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      Weight Gain and Height Growth during Infancy, Childhood, and Adolescence as Predictors of Adult Cardiovascular Risk

      research-article
      , PhD 1 , * , , MD, PhD 2 , * , * , , PhD 3 , , MSc 1 , , MSc 1 , , PhD 1 , , MD 4 , , MD, PhD 2 , 5 , , PhD 6 , , MD, PhD 6
      The Journal of Pediatrics
      Mosby
      children, weight gain, height gain, conditional growth analysis, cardiovascular risk markers, Asian Indians, BMI, Body mass index, BP, Blood pressure, CVD, Cardiovascular disease, DBP, Diastolic blood pressure, HOMA-IR, Homeostatic model assessment-insulin resistance, LMIC, Low and middle income countries, SBP, Systolic blood pressure, T2DM, Type 2 diabetes mellitus, WC, Waist circumference

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          Abstract

          Objectives

          To investigate independent relationships of childhood linear growth (height gain) and relative weight gain to adult cardiovascular disease (CVD) risk traits in Asian Indians.

          Study design

          Data from 2218 adults from the Vellore Birth Cohort were examined for associations of cross-sectional height and body mass index (BMI) and longitudinal growth (independent conditional measures of height and weight gain) in infancy, childhood, adolescence, and adulthood with adult waist circumference (WC), blood pressure (BP), insulin resistance (homeostatic model assessment-insulin resistance [HOMA-IR]), and plasma glucose and lipid concentrations.

          Results

          Higher BMI/greater conditional relative weight gain at all ages was associated with higher adult WC, after 3 months with higher adult BP, HOMA-IR, and lipids, and after 15 years with higher glucose concentrations. Taller adult height was associated with higher WC (men β = 2.32 cm per SD, women β = 1.63, both P < .001), BP (men β = 2.10 mm Hg per SD, women β = 1.21, both P ≤ .001), and HOMA-IR (men β = 0.08 log units per SD, women β = 0.12, both P ≤ .05) but lower glucose concentrations (women β = −0.03 log mmol/L per SD P = .003). Greater height or height gain at all earlier ages were associated with higher adult CVD risk traits. These positive associations were attenuated when adjusted for adult BMI and height. Shorter length and lower BMI at birth were associated with higher glucose concentration in women.

          Conclusions

          Greater height or weight gain relative to height during childhood or adolescence was associated with a more adverse adult CVD risk marker profile, and this was mostly attributable to larger adult size.

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          Most cited references26

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          Global and regional patterns in cardiovascular mortality from 1990 to 2013.

          There is a global commitment to reduce premature cardiovascular diseases (CVDs) 25% by 2025. CVD mortality rates have declined dramatically over the past 2 decades, yet the number of life years lost to premature CVD deaths is increasing in low- and middle-income regions. Ischemic heart disease and stroke remain the leading causes of premature death in the world; however, there is wide regional variation in these patterns. Some regions, led by Central Asia, face particularly high rates of premature death from ischemic heart disease. Sub-Saharan Africa and Asia suffer disproportionately from death from stroke. The purpose of the present report is to (1) describe global trends and regional variation in premature mortality attributable to CVD, (2) review past and current approaches to the measurement of these trends, and (3) describe the limitations of existing models of epidemiological transitions for explaining the observed distribution and trends of CVD mortality. We describe extensive variation both between and within regions even while CVD remains a dominant cause of death. Policies and health interventions will need to be tailored and scaled for a broad range of local conditions to achieve global goals for the improvement of cardiovascular health.
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            Unravelling the fetal origins hypothesis: is there really an inverse association between birthweight and subsequent blood pressure?

