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Early determinants of cardiovascular disease: the role of early diet in later blood pressure control^1,2,3,4

¹ From the Centre for Reproduction and Early Life, the Institute of Clinical Research, the University of Nottingham, Nottingham, United Kingdom.

² Presented at the workshop "Early Risk Determinants and Later Health Outcomes: Implications for Research Prioritization and the Food Supply," held in Washington, DC, July 8–9, 2008.

³ Supported by the British Heart Foundation and the European Union Sixth Framework Programme for Research and Technical Development of the European Community–The Early Nutrition Programming Project (FOOD-CT-2005-007036). Funds to support the writing of this manuscript were provided in part by the Project Committee on Early Nutrition of the International Life Sciences Institute North American Branch.

⁴ Reprints not available. Address correspondence to ME Symonds, Academic Division of Child Health, School of Human Development, Queen's Medical Centre, University Hospital, Nottingham NG7 2UH, United Kingdom. E-mail: michael.symonds{at}nottingham.ac.uk.

ABSTRACT

It is now widely accepted that a gross change in the maternal diet during pregnancy results in offspring with raised blood pressure. More recently, results from human intervention studies and a range of animal experiments have questioned this concept. It thus appears that, when blood pressure is measured directly or by telemetry, the extent to which blood pressure is raised is largely dependent on the magnitude of the postnatal catch-up growth. In addition, such effects can be lost when appropriate corrections are made for current body weight. Consequently, offspring born to nutritionally manipulated mothers can actually have a lower blood pressure than control group offspring. At the same time, studies of the offspring born to contemporary women in developed countries show very little, if any, effect of changes in maternal diet on blood pressure in the offspring when assessed during childhood. In small animal studies, at least, the cardiovascular outcomes linked to small size at birth can differ between the sexes, which may be related in part to differences in kidney function between males and females. With respect to large animal studies, significant effects on blood pressure are less apparent and may relate to the much slower onset of hypertension. The challenge is to use our increased knowledge of the critical windows in early development to optimize later health. One clear priority is the prevention of excess adiposity and to determine how epigenetic mechanisms may provide novel strategies in this regard.

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