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1. Changing genetic architecture of body mass index from infancy to early adulthood: an individual based pooled analysis of 25 twin cohorts

Author

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 I., Sørensen, Thorkild I. A., and Kaprio, Jaakko

Published
2022
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4. Familial Risk and Heritability of Colorectal Cancer in the Nordic Twin Study of Cancer

Author

Graff, Rebecca E, Möller, Sören, Passarelli, Michael N, Witte, John S, Skytthe, Axel, Christensen, Kaare, Tan, Qihua, Adami, Hans-Olov, Czene, Kamila, Harris, Jennifer R, Pukkala, Eero, Kaprio, Jaakko, Giovannucci, Edward L, Mucci, Lorelei A, and Hjelmborg, Jacob B

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Genetics, Digestive Diseases, Human Genome, Cancer, Genetic Testing, Clinical Research, Colo-Rectal Cancer, Prevention, Adolescent, Adult, Aged, Aged, 80 and over, Child, Child, Preschool, Colonic Neoplasms, Europe, Family Health, Female, Genetic Predisposition to Disease, Humans, Individuality, Infant, Male, Middle Aged, Rectal Neoplasms, Risk Assessment, Twins, Dizygotic, Twins, Monozygotic, Young Adult, Biometric Modeling, Genetic Susceptibility, Zygosity, Concordance Relative Risk, Gastroenterology & Hepatology, Clinical sciences
Abstract

Background & aimsWe analyzed data from twins to determine how much the familial risk of colorectal cancer can be attributed to genetic factors vs environment. We also examined whether heritability is distinct for colon vs rectal cancer, given evidence of distinct etiologies.MethodsOur data set included 39,990 monozygotic and 61,443 same-sex dizygotic twins from the Nordic Twin Study of Cancer. We compared each cancer's risk in twins of affected co-twins relative to the cohort risk (familial risk ratio [FRR]). We then estimated the proportion of variation in risk that could be attributed to genetic factors (heritability).ResultsFrom earliest registration in 1943 through 2010, there were 1861 individuals diagnosed with colon cancer and 1268 diagnosed with rectal cancer. Monozygotic twins of affected co-twins had an FRR for colorectal cancer of 3.1 (95% confidence interval [CI], 2.4-3.8) relative to the cohort risk. Dizygotic twins of affected co-twins had an FRR for colorectal cancer of 2.2 (95% CI, 1.7-2.7). We estimated that 40% (95% CI, 33%-48%) of the variation in colorectal cancer risk could be attributed to genetic factors; unique environment only accounted for the remaining liability. For colon cancer, the FRR was 3.3 (95% CI, 2.1-4.5) for monozygotic twins and 2.6 (95% CI, 1.7-3.5) for dizygotic twins. For rectal cancer, comparable estimates were 3.3 (95% CI, 1.5-5.1) for monozygotic twins and 2.6 (95% CI, 1.2-4.0) for dizygotic twins. Heritability estimates for colon and rectal cancer were 16% (95% CI, 0-46%) and 15% (95% CI, 0-50%), common environment estimates were 15% (95% CI, 0-38%) and 11% (95% CI, 0-38%), and unique environment estimates were 68% (95% CI, 57%-79%) and 75% (95% CI, 61%-88%), respectively.ConclusionsInterindividual genetic differences could account for 40% of the variation in susceptibility to colorectal cancer; risk for colon and rectal cancers might have less of a genetic component than risk for colorectal cancer. Siblings, and particularly monozygotic co-twins, of individuals with colon or rectal cancer should consider personalized screening.

Published
2017

15. Stoppage in Autism Spectrum Disorders

Author

Grønborg, Therese K., Hansen, Stefan N., Nielsen, Svend V., Skytthe, Axel, and Parner, Erik T.

Abstract

Stoppage refers to changes in reproductive behavior following the birth of a child with a severe disease. The presence of stoppage can bias estimates of sibling recurrence risk if not properly addressed. If stoppage occurs non-randomly (differential stoppage), it is possibly an additional source of bias in sibling recurrence risk estimation. This study investigated whether stoppage occurs in Danish families with a firstborn child diagnosed with autism spectrum disorders, and if stoppage was differential. We found that stoppage occurs moderately in Danish families affected by autism spectrum disorders, and that stoppage is differential. However, differential stoppage is a minor source of estimation bias in Danish sibling recurrence risk studies of autism spectrum disorders.

Published
2015
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30. Stoppage in Autism Spectrum Disorders

Author

Grønborg, Therese K., Hansen, Stefan N., Nielsen, Svend V., Skytthe, Axel, and Parner, Erik T.

Subjects
Communication disorders -- Research -- Risk factors, Pervasive developmental disorders -- Research -- Risk factors -- Care and treatment -- Development and progression, Health
Abstract

Stoppage refers to changes in reproductive behavior following the birth of a child with a severe disease. The presence of stoppage can bias estimates of sibling recurrence risk if not properly addressed. If stoppage occurs non-randomly (differential stoppage), it is possibly an additional source of bias in sibling recurrence risk estimation. This study investigated whether stoppage occurs in Danish families with a firstborn child diagnosed with autism spectrum disorders, and if stoppage was differential. We found that stoppage occurs moderately in Danish families affected by autism spectrum disorders, and that stoppage is differential. However, differential stoppage is a minor source of estimation bias in Danish sibling recurrence risk studies of autism spectrum disorders., Author(s): Therese K. Grønborg[sup.1] , Stefan N. Hansen[sup.1] , Svend V. Nielsen[sup.2] , Axel Skytthe[sup.3] , Erik T. Parner[sup.1] Author Affiliations: (1) Section for Biostatistics, Department of Public Health, Aarhus [...]

Published
2015
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36. Changing genetic architecture of body mass index from infancy to early adulthood: an individual based pooled analysis of 25 twin cohorts

Author

Genética, antropología física y fisiología animal, Genetika,antropologia fisikoa eta animalien fisiologia, Silventoinen, Karri, Li, Weilong, Jelenkovic Moreno, 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 I., Sørensen, Thorkild I. A., Kaprio, Jaakko, Genética, antropología física y fisiología animal, Genetika,antropologia fisikoa eta animalien fisiologia, Silventoinen, Karri, Li, Weilong, Jelenkovic Moreno, 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 I., Sørensen, Thorkild I. A., and Kaprio, Jaakko

Abstract

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.

Published
2022

37. Changing genetic architecture of body mass index from infancy to early adulthood:an individual based pooled analysis of 25 twin cohorts

Author

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, 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., and Kaprio, Jaakko

Abstract

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.

Published
2022

40. Risk of Oral Clefts in Twins

Author

Grosen, Dorthe, Bille, Camilla, Petersen, Inge, Skytthe, Axel, von Bornemann Hjelmborg, Jacob, Pedersen, Jacob Krabbe, Murray, Jeffrey Clark, and Christensen, Kaare

Published
2011
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