Nutrition in early life and the programming of adult disease: a review

• Published in: Journal of human nutrition and dietetics 2015-01, Vol.28 (s1), p.1-14
• Main Author: Langley‐Evans, S. C
• Format: Article
• Language: English
• Subjects: adulthood; adults; Breast Feeding; Cardiovascular disease; Cardiovascular Diseases - etiology; Cardiovascular Diseases - genetics; cell cycle; coronary disease; Diabetes Mellitus, Type 2 - etiology; Diabetes Mellitus, Type 2 - genetics; Diet; Epigenesis, Genetic; epigenetics; Female; Fetal Development; foetal programming; foods; gene expression; genotype; Humans; infancy; infants; longevity; Malnutrition - complications; Maternal Nutritional Physiological Phenomena; metabolic syndrome; Mortality; mothers; noninsulin-dependent diabetes mellitus; nutrients; Nutritional Status; obesity; Pregnancy; risk factors; tissues; weaning
• ISSN: 0952-3871; 1365-277X
• DOI: 10.1111/jhn.12212

Foetal development and infancy are life stages that are characterised by rapid growth, development and maturation of organs and systems. Variation in the quality or quantity of nutrients consumed by mothers during pregnancy, or infants during the first year of life, can exert permanent and powerful effects upon developing tissues. These effects are termed ‘programming’ and represent an important risk factor for noncommunicable diseases of adulthood, including the metabolic syndrome and coronary heart disease. This narrative review provides an overview of the evidence‐base showing that indicators of nutritional deficit in pregnancy are associated with a greater risk of type‐2 diabetes and cardiovascular mortality. There is also a limited evidence‐base that suggests some relationship between breastfeeding and the timing and type of foods used in weaning, and disease in later life. Many of the associations reported between indicators of early growth and adult disease appear to interact with specific genotypes. This supports the idea that programming is one of several cumulative influences upon health and disease acting across the lifespan. Experimental studies have provided important clues to the mechanisms that link nutritional challenges in early life to disease in adulthood. It is suggested that nutritional programming is a product of the altered expression of genes that regulate the cell cycle, resulting in effective remodelling of tissue structure and functionality. The observation that traits programmed by nutritional exposures in foetal life can be transmitted to further generations adds weight the argument that heritable epigenetic modifications play a critical role in nutritional programming.