Heart Rate Variability and Inflammatory Stress Response in Young African American Men: Implications for

Dina Tell1, Robert L Burr2, Herbert L Mathews3

  • 1Department of Health Systems and Adult Health, Marcella Niehoff School of Nursing, Loyola University Chicago, Chicago, IL, United States.

Insights

Childhood adversity in African American men is linked to altered autonomic nervous system (ANS) activity and increased inflammation (IL-6) during stress, raising cardiovascular disease (CVD) risk.

Area of Science:

  • Psychoneuroimmunology
  • Cardiovascular Disease Research
  • Stress and Health

Background:

  • African American men face disproportionately high cardiovascular disease (CVD) rates and mortality.
  • Inflammation is a key factor in CVD pathogenesis, influencing plaque development and instability.
  • Adverse childhood experiences (ACEs) are linked to adult inflammatory diseases, including CVD, potentially mediated by autonomic nervous system (ANS) activity.

Purpose of the Study:

  • To investigate if altered ANS activity, measured by heart rate variability (HRV), mediates a heightened proinflammatory response to stress in African American men with a history of childhood adversity.
  • To determine the relationship between childhood adversity, ANS regulation during stress, and inflammatory markers.

Main Methods:

  • Thirty-four African American men underwent the Trier Social Stress Test (TSST) with continuous heart rate monitoring for HRV analysis.
  • Heart rate variability (HRV) was quantified using the low frequency (LF) to high frequency (HF) ratio (LF/HF) as an indicator of sympathetic-parasympathetic balance.
  • Salivary IL-6 levels and childhood adversity (via Childhood Trauma Questionnaire) were assessed pre- and post-TSST.

Main Results:

  • Higher levels of physical abuse correlated with a greater increase in the LF/HF ratio during the TSST.
  • An elevated LF/HF ratio, combined with emotional and physical abuse, was associated with a significantly larger IL-6 response to acute stress.
  • These findings indicate a link between ACEs, stress-induced ANS dysregulation, and elevated inflammation.

Conclusions:

  • Adverse childhood experiences are associated with an adult phenotype of altered ANS response to stress and increased proinflammatory cytokine IL-6 release.
  • This heightened inflammatory response to stress, potentially mediated by ANS alterations, may contribute to the increased CVD risk observed in individuals with a history of childhood adversity.
  • The study highlights the role of the ANS in the neurobiological pathways linking childhood adversity to exaggerated inflammatory responses in adulthood.

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