Tylenol in pregnancy is back in the headlines, and this time the concern has nothing to do with autism or neurodevelopment. A new study is asking a very different question: could taking Tylenol during pregnancy affect the future reproductive health and fertility of a daughter?
The study, from a Danish research group following approximately 300 infant girls, reported small differences in ovarian size, uterine volume, follicle counts, and, in one subgroup, AMH levels depending on when their mothers were exposed to paracetamol (acetaminophen, or Tylenol) during pregnancy. Put “Tylenol,” “pregnancy,” “ovaries,” and “future fertility” together in a headline, and it’s understandably going to sound alarming.
I’m Dr. Lucky Sekhon, a double board-certified Reproductive Endocrinologist and Infertility specialist practicing in New York City. Through my work with fertility patients, my Instagram @lucky.sekhon, my newsletter The Lucky Egg Drop, and my book The Lucky Egg: Understanding Your Fertility and How to Get Pregnant Now, I spend a lot of time cutting through exactly this kind of reproductive-health noise. I’ve discussed Tylenol in pregnancy before, particularly during the debate over its purported association with autism, and the same fundamental principle applies here: finding an association does not prove that a medication caused the outcome. I also recorded a full video breaking down this new study if you want to hear me walk through the research in more detail.
TLDR: This is far from proof that taking Tylenol during pregnancy can damage your daughter’s future fertility. Absolutely not.
This is a real study asking a reasonable scientific question, and its findings are worth investigating further. But it does not change how I currently counsel patients about Tylenol use during pregnancy. Let’s look at what the researchers actually found, the significant limitations in how those findings were measured, and why a difference that is statistically significant on paper may have little to no clinical significance in the real world.
What the new Tylenol pregnancy study actually found
The COPANA study, published in Human Reproduction Open, examined prenatal paracetamol exposure and markers of reproductive development in infant girls. At around three months of age, researchers performed transabdominal ultrasounds to measure the babies’ ovaries and uterus, count ovarian follicles, and assess breast tissue. They also measured reproductive hormones. The researchers reported that exposure earlier in pregnancy was associated with slightly smaller ovaries and reduced uterine volume, while exposure after 17 weeks was associated with approximately one fewer ovarian follicle. In one relatively small subgroup exposed very early in pregnancy, AMH, a hormone produced by ovarian follicles, was also lower.
The biological hypothesis behind this is interesting. Animal studies have suggested that prenatal paracetamol exposure may interfere with the formation of primordial follicles, the microscopic structures containing immature eggs that develop while a female fetus is still in the womb. The theory is that fewer follicles could lead to lower estrogen production, which might then affect estrogen-responsive organs like the uterus and breast tissue. Evidence tier: suggestive but inconclusive. This is an interesting biological hypothesis! BUT, it is not evidence that prenatal Tylenol exposure reduces fertility in human daughters!
| What the study found | What it does not establish |
|---|---|
| Slightly smaller ovarian measurements with some exposure windows | That Tylenol damaged the ovaries |
| Reduced uterine volume with some early exposure | That the difference affects reproductive function |
| About one fewer follicle with exposure after 17 weeks | That a daughter has meaningfully fewer eggs or lower fertility |
| Lower AMH in a small early-exposure subgroup | That she will have diminished ovarian reserve as an adult |
| Associations between exposure and infant measurements | Cause and effect |
What this study does NOT prove
Established evidence: this was an observational cohort study. Observational research can identify associations, but it cannot establish cause and effect. That distinction matters enormously here because the absolute differences were small, and we have no evidence that they translate into anything clinically relevant when it comes to infertility. Does the difference of one follicle mean anything, really? Independent experts reviewing the research raised the same concern: it remains unknown whether these small differences persist into adulthood or affect fertility at all.
Then there is the measurement problem, which jumped out at me immediately as a fertility doctor who has lost count of the number of ultrasounds I have done in my career. Anyone who has ever performed a transabdominal ultrasound will tell you it is nowhere near as precise as a vaginal ultrasound when it comes to measuring ovaries or follicles. Measuring tiny ovaries and trying to count follicles in three-month-old babies with an abdominal ultrasound is technically difficult. In many babies, both ovaries could not be visualized. When only one ovary was seen, the researchers estimated the total follicle count based on the visible ovary. When your headline finding is roughly “one fewer follicle,” those measurement limitations really matter. As I put it in my original discussion of this study: garbage in, garbage out. If measurements aren’t reliable or accurate, we can’t build solid conclusions from them.
Exposure measurement was imperfect, too. One seemingly strong feature of the study was that researchers did not rely exclusively on mothers remembering whether they had taken Tylenol. They also measured paracetamol in urine at around 14 weeks. But that is one snapshot during a nine-month pregnancy, not a reliable measure of exposure throughout pregnancy. Some women had detectable paracetamol despite not reporting early pregnancy use, further complicating the question of exactly who was exposed, when, and by how much.
