AUTONOMIC REGULATION AND SUBCLINICAL CARDIOVASCULAR RISK IN YOUNG ADULTHOOD: A GENE-ENVIRONMENT PERSPECTIVE

Early-life adversity is recognized as a contributor to cardiovascular vulnerability, yet the neurobiological pathways linking environmental and biological factors to early physiological markers of cardiovascular health remain unclear. This study examined gene-environment contributions to autonomic regulation and subclinical cardiovascular risk in healthy young adults.

A sample of 218 healthy young adults (172 females, 46 males; mean age ± SD = 20.94 ± 2.50 years) completed self-report questionnaires assessing early adversity (Childhood Trauma Questionnaire–Short Form; Adverse Childhood Experiences Questionnaire), parental care and overprotection (Parental Bonding Instrument), and perceived stress (Perceived Stress Scale). Cardiovascular risk factors and blood pressure were assessed. Heart rate variability (HRV) was recorded at rest and during standardized stress-inducing tasks. Buccal swabs were collected for DNA extraction and genotyping of candidate cardiovascular risk variants, with ongoing analyses aimed at deriving a composite genetic risk score.

Greater exposure to childhood trauma and less supportive caregiving were associated with altered physiological markers of cardiovascular regulation, including higher diastolic blood pressure and reduced HRV. Emotional abuse was associated with overall lower HRV across conditions, consistent with a downward shift in autonomic set-point. Conversely, emotional neglect was characterized by a flattened HRV response profile across rest, stress, and recovery phases, suggesting reduced dynamic modulation of autonomic activity. Genetic susceptibility to cardiovascular risk was examined in relation to the observed physiological markers.

These findings suggest that early relational and traumatic experiences contribute to latent cardiovascular vulnerability in young adulthood through long-lasting alterations in autonomic regulation, highlighting the relevance of individual biological susceptibility.