A 2025 study suggests that acetaminophen (Tylenol), at levels reached after a standard dose, can disrupt embryo development in experimental models, raising questions about its potential impact on IVF outcomes, although better research in humans is needed before changing clinical practice.
Many human embryos arrest or are lost around the time of implantation, and while chromosomal abnormalities explain some cases, many donโt have a clear explanation. Environmental factors like alcohol, smoking, or even medications, have been suspected but are harder to prove.
Acetaminophen (Tylenol, paracetamol, APAP) is one of the most widely used pain relievers worldwide and has long been considered safe for women trying to conceive or during pregnancy.
A new study by Nielsen et al. (2025) set out to test whether acetaminophen could harm embryo development.
For more background, check out my post on embryo arrest.
๐ Original studies are referenced in this post or within the linked Remembryo posts.
๐ก Reminder: Terms underlined with a dotted black line are linked to glossary entries. Clicking these does not count toward your paywall limit.
The team used a wide-ranging experimental approach, testing acetaminophen exposure across several systems: yeast, human cell lines, mouse embryos, and donated human embryos.
Acetaminophen exposure consistently slowed or blocked cell division across the models tested. In yeast and human cells, the drug appeared to act on ribonucleotide reductase, an enzyme needed for DNA synthesis. By blocking this enzyme, acetaminophen can slow DNA synthesis, which in turn could prevent normal cell division.
Acetaminophen reduces implantation in mouse models
In mouse embryos, exposure of acetaminophen above a concentration of 25 ฮผM delayed division of cleavage stage embryos, and higher doses (100โ200 ฮผM) prevented blastocyst formation, suggesting acetaminophen was causing embryo arrest. Even when embryos reached the blastocyst stage, the number of cells in the ICM was reduced.
Importantly, when embryos pre-exposed to acetaminophen were transferred into recipient mice, implantation rates dropped and pregnancy losses increased.
Acetaminophen disrupts human embryo growth
They also measured real drug concentrations in womenโs reproductive tissues after a standard oral dose of acetaminophen.
In humans, a single therapeutic dose (1 g) of acetaminophen was detected in womenโs reproductive tissues within an hour, reaching average levels of ~38 ฮผM in follicular fluid, ~80 ฮผM in endometrium, and ~125 ฮผM in uterine fluid, with one case as high as 291 ฮผM. These doses overlapped with what delayed embryo development in the mouse experiments.
Human cleavage stage embryos exposed to 100โ200 ฮผM showed fewer cells, slower development, or outright cell death with higher doses. Blastocysts exposed for only 6 hours had reduced DNA synthesis within ICM cells, suggesting even brief exposure can disrupt growth.
Conclusions and limitations
This study suggests that acetaminophen, at concentrations measurable in the reproductive tract after a standard dose, can slow DNA synthesis and impair early development.
However, this was a lab-based study with only a few human embryos, and pregnancy loss was shown only in mice; regulatory agencies like the FDA and EMA still consider acetaminophen safe in pregnancy when used as directed.
The results suggest that if acetaminophen is taken around the time of embryo transfer, it is possible that day 3 embryos could be delayed in reaching the blastocyst stage and risk missing the implantation window. Blastocyst transfers might also be affected if ICM quality or DNA synthesis is reduced, and very high doses could be lethal to embryos. However, this has only been shown in lab models, and acetaminophen use around embryo transfer may not be common.
Acetaminophen is more often given before egg retrieval, but the study did not examine whether this affected egg quality or later embryo development. As far as I know, there is no evidence that taking acetaminophen before retrieval causes problems.
Other limitations of the study:
- The exact mechanism is uncertain, since acetaminophen may act on multiple targets (such as PTGS1, PTGS2, CB1, or through its metabolite NAPQI), and while the evidence points to inhibition of ribonucleotide reductase, this was inferred rather than directly proven.
- Small number of human embryos were tested
- Embryo culture conditions differ from the uterine environment and may change how acetaminophen acts
- Evidence for pregnancy loss came only from mouse models and it is unknown if the same occurs in humans
- Concentrations tested on embryos were on the higher end of what was measured in tissues, though some patients did reach those levels
- Drug levels were measured only one hour after administration and it is unknown how concentrations change over time, though repeated dosing could maintain higher levels. The experiments presented here exposed embryos to constant levels for 6 to 48 hours, which arenโt realistic in the body since the drug would be metabolized/eliminated over time (acetaminophen has a half-life of about 2 hours, Mazaleuskaya et al. 2016)
Whatโs ultimately needed are human studies that track acetaminophen use in people trying to conceive and measure pregnancy outcomes directly. Until this data is available, the clinical relevance of these findings remains unclear.
Important: I hesitated to share this study because the findings are concerning, but it was published in a leading fertility journal by a large research team and could eventually inform how a common drug is used in IVF. That said, we are far from that point and much more work is needed! I donโt want to alarm anyone who has had a transfer or is pregnant: right now there is no evidence that acetaminophen affects IVF outcomes, and both the FDA and EMA continue to consider it safe in pregnancy when used as directed. This was a small study with limited human embryo testing, and pregnancy loss was observed only in mice. These results must be confirmed in human patients before any conclusions can be drawn!
Want to read more about embryo arrest or implantation failure?
Embryo arrest is when an embryo stops developing, usually before reaching the blastocyst stage. This post explains possible causes, including embryonic genome activation, maternal effect genes, the subcortical maternal complex, aneuploidy, mitochondrial dysfunction, oxidative stress, lab conditions, and sperm DNA fragmentation. Read more.
This post covers the variety of reasons embryos can fail to implant or miscarry, including as a result of advanced maternal age, chromosomal translocations, lifestyle, endometritis, the microbiota, immunological issues, endometrial receptivity, the clinic, and more. Note that this is not a complete list, and will be updated periodically. Read more.
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About Embryoman
Embryoman (Sean Lauber) is a former embryologist and the founder of Remembryo, an IVF research and fertility education website. After working in an IVF lab in the US, he returned to Canada and now focuses on making fertility research more accessible. He holds a Masterโs in Immunology and launched Remembryo in 2018 to help patients and professionals make sense of IVF research. Sean shares weekly study updates on Facebook, Instagram, and Reddit regularly. He also answers questions on Reddit or in his private Facebook group.
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