Discussion in 'Other Health News and Research' started by kaffiend, Jun 14, 2013.
A very sad, and familiar story of treatment by the authorities...
This is the study the article is based on...
Exercise Challenge in Gulf War Illness Reveals Two Subgroups with Altered Brain Structure and Function
Rayhan RU, Stevens BW, Raksit MP, Ripple JA, Timbol CR, et al.
June 14, 2013
PLoS ONE 8(6): e63903.
This is the study described by Rayhan at Invest in ME (see my article for very brief summary, somewhat truncated in case it should be embargoed). He said it'd be out in a couple of weeks, and indeed it is - to the day. Small study, but extremely interesting to me. The idea of subgroups for post-exercise pain and post-exercise fatigue, caused by different areas of compensatory brain activity in response to...what? the same cause perhaps?...is intriguing. This is in GWI, but similar studies in ME/CFS would be extremely interesting. They would like to do that, but it is much harder to get funding for ME/CFS than for GWI. I do hope they are able to follow this up with larger studies, and even better, somebody else replicate it. Such a small study is not sufficient for establishing this as proven, far too many such findings evaporate on attempted replication, but if they are right it could be a major breakthrough because finding such subgrouping of response could explain previous conflicting findings and find a way to untangle heterogeneity in the condition(s).
two groups within GWS: what's the bet one is organophosphate triggered, the other, by vaccines?
I wouldn't want to bet on this. However I also wouldn't want to presume that is right, or entirely right. I still think we might have surprises awaiting for us in this area of medical science. In particular we need to know, not just speculate on, why some people with rapid vaccination schedules or exposed to low levels of nerve gas or high levels of insecticides (the US Army uses them) get sick and not others.
I've been plugging the work of Beatrice Golomb (previously scientific director and chief scientist at the Dept for Veteran Affairs) for some time now.
She sets out a very plausible model for how the various putative triggers for GWI (and other 'overlap' conditions) may result in the same pathophysiology (and also why some get sick and most don't).
Oxidative Stress and Mitochondrial Injury in Chronic Multisymptom Conditions: From Gulf War Illness to Autism Spectrum Disorder .
Re this paper I don't think its safe to conclude that a different pathology underlies the two groups they identified. You can't rule out the possibility that the same mechanism affects different brain areas in different people or that they represent a disease progression rather than discrete sub-groups.
A good paper though and consistent with some ME/CFS research I've been reading lately.
Oooppss I posted the research paper here. Not ME but figured it had ME implications and ought to be repeated in ME populations especially as it includes PEM as a symptom for GWI and exercise formed a key component of the test and scan. Some good imaging results shown also and it's been a while since I've seen any from an ME-specific paper. What's the difference between GWI and ME - that they are Veterans? Symptom presentations are obviously very similar and this relationship to PEM (that I always thought was sold by some as a unique marker in ME) makes me want to see similar studies conducted on this patient population too.
Could GWI be more similar to cases of ME than has been thought? Or vice-versa? A similar study of ME and GWI and healthy controls would be very interesting I think. Can someone who is a Veteran have ME or are they excluded because they are a Vet? Interesting.
Answers my last question then I guess.
Researchers cite new findings on Gulf War Illness
Nice start, "it's legitimate" - now find the underlying biological pathologies and cause.
I like the idea of piggybacking on GWI research.
I assume they've got more funding than me/cfs researchers can dream about.
If the pathology is similar or the same, any relevant progress in their field could be transitioned to me/cfs patients,
doubtless quicker than through me/cfs channels.
Neurodegeneration doesnt sound like much fun though. How does one rehabilitate that?
The PLoS One paper states that all the GWI patients are CFS too
Does anyone think this paper is worth me blogging about?
Hi Simon , yes I think its worth blogging about. Aside from possible links to ME, there are two good reasons to blog about it. First, we should be concerned about all neuroimmune illnesses. All of us get poor research, poor research funding, and poor support. Second, this paper sends another message to proponents of psychogenic views: yet again you are wrong, its not psychosomatic. Best wishes, Alex.
