Background Identifying symptom clusters in Long COVID is necessary for developing effective therapies for this diverse condition and improvi
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Background Identifying symptom clusters in Long COVID is necessary for developing effective therapies for this diverse condition and improvi
Hi in your post about covid studies you've put that adolescents' risk of diabetes is increased by 584% ik it's meant to say 84%, just letting you know the typo is there.
Yeah I'm afraid that's not a typo anon. The risk in 0-1 year olds does increase by over 6x, or 584%.
Long-term effects of COVID-19
Long-term effects of #COVID-19
🔗 https://www.nature.com/articles/s41598-021-95565-8#Fig2
Oxidative stress is a shared characteristic of ME/CFS and Long COVID
Proceedings of the National Academy of Sciences (PNAS), a peer reviewed journal of the National Academy of Sciences (NAS) - an authoritative
AI summary:
Long COVID (LC) and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) share symptoms like fatigue, post-exertional malaise, and cognitive issues.
Both conditions lack approved treatments or reliable diagnostic markers, necessitating molecular research.
Study reveals elevated oxidative stress in lymphocytes of ME/CFS and LC patients, linked to mitochondrial damage and energy overconsumption.
Oxidative stress is sex-specific: females show higher reactive oxygen species (ROS) and mitochondrial calcium, while males exhibit lipid oxidative damage.
Elevated ROS in females correlates with T cell hyperproliferation, potentially contributing to fatigue.
Males show mitochondrial lipid oxidative damage, impairing mitochondrial function and energy production.
Antioxidant pathways, including glutathione and superoxide dismutase, are disrupted in both conditions.
Memory T cells in ME/CFS and LC patients exhibit oxidative stress, suggesting adaptive immune dysfunction.
T cell hyperproliferation in females is linked to higher energy demands, potentially acting as an "energy sink."
Metformin, an FDA-approved drug, reduces T cell hyperproliferation in ME/CFS females, showing potential as a treatment.
LC and ME/CFS patients exhibit distinct but overlapping oxidative stress pathways, with LC showing lower mitochondrial superoxide dismutase and ATP levels.
Sex hormones may influence the observed sex-specific oxidative stress differences.
Lipid peroxidation and fatty acid metabolism abnormalities are more pronounced in males, linked to mitochondrial dysfunction.
LC and ME/CFS patients show differences in ROS profiles, with LC exhibiting a heavy-tailed oxidative stress distribution.
Persistent oxidative stress in lymphocytes may result from prolonged immune activation post-infection.
Study suggests oxidative stress and mitochondrial dysfunction as shared mechanisms in LC and ME/CFS.
Findings highlight the need for sex-specific diagnostics and treatments for these conditions.
Precision medicine approaches, like ROS-modulating drugs, could help tailor treatments for ME/CFS and LC patients.
Further research is needed to explore the triggers, sex-specific mechanisms, and long-term effects of oxidative stress in these diseases.
Results provide a foundation for developing diagnostics and therapies targeting oxidative stress and immune dysfunction in ME/CFS and LC.
We discuss the paper recently published in Rheumatology Internationa. This article reflects on the prevalence of autoimmune rheumatic diseases (ARD) during the COVID-19 pandemic (2020–2023) and compares the same with the pre-pandemic period (2016–2019). We assume that SARS-CoV-2 triggers ARD. This study concerns the 10 million population of Greece, and this work convincingly confirms our hypothesis. Besides, four large cohort studies have demonstrated an increased incidence of autoimmune diseases after surviving COVID-19. Compared to the prepandemic period, all ARD increased, and RA growth in the index study reached a level of more than 20% during the pandemic. A similar trend was observed in our report covering four Central Asian republics, namely Kazakhstan, Kyrgyzstan, Uzbekistan, and Tajikistan. The alarming growth of ARDs due to the consequences of the pandemic can still be predicted for the coming years. Healthcare professionals worldwide should be aware of this hypothesis to plan their COVID-19, long COVID, and ARD diagnostic and therapeutic strategies. We agree with the authors of the index article that more resources and research studies are warranted to optimize the diagnosis and treatment of ARDs in this challenging time.
Autoantibody immune responses could contribute to acute and post-COVID-19 symptoms. Here, the authors describe longitudinal autoantibody res
Several of the most prevalent new-onset autoantibodies have, to our knowledge, not been described previously, including the three with the highest prevalence, i.e., anti-CCDC63 (coiled-coil domain-containing protein 63), anti-TRIM63 (E3 ubiquitin-protein ligase TRIM63), and anti-SNURF (SNRPN upstream reading frame protein)
The virus may be making us more susceptible to certain cancers
Recent studies indicate that the coronavirus is triggering many new autoimmune and neurological diseases. That's good news for chronic fatig
The field of post-infectious diseases didn’t (except for ME/CFS) exist prior to the coronavirus. The medical field focused on treating infections – not dealing with their aftermath. Recent studies indicate why that’s not going to fly anymore – and it’s not just because of ME/CFS. It’s because large studies are indicating that a coronavirus infection – whether it’s mild or severe – is upping the risk for all sorts of diseases.
Most of these studies are very large – running into the millions of participants – that rely on electronic health records. They’re comparing the incidence of new diagnoses in people who were infected with the coronavirus with those who weren’t.
Eric Topol recently wrote a blog on the autoimmune implications of COVID-19. Three recently published large studies lead Topol to report a “substantially increased risk of developing a diverse spectrum of new-onset autoimmune diseases.“
The increased risk was not low – a 20-40% increase in the likelihood of coming down with one of these illnesses – and the range of autoimmune illnesses affected was diverse indeed: the studies pointed to dramatic increases in the diagnosis of almost 20 autoimmune diseases. (See blog for the diseases). Since autoimmune disease can take a while to show up after an infection, one can only assume that this number will rise over time.
Other studies have found a marked increase in neurological diseases, including some one might not have thought. Besides things like cognitive disorders, sharp increases in the rates of psychotic disorders, epilepsy, stroke, and parkinsonism as well as others.
Cardiovascular and metabolic diseases have not been as well assessed but increases in asthma, type I and type II diabetes, respiratory diseases, heart failure, and stroke have been seen.
Oddly enough, none of these studies have assessed increased incidences of the one disease long COVID has been most associated with – ME/CFS. Nor have they assessed new diagnoses of fibromyalgia, IBS, dysautonomia, postural orthostatic tachycardia syndrome (POTS), or gynecological diseases.
If you want more research into post-infectious illnesses, then linking an infectious event to dozens of serious illnesses can only help.
The study makes one wonder how many chronic illnesses were triggered by an infectious event.
For all of its horrendous impact, the coronavirus pandemic is clearly going to force the medical profession to take a very close look at what happens during an infectious event – and afterward – and that is good news for anyone with a post-infectious illness like ME/CFS.