Discussion in 'Phoenix Rising Articles' started by Mark, May 21, 2013.
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Thanks for this, excellent article - very interesting to get all this detail on what Prof Newton is doing. I can't think of another researcher in the UK who has a research programme remotely like this.
Thank you, Clark, for a fascinating article. When Dr Newton's group came out with the article on endothelial dysfunction in ME/CFS, I was already hooked. But her subsequent work on lactate production in "CFS", clear intention to do translational work and repurpose drugs to treat this lactate buildup; her interest in involving young researchers in this field, and her political astuteness in recognizing the stigma of even working with our collection of diseases, has my respect.
Dr Newton strikes me as a researcher with genuine intellectual curiosity; a politically savvy person with emotional intelligence, who may do great things for our fields in ME and CFS. It was wonderful to get some more granularity on her research, through this interview. Thank you!
P.S. I was especially struck by her comment about leveraging patient feedback on the seriousness of the symptom of fatigue, to get a grant for Primary Biliary Cirrhosis. In other words, patient's stories about disease can help open wallets! Indeed, I referenced this in my plea for folks to sign a Thank You Card to the latest foundation to give money to the Open Medicine Institute here: http://forums.phoenixrising.me/index.php?threads/one-minute-advocacy-2-and-great-feedback-on-thank-you-card.23255/#post-356660. And you can sign the card here: http://www.groupcard.com/c/ZjA2X_lwClv
Great article - after all "fatigue" is there for a reason and not the simple run round the block too often or depression beloved by the psyches - obviously not that simple and has to do with pathologies.
Thanks for this Clark. I am going to take more time to read through it. Very detailed and highly interesting
And I must add - superb work and opening up medicine to past ignorances by Dr Newton. My own brother (Prof Neurology) knows the same.
I've just read the interview for a second time, and it was even more fascinating the second time!
Two paragraphs struck me as having incredibly promising implications and potential, as follows...
(I've bolded some sentences that particularly caught my eye.)
“So the muscle MRI studies in a nutshell showed that people with ME/CFS accumulate large amounts of acid within their muscles and have difficulty getting rid of acid after exercise. The heart MRI scans showed that a third of people with ME/CFS have impaired bioenergetic function in their hearts which has a knock on effect upon the function of their hearts. In terms of the brain we have been able to show that people perform badly on memory tests, the degree of this associates with changes in cerebral blood flow during stress of the autonomic nervous system. Interestingly, when we look at the muscle, brain and hearts of those who have had all three of these investigations there is a relationship between the abnormalities that we have found suggesting that any problem is not just related to one organ but is generalised across a number of organs. Our muscle studies have now extended into taking muscle biopsies from people and growing the muscle cells and we have also recently been looking at mitochondria.”
“There are a number of strands to the muscle biopsy work. We have been able to show that we can exercise muscle cells in the laboratory and get similar findings in the laboratory as we have seen in the MRI scans. So we have been exercising muscles and looking at what happens to these and whether or not any acid that we accumulate is potentially reversible. We are confident that the acid accumulation is reversible but the Action for ME funding is now directed at a 50% PhD student who is going to start looking at other drugs in this muscle system so that we can begin to tease out where the abnormality might lie and whether it is amenable to currently available drugs. So the initial development of the model and showing that it replicates the MRI is almost finished and we are in the process of writing this up at the moment and the next stage is to really begin to drill down in this model where interventions could best be directed.”
Where Julia talks about heart issues, this is something that I've heard discussed (I think by Hyde and Cheney, but I might be wrong) ever since I became ill. But I think this is the first time that I've seen research evidence, confirming it, which has real potential, and a number of objective markers/measurements for it.
Regarding the muscle acid: If there are any drugs that can reduce lactic acid, or can be re-purposed to do this, it might be a really promising direction to travel, in terms of significantly relieving symptoms.
They are going to look at drugs to see if they can work out where the abnormality lies, in relation to the muscle acid. (The abnormality that causes excess acid.) This could be interesting and fruitful.
There is so much evidence here, whereby many of the symptoms that ME patients report, have been reproduced objectively in the lab. This is fascinating and very helpful stuff!
Sasha, parvofighter, Enid, @Firestorm, Bob - thanks for your appreciation. I found the answers fascinating as well and Dr. Newton was a pleasure to interview.
I think she is leading the ME/CFS field in the UK and is very smart and politically astute too (as one of you mentioned already). She is determined and resourceful too - I also loved the fact that she didn't give up when faced with a knock-back on the PBC/Rituximab trial, but instead went and gathered the necessary evidence to support her view and got the grant as a result. We need that kind of resourcefulness in our field.
Parvo - those cards are an excellent idea. I tweeted about them to help spread the word. I think they deserve promotion and it just goes to show that we patients can do some small things to make a big difference.
