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      Estimation of Newborn Risk for Child or Adolescent Obesity: Lessons from Longitudinal Birth Cohorts

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          Abstract

          Objectives

          Prevention of obesity should start as early as possible after birth. We aimed to build clinically useful equations estimating the risk of later obesity in newborns, as a first step towards focused early prevention against the global obesity epidemic.

          Methods

          We analyzed the lifetime Northern Finland Birth Cohort 1986 (NFBC1986) (N = 4,032) to draw predictive equations for childhood and adolescent obesity from traditional risk factors (parental BMI, birth weight, maternal gestational weight gain, behaviour and social indicators), and a genetic score built from 39 BMI/obesity-associated polymorphisms. We performed validation analyses in a retrospective cohort of 1,503 Italian children and in a prospective cohort of 1,032 U.S. children.

          Results

          In the NFBC1986, the cumulative accuracy of traditional risk factors predicting childhood obesity, adolescent obesity, and childhood obesity persistent into adolescence was good: AUROC = 0·78[0·74–0.82], 0·75[0·71–0·79] and 0·85[0·80–0·90] respectively (all p<0·001). Adding the genetic score produced discrimination improvements ≤1%. The NFBC1986 equation for childhood obesity remained acceptably accurate when applied to the Italian and the U.S. cohort (AUROC = 0·70[0·63–0·77] and 0·73[0·67–0·80] respectively) and the two additional equations for childhood obesity newly drawn from the Italian and the U.S. datasets showed good accuracy in respective cohorts (AUROC = 0·74[0·69–0·79] and 0·79[0·73–0·84]) (all p<0·001). The three equations for childhood obesity were converted into simple Excel risk calculators for potential clinical use.

          Conclusion

          This study provides the first example of handy tools for predicting childhood obesity in newborns by means of easily recorded information, while it shows that currently known genetic variants have very little usefulness for such prediction.

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          Most cited references19

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          Six new loci associated with body mass index highlight a neuronal influence on body weight regulation.

          Common variants at only two loci, FTO and MC4R, have been reproducibly associated with body mass index (BMI) in humans. To identify additional loci, we conducted meta-analysis of 15 genome-wide association studies for BMI (n > 32,000) and followed up top signals in 14 additional cohorts (n > 59,000). We strongly confirm FTO and MC4R and identify six additional loci (P < 5 x 10(-8)): TMEM18, KCTD15, GNPDA2, SH2B1, MTCH2 and NEGR1 (where a 45-kb deletion polymorphism is a candidate causal variant). Several of the likely causal genes are highly expressed or known to act in the central nervous system (CNS), emphasizing, as in rare monogenic forms of obesity, the role of the CNS in predisposition to obesity.
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            Interventions for preventing obesity in children.

            Prevention of childhood obesity is an international public health priority given the significant impact of obesity on acute and chronic diseases, general health, development and well-being. The international evidence base for strategies that governments, communities and families can implement to prevent obesity, and promote health, has been accumulating but remains unclear. This review primarily aims to update the previous Cochrane review of childhood obesity prevention research and determine the effectiveness of evaluated interventions intended to prevent obesity in children, assessed by change in Body Mass Index (BMI). Secondary aims were to examine the characteristics of the programs and strategies to answer the questions "What works for whom, why and for what cost?" The searches were re-run in CENTRAL, MEDLINE, EMBASE, PsychINFO and CINAHL in March 2010 and searched relevant websites. Non-English language papers were included and experts were contacted. The review includes data from childhood obesity prevention studies that used a controlled study design (with or without randomisation). Studies were included if they evaluated interventions, policies or programs in place for twelve weeks or more. If studies were randomised at a cluster level, 6 clusters were required. Two review authors independently extracted data and assessed the risk of bias of included studies.  Data was extracted on intervention implementation, cost, equity and outcomes. Outcome measures were grouped according to whether they measured adiposity, physical activity (PA)-related behaviours or diet-related behaviours.  Adverse outcomes were recorded. A meta-analysis was conducted using available BMI or standardised BMI (zBMI) score data with subgroup analysis by age group (0-5, 6-12, 13-18 years, corresponding to stages of developmental and childhood settings). This review includes 55 studies (an additional 36 studies found for this update). The majority of studies targeted children aged 6-12 years.  The meta-analysis included 37 studies of 27,946 children and demonstrated that programmes were effective at reducing adiposity, although not all individual interventions were effective, and there was a high level of observed heterogeneity (I(2)=82%).  Overall, children in the intervention group had a standardised mean difference in adiposity (measured as BMI or zBMI) of -0.15kg/m(2) (95% confidence interval (CI): -0.21 to -0.09).  Intervention effects by age subgroups were -0.26kg/m(2) (95% CI:-0.53 to 0.00) (0-5 years), -0.15kg/m(2) (95% CI -0.23 to -0.08) (6-12 years), and -0.09kg/m(2) (95% CI -0.20 to 0.03) (13-18 years). Heterogeneity was apparent in all three age groups and could not explained by randomisation status or the type, duration or setting of the intervention.  Only eight studies reported on adverse effects and no evidence of adverse outcomes such as unhealthy dieting practices, increased prevalence of underweight or body image sensitivities was found.  Interventions did not appear to increase health inequalities although this was examined in fewer studies. We found strong evidence to support beneficial effects of child obesity prevention programmes on BMI, particularly for programmes targeted to children aged six to 12 years. However, given the unexplained heterogeneity and the likelihood of small study bias, these findings must be interpreted cautiously. A broad range of programme components were used in these studies and whilst it is not possible to distinguish which of these components contributed most to the beneficial effects observed, our synthesis indicates the following to be promising policies and strategies:·         school curriculum that includes healthy eating, physical activity and body image·         increased sessions for physical activity and the development of fundamental movement skills throughout the school week·         improvements in nutritional quality of the food supply in schools·         environments and cultural practices that support children eating healthier foods and being active throughout each day·         support for teachers and other staff to implement health promotion strategies and activities (e.g. professional development, capacity building activities)·         parent support and home activities that encourage children to be more active, eat more nutritious foods and spend less time in screen based activitiesHowever, study and evaluation designs need to be strengthened, and reporting extended to capture process and implementation factors, outcomes in relation to measures of equity, longer term outcomes, potential harms and costs.Childhood obesity prevention research must now move towards identifying how effective intervention components can be embedded within health, education and care systems and achieve long term sustainable impacts.  
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              Genome-wide association study for early-onset and morbid adult obesity identifies three new risk loci in European populations.

