Young adults who were exposed to adverse experiences as children have greater signs of unhealthy blood vessel function than young people without a traumatic past, a new study finds.
The results suggest that early-life stress may raise the risk of heart disease later on by affecting blood vessel function and blood pressure in ways that can be detected during young adulthood, the authors say.
“We have translated ideas that we had from animal research and found that it’s true in humans,” Jennifer Pollock told Reuters Health.
She and her colleagues looked for elevations in blood pressure and other indicators of how well blood vessels constrict or relax, as well as signs of stiffness in blood vessel walls.
“All of this was highly correlated with people who have more of these stresses during childhood than the people who had no stressors in childhood,” she said.
Pollock said that household dysfunction was the most common adverse event, followed by neglect and abuse.
For their study, which was published in the journal Hypertension, Pollock and her colleagues analyzed data on 221 healthy adolescents and young adults recruited for a study of cardiovascular risk factors that started in 1989.
The research team looked at markers of blood vessel health including blood pressure, the heart’s output of blood, characteristics of the pulse and levels of a substance called endothelin-1, a protein that constricts blood vessels and increases blood pressure.
They calculated adverse childhood event (ACE) scores based on a questionnaire answered when the participants were about 21 years old. Those who reported one traumatic event were classified as having mild ACE and those with two or more traumatic events were classified as moderate or severe ACE.
The researchers found that participants who had one traumatic event in childhood had plasma endothelin-1 levels that were an average of 18% higher than those who had reported no traumatic events, and those who had two or more traumatic childhood events had levels that were 24% higher.
Participants with two or more adverse events also had elevated measures of blood pressure and blood vessel stiffness.
The study didn’t follow up to see if those young people ended up having more heart attacks, strokes or other illnesses. And it cannot prove that the early-life traumas were the cause of the cardiovascular differences.
Nonetheless, Pollock said that in the future she’d like to determine if behavioral therapies may change the course of the cardiovascular risk factors in people who have these early life stressors.
“Exposure to psychosocial stress triggers a biological response aimed at improving adaptation to challenges,” said Dr. Andrea Danese, of the Institute of Psychiatry, King's College London.
“Although the biological responses to stress are vital in the short term, they may become detrimental when chronically activated,” he told Reuters Health in an e-mail. “For example, immune mediators including inflammation proteins can damage blood vessels leading to atherosclerosis and cardiovascular disease.”
Danese, who was not involved in the new study, said researchers are increasingly interested in finding ways to reverse such damage to help individuals who experienced childhood adversity.
“We know little on the topic at present, but once we are able to confidently point to mechanisms through which child stress is translated into biological risk for disease, we will be able to target biological abnormalities before the onset of clinical symptoms,” he said.
This does not necessarily mean giving children medications, he said. “In contrast, we can also use this information to see if psychosocial interventions, such as psychotherapy, could help remediate the detrimental effects of childhood adversity on physical health as they often do for mental health.”
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