Experiencing trauma, abuse, neglect, and family dysfunction in childhood increases the risk of middle age cardiovascular disease (CVD), according to results published in the Journal of the American Heart Association. In fact, researchers found that adults exposed to the highest levels of adversity in childhood through dysfunctional family environments were over 50% more likely to experience a CVD event such as myocardial infarction or stroke, over a 30-year follow-up. Even moderate adversity during childhood significantly increased the risks for all-cause mortality in adulthood.
“Exposure to adverse emotional or traumatic experiences during childhood and adolescence is increasingly recognized as having a profound impact on cardiometabolic disease throughout the life course. These experiences are thought to affect emotional and behavioral regulation, predisposing individuals to higher rates of behavioral cardiovascular disease (CVD) risk factors that persist into adulthood such as smoking, anxiety, depression, and sedentary lifestyle,” noted Jacob B. Pierce BA, of Northwestern University Feinberg School of Medicine, Chicago, IL and colleagues.
Using data from the Coronary Artery Risk Development in Young Adults (CARDIA) study, these researchers sought to assess how childhood psychosocial environment affects the incidence of CVD and all-cause mortality in middle age. They used data from CARDIA — a population-based, epidemiological, longitudinal study — which followed participants from 1985-1986 through 2018.
Between 2000 and 2001, 3,546 participants (mean age: 25.1 years; 47% black; 56% female) completed the Childhood Family Environment (CFE) questionnaire, which was designed to assess how often respondents experienced seven elements of family environments: parental love/support, physical affection, verbal abuse, physical abuse, presence of an alcohol/drug abuser in the home, and whether the household was well-organized/well-managed, and parental knowledge of what children were doing during childhood.
Pierce and colleagues grouped these participants according to high, moderate, or low CFE adversity scores. Using sequential multivariable regression models, they estimated the hazard ratios of incident CVD and all-cause mortality.
During a median follow-up of 30.9 years, 198 participants developed CVD. The incidence of CVD was over 50% higher for those in the high CFE adversity group compared with those placed in the low adversity group.
Participants in the moderate CFE adversity group had a higher incidence of CVD over the follow-up period (20.1 events/10,000 person-years), as did those in the high CFE adversity group (22.2 events/10,000 person-years), compared with those in the low CFE adversity group (14.7 events/10,000 person-years). In those reporting high CFE adversity, the CVD hazard ratio was 1.40 (95% CI: 0.98-2.11) compared with those reporting low CFE adversity; and 1.25 (95% CI: 0.89-1.75) in those reporting moderate CFE adversity. Adjusted hazard ratios for all-cause mortality were 1.68 (95% CI: 1.17-2.41) in those with high CFE adversity scores and 1.55 (95% CI: 1.11-2.17) in those with moderate scores.
In the multivariable adjusted models, including those adjusted for demographic, socioeconomic, clinical and psychological characteristics, this relationship remained significant. In the fully adjusted model, however, it was not significant (HR: 1.40; 955 CI: 0.98-2.01).
Also, in the fully adjusted model, researchers found that black race, examination center, older age, lower education, smoking status, higher systolic blood pressure, and higher fasting baseline glucose were significantly associated with a greater risk of CVD. Male sex and depressive symptoms at year 5 were not, and those with moderate CFE adversity scores did not have a greater risk for CVD events compared with those with low scores.
As CFE adversity scores increased, rates of coronary artery disease (CAD) were significantly higher. Among those with high CFE adversity scores, 3.8% had CAD, compared with 2.7% of those with moderate CFE scores and 1.9% of those with low CFE scores (P ˂ 0.01). The incidence of stroke, heart failure, carotid artery disease, and peripheral artery disease were all less frequent than CAD, and across CFE adversity score groups, were not statistically significantly higher.
Fifteen years after the questionnaire was administered, 201 participants died. Those with moderate or high CFE adversity scores had higher rates of all-cause mortality (439 and 45.5 deaths/10,000 person-years, respectively), compared with those with low CFE adversity scores (25.8 deaths/10,000 person-years).
Upon fully adjusted regression analysis, researchers found that those in both the moderate (HR: 1.55; 95% CI: 1.11-2.17) and high CFE adversity groups (HR: 1.68; 05% CI: 1.17-2.41) were at greater risk for mortality compared with the low CFE adversity group. Greater mortality was significantly associated with older age, smoking status, higher systolic blood pressure, higher fasting baseline glucose levels, and examination center.
“These results suggest that unfavorable childhood psychosocial environment not only affects baseline health in young adulthood, but also continues to increase risk well into middle age. This is particularly concerning given the remarkable prevalence of childhood adversity; > 20% of our sample reported 4 or more out of 7 indicators of adverse childhood environment,” wrote Pierce and fellow researchers.
Study limitations include the exclusion of mortality events before the year-15 examination of participants in the CARDIA study, and the retrospective and possibly biased nature of self-reported data on childhood environments.
In an accompanying editorial, Donald A. Barr, MD, PhD, of Stanford University Medical School, Stanford, CA, focused on the lack of statistical significance of the association between childhood adversity and CVD when demographic, socioeconomic, clinical and psychological variables were included. Specifically, he noted that education had perhaps the greatest effect on future risks.
“On the basis of the authors’ multivariate analysis, perhaps the strongest mediating factor in affecting CVD risk is participant education. There is a striking difference in the highest level of education attained among subjects having experienced different levels of childhood adversity. As shown in table 1 of the article, >45% of those in the highest level of adversity had either dropped out of high school or stopped with graduation from high school. By contrast, <30% of those in the lowest level of adversity had stopped at high school, with >70% having enrolled in college,” he wrote.
He also points out the association between the level of childhood adversity experienced and subsequent rates of smoking.
“At the average age of 25 years, 34.9% of those having experienced high levels of adversity were current smokers, whereas 22.8% of those with low levels of adversity were smokers,” he wrote.
Barr concedes, however, that Pierce and colleagues have confirmed — with 30 years of longitudinal data — that child adversity can lead to long-term health consequences, but added an important caveat:
“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 physiologic impacts of adversity.”
An adverse childhood environment significantly impacts future risks for cardiovascular events and mortality.
Other more traditional cardiovascular disease risk factors may explain and even mitigate these risks in those growing up in an adverse childhood environment, including education levels and smoking status.
E.C. Meszaros, Contributing Writer, BreakingMED™
Pierce reported no conflicts of interest.
Barr has received royalties from Johns-Hopkins University Press for textbooks he has written.
The CARDIA study was conducted and supported by the National Heart, Lung, and Blood Institute in collaboration with the University of Alabama at Birmingham, Northwestern University, University of Minnesota, and the Kaiser Foundation Research Institute.
Cat ID: 138
Topic ID: 85,138,585,730,914,138,192