Patrick

@scott_scientist @chydorina Where did you get this?

@chydorina Certainly a clue there…

I cannot stress this enough. To handle many interventions there is a critical layer of system support that must be in place or you will react negatively. How does this not make sense?

@sunsopeningband Truly agree!

We wouldn’t put the chart of a metabolic pathway up on the wall, blindfold ourselves, throw a dart at the chart, and then push a drug at whatever step the dart lands. Not hard to see why drug repurposing, this strategy for speed and convenience, is yielding disappointing results.

@SoMammoth Tage

Name a superstar trade in the NHL the buying team didn’t overpay for:

@sunsopeningband @AnsamGroshong @rhymeswithvery @MelanieWeckert Okay but you have to also emphasize the permanent decline that can result from PEM

@rhymeswithvery @MelanieWeckert PESE = symptoms worsen with exertion, says nothing about latency between onset and stressor nor recovery period PEM = delayed symptoms after stressor, prolonged recovery PEM is an energy problem. Signs/symptoms also may coincide with dysfunction in a number of other systems.

Today’s unpopular opinion is maybe the worst development in Long Covid research has been confusing PESE with PEM. Just because a person may have unusual and disabling symptoms and signs after an exertion (PESE) doesn’t necessarily make it PEM. Please see the ICC-ME for details.

The Boston Globe published an article about Long COVID in kids last week. I'm glad they're covering it, but as you'd expect, it's full of the typical propaganda. I'll break it down: 1. A neurologist at Boston Children's Hospital describes Long COVID as "like a salad bar". This framing makes the disease sound quirky and varied rather than devastating. Imagine an oncologist saying "I describe cancer like a salad bar." The casualness trivializes the severity. 2. "Research shows vaccination may reduce the risk." Typical "vaxx and relax" propaganda. No discussion of infection prevention, clean air, masking, or the fact that this child was unvaccinated when infected because she was 12 and vaccines weren't yet available for her age group. No discussion of whether subsequent infections could worsen her condition. No mention of ongoing risk. 3. "Social factors may also play a role... low social support or high levels of discrimination." This is the psychosocial creep. A virus damaged this child's body and now researchers are exploring whether discrimination contributed. This shifts causation from the virus to the social environment, reinforcing the ongoing pandemic denial and delusion. 4. "There is no single cure... care is typically tailored to each symptom." This normalizes symptom management as the expected standard of care rather than presenting it as a failure. The framing is "this is how we treat Long COVID" rather than "this is all we have because we haven't done the mechanistic research." 5. "She pushes herself to show up, even on the hard days." The child is framed as heroic for enduring (to be clear, I think she is). But the system that failed to prevent her infection, failed to develop diagnostics, and failed to find treatments is invisible. The burden is on the 16yo to live with it. 6. "Chiropractic treatment helped ease her pain" is presented without any skepticism. No mention that chiropractic was invented by a guy who said he got it from ghosts. This reinforces the DIY, alternative medicine, symptom management approach as normal. 7. Of course, there is no mention of SARS2 as an ongoing threat. No mention of reinfection risk. No demand for better research, better funding, or actual treatments. The article presents a child whose life was destroyed by a preventable infection and frames it as a human interest story about resilience rather than a government failure demanding systemic change. 8. Worst of all, the article makes you feel sad for Kaylee while accepting her situation as inevitable. It never asks why a 16yo at 45% capacity years after infection has no treatments. It never asks who are the people that failed her. It never asks what should have been done differently.

@kirstymecfslife It’s more that ME = the capacity to induce PEM

@TomKindlon Such a beautiful nice school. I’m so sorry

I had to drop out of college (Trinity College Dublin) in my early 20s (actually got straight firsts in my last exams). Still cared for by my parents at age 53 when both my parents are in their 80s. #MEcfs #PwME

What’s interesting about severe ME/CFS is that when you explain your life to people, they never seem to actually digest how ill you are and how you live. I haven’t left my house in 4 years and eat ONLY sweet potatoes and beef. When I’ve told people this, later in the conversation they’ll mention me eating different types of food or seeing friends occasionally, as if they thought I was joking or exaggerating about how I live. Once they realise it’s actually that minimal, their brain seems to break and they just have no way to process it. They remain in disbelief.

