The epidemiological study noted here makes use of phenotypic age, a simple biomarker-based aging clock. The calculation used to derive a phenotypic age based on common biomarkers can be in the methods section of the paper, for those interested. It is a mortality-related calculation, and a higher phenotypic age is presumed to indicate a greater risk of age-related disease and death. Where phenotypic age is greater than chronological age, this may represent a faster pace of aging in that individual, as is the case for epigenetic clocks and epigenetic age acceleration.
The conclusion reached in the study here is that unhealthy lifestyle choices, such as becoming overweight, mediate much of the relationship between childhood adversity and shorter life expectancy, which we might compare with past research suggesting that early life adversity raises the chance of early exposure to cytomegalovirus and thus leads to a higher lifetime burden of inflammation and immune dysfunction.
Accelerated aging makes adults more vulnerable to chronic diseases and death. Whether childhood adversity is associated with accelerated aging processes, and to what extent lifestyle mediates the association, remain unknown. Out objective was to examine the associations of childhood adversity with a phenotypic aging measure and the role of unhealthy lifestyle in mediating these associations. A retrospective cohort analysis was conducted using data from adult participants in the UK Biobank baseline survey (2006-2010) and online mental health survey (2016). Childhood adversity, including physical neglect, emotional neglect, sexual abuse, physical abuse, and emotional abuse, was assessed retrospectively through the online mental health survey (2016).
A phenotypic aging measure, phenotypic age acceleration, was calculated, with higher values indicating accelerated aging. Body mass index, smoking status, alcohol consumption, physical activity, and diet were combined to construct an unhealthy lifestyle score (range, 0-5, with higher scores denoting a more unhealthy lifestyle). A total of 127,495 participants aged 40 to 69 years were included. Each individual type of childhood adversity and cumulative childhood adversity score were associated with phenotypic age acceleration. For instance, compared with participants who did not experience childhood adversity, those who experienced 4 (β = 0.296) or 5 (β = 0.833) childhood adversities had higher phenotypic age acceleration in fully adjusted models. The formal mediation analysis revealed that unhealthy lifestyle partially mediated the associations of childhood adversity with phenotypic age acceleration by 11.8% to 42.1%.
In this retrospective cohort study, childhood adversity was significantly associated with acceleration of aging and, more importantly, unhealthy lifestyle partially mediated these associations. These findings reveal a pathway from childhood adversity to health in middle and early older adulthood through lifestyle and underscore the potential of more psychological strategies beyond lifestyle interventions to promote healthy aging.