Dangerous garbage being presented “science writing”. Two *actual* facts surrounding #COVID infection: 1. Your risk of #LongCOVID, a currently incurable chronic illness, after surviving an acute COVID infection currently sits conservatively at ~6-7% 2. Your risk of LC increases 1/
Now, in the face of this information, there are really five (or so) types of reactions: 1. Disbelief and denial 2. Being unaware or uninformed of the risk 3. Believing appropriate caution is necessary to avoid Long COVID 4. Believing it is worth the risk 2/
to yourself AND OTHERS to live your best pre-COVID life 5. Not having the financial freedom to not risk yourself and others by not taking precautions
Regardless of which of these 5 lanes you live in, won’t change the first two FACTS. So, as a person of questionable influence, 3/
let me remind you: #LongCOVID is life-changing and incurable. LongCOVID is caused by #COVID. We still have no way of predicting who will emerge unscathed from a COVID infection. The only way to avoid getting LongCOVID is to not get COVID. Let me also remind you that while 4/
@ClareWilsonMed ridicules people “putting sticks up their nose” if you should, god forbid, get #LongCOVID and you don’t have evidence of infection, things get harder for you to access good care. They shouldn’t, but they do. So since the “science writer” who penned this opinion 5/
didn’t lay it all out honestly in favor of publishing a bit of clickbait that hurts public health, next time you hear drivel like this, think about the 5 lanes of people and which lane you want to be in. Think about the fact that those minimizing COVID have been minimizing it 6/
since 2020 and have been consistently wrong since 2020. Magical thinking doesn’t make you safe and speaking realistically and quantitatively about risk stratification doesn’t make you a fearmonger. Writing junk like this DOES make you dangerous. Grow up, Clare.
/end
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Excited to finally get this one out in @Nature_NPJ! In the largest study of its kind to date, we used data from the @visible_health platform to answer a simple question: can we predict symptom fluctuations and crashes from both the physiological and
patient-reported data? The answer to this question is yes. Not perfectly, but actually quite well. A few important takeaways: 1) Just as we have seen previously in people living with chronic pain, the ability to predict symptom flares and crashes in ppl with #LongCOVID,
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#MECFS and other complex chronic illnesses can represent a massive life upgrade. The ability to prepare for or expect a crash or a bad symptom day is preferable to many than these things just seemingly randomly appearing with no warning. 2) The fact that physiological signal
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I want to thank everyone for the interest in this work that we completed in a #LongCOVID cohort with this novel device. I always appreciate feedback and want to thank folks for holding me accountable to a high standard of communication. To that end, I want to re-clarify this 1/
thread: this was a safety/feasibility trial which means that our primary endpoints were related to safety and feasibility. In the paper, we state clearly that we hit those endpoints: no device-related adverse events and 100% adherence to the protocol in all participants. That
2/
is great for a safety/feasibility trial. I then went on to express excitement that some cognitive scores moved. I understand that folks have (rightly) pointed out that without a larger sample size and correcting for multiple comparisons we can’t make definitive statements
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Excited to get this out in preprint: triple-blind, placebo-controlled microtesla magnetic therapy (MMT) is safe, feasible and effective in reducing cognitive impairment in people with #LongCOVID. I get excited about interventions for cognitive symptoms
as they can be so disabling and frightening because you don't know if the symptoms are going to be permanent. This paper makes us feel hopeful that Long COVID cognitive impairment related to neuroinflammation is something that is treatable. This was a first-in-human safety-
2/
feasibility trial. Typically in trials like this, because they haven't been done in humans and only in animals, we're happy if we see safety and good adherence to the protocol, but we're not usually expecting to see efficacy because the dosage is a bit of a "best guess". 3/
Proud to have worked with the brilliant @drmfreire on this new study looking into spike protein in #LongCOVID. The most important part of this study that doesn't just look for spike protein in folks with LC and healthy controls, but it also uses a technique called 1/
spatial transcriptomics to better understand how spike protein might be interacting with the tissue around it. Here's what is interesting about this trial: lots of gut tissue samples, in both healthy controls and #LongCOVID showed evidence of persistent spike protein. However,
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in the folks with #LongCOVID that persistent spike protein was causing problems in the tissue: pro-inflammatory, tissue-damaging trouble. So not only do folks with LC have more spike, but the spike is actively irritating and damaging the surrounding tissue compared to healthy
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Crucial paper published Friday that deserves much more attention in the #LongCOVID world: .
TLDR: 13/15 immunocompromised patients who had chronic COVID infections (>200 days) cleared the virus in under 2 weeks when given combo antivirals/monoclonals
The caveat: yes these were cancer patients who were severely immunocompromised, and the "haters" are going to say that it isn't appropriate to draw parallels between this patient group and folks with #LongCOVID.
That's incorrect.
It is perfectly acceptable to draw such
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parallels and here is why: we (and others) have shown over and over again that immune dysregulation is associated with #LongCOVID, and T Cell Exhaustion, specifically, is a key feature of this dysregulation (first paper here: ). Why is T Cell exhaustion
3/nature.com/articles/s4158…
Great win early in the year to receive notification that our case series looking into Dr Pridgen’s Valacyclovir, Celecoxib and Paxlovid protocol seems to really help some folks with #LongCOVID. This paper is a start, not the be-all and end-all:
It is a small, open-label case series, but there are some interesting things that are worth noting that give me hope that what we are seeing is real and will hold up in a larger trial 1) People got to choose between Val/Cel only (called ‘IMC-2’ in the paper) and Val/Cel + Pax
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The people who chose the latter reported greater benefit. 2) The subset of people who started with Val/Cel only but then chose to retry the protocol with Paxlovid added experienced more benefit with the three drugs together than they did with the two drugs 3) The follow-up
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