How much TUDCA does your wife take daily in mg? How much is each pill? Have you considered taking more? It would be interesting to see if a higher dose leads to an even lower ALP.
Ora Biomedical tested UDCA and TUDCA on worms btw: Ora Biomedical Million Molecule Challenge Results - #352 by adssx
The results don’t confirm the 2024 Chinese paper: UDCA (ursodiol) / TUDCA for healthspan and lifespan? - #4 by adssx
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Ok, I may have overstated. Just asked her and she takes 2 pills when it hurts. She has done that twice a day, but not usually. But there is a twist.
I bought the body bio, which costs twice as much and has half the TUDCA. Because like I said I’m a bad shopper and I happened to be on fullscript. She says it works much better and she quit taking hers. Hers was the VINATURA, which has 1000mg plus milk thistle. She says it doesn’t work at all. Also it doesn’t smell or taste like bile, which the bodybio does. So there is a big difference in product here according to her.
WOW! wish I had come across this earlier! i.e that weight loss can catalyze? cause? gallstones.
After taking only the "trainer"dose of Rybelsus for about two weeks, had severe back pain, and ran sky high WBC. A CRT showed incipient gallstones and there may have been a small kidney stone passed.
I associated this with the Rybelsus, but now I see that it was the weight loss (went from 104 to about 97 in just a couple of weeks) might well have been the absolute causal.
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If this keeps up, TUDCA will soon be a prescription -only drug. I wonder if this is why the big-name nutritional supplement companies aren’t yet manufacturing it – fear of lawsuits by big pharma(?)
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Incredible! Thanks for sharing. (How did I miss this paper? 
)
A double-blind, placebo-controlled trial was completed in people with progressive MS (PMS), randomized to receive either TUDCA (2 g/day) or placebo for 16 weeks.
In the observational cohort, higher primary bile acid levels at baseline predicted slower whole-brain atrophy, brain substructure atrophy, and specific retinal layer atrophy. In the clinical trial, 47 participants were included in our analyses (21 in placebo arm, 26 in TUDCA arm). Adverse events did not differ significantly between arms (p = 0.77). The TUDCA arm demonstrated increased serum levels of multiple bile acids. No significant differences were noted in clinical or fluid biomarker outcomes. Central memory CD4+ and Th1/17 cells decreased, while CD4+ naive cells increased in the TUDCA arm compared to placebo. Changes in the composition and function of gut microbiota were also noted between the two groups.
BTW, I tried TUDCA in November and March and it caused very mild skin rash so I stopped after a couple of days. I mentioned it to @John_Hemming who said it might actually a good sign: the body clearing an infection previously ignored by the immune system. So I decided to give another try to TUDCA and third time lucky… I got a skin rash again but time it wasn’t mild it was… shingles! 
Any joking aside I don’t know if TUDCA caused my shingles or if John theory is correct but together with the above paper and TUDCA’s immuno-modulatory effects, that’s… Interesting.
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I ordered from Vitality Pro as they seem reliable + third party tested: https://vitality-pro.com/product/tudca/
How good is Nutricost as a brand?
Seems like a mixed bag after a brief perusal of various tested products on ConsumerLab. Most tested products passed, but (for instance) their goldenseal extract failed (only 1mg berberine detected per capsule instead of 30mg expected).
I’d stick with the Vitality Pro if I were you.
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Numerous secreted bacterial metabolites were identified with bioactivity in various neoplasias, including ovarian cancer. One such metabolite is ursodeoxycholic acid (UDCA), a secondary bile acid that has widespread beneficial effects in neoplasias. Hereby, we assessed the bioactivity of UDCA in cell models of ovarian cancer, by applying UDCA in concentrations corresponding to the serum reference concentrations of UDCA (300 nM). UDCA induced epithelial-to-mesenchymal transition (EMT), increased the flux of glycolysis and reduced the naturally occurring oxidative stress in ovarian cancer cells. These changes were dependent on the activation of NRF2. The tumoral overexpression of UDCA-induced genes in humans correlated with worse survival. These results point out that bacterial metabolites may have opposite effects in different neoplasias and raise the possibility that UDCA-containing remedies on the long run may support cancer progression in ovarian cancer patients.
Osteoarthritis treatment via the GLP-1–mediated gut-joint axis targets intestinal FXR signaling 2025
Additionally, C. bolteae showed the strongest positive correlation with GUDCA within the same cohort. In mice, colonization with C. bolteae increased the levels of ursodeoxycholic acid (UDCA) (a precursor of GUDCA) and alleviated the progression of osteoarthritis. Notably, UDCA (an FDA-approved drug) supplementation mitigated osteoarthritis progression through this gut-joint axis in mice, and UDCA use was also associated with a lower risk of clinically relevant end point of osteoarthritis-related joint replacement in a cohort of 5972 individuals.
