Tec. Lab Clinicos

UKPMC Funders Group
Author Manuscript
Br J Nutr. Author manuscript; available in PMC 2009 March 1.
Published in final edited form as:
Br J Nutr. 2009 March ; 101(5): 619–630. doi:10.1017/S0007114508145883.

UKPMC Funders Group Author Manuscript

Nutrition in early life, and risk of cancer and metabolic disease:
alternative endings in an epigenetic tale?
Graham C Burdge1, Karen ALillycrop2, and Alan A Jackson1
1Institute of Human Nutrition, University of Southampton, Southampton, UK
2Developmental and Cell Biology, University of Southampton, Southampton, UK

Abstract
There is substantial evidence which shows that constraints in the early life environment is an
important determinant of risk of metabolic and cardiovascular disease. There is emerging evidence
that higherbirth weight, which reflects a more abundant prenatal environment, is associated with
increased risk of cancer, in particular breast cancer and childhood leukaemia. Using specific examples
from epidemiology and experimental studies, this review discusses the hypothesis that increased
susceptibility to cardiovascular, metabolic disease and cancer have a common origin in
developmental changesinduced in the developing fetus by aspects of the intra uterine environment
including nutrition which involve stable changes to the epigenetic regulation of specific genes.
However, the induction of specific disease risk is dependent upon the nature of the environmental
challenge and interactions between the susceptibility set by the altered epigenome and the
environment throughout the life course.UKPMC Funders Group Author Manuscript

Introduction
Cancer is the result of derangement of cellular processes which control cell division and
apoptosis(1). There is a large body of information which shows that environmental exposures,
including nutrition, play a significant role in the aetiology of the disease. Such exposures
usually precede the appearance of clinical disease by aprolonged period of time, often several
decades(1). While gene mutation has a role in the aetiology of cancer, there is increasing
evidence which shows that epigenetic processes such as DNA methylation and covalent
modifications to histones are also involved(2). Such epigenetic changes represent potential for
altered gene activity and hence cellular dysregulation, but these may only be manifest whenthe gene is exposed to an appropriate environmental signal which is enhanced or diminished
as a consequence of the epigenetic change compared to normal cells. This suggestion is
consistent with a life-course perspective on cancer risk. The early life environment has been
shown to be an important factor in determining risk for some types of cancer. Measures of
growth in early life showstatistical associations with risk of specific cancers. In this context,
there appear to be parallels between causal processes in cancer with metabolic and
cardiovascular disease in which the early life environment and epigenetic processes lead to a
susceptibility which increases the risk to later specific environmental exposures(3). The
purpose of this review is to discuss the hypothesis that theearly life environment, in particular
nutrition, induces changes in the development of the offspring which lead to increased risk of
Correspondence to:- Dr GC Burdge, Institute of Human Nutrition, Institute of Developmental Sciences Building, Southampton General
Hospital, MP 887, Tremona Road, Southampton, SO16 6YD, UK. Telephone +44 (0)23 80798663; FAX +44 (0)23 80795225; e-mailg.c.burdge@southampton.ac.uk.
Author contributions and conflict of interest statement
GCB wrote the manuscript with substantial contributions from KAL and AAJ. All authors declare no conflict of interest.

Burdge et al.

Page 2

cancer, or metabolic and cardiovascular disease. The extent to which altered epigenetic
processes established during development represent a common mechanism in cancer and...