Mauritio
Member
- Joined
- Feb 26, 2018
- Messages
- 5,669
I found some cool studies on the ,in my opinion, unappreciated role of Vitamin A against Endotoxin and therefore against Serotonin.
@Koveras has already posted that a single big dose dose of Vitamin A may be a treatment for autism(Vitamin A May Be A Viable Therapy For Autism (human Study)) Since there is high chance that endotoxin/serotonin is a big part in the origin of autism (Gut Dysbiosis May Cause Autism Through Cortisol And Serotonin) Vitamin A might be a viable anti-serotonin / anti-endotoxin chemical.
Besides that Serotonin might be the master trgulator of metabolism ,so it's probably beneficial for most if not everybody to have another cheap OTC anti-serotonin substance in their arsenal (Gut serotonin (due to bacteria) is the master regulator of metabolism, insulin sensitivity, and weight – To Extract Knowledge from Matter)
I already posted 1 study in koveras thread,but the forum can be confusing so I want them to be at one place , so It's easier for new members ,or if you just want to look it up quickly...
Acute effects of vitamin A on the kinetics of endotoxin in conscious rabbits. - PubMed - NCBI
CONCLUSION:
A fairly low dose of vitamin A reduced the half-life of endotoxin.
Vitamin A inhibits the action of LPS on the intestinal epithelial barrier function and tight junction proteins. - PubMed - NCBI
In conclusion, Vitamin A improves the intestinal barrier function and reverses LPS-induced intestinal barrier damage via enhancing the expression of tight junction proteins.
https://www.tandfonline.com/doi/full/10.1080/1828051X.2018.1453757
In conclusion, RA ameliorated the LPS-induced BMECs damage by improving levels of antioxidant markers and reducing inflammatory cytokines contents, indicating that RA has the potential to counter measure the immunosuppressive condition on BMECs oxidative damage and to improve antioxidative function. However, further studies are still required to elucidate the molecular mechanisms underlying the protective effects of RA as an antioxidant.
Retinol suppresses the activation of Toll-like receptors in MyD88- and STAT1-independent manners. - PubMed - NCBI
Together, the results demonstrate that retinol suppresses the activation of TLRs in macrophages resulting in downregulation of inflammatory gene expression and further suggest that beneficial effect of retinol is mediated through regulation of TLR-mediated inflammatory responses.
Vitamin A and Response to Endotoxin - Full Text View - ClinicalTrials.gov
Interesting clinical trial . Can somebody find the results? It should have ended 2014.
@Koveras has already posted that a single big dose dose of Vitamin A may be a treatment for autism(Vitamin A May Be A Viable Therapy For Autism (human Study)) Since there is high chance that endotoxin/serotonin is a big part in the origin of autism (Gut Dysbiosis May Cause Autism Through Cortisol And Serotonin) Vitamin A might be a viable anti-serotonin / anti-endotoxin chemical.
Besides that Serotonin might be the master trgulator of metabolism ,so it's probably beneficial for most if not everybody to have another cheap OTC anti-serotonin substance in their arsenal (Gut serotonin (due to bacteria) is the master regulator of metabolism, insulin sensitivity, and weight – To Extract Knowledge from Matter)
I already posted 1 study in koveras thread,but the forum can be confusing so I want them to be at one place , so It's easier for new members ,or if you just want to look it up quickly...
Acute effects of vitamin A on the kinetics of endotoxin in conscious rabbits. - PubMed - NCBI
CONCLUSION:
A fairly low dose of vitamin A reduced the half-life of endotoxin.
Vitamin A inhibits the action of LPS on the intestinal epithelial barrier function and tight junction proteins. - PubMed - NCBI
In conclusion, Vitamin A improves the intestinal barrier function and reverses LPS-induced intestinal barrier damage via enhancing the expression of tight junction proteins.
https://www.tandfonline.com/doi/full/10.1080/1828051X.2018.1453757
In conclusion, RA ameliorated the LPS-induced BMECs damage by improving levels of antioxidant markers and reducing inflammatory cytokines contents, indicating that RA has the potential to counter measure the immunosuppressive condition on BMECs oxidative damage and to improve antioxidative function. However, further studies are still required to elucidate the molecular mechanisms underlying the protective effects of RA as an antioxidant.
Retinol suppresses the activation of Toll-like receptors in MyD88- and STAT1-independent manners. - PubMed - NCBI
Together, the results demonstrate that retinol suppresses the activation of TLRs in macrophages resulting in downregulation of inflammatory gene expression and further suggest that beneficial effect of retinol is mediated through regulation of TLR-mediated inflammatory responses.
Vitamin A and Response to Endotoxin - Full Text View - ClinicalTrials.gov
Interesting clinical trial . Can somebody find the results? It should have ended 2014.