TUDCA dosage and evidence
Written by Aaron CuhaReviewed Sep 2026
The short answer
In twenty obese adults over four weeks, insulin sensitivity in the liver and muscle rose about 30 percent on a detailed lab test.
Evidence grade for TUDCA: Limited. The rule: people have taken it in a published study, but fewer than 100 of them. The sum on this page: 3 completed trials, 54 people given it. A grade counts how much has been done to people, not whether it works.
- People given it
- 54
- Human studies
- 3
- Found nothing
- 2
Dose
No human dose established
Amounts that were given in studies sit in Human evidence on this page. None of them is a personal dose.
3 completed trials, 54 people given it
7 effects reported, 4 unwanted, 3 wanted, by people using it, not a trial
Goal pages: Fat loss and metabolism, Ageing and longevity, Gut health
In plain English
In plain English, from Aaron
This is how I would explain it to a friend. The evidence, with the numbers, is further down the page.
TUDCA is a bile acid, a natural helper your liver makes to digest fat. It is sold as a liver and cell-health supplement. It is not the same as UDCA, the prescription liver drug.
What people take it for
- Protecting the liver, especially on steroids or oral hormones.
- Better insulin sensitivity.
- Brain protection, based on ALS research.
- Living longer.
What studies in people showed
The biggest study was in 664 people with ALS. A drug that combined it with sodium phenylbutyrate made no difference to function, and it was pulled from sale. A smaller study of 137 people had looked good and won approval first. In 20 obese adults, four weeks of TUDCA raised insulin sensitivity in the liver and muscle by about 30 percent. The cell stress it was meant to fix did not change. No study has tested it as liver support in healthy people.
What people report
Reports, not study results
The good
- On steroid forums, people say their liver enzymes fell quickly while on it.
- One person tracked six months of blood work and saw liver and iron markers shift, though a second supplement was added partway through.
- Side effects reported are few and mild.
The bad
- Someone who used it for more than two years says their blood work did not change at all.
- Stomach upset, gut noise and feeling briefly unwell after a capsule are reported.
- Skeptics argue there is no evidence for using it to prevent damage, which is how almost everyone uses it.
- Cost is a common reason people drop it.
Where these come from: Threads on ExcelMale and Bluelight, plus search extracts from MESO-Rx and LongeCity, read in September 2026, and the studies on this page. Forum reports are not from a study.
My bottom line
If your liver numbers are fine, I see no proof it does anything for you. If you are on oral steroids, get your liver enzymes tested, and do not treat this as a free pass.
An opinion, not a finding. I am a coach, not a doctor.
What it has been measured to do
Measured in people
Goals TUDCA has been tested for in people, biggest studies first. We count only what the studies on this page say, so the real numbers may be higher.
- Losing fat specifically20 people · 1 study · 1 found nothing
- Blood sugar and insulin20 people · 1 study · 1 found nothing
- Liver fat and liver health20 people · 1 study · 1 found nothing
- Living longerno headcount stated · 1 study · 1 found nothing
What people using it report
Real people telling you what happened to them. Nobody checked it, and the people who post are not a fair sample, so it cannot prove anything works. It is still the best guide on this page to what people actually do with TUDCA, what they expect, and what goes wrong. The full account, including the negative reports, is below.
29 of the 36 indexed goals have no study of any kind behind TUDCA
No study in people, animals or cells on this page reports a result for these. That does not prove TUDCA does nothing for them. It does mean anything you have heard about TUDCA and one of these did not come from a study cited here.
Show full evidence
What is TUDCA?
In twenty obese adults over four weeks, insulin sensitivity in the liver and muscle rose about 30 percent on a detailed lab test. Fat tissue did not respond. The cell stress markers the drug was meant to fix did not change either. In ALS, a large final-stage study of TUDCA combined with sodium phenylbutyrate missed its goal, and the maker pulled the approved product from the market.
TUDCA is a bile acid. It is UDCA with the amino acid taurine attached. UDCA has its own page on this site. The two are not the same, though supplement marketing often treats them as if they were. TUDCA is the form most brain-protection research uses. UDCA is the form with the liver approvals, and with the mouse lifespan test that found nothing.
The human evidence for TUDCA itself splits into two parts. One small metabolism study. And one long drug story that ended badly.
