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Adverse childhood experiences and leukocyte telomere maintenance in depressed and healthy adults.

aging

genetics

lifestyle

senescence

telomerase activation

telomere length

Authors: Stephen H SH. Chen, Elissa S ES. Epel, Synthia H SH. Mellon, Jue J. Lin, Victor I VI. Reus, Rebecca R. Rosser, Eve E. Kupferman, Heather H. Burke, Laura L. Mahan, Elizabeth H EH. Blackburn, Owen M OM. Wolkowitz
Published: 08/05/2014, Journal of affective disorders

Background

Adverse childhood experiences (ACEs) are associated with poor physical and mental health outcomes in adulthood. Adverse childhood experiences are also associated with shortened leukocyte telomere length (LTL) in adults, suggesting accelerated cell aging. No studies have yet assessed the relationship of ACEs to LTL in individuals with major depressive disorder (MDD), despite the high incidence of antecedent ACEs in individuals with MDD. Further, no studies in any population have assessed the relationship of ACEs to the activity of telomerase, the major enzyme responsible for maintaining LTL, or the relationship between telomerase and LTL in individuals with ACEs.

Methods

Twenty healthy, unmedicated adults with MDD and 20 healthy age-, sex- and ethnicity-matched controls had ACEs assessed and had blood drawn for LTL and peripheral blood mononuclear cell (PBMC) resting telomerase activity.

Results

In healthy controls, greater ACE exposure was associated with shorter LTL (p<.05) but was unassociated with telomerase activity. In MDD, however, the opposite pattern was seen: greater ACE exposure was unrelated to LTL but was associated with increased telomerase activity (p<.05) and with a higher telomerase:LTL ratio (p=.022).

Limitations

Study limitations include the small sample size, a single timepoint assessment of telomerase activity, and the use of retrospective self-report to assess ACEs.

Conclusions

These results replicate prior findings of shortened LTL in healthy adults with histories of multiple ACEs. However, in MDD, this relationship was substantially altered, raising the possibility that activation of telomerase in ACE-exposed individuals with MDD could represent a compensatory response to endangered telomeres.

Copyright © 2014 Elsevier B.V. All rights reserved.
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