Telomere Length and Psychopathology: Specificity and Direction of Effects Within the Bucharest Early Intervention Project.

ABSTRACT:

Objective

Telomere length (TL) has been linked to several psychiatric conditions in children and adults. Telomere shortening is accelerated by early adversity, including maltreatment and psychosocial deprivation. These experiences also increase the risk of psychopathology in many domains. Two fundamental issues remain unresolved. The first concerns the specificity of the relations between TL and different dimensions of psychopathology; and the second relates to the direction of association between TL and psychopathology.

Method

This study addressed these shortcomings in a 2-fold manner. First, the association between TL and statistically independent general, internalizing, and externalizing psychopathology factors was examined to determine the specificity of this relation. Second, a 2-wave longitudinal cross-lagged model was used to explicitly examine the direction of the relation between TL and each psychopathology factor. Data were drawn from the Bucharest Early Intervention Project, a longitudinal study exploring the impact of severe psychosocial deprivation on child health and development (N = 195). At 8 to 10 and 12 to 14 years of age, buccal DNA was collected and teachers and/or caregivers reported on different domains of psychopathology.

Results

Longitudinal path analyses showed that shorter TL was specifically associated with higher internalizing psychopathology at 8 to 10 years of age. In contrast, at 12 to 14 years, shorter TL was associated with higher general psychopathology. Most telling, internalizing psychopathology at 8 to 10 years predicted shorter TL at 12 to 14 years, with no reciprocal effects.

Conclusion

Results suggest that telomere erosion could be a consequence of distress-related psychopathology rather than a selection mechanism for later psychiatric problems.

Clinical trial registration information

The Bucharest Early Intervention Project; https://clinicaltrials.gov/; NCT00747396.

SUBMITTER: Wade M 

PROVIDER: S-EPMC8056885 | biostudies-literature |

REPOSITORIES: biostudies-literature