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May 27 13 tweets 5 min read
Some long weekend reflection as we work to build effective research infrastructure around #LongCovid and other infection-associated chronic illnesses like #MECFS and #Lyme. For those who don't know, I was born and raised in Perth, Western Australia, so here's a "local" story. 1/
Apologies if this is a familiar story to many, but I think there is much wisdom to be gained. For the longest time, gastric ulcers were thought to be related to excess acid in the stomach and worsened by stress/lifestyle. People were treated for peptic ulcers with antacids and 2/
the recommendation to reduce stress in their lives. This went on for decades until a Perth-based physician/scientist, Dr Barry Marshall, made an accidental discovery that led him to believe that gastric ulcers may not be stress-related at all: in fact they might be a result of 3/
bacterial infection from a bug called "h. pylori". This theory was roundly ignored, derided and dismissed: the conventional science was clear - Dr Marshall was dead wrong. Since he couldn't get any funding support for his research and no one was paying attention he did the 4/
only thing he could think of to take his theory to the next level - he scoped himself to show he had no ulcers, he infected himself with h. pylori, he scoped himself again to prove that ulcers had formed and then he cured himself of those ulcers with antibiotics. He took this 5/
pilot data and applied for a $15k NHMRC grant (the Australian NIH). Naturally, the folks on the review panel thought he was insane and he almost didn't get the money, but apparently a single reviewer (legend has it, one Ismail Kola though this has never been verified) made the 6/
argument that if they funded this one small grant (and a few other smaller grants) in favor of a larger one that was going to be funded instead, they could get more "bang for their buck". The logic succeeded, the grant was funded. At the conclusion of Dr Marshall's "crazy" 7/
project it was clear: the conventional therapy and thought around gastric ulcers was total bunk. It was bacteria, not stress, that caused ulcers. Let me reiterate: for decades, getting ulcers was a dreaded fate because all available treatments were pretty terrible - MAYBE you 8/
experienced some symptomatic relief from antacids and cutting out stress, but not really: usually you just suffered in silence and kept seeing the doctor who kept reminding you to "take it easy" (and collected their cash for the appointment). Dr Marshall went on to win the 9/
Nobel Prize for his discovery but the point of today's story is this: #medtwitter #ScienceTwitter - if the answer to #MECFS, #LongCOVID, #Lyme, #EDS, #dysautonomia was just "doing what has always been done" or building on the existing conventional wisdom of these conditions, 10/
we would have solved it by now. The solution to these problems will come from those with the curiosity, creativity and bravery to think outside of the box, to not be afraid to look "silly" in front of their colleagues and to ask the questions that others aren't asking. 11/
Cookie-cutter science may win you grants and get you accolades amongst your mainstream colleagues, but taking the path less-traveled, LISTENING to you patients and chasing the "crazy" ideas that make intuitive and scientific sense DESPITE conventional wisdom will save lives, 12/
shift paradigms and create disruptive innovation. #MedTwitter and #AcademicTwitter: make no mistake, this is a red pill/blue pill moment. WHO do you want to be? Think on it, but remember that symptoms of infection associated chronic illnesses don't take the weekend off /end/

