There is ongoing scientific investigation into whether a link exists between the use of antidepressants during pregnancy—particularly selective serotonin reuptake inhibitors (SSRIs)—and autism spectrum disorder (ASD) in newborns. The relationship is complex and not fully understood, with research showing mixed findings and emphasizing the importance of considering multiple factors including maternal mental health, genetics, and placental biology.
One key area of research focuses on the role of serotonin, a neurotransmitter that SSRIs affect, and how it is regulated during fetal development. A recent study from Yale University revealed that the placenta plays a critical role in controlling serotonin delivery to the fetus, rather than producing serotonin itself. This regulation can influence fetal brain development and growth. The study found that altered serotonin transport through the placenta might impact the risk of developmental disabilities such as autism. Specifically, increased serotonin levels delivered to the fetus were associated with larger babies and bigger brains but also a higher risk of autism, while SSRIs, which reduce serotonin transport, were linked to smaller babies[1][2].
This research suggests that the fetus’s genetics largely determine placental serotonin transport characteristics, which may predispose to autism independently of external factors like vaccines, a claim that has been scientifically debunked[2]. The findings open the possibility that SSRIs might one day be used pharmacologically during pregnancy to modulate serotonin delivery and potentially reduce autism risk in high-risk pregnancies, although no clinical recommendations currently exist[2].
On the other hand, epidemiological studies have reported associations between prenatal antidepressant exposure and increased rates of autism or other neurodevelopmental issues in children. For example, a study published in the BMJ found that children exposed to antidepressants in utero had higher autism rates compared to children of mothers with mental health disorders who did not take antidepressants. Animal studies also support the idea that SSRIs can affect offspring behavior and social interactions[3]. However, these studies often face challenges in fully accounting for confounding factors such as the underlying maternal mental illness itself, which independently affects fetal development and child outcomes.
Importantly, large-scale and well-controlled studies have also found no significant increase in neurodevelopmental disorders, including autism, following prenatal SSRI exposure. Expert panels and perinatal psychiatrists emphasize that untreated maternal depression carries serious risks such as preterm birth, low birth weight, neonatal intensive care admissions, and even maternal suicide. Moreover, untreated depression can negatively affect fetal brain development through stress hormone dysregulation, which may have lasting effects on the child’s mental health[4][5].
There is also a rare but serious neonatal complication linked to antidepressant use in pregnancy called persistent pulmonary hypertension of the newborn (PPHN), which affects lung blood vessels and oxygen delivery. While uncommon, it has a notable mortality rate and occurs more frequently in babies exposed to antidepressants[3].
In summary, the current scientific consensus is that while some studies suggest a possible association between prenatal antidepressant use and autism, the evidence is not definitive and is complicated by confounding factors. The placenta’s regulation of serotonin is a promising area of research that may clarify mechanisms behind autism risk and guide future interventions. Meanwhile, the risks of untreated maternal depression are well-established and significant, underscoring the need for careful, individualized treatment decisions during pregnancy.
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[1] Yale News, 2025: “Serotonin shield”: The placenta’s critical role in the health of babies
[2] Connecticut Public Radio, 20
