Display options
Cite
Shenk CE, Felt JM, Ram N, et al. Cortisol trajectories measured prospectively across thirty years of female development following exposure to childhood sexual abuse: Moderation by epigenetic age acceleration at midlife. Psychoneuroendocrinology. 2021;136:105606doi: 10.1016/j.psyneuen.2021.105606.
Shenk, C. E., Felt, J. M., Ram, N., O'Donnell, K. J., Sliwinski, M. J., Pokhvisneva, I., Benson, L., Meaney, M. J., Putnam, F. W., & Noll, J. G. (2022). Cortisol trajectories measured prospectively across thirty years of female development following exposure to childhood sexual abuse: Moderation by epigenetic age acceleration at midlife. Psychoneuroendocrinology, 136105606. https://doi.org/10.1016/j.psyneuen.2021.105606
Shenk, Chad E, et al. "Cortisol trajectories measured prospectively across thirty years of female development following exposure to childhood sexual abuse: Moderation by epigenetic age acceleration at midlife." Psychoneuroendocrinology vol. 136 (2022): 105606. doi: https://doi.org/10.1016/j.psyneuen.2021.105606
Shenk CE, Felt JM, Ram N, O'Donnell KJ, Sliwinski MJ, Pokhvisneva I, Benson L, Meaney MJ, Putnam FW, Noll JG. Cortisol trajectories measured prospectively across thirty years of female development following exposure to childhood sexual abuse: Moderation by epigenetic age acceleration at midlife. Psychoneuroendocrinology. 2022 Feb;136:105606. doi: 10.1016/j.psyneuen.2021.105606. Epub 2021 Nov 26. PMID: 34896740; PMCID: PMC8724404.
Copy Download .nbib Format: NLM
Share it on

Psychoneuroendocrinology. 2022 Feb;136:105606. doi: 10.1016/j.psyneuen.2021.105606. Epub 2021 Nov 26.

Cortisol trajectories measured prospectively across thirty years of female development following exposure to childhood sexual abuse: Moderation by epigenetic age acceleration at midlife.

Psychoneuroendocrinology

Chad E Shenk, John M Felt, Nilam Ram, Kieran J O'Donnell, Martin J Sliwinski, Irina Pokhvisneva, Lizbeth Benson, Michael J Meaney, Frank W Putnam, Jennie G Noll

Affiliations

  1. Department of Human Development and Family Studies, The Pennsylvania State University, United States; Department of Pediatrics, The Pennsylvania State University College of Medicine, United States. Electronic address: [email protected].
  2. Department of Human Development and Family Studies, The Pennsylvania State University, United States.
  3. Department of Communications, Stanford University, United States; Department of Psychology, Stanford University, United States.
  4. Child Study Center, Yale University, United States; Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University, United States.
  5. The Douglas Hospital Research Centre, Department of Psychiatry, McGill University, Canada.
  6. The Douglas Hospital Research Centre, Department of Psychiatry, McGill University, Canada; Child and Brain Developmental Program, Canadian Institute for Advanced Research, Canada; Singapore Institute of Clinical Sciences, Singapore.
  7. Department of Psychiatry, University of North Carolina School of Medicine, United States.

PMID: 34896740 PMCID: PMC8724404 DOI: 10.1016/j.psyneuen.2021.105606

Abstract

Lasting changes in the hypothalamic-pituitary-adrenal (HPA) axis are a potential indication of the biological embedding of early life adversity, yet, prospective and repeatedly collected data are needed to confirm this relation. Likewise, integrating information from multiple biological systems, such as the HPA axis and the epigenome, has the potential to identify individuals with enhanced embedding of early life adversity. The current study reports results from the Female Growth and Development Study, a 30-year prospective cohort study of childhood sexual abuse (CSA). Females exposed to substantiated CSA and a demographically-similar comparison condition were enrolled and resting state cortisol concentrations were sampled on seven subsequent occasions across childhood, adolescence, and adulthood. Differences in participants' cortisol trajectories were examined in relation to prior CSA exposure and DNA methylation-derived epigenetic age acceleration at midlife. Bilinear spline growth models revealed a trajectory where cortisol secretion increased until approximately age twenty and then declined into mid-life, consistent with normative trends. However, cortisol concentrations peaked at a lower level and transitioned to the decline phase at an earlier age for females in the CSA condition with increased epigenetic age acceleration. Robustness tests across three independent measures of epigenetic age acceleration demonstrated similar results for lower peak cortisol levels and earlier ages at transition. Results suggest that CSA is associated with significant changes in HPA-axis activity over extended periods of time with these changes most pronounced in females with accelerated epigenetic aging in mid-life. Implications for biological embedding models of early life adversity and adulthood health are discussed.

Copyright © 2021 Elsevier Ltd. All rights reserved.

