J Peace 3

Can anyone tell me is there such a thing as Spiky-Leaky Syndrome but in the serous fluid cavities? Would this differ from an effusion?

@Dfrizz007 i feel like we are pawns all trying to drag ourselves to the other side of the board so we can change into whatever will let us get back into the game again. Without reaching that point theres no point in thinking about how to win it, it's just a matter of slow steps to survival.

@JPeaceJPeace no this refers to anything we do results in a loss. this is the moment before the realization you know you are about to be checkmate. it applies to my (our) life anyways with this illness. at least in my opinion

zugzwang.......technically a chess term or game theory. sums up our lives huh? "when a player is forced to move but any action results in a worse position or loss. It is essentially a "forced move" where simply having to move turns a winning or drawing position into a losing one"

@nick_boileau @kirstymecfslife

@kirstymecfslife @JPeaceJPeace 😂

@sanilrege @rhymeswithvery @psycheureka Anyone who wants to oversimplify the complex and uncertain in health is doing all a disservice. The problem is influencers & clinicians get away with it in a vacuum of accurate widely understood knowledge of these conditions. e.g. Not much need for "oncongeniacs".

@rhymeswithvery @psycheureka I had influencers and clinicians in mind here .

Mitochondriac (n.): A person with a disproportionate tendency to invoke mitochondrial dysfunction as a preferred explanatory model for nonspecific symptoms, impaired functioning, or complex clinical phenomena. *inspired by a comment by a subscriber on my YouTube channel who came up with this term.

@seanstidston It's interesting to me how neutrophils seem to be so key to LC. More and more evidence seems to be showing this. nature.com/articles/s4139…

@JPeaceJPeace No I am referring to those who think reframing beliefs alter illness.

This is brilliant work from TeamClots colleagues @resiapretorius & @DrMark_Faghy.Again yet another paper clearly demonstrating pathobiological changes in PEM. The fact that some few individuals still believe PEM in LC &ME can be treated by reframing illness beliefs beggars belief

@seanstidston Ah yeah. Got you mate sorry. That is a whole other question I'd agree for alot of them it is a matter of insentive rather than inquiry.

@seanstidston There is a lot more research that is needed to prove microclots are the cause of symptoms, but the research into them has been long overdue in ME/CFS like conditions. Something similar was first described in the 1980s. x.com/JPeaceJPeace/s…

@seanstidston Sean I hope you're not talking about the researchers who released this preprint?

@kirstymecfslife @seanstidston @Dfrizz007 Shit, I didn't know that was an actual thing. George Lazenby is defs the best bond, and I'm not biased AT ALL

non illness related MOVIE question. for those that like or love the James Bond films over many of years, who was your favorite bond actor? also who would you like to see in the future? Sean Connery David Niven George Lazenby Roger Moore Timothy Dalton Pierce Brosnan Daniel Craig

@DavidJoffe64 @DrMark_Faghy Is it shortsighted of me to feel a little bit frustrated that it seems this sort of testing has not been done more widely in LCers prior to now? I'm thankful that science is starting to shine a light on this. But there are so many layers to peel back to get to the bottom of it!

I've been waiting for this paper to drop for several months 👏🏻👏🏻😎 The honour of sitting with the grown-ups is seeing the science in its raw form Now peer reviewed and published🏁 @DrMark_Faghy and Team... Bloody FANTASTIC science🏆🏆 Things that aren't "PSYCHOSOMATIC"‼️

@DrMark_Faghy @CallumThomas96 what happens if this test is run over hours rather than minutes? Are LCers vs controls likely to diverge futher IYO? It would also be interesting to see what happened at day 3 or further into this protocol. My guess the trend would be an even greater split btwn the two groups.

Latest paper from @CallumThomas96 and our research group showing a reduction in oxygen extraction in the calf muslces during low intensity exercise/activity. This has important implications for energy production and functional status... physoc.onlinelibrary.wiley.com/doi/10.14814/p… #longcovid

@jaymie_hu 💙

Feel pretty good today

#MedTwitter This needs to stop. The End/

There’s a common argument that we need validated biomarkers before running clinical trials in Long COVID and ME/CFS. I think this is wrong. First, you don’t need disease-specific biomarkers to track whether a treatment is working. Nearly all clinical trials across medicine rely on symptom-based endpoints. Change in disease status is measured through patient-reported outcomes, functional capacity, and clinical assessments. This is standard. It’s also what we care about, do we care if biomarker X improved if function is still the same? Yes for research, no for approving that drug, which is the purpose of the trial. Second, biomarkers can help guide which drugs are worth trialing, but their absence isn’t a blocker. We already have plausible mechanistic targets. There’s evidence pointing to mitochondrial dysfunction, so there’s logic to try mitochondrial drugs etc. Where biomarkers genuinely matter is in identifying responding subgroups, and this is a different problem than having a “disease biomarker.” It’s exploratory, study-specific work: you run omics-based blood profiling on trial participants, or leverage established subgrouping frameworks, and look for signatures that predict who responds and who doesn’t. That’s valuable post analysis, not a prerequisite. What actually needs to change is the study design itself. Trials in this space need to stop recruiting patients too early in their illness. Enrolling people within the first year creates artificially inflated placebo response rates, because natural improvement is still occurring. Trials also need to run far longer than the one-to-three-month durations that are common now. Six to twelve months is more realistic for detecting meaningful therapeutic effects. In mastocytosis, a disease with mast cell involvement that parallels the theorized mast cell dysfunction in Long COVID and ME/CFS, the most promising therapeutics showed significantly greater improvements at six months and one year compared to short-term endpoints. Combine longer trials and later-stage recruitment with the subgroup biomarker exploration described above, and the clinical trial landscape in these diseases improves dramatically. The framing that biomarkers must come first risks becoming an excuse for inaction in diseases where patients are waiting for trials that could start today.

@sanilrege @psycheureka Maybe we could get your brave youtube commentator to mainline some IgGs from some patients with diverse, nonspecific or insufficiently characterised symptoms just to make sure it isn't a mitochondrial issue? If they aren't scared of course... sciencedirect.com/science/articl…

@sanilrege @psycheureka I'm not suggesting we take endomyocardial biopsies of everyone looking for mitochondrial damage, but if we had a safe test for it we'd have a much better chance of correctly characterising "diverse, nonspecific" symptoms. Instead of blindly sacrificing people to the "iac gods"