Nutrition in early life, and risk of cancer and metabolic disease: alternative endings in an epigenetic tale?
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.
Burdge
Graham C
GC
Institute of Human Nutrition, Southampton General Hospital, Tremona Road, Southampton, UK. g.c.burdge@southampton.ac.uk
Lillycrop
Karen A
KA
Jackson
Alan A
AA
D000818:Animals; D001724:Birth Weight; D004195:Disease Models, Animal; D044127:Epigenesis, Genetic; D005260:Female; D047109:Fetal Development / Q000502:physiology; D006801:Humans; D007231:Infant, Newborn; D008659:Metabolic Diseases / Q000196:embryology*; D009369:Neoplasms / Q000196:embryology* / Q000235:genetics; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D039401:Prenatal Nutritional Physiological Phenomena / Q000502:physiology*; D012307:Risk Factors