Keywords: Childhood sexual abuse; Cortisol; Epigenetic age acceleration

References

  1. Psychiatry Res. 2018 Dec;270:744-748 - PubMed
  2. Psychoneuroendocrinology. 2016 Nov;73:16-23 - PubMed
  3. Psychoneuroendocrinology. 2015 Jun;56:45-51 - PubMed
  4. Neurosci Biobehav Rev. 2017 Mar;74(Pt B):356-365 - PubMed
  5. BMC Pediatr. 2018 Feb 23;18(1):83 - PubMed
  6. Genome Biol. 2013;14(10):R115 - PubMed
  7. Genome Biol. 2015 Dec 17;16:266 - PubMed
  8. Lancet Public Health. 2017 Aug;2(8):e356-e366 - PubMed
  9. Psychoneuroendocrinology. 2017 Apr;78:57-67 - PubMed
  10. Psychoneuroendocrinology. 2021 Jul;129:105254 - PubMed
  11. BMC Bioinformatics. 2012 May 08;13:86 - PubMed
  12. Psychoneuroendocrinology. 2005 Nov;30(10):1010-6 - PubMed
  13. J Pediatr Endocrinol Metab. 2002 Feb;15(2):197-204 - PubMed
  14. Nat Genet. 2016 Oct;48(10):1279-83 - PubMed
  15. Dialogues Clin Neurosci. 2019 Dec;21(4):389-396 - PubMed
  16. Aging (Albany NY). 2018 Apr 18;10(4):573-591 - PubMed
  17. J Am Acad Child Adolesc Psychiatry. 1988 Nov;27(6):748-50 - PubMed
  18. Psychoneuroendocrinology. 2018 Dec;98:39-45 - PubMed
  19. Transl Psychiatry. 2017 Aug 29;7(8):e1223 - PubMed
  20. Exp Biol Med (Maywood). 2020 Nov;245(17):1532-1542 - PubMed
  21. Cell Metab. 2014 Jun 3;19(6):910-25 - PubMed
  22. J Pediatr Psychol. 2016 Jan-Feb;41(1):37-45 - PubMed
  23. Pediatrics. 2007 Mar;119(3):509-16 - PubMed
  24. BMC Psychiatry. 2018 Oct 5;18(1):324 - PubMed
  25. Mol Cell. 2013 Jan 24;49(2):359-367 - PubMed
  26. Gigascience. 2015 Feb 25;4:7 - PubMed
  27. Psychoneuroendocrinology. 2005 Jun;30(5):483-95 - PubMed
  28. Neurosci Biobehav Rev. 2011 Jun;35(7):1562-92 - PubMed
  29. Dev Psychobiol. 2015 Sep;57(6):670-87 - PubMed
  30. Psychol Med. 1996 Mar;26(2):245-56 - PubMed
  31. Psychoneuroendocrinology. 2013 Sep;38(9):1630-8 - PubMed
  32. Front Neuroendocrinol. 2014 Apr;35(2):197-220 - PubMed
  33. Dialogues Clin Neurosci. 2014 Sep;16(3):321-33 - PubMed
  34. Nat Commun. 2018 Jan 26;9(1):387 - PubMed
  35. Nucleic Acids Res. 2013 Apr;41(7):e90 - PubMed
  36. Psychol Bull. 2007 Jan;133(1):25-45 - PubMed
  37. J Nerv Ment Dis. 2007 Nov;195(11):919-27 - PubMed
  38. Neuropsychopharmacology. 2016 Jan;41(1):3-23 - PubMed
  39. Dev Psychopathol. 2010 Winter;22(1):165-75 - PubMed
  40. Genome Biol. 2015 Jan 30;16:25 - PubMed
  41. Aging (Albany NY). 2016 Sep 28;8(9):1844-1865 - PubMed
  42. Aging (Albany NY). 2019 Jan 21;11(2):303-327 - PubMed
  43. PLoS Genet. 2006 Dec;2(12):e190 - PubMed
  44. Br J Psychiatry. 2014;204:335-40 - PubMed
  45. Psychoneuroendocrinology. 2017 Sep;83:25-41 - PubMed
  46. Dev Psychopathol. 2021 Aug;33(3):1107-1137 - PubMed
  47. Psychoneuroendocrinology. 2006 Oct;31(9):1131-7 - PubMed
  48. Dev Neurosci. 2018;40(1):13-22 - PubMed
  49. J Adolesc Health. 2017 Jan;60(1):65-71 - PubMed
  50. Viral Immunol. 2005;18(1):41-78 - PubMed
  51. Dev Psychopathol. 2011 May;23(2):453-76 - PubMed
  52. Am J Psychiatry. 2020 Jan 1;177(1):20-36 - PubMed
  53. Lancet. 2009 Jan 3;373(9657):68-81 - PubMed
  54. Psychoneuroendocrinology. 2020 Nov;121:104835 - PubMed
  55. Physiol Rev. 2007 Jul;87(3):873-904 - PubMed
  56. Crit Rev Neurobiol. 1995;9(4):371-81 - PubMed

Publication Types

Grant support