Eats shoots and leaves, not necessarily in that order || Filmmaker/DP/Videographer from Hong Kong || Appalled by our response to Covid-19 & climate change
Joined June 2011
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Yuling Chow retweeted
'If the worst comes to pass, the Trump Administration has gone out of its way so that the country—and the rest of the world—will be vulnerable to the virus'.
Excellent overview of where we are with H5N1.
We are giving this beast too much room.
Humans Might Have a Serious Bird Flu Problem on Their Hands popularmechanics.com/science…
Yuling Chow retweeted
This is absolute insanity.
They're planning to delete the electronic info collected on 36,000 Long COVID patients over the past years.
That means it won't be possible to use it for research, or to follow with patients later wrt health outcomes after specific treatments.
"Donderdag komen partijen opnieuw bij elkaar, een dag voordat wordt begonnen met de vernietiging van de dossiers."
Sla #PAIS data op, zoek ondertussen een oplossing @MinVWS
Dit is onomkeerbaar, stelletje klunzen.
En anders een kort geding? @NMCB_studie
volkskrant.nl/wetenschap/ver…
Yuling Chow retweeted
The new German guideline for Long Covid is out.
Given the medico-political landscape there, I'm impressed with its references and nuance.
I'm very thankful to those who've sacrificed their energy, political capital and even health to get this through.
register.awmf.org/de/leitlin…
Yuling Chow retweeted
Country music legend Willie Nelson, 93, reveals he nearly died from COVID in 2022. He struggled to breathe and felt powerless. Paxlovid didn't seem to help much. His wife Annie, who had prepared months ahead, arranged monoclonal antibody treatment that may have saved his life.
ALT Screenshot of a New York Daily News article titled “Willie Nelson was ready to die from Covid, but his wife said no.” • Headline refers to country music legend Willie Nelson's serious COVID-19 illness in 2022. • Main photograph shows Willie Nelson smiling, wearing a brown cowboy hat and black T-shirt, pointing towards a crowd. • His wife, Annie D'Angelo, stands beside him wearing sunglasses, a black face mask and black clothing. • Several masked people are visible around them. • Photo taken at a voting rights rally at the Texas State Capitol in Austin on July 31, 2021. • Article written by Brian Niemietz. • Published November 10, 2026, at 6:40 PM EST. • Photo credit: Suzanne Cordeiro/AFP via Getty Images. • Source: New York Daily News.
Yuling Chow retweeted
Patients with hypermobile Ehlers-Danlos syndrome (hEDS) face nearly 3x the risk of developing Long COVID, according to a major U.S. nationwide study of 19+ million health records.
Despite similar COVID infection rates, the elevated risk of developing Long COVID was heavily concentrated in hEDS patients who were also diagnosed with:
- POTS
- MCAS
- ME/CFS
The study also found hEDS is far more common than previously thought (~1 in 800 people).
Better screening, earlier diagnosis, and integrated care are urgently needed for this underdiagnosed group.
#hEDS #LongCOVID #POTS #MCAS #EhlersDanlos
Read more: buff.ly/SphJNeW
Yuling Chow retweeted
This new study is particularly interesting because it connects with something I’ve been reflecting on recently.
What if people with Long COVID and ME/CFS have a persistently altered inflammatory baseline?
The fact that immune biomarkers don’t correlate with symptom severity doesn’t necessarily mean these alterations are irrelevant. Perhaps measuring inflammation at a single point in time isn’t enough.
What if the key lies in how an already activated immune system responds to additional stimuli, and what happens when that response subsides?
In my recent Substack article, I explored this possibility by drawing parallels with autoinflammatory diseases such as familial Mediterranean fever.
My hypothesis is that persistent immune activation could make relatively small triggers more likely to cause severe exacerbations. And when the flare ends, patients may simply return to their chronically altered inflammatory baseline rather than normal physiological homeostasis.
Perhaps we need to study not only baseline inflammation, but also how immune activity changes before, during, and after symptom flares.
I explore this idea in more detail here:
manruipa.substack.com/p/are-…
Long-COVID: Ultrasensitive multiplex protein biomarker profiling reveals subclinical neuroinflammatory and innate immune dysregulation without correlation to symptom severity
🚨LongC0VID patients show a hidden cytokine-storm + neuroinflammation signature that only ULTRA-SENSITIVE PROTEOMICS can detect. Yet the biology doesn’t match how sick they feel. The real driver may be central sensitisation or brain rewiring.🤔
➡️Very interesting small Norwegian study, bear with me!
