British Journal of Nutrition

Horizons in Nutritional Science

Nutrition in early life, and risk of cancer and metabolic disease: alternative endings in an epigenetic tale?

Graham C. Burdgea1 c1, Karen A. Lillycropa2 and Alan A. Jacksona1

a1 Institute of Human Nutrition, Institute of Developmental Sciences Building, Southampton General Hospital, MP 887, Tremona Road, Southampton SO16 6YD, UK

a2 Developmental and Cell Biology, Biomedical Sciences Building, University of Southampton, Bassett Crescent East, Southampton SO16 7PX, UK


There is substantial evidence which shows that constraints in the early life environment are an important determinant of risk of metabolic disease and CVD. There is emerging evidence that higher birth 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 CVD, metabolic disease and cancer have a common origin in developmental changes induced 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.

(Received June 04 2008)

(Revised August 28 2008)

(Accepted October 07 2008)

(Online publication December 12 2008)


c1 Corresponding author: Dr Graham C. Burdge, fax +44 23 80795225, email


Abbreviations: Dnmt, DNA methyltransferase; GR, glucocorticoid receptor; IGF, insulin-like growth factor; HRad, adjusted hazard ratio; MeCP2, methyl CpG binding protein; PR, protein-restricted