Changing genetic architecture of body mass index from infancy to early adulthood: an individual based pooled analysis of 25 twin cohorts
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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. / Silventoinen, Karri; Li, Weilong; Jelenkovic, Aline; Sund, Reijo; Yokoyama, Yoshie; Aaltonen, Sari; Piirtola, Maarit; Sugawara, Masumi; Tanaka, Mami; Matsumoto, Satoko; Baker, Laura A.; Tuvblad, Catherine; Tynelius, Per; Rasmussen, Finn; Craig, Jeffrey M.; Saffery, Richard; Willemsen, Gonneke; Bartels, Meike; van Beijsterveldt, Catharina E. M.; Martin, Nicholas G.; Medland, Sarah E.; Montgomery, Grant W.; Lichtenstein, Paul; Krueger, Robert F.; McGue, Matt; Pahlen, Shandell; Christensen, Kaare; Skytthe, Axel; Kyvik, Kirsten O.; Saudino, Kimberly J.; Dubois, Lise; Boivin, Michel; Brendgen, Mara; Dionne, Ginette; Vitaro, Frank; Ullemar, Vilhelmina; Almqvist, Catarina; Magnusson, Patrik K. E.; Corley, Robin P.; Huibregtse, Brooke M.; Knafo-Noam, Ariel; Mankuta, David; Abramson, Lior; Haworth, Claire M. A.; Plomin, Robert; Bjerregaard-Andersen, Morten; Beck-Nielsen, Henning; Sodemann, Morten; Duncan, Glen E.; Buchwald, Dedra; Burt, S. Alexandra; Klump, Kelly L.; Llewellyn, Clare H.; Fisher, Abigail; Boomsma, Dorret; Sorensen, Thorkild I. A.; Kaprio, Jaakko.
In: International Journal of Obesity, Vol. 46, 2022, p. 1901–1909.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Changing genetic architecture of body mass index from infancy to early adulthood
T2 - an individual based pooled analysis of 25 twin cohorts
AU - Silventoinen, Karri
AU - Li, Weilong
AU - Jelenkovic, Aline
AU - Sund, Reijo
AU - Yokoyama, Yoshie
AU - Aaltonen, Sari
AU - Piirtola, Maarit
AU - Sugawara, Masumi
AU - Tanaka, Mami
AU - Matsumoto, Satoko
AU - Baker, Laura A.
AU - Tuvblad, Catherine
AU - Tynelius, Per
AU - Rasmussen, Finn
AU - Craig, Jeffrey M.
AU - Saffery, Richard
AU - Willemsen, Gonneke
AU - Bartels, Meike
AU - van Beijsterveldt, Catharina E. M.
AU - Martin, Nicholas G.
AU - Medland, Sarah E.
AU - Montgomery, Grant W.
AU - Lichtenstein, Paul
AU - Krueger, Robert F.
AU - McGue, Matt
AU - Pahlen, Shandell
AU - Christensen, Kaare
AU - Skytthe, Axel
AU - Kyvik, Kirsten O.
AU - Saudino, Kimberly J.
AU - Dubois, Lise
AU - Boivin, Michel
AU - Brendgen, Mara
AU - Dionne, Ginette
AU - Vitaro, Frank
AU - Ullemar, Vilhelmina
AU - Almqvist, Catarina
AU - Magnusson, Patrik K. E.
AU - Corley, Robin P.
AU - Huibregtse, Brooke M.
AU - Knafo-Noam, Ariel
AU - Mankuta, David
AU - Abramson, Lior
AU - Haworth, Claire M. A.
AU - Plomin, Robert
AU - Bjerregaard-Andersen, Morten
AU - Beck-Nielsen, Henning
AU - Sodemann, Morten
AU - Duncan, Glen E.
AU - Buchwald, Dedra
AU - Burt, S. Alexandra
AU - Klump, Kelly L.
AU - Llewellyn, Clare H.
AU - Fisher, Abigail
AU - Boomsma, Dorret
AU - Sorensen, Thorkild I. A.
AU - Kaprio, Jaakko
PY - 2022
Y1 - 2022
N2 - 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.
AB - 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.
KW - ANTHROPOMETRICAL MEASURES
KW - ENVIRONMENTAL VARIATION
KW - COLLABORATIVE PROJECT
KW - METABOLIC SYNDROME
KW - CHILDHOOD
KW - OBESITY
KW - AGE
KW - WEIGHT
KW - BMI
KW - HEIGHT
U2 - 10.1038/s41366-022-01202-3
DO - 10.1038/s41366-022-01202-3
M3 - Journal article
C2 - 35945263
VL - 46
SP - 1901
EP - 1909
JO - International Journal of Obesity
JF - International Journal of Obesity
SN - 0307-0565
ER -
ID: 317510127