Bob - I too am pleased that she is looking at Mitochondria. It seems like a natural place to look given the acid accumulation. Cheney talked about the mitochondria and heart in his March talk which can be found online.
Hi Clark, a very big welcome to the forum, and thanks again for such an interesting interview.
I found the lactic acid issue to be particularly interesting. I remember reading someplace that lactic acid can be used as a fuel in place of ATP. I have the impression that there is pretty good evidence that we are unable to make ATP properly, so I have to wonder, is excess lactic acid the body's attempt to compensate for a lack of ATP?
Bob - thank you!
Yes it is certainly interesting. Most of your ATP production comes via cellular respiration and is aerobic. But when oxygen is limited, like when you exercise, you can create a small amount of ATP via lactic acid fermentation which is an anaerobic process. ATP production has many influencing factors, and there is plenty of room for it to be dysfunctional in diseases like ours and so that could be related to acid accumulation for sure.
Finally got round to reading this feature-length version of your interview: epic, and very interesting too.
One thing that did surprise me slightly, though, was Julia's view that all fatigue was the same - was the issue of post-exertional fatigue/malaise discussed? I'd thought that was far more unusual and was one feature that differentiated ME/CFS fatigue from that in many other illnesses. PEM after cognitive activity, rather than physical exercise, is again something that I thought was unusual in illnesses. There again, I know next to nothing about PBC or Sjorgren's syndrome so maybe fatigue in these illnesses is similar to ME/CFS.
I admit to being a bit surprised by that as well. Personally, I cringe every time I read a journal paper that opens with something along the lines of "Chronic fatigue syndrome (CFS) is characterized by fatigue lasting 6 months or longer," to quote a recent publication (not a Newton one)...
I think PEM is indeed a more accurate sign of the disease, and that is probably followed by immune dysfunction, before fatigue. I don't believe that fatigue characterizes the disease, for the simple reason that it is not exclusive to ME/CFS. Nevertheless, I think the vast majority of us have fatigue as a symptom, so focusing research on this symptom may well lead to significant findings, perhaps building on knowledge from other diseases with a fatigue component.
It is very interesting, I think, that PBC appears to respond to Rituximab and that may suggest some similarity between the two diseases. PBC has a known autoimmune component where B-cells produce anti-mitochondrial antibodies (which of course provides an understanding as to why depleting B-cells brings benefit there), and perhaps something similar, but yet undiscovered, is occurring in ME/CFS.
Something which really came across to me though was that 'fatigue' was what attracted Julia to CFS - it was why she got involved. And I think it has been one of the reasons (among many) why she has been successful in gaining funding, as findings related to fatigue can be applied, potentially, to many different diseases.
I am pleased that other researchers are focusing on other areas like PEM or the immune system though, as any of these areas could equally result in significant findings, but it looks like fatigue is Julia's primary focus.
Does anyone happen to have any more detail about this study from Crawley, please:
Only I hadn't come across it before. Maybe it isn't a study but part of her investigative procedure? Many thanks in advance
Thanks for that.You've made me realise that I probably should have separated post-exertional fatigue from post-exertional Malaise in my question.
Not sure if you are aware that Lenny Jason has done a lot of work characterising ME/CFS fatigue, particularly with his ME/CFS Fatigue Type Questionnaire? Basically, he argues that ME/CFS fatigue is different, at least from some illnesses eg empahsising post-exertional fatigue as opposed to 'Tired All the Time', and has used the Questionnaire to separate patients with CFS from those with Depression.
Part of the Q does relate to Malaise, but most of it does not, and I'm not convinced there's good evidence that all fatigue is the same. Interestingly, PEM is not unique to ME/CFS eg there is a similar problem in at least some types of Chronic Pain (as well as fatigue).
Am I right in thinking that Julia argues all fatigue is pretty-much the same, which would also tie in with transferring knowledge from fatigue in one illness to another. As opposed to, say, arguing that there are different types of fatigue but that fatigue in PBC etc has been examined and found to be similar to ME/CFS fatigue? It probably didn't come up in your interview but I'm curious to learn anything you may have gleaned.
There is nothing much beyond what was in the CMRC press release, though I now know the work is done by Jade Thai at Bristol. Think they looked at attention and discovered that CFS patients activated more brain areas than controls to achieve the same results, though fMRI studies tend to be tiny. No published resutls as yet.
I am so pleased that someone is finally investigating fatigue.
Recently I had an abnormal fibroscan - I would love to know if Dr Newton has considered conducting fibroscan tests on people with ME to see if they show similar results to those with PBC. Blood tests and an ultrasound have shown nothing to account for my abnormal result.
One of my acquaintances with ME has been able to get a prescription for ME, they are one of the few who had severe symptoms able to continue working.
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