Social scientists generally agree that health disparities are produced, at least in part, by adverse social experiences, especially during childhood and adolescence. Building on this research, we use an innovative method to measure early adversity while drawing upon a biopsychosocial perspective on health to formulate a model that specifies indirect pathways whereby childhood and adolescent adversity become biologically embedded and influence adult health.

Using nearly 20 years of longitudinal data from 382 Black Americans, we use repeated-measures latent class analysis (RMLCA) to construct measures of childhood/adolescent adversities and their trajectories. Then, we employ structural equation modeling to examine the direct and indirect effects of childhood/adolescent adversity on health outcomes in adulthood through psychosocial maladjustment.

RMLCA identified two classes for each component of childhood/adolescent adversity across the ages of 10 to 18, suggesting that childhood/adolescent social adversities exhibit a prolonged heterogeneous developmental trajectory. The models controlled for early and adult mental health, sociodemographic and health-related covariates. Psychosocial maladjustment, measured by low self-esteem, depressive and anxiety symptoms, and lack of self-control, mediated the relationship between childhood/adolescent adversity, especially parental hostility, racial discrimination, and socioeconomic class, and both self-reported illness and blood-based accelerated biological aging (with proportion mediation ranging from 8.22% to 79.03%).

The results support a biopsychosocial model of health and provide further evidence that, among Black Americans, early life social environmental experiences, especially parenting, financial stress, and racial discrimination, are associated with adult health profiles, and furthermore, psychosocial mechanisms mediate this association.

Depression is the mental disorder with the largest disease burden impact. That is due to its high prevalence, chronicty, early onset but also due to its impact on various aging-related somatic morbidities and mortality. This talk will describes to what extent depression characteristics are related to chronologial and biological aging patterns.

Data will be shown from the Netherlands Study of Depression and Anxiety (NESDA, www.nesda.nl). In this study, a large cohort of over 3000 individuals (18-65 years), among which over 1200 with a DSM-based major depressive disorder (MDD), are now followed for 9 years. The association between depression characteristics and chronological and biological age will be described. Biological age was determined at various biological system-levels, including telomere length, epigenetics, transcriptomics, metabolomics and proteomics.

Older persons with a current MDD do not differ in overall disease severity as compared to younger persons with a current MDD. However, older depressed persons do differ in the types of symptoms they experience (more neurovegetative, somatic symptoms and less mood symptoms) and in their chronic course (with twice more chronicity in the oldest depressed persons compare to the younges depressed persons). At all biological system-levels, there was evidence for more advaned biological aging among persons with depression. This was not differential across chronological age groups. Discussion: Findings suggest that depression characteristics are linked to both chronological and biological age. It will be discussed what this could mean for clinical practice and intervention.

No significant relationships.