Thread attached about how the “confused” immune system drives covid / long covid and some things that can be done now to help reverse it. #LongCovid #Treatment #Science

A recent review proposes integrating POTS, ME/CFS, and Long COVID into the neuroimmunology subspecialty. Here is their compelling case. \ Overlapping Drivers of Disease: The authors outline several major overlapping pathophysiological mechanisms shared by POTS, ME/CFS, and Long COVID. This includes: 1. Autonomic Dysfunction (Dysautonomia) 2. Mitochondrial Dysfunction 3. Cerebral Hypoperfusion 4. Immune Dysregulation 5. Neuroinflammation 6. Autoimmunity \ The Harm of Psychiatric Misdiagnoses: For decades, patients have been wrongly labeled with "functional neurological disorder," anxiety, or somatization because routine tests often look normal. \ A Call for Better Diagnostics: Researchers and clinicians urgently need advanced tools such as: - 7T MRIs - Targeted PET scans - Autoantibody and cytokine panels - Comprehensive autonomic function testing Routine tests are simply not enough. \ The Authors’ Core Proposal: Classify and treat POTS, ME/CFS, and Long COVID as neuroimmune disorders under the subspecialty of neuroimmunology. This shift would: • Improve clinical care • Accelerate research • Enable effective neurotherapeutics (including repurposed immunomodulatory and anti-inflammatory treatments) Thanks, Dysautonomia Clinic, for the awesome paper! #MECFS #POTS #LONGCOVID #PASC Read more here: buff.ly/HqR7NKH

We’re a primary care practice in Vermont. We implemented a practice-wide protocol screening every patient at every encounter for recent SARS-CoV-2 infection history. What we’re observing in our panel is not consistent with a psychosomatic framework. We’re seeing measurable, objective increases in new-onset hypertension, acute cardiovascular events, new-onset allergic disease, and new-onset type 2 diabetes mellitus, all temporally correlated with infection history. These are not symptom reports. These are clinical findings.

Dr. Bramante for the win again 🎉 Less long covid with Metformin tx. Study of 3k people who had covid in 2023 and 2024. Metformin for 14 days vs placebo. Clinician dx’d long covid at 6 Months = 0.56% vs 1.17%. 🔔 so, 1️⃣there is less new long covid overall in 2023 vs earlier ~2020 (viruses tend to get more contagious and less host disruption as they evolve) 🔔 2️⃣14 days of metformin still protective. (Metformin helps clear virus faster, decreases innate immune driven inflammation). Metformin decreases Mtor via ampk increase. Sarscov2 increases Mtor.

One of the concerning framings of the Levinovitz WIRED article is the deep lack of understanding about PEM (& outing a professor in the process)! Dr Elke Hausmann (retired GP & with lived experience) addresses this brilliantly in her article. longcovidadvoc.com/post/comm…

Worth reading: x.com/i/status/2062098595042…

Microplastic increase inflammatory surface receptors, such as TLR4. Same Mechanism is also called out in many of the post infective conditions. 🔔Each expected to increase the impact of the other. Example reference… sciencedirect.com/science/ar……

Real care. Real improvement. And takes Real time.

Takes a few minutes to read. Worth the investment in time and thought. Long Covid (and MECFS and Long Lyme and …) are conditions our current system of care were not designed to identify and treat. But these conditions impact millions and also millions more who are impacted without realizing it.

Another study where long COVID does not look like a small residual problem after infection, but like broad chronic illness scattered across everyday medicine. And that is exactly why the system often fails to see it🧵

A Spanish multicentre cohort study followed patients for up to 5 years after SARS-CoV-2 infection. At the 1-2 year follow-up, 56% of participants reported at least one persistent symptom. The prevalence was similar in hospitalized and non-hospitalized patients, 57.6% vs 53.0%. The key finding comes from the 5 year follow-up. 14.3% of the entire cohort sought medical care for symptoms compatible with a post-COVID condition. Despite this, a formal diagnosis of long COVID was recorded in the medical records of only 3.4% of the whole cohort. The study shows a clear gap between the number of people with persistent symptoms or post-COVID compatible healthcare needs and the number of cases formally documented as long COVID. The healthcare system often fails to recognize these symptoms, link them to prior infection, or code them as long COVID. And this is not a trivial burden for the healthcare system. It may be dispersed across ordinary clinical encounters, without being recognized. An additional 15% of people seeking care years after infection has the potential to create a long-term, difficult-to-absorb burden for the healthcare system. @adamvojtech86 An exceptional performance @szupraha @vlvalek @ZdravkoOnline

Looking for root causes to fix = better, sustainable care. Amy shares a study looking at chronic pain not just as a symptom to treat, but also as a marker of “out of wack” nerve-immune system coordination (signaling). @remissionbiome

‼️ This needed to be stated on record: autonomic dysfunction (aka #dysautonomia) is a key feature of h #EDS and other complex disorders with chronic fatigue. ‼️ sciencedirect.com/science/ar…

