Child Development

Can Childhood Trauma Make the Body and Brain Age Faster?

A new study reveals surprising results.

Posted Aug 06, 2020

 Photo by Heike Mintel on Unsplash
Source: Photo by Heike Mintel on Unsplash

A long-standing body of research shows that adverse childhood experiences such as child abuse, trauma, sexual assault, and chronic poverty can negatively affect people well into adulthood. Adult experiences that have been associated with adverse childhood experiences include post-traumatic stress disorder, depression, dissociative symptoms, and other psychiatric disorders, plus physical illnesses such as diabetes, cancer, and cardiovascular disease.

A recent study found evidence that children who experience abuse and violence age faster, biologically, than children with no such history.

Scientists have known that the wear and tear of stress, and the way we handle it, can make the mind and body "older" or "younger." Nobel Prize-winning scientist Elizabeth Blackburn and health psychologist Elissa Epel researched the psychological factors that may damage our telomeres—the protective tips that reside at the end of chromosomes. When telomeres become too short, they stop dividing, and cells grow old. In addition to shortening, however, the scientists discovered that telomeres also lengthen, which slows down the aging process.

Some of the factors that may determine the aging of the telomeres and prevent premature aging at the cellular level are a healthy diet, genetics, how you respond to stress, ample sleep, and regular exercise. But in addition to these factors, the scientists identified five toxic thought patterns that might also lead to shorter telomeres and premature aging: pessimism, cynical hostility, rumination, thought suppression, and mind straying.

But previous research has reported mixed results on whether childhood adversity is linked to accelerated aging. In the newest study, published in the recent issue of the Psychological Bulletin, the researchers examined two categories of adversity among 116,000 participants: threat-related adversity, such as abuse and violence, and deprivation-related adversity, such as physical or emotional neglect or poverty. They found that children who suffered threat-related trauma were more likely to enter puberty early and also showed signs of faster aging on a cellular level—including shortened telomeres. But children who experienced poverty or neglect did not show either of those signs of early aging.

Next, the scientists examined data from 3,253 participants in 25 other studies to pinpoint associations between early life adversity and brain development. They found that childhood adversity was indeed associated with cortical thinning—a sign of aging, as the cortex thins as people age. Trauma and violence were related to thinning in the ventromedial prefrontal cortex (involved in social and emotional processing) and deprivation was associated with reduced cortical thickness in the frontoparietal, default mode, and visual networks, which are involved in sensory and cognitive processing.

The implications of the results, according to the study’s authors: “These findings suggest specificity in the types of early environmental experiences associated with accelerated biological aging and highlight the importance of evaluating how accelerated aging contributes to health disparities and whether this process can be mitigated through early intervention.”

LinkedIn and Facebook Image: sukra13/Shutterstock

References

Colich, N. et al. (2020). Biological aging in childhood and adolescence following experiences of threat and deprivation: A systematic review and meta-analysis. Psychological Bulletin. DOI: 10.1037/bul0000270

McLaughlin, K. A., et al. (2016). Childhood exposure to violence and chronic physical conditions in a national sample of U.S. adolescents. Psychosomatic Medicine, 78, 1072–1083. http://dx.doi.org/10.1097/PSY.0000000000000366

McLaughlin, K. A., et al. (2012). Socioeconomic status and adolescent mental disorders. American Journal of Public Health, 102,1742–1750. http://dx.doi.org/10.2105/AJPH.2011.300477