Danick Goulet, Michel Boivin, Christopher A Gravel, Julian Little, Beth K Potter, Lise Dubois
{"title":"儿童饮食行为对肥胖遗传易感性的调节作用。","authors":"Danick Goulet, Michel Boivin, Christopher A Gravel, Julian Little, Beth K Potter, Lise Dubois","doi":"10.1111/ijpo.13180","DOIUrl":null,"url":null,"abstract":"<p><strong>Background/objectives: </strong>Few studies have examined the putative mediating role of eating behaviours linking genetic susceptibility and body weight. The goal of this study was to investigate the extent to which two polygenic scores (PGSs) for body mass index (BMI), based on child and adult data, predicted BMI through over-eating and fussy eating across childhood.</p><p><strong>Subjects/methods: </strong>The study sample involved 692 participants from a birth cohort study. Height and weight were measured on six occasions between ages 6 and 13 years. Over-eating and fussy eating behaviours were assessed five times between ages 2 and 6 years. Longitudinal growth curve mediation analysis was used to estimate the contributions of the PGSs to BMI z-scores mediated by over-eating and fussy eating.</p><p><strong>Results: </strong>Both PGSs predicted BMI z-scores (PGS<sub>child</sub>: β = 0.26, 95% CI: 0.19-0.33; PGS<sub>adult</sub>: β = 0.34, 95% CI: 0.27-0.41). Over-eating significantly mediated these associations, but this mediation decreased over time from 6 years (PGS<sub>child</sub>: 18.0%, 95% CI: 3.1-32.9, p-value = 0.018; PGS<sub>adult</sub>: 14.2%, 95% CI: 2.8-25.5, p-value = 0.014) to 13 years (PGS<sub>child</sub>: 11.4%, 95% CI: -0.4-23.1, p-value = 0.057; PGS<sub>adult</sub>: 6.2%, 95% CI: 0.4-12.0, p-value = 0.037). Fussy eating did not show any mediation.</p><p><strong>Conclusions: </strong>Our results support the view that appetite is key to translating genetic susceptibility into changes in body weight.</p>","PeriodicalId":217,"journal":{"name":"Pediatric Obesity","volume":null,"pages":null},"PeriodicalIF":2.7000,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Mediation of genetic susceptibility to obesity through eating behaviours in children.\",\"authors\":\"Danick Goulet, Michel Boivin, Christopher A Gravel, Julian Little, Beth K Potter, Lise Dubois\",\"doi\":\"10.1111/ijpo.13180\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background/objectives: </strong>Few studies have examined the putative mediating role of eating behaviours linking genetic susceptibility and body weight. The goal of this study was to investigate the extent to which two polygenic scores (PGSs) for body mass index (BMI), based on child and adult data, predicted BMI through over-eating and fussy eating across childhood.</p><p><strong>Subjects/methods: </strong>The study sample involved 692 participants from a birth cohort study. Height and weight were measured on six occasions between ages 6 and 13 years. Over-eating and fussy eating behaviours were assessed five times between ages 2 and 6 years. Longitudinal growth curve mediation analysis was used to estimate the contributions of the PGSs to BMI z-scores mediated by over-eating and fussy eating.</p><p><strong>Results: </strong>Both PGSs predicted BMI z-scores (PGS<sub>child</sub>: β = 0.26, 95% CI: 0.19-0.33; PGS<sub>adult</sub>: β = 0.34, 95% CI: 0.27-0.41). Over-eating significantly mediated these associations, but this mediation decreased over time from 6 years (PGS<sub>child</sub>: 18.0%, 95% CI: 3.1-32.9, p-value = 0.018; PGS<sub>adult</sub>: 14.2%, 95% CI: 2.8-25.5, p-value = 0.014) to 13 years (PGS<sub>child</sub>: 11.4%, 95% CI: -0.4-23.1, p-value = 0.057; PGS<sub>adult</sub>: 6.2%, 95% CI: 0.4-12.0, p-value = 0.037). Fussy eating did not show any mediation.</p><p><strong>Conclusions: </strong>Our results support the view that appetite is key to translating genetic susceptibility into changes in body weight.</p>\",\"PeriodicalId\":217,\"journal\":{\"name\":\"Pediatric Obesity\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":2.7000,\"publicationDate\":\"2024-10-10\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Pediatric Obesity\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1111/ijpo.13180\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"PEDIATRICS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Pediatric Obesity","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1111/ijpo.13180","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"PEDIATRICS","Score":null,"Total":0}
Mediation of genetic susceptibility to obesity through eating behaviours in children.
Background/objectives: Few studies have examined the putative mediating role of eating behaviours linking genetic susceptibility and body weight. The goal of this study was to investigate the extent to which two polygenic scores (PGSs) for body mass index (BMI), based on child and adult data, predicted BMI through over-eating and fussy eating across childhood.
Subjects/methods: The study sample involved 692 participants from a birth cohort study. Height and weight were measured on six occasions between ages 6 and 13 years. Over-eating and fussy eating behaviours were assessed five times between ages 2 and 6 years. Longitudinal growth curve mediation analysis was used to estimate the contributions of the PGSs to BMI z-scores mediated by over-eating and fussy eating.
Results: Both PGSs predicted BMI z-scores (PGSchild: β = 0.26, 95% CI: 0.19-0.33; PGSadult: β = 0.34, 95% CI: 0.27-0.41). Over-eating significantly mediated these associations, but this mediation decreased over time from 6 years (PGSchild: 18.0%, 95% CI: 3.1-32.9, p-value = 0.018; PGSadult: 14.2%, 95% CI: 2.8-25.5, p-value = 0.014) to 13 years (PGSchild: 11.4%, 95% CI: -0.4-23.1, p-value = 0.057; PGSadult: 6.2%, 95% CI: 0.4-12.0, p-value = 0.037). Fussy eating did not show any mediation.
Conclusions: Our results support the view that appetite is key to translating genetic susceptibility into changes in body weight.
期刊介绍：
Pediatric Obesity is a peer-reviewed, monthly journal devoted to research into obesity during childhood and adolescence. The topic is currently at the centre of intense interest in the scientific community, and is of increasing concern to health policy-makers and the public at large.
Pediatric Obesity has established itself as the leading journal for high quality papers in this field, including, but not limited to, the following:
Genetic, molecular, biochemical and physiological aspects of obesity – basic, applied and clinical studies relating to mechanisms of the development of obesity throughout the life course and the consequent effects of obesity on health outcomes
Metabolic consequences of child and adolescent obesity
Epidemiological and population-based studies of child and adolescent overweight and obesity
Measurement and diagnostic issues in assessing child and adolescent adiposity, physical activity and nutrition
Clinical management of children and adolescents with obesity including studies of treatment and prevention
Co-morbidities linked to child and adolescent obesity – mechanisms, assessment, and treatment
Life-cycle factors eg familial, intrauterine and developmental aspects of child and adolescent obesity
Nutrition security and the "double burden" of obesity and malnutrition
Health promotion strategies around the issues of obesity, nutrition and physical activity in children and adolescents
Community and public health measures to prevent overweight and obesity in children and adolescents.
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