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

[snowathlete]

Problem 1:
The UK is the birth place of the cruel Psych Lobby denial of ME, and should play no part in deciding anything to do with CFS or ME, because they created the suffering for patients. (Unlike independent American researchers who do the exact opposite). Ergo, they could never be independent.

Problem 2:
The UK has no independent researchers like Scientists Navieux and Ron Davis, for CFS/ME it only has the MRC.

Problem 3:
The MRC orchestrated the PACE trial and historically backed pro psychiatric views on ME as CFS.

Problem 4:
The MRC continues to enable GET studies for Children.

Problem 5:
The UK has never mailed CFS/ME patients to inform them they cannot donate blood/tissue, they have also not informed doctors!!! How many babies are now infected? 1 or 1 milliion? No one knows. How safe!

Are we to think, the UK would produce an honest study, using classic 'ME sufferers' that proves they were wrong all along?

No, their current research based on psycho-social theory of fear avoidance on exercise and activity would then have to be disbanded. That will never be allowed to happen by those who deny ME (World Health Organisation disease) even exists, as then they are proven to be wrong and need to pay compensation for injuries and deaths to PWME who've died since the 'idea' CFS = ME was established by them.

What will happen is private American researchers selling private tests (that other countries with socialised medical health care systems ignore, not just UK), will cause the development of a time-wasting long drawn out legal process in which via very costly private testing, European, Canadian and Australian ME sufferers will have to take personal legal action against the various health agencies that produce scientifically fraudulent, non evidence based research.

CBT/GET, is blueprinted in the UK and exported around the world, to be sold to (ironically) America where it is sold to American insurance companies for profit.

In terms of game changing for patients, Americans can change the status quo: America is a free nation (bill of rights, constitution, 2nd amendment etc), that has no tax payer funded, pro psychiatric state run health service. UK has no choice, it's psychiatry or nothing.(socialism). In America, you pay with your credit card for choice (capitalism)

America has choice, the UK has a dictatorship of psychiatrists who 'believe' patients 'believe' in a disease that doesn't exist as this is cost effective, and thus fits the model for communism precisely.

No escape from that, when it's state lead. UK research is also state lead and state influenced, not independent private research. Why do you think it was the MRC who just happened to need the PACE trial so much? Think why it was so important to blow $8 million on psych patients, and refer to them as 'ME'? As it de legitimizes ME.

Why then, in heaven's name, would the MRC or anyone else in power, want to then legitimize ME, by honestly replicating Navieux or Davis's work? Of course they won't.

Conversely, in America, you have human rights and an excellent ability to take legal action against people who steal your human rights, when medical evidence surfaces this is happening.

The idea that the UK will perform good quality honesty science to prove ME exits outside of psych CFS, is not going to happen, ever, as if it does, the NHS (National Health Service) would be sued for millions of pounds, by each and every patient. They would go bust, and there would be no health service left.

Thus it cannot happen.

There are metabolomics experts in the UK who are waking up today and for the first time ever they have a big interest in ME/CFS. They have no BPS baggage, no history with CFS, and probably no ties with the BPS crowd. They have access to the technology and know how to use it. The big stumbling block, in my view, is funding - hopefully charities can help, but patients will have to fund this themselves. But that is worth doing.

 

[AndyPR]

Full SMC response

A group of researchers publishing in the journal Proceedings of the National Academy of Sciences (PNAS) have examined the metabolic features of patients with chronic fatigue syndrome (CFS/ME) and report a number of differences in various metabolic pathways.

Prof. Andrew McIntosh, Chair of Biological Psychiatry, University of Edinburgh and Honorary Consultant Psychiatrist, said:

“Naviaux et al. discovered that the levels of blood metabolites were so markedly affected in Chronic Fatigue Syndrome that they could potentially be used to completely separate the affected individuals from unaffected participants in their sample. Intriguingly, the chemicals altered in their study of CFS belonged to pathways affecting a number of bodily processes and functions previously implicated in CFS, including the gut microbiome (gut bacterial genome) and cellular energy production. The study establishes that this approach is likely to yield new findings and possible insights in the study of a number of complex and highly heterogeneous disorders, including CFS.

“Whilst interesting, however, it is difficult to know whether the changes reported are a cause or an effect of CFS. There is also a lot more to be done before there can be any clinical or diagnostic impact from this relatively new technology. I think it is essential that readers of this paper interpret the assessment of metabolomics as a diagnostic test with particular caution. Further genomic and metabolic studies, independent replications and much larger samples, will be needed to address these and other issues, before any assessment of clinical impact can be made. Nevertheless, this is a promising start to a young and rapidly growing area of research with broad application to a number of common diseases.”

