Babies born very preterm—before 32 weeks—grow up with bodies and brains that age faster than their full-term peers, but a supportive environment may slow that accelerated ageing. This project treats very preterm birth as a natural experiment to understand how early-life adversity interacts with social environment across the entire lifespan. The core question is why some preterm individuals develop chronic disease and die younger, while others, given the right conditions, adapt successfully. The researcher will combine data from multiple birth cohorts spanning childhood to adulthood, plus intensive brain imaging, epigenetic analysis, and measures of social environment in one cohort. She will test whether protective environments can reduce accelerated brain ageing, physiological decline, and epigenetic changes. The work also asks whether very preterm adults have fewer children, biased sex ratios, or receive less parental investment in their own offspring. This is fundamental science about developmental plasticity—how early insults and later environment jointly shape health trajectories. If successful, it could inform interventions—such as targeted family support or neonatal care practices—that shift preterm individuals toward healthier ageing rather than early disease.
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Developmental theories of origin of diseases propose that individual differences in development and longevity start in the womb. These pathogenetic theories predict that adversity to the body early in life may lead to disease and early mortality. In contrast, Life History theories propose that early childhood adversity change the speed of development with trade-offs such as earlier ageing. But how can developmental trajectories heading towards disease or trade-offs be altered? We propose VP birth (<32 weeks' gestation) as a natural experiment of how early adversity may nevertheless lead to developmental plasticity across the life course. I will use radically new approaches to study the core question: How does VP birth result in either long term maladaptation or alternatively, under the right environmental conditions, to adaptive development? The first key challenge is to identify what are the right environmental conditions and what are the mechanisms of how they relate to early adversity? The second challenge is the study of whether risk or protective environments get into the brain and alter brain structure? Thirdly, can protective environments reduce accelerated brain, physiological, and epigenetic ageing? The fourth challenge is to investigate how early adversity affects the next generation. Do VP have lower reproductive success, a different sex-ratio (Trivers-Willard hypothesis), and do parents invest less in VP offspring? To address these questions, I will combine study of VP and term born from birth into adulthood across various cohorts with an intensive study of brain, environment, epigenetics and functional development within one cohort. I test alternative developmental models where they make different predictions of how the environment may interact with early adversity. The increased understanding of the mechanisms of how early childhood adversity and environment accounts for lifespan adaptations has implications for life course theory and interventions.
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