John C Mathers1. 1. Human Nutrition Research Centre, School of Clinical Medical Sciences, University of Newcastle, Newcastle, UK.
Abstract
BACKGROUND/AIMS: (1) To outline the findings that alterations in nutrition in utero and in early postnatal life influence health in later life. (2) To review the evidence that alterations in epigenetic markings may be a means by which the genome records environmental (including nutritional) exposure resulting in changes in gene expression and cell function which underlie susceptibility to disease. METHODS: Literature review. RESULTS: There is strong evidence that low birth weight, especially when followed by accelerated growth in childhood and greater central adiposity in adulthood, is a risk factor for a range of common diseases including cardiovascular disease and type 2 diabetes. Such observations provide the basis for the 'programming' hypothesis and present a challenge to discover the mechanisms by which nutritional insults in early life are received, recorded, remembered and then revealed in later life. Emerging evidence suggests that alterations in epigenetic marking of the genome may be a key mechanism by which nutritional exposure in utero can influence gene expression, and therefore, phenotype. CONCLUSION: Early life nutrition has the potential to change chromatin structure, to alter gene expression and to modulate health throughout the life course. Whether later interventions can reverse adverse epigenetic markings remains to be discovered.
BACKGROUND/AIMS: (1) To outline the findings that alterations in nutrition in utero and in early postnatal life influence health in later life. (2) To review the evidence that alterations in epigenetic markings may be a means by which the genome records environmental (including nutritional) exposure resulting in changes in gene expression and cell function which underlie susceptibility to disease. METHODS: Literature review. RESULTS: There is strong evidence that low birth weight, especially when followed by accelerated growth in childhood and greater central adiposity in adulthood, is a risk factor for a range of common diseases including cardiovascular disease and type 2 diabetes. Such observations provide the basis for the 'programming' hypothesis and present a challenge to discover the mechanisms by which nutritional insults in early life are received, recorded, remembered and then revealed in later life. Emerging evidence suggests that alterations in epigenetic marking of the genome may be a key mechanism by which nutritional exposure in utero can influence gene expression, and therefore, phenotype. CONCLUSION: Early life nutrition has the potential to change chromatin structure, to alter gene expression and to modulate health throughout the life course. Whether later interventions can reverse adverse epigenetic markings remains to be discovered.
Authors: Cathrine Hoyo; Amy P Murtha; Joellen M Schildkraut; Randy L Jirtle; Wendy Demark-Wahnefried; Michele R Forman; Edwin S Iversen; Joanne Kurtzberg; Francine Overcash; Zhiqing Huang; Susan K Murphy Journal: Epigenetics Date: 2011-07-01 Impact factor: 4.528
Authors: Elizabeth W Triche; Lisbet S Lundsberg; Paige G Wickner; Kathleen Belanger; Brian P Leaderer; Michael B Bracken Journal: Ann Allergy Asthma Immunol Date: 2011-01-08 Impact factor: 6.347
Authors: Susan K Murphy; Abayomi Adigun; Zhiqing Huang; Francine Overcash; Frances Wang; Randy L Jirtle; Joellen M Schildkraut; Amy P Murtha; Edwin S Iversen; Cathrine Hoyo Journal: Gene Date: 2011-12-20 Impact factor: 3.688
Authors: Carolyn F McCabe; Jennifer L LaBarre; Steven E Domino; Marjorie C Treadwell; Ana Baylin; Charles F Burant; Dana C Dolinoy; Vasantha Padmanabhan; Jaclyn M Goodrich Journal: J Nutr Biochem Date: 2022-01-10 Impact factor: 6.048
Authors: Carrie V Breton; Hyang-Min Byun; Made Wenten; Fei Pan; Allen Yang; Frank D Gilliland Journal: Am J Respir Crit Care Med Date: 2009-06-04 Impact factor: 21.405