The metabolism study is the best-run human study this compound has. Twenty obese adults, average BMI 37, took 1,750 mg of TUDCA a day or a dummy pill for four weeks. They had a detailed lab test of how well insulin works, plus small samples of muscle and fat. Insulin sensitivity in the liver and muscle rose about 30 percent. The dummy group did not change. Insulin signalling in muscle improved. And here is the finding that matters for everything else. Markers of cell stress in muscle and fat did not change on TUDCA. Easing that cell stress was the whole idea the study was built to test. Something happened, but the proposed reason was not shown.
The drug story starts with a 34-patient study in ALS. People took 1 gram twice a day on top of riluzole for 54 weeks. 87 percent counted as responders, against 43 percent on a dummy. Then came CENTAUR, a mid-stage study of TUDCA combined with sodium phenylbutyrate. It looked good enough on function, and on survival numbers worked out afterwards, to win FDA approval. Then the large final-stage PHOENIX study showed no change on the ALS function scale at 48 weeks. The maker then pulled the drug from sale with the US and Canadian regulators.
That sequence is the single most useful thing to know about this compound. A small positive study, a positive mid-stage study, an approval, a failed final-stage study and a withdrawal. Almost no supplement listing mentions it.
How does TUDCA work?
TUDCA is a water-loving bile acid that acts as a chemical helper for proteins. It helps them fold properly, and it eases a kind of stress in the part of the cell that makes proteins. Separately, it makes the cell's power plants less likely to leak the signals that tell a cell to self-destruct. Attaching taurine makes it more water-soluble. It also changes how the body recycles it between gut and liver, compared with plain UDCA. That is why the two are studied separately. The honest catch is this. The protein-helper idea was tested directly in the one human study built to look for it. The cell stress markers in muscle and fat did not move, while insulin sensitivity did. The authors said as much. More studies are needed to find which cells and which mechanisms are responsible.
What have studies in people found about TUDCA?
Real but narrow. One carefully measured four-week metabolism study in 20 people. One 34-patient early study in ALS. And a drug program in which the combination product was approved on mid-stage data, then pulled after the large final-stage study.
- PHOENIX, the large final-stage study of the combination in 664 people, showed no change on the ALS function scale at 48 weeks. The maker withdrew the drug from sale.
- CENTAUR, the mid-stage study of the combination with sodium phenylbutyrate in 137 people, supported an FDA approval.
- 34 ALS patients, 1 gram twice a day for 54 weeks on top of riluzole: 87 percent counted as responders, against 43 percent on a dummy, with slower decline on the ALS function scale.
- 20 obese adults, 1,750 mg a day for 4 weeks: insulin sensitivity in liver and muscle up about 30 percent on a detailed lab test. Fat tissue and cell stress markers did not change.
- A European final-stage study of TUDCA alone is registered as NCT03800524. The registry lists its status as unknown, and no results paper was found.
- No human study has measured lifespan, healthy ageing, thinking in healthy people, or any ageing measure with TUDCA.
What this does not tell you: The insulin result is four weeks in twenty people, measuring a stand-in marker, however carefully. That lab test tells you how the body handled sugar on the day of the test. It does not tell you whether anyone developed diabetes. The ALS pilot counted responders by comparing each person's decline with their own earlier rate. That is a fragile measure in a small study, and the bigger program built on that signal failed at the final stage. Nothing here supports the liver support, cell energy or long-life uses it is actually sold for.
What do people who took TUDCA report?
This is what real people say happened to them, good and bad. Nobody measured it. A report cannot tell a real effect from the lift people get just from expecting it to work, from a diet or training change made at the same time, or from what was really in the vial. We still put it near the top. It is the next best thing to a study in people: what happens when real people use it, including what goes wrong.
- Two separate populations discuss it and they do not agree. In steroid and testosterone forums it is taken as liver insurance, commonly at 250 to 750 mg a day and sometimes 1 to 2 g alongside oral compounds, and people report liver enzyme values falling quickly. In longevity and harm reduction discussion the same doses are treated as unproven for anyone whose liver is healthy.
- The most detailed self-experiment described tracks iron, ferritin, liver enzymes, kidney markers and free T3 falling or shifting over roughly six months on a small daily dose, with a second supplement added partway through, so nothing in it isolates this compound. The person running it reports no change in testosterone or oestrogen.
- Directly against that, someone describing more than two years of consistent use reports no difference in bloodwork before or after, which is the clearest no effect report in the discussion and sits in a thread about whether it aids thyroid hormone conversion.
- The central disagreement is whether it prevents damage or only treats damage already present. The sceptical position, argued at length, is that there is no evidence for the preventive use that almost everyone is actually making of it, and a related argument holds that raised enzymes after heavy lifting are not liver injury in the first place.
