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Variation in the form, pattern and pace of ageing is studied by scientists in multiple disciplines and there is much to be gained from more cross-disciplinary communication. This chapter suggests here that the framework provided by Tinbergen’s ‘Four Questions’ is useful in integrating ageing research. It emphasizes the need to separate biological and chronological age and describe several markers of age-related deterioration that could be used more widely to measure biological age, with a focus on those that can be deployed outside of the standard laboratory setting and be used repeatedly in individuals to enable longitudinal studies. Whole organism frailty measures are currently little used by evolutionary ecologists and this chapter describes how these could be used more extensively. Telomere attrition and mitochondrial function are highly conserved processes and have been studied in an increasingly wide range of taxa in recent years. The chapter also discusses other markers, including those related to immune function, oxidative damage, inflammation and DNA methylation. Great progress is currently being made in the use of epigenetic alterations to provide information on chronological and biological age in a range of (predominantly) vertebrate taxa. The chapter outlines how this integrative approach could be developed further and highlight future directions.
The current study examined if early adversity was associated with accelerated biological aging, and if effects were mediated by the timing of puberty.
Methods
In early mid-life, 187 Black and 198 White (Mage = 39.4, s.d.age = 1.2) women reported on early abuse and age at first menstruation (menarche). Women provided saliva and blood to assess epigenetic aging, telomere length, and C-reactive protein. Using structural equation modeling, we created a latent variable of biological aging using epigenetic aging, telomere length, and C-reactive protein as indicators, and a latent variable of early abuse using indicators of abuse/threat events before age 13, physical abuse, and sexual abuse. We estimated the indirect effects of early abuse and of race on accelerated aging through age at menarche. Race was used as a proxy for adversity in the form of systemic racism.
Results
There was an indirect effect of early adversity on accelerated aging through age at menarche (b = 0.19, 95% CI 0.03–0.44), in that women who experienced more adversity were younger at menarche, which was associated with greater accelerated aging. There was also an indirect effect of race on accelerated aging through age at menarche (b = 0.25, 95% CI 0.04–0.52), in that Black women were younger at menarche, which led to greater accelerated aging.
Conclusions
Early abuse and being Black in the USA may both induce a phenotype of accelerated aging. Early adversity may begin to accelerate aging during childhood, in the form of early pubertal timing.
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