There is a cluster of studies in which TUDCA improved embryo development, implantation rates and live births. Search for TUDCA and fertility and you will find them summarised as though they describe a fertility supplement. They do not, and the reason is a single detail that changes the meaning of the entire literature.
In every one of these studies, TUDCA was added to the culture medium the embryos were growing in. Not to an animal’s food, not by injection, not to a person. Into the dish. That distinction is the whole point of this page, and it is worth understanding properly rather than being warned about vaguely.
Key Takeaways
- Mouse two-cell embryos cultured with 50 micromolar TUDCA for 52 hours and then transferred to foster mothers produced significantly higher pregnancy and implantation rates and more live pups per surrogate than untreated controls[1].
- In that study there was no difference in the mean weights of the pups or the placentas[1], so the benefit was in how many embryos survived, not in how they grew afterwards.
- In embryos created by intracytoplasmic sperm injection, 200 micromolar TUDCA reduced the ER stress marker BIP and improved developmental competence, implantation and birth rate[2].
- TUDCA improved blastocyst quality in pig embryos made from in vitro matured oocytes and dried sperm, reducing reactive oxygen species and DNA fragmentation and shifting the balance of Bax and Bak against Bcl-2 and Bcl-XL[3].
- The receptor involved is TGR5. TUDCA acting through TGR5 rescued development in glucose-stressed pig embryos[4] and facilitated DNA damage repair after ultraviolet stress[5].
- In postovulatory aged pig oocytes, TUDCA in the maturation medium preserved spindle structure and cortical granule distribution and raised blastocyst rates[6].
- No study has given TUDCA to a person, or to an animal, for a fertility outcome. This is laboratory embryo culture research, largely veterinary and assisted reproduction focused.
What These Studies Actually Did
The cleanest example is a 2015 paper in Reproductive Biology[1]. Mouse two-cell embryos were collected by flushing the oviduct, then cultured for 52 hours either with or without 50 micromolar TUDCA. The resulting blastocysts were transferred into 2.5-day pseudopregnant foster mothers, and the researchers counted pregnancies, implantations and live pups.
The TUDCA group did better on all three. The authors noted it was the first report that supplementing the embryo culture medium with TUDCA increased implantation and live birth rates of transferred embryos. They also reported that pup and placental weights did not differ, which is a useful negative: the treatment changed survival, not growth.
Read that sequence again and notice where TUDCA was. It was in the dish, for 52 hours, before transfer. The foster mother never received it. Nothing in this experiment tells you what happens if a mammal ingests TUDCA and then tries to conceive, because that experiment was not performed.
A 2020 study in Journal of Assisted Reproduction and Genetics followed the same design in ICSI embryos, using 200 micromolar TUDCA[2]. ICSI embryos showed higher BIP expression than conventional IVF embryos, indicating more ER stress, and TUDCA reduced it while improving the inner cell mass to trophectoderm ratio, pregnancy, implantation and birth rates. Again: added to the embryo, not to the parent.
The Mechanism Is Consistent and the Receptor Is Known
Early embryos are unusually vulnerable to ER stress. They have no maternal blood supply yet, they are dividing rapidly, and in the laboratory they sit in artificial media under conditions that are at best an approximation of an oviduct. Anything that reduces stress-induced apoptosis at that stage has an obvious route to improving how many embryos survive to blastocyst.
Several studies establish TGR5 as the receptor. In glucose-stressed pig embryos, a model motivated by the association between diabetes, obesity and infertility, TUDCA acting through TGR5 promoted survival and early development[4]. In pig embryos given ultraviolet-induced nuclear stress, TUDCA reduced DNA damage measured by gamma-H2AX and ER stress measured by GRP78, again via TGR5, and rescued early development[5]. That is the same receptor that turns up in the gut barrier work, which is a reassuring sign of a coherent mechanism rather than a scattering of unrelated findings.
The antioxidant side appears too. In pig embryos produced from in vitro matured oocytes and evaporatively dried boar sperm, a preservation technique that damages sperm DNA, TUDCA in the culture medium reduced reactive oxygen species, DNA degradation and fragmentation, lowered Bax and Bak and raised Bcl-XL and Bcl-2, and improved blastocyst quality[3]. A 2025 study in postovulatory aged pig oocytes reported preserved oocyte morphology, cortical granule distribution and spindle structure, higher blastocyst rates and cell numbers, lower ROS and higher glutathione[6].
Notice what most of these have in common. Dried sperm, aged oocytes, ultraviolet damage, high glucose: they are all deliberately compromised starting material. TUDCA is repeatedly rescuing embryos that were damaged on purpose, which is the right way to test a protective compound and a poor basis for claiming it improves healthy reproduction.
