Experimental evidence for early nutritional programming of later health in animals.
OBJECTIVE
The developmental origins of adult disease represent a burgeoning area of research for which it has been suggested that up to 50% of the current incidence of later adult disease may be explained or even alleviated. Therefore, it is not surprising that there has been a substantial increase in the number of publications on this subject. In this review, some of the most important recent publications will be highlighted, particularly those focusing on the consequences for later cardiovascular control and obesity.


RESULTS
The review will consider the extent to which both increased and decreased maternal nutrient intake in relevant animal models can result in offspring that are at greater risk of later disease, and will indicate the potential mechanisms involved. Particular focus will be given to effects on glucocorticoids, potential epigenetic effects, and the extent to which male or female offspring may be differentially programmed. In addition, the potential for nutritional or endocrine interventions during lactation in order to overcome these adverse outcomes will be covered.


CONCLUSIONS
Inappropriate growth during pregnancy, lactation and/or childhood can result in individuals whose risk of later cardiovascular disease is greatly increased. By considering the critical importance of the maternal diet from before conception through to lactation, there is a clear potential to substantially improve the health of all children and adults.
Symonds
Michael E
ME
Centre for Reproduction and Early Life, Institute of Clinical Research, University of Nottingham, UK. michael.symonds@nottingham.ac.uk
Gardner
David S
DS
D000328:Adult; D000818:Animals; D001724:Birth Weight / Q000502:physiology; D002318:Cardiovascular Diseases / Q000196:embryology / Q000517:prevention & control; D002648:Child; D002664:Child Nutritional Physiological Phenomena / Q000502:physiology*; D002675:Child, Preschool; D002908:Chronic Disease / Q000453:epidemiology*; D005260:Female; D006801:Humans; D007223:Infant; D007227:Infant Nutritional Physiological Phenomena / Q000502:physiology*; D007231:Infant, Newborn; D008297:Male; D039382:Maternal Nutritional Physiological Phenomena / Q000502:physiology*; D009765:Obesity / Q000196:embryology / Q000517:prevention & control; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D039401:Prenatal Nutritional Physiological Phenomena; D012737:Sex Factors