Of course, they are led by Peter White, the lead investigator of the PACE trial that NICE thoroughly debunked, and members of a (bio)psychosocial collaboration for “post-infectious fatigue” called COFFI.
If you have #LongCovid, I’m sure some of these names will be familiar to you already.
Be warned, #pwLC: that many proponents of “functional neurological disorders” (FND) co-authored this paper shows how much they want to get their hands not just on #MECFS but on LC too.
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My GP is amazing but, for the hundredth time, he really needs to be more careful. He prescribed me erithromycin for gastroparesis, which interacts with a lot of drugs (CYP inhibitor)… including domperidone, which he told me I could continue taking. 😬
Disappointed that @SBMPediatrics abides by the biopsychosocial (psychosomatic) model of chronic pain, despite all its evidence base being a tangled mess of confusion between correlation and causation.
The blog post is a fair critique of this intervention. But no, psychosocial factors *do not* explain chronic pain. The evidence for psychosomatic treatments (exercise, CBT..) consistently shows modest effect sizes despite high risk of bias: no blinding + only subjective outcomes.
The reported modest improvement in trials of psychosomatic interventions can be explained solely by a combination of response bias on questionnaires because of behaviour modification, attention bias for therapist-delivered interventions due to inadequate control groups, —
Important caveat: of course, not all people with durable #LongCovid have developed #MECFS.
The @ONS stats include people with well recognized organ damage from Covid, and some may have developed post-infectious conditions with symptoms that overlap those of ME but aren’t ME, etc
Regardless of the condition people with #LongCovid develop, these data are just terrible. Nearly 1.5 million people disabled in their daily activities.
“Long COVID symptoms adversely affected the day-to-day activities of 1.4 million people (72% of those with self-reported —
81 healthy controls & 116 #POTS pts had similar levels of autoantibodies against G-protein coupled receptors, suggesting GPCR AAB tests are “not useful for establishing the role of autoimmunity in POTS”