Childhood adversity, trauma increase CVD, mortality risk later in life
Click Here to Manage Email Alerts
People with an adverse childhood family environment had elevated risk for CVD and all-cause mortality at middle age, according to a study published in the Journal of the American Heart Association.
“Our study highlights that patients who have had challenging childhoods are at higher risk for cardiovascular disease regardless of their health status as young adults,” Jacob B. Pierce, BA, a fourth-year MD/MPH student at Northwestern University Feinberg School of Medicine, told Healio.
CARDIA study data
Researchers analyzed data from 3,646 participants (mean age, 25 years; 56% women; 47% black) from the Coronary Artery Risk Development in Young Adults (CARDIA) study who completed a questionnaire in 2000-2001 to assess childhood family environment adversity.
“The CARDIA cohort is an extremely well-studied cohort and allowed us to control for cardiovascular risk factors in young adulthood,” Pierce said in an interview. “In doing so, we were better able to characterize the lifelong risk posed by childhood psychosocial adversity.”
The questionnaires assessed how often participants experienced seven elements of family environment such as verbal abuse, parental love and support, physical abuse, physical affection, and organization and management of their household.
Participants were followed up annually by phone and periodically with an in-person examination to learn more about recent hospitalizations, outpatient medical procedures, vital status and other items within their medical history. Follow-up was conducted for a median of 30.9 years.
The primary outcome was a composite of CVD events including non-MI ACS, fatal and nonfatal MI, HF, stroke, peripheral artery disease, carotid artery stenosis and other fatal CVD or atherosclerotic events. The secondary outcome was all-cause mortality.
During follow-up, 198 participants developed CVD, which equated to a rate of 17.9 per 10,000 person-years. The incidence of CVD was more than 50% higher in participants with high childhood family environment adversity vs. those with low childhood family environment adversity.
Compared with participants with low childhood family environment adversity, CVD was more likely in those with higher (HR = 1.4; 95% CI, 0.98-2.11) and moderate childhood family environment adversity (HR = 1.25; 95% CI, 0.89-1.75).
All-cause mortality was also more likely in participants with high (HR = 1.68; 95% CI, 1.17-2.41) and moderate childhood family environment adversity scores (HR = 1.55; 95% CI, 1.11-2.17) vs. those with low childhood family environment adversity scores.
“The next step in this field of research is gaining a mechanistic understanding of the relationship between childhood psychosocial dysfunction and cardiovascular disease, and how to clinically intervene to reduce subsequent risk,” Pierce told Healio. “A really interesting field of research is the neurohormonal axes that might be at play in these patients. There is an opportunity for paradigm-shifting discoveries in the field on the mechanisms that underlie this association.”
Potential to reverse impact
In a related editorial, Donald A. Barr, MD, PhD, professor of pediatrics and of education (by courtesy) at Stanford University, wrote: “This is not to say, however, that a child experiencing early adversity is irreversibly destined to experience increased CVD and early mortality. ... Rather than viewing the child as permanently damaged by the experience of adversity, we need to appreciate the child’s capacity to respond to subsequent emotional and personal support in ways that can reverse the behavioral and psychological impacts of adversity.” – by Darlene Dobkowski
For more information:
Jacob B. Pierce, BA, can be reached at jacob.pierce@northwestern.edu.
Disclosures: The authors report no relevant financial disclosures. Barr reports he receives royalties from Johns Hopkins University Press.
Collapse
Barr DA. J Am Heart Assoc. 2020;doi:10.1161/JAHA.120.016162.
Pierce JB, et al. J Am Heart Assoc. 2020;doi:10.1161/JAHA.119.015326.
Click Here to Manage Email Alerts