I hope there is plenty of attention paid by researchers to the issue of hyperpermeable biological barriers, e.g. and especially gut wall/mucosa and blood-brain barrier. Permeability can increase with a range of stressors both physical and mental, which can include chemicals and infectious agents. This excessive permeability can let inappropriate substances into the bloodstream and/or brain and trigger the production of autoantibodies. Which autoantibodies are triggered would depend on environmental factors and genetic predisposition and could account for why the same process can lead to a range of different autoimmune conditions, and why the conditions can change over time.
This scientific paper explains how:
Recently I have come increasingly to the view that the Western model of disease is a very poor one. Numerous quite different conditions can be caused - and treated - in similar ways.
Has anyone read the Golomb paper I linked to?
Marco, I read the Golomb paper some time ago. Its more of the same of research I have been reading since 2005 or prior. Its not that impressive, and leaves lots of things open. This kind of research needs a lot more funding and investigation before we draw conclusions. One issue I have with many of these papers, and I mean all over the ME issue, is how do we know they are investigating secondary or primary mechanisms? We don't.
For example they are saying this will depress Vit D conversion, yet we have very high Vit D conversion if you believe KDM. In other words, and I can list other examples if I could go back and review a few things, they explain some of the pathophysiology but its important not to over-interpret this to full causation. That can be said of many other topics too, from autoantibodies (we have loads) to tissue viral loads or methylation issues.
Marty Pall wrote an entire book on this in 2005, and I reviewed it.
I accept your point Alex although I'm not sure that and apparently isolated finding (such as KDM's) invalidates the model.
The main point I was making was that increasingly, particularly in psychiatry, pathological mechanisms are seen to transcend traditional diagnostic labels. Yes, there may be a danger of over-interpretation or over-extending the reach of these models but I much prefer that to the under-interpretation that appears to go along with treating each 'label' as a discrete self-contained box.
How many times have you heard phrases like 'Yes there may be similarities but CFS isn't multiple sclerosis' as if that represents sufficient logical grounds to rule out any potential for shared pathology?
PS - Pardon my French - bad day yesterday
Marco , the issue is that these findings and models present alternative explanations, and nearly all of them have more objective evidence for them than any psychiatric diagnosis, and some have a lot more evidence for them. The take home lesson for me is that we need to consider all the possibilities until we can nail one (or more) down and throw the others into the trashbin. That means more research, which requires more funding, which relies on funding being available.
I am a big fan of OS & NS models, have been since about 2000 or so. They also tie in closely with methylation research. From about 1998 I was interested in the impact of glutathione on ME. Thats how far back the science clearly showed there might be a major issue there, but even now we don't know enough to make definitive statements.
One thing I keep saying (since maybe 2000) but most do not consider is that glutathione is not just an antioxidant, its a sulphur source and is critical for proper protein folding. Insufficient glutathione leads to bad proteins, which may impair cell function and possibly accumulate. There has been a little research along these lines in ME, but again nothing definitive.
One I investigated in some detail way back when was the enzyme aconitase which is essential for mitochondrial function. Its imported to mitochondria from the cell, and without glutathione will not function as it wont be folded properly. Now the cell should have mechanisms that destroy unfolded aconitase before it becomes a problem, and the evidence of a block at aconitase is not strong in ME, but it still remains a concern. Under normal physiological conditions we might have enough aconitase. Under exercise demand however we might rapidly reach a limit due to insufficient aconitase.
Nitric oxide inactivates aconitase, and peroxynitrite destroys it. Nerve cells are very vulnerable to even a small decline in energy production.
Will we hear anything from Mr Wessley do you think - given he was the expert at one point informing both the USA and the UK about the mental health of GW vets? I think not....
Luckily he's had extensive experience in avoiding biomedical research - I'm sure he's already got a mechanism in place to ignore this or explain why CBT is still the One True Cure
Didn't he get some kind of merit badge for his services in this area?
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