Lipkin's Microbiome Research -- new or old topic? (split thread)

[Valentijn]

@Valentijn
Why does it matter what she calls it? We all know what we are referring to here. Instead of picking out such a small detail, focus instead on any ideas we can share regarding studies and treatment for the disease. N.B I've always called it CFS too.

She was calling it "chronic fatigue", not CFS. While CFS can easily be understood to mean ME/CFS, CF is a different matter as it has a completely different definition and is a symptom rather than an illness. For the sake of clarity, it's very problematic when someone repeatedly says "chronic fatigue" when talking about the illness, as it's hard to figure out if they mean the illness or the symptom.

 

[vli]

Another good reason not to just say 'chronic fatigue' is that the letters actually stand for Cystic Fibrosis in the patient community, a completely different condition altogether.

 

[MeSci]

Anyone want to raise funds for me so as I can buy a Mars bar? Am feeling a bit peckish

No - because they are BAD for you! We want to make people better, not worse.

 

[Daffodil]

wpi campaigns all the time..the KDM/Lombardi work is done there..isn't it?

we may as well stop wishing scientists will all call eachother to share knowledge and collaborate...it won't happen

 

[Sushi]

wpi campaigns all the time..the KDM/Lombardi work is done there..isn't it?

we may as well stop wishing scientists will all call eachother to share knowledge and collaborate...it won't happen

I believe that they are researching through grants, not from WPI fund-raising--though obviously I haven't seen the books!

Many of the docs who are not collaborating in open studies and partnerships, are collaborating through on-going conversations. This is heartening!

And yes--we need all the research we can get, no matter who the principal researchers are and how they get funding.

Sushi

 

[SOC]

wpi campaigns all the time..the KDM/Lombardi work is done there..isn't it?

we may as well stop wishing scientists will all call eachother to share knowledge and collaborate...it won't happen

Not true. Scientists researching our illness have done a more than usual amount of collaboration and sharing knowledge. Witness both public conferences and several researcher-only conferences.

It is true that scientists have different areas of interest and research. That's good, we want a variety of approaches because we don't know where the final answer is going to come from. Researchers work in the area in which they're trained -- immunology, infectious disease, systems analysis, whatever. I'm fine with researchers working within their area of expertise. That's where they're going to make the most impact.

 

[Daffodil]

well lets hope lipkin finds something the others didn't.

 

[SOC]

well lets hope lipkin finds something the others didn't.

Yes, let's hope so. Let's hope other researchers get money to do their research as well. The more the merrier!

 

[August59]

I believe this study is continuing:

Plasmacytoid Dendritic Cells in the Duodenum of Individuals Diagnosed with Myalgic Encephalomyelitis Are Uniquely Immunoreactive to Antibodies to Human Endogenous Retroviral Proteins

http://iv.iiarjournals.org/content/27/2/177.full

My opinion, being a patient, is that this looks like a very promising avenue to approach. One sentence made the whole study seemingly insignificant to the majority of the research community. If it had read that "80 out of 100 patients", instead of "8 out of 10 patients" would have made an extensive difference in the perception of the study when presented to the scientific/research community. Probably even 40 out 50 would have made a drastic difference since the study samples were intestinal biopsies, instead of blood samples.

This just an example, in my opinion, of how the trend has been with ME/CFS studies since I was diagnosed in 2006 after being ill for 3 years prior. The funding has just been so poor or non-existent that even good valid studies don't carry any clout due to the extremely low "numbers" involved in the studies, but we are at the point where we have to take what we can get!

This study should definitely get more funding for a larger cohort so that it can get the recognition that the study, researchers and we as patients deserve. This would be a good study to get replication on as it has potential to move toward a possible diagnosis or treatment.

I also don't have any negative feelings toward the WPI because the proof is in the pudding and I don't care where the pudding comes from. I'll gladly donate a biopsy from any part of my body (well almost any part) for any study that will potentially advance the knowledge of a disease that has stolen the last 10 years of my life!

I'm throwing out this question because I don't know what the full detailed study states for Dr. Lipkins "Microbiome Study", but is there as possibility that the "Microbiome Study" could attempt to replicate this study? Or are we talking about an endoscopy, instead of colonoscopy/sigmoidoscopy?

Prayers and wishful thinking,
Jerry

 

[vli]

@August59, please see the original article thread for details of the study. I wanted to include paragraphs from that first post in this reply, but can't because that thread is separate.

 

[Sasha]

I'm throwing out this question because I don't know what the full detailed study states for Dr. Lipkins "Microbiome Study", but is there as possibility that the "Microbiome Study" could attempt to replicate this study? Or are we talking about an endoscopy, instead of colonoscopy/sigmoidoscopy?

Hi Jerry - it's neither - it's faecal matter collected in a special cup to give a sample of the gut microbiome.

 

[vli]

HERV proteins are being cranked out - and the only group I know who is looking into why, is KDM/Lombardi/WPI.