Both trigger/pathogen-specific mechanisms and the convergence of different triggers onto shared biological pathways are plausible and complementary models. Different triggers do not act equivalently: they have distinct biological properties and are associated with different symptom profiles, likelihoods, and severities, reflecting, among other factors, differences in tissue tropism and host response. At the same time, distinct triggers can converge on overlapping downstream pathophysiological processes, leading to similar/same clinical phenotypes despite differences in upstream biology. Which pathways predominate may be shaped both by the nature of the trigger and by host-specific factors. The relevant question is therefore not whether trigger-specificity or convergence exists, but how much of each is present, at which level, and in which patient. Accordingly, research into ME/CFS should integrate trigger-specific or pathogen-specific approaches where appropriate, together with pathway-level convergence approaches, rather than treat them as mutually exclusive.

@FabulousBS @JayManCroft Wallstedt

@JayManCroft Find me a Stanley Cup contender whose starting goalie started the year in the AHL. It doesn’t happen. Ingram is a backup at best. Kap✅ Dickinson✅ Jones❌ Murphy❌ (unless he’s cheap) Lazar❌ Hamblin✅ Dineen✅ Biggest needs: GOALIE Nurse EXIT Walman EXIT PK specialists

Depending on money I’d bring back UFAs - Dickinson, Kapanen, Jones, Lazar, Murphy, Ingram, Poulin, Hamblin, Dineen RFAs - Dach, Jarventie, Stastney, Ungar I could see Dickinson/Murphy signing for cheaper in order to take a run at a Cup.

A group of my very dear friends came together to make this post, thank you to @alexandrite113 & Fran I’m not sure you’re on Twitter, and everyone who contributed. #longcovidawareness #longcovid

Sometimes I see people defend researchers from criticism to the tune of "we don't want to scare them away" or "they're on our side". Understandable, but... If I get something wrong I want it to be corrected. This is me saying that it is GOOD to give constructive criticism.

@RattusFlattus @marinaflares Yes, it is like swimming with a 50ft anchor on your foot. It does not matter how much you struggle, to what extent, if you do not take off the anchor.

@marinaflares It’s so insulting. It’s the wrong emphasis. We are already as active as we can be and usually too active. It’s not like there’s a bunch of patients out there that are always under their energy envelope and just don’t get enough activity. That just doesn’t happen.

Let us talk about the "be as active as possible without triggering PEM" that has recently been perpetuated again - in a Nature publication no less. I used to be a marathon runner, so I'll use this example to illustrate my point. 1/

@spritesfly @marinaflares "The paradox is that better fitness level can raise the baseline for some." For whom? Where?

@marinaflares The paradox is that better fitness level can raise the baseline for some. To do that you have to accept the PEM. Exercising (anaerobic, not aerobic), three days a week &aggressively resting (supine, blindfolded) on intermittent days, can raise fitness, &baseline on active days.

@_VFK_DAA @BayouMystere E.g. was a big fad for anticoagulation earlier in pandemic because of "spike protein in blood", when there are elevated albumin transudation rates, NETs, low blood volume, basement membrane thickening, etc, in non-covid ME cohorts as well. I hope I am not crazy :) Best regards

@_VFK_DAA @BayouMystere I know people who have very bad lung epithelial and lung fibrosis as part of their LC cases, it is very bad. And it is specific to COVID. It is abject. All my post was doing was pointing out that vascular symptoms (like in original post) can exist from other sources as well.

FFS can people please read up on what ME/CFS is, what severe and very severe ME/CFS looks like and which body systems it affects That’s sort of necessary in order to recognise it, you know

@elle_carnitine If I find the energy I’ll email these guys

"While there is emerging evidence supporting the role of physical therapy in managing PEM (REF)" sometimes you have to laugh nature.com/articles/s4385…