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• W2000750573 abstract "Monitoring growth is an essential part of good pediatric care. The pattern of growth is not only a marker of the immediate physical and emotional well-being of the child but also has long-term implications for health. Previously, however, research and clinical practice in pediatrics have focused almost exclusively on achieving adequate growth and the prevention of growth faltering. More recently, compelling evidence has emerged for the adverse long-term consequences of “accelerated” or too fast growth. The present review considers this evidence, focusing on the role of accelerated weight gain in infancy on the long-term risk of obesity. The concept that the pattern of growth in early life could have long-term biological effects first emerged in the 1930s (1). McCay (1) showed that rats whose growth was stunted by restricting their food intake had a lower incidence of tumors, kidney disease, vascular calcification, and chronic pneumonia, and consequently a substantial 35% increase in life span. The idea that manipulation of early growth could affect the later risk of obesity was first demonstrated by McCance in the 1960s. He found that overfeeding rats, during a critical window in early postnatal life, permanently increased later body size. Subsequently, Lewis showed that male infant baboons given a nutrient-enriched formula, which provided >30%, more energy, had greater mesenteric and omental fat depots, an effect that emerged only after adolescence. Evidence that early weight gain could influence, or program, the long-term risk of obesity in humans, as in animal models, was first obtained in 1970. Eid (2) showed that faster weight gain in the first 6 months after birth was associated with obesity at ages 6 to 8 years. Specifically, the prevalence of obesity, defined as >20% of expected weight for height and sex, was 9.4% in children with rapid weight gain (>90th centile for sex) in the first 6 postnatal months compared with 1.9% in those with slower weight gain (<10th centile) (2). Importantly, the main findings from this early research have been confirmed by subsequent studies. For instance, infants born at low birth weight showed the most rapid infant weight gain; the critical window for the effects of faster weight gain was as early as the first 6 weeks of life; rapidity of weight gain in infancy was a better guide to the risk of overweight in later childhood than the weight of the parents; and the effects of infant growth were independent of the whether infants were bottle-fed or breast-fed (2). The work of Eid (2) was not replicated in a large modern cohort study until 2002. Stettler et al (3) showed in 19,397 children that each 100-g increase in weight per month during the first 4 postnatal months increased the risk of overweight status at age 7 years by approximately 30%. Subsequently, based on follow-up of randomized studies, initially in preterm infants and then in infants born at term, we proposed in 2003 that faster infant growth not only influenced obesity but also programmed the risk of cardiovascular disease (CVD) (4,5). This “growth acceleration hypothesis” suggested that rapid infant growth programmed obesity, insulin resistance, higher blood pressure, and higher cholesterol concentration, the main components of the metabolic syndrome and the major cause of morbidity and mortality in the Western world. Furthermore, a slower rate of weight gain as a consequence of relative under-nutrition in breast-fed compared with formula-fed infants, particularly in the first few weeks of life, could explain the greater tendency to obesity in infants fed formula rather than breast milk (5). Since this early work, more than 50 studies now support the growth-acceleration hypothesis. For instance, faster weight gain (upward centile crossing for weight) in infancy is associated with a greater risk of long-term obesity in more than 27 studies (as summarized in several systematic reviews) (6,7). This association has been seen for obesity in adults and children, in breast-fed and formula-fed populations, for faster length gain as well as weight gain in infancy, in high-income and low-income countries, and is consistent for cohorts during the last 80 years. This association is strong, shows a dose-response effect, is biologically plausible, and is experimentally reproducible in animal models (7). The association is consistent (few studies have not found a significant link between rapid infant growth and later obesity (6)), is independent of birth weight, and is seen across the birth weight spectrum (ie, is not confined to infants born at low birth weight) (6). Interestingly, faster weight gain in infancy (during first 3 months) appears to have stronger programming effects on fat mass rather than lean mass, assessed using the 4-component model. Finally, recent data suggest that rapid infant weight gain has stronger programming effects on visceral or peritoneal fat (a major risk factor for CVD) compared with subcutaneous fat. Nevertheless, despite extensive research, 3 key questions remain unanswered. First, it is uncertain whether the link between infant growth and later obesity is causal, as suggested previously for CVD risk factors (5), or is confounded by factors that influence both postnatal weight gain and later adiposity. For instance, genetic factors, a major influence on postnatal growth rate (8), could influence appetite and hence both the risk of overfeeding in infancy and later obesity. We are addressing this issue with follow-up of children born small-for-gestational age who were randomly assigned at birth to receive a standard- or nutrient-enriched formula that promoted growth. Such a causal link would strongly support interventions aimed at modifying infant growth to prevent long-term obesity. Second, the most sensitive window for programming effects of postnatal weight gain is uncertain. Faster weight gain throughout the first year appears to program later obesity, with a longer exposure to rapid weight gain (eg, 9 months compared with 6 months) having a stronger effect (6). However, consistent with our data on programming of insulin resistance, inflammatory markers, cholesterol concentration, and endothelial function by weight gain in the first postnatal weeks (5), Stettler (7) found that faster weight gain in the first week adversely affected overweight status up to 32 years later. Therefore, relative undernutrition and slower growth associated with breast-feeding in the first postnatal week could explain the long-term advantage for obesity and CVD for breast-fed compared with formula-fed infants (5). Finally, the mechanisms linking infant weight gain with later obesity are poorly understood. Of particular interest are effects of infant nutrition on programming of appetite and hormonal systems relevant to appetite and energy metabolism (9). Moreover, as first suggested by McCay (1), early growth may program long-term aging and age-related processes. In fact, the hypothesis that programming of obesity, CVD, and aging may represent similar processes and have common underlying mechanisms in humans (5), as in animals (10), is a current focus of research. Clearly, additional experimental data are required to define the risks/benefits of promoting growth in infancy. However, epidemiological evidence suggests a large effect of infant growth on later obesity. For instance, in a contemporary Western environment, approximately 20% of the population risk of overweight in childhood can be attributed to both infant nutrition (formula feeding rather than breast-feeding) and being in the highest quintile for weight gain in infancy (7). Interventions aimed at modifying infant growth could therefore play a key role in the primary prevention of long-term obesity." @default.
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• W2000750573 date "2010-12-01" @default.
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• W2000750573 title "Does Weight Gain in Infancy Influence the Later Risk of Obesity?" @default.
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