LinkedIn saw it first, but I’m proud to announce that, as of yesterday, I’ve finished a PhD (Publication) at @portsmouthuni @UoPSportScience. It was a winding and unorthodox route to develop content expertise and demonstrate the relevant scholarly skills, but worth every second.
The title of my thesis is “From Function to Physiology and Back in Adults with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.” It consolidated findings from 11 publications over the last decade of work in this area to tell the story of post-exertional symptoms and signs.
All of the publications in the thesis are out in the public domain, so you may have read them already.
And, there’s a discussion of what comes next for this line of research. Many of those recommendations already have been put in motion by my @4workwell and @4workwellhealth, as @dsethlewis put it so well the other day, in the spirit of going slow and fixing things.
@4Workwell @4WorkwellHealth @dsethlewis Obviously none of this is worthwhile without people living with ME, and now Long Covid, and their carers and none of this is possible without my @4Workwell @4WorkwellHealth colleagues, other collaborators and friends, and mentors along the way. All of this takes a village.
@4Workwell @4WorkwellHealth Onward.
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Hi, @ChrisCuomo. I know you’re committed to getting this right and
@mjsportspt is a friend. But as a physio working with (commonly) infection associated complex chronic disease, I hope you’ll take this video down. It’s riddled with inaccuracies and may wind up hurting people.
I’ve watched this video three times already and it’s making my head hurt.
Point 1: "People with a wide variety of illness demonstrate oxidative stress."
--Sure. I'll buy that. Oxidative stress is a known effect of many different types of conditions, including inflammatory ones. Long Covid is a lot of things, and inflammatory is one of those things.
Dr. Putrino is outstanding in so many ways, but even regular people with a standard commitment to solid science and humane clinical practice quickly find themselves in the position of remediating deep and long-standing injustices in infection-associated chronic complex diseases.
It doesn't have to be a motivation to enter and stay in the field, but once you're here, it's hard to miss. Some folks just want to do the science and practice and avoid the rest of it, but that's not how it works. Just a presence as a scholar and clinician makes you an advocate.
Imagine a clinical population in whom the science and practice is so historically non-existent that just doing anything to move either forward is a big deal. That's infection-associated chronic disease. Under-diagnosed, under-recognized, under-treated, under-funded. For years.
I’m a small account @EricTopol but I just want to underline the importance of including post exertional malaise in any analysis of exercise in PASC. This latest article you reviewed didn’t and should’ve. We know too much about exertional intolerance to be able to claim ignorance.
Any article published in 2024 citing the PACE Trial as evidence of safety and efficacy of graded exercise should not be taken seriously. It’s one citation, so maybe that seems unfair. But to neglect that level of scientific misconduct calls into question the authors’ judgement.
Aerobic exercise particularly involving scheduled benchmarks of volume to be achieved regardless of symptoms is contraindicated in people living with ME. Certain types of exercise may be beneficial depending on severity and whether PENE/PEM is/can be effectively self-managed.
Turns out there’s a lot of gray area after we dismiss the kind of exercise that is consistently harmful based on what we know about post-exertional metabolism in PENE/PEM from ME, actually.
I totally understand why we often and purposefully engage in false binaries surrounding exercise in PEM—many clinicians are generally clueless about something they zealously but incorrectly “prescribe” and it’s really hurt a lot of people—but that doesn’t mean I have to like it.
This might be unpopular but here's a connection I think a lot of people still haven't made: PEM isn't deconditioning, but that doesn't mean that people with PEM can't have deconditioning, too. You just can't address the deconditioning in the normal way (i.e., exercise) with PEM.
So when I see "PEM isn't deconditioning," it gets a vigorous head nod. Then when I see studies in ME/Long Covid using single CPET and histology that have findings suspicious for changes associated with deconditioning, no biggie, there's space in the thought process for that too.
When I see study results in people with ME and Long Covid consistent with deconditioning (🔽 VO2, 🔽 capillary density, 🔽 mitochondrial density, and myosin heavy chain isoform shift to fast glycolytic fibers), it's not a total surprise. But that's also not where it ends for me.
@EnyaDaynesPT Thanks for the chance to contribute here. I'll highlight five papers here and give honorable mention to several others. This might be a long-ish thread, so please bear with me.
@EnyaDaynesPT In many ways, the first paper describing the prevalence of PEM in Post Covid Condition is still the best. Cross sectional work from the early days on an international cohort of about 3,750 people with lab confirmed and suspected wild type COVID-19 infection. Patient led research.
@EnyaDaynesPT The overall prevalence of self-reported Post Covid Condition signs and symptoms went down in this cohort over time through 7 months postinfection, but PEM is notable for going up in prevalence. PEM was experienced by 88% of the cohort at some point in their illness. That's a lot.