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More from @PutrinoLab

May 19
@sunsopeningband Great question! Our data also supports that the majority of folks we see with LC have both metabolic and autonomic components (we see kind of a distribution of 15-20% of autonomic or metabolic alone, and 60-70% of a mix of both). I think the main point is that you can have 1/
@sunsopeningband both processes at play, but I don't have evidence at this stage that the processes are linked, they're likely separate: you have metabolic PEM AND autonomic PEM and one doesn't influence the other. For autonomic we take careful physical and physiological measurement at each 2/
@sunsopeningband session in order to measure the extent to which someone's ANS is activated on the day, as well as to track progress (10m stand, HRV (SDNN), HR/BP changes through positional transitions), for metabolic it is very tough (we're going to release some research on this ASAP), but 3/
Read 8 tweets
May 13
Today's 🧵 is about autonomically-led post-exertional symptom exacerbation (PESE) in #LongCovid, #MECFS and other infection-associated chronic illnesses. This form of PESE is different to metabolically-led PESE, but it is also possible to have both occurring at the same time (1/)
Autonomic dysfunction happens a lot in #LongCovid and #MECFS and can be highly debilitating. The autonomic nervous system (ANS) manages a lot of intricate body physiology. For instance, every time you change position from laying down to sitting up, your ANS makes changes to (2/)
your blood pressure and heart rate to make sure that blood can travel all the places it needs to (e.g. the brain) despite the new position. The ANS does 1000 little ingenious, complex and entirely automatic functions like this on the daily. As such, when people experience (3/)
Read 18 tweets
May 8
Time for a 🧵 about metabolically-led post-exertional symptoms. This is quite possibly the most dangerously misunderstood piece of #LongCovid, #MECFS and infection-associated chronic illness puzzle (including non-viral pathologies that involve mitochondrial damage). (1/n)
First: many things can cause post-exertional symptoms, especially in the case of #LongCovid, where a large % of people have associated #dysautonomia. Understanding this is crucial to maximizing the utility of interventions such as autonomic rehabilitation and pacing (2/n)
without doing more harm than good. However, today is about metabolically-driven #PEM/#PESE. It should be fairly well-established at this point that many people with conditions like #LongCOVID and #MECFS have evidence of mitochondrial dysfunction, oxidative stress and (3/n)
Read 21 tweets
May 6
Short 🧵on symptom measurement in #LongCovid / #MECFS and other chronic illnesses. We need to do better. Many of the symptoms that we're trying to track don't have a physical biomarker, and while patient-reported outcomes (PROs) are helpful, then need to be far more (1/n)
rigorously developed. Let's pick on fatigue as a #LongCovid symptom, because it is incredibly disabling for most folks with LC and it is not well characterized. To measure fatigue, my team uses the Fatigue Severity Scale. Why? Because it is well-validated and allows us to (2/n)
reliably track change in response to interventions. Is it perfect? Far, far from it. The FSS gives us a reliable, but basic understanding of fatigue severity and how it is impacting daily life. What it doesn't do, however, is help us to differentiate different causes and (3/n)
Read 11 tweets
May 4
Ok. Another request, another 🧵. Today, we address the strained relationship between psychology, psychiatry and #LongCovid. Much of this may also apply to #pwME and other infection-associated chronic illnesses (h/t again @microbeminded2) and other “invisible” illnesses (1/n)
Psychology and psychiatry have a complex history with syndromic illnesses. Why? When illnesses are diagnosed on the basis of symptoms rather than “objective” tests, some clinicians will doubt the reality of the condition. Let’s start by psychoanalyzing them, shall we? (2/n)
This behavior is not justifiable, scientific or ethical. But it is also is not new: in the 1800s, tuberculosis was regarded by most physicians as the “disease of the sensitive” before tubercule bacillum was discovered, the “cancer personality” was touted for decades (3/n)
Read 22 tweets
May 1
Ok. As promised, here is a super-🧵 on cognition and #LongCovid. This will be a combination of published material and things that we have observed in-clinic. This is not intended to be definitive nor epidemiological and so it is highly likely that your personal experience (1/n)
may deviate significantly. This is about my reading and experience of cognition and #LongCovid but from what I have seen shared in the comments of my tweet yesterday, it seems that much of this may apply to other infection-associated chronic illnesses (h/t @microbeminded2) (2/n)
such as #MECFS, #Lyme and #dysautonomia/#POTS to name a few. Let’s start out with naming. I try not to use the term “brain fog” because I don’t think it conveys the seriousness. People with LC are experiencing cognitive dysfunction that often results in cognitive impairment (3/n)
Read 25 tweets

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