Biological age, of which the calculation primarily involves the use of epigenomic data, such as methylation, could predict the health status and disease risk in humans, and show substantial differences between individuals in early life, sometimes even from birth. Numerous studies have demonstrated that accelerated biological ages were related to increased disease risk and mortality, whereas conversely, deceleration relates to better health and longevity.
The Developmental Origins of Health and Disease (DOHaD) hypothesis suggests that the health and disease risk of offspring could be influenced by exposures during parental pregnancy and early-life experiences. Current research also indicates that parental lifestyle and environmental exposures during early fetal development may have profound and lasting effects on the health of offspring. However, there are still gaps in our understanding of whether and how early-life modifiable exposures during parental pregnancy and early life, such as socioeconomic factors, education, etc., may impact the biological age of offspring, thereby influencing disease risk.
This project aims to investigate the causal relationship between early-life modifiable exposures with the biological age and the disease risk of offspring using data from the ALSPAC cohort. We will employ a multi-omics approach and longitudinal data analysis to explore the underlying biological mechanisms, providing new opportunities and valuable guidance for early detection and health interventions.