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Biological embedding of early‐life exposures and disease risk in humans: a role for DNA methylation
Author(s) -
Demetriou Christiana A.,
Veldhoven Karin,
Relton Caroline,
Stringhini Silvia,
Kyriacou Kyriacos,
Vineis Paolo
Publication year - 2015
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/eci.12406
Subject(s) - dna methylation , epigenetics , causality (physics) , disease , mechanism (biology) , biology , psychology , bioinformatics , medicine , genetics , gene , pathology , philosophy , gene expression , physics , epistemology , quantum mechanics
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.