- Side effect reports are mild and few, mostly stomach upset, gut noise and feeling briefly unwell after a capsule, with caution raised about sustained high doses on the basis of bile acid work rather than anyone's experience.
- Cost and the view that a healthy person gets nothing for it are the usual reasons given for not bothering.
Sources: Threads on ExcelMale and Bluelight, found by site-restricted search and read directly, September 2026, with MESO-Rx and LongeCity material seen only through search extracts because those boards were not directly fetchable from this environment. Nothing above is attributed to any specific post and no post is reproduced.
The state of the research
Read this page next to the ursodeoxycholic acid (UDCA) page, which covers the parent compound. The difference is not nit-picking. UDCA has the liver approvals, a Parkinson's disease study, and a mouse lifespan test that found nothing. TUDCA has the insulin study and the ALS program. Evidence for one does not carry over to the other. Products sold as bile acid support blur the two all the time.
The ALS story deserves to be told bluntly. It is a complete worked example of how an idea becomes a product and then stops being one. A believable protein-helper idea, a small positive study, a positive mid-stage study, an approval, a failed final-stage study, a withdrawal. The compound did not change during that sequence. What changed was the size and strength of the test. A supplement buyer who reads only the first three steps is reading a version of the evidence that went out of date in 2024.
A stand-in marker is a lab number used in place of the thing you actually care about. The idea is that if you move the number, you move the health result. That idea has failed often enough that it should be treated as a claim, not a fact. Homocysteine is the classic case. In studies that watch people, high homocysteine strongly predicts heart disease. Several cheap supplements can lower it reliably. But when studies lowered it and then counted heart attacks, the heart attacks did not go down. The lesson is not that markers are worthless. It is that a study reporting a marker has answered a smaller question than the one the buyer is asking. The page should say which question was answered.
The evidence, in charts
Fig. 1a · how many people
54people, across 2 studies in people cited here
| Study | People | Share |
|---|---|---|
| European Journal of Neurology 2016 | 34 | 63% |
| Diabetes 2010 | 20 | 37% |
One study holds 63% of these people, so the total rests more on one study than its size suggests. Counts are the number of people each study on this page says it signed up. That includes studies that only watched people and gave nobody the compound. 3 more studies in people give no headcount and are not counted here. Studies still signing people up are left out, and only studies cited on this page are counted.
Fig. 1b · evidence mix
5 of 6 sources here are studies in people. The rest is not.
- Study in people · done in people583%
- Review of studies · sums up other studies117%
Counted from the list of sources on this page. It counts only what we cite, so there may be more studies out there. A review counts once, however many studies it sums up.
Fig. 2 · evidence over time
The studies cover 6 different years, 2010 to 2024, counted from the list of sources on this page.
Fig. 3 · legal status at a glance
US
Not approved
UK
Not approved
AU
Not approved
CA
Not approved
Not approved in any of the four countries shown. This is what the law says, not a verdict on the science. See Legal status below for the full text and any notes.
Fig. 4 · how much does what
Nobody has tested different amounts in people
This chart would show how the effect changes as the amount goes up. For this compound, nobody has measured that in people. So we leave it empty. We will not borrow an animal chart and pretend it works the same in people.
Fig. 5 · what the molecule is
- Kind of compound
- Supplement
- Molecule weight
- 499.7 Da. A taurine-conjugated bile acid, not a peptide.
- Half-life
- Stated in words, not a numbersee the exact wording below
- Chain length
- None on file
Half-life as stated on file: Not established for supplemental dosing. Bile acids recirculate between gut and liver many times over, so a single plasma figure does not describe exposure.
No amino acid sequence is on file for TUDCA, which is expected: a supplement is not built from amino acids.
The studies we cite
- Study in people2010Tauroursodeoxycholic Acid may improve liver and muscle but not adipose tissue insulin sensitivity in obese men and women.
Four weeks of TUDCA improved insulin sensitivity in liver and muscle, and not in fat. 20 obese adults took 1,750 mg a day or a dummy for four weeks, with detailed infusion tests and samples from muscle and fat. Liver and muscle insulin sensitivity rose by roughly 30 percent while the dummy group did not change. The cell stress markers that were meant to explain all this did not move in either tissue. NIH funded. Twenty people over four weeks is a mechanism study.