- Routine labs are normal in longC0VID, yet patients have persistent fatigue, cognitive issues, depression, and other symptoms more than a year after infection.
- In this matched case-control study (48 longC0VID patients vs 48 fully recovered controls, median ~65–72 weeks post-infection), ultrasensitive NULISAseq proteomics (123 CNS/immune biomarkers at attomolar sensitivity) detected clear biological differences invisible to standard tests.
- 19 proteins were significantly dysregulated; top upregulated markers included CCL22, IL-6R and CST3. Pathway analysis showed activated Pathogen-Induced Cytokine Storm, Neuroinflammation, and IL-10 signalling pathways, pointing to low-grade innate immune activation and neuroinflammatory signals.
- Hierarchical clustering split longC0VID patients into two biological subgroups (one dominated by metabolic reprogramming/mitochondrial dysfunction and cytokine-storm features, the other by neuroinflammation and related signalling).
- Critically, neither the protein levels nor the biological clusters correlated with symptom severity, fatigue, depression, cognitive scores, or any patient-reported outcomes. Conventional PCA also showed no clear patient-control separation.
- The study does not examine reinfection or vaccination status. It simply compares people with ongoing longC0VID symptoms versus people who fully recovered, both more than one year after documented SARSCoV2 infection.
➡️The authors conclude that subclinical immune/neuroinflammatory dysregulation is present but does not map directly onto how sick patients feel, implying additional mechanisms (central sensitisation, epigenetic changes or similar) convert peripheral signals into the clinical picture.
‼️So, according to these authors, LongC0VID harbours a real but hidden biological footprint of innate immune activation and neuroinflammation that standard medicine cannot see and that does not match the intensity of patients’ symptoms, pointing to brain-level amplification mechanisms as the missing link.
‼️Important take-away:
1. For the millions still living with longC0VID, this matters because it shows why ordinary blood tests are repeatedly “normal” while people remain disabled. It validates that low-level immune and neuroinflammatory changes can persist >1 year and explains the frustrating mismatch between lab results and lived experience. Clinically it argues against relying solely on symptom scores or standard inflammatory markers for diagnosis or trial endpoints, and it supports research into treatments that address both residual immune signalling and central sensitisation/pain-processing pathways. It also reinforces that longC0VID is heterogeneous at the molecular level even when symptoms look similar.
2. Finally, this study doesn’t contradict earlier ultrasensitive findings, actually, it confirms and extends them. The attomolar view of longC0VID as a state of low-grade, heterogeneous innate immune and neuroinflammatory dysregulation that is largely invisible to routine labs and poorly linked to symptom intensity is holding up across platforms and other cohorts.
We’re getting somewhere!
#AvoidSars2 #AvoidReinfection
nature.com/articles/s41598-0…
Yuling Chow retweeted
The pandemic is managed according to healthcare capacity. As long as there is still room in the ICU for more critically ill COVID patients, governments and public health institutions see no problem. The dead and the permanently disabled are no longer a problem.
Yuling Chow retweeted
It’s fair to say the so-called flatten the curve strategy had a crushing effect on how governments and the public see public health and healthcare.
I wrote this thread in 2023, based on a John Snow Project paper. Nothing at all has changed since then, so it's worth publishing again. Retro🧵
Yuling Chow retweeted
Four months on, this important paper is peer reviewed, out in Frontiers in Immunology.
Only one correction - the fibrosis difference between mice with and without human immune cells didn’t reach significance. The direction holds.
Yuling Chow retweeted
The people have spoken. A new UK Grassroots ME Activism Discord has been created to plan the protest and future advocacy:
discord.gg/8MmNMCum8G
If you have any of the following, join the cause and help make history in the UK:
- Connections to politicians
- Journalism experience and media contacts
- Previous protest and activism experience
- Event organizing experience
- Leadership skills
- Project management
- Design and branding
- Ability to reach large audiences of patients
People in the UK with Long COVID and ME:
Where @BethDobbin is bringing the smoke, let there be fire:
Now is the perfect time to arrange an in-person protest to show Downing Street the visual of how many people are affected by this illness, and also bringing attention to the current mistreatment of Savannah Victoria-May at Queen Elizabeth Hospital.
Needed to lead the organization are 2-3 patients and the same number of healthy (or mild) people committing just 4-6 hours a week.
Organizers in the Netherlands just pulled off a successful protest vigil, leading to numerous news stories, talk show program discussions, and finally forcing parliament's hand to pass a motion for action.
