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The effect of early-life adversity on telomere length and psychosocial well-being

Year: 2022
Type: dissertation
Abstract: Early-life adversity is well-documented to influence health and well-being throughout life. Anxiety and depressive disorders are common psychiatric disorders observed in childhood and adolescence. One theory behind this relationship is the first 1000 days hypothesis which suggests children before the age of two are sensitive to environmental exposures due to the rapid development and adaptability to stimuli during this period. Whilst the biological mechanism driving this association remains unresolved, the relationship between adversity and telomere length may help explain and potentially mediate this association. Telomeres are repetitive regions of DNA located at the ends of chromosomes that protect genetic material from damage. However, telomeres undergo natural shortening during cell division and are therefore negatively associated with ageing. There is increasing evidence that environmental factors that cause oxidative stress and inflammation may also accelerate telomere attrition. These factors are also linked to the development of psychosocial outcomes. This research aims to explore associations between early-life adversity, telomere length and psychosocial outcomes. This study utilised data and biological samples from the Growing Up in New Zealand longitudinal study. Psychosocial outcomes were measured at age eight with the PROMIS anxiety and CES-DC depression scales. DNA was extracted from saliva samples at age four, and telomere length was measured by qPCR. An adversity score was created utilising measures associated with adversity and factors known to influence telomere length. Associations between adversity, telomere length, and each psychosocial outcome were assessed, and interaction analysis and mediation analyses were performed. Results show a positive association between adversity, telomere length and psychosocial wellbeing, and a positive relationship between telomere length and psychosocial wellbeing. However, telomere length did not mediate the association between adversity and psychosocial outcomes. Confounding interactions between covariates may explain this result. These findings demonstrate childhood as being a sensitive period to adversity which may initiate the onset of health outcomes. We propose telomere length acts as a compensatory mechanism to regulate the effects of accelerated telomere attrition in response to adversity. Further research is needed to understand these relationships and help improve the incidence of negative health effects of adversity on New Zealand children.
Language: English
Field: Psychology
Open Access status: green
OpenAlex ID: W7028069460
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