New research establishes a link between adverse childhood experiences and alterations in mitochondrial bioenergetics later in life, underscoring how early-life stress impacts cellular health. The study also revealed that different types of childhood stressors leave distinct biological imprints. Published in Biological Psychiatry, these findings deepen our understanding of how negative events in early childhood can shape mental and physical health across the lifespan, paving the way for improved screening and intervention strategies.
Adverse childhood experiences encompass situations that deviate from expected environments and demand adaptation, including abuse, food scarcity, and physical neglect. Recent data indicates that 64% of adults in the United States have encountered at least one such adverse event during childhood or adolescence, with nearly one in five (17.3%) reporting four or more.
“Stressful and traumatic experiences affect both mental and physical health,” explains lead author Jennifer A. Sumner from the University of California, Los Angeles. “In this study, we focused on mitochondrial function as a potential pathway through which stress becomes biologically embedded. Mitochondria are often called the ‘powerhouses of the cell,’ but they do much more and play a key role in stress-related disorders and biological aging.”
Despite growing awareness of how psychosocial stress influences mitochondrial function, very few studies have examined the impact of early-life adversity on mitochondrial activity in living cells. This research is the first to explore how such adversity affects mitochondrial bioenergetics in a diverse group of adult men and women.
Given the high prevalence of adverse childhood experiences and their significant effects on mental and physical health, researchers investigated how early adversity might impact mitochondria. In a sample of 143 adults who had experienced trauma, they measured various bioenergetic parameters of living mitochondria using a mitochondrial stress test. They found that cumulative adverse childhood experiences were linked to mitochondrial bioenergetic patterns marked by increased respiratory (energy-producing) capacity.
The team distinguished between trauma types: experiences characterized by threat, such as abuse or violence, and those involving deprivation, like neglect or food scarcity, were associated differently with markers of mitochondrial function. This suggests that the nature of adversity uniquely influences biological health. Threat was linked to lower cellular energy demand and a shift away from glycolysis (the process of breaking down sugar [glucose] for energy), whereas deprivation was tied to higher glycolytic activity and less efficient energy production, potentially indicating greater dysfunction.
By examining distinct aspects of early-life adversity—specifically threat and deprivation—in relation to mitochondrial function, the study offered more nuanced insights into the connection between childhood hardships and mitochondrial health.
“We were particularly struck by the different mitochondrial functioning patterns observed depending on whether participants had experienced threat or deprivation in early childhood,” comments co-author Shilo Cleveland from UCLA. “Understanding how adverse events during childhood and adolescence relate to mitochondrial function could help design targeted interventions earlier in life to improve health outcomes before age-related diseases set in.”
Sumner adds, “Our findings suggest that taking a more refined approach to conceptualizing experiences of early-life adversity may help uncover distinct mechanisms of biological stress embedding.”
The researchers note that future studies should continue exploring the mechanisms through which early adversity influences lifelong health, aiming to develop more effective prevention and intervention strategies.
“There is growing interest in how cellular dysfunction impacts mental health. This study demonstrates that childhood trauma leaves a lasting mark on mitochondrial function in adulthood, highlighting a key mechanism through which early-life stress contributes to the biological underpinnings of psychiatric disorders,” concludes John Krystal, editor of Biological Psychiatry.
About the Author