I have confirmed with the Dutch organizers that they are willing to consult and share their entire playbook.
The template is there. The moment is ripe. The next step is for willing organizers to take the lead.
Please DM me or reply if you have any interest in capitalizing on this historic moment (even if you're unsure - we can talk through it!) I will connect all those interested and we can let structure emerge organically.
For those that don't have the capacity, you can greatly help by spreading the word or connecting me with people that may be interested in organizing.
Yuling Chow retweeted
Some incredible science coming out of the Long COVID conference in France this week.
Viral persistence, autoimmunity, immune dysregulation, biomarkers, and clinical trials.
It’s crazy how far this field has come in just five years.
academicmedicaleducation.com…
Yuling Chow retweeted
Millions of chronically ill patients have been living for decades with persistent infections that no one is looking for.
Chronic fatigue. Unexplained pain and stiffness. Brain fog. Shortness of breath. Palpitations. Disability.
The official position remains stuck on a simplistic formula:
👉 “acute infection + short course of antibiotics = cure.”
But the biological evidence shows a different reality:
🔬 Active DNA and RNA in tissues
🔬 Biofilms that protect the microbes
🔬 Persistent forms of Bartonella, Babesia and Borrelia (the “3 Bs”) and other co-infections
…that do not respond to short-course monotherapy.
Studies that repeatedly investigate symptoms and other consequences in the body are preferentially funded, while research aimed at eradicating the root cause is blocked.
The result: patients who remain ill for decades without an etiological diagnosis, labeled as “somatization,” chronic fatigue syndrome (ME/CFS), fibromyalgia, multiple sclerosis, stiff-person syndrome, or psychiatric disorders… while combination protocols already used in clinical practice (such as those of Dr. Horowitz and other leading physicians) wait for a formal evaluation that never arrives.
In Australia the situation has reached extremes. To the denial of persistent infections has been added the defunding of etiological research and a deterrent effect on physicians, so that many have chosen to avoid diagnosing these infections or to treat them in silence. The price: thousands of patients without access to treatments directed at the cause.
This is no longer just a scientific debate.
It is a bioethical failure that prolongs the suffering of millions.
We have published several papers on this topic:
🔗 researchgate.net/publication…
researchgate.net/publication…
researchgate.net/publication…
researchgate.net/publication…
researchgate.net/publication…
🤖 Made with AI
Yuling Chow retweeted
CFS/ME, fibromyalgia, long COVID, dysautonomia/POTS and MCAS all share similar pathologies because of the interactions between the nervous, lymphatic, circulatory, respiratory, digestive, and immune systems.
The major symptoms in these conditions are nerve and immune related (eg., chronic pain, immune flares, insomnia/wired-but-tired, brain fog, migraines, etc.) which ties into the deep effects the neuro-immune system/loop can drive.
The immune system has very various triggers (DAMPs, PAMPs) that act on receptors in every tissue to drive a pro-inflammatory environment (IL-6, TNF-a etc.). Once inflammation hits the brain due to BBB disruption, microglia will hyperactivate and become hypersensitive.
If we cannot clear toxins, wastes, and debris from the brain, then they pool within the ISF and further drive microglial priming to further create a self-perpetuating loop of chronic neuroinflammation, mitochondrial dysfunction, and glymphatic impairment.
The digestive system has major influence on this due to its deep bidirectoinal relationship with the nervous system through the vagus nerve, enteric nervous system, gut microbial metabolites, and immune control via the GALT.
The circulatory and respiratory system both influence the nervous and glymphatic system. If there's a lack of cerebral blood flow or lower respiratory rhythms, brain detoxification is halted and toxins accumulate causing chronic neuroinflammation.
All of these systems feed into one another, where one system starts to fail, then the others collapse. An example is that gut dysbiosis/infections and leaky gut drive pro-inflammatory shifts in the immune system which then causes the BBB to become leaky and then cytokines inhibit the glymphatic system which is tied to brain detoxification. One of the most underlooked factors around these diseases is the brain's detoxification system.
The opening of the BBB is an attempt to clear the perceived threat. Whilst also allowing a large amount of peripheral immune cells to house themselves within the brain in an attempt to restore homeostasis.
Sadly, severe health conditions such as chronic fatigue syndrome, fibromyalgia, long COVID, dysautonomia/POTS, gut dysbiosis, and mast cell activation are now more common than ever. They are all branches of the same tree. Whilst each branch is able to feed into one another and further manifest symptoms.
