Discussion in 'ME/CFS research news' started by Andy, Oct 14, 2020.
Glad to see Nath involved more in these things. Sometimes I wonder if this was some sort of punishment to him, but this may end up defining his career in a positive way.
Bumping this as it's taking place today
I've just listened to it. It seemed more targeted at clinicians, and so there wasn't a lot that would be new to most of us here. There was emphasis on Me/CFS being a physical illness, with the material presented being quite convincing on that. It also had a wide scope, so the presentations covered a lot of ground quickly and lightly.
There were presentations by Maureen Hanson, Ian Lipkin and Avindra Nath. If you are going to just listen to a bit, I think you'll find Nath's presentation most interesting, because of the reason I just mentioned.
Presented some research findings of ME/CFS differences as facts e.g. impaired natural killer function - that I would be more cautious about.
Finding of less bacterial diversity in ME/CFS - paper by Giloteaux et al
T cell study - paper by Mandarin et al - altered T-cell metabolism and cytokine associations. There was a slide there that was interesting, but it was too quick for me. Something about t-cells having different energy mechanisms when proliferating
Current research is focussed on samples from before and after exercise. They are working with Betsy Keller. In 94 patients, 29% were able to reproduce CPET results normally on the 2nd CPET, but these tended to be younger and have had ME/CFS for a short time (I wonder if perhaps the exercise provocation wasn't big enough to induce PEM?). They are analysing plasma metabolites; of 933 metabolites, only 7 were different between ME/CFS patients and healthy controls before exercise, but there were 56 different before the second exercise test.
Maureen is a strong advocate for people with ME/CFS, she criticised GET and the PACE trial and emphasised the physical nature of the disease. She said that unmonitored aerobic exercise can result in a permanent worsening (I don't know if she has more than patient anecdote to base that on).
I watched. Dr Lipkin shared that he still had after effects of COVID, mostly fatigue. He is rehabbing through exercise. Said he didn’t get COVID while in China, but believes he got it during a television interview.
From the presentation of Dr Avi Nath, there will be a study examining the long term symptoms of COVID. I have taken screen shots, will share Dr Nath’s slides for now.
Part 2 of Dr Nath’s presentation:
He had a slide showing that 11% develop ME/CFS from EBV, Ross River fever and Q fever; 50% develop it after SARS and MERS, but none developed after some other infections. He threw XMRV in there, which seemed a bit confusing, but helped to make his point of doing work in the field for a long time.
He noted that faecal bacteria differ between ME/CFS and healthy controls, particularly that there are fewer species responsible for butyrate production. He doesn't know if it is cause or effect but it seems to be a biomarker. And that the substances these bacteria produce, butyric acid etc are decreased in ME/CFS.
Plasma proteomic profiling suggest differences - changes in immunoglobulins, associations with lymphoma. (the slide went too fast)
He also believes that it is important to look at the effect of exercise - before and after. His team have some findings that will be published, they are finding (metabolomic, I think it was) differences.
He mentioned Ampligen - he seemed to think it had helped some people. I think.
He said that he thinks Gulf War Illness is in fact ME/CFS. There is a publication 'Gulf War and Health'. I think he has a chapter in it.
Lipkin has not yet recovered from Covid-19. He said that he has personally found it very useful to get on an exercise bike with a trainer, to push himself, to recover. Which was a bit odd.
He concluded with "There is symptom overlap with Gulf War Illness and possibly a post Covid-19 syndrome".
If he can push himself on an exercise bike and recover, he presumably doesn't have PEM. Not everyone with post viral fatigue develops ME. And Covid fatigue for some may be more related to ongoing lung problems.
He focussed largely on post-Covid19 neurological impacts. He noted that all human coronaviruses cause neurological complications. Showed images showing effectively brain damage, microhaemorrhages, macrophage infiltration into brain tissue and quoted a recent study that found that altered mental status in discharged hospitalised Covid-19 patients was common.
He noted that the symptoms of 'Long-haul Covid' overlap with ME/CFS. But that no one should rush to label a person with the symptoms as having ME/CFS, as they are non-specific. The illness may have unmasked a co-morbidity (e.g. thyroid disease), there might be residual damage from the infection, there might be persistent viral replication, there might be persistent immune activation (and he seemed to be suggesting that this is what ME/CFS is), or it might be something else.
There are two studies, building off a review of 1000 people with neurological issues post-Covid. Phone screening and questionnaires will characterise them.
Those meeting ME/CFS criteria will go into a study led by Brian Walitt and they will go through the existing ME/CFS study protocol. Others (50) will go into another study that will investigate their issues with MRIs and autonomic testing led by Bryan Smith.
