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Accelerated Biologic Aging, Chronic Stress, and Risk for Sepsis and Organ Failure Following Trauma.

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Chronic stress accelerates aging, increasing trauma patients' risk for sepsis and organ failure. Understanding this link can help identify high-risk individuals and inform preventative interventions.

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Area of Science:

  • Trauma research
  • Gerontology
  • Immunology

Background:

  • Chronic stress and accelerated aging are linked to inflammation and poor outcomes like sepsis.
  • Limited data exist on these factors within trauma literature.
  • Pretrauma stress may increase susceptibility to posttrauma complications.

Purpose of the Study:

  • To investigate the relationship between pretrauma stress and posttrauma outcomes.
  • To test the hypothesis that chronic stress accelerates aging, increasing sepsis and organ failure risk.
  • To explore associations between chronic stress, biologic aging, and inflammatory markers in trauma patients.

Main Methods:

  • Prospective, correlational study design.
  • Inclusion of trauma patients aged 18-44 years.
  • Comparison of chronic stress and accelerated biologic aging with systemic inflammatory response syndrome, sepsis, and organ failure incidence.

Main Results:

  • Significant associations found between accelerated biologic aging and sepsis susceptibility (n=142).
  • Negative associations observed between mean cytokine levels and chronic stress.
  • Strongest correlation: Interleukin-1β (IL-1β) and human telomerase reverse transcriptase (hTERT) (r = -0.28, p = .004).
  • Significant negative associations between IL-12p70, TNF-α, and positive life events via chronic stress measure.

Conclusions:

  • Pretrauma chronic stress and accelerated aging increase sepsis and organ failure risk in trauma patients.
  • Cytokine levels show complex associations with stress and positive life events.
  • Findings can aid in identifying at-risk individuals and developing interventions to mitigate trauma complications.