Other offtopic improvements that may be related may be not: lowest acid uric value ever & lowest homocisteine ever.
Cofounders: artichoke extract (also known to improve bile flow), increase astaxanthin from 12 to 18mg, k2 from 100 to 200mg)
Overall I would say that this has move the needle more than Rapa, 17alphaestradiol or astaxanthin, all 3 didn’t show any effect in my data. Unless someone convinces me this is doing some kind of harm I will continue. I may wait for the next test to reconfirm these results without increasing dose.
IMPORTANT: if anyone wants to try this supplement you have to know this is the most horrible tasting supplement you will ever know (and I tried all of them). You HAVE to take it in pill form.
Interesting, thanks for sharing your experience! Did you notice any impact on blood pressure? At what time(s) did you take TUDCA? Have you also tried UDCA?
MR analysis revealed a negative association between ED and the gut microbial genera Alistipes, Butyricicoccus, and Dialister, suggesting a potential protective role. Machine learning predictions indicated strong binding affinities between target genes (NFKB1, TLR4, CYP3A4) and bile acid derivatives (Tauroursodeoxycholic acid and Taurochenodeoxycholic acid). Molecular docking confirmed high binding affinities of NFKB1 to Tauroursodeoxycholic acid (−9.81 kcal/mol) and Taurochenodeoxycholic acid (−9.35 kcal/mol).
The molecular docking analysis conducted in this study further validates the interactions between NFKB1 and Tauroursodeoxycholic acid, as well as Taurochenodeoxycholic acid. As a key transcription factor in inflammatory responses, NFKB1 may play a central role in the pathogenesis of ED. Studies have shown that the activation of NFKB1 is closely associated with inflammatory responses in various chronic diseases, including ED.30–32 By binding to NFKB1, Tauroursodeoxycholic acid and Taurochenodeoxycholic acid may modulate its activity, thus influencing local inflammatory environments and promoting the recovery of endothelial cell function. Given the pivotal role of NFKB1 in immune and inflammatory responses, this finding offers potential therapeutic targets for new ED treatment strategies. Moreover, as metabolites of gut microbiota, Tauroursodeoxycholic acid and Taurochenodeoxycholic acid may exert anti-inflammatory effects through their interactions with NFKB1, consistent with previous studies on the immune-modulatory functions of bile acids.33,34 These metabolites may hold therapeutic potential in regulating immune responses, alleviating local oxidative stress, and restoring vascular endothelial function, warranting further investigation.
I stopped Tudca recently. A quick glance at my results would not imply this. I think if the k2 is mk7 (which it probably is given the dose) that is more likely to have such an effect. Because I also stopped drinking alcohol (not permanently, but on an experimental basis) I would like to wait a while before analysing my results as I need to slot in the various changes.
