Discussion in 'Active Clinical Studies' started by Kati, Dec 9, 2016.
Let's hope some early results might persuade them to speed things up
From the article
by Miriam Tucker
She states that Dr. Nath said:
"We want to keep an open mind, and not bias ourselves. We're looking at a very broad panel,"
Yet, Dr. Nath starts off with a specific hypothesis - not shared by many ME experts.rming this NIH study.
As Miriam Tucker quoted Dr. Nath:
"The current hypothesis, Nath says, is that, in contrast to people with normal immune systems that act to quell an infection and then subside, there is "a subset of individuals whose immune systems over-react and do a lot of collateral damage."
"We think it's unlikely there's persistent infection going. Our hypothesis is that there's an infectious process that triggers it, and after that the infection is gone but the symptoms persist."
Many ME experts believe there is an ongoing persistent viral/enteroviral/retroviral infection going on impacting patients.
So, the statement that they are not starting with any bias about the disease yet, choose one specific hypothesis, is not consistent.
Does a hypothesis automatically introduce bias?
My guess, from what I've observed, is that none of the multisite cohort doctors (the source for patients for the NIH study as far as I understand) properly test their patients for enterovirus infection, so either the patients in the NIH study don't have enterovirus infections, or do and we'll never know about it since NIH isn't testing for enteroviruses either. Dr. Chia isn't part of the multisite cohort and the majority of his patients would be excluded from the study as most have serological and histopathological evidence of active enterovirus infection, active infection being one of the exclusion criteria for the study.
This was what I was told about looking for Enterovirus or other chronic infections. Researchers feel Dr Lipkin looked for chronic infections in Dr Montoya's patients without finding clear evidence. I am not familiar with exact methods used by Dr Lipkin or characteristics of Dr Montoya's patient cohort. However, I suspect Dr Nath could look for infectious agents in CSF with mass spectrometry in NIH post infection patients. Perhaps @viggster could pose this question to Dr Nath. I could also possibly email Dr Nath and ask him directly.
Does anyone know if Dr Chia ever examined CSF samples looking for Enterovirus? Obviously, obtaining brain tissue samples may not be feasible but I would willing to provide muscle punch biopsy sample if needed.
They only looked at plasma, it was far from a complete study. I assume that's why it has never been published. Nobody should assume anything based on this.
It's actually quite rare to isolate enteroviruses from blood or CSF in non-hypogammaglobulinemic patients, even during acute infection. Here are two cases where PCR of CSF were false-negative and brain biopsies were positive (1,2). Obviously we're not going to get brain biopsies for the NIH study, but at a minimum they need to be performing neutralizing serology for coxsackie B and echovirus which they aren't. We already know ME patients have enterovirus infection in their brains, it's been proven three times at autopsy by three different groups. I'm not sure how many more people have to die to get the NIH to take notice of this evidence.
These ME experts may be incorrect in their assumptions about ongoing infections. Thats exactly why we need researchers that are looking at different things.
Lipkin and Hornig are trying to do just that but like everybody else they need more funding.
I'm curious how you know for certain this isn't being done. I can ask about it. The study has flexibility to add things.
I have spoken with Dr Chia in the past and he told me how difficult it is to find evidence of Enterovirus in tissue using PCR. Mass spectrometry may be much more sensitive. I do wish NIH could work to resolve this long drawn out issue.
My own opinion is that the longer I have this disease and try to "educate" myself about ME/CFS, the more I appreciate the lack of good quality scientific data.
I also wonder about my own bias as a patient. The concept of a smouldering undetectable viral infection is alluring because it implies a tidy and satisfying answer. If we can just find the offending agent, we can work on an anti-viral cure.
However, what if the initial viral trigger is just a red herring. I think anyone "entrenched" in their belief of a specific mechanism of disease (smouldering infection, auto antibodies, toxic mold, channelopathy, etc) is not standing on terra firma. Which is exactly why we need more quality studies. At least the intramural study at NIH is a good start. It may not be perfect but it has the potential to uncover a biomarker. A biomarker that can point to a direction for further research.
