unfamiliar with and did not look into.

Its very possible lemtrada would work for us too. Beta interferon might or might not, or might work on a subset.

 

[NK17]

Don't want to hijack this thread, but I need to mention and suggest to @Kati and @alex3619 Prof. Gavin Giovannoni's MS blog:
www.multiple-sclerosis-research.blogspot.com
for all of the most insightful news on everything, really every aspect of MS and its impact on patients' lives and for a different take on the possible trigger/s and potential therapeutical drugs repurposing in MS.

 

[Kati]

Don't want to hijack this thread, but I need to mention and suggest to @Kati and @alex3619 Prof. Gavin Giovannoni's MS blog:
www.multiple-sclerosis-research.blogspot.com
for all of the most insightful news on everything, really every aspect of MS and its impact on patients' lives and for a different take on the possible trigger/s and potential therapeutical drugs repurposing in MS.

Hi @NK.17 the link is broken but I found it and it is very interesting indeed.
Definitely not off-topic.

 

[heapsreal]

@alex3619

I spent a short amount of time on an MS forum and at the time there were a few of them using valtrex and getting a good response. The theory was that ebv was somehow involved in MS.

The other treatment alot of MSers use is interferon, not commonly used in cfs/me but is used by dr chia for enteroviruses. Than there is the interferon inducers commonly used by many cfs docs, ampligen being the big gun and the other being immunovir.

Another drug i noticed used by quite a few was modafinil. There is some research showing it is neuroprotective, but cant recall if this study was in relation to MS or not.

The other treatment thats still in research stage for MS that i found interesting was that they extracted patients T cells and exposed them to an ebv vaccine, therefore strengthening its response to ebv. Then they infused it back in the patient. Apparently this patient improved remarkedly. http://www.msaustralia.org.au/news/queensland-researchers-make-major-breakthrough-ms-treatment