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Sept 10: CDC 'conference call' including Unger and Lipkin

Bob

Senior Member
Messages
16,455
Location
England (south coast)
Without ever naming it, Dr. Unger is referring to the ICC domain of post-exertional neuroimmune exhaustion: “When an exercise test was given on two consecutive days, some patients experienced up to a 50% drop in their ability to produce energy on the second evaluation [62].” PENE is described as the cardinal feature of ME, a subset that should be treated as separate and distinct from CFS. Dr. Unger must be familiar with the test for PENE prescribed by the ME Primer:
PENE: A 2 consecutive day comprehensive 8-12 minute cardiopulmonary exercise stress test (measuring heart, lung, and metabolic function) - only ME patients have significantly worse scores the second day & abnormal recovery from exertion. * Exercise tolerance test with expired gas exchange - (2 consecutive days) – measure cardiovascular, pulmonary & metabolic responses at rest & during exercise: □ peak oxygen consumption VO2 or VO2 at anaerobic threshold (AT) - decline of 8% or greater on test 2 indicates metabolic dysfunction, □ post-exercise blood analysis - increase in sensory, adrenergic and immune genes - increase in metabolite receptors unique to ME
Considering that Dr Snell's latest paper supersedes his 2005 paper which is cited in the ME primer, and the results for VO2 peak do not seem significant in the latest paper (if I've interpreted it correctly), do you think the primer now needs updating?

By tapping the domains of earlier case definitions, Dr. Unger is turning the clock back a decade, despite professing:
I share your concern about patient heterogeneity. My question is whether any one case definition is going to solve the problem. Part of what I think we need to do is decide what the measures are that are going to yield us meaningful subgroups of this illness. I think even the Canadian case definition allows for heterogeneity.

But she's actively trying to define subsets, based on her data. Yes, I agree that she needs to include objective tests. But if she does include objective tests, then I can't fault her approach of actively trying to define subsets, with large amounts of data. That is exactly what is needed, in my opinion. Of course it all depends on the honest intentions of the investigators, which is yet to be proven.

Assuming honest intentions, for the sake of discussion, how would such a study not be beneficial, in your opinion, if it included two day CPET tests?

Dr. Unger could address her research questions by gathering the data that the Stevens Protocol provides.
Agreed, as long as Unger is aware of Dr Snell's 2013 CPET research results, and not just the 2005 paper which is referenced in the ME primer. But I still think her post-exertion cognition tests may prove to have some merit. Cognitive tests are a fairly objective indicator of cognitive performance, aren't they? (I do not know much about the merits of cognitive tests, but I assume that they can be helpful objective indicators of cognitive function. And if they are, then they may provide a useful objective indication of post-exertional symptom exacerbation.)
 

patient.journey

Senior Member
Messages
443
Even when i think this study is good but there are some questions about it that needs an answer :

1) Prof. Paterson CSF samples used to be tested positive by PCR for HHV6 and now they said they didnt find that !! is that because the long time of frozen ?

2) Dr. Montay used to test his patients under the HHV6 foundation instructions as i know because they were funding his studies and now his all samples too were clean for HHV6 ?

3) If no herpes virus was in the blood why the antivirals had a good effect on patient ?

4) How can they just ditch the 85% of positive samples for retroviruses and we know that retroviruses are accountable on one hand !! so what was that retro virus ? specially that a lot of patient who tried anti retro viral had positive results !

I dont say Prof. Lipkin study is not good in anyway but some questions should have an answer :)

Some times i feel like they want to find some common out come of all patients so they can provide a treatment one day without knowing the real cause of our illness
 

Andrew

Senior Member
Messages
2,513
Location
Los Angeles, USA
4) How can they just ditch the 85% of positive samples for retroviruses and we know that retroviruses are accountable on one hand !! so what was that retro virus ? specially that a lot of patient who tried anti retro viral had positive results !

I was wondering about this too. The first question would be whether the controls had this level too. And my second question is whether these appear to be working retroviruses, as opposed to retrovirus remnants that litter our genome.
 

Firestormm

Senior Member
Messages
5,055
Location
Cornwall England
Even when i think this study is good but there are some questions about it that needs an answer :

1) Prof. Paterson CSF samples used to be tested positive by PCR for HHV6 and now they said they didnt find that !! is that because the long time of frozen ?

2) Dr. Montay used to test his patients under the HHV6 foundation instructions as i know because they were funding his studies and now his all samples too were clean for HHV6 ?

3) If no herpes virus was in the blood why the antivirals had a good effect on patient ?

4) How can they just ditch the 85% of positive samples for retroviruses and we know that retroviruses are accountable on one hand !! so what was that retro virus ? specially that a lot of patient who tried anti retro viral had positive results !

I dont say Prof. Lipkin study is not good in anyway but some questions should have an answer :)

Some times i feel like they want to find some common out come of all patients so they can provide a treatment one day without knowing the real cause of our illness
I was wondering about this too. The first question would be whether the controls had this level too. And my second question is whether these appear to be working retroviruses, as opposed to retrovirus remnants that litter our genome.

In addition to what was said on the transcript (see links in my signature) we heard this from Lipkin in reply to a question from Wildaisy.
 

patient.journey

Senior Member
Messages
443
In addition to what was said on the transcript (see links in my signature) we heard this from Lipkin in reply to a question from Wildaisy.


What about if this new retrovirus is causing some people sick but not all of us as many other viruses ?

The percentage for this virus in healthy people should e known and this high number of CFS/ME patients infected with it should not be ignore.

