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Published on: October 22, 2014
Perinatal determinants of adult cardiovascular disease and cancer
L B Signorello1, D Trichopoulos
1Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA.
Insights
Perinatal factors like birthweight influence adult diseases. Genomic imprinting may explain how early life conditions impact health across generations, requiring further research.
Area of Science:
- Reproductive biology
- Developmental origins of health and disease (DOHaD)
- Epigenetics
Background:
- Growing evidence links perinatal factors, particularly birthweight, to adult-onset diseases.
- Low birthweight is associated with cardiovascular disease risk; high birthweight with increased cancer risk.
- Existing hypotheses often cite physiological programming during fetal development.
Purpose of the Study:
- To explore genomic imprinting as a potential mechanism explaining the link between perinatal conditions and adult-onset diseases.
- To highlight the need for robust evidence to validate biological theories on the perinatal origins of adult disease.
Main Methods:
- Review of existing literature on perinatal factors and adult-onset diseases.
- Discussion of genomic imprinting as a candidate mechanism.
- Emphasis on the need for assembling reliable evidence.
Main Results:
- Birthweight is a significant perinatal factor linked to distinct adult disease risks.
- Genomic imprinting, involving non-permanent DNA modifications, offers a biologically plausible programming mechanism.
- This epigenetic mechanism can influence health outcomes across multiple generations.
Conclusions:
- Perinatal factors, including birthweight, play a crucial role in determining adult health outcomes.
- Genomic imprinting presents a compelling avenue for understanding how early life exposures program long-term disease risk.
- Further research is essential to build a strong evidence base for these developmental origins of health and disease theories.
Abstract:
Interest in perinatal factors, especially birthweight, as determinants of adult-onset diseases has been steadily growing. Low birthweight has been associated with increased risk of cardiovascular disease, and high birthweight has been linked to higher risk of breast and possibly other cancers. Most mechanistic hypotheses that have been advanced to explain the empirical evidence linking perinatal conditions to adult-life disease in humans have invoked modulation of physiological processes by exogenous factors or poorly specified "programming" during fetal life. A form of programming that has a strong biological foundation and has recently been suggested for further study is genomic imprinting, which involves non-permanent DNA modifications and allows for influences that span three generations. The subject of the perinatal origin of adult-onset disease has profound implications and a large and reliable body of evidence needs to be assembled for biological theories to be validly evaluated against.
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