One of the deepest biochemical layers of this pathology is through the inability of the nervous system (and also the peripheral body) to clear protein aggregates through the brain's glymphatic detoxification system and autophagy. I'll outline the details and the interventions below to aid in resolution.
The brain is 2% body weight and uses 20% of the body's energy. Neurons are extremely rich in mitochondria. Neurons can't divide either, so they rely deeply on autophagy to clear damaged mitochondria and misfolded proteins.
Autophagy = intracellular clearance
Glymphatic system = extracellular clearance
2 exit routes. Both are important and they act as a cooperative network.
Essentially, what happens in a healthy system:
> neuronal activity during the day generates waste (eg., misfolded proteins, lactate, glutamate)
> waste must be cleared by 2 major systems: glymphatic system and autophagy
> the biochemical and physiological levers that optimize these systems prevents protein aggregation and misfolding are deep sleep, fasting, movement, meditation, optimal breathing, healthy posture, dietary/nutrient factors, supporting inflammation, and more.
In an unhealthy system:
> neuronal activity during the day leads to accumulation of waste
> glymphatic system and autophagy are no longer active due to various factors (below)
> protein aggregates, metabolic wastes, and toxins act like a wrecking ball to cell membranes, signalling and proteins, organelles, and mitochondrial function
> poor cerebral blood flow, high blood pressure, heightened neuroinflammation, mitochondrial dysfunction, mast cell activation, demyelination, endothelial/BBB disruption/leaky gut, irregular nerve impulses, hypoxia, lactic acidosis, and platelet hyperactivation can all occur; all found to some degree in the conditions above.
> these all act to continue to influence each other in a continuous web of positive feedback loops, amplifying disease.
This is what further inhibits the clearance processes or generates more protein misfolding:
- gut endotoxins (eg., LPS, LTA)
- low magnesium-ATP (cofactor for HSP70 + HSP90)
- dysregulated meal timing
- low melatonin (key for regulating LLPS alongside Mg-ATP)
- free radicals (ROS, RNS)
- viral antigens such as EBV, CMV, spike protein (from SARS-CoV-2)
- pro-inflammatory cytokines (eg., IL-1B, TNF-a)
- hyperammonemia (due to impaired mitochondrial function)
- protein aggregates themselves, acting in a positive feedback loop via "cross-seeding" prions
- environmental toxins (eg., phthalates, VOCs, heavy metals, etc.)
Protein aggregates can be super nasty. They can be found in their "prion" form, which stands for "proteinaceous infectious particle." They are incredibly resistant to degradation (due to their rigid beta-sheets, tied to their different hydrogen bonding in comparison to healthy-formed alpha helix proteins) and can further reinforce protein aggregation, inhibit autophagy and glymphatic detoxification.
You will find low neutrophils + WBCs on blood work as a major clue that this pathology may be happening if symptoms reflect it (anecdotally, I've seen this, won't always be this rule as blood work is limiting). If you see a trend with high levels of these trending downwards whilst symptoms are not improving and may be getting worse, even more so.
Here are some interventions to support with the process:
- sunlight exposure throughout phases of the day with huge emphasis of darkness at night, mitigating both nnEMFs and artificial blue light to best of your ability to enhance deep sleep/SWS.
- to further enhance deep sleep explore mouth taping, nasal strips, organic bed sheets/pillow cases, multiform magnesium, herbal teas (eg., chamomile, lavender, valerian, licorice root, tulsi, passionflower, skullcap) 1/2 tsp of baking soda (esp. if you have apnea), and a high-quality lavender spray for your pillow
- all the B vitamins, CoQ10, electrolytes, iron, copper, sulfur are needed for mitochondrial respiration; whilst vitamin C, E, glutathione, selenium, and manganese are involved in dealing with excess oxidative stress.
- tryptophan, B1, B2, B3, B5, B6, B9, B12, iron, vitamin C, and a methyl group from either methionine/choline is required to make melatonin.
- elimination diet framework + digestive aid support to deal with microbiome dysbiosis.
- support inflammation through specific herbs and supplementation catered to your specifics, but a few to name are black seed oil, frankinscense, ginger, taurine, palmitoylethanolamide, turmeric, triphala.
