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
AI–Assisted Updates (see footnote below)
A 2016 study found that early life stress affects growth and cardiovascular risk through autonomic nervous system imprinting. This study investigated heart rate variability (HRV) in 101 children with height below the third percentile, who experienced early life stress due to conditions like intrauterine growth retardation or heart failure. Compared to a healthy control group, these children exhibited reduced HRV, specifically lower RMSSD and High Frequency (HF)-Power, indicating reduced vagal activity and autonomic imbalance. This dysfunction was linked to groups born small for gestational age (SGA), with cardiac growth failure, and congenital syndromes, but not constitutional growth delay, suggesting that underlying diseases, not short stature itself, drive this risk.
The findings imply these children have a higher risk for cardiovascular diseases in later life. These high risk children—allocated in the groups with an adverse autonomic imprinting in utero or infancy (SGA, congenital heart disease and congenital syndromes)—have the highest risk for ‘stress diseases’ such as cardiovascular disease in later life.
A 2017 review confirmed that early life stress is a significant risk factor for cardiovascular disease, supported by both human and animal studies. This review synthesizes epidemiological data and animal model research to demonstrate that early life stress (ELS) is an independent risk factor for cardiovascular disease (CVD). Human cohort studies, such as the ACE study and National Comorbidity Survey, show a dose-response relationship between adverse childhood experiences (ACEs) and increased risk of ischemic heart disease, hypertension, stroke, respiratory disease, diabetes, and cancer.
For instance, the ACE study (n=17,337) found a clear link, while Finnish war evacuees (n=1,361) separated at ages 4–7 had 9 mmHg higher systolic blood pressure as adults. Animal models, particularly maternal separation (MatSep) in rodents (3 hours/day, postnatal days 2–14), mimic ELS, priming systems for overreaction to secondary stressors, leading to hypertension without baseline changes in young adults.
Molecular mechanisms include alterations in the central nervous system (e.g., frontal cortex, hippocampus, amygdala), hypothalamic-pituitary-adrenal (HPA) axis, sympathetic nervous system (SNS), renin-angiotensin-aldosterone system (RAAS), inflammation (increased IL-1β, IL-6), and epigenetic changes (e.g., DNA methylation of GR, Nr3c1 promoter), all contributing to CVD risk.
A 2023 study found that early life stress is associated with lower heart rate reactivity to acute social stress, and coping styles moderate this relationship. This study examined the relationship between early life stress (ELS), coping styles, and cardiovascular reactivity to acute social stress in a diverse sample of 1,027 adolescents and young adults (mean age 19.29 years). Participants completed the Trier Social Stress Test (TSST), with heart rate (HR) and blood pressure (BP) measured before, during, and after. ELS was associated with lower HR stress reactivity (β = -0.09, p = .003, after adjusting for covariates). Coping styles significantly influenced outcomes: emotion-oriented coping predicted higher emotional stress reactivity (β = .22, p < .001), while task-oriented coping predicted lower emotional reactivity (β = -0.08, p = .013). Avoidant coping was related to lower systolic BP (SBP) and diastolic BP (DBP) during stress.
The interaction between ELS and emotion-oriented coping was notable: at high levels (1.39–3.14 SD above mean), ELS linked to higher resting HR, greater emotional reactivity, and lower SBP/DBP recovery; at low levels (below 1.85 SD), linked to lower resting HR, lower emotional reactivity, average HR/SBP reactivity, but higher DBP stress and SBP/DBP recovery. Effects were most robust for interpersonal, illness-related, and financial/job/other stressors. The study suggests interventions like cognitive-behavioral therapy (10 sessions) or mindfulness training could reduce emotion-oriented coping, mitigating ELS effects on cardiovascular health.
Discussion and Implications
These studies collectively reinforce the original article’s premise that early life stress is a critical driver of cardiovascular risk in later life, extending the understanding through new evidence on autonomic dysfunction, molecular mechanisms, and the role of coping styles. The 2016 study highlights the long-term impact on autonomic nervous system function, particularly in vulnerable populations like those with SGA or congenital conditions, suggesting early identification and intervention could be crucial.
The 2017 review provides a comprehensive framework, integrating human and animal data to elucidate pathways such as HPA axis dysregulation and epigenetic changes, which are vital for developing personalized therapeutics. The 2023 study introduces a novel perspective by linking coping mechanisms to cardiovascular reactivity, offering practical intervention strategies like reducing emotion-oriented coping, which could be an unexpected but promising approach for prevention.
The findings underscore the need for public health strategies that address early life stress, potentially through enhanced screening for ACEs and support for emotional development in childhood. This aligns with the original article’s recommendations for considering psychological stress across the lifespan in cardiovascular risk assessment, now supported by more robust, recent evidence.
Professional AI assistance:
Updates assisted and generated by an Artificial Intelligence (AI) using the professional services of Zlatin Balevsky (contact@balevsky.ai).
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 https://commons.wikimedia.org/wiki/File:Ralph_Hedley_The_tournament_1898.jpg
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