Early Growth Patterns Associated with Cardiovascular Disease
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OBESITY AND DIET (G RAO, SECTION EDITOR)
Early Growth Patterns Associated with Cardiovascular Disease Kate Kirley & Madeleine Shalowitz
Published online: 1 February 2013 # Springer Science+Business Media New York 2013
Abstract Clearly, the development of cardiovascular disease in adulthood is influenced by growth very early in life, even prior to birth. Substantial evidence indicates that impaired fetal growth and subsequent low birth weight are associated with adult cardiovascular disease and related mortality, and there is emerging evidence that elevated birth weight has similar associations. Patterns of rapid and slow infant growth are each associated with multiple cardiovascular disease processes, and rapid growth during childhood is also predictive of adult cardiovascular disease. Additionally, early adiposity rebound is linked to obesity and diabetes mellitus later in life. Keywords Cardiovascular disease . Early growth . Birth weight . Infant growth . Childhood growth . Adiposity rebound . Obesity
worldwide [1, 2]. Major prevention efforts are targeted at reducing the risk factors for CVD, including obesity, hypertension, hyperlipidemia, smoking, and type 2 diabetes mellitus. While the bulk of preventive efforts focus on adults, increasing attention is being paid to preventive interventions beginning earlier in life. At least three decades of research suggest that adult cardiovascular disease can be linked to patterns of growth in utero, during infancy, and throughout childhood. The bulk of this data is derived from cohort studies from England or Finland. Within recent years, data from other populations in Europe, North America, and Asia have reinforced these associations. These studies have also identified new early growth patterns associated with cardiovascular disease. Furthermore, new research has begun to identify the mechanisms which link specific patterns of early growth to later cardiovascular disease.
Introduction The National Vital Statistics Reports (October, 2012), recently confirmed that cardiovascular disease (CVD) remains the number one cause of death both in the United States and
Fetal Growth and Birth Weight
K. Kirley Department of Family Medicine, NorthShore University HealthSystem, Evantson, IL and Pritzker School of Medicine, University of Chicago, Chicago, IL, USA
The fetal origins hypothesis proposed by Barker and colleagues states that CVD is associated with patterns of suboptimal fetal growth which are the result of fetal under-nutrition during gestation [3]. Insufficient nutrition over the course of pregnancy can impair fetal growth to a degree related to the duration of undernutrition. Short-term deficiency results in an underweight, but otherwise normal sized infant, while longerstanding deprivation results in linear growth deceleration, socalled intrauterine growth retardation (IUGR), with the subsequent birth of a low birth-weight or small for gestation age (SGA) infant [4]. IUGR and SGA are generally defined as estimated fetal weight or birth weight, respectively, below th
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