- support cerebral blood flow and neuroinflammation with some of the above, alongside brahmi/bacopa, gotu kola, ginkgo biloba, ashwaghanda, cordyceps (which also helps boost WBCs)
- medicinal mushrooms, astragalus, vitamin C, dietary copper, lactoferrin, dark chocolate, dessicated thymus, zinc are all immunostimulants for boosting WBCs
- whilst nutrients to support immune response are vitamin A/C/D/E, B1, B2, B3, B6, B9, B12, omega 3/6, iron, iodine, magnesium, arginine, zinc, copper, selenium, glycine, cysteine, glutamine, glutamate, and chloride.
- I'm mentioning a LOT of nutrients so this just reinforces that Cronometer nutrient tracking should be as close to perfect as possible without the stress and perfectionism that can be attached to it.
- ayurveda morning routine encompassing neti pot, tongue scraping, tooth brushing, facial/lymphatic massages, pranayama, and meditation.
- qigong is best suitable for exercise intolerance which further supports lymphatics, movement, meditation, and breath
- boosting AMPK (and adjacent pathways such as PINK1/Parkin, SIRT1, etc.) through fasting, exercise, mild heat/cold therapies (if tolerated), and herbs such as japanese knotweed, turmeric, ginseng, goldenseal/berberine, black seed oil, butyrate, sichuan pepper, ACV, jiaogulan.
- if there's emotional trauma, this can further manifest as physiological dysfunctions within the body and must be addressed through either of the eastern or western modalities.
- for further information around lymphatic support, read this one: teapaw.org/jack_schroder_/status/…
I'm not expecting you to do all of this as each individual is different in terms of their requirements. I'm just sharing everything. This is incredibly important for those with hypersensitivity.
For further readings:
- if MCAS issues refer to my post here: teapaw.org/jack_schroder_/status/…
- if gut issues refer to my post here: teapaw.org/jack_schroder_/status/…
- more on glymphatic system: teapaw.org/jack_schroder_/status/…
- even more on glymphatic system: teapaw.org/jack_schroder_/status/…
- more on immune dysregulation/supression: teapaw.org/jack_schroder_/status/…
Yuling Chow retweeted
Scientists found a way to flush Alzheimer’s plaque out of the brain in minutes.
Without any surgery and drugs.
Your brain has a waste-clearance network called the glymphatic system. It flushes out toxic proteins and dead cells.
But it only really activates during deep, slow-wave sleep.
If you don't sleep, the trash piles up. Over time, that buildup leads to cognitive decline and Alzheimer's.
Until today.
Researchers just published a paper proving they can manually trigger this cleaning cycle.
Without you ever going to sleep.
They used 40.68 MHz ultrashort waves (USW) beamed non-invasively into the brain.
Within 10 minutes, the brain's fluid flow rapidly accelerated.
The waves artificially synchronized the neurons into a Delta state, the exact frequency of deep sleep. This forced the brain's water channels to open and start flushing out the system.
They tested it on mice with traumatic brain injuries and Alzheimer's pathology.
The brain swelling dropped. The toxic proteins were cleared out. Cognitive deficits actually improved.
No surgery. No massive chemical interventions. Just a frequency.
Yuling Chow retweeted
Long-COVID: Ultrasensitive multiplex protein biomarker profiling reveals subclinical neuroinflammatory and innate immune dysregulation without correlation to symptom severity
🚨LongC0VID patients show a hidden cytokine-storm + neuroinflammation signature that only ULTRA-SENSITIVE PROTEOMICS can detect. Yet the biology doesn’t match how sick they feel. The real driver may be central sensitisation or brain rewiring.🤔
➡️Very interesting small Norwegian study, bear with me!
- Routine labs are normal in longC0VID, yet patients have persistent fatigue, cognitive issues, depression, and other symptoms more than a year after infection.
- In this matched case-control study (48 longC0VID patients vs 48 fully recovered controls, median ~65–72 weeks post-infection), ultrasensitive NULISAseq proteomics (123 CNS/immune biomarkers at attomolar sensitivity) detected clear biological differences invisible to standard tests.
- 19 proteins were significantly dysregulated; top upregulated markers included CCL22, IL-6R and CST3. Pathway analysis showed activated Pathogen-Induced Cytokine Storm, Neuroinflammation, and IL-10 signalling pathways, pointing to low-grade innate immune activation and neuroinflammatory signals.
- Hierarchical clustering split longC0VID patients into two biological subgroups (one dominated by metabolic reprogramming/mitochondrial dysfunction and cytokine-storm features, the other by neuroinflammation and related signalling).
