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.

New thinking has arisen about the origin of adult onset diseases stemming from a collective body of evidence commonly referred to as the developmental origins of health and disease. This conceptual paradigm posits that certain adult onset diseases arise during critical or sensitive windows of human development or even transgenerationally. The testicular dysgenesis hypothesis (TDS) postulates an in utero origin for adverse male reproductive outcomes, and is an excellent example of the early origins of the paradigm. Despite similarities in the development of the male and female reproductive tracks, noticeably absent is a collective body of evidence focusing on the plausibility of an early origin for gynecologic outcomes and later onset of adult diseases. Using the TDS paradigm, we synthesized the available literature relative to the ovarian dysgenesis syndrome (ODS), which we define as alterations in ovarian structure or function that may manifest as fecundity impairments, gynecologic disorders, gravid diseases or later onset adult diseases. We evaluated environmental exposures, particularly the role of endocrine disrupting chemicals, in relation to these outcomes, and found evidence (although fragmented) consistent with an in utero origin of gynecologic outcomes, which in turn is associated with later onset of adult diseases. The findings are interpreted within the ODS paradigm while delineating methodological challenges and future research opportunities designed to answer critical data gaps regarding the origin of fecundity, gravid health and chronic diseases affecting the female population.