‘Metabolic features of chronic fatigue syndrome’ by Naviaux et al. published in Proceedings of the National Academy of Sciences (PNAS) on Monday 29th August.

Declared interests

Prof. McIntosh: “I have received grant support from Pfizer, Lilly and Janssen. I am currently supported by the Wellcome Trust.”

You can read it at http://www.sciencemediacentre.org/expert-reaction-to-metabolic-features-of-chronic-fatigue-syndrome-cfsme/ if you must but, as it's the SMC, I didn't see any reason to encourage web traffic to them.

 

[msf]

´Protean´ - I like the guy already.

 

[mermaid]

He speaks about it here from 22:00 onwards:

@Chris @M Paine Some of us are unlucky enough to have both hypothyroidism and ME (my hypothyroidism is the genuine variety as TSH rose, and was diagnosed long before ME began. Luckily I don't have a severe form of ME though.

Edit: apologies I meant to quote from Chris's post also but failed due to brain malfunction of knowing how to....this is what Chris wrote....
're hypothyroidism--I do recall that Paul Cheney mentioned that he thought that thyroid replacement therapy might be the most dangerous thing that could be prescribed for ME--he clearly shared much of the basic model that emerges from this terrific study, and may well have had a real share in the basic thinking that went into it--he is thanked.'

 

[Forbin]

It will be interesting to see if critics use the usual fallback position that ME/CFS is so heterogeneous that no single mechanism can be attributed to all patients. That's no doubt true, but the paper did use a variety of diagnostic criteria:

Forty-five subjects (n = 22 men and 23 women) met diagnostic criteria for ME/CFS by Institute of Medicine, Canadian, and Fukuda criteria.

From the language, I can't tell if they mean that all the patients met all of those criteria, or if they mean that individual patients met just one (or more) of those criteria.

Never-the-less, there's this interesting quote from the ScienceDaily article that addresses heterogeneity...

"Despite the heterogeneity of CFS, the diversity of factors that lead to this condition, our findings show that the cellular metabolic response is the same in patients," said Naviaux. https://www.sciencedaily.com/releases/2016/08/160829163253.htm

Obviously, not everyone ever diagnosed with CFS is going to show this cellular metabolic response, but it does seem to say that people who may have diverse symptoms under those three criteria (and within a criteria as well) are apparently displaying a common dysfunction. In other words, ME/CFS may be less heterogeneous than has been thought.

 

[Tuha]

Are these metabolic findings similar to the findings of other teams? Can we say that Naviaux replicated some findings?

 

[Ben H]

It will be interesting to see if critics use the usual fallback position that ME/CFS is so heterogeneous that no single mechanism can be attributed to all patients. That's no doubt true, but the paper did use a variety of diagnostic criteria:


From the language, I can't tell if they mean that all the patients met all of those criteria, or if they mean that individual patients met just one (or more) of those criteria.

Never-the-less, there's this interesting quote from the ScienceDaily article that addresses heterogeneity...


Obviously, not everyone ever diagnosed with CFS is going to show this cellular metabolic response, but it does seem to say that people who may have diverse symptoms under those three criteria (and within a criteria as well) are apparently displaying a common dysfunction.

Hopefully with the OMF replication study, and the followup study against other illnesses and severity of ME/CFS, the biomarker that was found will be unique to ME/CFS.

These implications are potentially huge. The sensitivity of this initial study managed to identify the ME/CFS patients at 94 and 96% for males and females respectively, which is incredible for a first 'go' per se. Replication is key here, but these findings really are incredibly exciting.

The fact that heterogeniety had a homogenous result is also incredible-perhaps the standout of the paper. Aside from the obvious biological findings themselves.

I personally think that metabolomics will be the key, based on certain collections of metabolites, to identifying 'real' ME/CFS, and other conditions that get lumped in due to no current diagnostic marker.


B

 

[msf]

The low sphingolipid profile in CFS appears to be an adaptive response that is opposite to the increased sphingolipids observed in metabolic syndrome (11) and the acute cell danger response (CDR) (7) and ultimately may represent a fundamental response to oppose the spread of persistent viral and intracellular bacterial infections.

Second reason to like this paper: it talks about both viruses and bacteria.

 

[Sean]

The big stumbling block, in my view, is funding - hopefully charities can help, but patients will have to fund this themselves.

