Markers of oxidative stress during post-COVID-19 fatigue: a hypothesis-generating, exploratory pilot study on hospital employees, 2023, Hofmann et al.

[SNT Gatchaman]

Markers of oxidative stress during post-COVID-19 fatigue: a hypothesis-generating, exploratory pilot study on hospital employees
Hofmann, Hanna; Önder, Alexandra; Becker, Juliane; Gröger, Michael; Müller, Markus M.; Zink, Fabian; Stein, Barbara; Radermacher, Peter; Waller, Christiane

Introduction
Post-COVID fatigue is common after recovery from COVID-19. Excess formation of reactive oxygen species (ROS) leading to oxidative stress-related mitochondrial dysfunction is referred to as a cause of these chronic fatigue-like symptoms. The present observational pilot study aimed to investigate a possible relation between the course of ROS formation, subsequent oxidative stress and post-COVID fatigue.

Methods
21 post-COVID-19 employees of the General Hospital Nuremberg suffering from fatiguelike symptoms were studied during their first consultation (T1: in average three months after recovery from COVID-19), which comprised an educational talk on post-COVID symptomatology and individualized outpatient strategies to resume normal activity, and 8 weeks thereafter (T2). Fatigue severity was quantified using the Chalder-Fatigue-Scale together with a health survey (Patient-Health-Questionnaire) and self-report on well-being (Short-Form-12 Health-Survey). We measured whole blood superoxide anion (O2• ‾) production rate (electron spin resonance, as a surrogate for ROS production) and oxidative stress-induced DNA strand-breaks (single cell gel electrophoresis: "tail moment" in the "comet assay").

Results
Data is presented as Mean±SD or Median (interquartile range) depending on data distribution, differences between T1 and T2 were tested using a paired Wilcoxon rank sign or t-test. Fatigue intensity decreased from 24±5 at T1 to 18±8 at T2 (p<.05), which coincided with reduced O2• ‾ formation (from 239±55 to 195±59 nmol/sec; p<.05) and attenuated DNA damage (tail moment from 0.67(0.36-1.28) to 0.32(0.23-0.71); p=.05.)

Discussion
Our pilot study shows that post-COVID fatigue coincides with i) enhanced O2 • ‾ formation and oxidative stress, which are ii) reduced with attenuation of fatigue symptoms.

Link | PDF (Frontiers in Medicine)

 

[SNT Gatchaman]

You might read the abstract and wonder why this is in the psychosomatic section. It starts off quite well.

Post-COVID-19 fatigue symptomatology resembles that of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) (8), and substantial overlap has been reported between post-COVID-19 and ME/CFS symptoms (9). Persistent neuroinflammation (10) and brain antioxidant capacity (11), redox imbalance (oxidative stress) (12), and consecutive mitochondrial dysfunction resulting from impaired mitochondrial respiratory activity and/or a reduced number of intact mitochondria (13) have been referred to as a possible link between post-COVID-19 fatigue and ME/CFS.

Given the fundamental role of oxidative stress during the acute phase of a SARS-CoV-2 infection, we aimed to assess a possible relationship between oxidative stress and sequelae in patients who had recovered from the disease.

But then

We collected psychosocial data and analyzed ROS concentration and oxidative DNA damage in blood cells at two different time points prior to and after psychosomatic counseling.

Employees with fatigue symptoms presented at the Department of Psychosomatic Medicine and Psychotherapy between 10 a.m. and 12 p.m. for about half an hour and were always treated by the same physician (C.W.).

The intervention consisted of an educational talk during which the clinician explained the typical symptoms of the post-COVID-19 syndrome and the relationship between both physical and psychosocial stress and symptom amplification in the recovery phase.

Concluding

Our data suggest a connection between oxidative cell stress and post-COVID-19 fatigue. This possible relationship warrants further investigation so that knowledge can be gained about pathophysiological processes (oxidative stress) in the development of fatigue.

Yes, definitely. But wait...

This implies psychosomatic treatment options, e.g., mindfulness-based interventions, that stimulate antioxidative targets through psychological and biomolecular mechanisms.

Despite

The relatively small cohort studied may have precluded more robust, statistically significant results. In addition, due to the observational, exploratory pilot nature of the study, we could not include a control group that did not undergo the educational talk on the typical symptoms of post-COVID19 syndrome or, in particular, the individualized outpatient procedure. Hence, we cannot discriminate between a possible effect of this procedure and a putative time-dependent resolution of the fatigue symptoms and/or the biological findings.

 

[Hutan]

Oh dear.

Nice commentary SNT.

 

[Hutan]

I suppose the only bright side to this is that the cohort was employees from one hospital. And surely some of the participants will understand that it's highly unlikely that it was the wonders of 30 minutes spent with Christiane Waller that was responsible for any real improvement over time?

So, perhaps this study will have informed a few more health professionals about the dross that is psychosomatic studies? And, hopefully, those informed health professionals will be able to support each other, and advocate.

 

[rvallee]

This implies psychosomatic treatment options, e.g., mindfulness-based interventions, that stimulate antioxidative targets through psychological and biomolecular mechanisms.

It's so simple, people, just think away your oxidative stress. Mindful away those reactive oxygen species, duh! You have to think that way. No, not this way, that way!

I really do wonder if the stress in oxidative stress isn't just causing some weird unconscious bias. They know what it means, but somehow just because stress is there, it screws up the whole thinking process.

It's just weird that they mixed this biomedical study with some weird nonsense about explaining symptoms and calling this an intervention. It just shows how there is simply no way the biopsychosocial model will ever achieve anything, it's just bizarre all the way, and kind of a logical conclusion that it would lead to nonsense like mindfully thinking away your oxidative "stress" just because stress is in the biomedical term.

And to think that medicine laughs at stuff like electromagnetic sensitivity, and knowing that infectious diseases causes long-term illness, but gullibly swallows all this stuff. Beliefs are so freaking weird.