Abdominal adiposity and cardiometabolic risk factors in children and adolescents: a Mendelian randomization analysis
Mendelian randomization studies in adults suggest that abdominal adiposity is causally associated with increased risk of type 2 diabetes and coronary artery disease in adults, but its causal effect on cardiometabolic risk in children remains unclear. We aimed to study the causal relation of abdomina...
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| Published in | The American journal of clinical nutrition Vol. 110; no. 5; pp. 1079 - 1087 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
01.11.2019
Oxford University Press American Society for Clinical Nutrition, Inc |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0002-9165 1938-3207 1938-3207 |
| DOI | 10.1093/ajcn/nqz187 |
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| Abstract | Mendelian randomization studies in adults suggest that abdominal adiposity is causally associated with increased risk of type 2 diabetes and coronary artery disease in adults, but its causal effect on cardiometabolic risk in children remains unclear.
We aimed to study the causal relation of abdominal adiposity with cardiometabolic risk factors in children by applying Mendelian randomization.
We constructed a genetic risk score (GRS) using variants previously associated with waist-to-hip ratio adjusted for BMI (WHRadjBMI) and examined its associations with cardiometabolic factors by linear regression and Mendelian randomization in a meta-analysis of 6 cohorts, including 9895 European children and adolescents aged 3–17 y.
WHRadjBMI GRS was associated with higher WHRadjBMI (β = 0.021 SD/allele; 95% CI: 0.016, 0.026 SD/allele; P = 3 × 10−15) and with unfavorable concentrations of blood lipids (higher LDL cholesterol: β = 0.006 SD/allele; 95% CI: 0.001, 0.011 SD/allele; P = 0.025; lower HDL cholesterol: β = −0.007 SD/allele; 95% CI: −0.012, −0.002 SD/allele; P = 0.009; higher triglycerides: β = 0.007 SD/allele; 95% CI: 0.002, 0.012 SD/allele; P = 0.006). No differences were detected between prepubertal and pubertal/postpubertal children. The WHRadjBMI GRS had a stronger association with fasting insulin in children and adolescents with overweight/obesity (β = 0.016 SD/allele; 95% CI: 0.001, 0.032 SD/allele; P = 0.037) than in those with normal weight (β = −0.002 SD/allele; 95% CI: −0.010, 0.006 SD/allele; P = 0.605) (P for difference = 0.034). In a 2-stage least-squares regression analysis, each genetically instrumented 1-SD increase in WHRadjBMI increased circulating triglycerides by 0.17 mmol/L (0.35 SD, P = 0.040), suggesting that the relation between abdominal adiposity and circulating triglycerides may be causal.
Abdominal adiposity may have a causal, unfavorable effect on plasma triglycerides and potentially other cardiometabolic risk factors starting in childhood. The results highlight the importance of early weight management through healthy dietary habits and physically active lifestyle among children with a tendency for abdominal adiposity. |
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| AbstractList | Background Mendelian randomization studies in adults suggest that abdominal adiposity is causally associated with increased risk of type 2 diabetes and coronary artery disease in adults, but its causal effect on cardiometabolic risk in children remains unclear. Objective We aimed to study the causal relation of abdominal adiposity with cardiometabolic risk factors in children by applying Mendelian randomization. Methods We constructed a genetic risk score (GRS) using variants previously associated with waist-to-hip ratio adjusted for BMI (WHRadjBMI) and examined its associations with cardiometabolic factors by linear regression and Mendelian randomization in a meta-analysis of 6 cohorts, including 9895 European children and adolescents aged 3–17 y. Results WHRadjBMI GRS was associated with higher WHRadjBMI (β = 0.021 SD/allele; 95% CI: 0.016, 0.026 SD/allele; P = 3 × 10−15) and with unfavorable concentrations of blood lipids (higher LDL cholesterol: β = 0.006 SD/allele; 95% CI: 0.001, 0.011 SD/allele; P = 0.025; lower HDL cholesterol: β = −0.007 SD/allele; 95% CI: −0.012, −0.002 SD/allele; P = 0.009; higher triglycerides: β = 0.007 SD/allele; 95% CI: 0.002, 0.012 SD/allele; P = 0.006). No differences were detected between prepubertal and pubertal/postpubertal children. The WHRadjBMI GRS had a stronger association with fasting insulin in children and adolescents with overweight/obesity (β = 0.016 SD/allele; 95% CI: 0.001, 0.032 SD/allele; P = 0.037) than in those with normal weight (β = −0.002 SD/allele; 95% CI: −0.010, 0.006 SD/allele; P = 0.605) (P for difference = 0.034). In a 2-stage least-squares regression analysis, each genetically instrumented 1-SD increase in WHRadjBMI increased circulating triglycerides by 0.17 mmol/L (0.35 SD, P = 0.040), suggesting that the relation between abdominal adiposity and circulating triglycerides may be causal. Conclusions Abdominal adiposity may have a causal, unfavorable effect on plasma triglycerides and potentially other cardiometabolic risk factors starting in childhood. The results highlight the importance of early weight management through healthy dietary habits and physically active lifestyle among children with a tendency for abdominal adiposity. Mendelian randomization studies in adults suggest that abdominal adiposity is causally associated with increased risk of type 2 diabetes and coronary artery disease in adults, but its causal effect on cardiometabolic risk in children remains unclear. We aimed to study the causal relation of abdominal adiposity with cardiometabolic risk factors in children by applying Mendelian randomization. We constructed a genetic risk score (GRS) using variants previously associated with waist-to-hip ratio adjusted for BMI (WHRadjBMI) and examined its associations with cardiometabolic factors by linear regression and Mendelian randomization in a meta-analysis of 6 cohorts, including 9895 European children and adolescents aged 3-17 y. WHRadjBMI GRS was associated with higher WHRadjBMI (β = 0.021 SD/allele; 95% CI: 0.016, 0.026 SD/allele; P = 3 × 10-15) and with unfavorable concentrations of blood lipids (higher LDL cholesterol: β = 0.006 SD/allele; 95% CI: 0.001, 0.011 SD/allele; P = 0.025; lower HDL cholesterol: β = -0.007 SD/allele; 95% CI: -0.012, -0.002 SD/allele; P = 0.009; higher triglycerides: β = 0.007 SD/allele; 95% CI: 0.002, 0.012 SD/allele; P = 0.006). No differences were detected between prepubertal and pubertal/postpubertal children. The WHRadjBMI GRS had a stronger association with fasting insulin in children and adolescents with overweight/obesity (β = 0.016 SD/allele; 95% CI: 0.001, 0.032 SD/allele; P = 0.037) than in those with normal weight (β = -0.002 SD/allele; 95% CI: -0.010, 0.006 SD/allele; P = 0.605) (P for difference = 0.034). In a 2-stage least-squares regression analysis, each genetically instrumented 1-SD increase in WHRadjBMI increased circulating triglycerides by 0.17 mmol/L (0.35 SD, P = 0.040), suggesting that the relation between abdominal adiposity and circulating triglycerides may be causal. Abdominal adiposity may have a causal, unfavorable effect on plasma triglycerides and potentially other cardiometabolic risk factors starting in childhood. The results highlight the importance of early weight management through healthy dietary habits and physically active lifestyle among children with a tendency for abdominal adiposity. Mendelian randomization studies in adults suggest that abdominal adiposity is causally associated with increased risk of type 2 diabetes and coronary artery disease in adults, but its causal effect on cardiometabolic risk in children remains unclear.BACKGROUNDMendelian randomization studies in adults suggest that abdominal adiposity is causally associated with increased risk of type 2 diabetes and coronary artery disease in adults, but its causal effect on cardiometabolic risk in children remains unclear.We aimed to study the causal relation of abdominal adiposity with cardiometabolic risk factors in children by applying Mendelian randomization.OBJECTIVEWe aimed to study the causal relation of abdominal adiposity with cardiometabolic risk factors in children by applying Mendelian randomization.We constructed a genetic risk score (GRS) using variants previously associated