Epigenetics and DOHaD: From Basics to Birth and Beyond
Open accessAbstract
Developmental origins of health and disease (DOHaD) is the study of how the early life environment can impact the risk of chronic diseases from childhood to adulthood and the mechanisms involved. Epigenetic modifications such as DNA methylation, histone modifications and non-coding RNAs are involved in mediating how early life environment impacts later health. This review is a summary of the Epigenetics and DOHaD workshop held at the 2016 DOHaD Society of Australia and New Zealand Conference. Our extensive knowledge of how the early life environment impacts later risk for chronic disease would not have been possible without animal models. In this review we highlight some animal model examples that demonstrate how an adverse early life exposure results in epigenetic and gene expression changes that may contribute to increased risk of chronic disease later in life. Type 2 diabetes and cardiovascular disease are chronic diseases with an increasing incidence due to the increased number of children and adults that are obese. Epigenetic changes such as DNA methylation have been shown to be associated with metabolic health measures and potentially predict future metabolic health status. Although more difficult to elucidate in humans, recent studies suggest that DNA methylation may be one of the epigenetic mechanisms that mediates the effects of early life exposures on later life risk of obesity and obesity related diseases. Finally, we discuss the role of the microbiome and how it is a new player in developmental programming and mediating early life exposures on later risk of chronic disease.
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Maternal malnutrition, whether undernutrition, overnutrition, or obesity, can induce persistent epigenetic modifications that alter gene expression without changing the DNA sequence.
“Maternal malnutrition (whether undernutrition, overnutrition, or obesity) can induce persistent epigenetic modifications that alter gene expression without changing the DNA sequence.”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [157]
microRNAs (miRNAs) are small non-coding RNAs that post-transcriptionally regulate gene expression.
“regulation by microRNAs (miRNAs), small non-coding RNAs that post-transcriptionally regulate gene expression.”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [157]
Together, DNA methylation, histone modifications, and miRNA regulation form the molecular basis of fetal programming, through which maternal nutritional imbalance can imprint lasting effects on gene regulation, metabolism, and disease vulnerability in later life.
“Together, these mechanisms form the molecular basis of fetal programming, through which maternal nutritional imbalance can imprint lasting effects on gene regulation, metabolism, and disease vulnerability in later life [157,158,159].”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [157]
DNA methylation, mediated by DNA methyltransferases (DNMTs), typically represses gene transcription when occurring in promoter regions.
“DNA methylation, mediated by DNA methyltransferases (DNMTs), which typically repress gene transcription when occurring in promoter regions;”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [157]
Histone modifications such as acetylation, methylation, and phosphorylation influence chromatin structure and the accessibility of transcriptional machinery.
“histone modifications (e.g., acetylation, methylation, phosphorylation) that influence chromatin structure and the accessibility of transcriptional machinery;”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [157]
Once established early in life, these epigenetic alterations are relatively stable and may exert lifelong effects on phenotype and disease risk.
“Once established early in life, these epigenetic alterations are relatively stable and may exert lifelong effects on phenotype and disease risk.”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [157]
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- Authors
- Bianco-Miotto, T., Craig, J. M., Gasser, Y. P., van Dijk, S. J., & Ozanne, S. E.
- Affiliations
- Royal Children's Hospital (AU)
- University of Cambridge (GB)
- Venue
- Journal of Developmental Origins of Health and Disease
- Publisher
- Cambridge University Press (CUP)
- Published
- 2017-09-11
- Volume
- 8
- Issue
- 5
- Pages
- 513-519
- ISSN
- 2040-1744 (ISSN-L)
- 2040-1752
- OpenAlex
- W2753407674
- Cited by
- 361
- References
- 7
- Citations by year
- 2026: 24 · 2025: 42 · 2024: 58 · 2023: 56 · 2022: 48 · 2021: 41 · 2020: 40 · 2019: 22 · 2018: 26 · 2017: 2 · 2016: 1
- FWCI
- 4.60
- Type
- journal article
- Language
- en
- Open access
- green
- figshare.com
- Licence
- Locations
- Journal of Developmental Origins of Health and Disease (publishedVersion)
- PubMed (publishedVersion)
- Adelaide Research & Scholarship (AR&S) (University of Adelaide) (submittedVersion)
- Figshare (submittedVersion, cc-by)
- Apollo (University of Cambridge) (submittedVersion)
- Apollo
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Syndromes and Imprinting
- Keywords
- developmental origins of health and disease, epigenetics, DNA methylation, histone modifications, non-coding RNA, early life environment, chronic disease risk, animal models, type 2 diabetes, cardiovascular disease, obesity, metabolic health, microbiome, developmental programming, gene expression
- MeSH terms
- Gastrointestinal Microbiome, Animals, Environmental Exposure, Feeding Behavior, Female, Health Status, Humans, Pregnancy, Prenatal Exposure Delayed Effects, DNA Methylation, Epigenesis, Genetic
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