Epidemiologic evidence for association between adverse environmental exposures in early life and epigenetic variation: a potential link to disease susceptibility?

Alexander Vaiserman

doi:10.1186/s13148-015-0130-0

Alexander Vaiserman

Open Access

https://doi.org/10.1186/s13148-015-0130-0

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Abstract

A growing body of evidence suggests that the risk of development and progression of a variety of human chronic diseases depends on epigenetic modifications triggered by environmental cues during early life sensitive stages. Exposures to environmental factors such as adverse nutritional, psychological, and social conditions, as well as pollutants and substance abuse in early life, have been shown to be important determinants of epigenetic programming of chronic pathological conditions in human populations. Over the past years, it has become increasingly clear due to the epigenome-wide association studies (EWASs) that early life adverse environmental events may trigger widespread and persistent alterations in transcriptional profiling. Several candidate genes have been identified underlying these associations. In this context, DNA methylation is the most intensively studied epigenetic phenomenon. In this review, the clinical and epidemiological evidence for the role of epigenetic factors in mediating the link between early life experiences and long-term health outcomes are summarized.

Highlights

During the past decades, the burden of chronic diseases is rapidly increasing worldwide
Overrepresentation of methylation changes in genes related to organ development, mineralization, and morphology of bone has been obtained, while in boys, the alterations in cell-death-linked genes have been demonstrated. In another methylome-wide association study (MWAS), prenatal cadmium exposure resulted in changed patterns of DNA methylation in leukocytes, with enrichment of genes involved in apoptosis and transcriptional regulation [16]
In a subsequent study within the same cohort, some other genes implicated in growth and metabolic disorders, such as ATP-binding cassette transporter 1 (ABCA1), paternally expressed antisense transcript of the G-protein alpha subunit complex locus (GNASAS), insulin/insulin-like growth factor (INSIGF), interleukin 10 (IL10), leptin (LEP), and maternally expressed gene 3 (MEG3), had differential levels of DNA methylation in exposed and unexposed siblings [78]

Summary

Introduction

The burden of chronic diseases is rapidly increasing worldwide. In another methylome-wide association study (MWAS), prenatal cadmium exposure resulted in changed patterns of DNA methylation in leukocytes, with enrichment of genes involved in apoptosis and transcriptional regulation [16].

Results

Conclusion