What we do
About our project
Epigenetic ageing
Epigenetics can affect gene transcript and is related to aging. So strongly, in fact, that the epigenetic signal at specific sites can be used to estimate a persons’ age through the use of so-called ‘epigenetic clocks’. Not only do the age estimates produced by epigenetic clocks relate highly to chronological age, but the extent to which they deviate from chronological age is an important predictor of health: in adults, epigenetic age acceleration (i.e. being epigenetically older than one’s age) relates to greater disease risk and mortality, whereas deceleration relates to better health and longevity.
When do we start ageing?
Intriguingly, research from our group suggests that an individual’s epigenetic age acceleration might be determined early on – we found that sites that make up epigenetic clocks already show substantial differences between individual in early life, sometimes even from birth. This raises the possibility that longevity differences apparent in old age may already be influenced by factors occurring at a young age, opening new opportunities for early detection and intervention strategies to promote healthy ageing. Hence in this project, we aim to identify the early origins and consequences of epigenetic aging.
Our research focus
Epigenetic clocks in early life
Leveraging two of the largest epigenetic datasets in the world with repeated measures across the first two decades of life, we found that epigenetic clocks are not a unified construct and do not change linearly with age. Instead, they contain sites with widely varying developmental trajectories. We discovered that over a third of these clock sites vary significantly already at birth, and these early differences are predictive of variations in epigenetic age at 18 years. These findings support the idea that aging processes are shaped from the earliest stages of life, opening new avenues for early detection and intervention.
Early origins of epigenetic clocks
By linking our results to openly accessible resources and published findings, we find that epigenetic clock sites show widespread genetic effects and are also more likely to associate with prenatal factors such as maternal smoking and BMI, compared to non-clock sites. In the next phase, we will use our longitudinal datasets to map out more systematically genetic and prenatal factors related to early epigenetic ageing.
Epigenetic clocks and early health outcomes
As a final step of the project, we will study if early differences and changes at epigenetic clock sites already show effects on children’s biological function and early health outcomes during development. Together, the new knowledge generated by this project may help to find better ways to promote healthy aging from an early age.
Funds & Grants
Collaborations
Internal collaborations
- Department of Child and Adolescent Psychiatry/Psychology
- The Generation R Study Group
- Department of Pediatrics
External collaborations
Publications
- Epigenome-wide change and variation in DNA methylation in childhood: trajectories from birth to late adolescence. Mulder, R. H., Neumann, A., Cecil, C. A., Walton, E., Houtepen, L. C., Simpkin, A. J., ... & Suderman, M. (2021). Human molecular genetics, 30(1), 119-134.
- What makes clocks tick? Characterizing developmental dynamics of adult epigenetic clock sites. Mulder, R. H., Neumann, A., Felix, J. F., Suderman, M., & Cecil, C. A. (2024). bioRxiv.
- Online tool to track epigenome-wide change and variation in DNA methylation in childhood.
Our team
- Charlotte A. M. Cecil, PhD – project lead
- Rosa H. Mulder, PhD – project co-lead and main analyst
- Alexander Neumann, PhD - collaborator
- Janine Felix, PhD - collaborator
- Esther Walton, PhD – external collaborator
- Matthew Suderman, PhD – external collaborator
