There is increasing evidence that the early life environment, of which nutrition is a key component, acts through developmental adaptations to set the capacity of cardiovascular and metabolic pathways, and ultimately the limits to physiological challenges in later life. Suboptimal maternal nutrition and fetal growth result in reduced microvascular perfusion and functional dilator capacity, which are strongly associated with later development of obesity, type 2 diabetes, and hypertension. These conditions are also linked to microvascular rarefaction and remodeling that together limit capillary recruitment, reduce exchange capacity and increase diffusion distances of metabolic substrates, and increase local and overall peripheral resistance. Changes in small vessel structure and function may be seen very early, long before the onset of overt cardiovascular and metabolic disease, and may thus be a target for early therapeutic and lifestyle intervention strategies. This article explores how a disadvantageous microvascular phenotype may result from perinatal priming and how developmental plasticity may become an important and additional risk determinant in susceptibility to cardiometabolic disease in adult life.
© 2011 John Wiley & Sons Ltd.