            The association between birthweight and subsequent blood pressure levels has been considered to provide some of the strongest, and most consistent, support for the "fetal origins" hypothesis of adult disease. It had been estimated that a 1 kg higher birthweight is typically associated with a 2-4 mm Hg lower systolic blood pressure. 55 studies that had reported regression coefficients of systolic blood pressure on birthweight (with 48 further studies that reported only the direction of this association), and seven such studies within twin pairs, were identified. Each study was weighted according to the inverse of the variance of the regression coefficient (ie, "statistical size"), and combined using a "fixed effects" approach. Among the 55 studies that reported regression coefficients, there was a clear trend (p<0.0001) towards weaker associations in the larger studies: -1.9 mm Hg/kg in those with less than about 1000 participants; -1.5 mm Hg/kg with about 1000-3000 participants; and -0.6 mm Hg/kg with more than 3000 participants. By contrast with the inverse associations reported in 52 of these 55 studies, only 25 of the 48 studies that did not report regression coefficients found an inverse association (p<0.0001 for heterogeneity). Almost all of these regression coefficients had been adjusted for current weight (whereas few were adjusted for potential confounding factors), and removal of this adjustment in the larger studies reduced the estimated association to -0.4 mm Hg/kg. For studies within monozygotic twin pairs, the combined estimate was -0.6 mm Hg/kg with adjustment for current weight, and was also reduced without this adjustment. Claims of a strong inverse association between birthweight and subsequent blood pressure may chiefly reflect the impact of random error, selective emphasis of particular results, and inappropriate adjustment for current weight and for confounding factors. These findings suggest that birthweight is of little relevance to blood pressure levels in later life.
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              Fetal, infant, and childhood growth are predictors of coronary heart disease, diabetes, and hypertension in adult men and women.

              Many human fetuses have to adapt to a limited supply of nutrients. In doing so they permanently change their structure and metabolism. These programmed changes may be the origins of a number of diseases in later life, including coronary heart disease, hypertension, and noninsulin- dependent diabetes. We review epidemiologic studies in which the incidence of these diseases has been related to the recorded, early growth of individuals, while considering factors in the adult lifestyle, such as obesity and socioeconomic status. We discuss possible mechanisms. For hypertension these mechanisms include placentation, maternal blood pressure, fetal undernutrition; childhood growth, activation of the renin-angiotensin system, renal structure, programming of the hypothalamic-pituitary-adrenal axis, vascular structure, and sympathetic nervous activity. For noninsulin-dependent diabetes we discuss mechanisms concerning both insulin resistance and insulin deficiency. We include a review of evidence for the programming of serum cholesterol and clotting factor concentrations. We address the timing of critical windows for coronary heart disease, reviewing studies that allow assessment of the relative importance of fetal, infant, and childhood growth. We argue for a research strategy that combines clinical, animal, and epidemiological studies.
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                Author and article information

                Contributors
                Journal
                J Pediatr
                J. Pediatr
                The Journal of Pediatrics
                Mosby
                0022-3476
                1097-6833
                1 January 2017
                January 2017
                : 180
                : 53-61.e3
                Affiliations
                [1 ]Department of Biostatistics, Christian Medical College, Vellore, India
                [2 ]Oxford Center for Diabetes, Endocrinology, and Metabolism, University of Oxford, Oxford, United Kingdom
                [3 ]Department of Clinical Biochemistry, Christian Medical College, Vellore, India
                [4 ]Department of Child Health, Christian Medical College, Vellore, India
                [5 ]National Institute for Health Research Oxford Biomedical Research Centre, Oxford University Hospital, Oxford, United Kingdom
                [6 ]Medical Research Council Lifecourse Epidemiology Unit, University of Southampton, Southampton, United Kingdom
                Author notes
                [** ]Reprint requests: Oxford Center for Diabetes, Endocrinology, and Metabolism, University of Oxford, Churchill Hospital, Oxford OX3 7LE, United Kingdom.Oxford Center for Diabetes, Endocrinology, and MetabolismUniversity of OxfordChurchill HospitalOxfordOX3 7LEUnited Kingdom. senthil.vasan@ 123456ocdem.ox.ac.uk
                [*]

                Contributed equally.

                Article
                S0022-3476(16)31043-5
                10.1016/j.jpeds.2016.09.059
                5179199
                27823768
                199dbd7d-2e27-4523-9962-0844de2d5cc1
                © 2016 The Authors

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

                History
                : 4 April 2016
                : 29 July 2016
                : 28 September 2016
                Categories
                Original Articles

                Pediatrics
                children,weight gain,height gain,conditional growth analysis,cardiovascular risk markers,asian indians,bmi, body mass index,bp, blood pressure,cvd, cardiovascular disease,dbp, diastolic blood pressure,homa-ir, homeostatic model assessment-insulin resistance,lmic, low and middle income countries,sbp, systolic blood pressure,t2dm, type 2 diabetes mellitus,wc, waist circumference

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