Size at birth, weight gain in infancy and childhood, and adult blood pressure in 5 low- and middle-income-country cohorts: When does weight gain matter?

University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
American Journal of Clinical Nutrition (Impact Factor: 6.77). 04/2009; 89(5):1383-92. DOI: 10.3945/ajcn.2008.27139
Source: PubMed


Promoting catch-up growth in malnourished children has health benefits, but recent evidence suggests that accelerated child weight gain increases adult chronic disease risk.
We aimed to determine how birth weight (BW) and weight gain to midchildhood relate to blood pressure (BP) in young adults.
We pooled data from birth cohorts in Brazil, Guatemala, India, the Philippines, and South Africa. We used conditional weight (CW), a residual of current weight regressed on prior weights, to represent deviations from expected weight gain from 0 to 12, 12 to 24, 24 to 48 mo, and 48 mo to adulthood. Adult BP and risk of prehypertension or hypertension (P/HTN) were modeled before and after adjustment for adult body mass index (BMI) and height. Interactions of CWs with small size-for-gestational age (SGA) at birth were tested.
Higher CWs were associated with increased BP and odds of P/HTN, with coefficients proportional to the contribution of each CW to adult BMI. Adjusted for adult height and BMI, no child CW was associated with adult BP, but 1 SD of BW was related to a 0.5-mm Hg lower systolic BP and a 9% lower odds of P/HTN. BW and CW associations with systolic BP and P/HTN were not different between adults born SGA and those with normal BW, but higher CW at 48 mo was associated with higher diastolic BP in those born SGA.
Greater weight gain at any age relates to elevated adult BP, but faster weight gains in infancy and young childhood do not pose a higher risk than do gains at other ages.

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    • "To date, the association of these three developmental periods on adolescent and adult blood pressure has varied in both reproducibility and magnitude. Low birth weight has been well established to predict higher adolescent and adult blood pressure (Eriksson et al., 2000; Adair & Dahly, 2005; Adair & Cole, 2003; Law et al., 2002; Adair et al., 2009; Huxley, Shiell & Law, 2000; Horta et al., 2003). However, the degree of association has differed across populations and some investigations were unable to replicate these findings (Hemachandra et al., 2006; Huxley, Neil & Collins, 2002; Menezes et al., 2007). "
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    ABSTRACT: Background. Longitudinal investigations into the origins of adult essential hypertension have found elevated blood pressure in children to accurately track into adulthood, however the direct causes of essential hypertension in adolescence and adulthood remains unclear. Methods. We revisited 152 Peruvian adolescents from a birth cohort tracked from 0 to 30 months of age, and evaluated growth via monthly anthropometric measurements between 1995 and 1998, and obtained anthropometric and blood pressure measurements 11–14 years later. We used multivariable regression models to study the effects of infantile and childhood growth trends on blood pressure and central obesity in early adolescence. Results. In regression models adjusted for interim changes in weight and height, each 0.1 SD increase in weight for length from 0 to 5 months of age, and 1 SD increase from 6 to 30 months of age, was associated with decreased adolescent systolic blood pressure by 1.3 mm Hg (95% CI −2.4 to −0.1) and 2.5 mm Hg (95% CI −4.9 to 0.0), and decreased waist circumference by 0.6 (95% CI −1.1 to 0.0) and 1.2 cm (95% CI −2.3 to −0.1), respectively. Growth in infancy and early childhood was not significantly associated with adolescent waist-to-hip ratio. Conclusions. Rapid compensatory growth in early life has been posited to increase the risk of long-term cardiovascular morbidities such that nutritional interventions may do more harm than good. However, we found increased weight growth during infancy and early childhood to be associated with decreased systolic blood pressure and central adiposity in adolescence.
    PeerJ 06/2014; 2(3):e381. DOI:10.7717/peerj.381 · 2.11 Impact Factor
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    • "Thus, in this proposed scenario, insulin resistance is serving as a metabolic defense mechanism to protect the organism against hypoglycemia [39]. In addition to insulin resistance and type 2 diabetes, accelerated weight gain in early life has been associated with elevated blood pressure [44, 45] and coronary heart disease [46]. "
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    ABSTRACT: Chronic diseases such as type 2 diabetes and cardiovascular disease are the leading cause of death and disability worldwide. Although the metabolic syndrome has been defined in various ways, the ultimate importance of recognizing this combination of disorders is that it helps identify individuals at high risk for both type 2 diabetes and cardiovascular disease. Evidence from observational and experimental studies links adverse exposures in early life, particularly relating to nutrition, to chronic disease susceptibility in adulthood. Such studies provide the foundation and framework for the relatively new field of developmental origins of health and disease (DOHaD). Although great strides have been made in identifying the putative concepts and mechanisms relating specific exposures in early life to the risk of developing chronic diseases in adulthood, a complete picture remains obscure. To date, the main focus of the field has been on perinatal and specific nutrient however, the current global health crisis of overweight and obesity demands that perinatal and specific nutrient be examined. This paper assembles current thoughts on the concepts and mechanisms behind the DOHaD as they relate to maternal nutrition, and highlights specific contributions made by macro- and micronutrients.
    Journal of pregnancy 02/2013; 2013(3):368461. DOI:10.1155/2013/368461
    • "Weight and length/height measured at different ages are strongly correlated, leading to problems with collinearity [3]. We therefore modeled the relationship between early weight and length/height and adolescent physical activity using conditional variables. "
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    ABSTRACT: The Developmental Origins of Health and Disease hypothesis suggests that intrauterine, infancy and early childhood variables play a key role at programming later health. However, little is known on the programming of behavioral variables, because most studies so far focused on chronic disease-related and human capital outcomes. The aim of the present study was to evaluate the effects of prenatal, infancy and childhood weight and length/height gains on objectively-measured physical activity (PA) in adolescence. This is a prospective birth cohort study in Pelotas, Brazil, including 457 adolescents (mean age: 13.3 years) with weight and length/height data at birth, one, three and six months, one and four years of age. PA was measured using a GT1M Actigraph accelerometer, and expressed as (a) minutes per day spent on sedentary, light, moderate, vigorous and very-vigorous activities; (b) total counts per day. 61.3% of the adolescents accumulated 60+ minutes of moderate-to-vigorous PA per day. Weight and length/height trajectories in infancy and childhood were similar between those classified as active or inactive at 13.3 years. However, those classified as inactive were heavier and taller at all ages; differences were statistically significant only in terms of length at three, six and 12 months. Weight gain in infancy and childhood did not predict variability in adolescent PA, but those active in adolescence showed somewhat smaller average gains in length in infancy. These findings suggest that PA may partially be sensitive to early hormonal programming, or that genetic factors may affect both early growth and later metabolism or predisposition for PA.
    International Journal of Behavioral Nutrition and Physical Activity 07/2012; 9(1):82. DOI:10.1186/1479-5868-9-82 · 4.11 Impact Factor
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