20 obese adults, mean age 48 and BMI 37, randomised to 1,750 mg a day of TUDCA or placebo for 4 weeks, with two-stage hyperinsulinaemic-euglycaemic clamps, tracer infusions and muscle and adipose biopsies. Hepatic and muscle insulin sensitivity rose approximately 30 percent (p < 0.05) with no change on placebo, and muscle insulin signalling improved. Markers of endoplasmic reticulum stress in muscle and adipose tissue did not change after either treatment, despite that being the hypothesised mechanism. NIH funded.
- Study in people2016Tauroursodeoxycholic acid in the treatment of patients with amyotrophic lateral sclerosis.
A promising small trial, and its own authors call it preliminary. 34 ALS patients already taking riluzole were split by chance to TUDCA at 1 gram twice a day or a dummy for 54 weeks. Nobody knew which. 87 percent of the TUDCA group counted as responders, meaning their decline slowed by at least 15 percent against their own earlier rate, against 43 percent on the dummy. Side effects were no worse on TUDCA. 34 people is a first look.
A proof of principle double blind placebo-controlled trial: 34 ALS patients already on riluzole randomised to TUDCA 1 gram twice daily or placebo for 54 weeks after a three-month lead-in. The proportion of responders, defined as at least a 15 percent improvement in ALSFRS-R slope against the lead-in, was 87 percent on TUDCA against 43 percent on placebo (p = 0.021). Well tolerated with no between-group difference in adverse events. The authors describe it as preliminary data indicating TUDCA is safe and may be effective.
- Study in people2020Trial of Sodium Phenylbutyrate-Taurursodiol for Amyotrophic Lateral Sclerosis.
The trial behind the approval slowed decline slightly, and nothing else it measured moved. 137 people with ALS whose symptoms began within 18 months were split by chance, two to one, to the combination or a dummy. Nobody knew which. Function fell 1.24 points a month on the drug and 1.66 on the dummy, across 24 weeks. Every other measure, including strength, breathing and time to death, came out the same. Side effects were mainly stomach ones. The approval this supported was later withdrawn.
CENTAUR, the phase 2 randomised trial of the fixed combination of sodium phenylbutyrate and taurursodiol, the form of TUDCA used in drug development. 137 people with ALS randomised 2 to 1, 89 to active and 48 to placebo, over 24 weeks. ALSFRS-R declined 1.24 points a month on drug against 1.66 on placebo, a difference of 0.42 points a month (95% CI 0.03 to 0.81, p = 0.03). The secondary outcomes did not differ significantly. Adverse events were mainly gastrointestinal. This functional result, together with post hoc survival analyses, supported the regulatory approval that was later withdrawn.
- Study in people2023A randomized double-blind clinical trial on safety and efficacy of tauroursodeoxycholic acid (TUDCA) as add-on treatment in patients affected by amyotrophic lateral sclerosis (ALS): the statistical analysis plan of TUDCA-ALS trial.
This is the plan for a trial, not its result. A European study is testing TUDCA on its own, added to riluzole, in people with ALS. This paper sets out in advance exactly how the numbers will be analysed, which is done so nobody can pick a flattering result afterwards. The registry lists the study status as unknown, with completion estimated for December 2023. No results paper has appeared. One author is the medical director of the company supplying the drug.
The published statistical analysis plan for a European phase 3 trial of TUDCA alone, rather than in combination, as an add-on to riluzole, registered as NCT03800524. On the registry the study status is listed as unknown with an estimated completion date of December 2023, and no results publication was located in PubMed for this entry. Disclosed conflicts include an author employed as medical director by the company supplying the investigational product.
- Study in people2021Phase III Trial of AMX0035 for Amyotrophic Lateral Sclerosis Treatment
The big version of the trial was run and it found nothing. This registry record covers PHOENIX, which enrolled 664 people and tested the sodium phenylbutyrate and taurursodiol combination against a dummy over 48 weeks from October 2021. Nobody knew which they were taking. Function scores came out the same in both groups. The maker then withdrew the drug from sale. A large properly built trial overturned the small one that had won the approval.
The registry record for PHOENIX, a phase 3 randomised double-blind placebo-controlled multicentre trial of AMX0035, the sodium phenylbutyrate and taurursodiol combination, against placebo over 48 weeks. Actual enrolment 664, started October 2021. This is the trial that showed no change in ALSFRS-R total score and led to the sponsor withdrawing the marketing authorisations.