This study is going to find things and inform the scientific basis of ME/CFS. All of the current research is adding to our knowledge. If it turns out to be ground-breaking...all the better.
However, the most important part of this study is that it will create a new entry for ME/CFS politically. A large NIH study that validates ME/CFS on a biological basis is going to be very influential for future funding. Also, it will open the door for new researchers to enter the field by getting others interested. It's a start and its larger impact may be profound. We need a fresh start with the research community...and open minds to support this effort.
Thank you to @viggster and @RYO for giving us updates.
I agree. And this round of Millions Missing will be held at only one city in the US, unfortunately after May 17th. This could send the message that we are loosing momentum in the US. (A big thanks to Marilyn Yu for organizing the upcoming Sacramento rally on June 2).
I don't know for certain and I'd love to be proven wrong. They've only specifically mentioned HIV testing to determine eligibility and herpesvirus serology. If they go beyond this I'm sure it will just be the same PCR of serum or CSF which will never come back positive. They need to test tissue samples or serology, anything else is a waste of time. Chronic enterovirus infections don't involve viremia except in cases of hypogammaglobulinemia.
It's not trivial, but it's clearly possible and again has been done repeatedly in ME patients brains, hearts, muscles, GI tract, and other organs, by numerous groups using numerous techniques. Isolating enterovirus from body fluids is impossible no matter how hard you look because there is nothing there to find.
It's not undetectable. It's alluring because there is solid evidence for it, both in the literature and in my own body. I would have to deny reality to believe anything else. I'd have to believe two different labs made a mistake, on three occasions, testing my blood. I'd have to ignore the fact that I have a micrograph of my own stomach tissue that is visibly riddled with enterovirus infection. Yes, none of this proves causation, but objectively, the virus remains in my body and I remain ill, I don't think this is a coincidence, and it can't be proven wrong until targeted antivirals become available.
I am not ruling out the possibility that a biomarker may point towards chronic enteroviral or other infection. If it does, it would make sense that the NIH would further study the mechanisms leading to chronic symptoms. However, the current study design is broad enough to possibly detect other possibilities (autoimmune, microbiome abnormality, neuroinflammation)
Doesn't it bother you that the response rate for Equilibrant and Rituximab are both roughly around 50%. (I also have elevated coxsackie B subtype 4 titers from ARUP. My stomach biopsy stained positive for VP1 protein. There are healthy controls who also stain positive for this protein.) I am sure you can find someone who will vehemently argue their disease is caused by HHV6 or EBV.
How does a scientist reconcile these findings? You start to question inclusion criteria. Since we currently don't have a biomarker, you use clinical symptom criteria. I think the NIH intramural study does a thorough job of trying to rule out confounding factors and obtaining as many objective findings as possible (MRI of the Brain, full sleep study with EEG, neuropsychiatric testing, microbiome study, etc)
We do have several studies pointing to bio markers but these have been ignored by HHS. NIH has refused to fund needed large scale replications so they make believe these studies don't exist.
This refusal to follow up on the bio marker studies has enabled the government government to repeatedly create and use overly broad criteria which continue to confuse scientific findings.
NIH Study Takes the Deepest Dive Yet Into Baffling Condition
by Maggie Fox
Inhaling insulin? That's one I haven't heard of. @viggster is that helping you?
Maggie is such a good reporter. She taught me a few things about the study and included a lot of great details. For instance, I did not know NIH is trying to make a mouse model with immune systems from ME/CFS patients. They're trying to get the human immune stem cells into the mice at the embryonic stage. Let's hope it works. Though I do feel bad for any mouse born with my immune system. I've been thinking about asking for a new one (immune system, that is) while I'm here, but those tend to be major procedures that they don't just hand out.
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