HHV6 doesnt have an answer from lipkin or Montaya now so whe should wait and see
 

Legendrew

Senior Member
Messages
541
Location
UK
I just cannot believe that millions of us are as good as dead and they are trying to test poo.


It sounds crazy but the gut microbiome is quite an interesting area of researcher both inside and outside of ME. I'm not sure it will bring out the answers to ME but I think it could tell us quite a bit.
 

natasa778

Senior Member
Messages
1,774
What about if this new retrovirus is causing some people sick but not all of us as many other viruses ?

The percentage for this virus in healthy people should e known and this high number of CFS/ME patients infected with it should not be ignore.

HHV6 doesnt have an answer from lipkin or Montaya now so whe should wait and see


I just posted this on another thread, reposting ...

The big finding was a decrease in levels of Interleukin’s IL-17, IL-2, IL-8 and in TNF-alpha – all of which have a role in pro-inflammatory responses. Lipkin believes these significant differences are worth follow-up in larger cohorts to better understand what they mean.​

Interesting that lowered production of these very cytokines are associated with disease progression and immunological damage in HIV patients – HIV+ long-term nonprogressors retain the ability to make these cytokines, while individuals with progressive disease start producing less of Il-17, TNF-α and IL-2 after a while…


Also interesting to read that this sudden downturn in cytokine levels happened after exactly 3.1 years in this patient
Patient maintained a stable/low viral set point for 3.1 years before control of viral replication was lost … Gradual loss of functionality was observed in these responses, characterized by early loss of IL-2 …



This paper could give us further clues on reduced IL-17 levels in chronic, long-term ME sufferers (also possibly linking to gut barrier breakdown)

Studies in nonhuman primate models of lentiviral infection and in HIV-infected human individuals highlight pathogenic infection to be associated with loss of Th17 cells. IL-17 serves to maintain the integrity of the mucosal barrier. Loss of Th17 cells may permit microbial translocation across the gastrointestinal mucosa and thereby promote immune activation driven by bacterial lipopolyscaacharide, which is associated with disease progression. We demonstrate that …. We demonstrate that …. reduced Treg and IL-17 numbers is a feature of chronic HIV infection
 

patient.journey

Senior Member
Messages
443
I just posted this on another thread, reposting ...

The big finding was a decrease in levels of Interleukin’s IL-17, IL-2, IL-8 and in TNF-alpha – all of which have a role in pro-inflammatory responses. Lipkin believes these significant differences are worth follow-up in larger cohorts to better understand what they mean.​

Interesting that lowered production of these very cytokines are associated with disease progression and immunological damage in HIV patients – HIV+ long-term nonprogressors retain the ability to make these cytokines, while individuals with progressive disease start producing less of Il-17, TNF-α and IL-2 after a while…​
Also interesting to read that this sudden downturn in cytokine levels happened after exactly 3.1 years in this patient
Patient maintained a stable/low viral set point for 3.1 years before control of viral replication was lost … Gradual loss of functionality was observed in these responses, characterized by early loss of IL-2 …
This paper could give us further clues on reduced IL-17 levels in chronic, long-term ME sufferers (also possibly linking to gut barrier breakdown)​
Studies in nonhuman primate models of lentiviral infection and in HIV-infected human individuals highlight pathogenic infection to be associated with loss of Th17 cells. IL-17 serves to maintain the integrity of the mucosal barrier. Loss of Th17 cells may permit microbial translocation across the gastrointestinal mucosa and thereby promote immune activation driven by bacterial lipopolyscaacharide, which is associated with disease progression. We demonstrate that …. We demonstrate that …. reduced Treg and IL-17 numbers is a feature of chronic HIV infection


Yes but all those number are high in the first 3 years nearly ! i think its up to the time the body stop fighting something and immune system got a lot of damage
 

natasa778

Senior Member
Messages
1,774
Yes but all those number are high in the first 3 years nearly ! i think its up to the time the body stop fighting something and immune system got a lot of damage

Yes same in HIV infection - high at first then plummet down

(except in 'non-progressors' - those who don't get ill maintain normal/elevated levels)
 

Dolphin

Senior Member
Messages
17,567
I don't think we should donate money until they agree to test gut biopsy tissue

I don't think we can really tell Ian Lipkin what to do. Unfortunately, especially after XMRV, I think he may be a bit wary of us. It's not like he doesn't have other things (nothing to do with ME/CFS) he could be doing.

That's not to say that we couldn't look for some other researcher to do gut biopsies.

The thing with research is that one has to look at various angles to see what will work: maybe what Ian Lipkin wants to do will give us big answers, maybe it won't. Me personally, I'm glad he's interested and if he has something he wants to explore, I'd like to keep him involved.
 

Kati

Patient in training
Messages
5,497
I don't think we can really tell Ian Lipkin what to do. Unfortunately, especially after XMRV, I think he may be a bit wary of us. It's not like he doesn't have other things (nothing to do with ME/CFS) he could be doing.

That's not to say that we couldn't look for some other researcher to do gut biopsies.

The thing with research is that one has to look at various angles to see what will work: maybe what Ian Lipkin wants to do will give us big answers, maybe it won't. Me personally, I'm glad he's interested and if he has something he wants to explore, I'd like to keep him involved.


He also gave us lots of cues as of what to do, talk to congressman and government representant and demand funding. Am pretty sure he would approve a mass protest :)
 

Dolphin

Senior Member
Messages
17,567
A possible problem with a protest in Washington is the numbers might not be too big: 500 (?) people (say) would be a great achievement in terms of the ME/CFS community but it's not exactly a huge march.

But if people could use that energy to lobby their politicians, that'd be great.