Chelsey Lee, M.P.H.

Research Description

Our capacity for health and disease is intimately tied with the environment and the experiences to which we are exposed. Early life adversity is highly and universally prevalent, and accounts for increased mortality, as well as increased rates of mental and physical morbidity. This is manifested in the incidence of mental health disorders and chronic medical conditions well into adulthood, including cardiovascular disease, inflammation, obesity, and cancer. The Centers for Disease Control and Prevention revealed that 60.9% of adults reported to have experienced a minimum of one type of adverse childhood exposures (ACE), and 15.9% experienced an alarming four or more ACEs. This recent statistic underscores the sheer prevalence and far-reaching consequences of ACEs on human health and behavior. The early timing of exposure may significantly alter the set point of future transcriptional responses. In excess, this imparts hyper- or hypo-sensitivity to stress, indelibly shaping an individual’s propensity to cope with cognitive challenges later in life. 

A rapidly developing area of research regarding the effects of environment on psychiatric outcomes has focused on epigenetic factors, such as DNA methylation, histone modification and non-coding RNA. A variety of environmental insults, including maternal stress and nutrition, heavy metals, pesticides, and air pollution have been linked to epigenetic alterations. However, the pathophysiological basis of how such epigenomic modifications occur and which are causally relevant to psychiatric phenotypes remains poorly understood. Chelsea's research focuses on identifying the phenotypic consequences occurring in a mouse model of ACE.