- Critically, neither the protein levels nor the biological clusters correlated with symptom severity, fatigue, depression, cognitive scores, or any patient-reported outcomes. Conventional PCA also showed no clear patient-control separation.
- The study does not examine reinfection or vaccination status. It simply compares people with ongoing longC0VID symptoms versus people who fully recovered, both more than one year after documented SARSCoV2 infection.
➡️The authors conclude that subclinical immune/neuroinflammatory dysregulation is present but does not map directly onto how sick patients feel, implying additional mechanisms (central sensitisation, epigenetic changes or similar) convert peripheral signals into the clinical picture.
‼️So, according to these authors, LongC0VID harbours a real but hidden biological footprint of innate immune activation and neuroinflammation that standard medicine cannot see and that does not match the intensity of patients’ symptoms, pointing to brain-level amplification mechanisms as the missing link.
‼️Important take-away:
1. For the millions still living with longC0VID, this matters because it shows why ordinary blood tests are repeatedly “normal” while people remain disabled. It validates that low-level immune and neuroinflammatory changes can persist >1 year and explains the frustrating mismatch between lab results and lived experience. Clinically it argues against relying solely on symptom scores or standard inflammatory markers for diagnosis or trial endpoints, and it supports research into treatments that address both residual immune signalling and central sensitisation/pain-processing pathways. It also reinforces that longC0VID is heterogeneous at the molecular level even when symptoms look similar.
2. Finally, this study doesn’t contradict earlier ultrasensitive findings, actually, it confirms and extends them. The attomolar view of longC0VID as a state of low-grade, heterogeneous innate immune and neuroinflammatory dysregulation that is largely invisible to routine labs and poorly linked to symptom intensity is holding up across platforms and other cohorts.
We’re getting somewhere!
#AvoidSars2 #AvoidReinfection
nature.com/articles/s41598-0…
Yuling Chow retweeted
H5N1 bird flu is at pandemic alert phase 3.
Increasing reports of avian and mammalian outbreaks from US 🇺🇸 to UK 🇬🇧.
⚠️H5N1 Bird Flu.
A Pandemic timeline 🇺🇸 :
✴️Birds: Largest modern outbreak. 2300 flocks & 212M birds since Feb 2022. Still active in 2026.
✴️Cattle: Unprecedented. 1230 herds across 22 states since Mar 2024 (B3.13), recent spread in WA & first case in IN.
✴️Mammals: 800+ detections. Utah mink farm outbreak (Aug 2026, same cattle lineage) still ongoing — no mandatory cull which is playing with fire.
✴️Humans: Dozens of cases. First 2026 death in WA linked to dairy exposure.
✴️Seasonal flu: H1N1 arrived unusually early (rising since Aug). Higher activity than normal.
✴️Sustained H5N1 in birds, cattle & mink + early seasonal H1N1 raises the risk of a recombinant, human-adapted virus. Gaps in control (especially mink) keep the risk elevated.
teapaw.org/richardhirschs1/status…
Yuling Chow retweeted
Schools: When the CO2 level exceeds 1000 ppm, the risk of Covid transmission nearly doubles
Eine Schweizer Studie hat gezeigt, dass die wichtigste Ursache für virale Ansteckung in Schulen nicht enger Kontakt ist, sondern schlechte Belüftung. Liegt der CO2-Wert über 1000 ppm (schnell erreicht), verdoppelt sich das Ansteckungsrisiko beinahe. 4/ nature.com/articles/s41467-0…
Yuling Chow retweeted
An important new study in @PLOS Digital Health of nearly 20 million patient records suggests hEDS may be substantially more common than previously recognized and is associated with nearly threefold higher odds of a Long COVID diagnosis.
This intersects directly with a central question we're investigating through CODA Craniocervical Dysfunction Initiative (CODA CCD): Is hypermobility a preexisting vulnerability, an additional consequence of disease, or something more complicated?
Could immune dysfunction contribute to acquired changes in connective tissue, or make existing hypermobility more pronounced? Could infection trigger a process in which inflammation, connective tissue abnormalities, and autonomic and vascular dysfunction reinforce one another?
@ImmunoFever @FranCarrilloPhD
journals.plos.org/digitalhea…
Yuling Chow retweeted
This is related to the cranial cervical instability we are considering remediating with surgery for Soren
nytimes.com/2026/11/09/well/…
Yuling Chow retweeted
👏👏Sjogrens is a serious multisystem disease not a mild dryness Syndrome
It doesn’t start with sicca and “progress”to systemic. Time for better data. Dump the dogma!
