Boy is it refreshing to read this thread that takes a close look at two studies being used to rationalize #vitamin D supplementation for #COVID-19. It explains how both studies have so many problems that the findings must be interpreted with great caution
2/ Why do I care? I spent part of my graduate work working on the molecular #biology of the vitamin D system (including how the various “vitamin” D metabolites impact Vitamin D Receptor activity/gene expression)
3/ Far from being simplistic “vitamins”, the various forms of “vitamin” D are actually secosteroid transcriptional activators, w/ 1-25-dihydroxyvitamin D (also called D3) also acting as a hormone
4/ We, and many other “vitamin” D research teams, spent years working with the IOM to challenge the model that a mere association b/t low 25-D levels on a blood test and X condition is a justification for high-dose supplementation
5/ That model is aggressively pushed forward by Michael Hollick’s team (who did the 2nd study in Alina’s thread). Hollick has, by the way, been featured in the NYT for his conflicts of interest tied to vitamin D research: google.com/amp/s/www.nyti…
6/ To counter what became known to many as the “Hollick argument” the IOM invested $$$ in high-quality RCTs to test whether long-term vitamin D supplementation is actually effective in many conditions
7/ Almost no RCT showed a positive effect for vitamin D supplementation long-term. This RCT even found that in older community-dwelling women, annual oral administration of high-dose vitamin D resulted in an INCREASED risk of falls and fractures: pubmed.ncbi.nlm.nih.gov/20460620/
8/ Part of the reason for the negative RCT outcomes is that both main forms of “vitamin” D have immunosuppressive effects under certain circumstances (not always great for long-term health)
9/ In fact, our modeling data suggests that 1,25-D (D3) can bind into the glucocorticoid nuclear receptor with a similar affinity to dexamethasone: onlinelibrary.wiley.com/doi/abs/10.100…
10/ In that sense D3 could potentially be useful to control the #COVID-19 cytokine storm, but way more work on the specifics of the molecular biology must take place!
11/ Overall, there are 2 main takeaways: 1. “#Vitamin” D research must be based in molecular biology and not on association studies 2. Vitamin D supplementation is a complex topic that should not be centered on a “one size fits all” paradigm
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If you are a patient that meets #ME/CFS and #PEM criteria, info on the specific #infections or exposures that led to onset or exacerbation of your symptoms is of major importance. That info will help you pursue personalized treatment.
2/ That is because many of the infections you've sustained may still be #persisting in your body - in your tissue or nerves. These persistent infections can cause PEM symptoms by driving #mitochondrial dysfunction, blood vessel/perfusion issues, or #vagus nerve dysfunction
3/ If your symptoms started - or were exacerbated - by a #herpesvirus infection, such viruses persist in your system for life. Thus, treatment with herpesvirus #antivirals (e.g. the Pridgen Protocol which uses valacyclovir and Celebrex) has helped certain ME/CFS patients improve
Jawdropping data here showing dozens of #viruses - many rarely even discussed or tested for on a regular basis - in sewage collected from wastewater in multiple USA cities. The viruses are identified via unbiased sequencing that can identify any viral genome in the samples.
2/ Because the viruses are being identified in wastewater it's possible that some viruses are harbored by animals - for example cattle or birds - whose feces end up in the wastewater
3/ However, it's likely that most of the viruses being shed into wastewater come from infected humans. Viruses like the enteroviruses A, B, C, D68, Rhinoviruses A, B, C, Rotaviruses, Noroviruses, Rotaviruses, Mastadenoviruses, Adenoviruses, Rhinoviruses, Influenza viruses, etc.
Glad to have contributed to this new preprint. We found that some PVS participants had higher levels of circulating spike protein compared to controls.
This parallels #LongCovid where persistence of the SARS-CoV-2 #virus in patient tissue may also cause spike to periodically leak into blood
2/ For example, this study found #SARS-CoV-2 proteins including spike up to 1 year post-COVID in up to 25% of people tested. But identified spike was not a result of the COVID vaccine, since nearly all study participants had not received the vaccine: thelancet.com/journals/lanin…
3/ The same team also found SARS-CoV-2 spike protein encoding double-stranded RNA in LongCovid #gut tissue almost 2 years post-#infection. Such RNA is produced during active viral replication and thus wld not be vaccine derived: science.org/doi/10.1126/sc…
Today I write for the @latimes: Long COVID is solvable, but we need more clinical trials.
These include trials of drugs to clear #SARS-CoV-2 reservoirs: small pockets of the virus - or parts of the virus - that can persist long-term in people’s bodies.
2/ We are living in an epidemic of chronic #disease, with a growing number of pesticides, chemicals and food additives implicated in the declining health of Americans.
3/ Since 2019, another factor has been at play as well: The #SARS-CoV-2 virus has driven a huge increase in chronic #health consequences, broadly referred to as long COVID.
Our new Viewpoint is out! We draw from treatment strategies in HIV, Hep C & other infections, to detail key considerations for #LongCovid clinical trials targeting persistent #SARS-CoV-2. These include combination trials of drugs that target both the virus and the immune system: authors.elsevier.com/a/1kayZ5E-UogX…
2/ To maximize these trials, we must develop validated #biomarkers to detect persistent virus or protein in accessible fluids like blood & saliva. Such biomarkers will allow targeted recruitment of participants w/ viral persistence into trials - helping trials to meet endpoints
3/ This persistence biomarker development - and the #LongCovid trials of immunotherapies, monoclonals, antivirals and other drugs delineated in our Viewpoint - are huge opportunities for the #biotech space. Agile, action-oriented agencies like @ARPA_H should also rapidly engage
@BaszkoM @RorPreston @polybioRF That is not correct. We are working very hard on ME/CFS projects in addition to LC, and almost every day we work with teams to determine how more of our LC projects can be pivoted to ME/CFS in the future
@BaszkoM @RorPreston @polybioRF 2/ ME/CFS projects include this collaborative study determining immune activity, microclotting and other infectious parameters in ME/CFS patients with peripheral neuropathy: polybio.org/projects/immun…
@BaszkoM @RorPreston @polybioRF 3/ This study of neuroinflammation via PET imaging and imaging to document changes in cognitive control (brain fog) in ME/CFS: polybio.org/projects/5272/