Cardiovascular disease remains a major cause of morbidity and mortality in developed societies. It is also an increasing problem in developing societies, especially those in which transitions are occurring—for example, the migration of young people from rural to urban environments or the increasing availability of fast food of high calorific content. It is clear that such rapid changes in the incidence of cardiovascular disease, in some instances within a generation, cannot be explained in purely genetic terms. This does not deny the role of genetic factors (for example, single nucleotide polymorphisms) which convey susceptibility to disease, but emphasises that additional environmental factors must also play a major role. This idea is of course not new, although for many years such environmental contributions to disease risk have been considered to be largely adult “lifestyle” factors such as smoking, diet, and physical activity level. However, the results of interventions aimed at reducing such risk factors in adults have so far been disappointing. Pharmacological interventions such as statins have been shown to confer benefit in reducing occurrence of cardiovascular episodes in those at high risk (for example, type 2 diabetes or after a previous myocardial infarction1) but their use more widely is debated.2 The question therefore arises of how to target such preventative measures or interventions in otherwise healthy individuals (or sections of the population) who are at high risk. Such considerations must take into account the full range of risk factors: the series of short papers in this symposium focus on the risks associated with the early environment, prenatally and in childhood.
The contribution of the environment to risk of disease has been widely discussed,3 particular emphasis usually being placed on the association between low birth weight and components of the metabolic syndrome such as hypertension or type 2 diabetes. The strength of the association has been challenged largely on the basis of the size of the correlation between birthweight and adult blood pressure.4 We believe that such debate is sterile as it centres around the use of surrogate measures, both of prenatal environment (birthweight) and later cardiovascular disease (blood pressure). When disease is the outcome measure, the outcome is clear.5 A wide range of mechanistic investigations in animals has shown that adult metabolic, endocrine, and cardiovascular function can be “programmed” by the prenatal environment in the absence of a change in birthweight, and of course blood pressure in middle age may not be significantly elevated even in those who will subsequently have cardiovascular incidents—for example, their renal capacity may be impaired but they may currently be able to compensate. It is therefore clear that aspects of the prenatal environment can programme risk of disease in later life without necessarily being manifest in middle age. This insight needs to be explored further if its implications for prevention of disease are to be exploited. The range of research currently being undertaken around the world into the developmental origins of disease can be seen from the papers presented at the Second World Congress on Fetal Origins of Adult Disease held in June 2003.6,7