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

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)

 

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

But then

Concluding

Yes, definitely. But wait...

Despite

 

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.