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.
I only follow BP once per year, so until the end of the year I won’t know. Regarding times, whenever I remembered to take it. Mostly either fasted or at least 1 h after a meal. I haven’t tried UDCA but the literature doesn’t seem to favored it that much.
The aim of our work was to study impact of tauroursodeoxycholic acid (TUDCA), 4-phenylbutyric acid (PBA) and their combination on mitochondrial functions and morphology. TUDCA, PBA and their combination have a significant impact on mitochondrial respiration. Although both TUDCA and PBA are considered to be chemical chaperones influencing endoplasmic reticulum (ER) stress, they affect mitochondrial respiration in a specific way. While TUDCA decreases ROUTINE, maximal, succinate-driven maximal, ATP-coupled and leak respirations; PBA increases spare respiratory capacity (SRC). Combination of TUDCA with PBA increases ROUTINE, maximal, succinate driven maximal and ATP-coupled respirations and SRC. TUDCA, PBA and their combination exhibits positive impact on mitochondria elongation and do not induce expression of proteins involved in mitochondrial fusion and unfolded protein response. Our results do not indicate the impact of either TUDCA or PBA on ER stress since pre-treatment of the cells with either TUDCA or PBA does not significantly affect tunicamycin-induced expression of HRD1, GRP78 and SEL1L. The impact of PBA and combination of TUDCA with PBA on mitochondrial functions might be associated with their possible neuroprotective effects. Although TUDCA exhibits positive effect on inner mitochondrial membrane, the possible neuroprotective effect of TUDCA might involve mechanism distinct from modification of mitochondrial functions.
Bile acids are essential mediators of gut-liver crosstalk. We found that supplementing human bile or the primary bile acid chenodeoxycholic acid inhibited HEV replication in organoids via the farnesoid X receptor (FXR) signaling pathway. The effects of the secondary bile acid, ursodeoxycholic acid, were opposite and promoted viral replication. In conclusion, this model provides a novel approach to study the gut-liver axis in HEV transmission and the impact of bile acids in modulating HEV infection.
To investigate the potential role of bile acids on HEV infection, we supplemented bile collected from liver organ donors, chenodeoxycholic acid (CDCA, a primary bile acid), and ursodeoxycholic acid (UDCA, a secondary bile acid) into our gut-liver axis model. Within this model, we found that human bile and CDCA inhibited HEV infection, whereas UDCA slightly enhanced the infection in intestinal organoids (Fig. 2F).
Next, we focused on the effects of bile acids in HIOs alone. Similarly, bile and CDCA inhibited HEV (Fig. 2H and I), while UDCA promoted HEV infection (Fig. 2J).
This trial demonstrated no difference in fasting glycemia for women with GDM treated with UDCA compared to placebo. However, those with elevated serum UDCA concentrations were more likely to have fasting blood glucose concentrations below recommended thresholds, suggesting potential benefit of further investigation.
Ursodeoxycholic acid (UDCA) ameliorates neuronal deficit in multiple sclerosis.
Effect of UDCA is regulated by TGR5 of microglia.
UDCA increases the expression of anti-neuroinflammation protein.
UDCA could be potential therapeutic option for multiple sclerosis.
Multiple sclerosis (MS) causes demyelination of the central nervous system (CNS) because of excessive inflammation of peripheral tissues. The pathophysiological mechanisms remain unclear because of disease background variability; therefore, antibody drugs and disease-modifying agents are ineffective therapeutic options. Alterations in bile acid metabolism correlate with the progression of MS. However, the effects of bile acid supplementation on the amelioration of MS have not been fully elucidated. Thus, in this study, we aimed to investigate the effects of ursodeoxycholic acid (UDCA) on the CNS in a mouse model of MS. Repeated high-dose administration of UDCA significantly improved disease scores and alleviated tissue damage in the spinal cord. The number of Iba1-positive cells increased in the MS spinal cord, which decreased after UDCA treatment. The effect of UDCA ceased with the activation of the TGR5 inhibitor in mice with MS. Proteomic analysis of UDCA-treated activated MG6 cells revealed that the TGR5 inhibitor significantly decreased the expression of 40 proteins, including anti-neuroinflammatory proteins (A2M, AHSG, ALB, APOA1, APOH, and SPP2), and significantly increased the expression of six proteins (Atxn7l3b, Basp1, Plekha3, Ptma, and Rrp15). UDCA may potentially regulate MS progression by modulating microglial activity via TGR5 in the spinal cord. Overall, these findings suggest that UDCA has potential applications as a novel therapeutic agent for MS.
