Jiao Fang1,2, Chun Gong1,2, Yuhui Wan1,2, Yuanyuan Xu1,2, Fangbiao Tao1,2, Ying Sun1,2. 1. Department of Maternal, Child and Adolescent Health, School of Public Health, Anhui Medical University, Hefei, China. 2. Anhui Provincial Key Laboratory of Population Health & Aristogenics, Anhui Medical University, Hefei, China.
Abstract
BACKGROUND: Both polygenic and unhealthy lifestyle factors contribute to individual-level risk of obesity during childhood. The extent to which increased polygenic risk can be offset by healthy lifestyle is unknown. OBJECTIVE: To examine whether increased polygenic risk of obesity is modified by a healthy lifestyle during childhood. METHODS: A total of 997 children (418 boys and 579 girls) who had complete DNA genotyping and body mass index (BMI) were eligible for the study were analyzed from an established prospective puberty cohort. The polygenic risk score (PRS) was computed based on 11 BMI-increasing single nucleotide polymorphisms (SNPs) derived from a published genome-wide association study (GWAS) for child obesity. Seven lifestyle factors were selected to determine a composite healthy lifestyle, such as food responsiveness, slowness in eating, satiety responsiveness, physical activity, screen time, sleep duration, and sugar-sweetened beverages consumption, and which was classified as healthy (<P25 ), intermediate (P25 -P75 ) and unhealthy (>P75 ) lifestyle. Linear and logistic regression analyses were conducted. RESULTS: Children carrying additional BMI susceptibility alleles increased the BMI by 0.11 kg/m2 , after adjusting gender, age and socio-economic status (SES). A healthy lifestyle was associated with a substantially lower risk of obesity than an unhealthy lifestyle, regardless of the polygenic risk category. Among children at high polygenic risk, a healthy lifestyle was associated with an 85% lower risk of obesity than an unhealthy lifestyle (odds ratio, 0.15; 95% CI, 0.04 to 0.59; p = 0.007). CONCLUSIONS: Our findings suggest that increased polygenic risk might be largely offset by healthy lifestyle as early as in childhood.
BACKGROUND: Both polygenic and unhealthy lifestyle factors contribute to individual-level risk of obesity during childhood. The extent to which increased polygenic risk can be offset by healthy lifestyle is unknown. OBJECTIVE: To examine whether increased polygenic risk of obesity is modified by a healthy lifestyle during childhood. METHODS: A total of 997 children (418 boys and 579 girls) who had complete DNA genotyping and body mass index (BMI) were eligible for the study were analyzed from an established prospective puberty cohort. The polygenic risk score (PRS) was computed based on 11 BMI-increasing single nucleotide polymorphisms (SNPs) derived from a published genome-wide association study (GWAS) for childobesity. Seven lifestyle factors were selected to determine a composite healthy lifestyle, such as food responsiveness, slowness in eating, satiety responsiveness, physical activity, screen time, sleep duration, and sugar-sweetened beverages consumption, and which was classified as healthy (<P25 ), intermediate (P25 -P75 ) and unhealthy (>P75 ) lifestyle. Linear and logistic regression analyses were conducted. RESULTS:Children carrying additional BMI susceptibility alleles increased the BMI by 0.11 kg/m2 , after adjusting gender, age and socio-economic status (SES). A healthy lifestyle was associated with a substantially lower risk of obesity than an unhealthy lifestyle, regardless of the polygenic risk category. Among children at high polygenic risk, a healthy lifestyle was associated with an 85% lower risk of obesity than an unhealthy lifestyle (odds ratio, 0.15; 95% CI, 0.04 to 0.59; p = 0.007). CONCLUSIONS: Our findings suggest that increased polygenic risk might be largely offset by healthy lifestyle as early as in childhood.
Authors: Benjamin W Domingue; Klint Kanopka; Travis T Mallard; Sam Trejo; Elliot M Tucker-Drob Journal: Behav Genet Date: 2021-12-02 Impact factor: 2.805
Authors: Miguel Seral-Cortes; Sergio Sabroso-Lasa; Pilar De Miguel-Etayo; Marcela Gonzalez-Gross; Eva Gesteiro; Cristina Molina-Hidalgo; Stefaan De Henauw; Frederic Gottrand; Christina Mavrogianni; Yannis Manios; Maria Plada; Kurt Widhalm; Anthony Kafatos; Éva Erhardt; Aline Meirhaeghe; Diego Salazar-Tortosa; Jonatan Ruiz; Luis A Moreno; Luis Mariano Esteban; Idoia Labayen Journal: Sci Rep Date: 2021-02-04 Impact factor: 4.379