Prenatal stress in humans is linked to epigenetic changes, particularly DNA methylation (DNAm), which may influence child health outcomes. This review summarizes current research on how prenatal stress affects DNAm and its implications for child development. Prenatal stress is defined broadly, encompassing both objective and subjective stressors, and includes psychosocial stressors like domestic violence and pregnancy-specific stressors such as concerns about fetal health. Epigenetic mechanisms, including DNAm, are thought to mediate the biological embedding of prenatal stress, with studies showing associations between prenatal stress and DNAm changes in genes related to the HPA axis, such as NR3C1, FKBP5, and 11BHSD2. These changes may affect stress reactivity, neurobehavioral outcomes, and mental health in children. Candidate gene studies and epigenome-wide association studies (EWAS) have identified links between prenatal stress and DNAm, though findings often lack replication. EWAS have revealed associations between maternal stress and DNAm in various tissues, but results are inconsistent. Epigenetic clocks suggest that prenatal stress may lead to age-related changes in DNAm, with sex and tissue-specific effects. Prenatal stress may also influence the child's epigenetic age, with implications for health outcomes. Future research should focus on refining the measurement and definition of prenatal stress, incorporating longitudinal and genomic data, and considering the interplay between prenatal and postnatal environments. The role of epigenetic modifications in adaptive programming is also highlighted, suggesting that moderate prenatal stress may have protective effects. Overall, while the evidence is growing, further studies are needed to clarify the mechanisms and implications of prenatal stress on epigenetic changes and child health.Prenatal stress in humans is linked to epigenetic changes, particularly DNA methylation (DNAm), which may influence child health outcomes. This review summarizes current research on how prenatal stress affects DNAm and its implications for child development. Prenatal stress is defined broadly, encompassing both objective and subjective stressors, and includes psychosocial stressors like domestic violence and pregnancy-specific stressors such as concerns about fetal health. Epigenetic mechanisms, including DNAm, are thought to mediate the biological embedding of prenatal stress, with studies showing associations between prenatal stress and DNAm changes in genes related to the HPA axis, such as NR3C1, FKBP5, and 11BHSD2. These changes may affect stress reactivity, neurobehavioral outcomes, and mental health in children. Candidate gene studies and epigenome-wide association studies (EWAS) have identified links between prenatal stress and DNAm, though findings often lack replication. EWAS have revealed associations between maternal stress and DNAm in various tissues, but results are inconsistent. Epigenetic clocks suggest that prenatal stress may lead to age-related changes in DNAm, with sex and tissue-specific effects. Prenatal stress may also influence the child's epigenetic age, with implications for health outcomes. Future research should focus on refining the measurement and definition of prenatal stress, incorporating longitudinal and genomic data, and considering the interplay between prenatal and postnatal environments. The role of epigenetic modifications in adaptive programming is also highlighted, suggesting that moderate prenatal stress may have protective effects. Overall, while the evidence is growing, further studies are needed to clarify the mechanisms and implications of prenatal stress on epigenetic changes and child health.