u/Caster_of_spells

“Conclusions

Tailored exercise did not outperform standard care in HRQoL and was associated with reduced upright time, while improvements in several secondary outcomes were observed in both groups. Heterogeneity supports an individualized approach to exercise, integrated with pharmacological and multimodal management strategies”

Another one we might’ve predicted: A Pots cohort that included many patients exhibiting PEM (measured through DSQ questionnaire) did not respond well to tailored exercise programs. Both objective outcome measures showed significant reductions which makes me very distrustful of their subjective “positive secondary measures” to boot.

Good data point to refer too though from now on I guess

Hannover Medical School, 992 people.

Among those with Long COVID in 2021 who returned in 2024, 77.4% still met criteria about 4 years after infection.

More than 95% were never hospitalized initially

“Dr. Janet Mullington and her team, in collaboration with OMF’s Computational Research Center for Complex Diseases, recently released a paper on their investigation of sleep electroencephalographic (EEG) microstructures—components of sleep data related to brain and body functions that are more granular than the more commonly studied macrostructure (sleep stages).
The team studied these microstructures in the context of non-restorative sleep and daytime fatigue in ME/CFS and Long COVID.

When comparing results from people with Long COVID and ME/CFS to healthy controls, there were differences identified in the sleep EEG microstructures, including slow oscillations (SO), spindle-SO coupling, and within-spindle frequency. These findings show objective, measurable changes in sleep EEG microstructures that are associated with the non-restorative sleep experienced in Long COVID and ME/CFS.”

From the OMF article about the study:
https://www.omf.ngo/sleep-eeg-microstructures-long-covid/

This study found that ME/CFS patients often have too low blood and low red blood cell volume.

But surprisingly, these measures weren't related to orthostatic intolerance as measured by a lean test. This suggest that hypovolemia isn't the main reason for orthostatic problems

Very interesting study about reactivations and connections to long covid / ms/ post exertional Malaise.

'Chronically infecting viruses are prevalent in the general population, with individuals carrying 8–12 viruses at any given time [...] emerging evidence suggests that their reactivation may contribute to autoimmune diseases, malignancies and chronic fatigue syndrome [...]'

He says here he is currently working on getting all the data he’s collected over the past five years on an NIH grant published. 6 papers are in the making. Excited to read them. He seems pretty confident they prove neuroinflammation among ME patients, let’s see!

“The first clinical trial in the series will test the monoclonal antibody Pemgarda, along with the immune-modulating drug hydroxychloroquine. The study will include arms with both drugs by themselves and the two in combination.”

Department of Defense grants always seem comparatively small but they have a good track record of being efficient with their money. It’s the same institution that funded the promising Bezisterim trial we’re waiting for results on. Very much a contrast to Recover imo.

It seems we might be starting to understand how the differences between sexes in Long Covid and acute Covid come about.

This new study found that females developed more persistent neuroinflammation, immune dysregulation and cognitive problems after SARS-CoV-2 clearance, despite showing similar viral replication and persistence as males.

The difference traced back to having two X chromosomes and increased activity of the X-linked TLR7 pathway—and blocking TLR7 during the post-COVID phase reversed the inflammatory and cognitive effects

So that seems like a plausible explanation on why people with two XX chromosomes seem to suffer more and more often from Long Covid while people with XY chromosomes seem more at risk during acute infection.

And excitingly this might pose a possibility for treatment as well.

This is of course an animal model so some caution is still needed. 🐁

“Multiple studies have found an increased response of the hormone prolactin to the drug buspirone in ME/CFS patients. While baseline prolactin levels are normal in ME/CFS, they rise much higher in the hours after buspirone than in controls. This is one of the most replicated findings in the field, but for years this line of research was forgotten and abandoned.”

“It might, for example, point to a difference in the dopamine system in ME/CFS, as this is the main regulator of prolactin. This would be intriguing, as (preliminary) genetic findings point to the striatum and its medium spiny neurons, which are also regulated by dopamine”

For anyone interested in what was discussed at the recent big Amsterdam conference. Recordings of presentations are sadly behind a paywall and posters are unavailable because data is still unpublished. But all abstracts that were handed in beforehand can be found for free here.

Retinal vasculature is like a window into the brain because the eyes and the brain share the same system.

In this study changes were detected that weren’t too different from MS in LC patients.

In PCS, three layers were significantly thinner. pRNFL (nerve fibre layer around the optic disc), GCIP (ganglion cells plus their synaptic layer), TMV (total macular volume). And the worse the symptoms, the thinner the tissue!
Neuroretinal tissue is being lost - and it scales with how sick the person is.

This exact pattern - pRNFL and GCIP thinning - is an established marker of axonal and neuronal loss in multiple sclerosis, where OCT is used as a proxy for what’s happening in the brain

The group around Putrino has successfully completed their first mitochondrial transplant in a patient with vision loss after a brain bleed with the help of other experts in the field.

This should pave the way to trialing mitochondrial transplants in Long Covid and ME which Putrino already has plans on trialing.

“Also, there are so many conditions that can benefit from this work - including other forms of brain injury and neurodegeneration, but also #LongCOVID, #MECFS and other complex chronic illness where energy limitation is a problem. We will be aiming to get an active research arm off the ground on this ASAP.”

Source: https://bsky.app/profile/putrinolab.bsky.social/post/3msqs6xrgkc2i

New brain MRI study which induced hypoxia (too little oxygen) to compare reactions in the brain of patients to controls.

Interestingly lactate levels were already elevated at baseline in patients. Under hypoxia conditions controls started to produce more lactate to match while ME patients levels stayed at the elevated levels they were already at.

Roughly lactate is a byproduct of the less efficient way our system produces energy when oxygen is lacking (though its role in the brain is more complex than just that).

In the German CoCo-Fakt study at Cologne and Ausberg, patients who later developed Long Covid reported doing more and more intense physical activity prior to infection than controls who had COVID-19 but no long term symptoms.

The researchers expected the opposite.

The paper concludes:

"Unexpectedly, participants with long-term symptoms reported a longer PA [physical activity] duration in the four weeks before quarantine than those without long-term symptoms, albeit with a trivial effect size."