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CONGENITAL HEART DISEASE
Fetal and infant markers of adult heart diseases
  1. Marjo-Riitta Järvelin
  1. Department of Public Health Science and General Practice, University of Oulu, Finland and Department of Epidemiology and Public Health, Imperial College School of Medicine, London, UK
  1. Professor Marjo-Riitta Järvelin, Department of Epidemiology and Public Health, Imperial College School of Medicine, Norfolk Place, London W2 1PG, UK email:m.jarvelin{at}ic.ac.uk

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There is growing evidence of an increasingly complex and multifactorial aetiology of heart diseases.1 w1 It seems likely that the large geographic variations in cardiovascular disease (CVD) morbidity and mortality,w2 even though at least partly genetic in origin, are influenced by factors acting prenatally and in early life, or by a combination of factors present throughout the life course. Changes in fetal growth pattern have been related to adult disease risk,1 and there are many theories about the underlying mechanisms affecting cell division during critical periods of tissue development. The critical periods vary according to the tissue in question, and that is why there have been attempts to explore the timing of exposure in order to predict more specifically the adult disease risk.

This article examines: firstly the historical evolution of theories on childhood factors which have an influence in adulthood; secondly what is known today about the effect of early life factors on heart disease risk; and thirdly the specific problems in longitudinal studies which explore these factors and adult disease risk.

Dawn of the “hypothesis of the 20th century”

Biological programming: a new theoretical model about the aetiology of heart disease

The dawn of modern epidemiology came after the second world war, first with ecological studies comparing CVD incidence and mortality, and subsequently multicentre cross sectional and follow up studies on CVD.w3 The studies showed that populations with high CVD mortality have high cholesterol and high blood pressure, and that smoking and obesity are common among these populations.w4This led to the lifestyle model in understanding the aetiology of chronic diseases, where the key issues are health behaviour and the interaction between genes and an adverse environment in adult life. This was consequently followed by intervention programmes, which have significantly improved heart disease risk status in many countries.w3 However, lifestyle factors only explain part of the heart disease risk, which is why …

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