Adverse Childhood Experiences: Why Cortisol Responses Matter

Source: Alexas Fotos/Pixabay

Accumulating evidence suggests that adverse childhood experiences may have long-term impacts on the brain. ACEs can also increase some adolescents' odds of experiencing learning difficulties and anxiety disorders in adulthood.

But not all kids who are exposed to adversity and psychological distress around the time of puberty (i.e., peripubertal stress) respond the same way. Why are some adolescents more vulnerable to stress-inducing experiences during this pivotal time window of brain development than others?

New research (Tzanoulinou et al., 2020) using animal models suggests that the capacity to bounce back and recover from elevated stress hormone (i.e., cortisol) levels—but not necessarily the amount of cortisol that is released during stress exposure—predicts the degree that early life adversity has long-term consequences on brain plasticity and cognition. These findings were recently published in the Neurobiology of Stress open-access journal.

"Our results suggest that the degree of stress-induced adaptation of the hypothalamus-pituitary-adrenal axis in the important transition period of puberty is related to the long-term programming of cognition, behavior, and endocrine reactivity," first author Stamatina Tzanoulinou of Switzerland's École Polytechnique Fédérale de Lausanne said in a news release.

For this research into the long-term consequences of stress exposure during the developmentally critical period around the time of puberty, an international team of scientists conducted water maze experiments using lab rats exposed to peripubertal stress during their adolescence. The researchers performed similar water maze tests again when the same lab rats were adults and compared the results.

"Testing spatial learning in rats is a way of assessing cognitive, memory, and learning skills in the laboratory. This learning goes beyond the academic knowledge and extends to all facets of daily life," senior author Cristina Márquez of Spain's Institute of Neurosciences noted.

Interestingly, lab rats that recovered less quickly to skyrocketing stress hormone levels in the early stages of life also showed hippocampal differences related to the expression of PSA-NCAM, a neuroplasticity marker.

According to the authors, this suggests "a neurobiological mechanism by which peripubertal stress would alter the normal maturation of plasticity processes in specific regions of the brain, such as the hippocampus, leading to a deterioration in cognitive performance and the appearance of anxiety-related behaviors later in life."

These findings open the door for better ways to spot adolescents who are particularly susceptible to the long-term consequences of adverse childhood experiences. Identifying adolescents who are more vulnerable to ACEs could facilitate earlier therapeutic interventions—such as counter-ACEs, a.k.a. positive childhood experiences (PCEs)—that might offset early childhood adversity risks. (See "Seven Early Experiences with Potential Benefits in Adulthood.")

"The programming effects of early stress may need an incubation period that can be reversed in young and more plastic brains, but not during adulthood," Márquez concluded. "Therefore, following early detection of individuals vulnerable to stress, there could be a window of opportunity for therapeutic intervention in adolescence to avoid the natural course into psychopathology and cognitive impairment."