Once the big hitters in biomedical fields start taking an interest, the money will follow. Won't happen immediately, but I am confident we are going to see some big research money coming into play before much longer.

 

[Ben H]

Are these metabolic findings similar to the findings of other teams? Can we say that Naviaux replicated some findings?

There has never been a study like this. The Australian study of last year was similar, but not on the same scale, mixed gender, or as many metabolites iirc. I believe Ron has said that the Australian findings were in keeping with his own, and Dr Naviaux's also were. But @Rose49 will have a better idea.

Metabolomics is the razor edge of science. The Naviaux study is unprecedented.


B

 

[A.B.]

Low serum sphingolipids in children with attention deficit-hyperactivity disorder
http://journal.frontiersin.org/article/10.3389/fnins.2015.00300/full

 

[Sidereal]

From the language, I can't tell if they mean that all the patients met all of those criteria, or if they mean that individual patients met just one (or more) of those criteria.

I read that to mean that all patients met all three diagnostic criteria.

I think this is the most insightful study ever conducted into this disease but then again I'm biased because I think this paper nicely confirms what I've always suspected which is that a) this is metabolic disease characterised by low availability of NADPH which has nothing to do with "brain loops" and b) despite its protean manifestations, it's all the one disease, and there are no meaningful "subsets" even though no two of us have exactly the same symptom constellation. There are probably a bunch of people misdiagnosed with CFS who have other conditions but the bona fide ME/CFS patients, when you meet them, you can really tell that they're dealing with the same thing you are dealing with even though on its surface they may have totally different symptoms and onset/triggers.

To my mind, the pressing question is, what is the underlying problem that perpetuates this state of torpor. Bacterial dysbiosis / leaky gut? I don't believe it's mistaken or accidental, I think it's protective against death. Whenever I've tried to act like I wasn't sick and just push through the symptoms, I ended up in a push-crash cycle, and if I really pushed it, I would end up nearly dead every time.

 

[snowathlete]

and b) despite its protean manifestations, it's all the one disease, and there are no meaningful "subsets" even though no two of us have exactly the same symptom constellation. There are probably a bunch of people misdiagnosed with CFS who have other conditions but the bona fide ME/CFS patients, when you meet them, you can really tell that they're dealing with the same thing you are dealing with even though on its surface they may have totally different symptoms and onset/triggers.

I second that. It's the same disease, I don't believe there are lots of subsets as in different diseases.

 

[Simon]

There are metabolomics experts in the UK who are waking up today and for the first time ever they have a big interest in ME/CFS.

let's hope so. What I'd really like to hear are the opinions of metabolomics experts on ts study. So far we only have reaction from a biological psychiatrist.

 

[TiredSam]

let's hope so. What I'd really like to hear are the opinions of metabolomics experts on ts study. So far we only have reaction from a biological psychiatrist.

Yeah, funny that the SMC didn't get a metabolomics expert to comment.

 

[aimossy]

I'm hoping we might hear Ron Davis thoughts on the data, I like how he explains things.
@Rose49 great to hear Ron is going to be doing a statement.

Has anyone had a chance to read all the coverage, which mainstream article has been the best objective coverage so far?

 

[Cheesus]

I've gotten way too overexcited about this and now I am exhausted. That's okay with me

My hope is that this will strongly support Lipkin's application to the NIH to fund the rest of his study. If we could just get that under way it would (hopefully) replicate the findings of this and potentially identify a microbial cause.

 

[Cheesus]

Has anyone had a chance to read all the coverage, which mainstream article has been the best objective coverage so far?

I haven't read all of the coverage, but I have been feverishly emailing large, well known news agencies to get them to sit up and take notice of this.

In each email I have politely asked that if they decide to run the story that they do not interview any psychiatrists

 

[Janet Dafoe]

I'm hoping we might hear Ron Davis thoughts on the data, I like how he explains things.
@Rose49 great to hear Ron is going to be doing a statement.

Has anyone had a chance to read all the coverage, which mainstream article has been the best objective coverage so far?

Ron finished his statement tonight. OMF will publish it tomorrow morning. Then I'm going to try to take him through some of these comments and get his responses. If he has time. He is at the lab every minute he's not with Whitney. We barely see each other except for dinner. Our dinners are pretty funny sometimes. LOL.

 

[Daisymay]

Once the big hitters in biomedical fields start taking an interest, the money will follow. Won't happen immediately, but I am confident we are going to see some big research money coming into play before much longer.

And let's really hope the flow of money for psychiatric research here in the UK will dry up.