Our latest work now posted as a pre-print on @researchsquare: "ME/CFS and Long COVID Demonstrate Similar Bioenergetic Impairment and Recovery Failure on Two-Day Cardiopulmonary Exercise Testing" @4Workwell researchsquare.com/article/rs-860…
Using two‑day cardiopulmonary exercise testing (CPET), we compared physiological responses in people living with #MECFS and #LongCovid with matched controls, stratifying by sex, to resolve the weaknesses of single tests in mixed-sex cohorts we've seen so far in CPET studies.
Here's what we learned:
👉 Both ME/CFS and Long COVID show similar failure to recover after exertion
👉 Largest impairments occur at the ventilatory anaerobic threshold, suggesting similar aerobic system impairments between ME/CFS and Long COVID
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👉 Females exhibited more pronounced post‑exertional CPET abnormalities than males, but were present in both sexes
👉 No meaningful differences were observed between ME/CFS and Long COVID on two-day CPET, suggesting they share a common bioenergetic pathophysiology
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👉 Severe functional impairment was common in both patient groups and was not explained by effort preference, deconditioning, ventilation, or hemodynamics
Maybe the most remarkable thing? We didn't purposefully select for a cohort with Post COVID ME. It was dealer's choice.
Normally you might expect noisy case definitions to wash out any effects, because as we know, Long COVID isn't just one thing. But, at least in our sample, it didn't seem to matter. CPET responses were statistically and functionally similar between ME/CFS and Long COVID anyway.
These results reinforce post‑exertional malaise (PEM) is a measurable physiological phenomenon. In an era where the 'lazy-crazy dichotomy' still gets pushed as explanations for ME/CFS and Long Covid, unfortunately this doesn't get to be a throwaway line yet.
It still matters.
The findings of this study also underscore the value of two‑day CPET as a useful tool to:
✅ Differentiate PEM from normal recovery using objective measures
✅ Inform disability evaluations in people who can and choose to have a CPET
✅ Improve precision in clinical trials
Anyway, thanks for reading. I'm grateful to my co‑authors and to the patients. Their generous engagement continues to advance our understanding of these terribly disabling yet largely ignored chronic conditions.
Mechanistic work is slow but worth it. More forthcoming. Onward.
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I was privileged to sign on to a recent op-ed appearing in Le Monde, arguing that medicine and science must finally move beyond the outdated mind–body divide. What follows is a quick summary and explainer for my English-speaking friends on here. @apresj20
🧵
While studying symptoms is important, treating a "science of symptoms” as separate from a “science of disease” risks perpetuating methodological dualism on top of inadvertently reinforcing the Cartesian dualism that terminology describing functional disorders aims to critique.
Of course, we know normal testing doesn’t mean nothing potentially detectable is wrong. Advanced neuro-imaging techniques and biological tools are increasingly revealing the structural and molecular changes behind diseases involving persistent but often hard-to-explain...
Sometimes I talk with folks who don’t know much about myalgic encephalomyelitis and are researching it, such as for a media piece or class assignment, for the first time. The dogs are walking slow this morning, so here I’ll share a couple observations here about that experience.
First observation: it is impossible to portray the level of disability, suffering, expense, and marginalization characterizing the experience of ME/CFS in a short conversation with someone who has never thought about it before. Even if they’ve spoken with patients before speaking
with me, there’s a sense of magnitude that is impossible to grasp on the first pass. It all sounds too much to be believable. And, in fairness, maybe it’s a lot to take in and sit with and process if you’re well and have no lived context for it. I like to force the issue.
Long COVID trials are struggling—not because of lack of effort or goodwill (mostly), but because of errors in trial design and poor endpoints. Our new paper, out today, lays out how to start fixing this. Now.
A short 🧵.
We recommend
* Thorough baseline disease characterization
* Longitudinal data collection
* Placebo arms to track natural history
* Measuring post-exertional malaise (PEM)
* Balancing severity and phenotypes across trial arms
These are challenges we can address. Together.
PEM eats Long COVID trials for breakfast. It’s the hallmark symptom of the Post COVID ME phenotype that can derail trial validity. We have tools to use! DSQ-PEM, FUNCAP, PAQ, 2-day CPET and others may be key. But we urgently need patient reported outcome measures and biomarkers.
Thank you for the opportunity to share this proof-of-concept work, @CPTJournal. @wearlumia @4Workwell
We've known that post-exertional malaise is correlated with reduction in cerebral blood flow (CBF) for many years. We think cerebral hypo-perfusion may account for some of the signs and symptoms we observe.
However, measuring CBF takes expensive equipment. 1/n
Trying to measure CBF in any position or movement besides sitting or laying down is practically a non-starter. It is also not the kind of thing a person can do and interpret for themselves. Enter the Lumia™ in-ear device. It's a reliable measure of blood flow to the head, 2/n
People on here like to discredit PEM symptoms as less credible or reliable, despite all evidence to the contrary. Assuming a trustworthy patient (we always should accept a trustworthy patient as a baseline clinical assumption until proven incorrect), this shouldn’t be a problem.
Besides, anyone making a bright line distinction between signs and symptoms is vastly oversimplifying clinical life. For example, what’s a “limp?” If you see it, a sign. If I say it, a symptom. The truth is never as clear as it initially seems. Too bad for deniers and minimizers.
Similarly, when I do consults with patients, I can usually tell when cognitive dysfunction has begun to set in about the same time or earlier than they do. I know if they’re having a crash day right from the jump. Symptom? Sign? No real difference to the astute clinical observer.
If exercise makes symptoms worse…you know that exercise makes symptoms worse.
You do not know if it’s PEM from that observation alone.
For example, I work with people who have low back pain. Sometimes the treatments I provide overload things enough they feel a little worse temporarily. There’s a school of thought that says exercising into a little pain might even be helpful because it gets even better over time.
Getting worse after activity is PESE. It makes no assumption about the underlying capacity of tissues and systems to respond, just things got worse. PEM is a worsening in function in response to activity over time, suggesting lost tissues’ and systems’ ability to respond to load.