Antidepressants, particularly selective serotonin reuptake inhibitors (SSRIs), can cross the placenta and influence fetal development, but the relationship between their use during pregnancy and autism spectrum disorder (ASD) in children is complex and not fully understood. The placenta plays a critical role in regulating serotonin levels delivered to the fetus, which is important because serotonin acts as both a neurotransmitter and a growth factor during development[1][2].
The placenta does not produce serotonin itself but controls how much maternal serotonin passes through to the fetus. Research from Yale University shows that the placenta’s serotonin transport mechanisms can affect fetal growth and brain development. Increased serotonin transport through the placenta has been hypothesized to be linked with larger fetal brain size and folding patterns, traits often observed in children with autism[1][2]. Conversely, SSRIs, which reduce serotonin uptake into the placenta, have been associated with smaller babies, indicating that altering serotonin levels can impact fetal growth[1].
At the molecular level, serotonin is transported into placental cells via the serotonin transporter (SERT). This serotonin can modify gene expression through a process called serotonylation, which affects placental and fetal development. Blocking SERT with SSRIs like escitalopram changes the expression of hundreds of genes involved in cell proliferation, growth, and survival in placental cells, suggesting that SSRIs can influence placental function and potentially fetal development[3].
Regarding autism risk, some studies suggest that altered serotonin levels during pregnancy might contribute to neurodevelopmental changes associated with ASD. However, the evidence is not definitive, and the placenta’s regulation of serotonin is influenced by fetal genetics rather than solely maternal environment[1]. This means that genetic factors in the fetus may determine how serotonin is transported and metabolized, complicating the direct attribution of autism risk to maternal SSRI use.
Clinical observations note that SSRIs carry some risks during pregnancy, such as neonatal adaptation syndrome and rare conditions like primary pulmonary hypertension, but these are generally considered manageable. Importantly, untreated maternal depression poses significant risks, including suicide, which is a leading cause of maternal mortality. Therefore, the decision to use SSRIs during pregnancy involves weighing the benefits of maternal mental health against potential fetal risks[2].
Other prenatal factors, such as iron deficiency and maternal stress, also influence neurodevelopment and may contribute to autism risk. For example, prenatal iron deficiency has been linked to increased risk of autism and other neurodevelopmental disorders, possibly through its effects on brain iron levels and development[4]. Maternal stress during pregnancy is associated with a higher likelihood of neurodevelopmental disorders including ASD, suggesting that multiple prenatal environmental factors interact with genetic predispositions to influence autism risk[5].
In summary, antidepressants like SSRIs do cross the placenta and affect serotonin transport, which plays a crucial role in fetal brain development. While altered serotonin levels have been hypothesized to relate to autism, current research indicates that fetal genetics and other prenatal factors also significantly contribute to this risk. The use of SSRIs during pregnancy requires careful clinical consideration to balance maternal and fetal health.
—
**Sources:**
[1] Yale News, “‘Serotonin shield’: The placenta’s critical role in the health of babies,” 2025.
[2] Connecticut Public Radio, “Yale study examines how the placenta regulates serotonin, with implications for autism research,” 2025.
[3] PMC, “Role of Serotonin on Gen
