Recent studies suggest an association between greater dietary inflammatory index (DII) and higher biological ageing. As α-Klotho has been considered as a longevity protein, we examined whether α-Klotho plays a role in the association between DII and ageing. We included 3054 participants from the National Health and Nutrition Examination Survey. The associations of DII with biological and phenotypic age were assessed by multivariable linear regression, and the mediating role of α-Klotho was evaluated by mediation analyses. Participants’ mean age was 58·0 years (sd 11·0), with a median DII score of 1·85 and interquartile range from 0·44 to 2·79. After adjusting for age, sex, race/ethnicity, BMI, education, marital status, poverty income ratio, serum cotinine, alcohol, physical activity, a higher DII was associated with both older biological age and phenotypic age, with per DII score increment being associated with a 1·01-year increase in biological age (1·01 (95 % CI: 1·005, 1·02)) and 1·01-year increase in phenotypic age (1·01 (1·001, 1·02)). Negative associations of DII with α-Klotho (β = –1·01 pg/ml, 95 % CI: –1·02, –1·006) and α-Klotho with biological age (β= –1·07 years, 95 % CI: –1·13, –1·02) and phenotypic age (β= –1·03 years, 95 % CI: –1·05, –1·01) were found. Furthermore, α-Klotho mediated 10·13 % (P < 0·001) and 9·61 % (P < 0·001) of the association of DII with biological and phenotypic age, respectively. Higher DII was associated with older biological and phenotypic age, and the potential detrimental effects could be partly mediated through α-Klotho.

Objective methods for assessing the cumulative lifetime experience of non-human animals would be valuable. We develop the hypothesis that biological age is a common currency that integrates the overall quality of an animal's lifetime experience across a range of types of exposure. Ageing is the result of the accumulation of somatic damage, and its rate is determined by the balance between experiences that cause damage and experiences that mitigate damage or promote repair. Negative affective states are associated with somatic damage via both direct causal and indirect pathways. Based on these premises, we predict that individuals that are biologically old for their chronological age will, on average, have experienced worse lives than individuals that are biologically younger, both in terms of their overall health and affective experience. Biological age is, thus, an attractive measure of cumulative experience because it requires no subjective decisions either about how a given exposure impacts an animal, or about how different dimensions of welfare should be weighted in an overall assessment. Biological age can be measured objectively using biomarkers. We argue that two biomarkers, namely leukocyte telomere length and hippocampal volume, are valid biomarkers of cumulative experience in humans, with potential for use in non-human vertebrates. We discuss how these biomarkers could be used to assess cumulative experience in animals, highlighting some of the limitations. We conclude that biomarkers of biological age offer a viable objective solution to the assessment of cumulative experience and their application in an animal welfare context deserves further exploration.