Naviaux et. al.: Metabolic features of chronic fatigue syndrome

funkyqueen

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Hutan

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It means that those who don't have it are more likely to die in the long run, which means that though it is harmful the benefits outweigh the harm on an evolutionary scale.
Well actually, we all die in the long run :). So, pedantically, in evolutionary terms, the key thing is the passing on of genes - and for social species like humans, I guess it can also be argued that the survival of elders can facilitate the survival of younger relatives.
 

Chris

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Looks fabulous to me--this is ME/me, best shot so far I think. Interesting that Paul Cheney is thanked--I recall that many years ago he was saying things like "you get CFS to save you from worse," and "you can't train what's broken." Glad to see he has found a new audience for his experience and intelligence. Great stuff, though I will have to wait for those with much more scientific knowledge than I possess to help fully articulate what is here.
 

TiredSam

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Something odd seems to have happened as he is also quoted in the Times.
He's a psychiatrist and not even well-known in CFS circles so it would be a big coincidence if he was contacted independently by 2 journalists to comment on this story.
Is he being hidden behind? How generous of his senior colleagues to give him his big break and allow him to be the spokesperson this time ;).

Also found this interesting in the Daily Mail:

Critics have argued the condition, also called ME, is all in the mind
Nice to see that now it's the psychobabblers who are being labelled as "critics" instead of us. Is the nematode turning?

EDIT: @Dolphin have you got the Times link?
EDIT AGAIN: found it meself :)
 
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TiredSam

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Times article is here:

http://www.thetimes.co.uk/edition/n...uld-be-the-body-trying-to-hibernate-3fzp2zgxv

And you can read it all as one of your free articles if you register.

Other scientists welcomed the research, but cautioned that it was too early to say what was going on. Andrew McIntosh, from the University of Edinburgh, said: “It is difficult to know whether the changes reported are a cause or an effect of CFS.”
"Other scientists" indeed - that lot demonstrate their difficulty in knowing anything about cause and effect at every opportunity.

Didn't like the following:

Academics involved in the trial said they had received abuse just for doing their jobs.
Because although it's followed by a mention of Alem Matthees forcing them to release the data, it should have added that the academics' reports of receiving abuse were described as utter bollocks by the judge (I paraphrase).
 

Esther12

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Because although it's followed by a mention of Alem Matthees forcing them to release the data, it should have added that the academics' reports of receiving abuse were described as utter bollocks by the judge (I paraphrase).
I agree that it would have been good to have the tribunal's criticism in there, but they only spoke on the claims before them, so did not say that all reports of abuse were bollocks... some were not assessed! I think that we need much longer pieces for any worthwhile coverage of PACE issues, but at least this wasn't terrible like all UK PACE coverage had been up until last year. Would have been nice to get more quotes from White - I wonder if he tried to bring up 'harassment'?
 

Forbin

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If it hasn't been mentioned yet, one reason this is going to be tough to ignore is that it was published in The Proceedings of the National Academy of Sciences of the United States of America (PNAS), the second most cited journal across all fields of science. [The first spot going to the Journal of Biological Chemistry].
 

Thomas

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I can just hear the critics now: Oh you've got that hibernation syndrome. Well I'm tired too and would love to hibernate in bed for a while also.

Seriously though, if ME is a way for the body to avoid death by regressing to a hypometabolic state okay, but then why doesn't it just sort of stay that way? Why do mild patients often end up bedridden? Why does the illness have to progress to such unbearable levels? I'm guessing it becomes a vicious cycle of sorts...
 

Research 1st

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Well if this pans out with some sort of hypo metabolism. It is pretty hard to exercise your way out of that!
Indeed, with a cellular defect in energy metabolism (presumably driven by infection/autoimmunity), if you performed a VO2 max exercise test, twice, you may find a drastic difference between Day 1 and Day 2 (as Snell et al did), because exercise increases immune response, specifically inflammation, which presumably slams ATP. This inflammation in 'CFS' can be Oxidative Stress. Immune response in CFS doesn't have to be a rampant infection which skeptical doctors are looking for (temperature, diahoreah, vomiting), instead it could be an infection lead autoimmune attack that (due to Mito defect) massively elevates ROS. NB: We don't have exercise based Oxidative Stress data on this in the severely affected or bedridden.