with waist-to-hip ratio adjusted for BMI (WHRadjBMI) and examined its associations with cardiometabolic factors by linear regression and Mendelian randomization in a meta-analysis of 6 cohorts, including 9895 European children and adolescents aged 3-17 y.METHODSWe constructed a genetic risk score (GRS) using variants previously associated with waist-to-hip ratio adjusted for BMI (WHRadjBMI) and examined its associations with cardiometabolic factors by linear regression and Mendelian randomization in a meta-analysis of 6 cohorts, including 9895 European children and adolescents aged 3-17 y.WHRadjBMI GRS was associated with higher WHRadjBMI (β = 0.021 SD/allele; 95% CI: 0.016, 0.026 SD/allele; P = 3 × 10-15) and with unfavorable concentrations of blood lipids (higher LDL cholesterol: β = 0.006 SD/allele; 95% CI: 0.001, 0.011 SD/allele; P = 0.025; lower HDL cholesterol: β = -0.007 SD/allele; 95% CI: -0.012, -0.002 SD/allele; P = 0.009; higher triglycerides: β = 0.007 SD/allele; 95% CI: 0.002, 0.012 SD/allele; P = 0.006). No differences were detected between prepubertal and pubertal/postpubertal children. The WHRadjBMI GRS had a stronger association with fasting insulin in children and adolescents with overweight/obesity (β = 0.016 SD/allele; 95% CI: 0.001, 0.032 SD/allele; P = 0.037) than in those with normal weight (β = -0.002 SD/allele; 95% CI: -0.010, 0.006 SD/allele; P = 0.605) (P for difference = 0.034). In a 2-stage least-squares regression analysis, each genetically instrumented 1-SD increase in WHRadjBMI increased circulating triglycerides by 0.17 mmol/L (0.35 SD, P = 0.040), suggesting that the relation between abdominal adiposity and circulating triglycerides may be causal.RESULTSWHRadjBMI GRS was associated with higher WHRadjBMI (β = 0.021 SD/allele; 95% CI: 0.016, 0.026 SD/allele; P = 3 × 10-15) and with unfavorable concentrations of blood lipids (higher LDL cholesterol: β = 0.006 SD/allele; 95% CI: 0.001, 0.011 SD/allele; P = 0.025; lower HDL cholesterol: β = -0.007 SD/allele; 95% CI: -0.012, -0.002 SD/allele; P = 0.009; higher triglycerides: β = 0.007 SD/allele; 95% CI: 0.002, 0.012 SD/allele; P = 0.006). No differences were detected between prepubertal and pubertal/postpubertal children. The WHRadjBMI GRS had a stronger association with fasting insulin in children and adolescents with overweight/obesity (β = 0.016 SD/allele; 95% CI: 0.001, 0.032 SD/allele; P = 0.037) than in those with normal weight (β = -0.002 SD/allele; 95% CI: -0.010, 0.006 SD/allele; P = 0.605) (P for difference = 0.034). In a 2-stage least-squares regression analysis, each genetically instrumented 1-SD increase in WHRadjBMI increased circulating triglycerides by 0.17 mmol/L (0.35 SD, P = 0.040), suggesting that the relation between abdominal adiposity and circulating triglycerides may be causal.Abdominal adiposity may have a causal, unfavorable effect on plasma triglycerides and potentially other cardiometabolic risk factors starting in childhood. The results highlight the importance of early weight management through healthy dietary habits and physically active lifestyle among children with a tendency for abdominal adiposity.CONCLUSIONSAbdominal adiposity may have a causal, unfavorable effect on plasma triglycerides and potentially other cardiometabolic risk factors starting in childhood. The results highlight the importance of early weight management through healthy dietary habits and physically active lifestyle among children with a tendency for abdominal adiposity. ABSTRACT Background Mendelian randomization studies in adults suggest that abdominal adiposity is causally associated with increased risk of type 2 diabetes and coronary artery disease in adults, but its causal effect on cardiometabolic risk in children remains unclear. Objective We aimed to study the causal relation of abdominal adiposity with cardiometabolic risk factors in children by applying Mendelian randomization. Methods We constructed a genetic risk score (GRS) using variants previously associated with waist-to-hip ratio adjusted for BMI (WHRadjBMI) and examined its associations with cardiometabolic factors by linear regression and Mendelian randomization in a meta-analysis of 6 