Abstract. This chapter examines the biological pathways through which prenatal maternal stress, triggered by natural disasters, affects maternal and foetal health. Key mechanisms include HPA axis dysregulation and increased cortisol exposure, which may alter foetal development and long-term stress regulation. The chapter also explores epigenetic modifications, particularly DNA methylation, as lasting markers of prenatal stress, as well as emerging evidence on immune and inflammatory responses. Together, these findings highlight how acute stressors during pregnancy may have lasting, systemic impacts on offspring health and development. While biological mechanisms underlie the effects of prenatal maternal stress, social factors—at both individual and contextual levels—also shape how natural disasters affect maternal and child health and contribute to heterogeneity in its impacts. Country-specific conditions like infrastructures and healthcare quality moderate child outcomes. Maternal socioeconomic resources show a moderating role too. Disadvantaged mothers tend to face greater exposure, display more limited coping strategies and overall show higher risk of adverse outcomes. Timing also matters: First trimester exposure is linked to shorter gestation and low birth weight. Sex differences exist too, with varying physiological responses. Long-term effects of these initial disadvantages induced by natural catastrophes include chronic disease and reduced educational attainment.