Why This Is Veterinary and Laboratory Research
Look at the journals. Reproductive Biology, Molecular Reproduction and Development, Biology of Reproduction, Veterinary Sciences. Look at the species: mouse and pig. Pig embryo work of this kind is usually aimed at livestock breeding and at the general problem of making embryo culture media better, and mouse work is the standard proving ground for techniques that might later be tried in human assisted reproduction.
That is a legitimate and valuable research programme. If TUDCA does eventually reach human fertility care, the realistic route is as an additive in an embryology laboratory’s culture medium, used under a clinic’s protocol with the concentration controlled to the micromolar and the exposure measured in hours. It would be a change to how embryos are handled, not something a patient buys.
The gap between that and an oral supplement is not a technicality. A concentration of 50 to 200 micromolar maintained in a droplet of medium around an embryo has no straightforward relationship to whatever fraction of a swallowed capsule survives first-pass metabolism and reaches a follicle or an oviduct, and TUDCA’s absorption and distribution have never been measured in reproductive tissue.
The Safety Question Nobody Has Answered
Anyone reading a fertility page is, by definition, thinking about becoming pregnant, which makes this the most important section here.
TUDCA has not been established as safe in human pregnancy. There is no trial, no registry, and no meaningful safety dataset in pregnant women, and the contraindications page treats pregnancy and breastfeeding as reasons to avoid it for exactly that reason. Absence of evidence of harm is not evidence of safety, particularly for a compound that acts on a receptor expressed in early embryos.
It is also worth naming the direction of risk properly. TUDCA works partly by inhibiting apoptosis, and programmed cell death is not an error during development; it is part of how embryos and fetuses are built. A compound that suppresses it, at an unknown tissue concentration, at an unknown developmental stage, is not something to assume is neutral.
If you are undergoing fertility treatment, tell the clinic about every supplement you take. That is not a formality here: some are contraindicated around specific protocols, and the clinic controls the embryo culture conditions these studies are actually about.
Nothing on this page is medical advice. TUDCA is not established as safe in pregnancy or while trying to conceive, and fertility treatment decisions belong with a clinician who knows everything you are taking.
Frequently Asked Questions
Does TUDCA improve fertility?
There is no evidence that taking TUDCA improves fertility in any species. The studies people cite added TUDCA to embryo culture medium in the laboratory, at 50 to 200 micromolar for a matter of hours, and then measured what happened to those embryos[1][2]. No study has given TUDCA to an animal or a person and measured a fertility outcome.
What did the mouse implantation study actually show?
Mouse two-cell embryos cultured with 50 micromolar TUDCA for 52 hours, then transferred to pseudopregnant foster mothers, produced significantly higher pregnancy and implantation rates and more live pups per surrogate than untreated embryos, with no difference in pup or placental weight[1]. The foster mothers received no TUDCA, so the result is about how the embryos were handled before transfer.
Is TUDCA safe to take while trying to conceive?
It has not been established as safe, and this site lists pregnancy and breastfeeding among the situations to avoid it. There is no human pregnancy safety data, and TUDCA acts partly by inhibiting apoptosis, which is a normal and necessary part of embryonic development. That combination is a reason for caution rather than reassurance. Ask the clinician managing your care.
Could TUDCA be used in IVF?
Possibly, as a culture medium additive rather than a patient supplement. The existing work is mostly in mouse and pig embryos and is aimed at improving embryo culture and livestock breeding[3][4][6], with the receptor identified as TGR5[5]. Any human use would have to be validated in a clinical embryology setting with controlled concentration and exposure, and that has not happened.
References
- Tauroursodeoxycholic acid improves the implantation and live-birth rates of mouse embryos. Reprod Biol (2015).
- Tauroursodeoxycholic acid (TUDCA) enhanced intracytoplasmic sperm injection (ICSI) embryo developmental competence by ameliorating endoplasmic reticulum stress. J Assist Reprod Genet (2020).
- Tauroursodeoxycholic acid enhances the development of porcine embryos derived from in vitro-matured oocytes and evaporatively dried spermatozoa. Sci Rep (2017).
- Tauroursodeoxycholic acid/TGR5 signaling promotes survival and early development of glucose-stressed porcine embryos. Biol Reprod (2021).
- Tauroursodeoxycholic acid acts via TGR5 receptor to facilitate DNA damage repair and improve early porcine embryo development. Mol Reprod Dev (2020).
- Tauroursodeoxycholic Acid Enhances the Quality of Postovulatory Aged Oocytes by Alleviating Oxidative Stress, Apoptosis, and Endoplasmic Reticulum Stress. Vet Sci (2025).
These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure, or prevent any disease. Content is for informational purposes only and is not medical advice; consult a qualified healthcare provider before starting any supplement. As an Amazon Associate we earn from qualifying purchases.