Discussion in 'Phoenix Rising Articles' started by Firestormm, Sep 12, 2013.
Do you have links Alex to the Leptin info you reference? TIA
I thought Dr. Chia's main point is we're not going to find the viruses unless we're also testing a broad set of tissue samples, kind of to heapsreal's points above about the herpes family of viruses. Yes it's great they are testing cerrebrospinal and plasma, but if there is something we don't catch there, and it's already in all your nerve cells in various tissues, GI tract, etc. their "new happy home" then you may not find the usual viral counts or antibodies because the body can't fight them once they are in the nerve cells?
I do find the new direction on gut biome encouraging. If we can at least strengthen that area with some of their findings, that should do a lot to give the body a fighting chance to correct any other imbalances on its own.
The article and transcript get a mention from AfME:
Thanks. I do get the impression that these new cytokine findings don't quite fit with earlier ones. That said, generally cytokine findings are all over the place in this field.
Re that Broderick paper: it's very interesting in that it looks at cytokines over time in 300 adolescents who had glandular fever, and compares those that recover with those that get CFS. That's a strong experimental design - except there are not many CFS cases to go at. There were 22 CFS cases at 24 months and just 13 at 12 months - compare that with 285 for the Montoya sample in this study.(Though maybe those figures are not so different from the '3 years and under' subgroup in the Lipkin study?).
What I would particularly like to see is how consistent findings are between patients eg are patients consistently low for IL2,8 &17 - or are some low for 2, others for 8 etc. And also how big the differences are between patients and controls? Certainly for other studies there has been a high degree of overlap between patients and controls despite group differences. Will be good to see the paper when it's published.
These abnormalities could just be an outcome from the illness - not necessarily a causative agent.
I think there's little doubt that cytokines are not the causative agent - to me they stand out more as footsteps in the sand which are worth following. Abnormal levels of cytokines mean disruption of normal immune function and possibly abnormal and harmful immune loops. The true question is whether these loops are perpetuated by the continuing presence of a pathogen or are self-perpetuating as is seen in autoimmune activation.
Simon, Firestormm..... Thank you for that very well written article And the transcript. you are providing a valuable service to this community.
I Wonder how the Lipkin study fits in with the autoimmune/rituximab info? I guess we'll see what Dr. Edwards has to say about the transcript information....
i also wonder if Dr. Chia is ever going to get money to do his tissue sample studies. He is certainly a Lonewolf out there.
I wonder if hhv6a aka human b cell lymphotropic virus or African swine fever virus was tested for
I followed a link on anellovirus and it came up with torque teno virus,it is a very common virus
Its everywhere. I just gave a summary of a points on a few papers. Run a search and you will be overwhelmed with links. If I find really good review articles I will post those however.
One key word you might like to know is hyperleptinemia. High leptin has its own name.
PS Here is a paper that shows in mice some of the impact of hyperleptinemia can be reversed by resveratrol:
PPS. My initial brief survey found no good reviews of leptin. Instead many papers will discuss it in their opening sections, and some will review a particular aspect of leptin. For example, the following paper discusses in its introduction the impact of leptin on the immune system, but the primary focus is breathing problems:
There are so many links with possible ME issues that a word of caution is advised: these are all possibilities, but they require a lot of research to validate and test them. For example, hypoxia is known to induce increased leptin levels. However leptin also interferes with NO, inducing vasoconstriction. Its all very complicated.
Another thing I noticed is Chromosomally integrated HHV-6 about the same as autism rates.
New study: http://www.ncbi.nlm.nih.gov/pubmed/24027260 "Cytokines do not change after exercise or sleep deprivation in chronic fatigue syndrome" Thread here. Made me wonder the circumstances under which the samples in Lipkin's study were taken. Of course we don't know them yet - but it might be prove interesting when we do.
Returning to the pathogen hunt, Lipkin said:
So then. Borrelia species bacteria. We hear an awful lot about people being told they have Lyme Disease and receiving treatment for it - or not; but it looks like there is not a role for this at least in this study.
Much more is said on the forums about various doctors testing folk for the bacteria and determining that this is the source of the CFS-like symptoms - how then can Borrelia not be a factor in Lipkin's results when those patients taking part were diagnosed using Fukuda and CCC?
Any thoughts? Or is this the beginning of the end for people with CFS being misdiagnosed with Lyme disease and receiving inappropriate treatments based on spurious testing?
I thought Nancy Klimas said in Dr Peterson's pre-FDA workshop workshop (the audio went out as podcasts) that if she tests her patients, a minority are positive by PCR (blood, presumably) but by the time they've done three or four repeat tests, most are. I wonder how that ties up with Dr Lipkin's findings?
The serology, which is looking for evidence of previous infections (which is where I think much of what we need to do in the future must focus), is not part of this first report that I am making to you today
The above quote by lipkin is what many seem to be missing when i mention viruses etc. Serology might be about past infections but he seems very interested in this and thinks it maybe of importance. If serology is tested very high then dr's such as Lerner will say there is an active infection going on but lerner also mentions that these are viral particles, something that i think was missed in this study.
So at the moment i wouldnt say serology is dead and gone.
I saw an infectious diseases specialist in the UK who told me my massive HHV-6 IgG titre didn't mean anything because the tests were enormously inaccurate, among other things. Given that almost everyone has been exposed to HHV-6 by adulthood, I wonder what Dr Lipkin can do with his serology tests that would be worth doing. Perhaps he's got better tests?
I am not ignoring this, far from it. What these 'shadows' will reveal is evidence of previous infections: possible triggers for the ME - if the same ones can perhaps be found across the cohort.
However, he did not detect them as 'active' infections and the theories that we have been discussing are in the main about previously 'dormant' viruses common to most people becoming 'reactivated' in people with ME.
If that had been the case: he would have detected them. So, in short, the shadows might reveal more about common pathogen triggers for ME - that might then tie-in with e.g. the over-stimulated immune system and/or 'looping' or B-cell influencing factors perhaps: but not infections that remain active.
I'm not too surprised about the differences in the disease after 3 years.
I can't say if it was exactly 3 years, but in the beginning I had horrible sore throats and didn't have muscle pain. Now, at fourth year I never get sore throat and pain is constantly present.
Does anyone know where we can donate money for the Lipkin's microbiome research?
Lipkin's team might have benefited from consulting the HHV-6 Foundation about HHV-6 testing:
Well I don't know if CSF counts as 'the brain'. What do you think?
Isn't Montoya connected with them? And Lipkin used Montoya's samples, I think.
You can also try a Google Site Search
Separate names with a comma.