Fetal and early childhood environment : long-term health implications
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Bibliographic Information
Fetal and early childhood environment : long-term health implications
（British medical bulletin, v. 53,
Published for the British Council by the Royal Society of Medicine Press, 1997
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Early environment and health
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Includes bibliographical references and index
Description and Table of Contents
Description
This series of review papers documents research into the foetal and early-childhood origins of adult health on an unusually broad front. The range of disciplines includes epidemiology and public health, nutrition, psychiatry, paediatrics, physical medicine, psychology, comparative ethology and the social sciences. Neurological disorders, lung development and disease, mental health, childhood growth, cardiovascular disease and early-childhood learning are some of the areas covered. Some studies identify critical periods in foetal or early-postnatal life, while others point to factors at various stages of development that serve to reinforce trajectories for disease in adult life. The influence of genes over the pattern and occurrence of disease in later life is still the subject of vigorous debate. The debate has, of late, taken a new form. There may be influences from early life that influence adult disease rates that are environmental, not genetic. These may act in utero or during infancy, childhood and adolescence, and their relative importance must be considered.
Where environmental effects have been neglected, the relative importance of genetic effects may be overestimated; genetic factors are important in asthma and atopy, but there has been an increase in the prevalance of asthma that must have some other explanation. Genetic effects cannot be understood without taking into account gene-environment interactions. The bulk of the evidence suggests that, as with genes and environment, there are interactions between effects from early life and influences operating later in life. These papers hold out the prospect that the pathways linking early life effects to adult disease may be interrupted.
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