P02 Early life adversity is associated with phenotypic age but not delay discounting in chronologically young people

Background

Early life adversity results in accelerated ageing, which has been detected using molecular markers of ageing such as telomere length and DNA methylation, even in chronologically young people. Animal models have shown that accelerated ageing leads to a decreased willingness to wait for delayed rewards – a relationship thus far not observed in humans. Our study aimed to develop a simpler and cheaper marker of phenotypic age, to investigate links between early-life adversity, ageing and delay discounting.

Methods

In 250 UK younger adults (ages 17–38, 121 females, 129 males), we measured early life adversity using subjective childhood socioeconomic status (cSES), index of multiple deprivation, and the Childhood Trauma Scale. We assessed phenotypic age using a composite of 9 markers of ageing and physical function, and took two measures of delay discounting (hypothetical and experiential). We measured perceived odds of surviving beyond 75, and self-rated health. Using linear models and mediation analyses in R, we assessed the associations between early life adversity, ageing, perceived health & survival odds, and delay discounting.

Results

Lower cSES was associated with greater phenotypic age for chronological age (r = -.27, p < 0.01). Participants of lower cSES, and those with higher childhood trauma scores had poorer self-rated health (r_cSES = -.32, p < 0.01, r_ChildTrauma = .28, p < 0.01) and believed that they were less likely to survive beyond 75 (r_cSES = .33, p < 0.01, r_ChildTrauma = -.23, p < 0.01). Greater phenotypic age predicted worse self-rated health (β_adjusted = 0.13, p < 0.001) and lower perceived survival odds (β_adjusted = -0.07, p < 0.05) and mediated the association between cSES and self-rated health (33%, β_indirect = -0.08, 95% CIs = -0.15, -0.02). Contrary to our predictions, there were no associations between either early life adversity or phenotypic age and delay discounting.

Conclusion

These findings demonstrate that accelerated ageing can be detected in chronologically young people, using non-invasive low-cost phenotypic age markers, suitable for use in field studies. The young adults in our sample who reported greater childhood adversity were not only aged according to our compound phenotypic marker, but also rated their own health as being poorer and believed that they were less likely to survive beyond the age of 75. However, our results did not support our predictions regarding the antecedents of delay discounting.