cohorts, including 9895 European children and adolescents aged 3–17 y. Results WHRadjBMI GRS was associated with higher WHRadjBMI (β = 0.021 SD/allele; 95% CI: 0.016, 0.026 SD/allele; P = 3 × 10−15) and with unfavorable concentrations of blood lipids (higher LDL cholesterol: β = 0.006 SD/allele; 95% CI: 0.001, 0.011 SD/allele; P = 0.025; lower HDL cholesterol: β = −0.007 SD/allele; 95% CI: −0.012, −0.002 SD/allele; P = 0.009; higher triglycerides: β = 0.007 SD/allele; 95% CI: 0.002, 0.012 SD/allele; P = 0.006). No differences were detected between prepubertal and pubertal/postpubertal children. The WHRadjBMI GRS had a stronger association with fasting insulin in children and adolescents with overweight/obesity (β = 0.016 SD/allele; 95% CI: 0.001, 0.032 SD/allele; P = 0.037) than in those with normal weight (β = −0.002 SD/allele; 95% CI: −0.010, 0.006 SD/allele; P = 0.605) (P for difference = 0.034). In a 2-stage least-squares regression analysis, each genetically instrumented 1-SD increase in WHRadjBMI increased circulating triglycerides by 0.17 mmol/L (0.35 SD, P = 0.040), suggesting that the relation between abdominal adiposity and circulating triglycerides may be causal. Conclusions Abdominal adiposity may have a causal, unfavorable effect on plasma triglycerides and potentially other cardiometabolic risk factors starting in childhood. The results highlight the importance of early weight management through healthy dietary habits and physically active lifestyle among children with a tendency for abdominal adiposity. Mendelian randomization studies in adults suggest that abdominal adiposity is causally associated with increased risk of type 2 diabetes and coronary artery disease in adults, but its causal effect on cardiometabolic risk in children remains unclear. We aimed to study the causal relation of abdominal adiposity with cardiometabolic risk factors in children by applying Mendelian randomization. We constructed a genetic risk score (GRS) using variants previously associated with waist-to-hip ratio adjusted for BMI (WHRadjBMI) and examined its associations with cardiometabolic factors by linear regression and Mendelian randomization in a meta-analysis of 6 cohorts, including 9895 European children and adolescents aged 3–17 y. WHRadjBMI GRS was associated with higher WHRadjBMI (β = 0.021 SD/allele; 95% CI: 0.016, 0.026 SD/allele; P = 3 × 10−15) and with unfavorable concentrations of blood lipids (higher LDL cholesterol: β = 0.006 SD/allele; 95% CI: 0.001, 0.011 SD/allele; P = 0.025; lower HDL cholesterol: β = −0.007 SD/allele; 95% CI: −0.012, −0.002 SD/allele; P = 0.009; higher triglycerides: β = 0.007 SD/allele; 95% CI: 0.002, 0.012 SD/allele; P = 0.006). No differences were detected between prepubertal and pubertal/postpubertal children. The WHRadjBMI GRS had a stronger association with fasting insulin in children and adolescents with overweight/obesity (β = 0.016 SD/allele; 95% CI: 0.001, 0.032 SD/allele; P = 0.037) than in those with normal weight (β = −0.002 SD/allele; 95% CI: −0.010, 0.006 SD/allele; P = 0.605) (P for difference = 0.034). In a 2-stage least-squares regression analysis, each genetically instrumented 1-SD increase in WHRadjBMI increased circulating triglycerides by 0.17 mmol/L (0.35 SD, P = 0.040), suggesting that the relation between abdominal adiposity and circulating triglycerides may be causal. Abdominal adiposity may have a causal, unfavorable effect on plasma triglycerides and potentially other cardiometabolic risk factors starting in childhood. The results highlight the importance of early weight management through healthy dietary habits and physically active lifestyle among children with a tendency for abdominal adiposity. |
| Author | Lakka, Timo A Kilpeläinen, Tuomas O Grarup, Niels Holm, Jens-Christian Fonvig, Cilius E Larnkjaer, Anni Hollensted, Mette Pahkala, Katja Kähönen, Mika Raitakari, Olli Atalay, Mustafa Heikkinen, Sami Frithioff-Bøjsøe, Christine Carrasquilla, Germán D Viitasalo, Anna Pedersen, Oluf Hansen, Torben Lehtimäki, Terho Nielsen, Tenna RH Michaelsen, Kim F Schnurr, Theresia M Pitkänen, Niina Lind, Mads V |