This echoes my own research, and my data shows the same cascade is observed in ME/CFS, LC, PVS and a wide range of progressive diseases - in some cases differentiated by localisation of pathogens in different tissues. It’s one of the reasons I’ve also suggested this is a form / mimic of “advanced aging”, albeit with some differences. bornfree.life/ One of the key intersections is methylation-glutathione-oxPPP. It dysregulates mitochondrial function and glycogen homeostasis, leading to progressive loss of parasympathetic metabolism and creating a compensatory sympathetic bias. A chronic inflammatory spiral leads to progressive mineral deficiencies and heavy metals accumulation, further dysregulating important systems, eg. immune, thyroid, hepatic gluconeogenesis and more. The microbiome appears to attempt for sympathetic excess by fermentation -> acetaldehyde, which triggers endogenous opioid synthesis, also seen in Parkinson’s disease, etc. This can become maladaptive and exacerbate barrier dysfunction, neurotransmitters and energy metabolism. A number of cycles are created. We can already measure and visualise all of this directly, in very high detail, using readily available lab testing. bornfree.life/learn/metaboli… If you’d like to learn more about this disease model, here’s a hot-off-the-press deep-dive into some of these key mechanisms and tools from a recent clinician training session: youtu.be/NlUh4ukMsNY

👏🏻🎯🙏🏻 “These patients deserve more than a physician who fits them into the margins of an already full week. They deserve a field.” Dr. Danilo Buonsenso is head of the Unit of Pediatric Infectious Diseases at Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome #LongCOVID

1.5 yrs ago - 🔔study (red in pics of mice below) proved S1 spike sets up throughout the body and can park for a long time in the skull, meninges and other locations. Vs. flu virus that does not do that. 🔔A different study showed S1 spike (3 spikes together) fit the toll like 4 receptor and increase innate immune inflammatory activity.

MIT researchers studying 8 COVID-19 decedents used a new imaging method to reveal nanoscale SARS-CoV-2 spike proteins clustering with amyloid in the brain, alongside signs of neuroinflammation linked to Alzheimer’s related pathways. biorxiv.org/content/10.64898…

Healthcare administration costs should never exceed patient care costs.

#MECFSis patients advocating for each other. #MillionsMissing

Congratulations and thank you to @DaniBeckman - helping / leading the way to see and understand the human brain. 👏👏👏👏👍☀️🙏 @renegaderesearch @PutrinoLab

Tissue-specific autoantibody signatures reveal immune alterations undetected by routine serology in long COVID 🚨83% of long COVID patients have rogue autoantibodies attacking their own heart, lungs & blood vessels, and every standard blood test misses it completely. VERY INTERESTING! ➡️In a UNIQUE Hungarian cohort of 114 long COVID patients versus 36 pre-pandemic controls, tissue-specific Western blotting detected autoantibodies in 83% of cases, with strong cardiovascular dominance, ➡️Vascular autoreactivity was markedly higher in long COVID (34% vs. 8%, p<0.05), cardiac (54%) and pulmonary (34%) signals trended elevated but did not reach significance( cohort size?), ➡️Autoantibodies were predominantly IgM-skewed, polyreactive (up to 8 bands per patient), and persisted longitudinally (mean 141 days), with new isotypes emerging over time, ➡️Standard ANA testing showed no group differences and zero clinical correlations, rendering it useless for detecting these alterations, ➡️Cardiac autoreactivity associated with hypertension and headache, overall autoreactivity correlated with anosmia/ageusia, female sex, CRP, BMI, creatinine, and troponin levels, ➡️The study used human cardiac, pulmonary, and vascular tissue homogenates. ➡️Findings were independent of routine serology and highlight an under-recognized immune component invisible to current diagnostics. ➡️“This persistent, IgM-skewed profile suggests ongoing immune dysregulation and may reflect a previously underrecognized component of the immunological response in long COVID, highlighting the need for targeted immunodiagnostic approaches beyond routine serology.” ‼️Why this is shocking: It proves that in 83% of long COVID patients, the immune system is actively producing autoantibodies that directly target their own heart, lung, and especially blood-vessel tissues, yet every standard blood test (ANA HEp-2) comes back normal. These rogue antibodies are polyreactive, IgM-dominant, persist for months, and keep evolving. They correlate with real symptoms (anosmia, hypertension, headache) and lab markers of damage (troponin, CRP). ‼️In other words: The majority of long COVID sufferers have smouldering, organ-specific autoimmunity that is completely invisible to routine diagnostics. Doctors are flying blind while patients’ tissues are quietly under autoimmune attack. 🤔As far as I know, this is the first direct evidence of hidden, cardiovascular-dominant tissue autoimmunity driving the chronic L0ngC0vid phase! #BookMark #AvoidSars2 #AvoidReinfections link.springer.com/article/10…