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LC is unique due to its chronic inflammation of the vessels (vasculitis). Just because some symptoms are shared, it doesn't mean the conditions are the same.
Sep 23 15 tweets 4 min read
1) 2020 JAMA Cardiology study (Puntmann et al.) revealed the devastating cardiac toll of COVID. On advanced MRI, a staggering 78% of recovered patients had heart abnormalities & 60% had ongoing inflammation, regardless of initial severity. 2) Dr. Puntmann's upcoming "myoflame" study is set to reveal further devastating insights into post-COVID heart damage, focusing on microvascular dysfunction, fibrosis, & resulting diastolic dysfunction, pathologies often invisible to standard diagnostics.
Aug 26 8 tweets 2 min read
1🅱️) How do you make a public health crisis disappear? First, you deny the suffering. When that fails, you declassify the event to downplay it. Fragmenting Long COVID is a masterclass in this political strategy. Here’s the 3-step process. A thread: 2🅱️) Step 1: De-link the effect from the cause. By calling post-COVID organ damage a "complication," you sever its tie to the pandemic. A heart attack is no longer a public policy failure: it's a personal tragedy. The system is absolved. Image
Aug 22 25 tweets 8 min read
1 ) Seriously? We can't even acknowledge that COVID causes SPECIFIC damage anymore?

ME/CFS can be progressive & multi-systemic, that's true. But COVID's unique vascular & neurological damage patterns are WELL-DOCUMENTED.

Different triggers ≠ identical diseases. 2) A virus that killed millions, left millions more fighting for their lives, that mutates constantly, that crosses every organ barrier...

...and we're supposed to pretend it causes the same damage as other post-viral conditions? Cognitive disonance?

Aug 11 8 tweets 2 min read
1) A new study analyzes immunoglobulin complexes from patients with ME/CFS and a Long COVID cohort who also meet ME/CFS criteria (PCS-CFS). Proteomics reveals they have fundamentally different molecular signatures, suggesting distinct pathologies. A thread on the findings. 2) The key commonality: When applied to healthy human endothelial cells (the lining of blood vessels) in vitro, antibodies (IgG) from BOTH patient groups induced significant mitochondrial fragmentation. This points to a shared autoimmune attack on cellular energy infrastructure.
Aug 10 6 tweets 2 min read
1) Study finds healthy lab-grown muscle exposed to ME/CFS or Long COVID blood quickly loses strength, temporarily boosts metabolism, then undergoes mitochondrial and structural collapse with prolonged exposure. Distinct metabolic and structural differences separate ME from LC. 2) ME/CFS muscles show heightened oxygen consumption and tissue remodeling focused on extracellular matrix repair, while Long COVID muscles rely on mitochondrial compensation but suffer from inefficient energy use and faster fatigue.