| AuthorAffiliation | 11 Faculty of Medicine and Health Technology, Finnish Cardiovascular Research Center, Tampere University , Tampere, Finland 15 Department of Clinical Chemistry, Fimlab Laboratories , Tampere, Finland 2 Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku , Turku, Finland 4 Department of Pediatrics, Copenhagen University Hospital Hvidovre , Hvidovre, Denmark 9 The Hans Christian Andersen Children's Hospital, Odense University Hospital , Odense, Denmark 5 Paavo Nurmi Centre, Sports and Exercise Medicine Unit, Department of Physical Activity and Health, University of Turku , Turku, Finland 13 Kuopio Research Institute of Exercise Medicine , Kuopio, Finland 3 The Children's Obesity Clinic, Department of Pediatrics, Copenhagen University Hospital Holbæk , Holbæk, Denmark 10 Department of Clinical Physiology, Tampere University Hospital , Tampere, Finland 14 Faculty of Health Sciences, University of Copenhagen , Copenhagen, Denmark 1 Novo Nordisk Foundation Center for |
| AuthorAffiliation_xml | – name: 10 Department of Clinical Physiology, Tampere University Hospital , Tampere, Finland – name: 15 Department of Clinical Chemistry, Fimlab Laboratories , Tampere, Finland – name: 6 Institute of Biomedicine, University of Eastern Finland , Kuopio, Finland – name: 12 Department of Clinical Physiology and Nuclear Medicine, Kuopio University Hospital , Kuopio, Finland – name: 4 Department of Pediatrics, Copenhagen University Hospital Hvidovre , Hvidovre, Denmark – name: 13 Kuopio Research Institute of Exercise Medicine , Kuopio, Finland – name: 8 Institute of Clinical Medicine, University of Eastern Finland , Kuopio, Finland – name: 9 The Hans Christian Andersen Children's Hospital, Odense University Hospital , Odense, Denmark – name: 16 Department of Clinical Physiology and Nuclear Medicine, Turku University Hospital , Turku, Finland – name: 5 Paavo Nurmi Centre, Sports and Exercise Medicine Unit, Department of Physical Activity and Health, University of Turku , Turku, Finland – name: 2 Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku , Turku, Finland – name: 11 Faculty of Medicine and Health Technology, Finnish Cardiovascular Research Center, Tampere University , Tampere, Finland – name: 14 Faculty of Health Sciences, University of Copenhagen , Copenhagen, Denmark – name: 7 Department of Nutrition, Exercise, and Sports, Faculty of Science, University of Copenhagen , Copenhagen, Denmark – name: 1 Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen , Copenhagen, Denmark – name: 3 The Children's Obesity Clinic, Department of Pediatrics, Copenhagen University Hospital Holbæk , Holbæk, Denmark |
| Author_xml | – sequence: 1 givenname: Anna surname: Viitasalo fullname: Viitasalo, Anna email: anna.viitasalo@uef.fi organization: Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark – sequence: 2 givenname: Theresia M orcidid: 0000-0002-6573-4959 surname: Schnurr fullname: Schnurr, Theresia M organization: Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark – sequence: 3 givenname: Niina orcidid: 0000-0001-7383-4987 surname: Pitkänen fullname: Pitkänen, Niina organization: Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, Turku, Finland – sequence: 4 givenname: Mette orcidid: 0000-0001-5572-3183 surname: Hollensted fullname: Hollensted, Mette organization: Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark – sequence: 5 givenname: Tenna RH orcidid: 0000-0002-0684-6651 surname: Nielsen fullname: Nielsen, Tenna RH organization: The Children–s Obesity Clinic, Department of Pediatrics, Copenhagen University Hospital Holbæk, Holbæk, Denmark – sequence: 6 givenname: Katja surname: Pahkala fullname: Pahkala, Katja organization: Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, Turku, Finland – sequence: 7 givenname: Mustafa orcidid: 0000-0001-8999-1426 surname: Atalay fullname: Atalay, Mustafa organization: Institute of Biomedicine, University of Eastern Finland, Kuopio, Finland – sequence: 8 givenname: Mads V orcidid: 0000-0002-4999-1218 surname: Lind fullname: Lind, Mads V organization: Department of Nutrition, Exercise, and Sports, Faculty of Science, University of Copenhagen, Copenhagen, Denmark – sequence: 9 givenname: Sami orcidid: 0000-0002-6083-2402 surname: Heikkinen fullname: Heikkinen, Sami organization: Institute of Biomedicine, University of Eastern Finland, Kuopio, Finland – sequence: 10 givenname: Christine surname: Frithioff-Bøjsøe fullname: Frithioff-Bøjsøe, Christine organization: Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark – sequence: 11 givenname: Cilius E orcidid: 0000-0002-5031-0125 surname: Fonvig fullname: Fonvig, Cilius E organization: Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark – sequence: 12 givenname: Niels orcidid: 0000-0001-5526-1070 surname: Grarup fullname: Grarup, Niels organization: Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark – sequence: 13 givenname: Mika surname: Kähönen fullname: Kähönen, Mika organization: Department of Clinical Physiology, Tampere University Hospital, Tampere, Finland – sequence: 14 givenname: Germán D orcidid: 0000-0002-7147-9421 surname: Carrasquilla fullname: Carrasquilla, Germán D organization: Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark – sequence: 15 givenname: Anni surname: Larnkjaer fullname: Larnkjaer, Anni organization: Department of Nutrition, Exercise, and Sports, Faculty of Science, University of Copenhagen, Copenhagen, Denmark – sequence: 16 givenname: Oluf orcidid: 0000-0002-3321-3972 surname: Pedersen fullname: Pedersen, Oluf organization: Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark – sequence: 17 givenname: Kim F surname: Michaelsen fullname: Michaelsen, Kim F organization: Department of Nutrition, Exercise, and Sports, Faculty of Science, University of Copenhagen, Copenhagen, Denmark – sequence: 18 givenname: Timo A surname: Lakka fullname: Lakka, Timo A organization: Institute of Biomedicine, University of Eastern Finland, Kuopio, Finland – sequence: 19 givenname: Jens-Christian surname: Holm fullname: Holm, Jens-Christian organization: Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark – sequence: 20 givenname: Terho surname: Lehtimäki fullname: Lehtimäki, Terho organization: Faculty of Medicine and Health Technology, Finnish Cardiovascular Research Center, Tampere University, Tampere, Finland – sequence: 21 givenname: Olli surname: Raitakari fullname: Raitakari, Olli organization: Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, Turku, Finland – sequence: 22 givenname: Torben surname: Hansen fullname: Hansen, Torben organization: Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark – sequence: 23 givenname: Tuomas O orcidid: 0000-0002-8349-3028 surname: Kilpeläinen fullname: Kilpeläinen, Tuomas O organization: Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31504107$$D View this record in MEDLINE/PubMed |
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| Copyright | 2019 American Society for Nutrition. Copyright © American Society for Nutrition 2019. 2019 Copyright © American Society for Nutrition 2019. Copyright American Society for Clinical Nutrition, Inc. Nov 2019 |
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| DOI | 10.1093/ajcn/nqz187 |
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| Keywords | WHR STRIP cardiometabolic risk GWAS cardiovascular disease risk YFS meta-analysis waist-to-hip ratio BMI-SDS GRS ALSPAC Mendelian randomization PANIC children WHRadjBMI TDCOB SKOT abdominal adiposity |
| Language | English |
| License | http://www.elsevier.com/open-access/userlicense/1.0 This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model) Copyright © American Society for Nutrition 2019. |
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| Snippet | Mendelian randomization studies in adults suggest that abdominal adiposity is causally associated with increased risk of type 2 diabetes and coronary artery... ABSTRACT Background Mendelian randomization studies in adults suggest that abdominal adiposity is causally associated with increased risk of type 2 diabetes... Background Mendelian randomization studies in adults suggest that abdominal adiposity is causally associated with increased risk of type 2 diabetes and... |
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| Title | Abdominal adiposity and cardiometabolic risk factors in children and adolescents: a Mendelian randomization analysis |
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