- Review of studies2024Sodium Phenylbutyrate and Tauroursodeoxycholic Acid: A Story of Hope Turned to Disappointment in Amyotrophic Lateral Sclerosis Treatment.
A review that tells the whole story. The mid-stage CENTAUR study showed a slower loss of function, and numbers worked out afterwards hinted at fewer deaths, hospital stays and breathing machines. Then the large final-stage PHOENIX study showed no change in function at 48 weeks. The maker began pulling the drug from sale in the US and Canada. The authors discuss what it means when a mid-stage win is overturned at the final stage.
Review tracing the arc: CENTAUR showed an effect on ALSFRS-R and, in post hoc analyses, on risk of death, hospitalisation and tracheostomy or permanent assisted ventilation. The phase 3 PHOENIX trial (NCT05021536) then showed no change in ALSFRS-R total score at 48 weeks, and the sponsor initiated voluntary withdrawal of the marketing authorisations with the US FDA and Health Canada. The authors discuss what conflicting phase 2 and phase 3 data mean for ALS and other neurological disorders.
Where to buy TUDCA
1 seller lists TUDCA in our latest read. They are ranked by trust score, then by archive rating, then by certificate tier, then by the lowest price per milligram. Archive evidence is counted before source-backed. Each path is out of 4, and the two are not added. A higher price does not raise the score. The letter is the certificate chip. 0 of them have a published certificate that names TUDCA.
Some seller links may pay this site when you buy through them. A payment never changes a seller's tier or rank, and no seller has a say in any page.
| Seller | Trust score | Vial sizes | From, per mg | Certificate for TUDCA | Seller link |
|---|---|---|---|---|---|
| Pure Health Peptides | 25 InsufficientSource-backed 1 of 4. Archive evidence 0 of 4.C | 500 mg | $0.118 | None found for TUDCA | View |
- LC Lab-confirmed: the issuing laboratory echoed this certificate back
- A Current certificate, independent laboratory named, laboratory not yet checked
- B Certificate published, but no laboratory link, older than a year, or the laboratory did not recognise the published lookup
- C No certificate could be read
Every listing and vial size for TUDCA · How the trust score is counted
Sellers named on the price pages are ranked by certificate tier, then price, and any affiliate income is disclosed there. Naming a seller is not a recommendation to buy or use anything.
Common questions
Has TUDCA been tested in people?
Yes. 54 people given it across 3 completed trials cited here, 2 of which found nothing. In twenty obese adults over four weeks, insulin sensitivity in the liver and muscle rose about 30 percent on a detailed lab test.
What is the TUDCA dosage?
No human dose established. Amounts that were given in studies sit in Human evidence on this page. None of them is a personal dose. 3 completed trials, 54 people given it
Is TUDCA FDA-approved?
Not approved on its own. A fixed mix of sodium phenylbutyrate and taurursodiol was FDA-approved for ALS. Its maker then chose to pull it from sale, after the final-stage PHOENIX study found no change in its main measure of how well patients could function. TUDCA on its own is sold as a dietary supplement.
Is TUDCA the same as UDCA?
No. TUDCA is UDCA with taurine attached. It is the form most brain-protection research uses, and the one sold as a supplement. UDCA is the plain parent form. It is an approved prescription medicine for liver diseases where bile does not flow properly. In testing at several labs, it did not change mouse lifespan. Evidence for one does not automatically carry over to the other.
Does TUDCA improve insulin sensitivity?
In the one study that measured it properly, yes. Using a detailed lab test, insulin sensitivity in liver and muscle rose about 30 percent in 20 obese adults over four weeks. Fat tissue did not respond. The cell stress markers that were supposed to explain it did not change. It is a strong marker result in a very small study, and nobody has followed it with a study that counts who gets diabetes.
What happened with the ALS drug?
A combination of sodium phenylbutyrate and taurursodiol was approved because of the mid-stage CENTAUR study. The large final-stage PHOENIX study then showed no change on the ALS function scale at 48 weeks. The maker then started pulling the drug from sale with the FDA and Health Canada. A separate European final-stage study of TUDCA alone is registered. Its registry status is unknown, and no results paper was found here.
Does TUDCA protect the liver?
The liver approvals belong to UDCA, for specific diseases where bile does not flow properly. They do not belong to TUDCA in healthy people. No study has tested TUDCA as liver support in anyone without liver disease, which is how most of it is sold.
Is there any evidence it slows ageing?
None in humans. The nearest result is for the parent compound. UDCA did not clearly change lifespan in either sex in the multi-lab mouse testing program.