Stress May Start Driving Cardiovascular and Metabolic Risk Early In Life: Evidence from the 1958 British Birth Cohort Study

Stress Driving Cardiovascular Risk Early Life
Cardiovascular and Metabolic Risk Early In Life

Ashley Winning et al. report in the the Journal of the the American College of Cardiology that stress may start driving cardiovascular risk early in life – psychological distress at any point in the life course is associated with higher cardiometabolic risk.

Thus, the psychological stress in childhood, adulthood or persistent across a person’s life can contribute to high cardiovascular and metabolic risk.

Cardiovascular medicine has increasingly recognized the childhood origins of adult disease and has begun to promote strategies for primordial prevention. Because psychological distress is theorized to influence disease risk both directly and indirectly, by inducing biophysical changes and catalyzing health risk behaviors, primordial prevention strategies may benefit from considering the role of distress in cardiometabolic disease development over the life course.

Many clinical and epidemiological studies have documented the link between psychological stress and cardiovascular disease. Moreover, in individuals with heart disease stress is the strongest predictor of future cardiac events (cf. a Mayo Clinic study).

The association between adult psychological distress and increased cardiometabolic risk (CMR) is documented by a substantial body of published reports; yet, little is known of the impact of psychological distress earlier in the life course (that may or may not persist through adulthood) on cardiometabolic risk.

Thus, recent evidence indicates that the origins of many adult diseases can be found among adversities in the early years of life. Yet, how and to what extent psychological stress in early childhood affects cardiovascular health remains poorly understood.

Childhood psychological distress is commonly characterized as internalizing (e.g., depression, anxiety) and externalizing (e.g., inattention, impulsivity) symptoms. Given that most prospective cohorts with psychological measures obtained early in life are still too young to present with clinical disease endpoints, researchers have looked to biomarkers as indicators of subclinical disease.

The strongest evidence linking distress to CMR is from studies of depression and inflammatory markers; however, much of this work is cross-sectional. One prospective study found that poor emotional functioning assessed at age 7 years was associated with higher C-reactive protein at age 42 years.

The Ashley Winning et al. study published in the Journal of the the American College of Cardiology aimed to assess whether life course patterns of psychological distress assessed at childhood and into adulthood predict biomarkers of CMR in adulthood, using longitudinal data from the 1958 British Birth Cohort Study. Specifically it evaluated whether effects of distress on CMR remained evident when distress appeared to be remitted by adulthood and whether effects of sustained distress differed from more limited exposure.

This study supports growing evidence that psychological distress contributes to excess risk of cardiovascular and metabolic disease and that effects may be initiated relatively early in life.

Participants in the 1958 British Birth Cohort Study who had psychological distress at any period in their lifetime were at increased risk for cardiometabolic diseases at age 45 years, as indicated by higher CMR scores.

This report is perhaps the first to suggest that “increased risk of cardiometabolic disease associated with distress in childhood may be maintained even if distress remits by adulthood”.

Considering severity, greater psychological distress in childhood was associated with higher CMR in adulthood, even when controlling for adult distress. Notably, because adult psychological distress is affected by child distress, analyses simultaneously adjusting for both child and adult distress scores likely underestimate the effects of child distress on CMR.

As per the mechanisms behind these relationships, the authors suggest that they may reflect effects of the hypothalamic-pituitary-adrenal axis and sympathetic nervous system on processes related to cardiometabolic and immune functioning, blood pressure and lipid metabolism.

The authors propose that psychological stress across the lifespan should be considered during cardiovascular risk assessment.

Moreover, the results in this study point to childhood distress as relevant for both screening and intervention related to adult cardiometabolic disease prevention, and they provide support for the importance of attending to early emotional development as a primordial prevention strategy.

Source: J Am Coll Cardiol, 2015, 66:1577. doi: 10.1016/j.jacc.2015.08.021.
Read More: J Am Coll Cardiol

Cover Image Credit: The tournament. Signed and dated R Hedley 98. Oil on canvas. 83 x 103 cm; 1898, Ralph Hedley, Public domain, via Wikimedia Commons.

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