Dr Lipkin’s slides (i may have missed one) part 1
Yes, I guess the oddness I mentioned was that Maureen had tried really hard to get across the idea of PEM to any clinicians listening. And Ian Lipkin didn't put his experience into context with that, at least I don't think he did. It would have been good if he had said, not all post-covid fatigue will be ME/CFS,, and so it's important to listen to what the patient is saying about how exercise affects them.
There was one question that said something about PEM being a lot like delayed muscle soreness. Maureen responded that no, it's not like delayed muscle soreness, it's not healthy muscles soreness after exercise.
Throughout, I thought there was evidence of good collaboration between the teams behind the speakers, which was encouraging. They are aware of what each other, and other labs, are doing.
Dr Lipkin part 2
Dr Lipkin part 3
Maureen Hanson spoke first and stressed the dangers and risk of permanent damage from exercise on people with ME. Then in Ian Lipkin's presentation he said he hadn't recovered from COVID-19 but that exercising with a personal trainer had helped him a lot. This was weird as given it was an ME & long COVID presentation it certainly would have made sense for him to explain further. Perhaps he thought it was self explanatory that he doesn't have ME? He did make some comments that I interpreted as him indicating that he had a better understanding of what ME feels like now though.
Here is Dr Hansen’s slides (part 1) and to be noted, indeed dr Hanson went first, then dr Lipkin, then dr Nath
Dr Hanson part 3
I think, for some people, ME takes a while to evolve. On my doctor's recommendation, I tried to exercise my way back to health on a stationary bike just a couple of months after onset. I desperately wanted to get better, so I really tried hard for more than a month [It didn't help at all]. I don't recall feeling PEM at this point, but I got significantly worse over the next year. It was really only several years later, after I had improved somewhat, that I began to notice PEM (probably because I was exerting myself more and it was easier for PEM to be noticed among "background" symptoms that had lessened in severity somewhat). To tell the truth, I wouldn't even hear of "PEM" until decades later. All I knew was that if I did anything out of the ordinary, especially if it involved prolonged standing, I would feel "wiped out" the next day, as if I was coming down with a bad flu. So one's susceptibility to PEM may depend on where you are in terms of the evolution of the disease - and the timeline may be different for different people.
It's just my two cents, but, if I were Dr. Lipkin, I wouldn't feel too sanguine about having the capability to exercise at this point. What he should be concerned about is if all the exercise is not leading to the level of improvement he would expect under normal circumstances.
I agree with you @Forbin. Back in the early days, because i was believed to be lazy and faking illness for secondary gains, i went for a run as i did in the pre-illness days. I was determined to prove them i was not lazy. It was really weird because i could not run as before, i had to alternate run- walk, highly unusual for me, considering i could run uphill for 20 minutes (i live at the bottom of a big hill). Also i remembered my first days of orthostatic intolerance. I figured i was feeling better laying down, and significantly worse when standing. When i got to explain this to my family doctor, she wanted to prescribe anti-depressants, that i was lazy and i was not sick.
i flew 7 hours to a competent physician to be diagnosed with POTS. And back home my GP still did not want to believe it.
I did not listen to the presentations, so perhaps it's folded into those, but I could not find anything definitive in terms of cohorts' distribution through the US. My sense, based on the slides, is that a majority are from within the US, and of those, most come from the NorthEast/MidAtlantic Regions, and Western US. Also, I appreciate some are post-covid patients.
Lipkin's slide on infectious causes of ME/CFS intrigued me for a couple reasons.
First, he rules out some diseases as causes of ME/CFS, and I'd be curious to know by virtue of what tests he reached those conclusions. Did he test tissue, for instance?
Secondly, he highlights - literally - New York State, but on his list of infectious diseases to explore as contributory to ME/CFS, no where do we see any number of Borrelia species and strains, or babesia, or rickettsia, or bartonella....Which as a group, and in some areas it can be argued, individually, are ravaging the NorthEast US, and in particular, New York State. I know he's familiar with these, as his Tick Borne Disease Serochip (sp) kit suggests. For all you folks from the UK, this may seem like an unfair question, but I can assure you, in the US, and specifically in the MidAtlantic/NorthEast US, NOT looking at all the different tick-borne pathogens as possible causes for ME/CFS seems like a giant head-scratcher. Afterall, many are endemic here. Lyme, babesia and a certain type of rickettsia were first stumbled upon, according to some, off Long Island, NY back in the late '60's. Pretty much everybody in the NE US knows somebody who had at least one of those infections.
I know Lipkin was looking at this whole TBD thing, as was what's-his-name from southern California. But, sorry, if they ruled all of them out, I don't remember ever being informed how those pathogens were ruled out, i.e, by what procedures.
I can assure you, in Lyme World, key Lyme investigators have been for close to 25 years claiming that patients thinking they had Lyme, didn't, but instead, after being infected with Lyme, were cured, and now had CFS. So, there is plenty of precedent for that sentiment. I'm left wondering why he didn't at least include one or two on his slide.
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