And then there is the confounding! The exposed and unexposed groups differed in clinically relevant ways, including more smoking in the first trimester in the exposed group. People also generally take Tylenol because something else is happening: fever, infection, migraine, or pain, any of which could itself be related to the outcome being studied. Statistical adjustment helps, but it cannot guarantee every meaningful difference between groups has disappeared. I often describe this to patients using the umbrella analogy: people carry umbrellas when it rains, but umbrellas don’t cause the rain.
Finally, when researchers test many different outcomes, we have to consider the possibility that some associations will appear statistically significant simply by chance. Independent statistical commentary on the COPANA paper specifically highlighted this problem: numerous outcomes were examined, while only a small number crossed the conventional threshold for statistical significance. Statistical significance does not automatically equal clinical significance. A measurable difference on a spreadsheet is not necessarily a meaningful difference in someone’s health.
So will Tylenol affect my daughter’s fertility?
My clinical opinion: based on this study, we cannot conclude that taking Tylenol during pregnancy will affect your daughter’s future fertility.
An ultrasound measurement taken from the tiny ovaries of a three-month-old baby is not a fertility test. A difference of approximately one observed follicle is not a diagnosis of diminished ovarian reserve, and it certainly cannot tell us how many healthy eggs that child will have decades later or whether she will have difficulty conceiving. I spend a significant amount of time counseling women who have been unnecessarily frightened by ovarian reserve numbers taken out of context, particularly AMH and antral follicle count. Those markers have specific clinical uses, but they are not crystal balls for future fertility. In The Lucky Egg, I make the same distinction repeatedly: egg quantity and egg quality are different concepts, and ovarian reserve measurements should never be treated as simple fertility scorecards.
Future fertility is shaped by many factors, including genetics, reproductive aging, ovulation, egg quality, sperm, the fallopian tubes, the uterus, and medical conditions that may develop over a lifetime. One technically difficult ultrasound performed during infancy cannot meaningfully predict that reproductive future.
Why this isn’t the autism scare all over again
This is a different study looking at a different biological question, but it illustrates the same problem we encounter repeatedly with observational research: association is not causation.
One of the strongest examples comes from the much-discussed question of Tylenol and autism. A huge 2024 Swedish study published in JAMA included nearly 2.5 million children. In standard population analyses, associations could appear between acetaminophen exposure and neurodevelopmental outcomes. But when researchers compared siblings, which helps account for genetic and environmental factors shared within families, there was no association between acetaminophen use during pregnancy and autism, ADHD, or intellectual disability. The authors concluded that the associations seen in less-controlled analyses were likely explained by familial confounding.
That study does not answer the ovarian-development question raised by COPANA, but it shows why we have to be so careful before jumping from “people who took this medication had a different outcome” to “this medication caused that outcome.”
What I actually tell my patients about taking Tylenol while pregnant
For my patients asking, “Can you take Tylenol while pregnant?”, this new study does not change my advice. Acetaminophen remains an important option for treating pain and fever during pregnancy — it is the first-line pain and fever reliever recommended by the American College of Obstetricians and Gynecologists in pregnancy. I recommend using medication when it is actually needed, at the lowest effective dose for the shortest necessary duration, and discussing prolonged or frequent use with your OB/GYN.
Importantly, not treating fever and pain isn’t automatically safer. The decision is always about balancing benefits and risks, including the risks of the condition you are trying to treat.
| Issue | Practical approach |
|---|---|
| Tylenol / acetaminophen | Can be used when clinically needed; use the lowest effective dose for the shortest necessary duration |
| Frequent or prolonged pain/fever | Speak with your OB/GYN and address the underlying cause rather than repeatedly self-treating |
| Ibuprofen / NSAIDs | Not a simple substitute for acetaminophen in pregnancy; NSAID use has important pregnancy-specific restrictions |
| Untreated fever or significant pain | “Doing nothing” is not automatically the safer option; seek medical advice |
This is also where pregnancy advice can become unnecessarily cruel. Pregnant women are constantly handed new lists of things to fear, avoid, and stop doing. I wrote in The Lucky Egg about how easy it is to fall into a “life-in-a-bubble” mentality when trying to conceive. The goal is sensible, evidence-based decisions, not an impossible standard where every exposure becomes another opportunity for guilt.
What I want you to take away from this study
We should absolutely keep studying medication exposures during pregnancy. If future, larger studies using more reliable measurements find consistent evidence that prenatal acetaminophen exposure alters reproductive development in a clinically meaningful way, then our counseling should change with the evidence.
But we are not there.
A small observational study with significant technical challenges should be used to generate a hypothesis for future research. It shouldn’t be used to terrify women into blaming themselves for treating their fever or migraine.
So if you took Tylenol while pregnant, this study is not a reason to look backward and wonder whether you harmed your daughter. And if you are pregnant now, it is certainly not a reason to panic, feel guilty, or suffer through pain and fevers because you are frightened to take Tylenol. Talk to your doctor, use medications thoughtfully, and remember that a scary headline and proof of harm are two very different things.
For more science-backed fertility and reproductive-health information, you can follow me @lucky.sekhon on Instagram, subscribe to The Lucky Egg Drop, or read my book, The Lucky Egg: Understanding Your Fertility and How to Get Pregnant Now.
