Burdge and colleagues discuss the substantial evidence which shows that constraints in the early life environment are an important determinant of risk of metabolic disease in adult life.. There is emerging evidence that higher birth weight, which reflects a more abundant prenatal environment, is associated with increased 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 induced in the developing fetus by aspects of the intra-uterine environment including nutrition which involve stable changes to the genetic regulation of specific genes. However, the induction of specific disease risk is dependent upon the nature of the environmental challenge interactions between the susceptibility set by the altered epigenome and the environment throughout the life course.
Cancer is the result of derangement of cellular processes which control cell division and apoptosis. 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 modification to histones are also involved. Such epigenetic changges represent potential for altered gene activity and hence cellular dysregulation. These may only be manifest when the gene is exposed to an appropriate environmental
signal which is enhanced or diminished as a consequence of epigenetic change compared to normal cells.
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 show statistical associations with risk of specific cancers. In this context, there appear to be parallels between causal processes in cancer with metabolic disease and CVD in which the early life environment and epigenetic processes lead to a susceptibility which increases the risk to later specific environmental exposures.
Burdge et al 2009 Nutrition in early life, and risk of cancer and metabolic disease: alternative endings in an epigenetic tale . Brit J Nutrition vol 101 p 619-30

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