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Interesting report on high-dose UDCA @John_Hemming:
Overlap syndromes are inflammatory rheumatic conditions in which patients have clinical manifestations suggestive of multiple distinct immune diseases. The diseases most commonly involved in overlap syndromes include rheumatoid arthritis, lupus, scleroderma, and myositis.
High-dose ursodeoxycholic acid successfully treats overlap syndrome 2025
Treatment of PBC with UDCA has been shown to have a beneficial effect and highly safe effect on the disease progression. Regarding the dose of UDCA in patients with PBC, 14–16 mg/kg/day of UDCA for at least 2 years has demonstrated significant biochemical and histological improvement. Another randomized trial conducted demonstrated that UDCA doses of 13–15 mg/kg/day showed the highest rates of biochemical improvements compared with higher levels (23–25 mg/kg/day) and lower (5–7 mg/kg/day) doses. However, this patient had to take 35 mg/kg/day (700 mg thrice daily) to significantly improve the biochemical values. Therefore, UDCA can be administered at a dose that “at least does no harm”, and if this therapy fails to elicit an adequate biochemical response, a corticosteroid (e.g., prednisone 10–15 mg/kg/day) is added. However, in this case, because the patient refused to take steroids, high doses of UDCA were administered to achieve a therapeutic biochemical response. To our knowledge, administration of such high doses of UDCA to treat PBC is the first to be reported.
Also interesting (Chinese paper in cell model): Tauroursodeoxycholic Acid Induces Liver Regeneration and Alleviates Fibrosis Through GATA3 Activation 2025
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Open label trial without a placebo group, but still encouraging:
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Chinese paper, fairly high dose and animal model but not great for UDCA: Thyroid hormone ameliorates ursodeoxycholic acid-induced heart damage in zebrafish embryos
Ursodeoxycholic acid (UDCA) is the most commonly prescribed treatment for intrahepatic cholestasis of pregnancy (ICP) worldwide. Clinical studies show that UDCA helps alleviate maternal pruritus and lowers serum bile acid levels. However, despite treatment, women with ICP still experience unpredictable fetal deaths and other serious pregnancy complications. In this study, we hypothesize that while UDCA improves maternal symptoms, it may have harmful effects on the fetus due to its placental barrier crossing, potentially leading to negative pregnancy outcomes. We found that UDCA concentrations above 150 mg/L can exert toxic effects on zebrafish embryos, including increased mortality, slower heart rates, and pericardial edema. At these concentrations, UDCA also triggered apoptosis and elevated oxidative stress in embryonic cardiomyocytes. Importantly, the thyroid hormone T4 was able to partially mitigate these toxic effects. These findings suggest that adverse pregnancy outcomes in ICP may be related to fetal heart damage caused by UDCA’s effects on circulation, providing a possible explanation for fetal death in clinical settings. This also underscores the need to optimize UDCA dosing in clinical practice and explore the use of thyroid hormones as a potential protective therapy for the fetus in ICP cases.
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TUDCA resulted in smaller lesion observed on days 1 and 7 MRIs post-TBI.
TUDCA therapy resulted in lower cortical edema on day 1 post-TBI.
Animals in TUDCA group exhibited lower level of anxiety on day 7 post-TBI.
I was under the impression that TUDCA was to be used intermittently as a liver cleanse. Maybe used a month or two in a row and then 3-4 month break would have a different result?
Here are my results from my TUDCA intervention (3 months, 500mg/day, normally 1h after a meal):
- My alkaline phosphatase, the objective of this intervention got a modest improvement:
- GGT+ALT+AST. my lowest data yet in all 3 biomarkers:
- LDL got my lowest reading with an improvement in HDL:
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.
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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?
Mendelian randomization: NFKB1-targeted metabolites as novel therapeutic approaches for erectile dysfunction: evidence from gut microbiota network pharmacology and machine learning 2025
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.
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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.
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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.
After reading a little bit more into the literature I have decided that for the next 3 months I am going to split my 500g/day into 2 pills of 250g/day. At least in this study, the bolus dose is not better (not related to my objectives but eitherway worth the experiment): Tauroursodeoxycholic acid attenuates progression of steatohepatitis in mice fed a methionine-choline-deficient diet - PubMed
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