              We analyzed genome-wide association data from 1,380 Europeans with early-onset and morbid adult obesity and 1,416 age-matched normal-weight controls. Thirty-eight markers showing strong association were further evaluated in 14,186 European subjects. In addition to FTO and MC4R, we detected significant association of obesity with three new risk loci in NPC1 (endosomal/lysosomal Niemann-Pick C1 gene, P = 2.9 x 10(-7)), near MAF (encoding the transcription factor c-MAF, P = 3.8 x 10(-13)) and near PTER (phosphotriesterase-related gene, P = 2.1 x 10(-7)).
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                Author and article information

                Contributors
                Role: Editor
                Journal
                PLoS One
                PLoS ONE
                plos
                plosone
                PLoS ONE
                Public Library of Science (San Francisco, USA )
                1932-6203
                2012
                28 November 2012
                : 7
                : 11
                : e49919
                Affiliations
                [1 ]Unité Mixte de Recherche 8199, Centre National de Recherche Scientifique (CNRS) and Pasteur Institute, Lille, France
                [2 ]Regional Centre for Juvenile Diabetes, Obesity and Clinical Nutrition, University of Verona, Verona, Italy
                [3 ]Department of Clinical Epidemiology and Biostatistics, McMaster University, Hamilton, Canada
                [4 ]Obesity Prevention Program, Department of Population Medicine, Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston, Massachusetts, United States of America
                [5 ]Institute of Health Sciences and Biocenter, University of Oulu, Oulu, Finland
                [6 ]Department of Children, Young People and Families, National Institute for Health and Welfare, Helsinki, Finland
                [7 ]Institute of Clinical Medicine/Obstetrics and Gynecology, University of Oulu, Oulu, Finland
                [8 ]Finnish Institute of Occupational Health, Helsinki, Finland
                [9 ]Department of Clinical Sciences and Clinical Chemistry, University of Oulu, Oulu, Finland
                [10 ]Department of Epidemiology and Biostatistics, School of Public Health, Imperial College, London, United Kingdom
                [11 ]Centre for Environment and Health, School of Public Health, Imperial College, London, United Kingdom
                [12 ]Department of Life Course and Services, National Institute for Health and Welfare, Oulu, Finland
                [13 ]Department of Genomics of Common Disease, School of Public Health, Imperial College, London, United Kingdom
                Scientific Directorate, Bambino Hospital, Italy
                Author notes

                Competing Interests: The authors have declared that no competing interests exist.

                Conceived and designed the experiments: AM DM PF. Performed the experiments: SL SG VV. Analyzed the data: AM KK SLR-S. Contributed reagents/materials/analysis tools: SL MK SG VV. Wrote the paper: AM. Cohort investigators: M-RJ CM MG KK SLR-S MK AP A-LH JL AR SD AAK. Supervised the study: PE M-RJ PF. Equally contributed as last authors: M-RJ PF. Equal corresponding authors: AM PF.

                Article
                PONE-D-12-23619
                10.1371/journal.pone.0049919
                3509134
                23209618
                210a7092-f6c1-4b38-a80b-4e18df7f1ba0
                Copyright @ 2012

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                : 7 August 2012
                : 15 October 2012
                Page count
                Pages: 9
                Funding
                The Northern Finland Birth Cohorts program is financially supported by the Academy of Finland (project grants 104781, 120315, 129269, 1114194 and SALVE), University Hospital Oulu, Biocenter, University of Oulu, Finland (75617), the European Commission (EURO-BLCS, Framework 5 award QLG1-CT-2000-01643), the Medical Research Council, UK (G05005539, G0600705, PrevMetSyn) and the Divisional Grant Imperial College London [G24038]. The genotyping was supported by the “Conseil Régional Nord Pas de Calais/FEDER” and the “Agence Nationale de la Recherche.” Project Viva is financially supported by the National Institutes of Health, the March of Dimes Foundation, and the U.S. Centers for Disease Control and Prevention. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Research Article
                Medicine
                Clinical Genetics
                Clinical Research Design
                Cohort Studies
                Endocrinology
                Pediatric Endocrinology
                Epidemiology
                Cardiovascular Disease Epidemiology
                Pediatric Epidemiology
                Non-Clinical Medicine
                Health Care Policy
                Health Risk Analysis
                Nutrition
                Obesity
                Pediatrics
                Neonatology

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                Uncategorized

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