11 years ago, Snell et al said this in their paper....
''These results implicate abnormal immune activity in the pathology of exercise intolerance in CFS and are consistent with a channelopathy involving oxidative stress and nitric oxide-related toxicity''.

Source:
In Vivo. 2005 Mar-Apr;19(2):387-90.
Exercise capacity and immune function in male and female patients with chronic fatigue syndrome (CFS).
Snell CR1, Vanness JM, Strayer DR, Stevens SR.
Then 3 years ago, Snell et al, discovered this also....(this is the infamous 2-day VO2 repeat exercise test):

''Multivariate analysis showed
no significant differences between control participants and participants with CFS for test 1. However, for test 2, participants with CFS achieved significantly lower values for oxygen consumption and workload at peak exercise and at the ventilatory or anaerobic threshold. Follow-up classification analysis differentiated between groups with an overall accuracy of 95.1%.

Source:
Phys Ther. 2013 Nov;93(11):1484-92. doi: 10.2522/ptj.20110368. Epub 2013 Jun 27.
Discriminative validity of metabolic and workload measurements for identifying people with chronic fatigue syndrome.
Snell CR1, Stevens SR, Davenport TE, Van Ness JM.
With a future 'test', Snell et al (and others) can repeat their findings, and find out who exactly has the hypometabolic state (percentage in a heterogenous cohort) and see if this correlates with the previous 2-day VO2 max drop off in CFS, that appears to be unique to the disease.

Not only that, but patients who have this novel hypometabolic disease confirmed, then exceed Fukuda Criteria CFS, they must then be given a new disease diagnosis (CDC criteria does not permit explained reasons for Fatigue). This means, the truth will gradually emerge that organic disease cohort 'CFS' patients who meet and exceed CCC CFS Criteria/ME-ICC are commonly affected by:

1) Dysautonomia and Autoimmune POTS - not officially recognised as it's the converse of bio-psycho-social theory.
2) Existing Autoimmune diseases in addition to the CFS, acquired over time since the diagnosis - ditto.
3) Rare allergy Syndromes (MCAS) with some even reporting Anaphalaxis - ditto.
4) Additional illnesses and Syndromes such as Ehlers Danlos, and PCOS in CFS females - ditto.

The above basic examples (1-4) is precisely what you would expect to find in chronic ME type conditions (inc 'Chronic Lyme'), if you allow the people with the original described condition, ME, to be researched, and don't foolishly exclude them from biomedical research studies, because they exceed Fukuda Criteria CFS!!!!
 

OverTheHills

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Just to be clear for the non scientists (like me), supposing this finding is replicated and there are no problems with other diseases producing similar results, do the specfic panels of metabolites mentioned (8 for men 13 for women? producing 90%+ confidence) have potential to be biomarkers for research and/or clinical use? They are not too obscure or difficult for that purpose?

OTH
 
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Let me guess, people who are new to ME symptoms tend to be hypermetabolic, while those with chronic symptoms show up as hypo.
I wondered about this too. It would be great if they did a sub-analysis looking at illness duration.

And I wonder how these findings relate to Hornig & Lipkin's study showing different plasma signatures in those who were ill less than 3 years vs those who were ill longer than 3 years?
 

Janet Dafoe

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Ron says this is the best research ever done on ME/CFS and will transform research, diagnosis and treatment. It is consistent with what Ron has been finding with Metabalon data, but Naviaux has analyzed a large number of patients and put it all together into a coherent theory with predictive value. It's amazing and we're so excited that the paper is finally out and we can talk about it. Ron and Naviaux are now collaborating, with funding from OMF, on a big study that will validate these results and add on a genetic component to try to explain variation in metabolites and symptoms. Stay tuned for a statement from Ron tonight or tomorrow! We're going to END ME/CFS!