9) Link to the paper:
Omdal et al. 2026. Long-COVID: assessment of circulating markers suggests no cerebral neuronal damage, neuroinflammation or systemic inflammation-a controlled study.
8 ) IMHO, this is further evidence that classical inflammatory markers do not seem to drive long-term symptoms in Long Covid, similar to what we have seen in ME/CFS.
Looks like there's some other mechanism at play.
7) This Norwegian cohort was tested a median of 69 weeks (15 months) after infection where the inflammatory markers seem to have largely decreased.
There was also no significant correlations between any inflammatory biomarker and symptom severity.
6) Several other LC studies did find these markers to be increased. This Norwegian teams thinks this is because they were conducted early, a few months after the SARS-CoV-2 infection. So the immune markers might still reflect the infection, organ damage, or viral persistence.
5) "While the magnitude of these changes is insufficient to indicate overt immune activation, they may reflect a chronic, extremely low-level immune activation, that contributes to fatigue, pain, and other sickness symptoms..."
4) They also measured some classical inflammation markers in the blood such as CRP, IL-6, and TNF-alpha. These showed a slight increase that was not statistically significant.
3) All these markers were measured using the ultrasensitive NULISA technology but showed no significant difference compared to the control group. The authors interpretation is that there's unlikely to be neural damage or neuro-inflammation in LC.
2) Here's what they measured:
- Neurofilament light (NfL): a marker for neuronal damage
- Glial fibrillary acidic protein (GFAP): an indicator for astrocyte-driven immune activation
- TREM2: a receptor on immune cells including those in the brain
1) "The absence of neuroinflammation markers is consistent with the hypothesis that persistent long-COVID symptoms are unlikely due to ongoing neuronal injury or central nervous system inflammation"
From a Norwegian study that tested 48 LC patients.
Image of Bluesky account of ME/CFS Science
Changed our handle to mecfsscience.org, which is the domain name for our website.
(previous handle was mecfsskeptic.bsky.social)
But as Simon said there's no reason to think that the 68% is due to some special placebo effect. It might largely be due to the natural course of the illness, regression to the mean, and response bias.
Thanks but I think in this case the image doesn't add much info that isn't already in the summary thread.
10) Link to the paper:
Fricke et al. 2026. ACHTSAM study protocol: outreach diagnostics and assessment of tolerability in severe ME/CFS -a pilot study.
9) A staged assessment protocol with rest periods and the option to pause/terminate procedures is used to minimise the risk of PEM during data collection.
The goal is to determine which procedures and measurements work in severe ME/CFS to inform future studies
8 ) The study is called ACHTSAM and takes place at the university of Freiburg. Recruitment began in September 2025 and is expected to be completed by the end of April 2026.
It's not clear to me if they will do all tests on each participant or only a subgroup of them.
7) Subjective perceived exertion is assessed after each procedure, allowing systematic characterisation of individual tolerability limits to inform future study protocols.
The study will also check if tests in supine position are better tolerated than seated/standing tests.
6)
- Near-infrared spectroscopy of muscle tissue (to check oxygenation and blood flow)
- Handgrip strength
- Standing test for orthostatic intolerance
- Assessment of endothelial function
5)
- LightMove 4 Activity Sensor (tracks sleep quality, physical activity, sunlight exposure, etc.)
- Diaphragm ultrasound
- Assessment of body composition
- Blood samples
- Saliva samples
4) The full lists of measurements that they plan to test:
- Resting electrocardiogram (ECG)
- Heart rate variability (HRV)
- Pupillography (gives an indication of daytime sleepiness)
- Cognitive assessments of attention and memory
- Osteosonography (bone mineral density)
3) They also note that home-based testing could lead to more reliable measurements: "Home-based assessments may reduce noise from clinic-induced stress, providing more ecologically valid data."
2) The authors argue that this is urgently needed because these patients are often excluded from research:
"A central limitation of the current body of research is the insufficient inclusion of patients with severe and very severe ME/CFS into clinical studies."
1) 🇩🇪 This German study will test the feasibility of home-based diagnostics in patients with severe and very severe ME/CFS (Bell score < 30).
They plan to take blood and saliva samples, questionnaires and measurements such as ECG, ultrasound, pupillary responses, HRV, etc.
8 ) Link to the paper (open-access):
Lim et al. Neither Metformin nor Ursodeoxycholic Acid Effectively Treats Postacute Sequelae of COVID19: A Randomized Clinical Trial.
www.acpjournals.org/...
7) In our view, however, the differences in cytokine levels look rather modest (see image below).
Regarding the high recovery rates, the authors argue that this might be due to their cohort being mostly young adults with mild Long Covid.
6) Although there was no difference in cytokines between groups, the study found correlations between changes in cytokine levels and improvements in symptoms. According to the authors this "strongly support the role of immune dysregulation in the pathophysiology of long COVID."
5) Not sure if that's a good definition of recovery though (patients could improve with only 1 point, from 12 to 11 and be recovered?). It might therefore be more useful to look at the change in mean PASC score.
These clearly show that all 3 groups improved similarly.
4) The main outcome was a questionnaire called the PASC index. The authors defined recovery as a PASC score improved from 12 or higher to less than 12.
They expected a recovery rate around 15% but even in the placebo group it was 68%.
3) This was quite a large trial with 396 patients (132 in each treatment group) recruited from two tertiary hospitals. Patients were screened 180 to 730 days after their infection which was confirmed by PCR or antigen testing.
2) Both drugs are suspected to have immunomodulatory and antiviral effect. Studies also showed that taking metformin during the acute phase of COVID-19 can reduce the risk of long COVID.
1) 🇰🇷 A study from South-Korea shows that Metformin (the diabetes drug) and Ursodeoxycholic Acid (a bile acid) are not effective in Long Covid.
Most patients improved at lot, even those in the placebo group.
