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Changing genetic architecture of body mass index from infancy to early adulthood : an individual based pooled analysis of 25 twin cohorts
Authors
Sari Aaltonen
Lior Abramson
+55 more
Catarina Almqvist
Laura A. Baker
Meike Bartels
Henning Beck-Nielsen
Morten Bjerregaard-Andersen
Michel Boivin
Dorret I. Boomsma
Mara Brendgen
Dedra Buchwald
S. Alexandra Burt
Kaare Christensen
Robin P. Corley
Jeffrey M. Craig
Ginette Dionne
Lise Dubois
Glen E. Duncan
Abigail Fisher
Claire M.A. Haworth
Brooke M. Huibregtse
Aline Jelenkovic
Jaakko Kaprio
Kelly L. Klump
Ariel Knafo-Noam
Robert F. Krueger
Kirsten O. Kyvik
Weilong Li
Paul Lichtenstein
Clare H. Llewellyn
Patrik K.E. Magnusson
David Mankuta
Nicholas G. Martin
Satoko Matsumoto
Matt McGue
Sarah E. Medland
Grant W. Montgomery
Shandell Pahlen
Maarit Piirtola
Robert Plomin
Finn Rasmussen
Richard Saffery
Kimberly J. Saudino
Karri Silventoinen
Axel Skytthe
Morten Sodemann
Masumi Sugawara
Reijo Sund
Thorkild I.A. Sørensen
Mami Tanaka
Catherine Tuvblad
Per Tynelius
Vilhelmina Ullemar
Catharina E.M. van Beijsterveldt
Frank Vitaro
Gonneke Willemsen
Yoshie Yokoyama
Publication date
1 January 2022
Publisher
Doi
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on
PubMed
Abstract
Publisher Copyright: © 2022, The Author(s).Background: Body mass index (BMI) shows strong continuity over childhood and adolescence and high childhood BMI is the strongest predictor of adult obesity. Genetic factors strongly contribute to this continuity, but it is still poorly known how their contribution changes over childhood and adolescence. Thus, we used the genetic twin design to estimate the genetic correlations of BMI from infancy to adulthood and compared them to the genetic correlations of height. Methods: We pooled individual level data from 25 longitudinal twin cohorts including 38,530 complete twin pairs and having 283,766 longitudinal height and weight measures. The data were analyzed using Cholesky decomposition offering genetic and environmental correlations of BMI and height between all age combinations from 1 to 19 years of age. Results: The genetic correlations of BMI and height were stronger than the trait correlations. For BMI, we found that genetic correlations decreased as the age between the assessments increased, a trend that was especially visible from early to middle childhood. In contrast, for height, the genetic correlations were strong between all ages. Age-to-age correlations between environmental factors shared by co-twins were found for BMI in early childhood but disappeared altogether by middle childhood. For height, shared environmental correlations persisted from infancy to adulthood. Conclusions: Our results suggest that the genes affecting BMI change over childhood and adolescence leading to decreasing age-to-age genetic correlations. This change is especially visible from early to middle childhood indicating that new genetic factors start to affect BMI in middle childhood. Identifying mediating pathways of these genetic factors can open possibilities for interventions, especially for those children with high genetic predisposition to adult obesity.Peer reviewe
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