Experience‐sensitive epigenetic mechanisms, developmental plasticity, and the biological embedding of chronic disease risk. (20th February 2015)

• Record Type: Journal Article
• Authors: Cunliffe, Vincent T.
• Is Part Of: Wiley interdisciplinary reviews. Volume 7:Number 2(2015)
• Page Start: 53
• Page End: 71
• Publication Date: 2015-02-20
• Subjects: Systems biology -- Periodicals; Medicine -- Periodicals; 610
• DOI: 10.1002/wsbm.1291
• Languages: English
• ISSNs: 1939-5094

Abstract

<abstract abstract-type="main" id="wsbm1291-abs-0001"> <title> <x xml:space="preserve">Abstract</x> </title> <p id="wsbm1291-para-0001">A wide range of developmental, nutritional, environmental, and social factors affect the biological activities of epigenetic mechanisms. These factors change spatiotemporal patterns of gene expression in a variety of different ways and bring significant impacts to bear on development, physiology, and disease risk throughout the life course. Abundant evidence demonstrates that behavioral stressors and adverse nutritional conditions are particularly potent inducers of epigenetic changes and enhancers of chronic disease risks. Recent insights from both human clinical studies and research with model organisms further indicate that such experience‐dependent changes to the epigenome can be transmitted through the germline across multiple generations, with important consequences for the heritability of both adaptive and maladaptive phenotypes. Epigenetics research thus offers many possibilities for developing informative biomarkers of acquired chronic disease risk and determining the effectiveness of preventive and therapeutic interventions. Moreover, the experience‐sensitive nature of these disease risks raises important questions about societal and individual responsibilities for the prevention of ill‐health and the promotion of well‐being during development, across the life course and between generations. Better understanding of how epigenetic mechanisms regulate developmental plasticity and mediate the biological embedding of chronic disease risks is therefore likely to shed important new light on the nature of the pathophysiological mechanisms linking social and health inequalities, and will help to inform public policy initiatives in this area. <italic>WIREs Syst Biol Med</italic> 2015, 7:53–71. doi: 10.1002/wsbm.1291</p> <p>For further resources related to this article, please visit the <ext-link ext-link-type="uri" xlink:href="http://wires.wiley.com/remdoi.cgi?doi=10.1002/wsbm.1291" xlink:type="simple" xmlns:xlink="http://www.w3.org/1999/xlink">WIREs website</ext-link>.</p> <p>Conflict of interest: The author has declared no conflicts of interest for this article.</p> </abstract>