Psychopharmacology

, Volume 212, Issue 3, pp 405–417

Putative biological mechanisms for the association between early life adversity and the subsequent development of PTSD

Authors

    • Department of PsychiatryJames J. Peters Veterans Affairs Medical Center
    • Department of Psychiatry and Neurobiology Mount Sinai School of Medicine
  • Janine D. Flory
    • Department of PsychiatryJames J. Peters Veterans Affairs Medical Center
    • Department of Psychology, Queens College and the Graduate CenterCity University of New York
  • Laura C. Pratchett
    • Department of PsychiatryJames J. Peters Veterans Affairs Medical Center
  • Joseph Buxbaum
    • Department of Psychiatry and Neurobiology Mount Sinai School of Medicine
  • Marcus Ising
    • Max Planck Institute of Psychiatry
  • Florian Holsboer
    • Max Planck Institute of Psychiatry
original investigation

DOI: 10.1007/s00213-010-1969-6

Cite this article as:
Yehuda, R., Flory, J.D., Pratchett, L.C. et al. Psychopharmacology (2010) 212: 405. doi:10.1007/s00213-010-1969-6

Abstract

Rationale

Early Life Stress (ELS) increases risk for both adult traumatization and posttraumatic stress disorder (PTSD). Adult PTSD may also reflect a continuation of a response to an earlier exposure to adversity. Given similarities between neuroendocrine aspects of PTSD and ELS, such as in reduced cortisol signaling and glucocorticoid receptor (GR) responsiveness, some aspects of the biology of PTSD may reflect biological correlates of risk.

Objectives

This paper will examine how empirical findings regarding the biological basis of ELS can inform our understanding of the neuroendocrinology of PTSD. This paper will also propose a hypothetical model to guide future research that integrates genetic, epigenetic, neuroendocrine, and psychological observations to understand the contribution of ELS neurobiology to PTSD.

Results

Recent genetic findings demonstrate heritable aspects of at least some of these cortisol-related disturbances. Furthermore, ELS may produce at least some of the PTSD-associated changes in glucocorticoid responsiveness through epigenetic mechanisms such as developmental programming. These, then, may contribute to enduring changes in stress responsiveness as well as enhanced risk for adult exposure and PTSD.

Conclusion

Molecular mechanisms associated with gene x environment interactions or GR programming are essential in explaining current observations in the neuroendocrinology of PTSD that have been difficult to understand through the lens of contemporary stress theory.

Keywords

PTSDEarly life stressCortisolGene × environment interactionGene expressionEpigeneticsGlucocorticoid receptor

Copyright information

© US Government 2010