My question is: has KDM told his patients about any one particular HERV that he finds is being expressed? For a specific pathology to be the result, like PEM, there must be a specific causal pathway. If ME is caused by HERVs, is it just one particular HERV that does it? e.g. it can't be HERV-W activation, which they hypothesise for MS. There must be a reason why some people get ME and others get MS.

Thank you for any help/explanation

 

[MeSci]

My question is: has KDM told his patients about any one particular HERV that he finds is being expressed? For a specific pathology to be the result, like PEM, there must be a specific causal pathway. If ME is caused by HERVs, is it just one particular HERV that does it? e.g. it can't be HERV-W activation, which they hypothesise for MS. There must be a reason why some people get ME and others get MS.

Thank you for any help/explanation

Genes? It seems to be the case that it's common for ME sufferers to have family members with other autoimmune diseases. If they have specific HERVs in common, they may however react differently to them due to genetic differences. So they may have in common a genetic predisposition to autoimmune disease, but also genetic differences which mean that the autoimmune disease is a different one, i.e the autoimmunity manifests itself differently, thus attacking different proteins, etc.

 

[Daffodil]

KDM/Lombardi have already published a paper on this and are going to publish another one, on new discoveries, likely in the second half of this year.

 

[Sushi]

My question is: has KDM told his patients about any one particular HERV that he finds is being expressed? For a specific pathology to be the result, like PEM, there must be a specific causal pathway. If ME is caused by HERVs, is it just one particular HERV that does it? e.g. it can't be HERV-W activation, which they hypothesise for MS. There must be a reason why some people get ME and others get MS.

Thank you for any help/explanation

He can't discuss any of this pre-publication.

Sushi

 

[Nielk]

He can't discuss any of this pre-publication.

Sushi

It seems like there are a few researchers at the cusp of publication. I hope at least one will fan out to be something exciting.

 

[vli]

He can't discuss any of this pre-publication.

Sushi

I don't understand. Have I got this right: so KDM published his paper on this Feb '13 and did not say which HERV was activated? I'm just trying to understand if KDM patients know something that we don't know.

 

[Sushi]

I don't understand. Have I got this right: so KDM published his paper on this Feb '13 and did not say which HERV was activated? I'm just trying to understand if KDM patients know something that we don't know.

Yes, he published in Feb 13 but is preparing to publish again. In Feb 13, the article said:

Immunochemical analyses of 12 ME gut biopsies probed for viral antigens showed that eight samples of the duodenum were immunoreactive to antibodies raised against HERV proteins (Figure 1A-D).

(http://iv.iiarjournals.org/content/27/2/177.full)

At that time they had confirmed that antibodies against HERV proteins had been found, but, at that point no specific HERV proteins were identified. The next article will, I'd guess, elucidate their further research.

Sushi

 

[biophile]

The prevalence of (idiopathic?) chronic fatigue is about 10-15%.

The prevalence of CDC 1994 defined CFS is about 0.4%, and Canadian criteria is about half that.

In other words, CFS is relatively rare by comparison to 'chronic fatigue'.

 

[vli]

I gather that identifying the exact HERVs is very difficult so thanks @Sushi it’s not surprising that KDM would take a while to do it.


But sorry, I have more questions…


I started reading your posts and trying to understand your views in the first place because I genuinely wanted to understand HOW as @Daffodil says KDM is “ten years ahead”.

we all have HERVs, but we don t know yet whether HERV expression is the cause rather than effect of the main pathology. For instance someone suggested that a virus say EBV may be causing the HERV to be expressed-in which case, the chain of causation (if I've understood correctly) would be: EBV causes HERV expression, which in turn causes ME. If the HERV is being expressed wouldn't something still have to be causing it to be expressed (be it a virus and/or toxin)?? And shouldn't you then be trying to find out what that virus is (and I'm not saying it's EBV; I'm just using it as an example?)??

​

So regarding what's causing the HERV expression, Chia has lots of tissue biopsies showing enteros, which is a big deal b/c unlike HERVs, enteros shouldn't be there—they are an outside pathogen, and Chia’s found them in tissue. Shouldn’t that be a smoking gun?


I’m trying to be fair, I really am… but the little more that I try to understand of this issue everyday, the more I feel there’s more evidence AT THE PRESENT TIME for enteros to be the cause of ME than there is for HERVs to be. AND just because I say that doesn't mean I'm saying HERVs and enteroviruses are mutually exclusive, (so please don't put words into my mouth--thanks!!), especially if an entero can be proved to be the trigger for the HERV expression. Apart from what I said about the smoking gun of an outside pathogen being found—I feel enteros could be the cause because they've already been shown to be able to cause a LOT of probs like polio and viral myocarditis, and it is veery interesting that post-polio syndrome is so incredibly similar to ME. OTOH, HERVs have yet to be shown to cause a human disease, ALTHOUGH I’m by no means ruling them out (again, I’m just trying to learn here!!!).

Can anyone here illuminate me a bit more??