Psychosocial stress has profound effects on physical and mental health. Recent evidence suggests that this association can be epigenetically mediated. Exposure to psychosocial stress, particularly early in life, might trigger alterations in the epigenome, such as changes in DNA methylation. In this chapter we will summarize human epigenetic research assessing DNA methylation changes related to psychosocial stress exposure, with a focus on early life adversities. Various epigenetic studies investigated maternal psychosocial stress or mood disturbances during pregnancy in relation to the offspring's epigenome at birth or later in life or child maltreatment, adverse socioeconomic conditions, or stressful life events during childhood in relation to DNA methylation, in postmortem brain tissue, peripheral blood, saliva, and buccal epithelial cells, later in life. Although many of these studies indicate that alterations in DNA methylation persist from early life until adolescence or even adulthood, recent evidence also suggests that the human methylome might remain dynamically regulated by psychosocial experiences even beyond childhood. Interestingly, psychosocial stress across different age ranges was linked to changes in DNA methylation of genes implicated in the stress response system, such as the glucocorticoid receptor gene (NR3C1); FK506 binding protein gene (FKBP5); serotonin transporter gene (SLC6A4); genes involved in development, including the brain-derived neurotrophic factor gene (BDNF); parentally imprinted genes; and genes involved in the immune system. We here review selected findings from this rapidly growing research field and discuss limitations as well as potential implications for research and clinical practice.