Biological embedding of early‐life exposures and disease risk in humans: a role for DNA methylation
Open accessAbstract
BACKGROUND: Following wider acceptance of 'the thrifty phenotype' hypothesis and the convincing evidence that early-life exposures can influence adult health even decades after the exposure, much interest has been placed on the mechanisms through which early-life exposures become biologically embedded. MATERIALS AND METHODS: In this review, we summarize the current literature regarding biological embedding of early-life experiences. To this end, we conducted a literature search to identify studies investigating early-life exposures in relation to DNA methylation changes. In addition, we summarize the challenges faced in investigations of epigenetic effects, stemming from the peculiarities of this emergent and complex field. A proper systematic review and meta-analyses were not feasible given the nature of the evidence. RESULTS: We identified seven studies on early-life socio-economic circumstances, 10 studies on childhood obesity and six studies on early-life nutrition all relating to DNA methylation changes that met the stipulated inclusion criteria. The pool of evidence gathered, albeit small, favours a role of epigenetics and DNA methylation in biological embedding, but replication of findings, multiple comparison corrections, publication bias and causality are concerns remaining to be addressed in future investigations. CONCLUSIONS: Based on these results, we hypothesize that epigenetics, in particular DNA methylation, is a plausible mechanism through which early-life exposures are biologically embedded. This review describes the current status of the field and acts as a stepping stone for future, better designed investigations on how early-life exposures might become biologically embedded through epigenetic effects.
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DNA methylation is a plausible mechanism through which early life exposures such as low SES and nutritional patterns become biologically embedded.
“DNA methylation is an enzymatically-catalyzed modification of DNA and is one plausible mechanism through which early life exposures (low SES, nutritional patterns) become biologically embedded [135].”
From Food Addiction and Psychosocial Adversity: Biological Embedding, Contextual Factors, and Public Health Implications (2020) · cites this paper as [135]
The impact of low SES can become embedded into inflammatory processes, the HPA axis, and neural function/structure, all of which are epigenetically controlled.
“The impact of low SES can become embedded into inflammatory processes, the HPA axis, and neural function/structure, all of which are epigenetically controlled [135].”
From Food Addiction and Psychosocial Adversity: Biological Embedding, Contextual Factors, and Public Health Implications (2020) · cites this paper as [135]
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Prenatal ambient air pollution exposure and SOD2 promoter methylation in maternal and cord blood
Zhou, G., He, T., Huang, H., Feng, F., Liu, X., Li, Z., Zhang, Y., & Ba, Y. (2019) · Ecotoxicology and Environmental Safety · doi:10.1016/j.ecoenv.2019.06.039 · Cited by 35 · see citing works
- Authors
- Demetriou, C. A., van Veldhoven, K., Relton, C., Stringhini, S., Kyriacou, K., & Vineis, P.
- Affiliations
- Imperial College London (GB)
- Department of Epidemiology and Biostatistics School of Public Health Imperial College London London UK
- University of Bristol (GB)
- Centre Hospitalier Universitaire Vaudois (CH)
- The Cyprus Institute of Neurology & Genetics - Postgraduate Education (CY)
- Corresponding author
- Demetriou, Christiana A.
- Venue
- European Journal of Clinical Investigation
- Publisher
- Wiley
- Published
- 2015-02-25
- Volume
- 45
- Issue
- 3
- Pages
- 303-332
- ISSN
- 0014-2972 (ISSN-L)
- 1365-2362
- OpenAlex
- W1970563986
- Cited by
- 95
- References
- 96
- Citations by year
- 2026: 2 · 2024: 11 · 2023: 12 · 2022: 14 · 2021: 9 · 2020: 9 · 2019: 8 · 2018: 9 · 2017: 10 · 2016: 11
- FWCI
- 1.52
- Type
- journal article
- Language
- en
- Open access
- Locations
- European Journal of Clinical Investigation (publishedVersion)
- PubMed (publishedVersion)
- Archive ouverte UNIGE (University of Geneva) (submittedVersion, cc-by)
- IRIS (submittedVersion)
- Bristol Research (University of Bristol) (submittedVersion)
- Explore Bristol Research (submittedVersion)
- SERVAL (Université de Lausanne) (submittedVersion)
- Funders
- EU-Europeaid grant (CRIS 2009/223-507)
- European Union’s Seventh Framework Programme (FP7/2007-2013) (Grant Agreement No 288328)
- Swiss National Science Foundation (SNSF) (Ambizione Grant, n° PZ00P3_147998)
- 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
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Health, Environment, Cognitive Aging
- Keywords
- biological embedding, early life exposure, DNA methylation, epigenetics, thrifty phenotype, childhood obesity, early life nutrition, socioeconomic conditions, disease risk, causality, publication bias
- MeSH terms
- Adolescent, Adult, Aged, Aged, 80 and over, Child, Child Nutritional Physiological Phenomena, Child, Preschool, Disease Susceptibility, Environmental Exposure, Female, Humans, Infant, Life Change Events, Male, Middle Aged, Risk Factors, Socioeconomic Factors, Body Mass Index, DNA Methylation, Epigenesis, Genetic, Young Adult, Pediatric Obesity
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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