The impact of early life stress
Growing up in poverty or an abusive or neglectful family environment has been shown to be a strong predictor of poor health in adulthood. Loyola University Chicago scientists Linda Janusek, PhD, RN, FAAN, and Herb Mathews, PhD, are investigating the mechanisms by which childhood adversity predisposes individuals to poor health.
One possibility by which an adverse childhood environment might increase risk for disease is epigenetic embedding. Epigenetics determine how a person’s genes are expressed, that is turned on or off, without changing the actual DNA sequence. Changes in epigenetic regulation of gene expression occur in response to one’s life experiences and environment. The epigenome, a network of chemical compounds that have a role in determining which genes are active in a particular cell, is especially sensitive to experiences in early life, including childhood and adolescence. Such epigenetic changes can become embedded into a person’s DNA and persist into adulthood.
Janusek, professor and the Marcella Niehoff School of Nursing Endowed Chair for Research, and Mathews, a professor of Microbiology and Immunology, recently reported findings in the journal Brain, Behavior, and Immunity that show African American men ages 18-25 exposed to traumatic experiences during childhood produce an exaggerated inflammatory response to stress, termed a “stress-vulnerable phenotype.” A phenotype is visible physical characteristics, such as eye or hair color. In this case, the phenotype is increased inflammation throughout the body.
Janusek and Mathews’ research also showed that the young men, recruited from Rogers Park and Maywood, who exhibited a stress-vulnerable phenotype also had epigenetic changes that resulted in increased expression of inflammatory genes. This suggests that an epigenetic mechanism links childhood adversity to abnormal stress-related inflammation during adulthood. Inflammation is a key component in eight of the top 10 leading causes of death in the United States, including heart disease, cancer, diabetes, and stroke—many of which disproportionately afflict disadvantaged African Americans.
The researchers also identified a specific stress-resilient phenotype within the group of African American men in their study. “This stress-resilient phenotype was found in men who experienced high levels of early life stress and adversity, but who did not produce a heightened inflammatory response to stress challenge,” says Janusek. “A stress-resilient phenotype is consistent with the idea that some individuals who experience a difficult childhood are able to adapt, thrive, and effectively respond to future environmental challenge.”
Their current research project, funded by the health disparities initiative of the University’s strategic plan, is focused on identifying epigenomic pathways impacted by early life stress and adversity. These pathways are hypothesized to result in the two contrasting adult phenotypes: stress-vulnerable and stress-resilient. The stress-vulnerable phenotype produces a greater pro-inflammatory response to stress, while the stress-resilient phenotype promotes a more adaptive stress response despite a difficult childhood.
For that study, Janusek and Mathews are focusing on a group of 74 genes previously shown to be responsive to stress and adversity. In addition, those genes are implicated in the development of heart disease and metabolic disorders, where excess stress exposure and elevations in inflammation play a role. Discovering epigenomic pathways associated with childhood adversity and risk for poor health throughout a person’s life will lead to the identification of biomarkers that can help determine which individuals are at risk for a stress-vulnerable phenotype. This could set in motion preventive measures targeted to people who are vulnerable to adverse early life experiences, but who do not yet have symptoms of inflammatory disease.
The field of epigenetics is rapidly evolving and has the potential to deepen our understanding of how the environment influences the genome and a person’s health over the lifespan.
“Other ongoing research suggests that an unfavorable epigenetic profile can be diminished or even reversed by lifestyle interventions, such as by modifying diet, increasing physical activity, lowering levels of psychological stress, and implementing strategies that enrich the early-life environment,” says Janusek.