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426 results on '"Rijsdijk F"'

8. Spatial Models in Epidemiology and Genetics

Author

Altenburg, Hans-Peter, Bühler, Wolfgang J., Aronson, Donald G., Bögel, Konrad, Diekmann, Odo, Fife, P. C., Peletier, L. A., Mollison, Denis, Rijsdijk, F. H., Zadoks, J. C., Rothe, F., Sawyer, Stanley, Schumacher, K., Thieme, Horst R., and Weinberger, Hans F.

Published
1980
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10. A high-density SNP linkage scan with 142 combined subtype ADHD sib pairs identifies linkage regions on chromosomes 9 and 16

Author

Asherson, P, Zhou, K, Anney, R J L, Franke, B, Buitelaar, J, Ebstein, R, Gill, M, Altink, M, Arnold, R, Boer, F, Brookes, K, Buschgens, C, Butler, L, Cambell, D, Chen, W, Christiansen, H, Feldman, L, Fleischman, K, Fliers, E, Howe-Forbes, R, Goldfarb, A, Heise, A, Gabriëls, I, Johansson, L, Lubetzki, I, Marco, R, Medad, S, Minderaa, R, Mulas, F, Müller, U, Mulligan, A, Neale, B, Rijsdijk, F, Rabin, K, Rommelse, N, Sethna, V, Sorohan, J, Uebel, H, Psychogiou, L, Weeks, A, Barrett, R, Xu, X, Banaschewski, T, Sonuga-Barke, E, Eisenberg, J, Manor, I, Miranda, A, Oades, R D, Roeyers, H, Rothenberger, A, Sergeant, J, Steinhausen, H-C, Taylor, E, Thompson, M, and Faraone, S V

Published
2008
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12. Genetic and environmental variation in educational attainment: an individual-based analysis of 28 twin cohorts

Author

Silventoinen, K, Jelenkovic, A, Sund, R, Latvala, A, Honda, C, Inui, F, Tomizawa, R, Watanabe, M, Sakai, N, Rebato, E, Busjahn, A, Tyler, J, Hopper, JL, Ordonana, JR, Sanchez-Romera, JF, Colodro-Conde, L, Calais-Ferreira, L, Oliveira, VC, Ferreira, PH, Medda, E, Nistico, L, Toccaceli, V, Derom, CA, Vlietinck, RF, Loos, RJF, Siribaddana, SH, Hotopf, M, Sumathipala, A, Rijsdijk, F, Duncan, GE, Buchwald, D, Tynelius, P, Rasmussen, F, Tan, Q, Zhang, D, Pang, Z, Magnusson, PKE, Pedersen, NL, Aslan, AKD, Hwang, AE, Mack, TM, Krueger, RF, McGue, M, Pahlen, S, Brandt, I, Nilsen, TS, Harris, JR, Martin, NG, Medland, SE, Montgomery, GW, Willemsen, G, Bartels, M, van Beijsterveldt, CEM, Franz, CE, Kremen, WS, Lyons, MJ, Silberg, JL, Maes, HH, Kandler, C, Nelson, TL, Whitfield, KE, Corley, RP, Huibregtse, BM, Gatz, M, Butler, DA, Tarnoki, AD, Tarnoki, DL, Park, HA, Lee, J, Lee, SJ, Sung, J, Yokoyama, Y, Sorensen, TIA, Boomsma, D, Kaprio, J, Silventoinen, K, Jelenkovic, A, Sund, R, Latvala, A, Honda, C, Inui, F, Tomizawa, R, Watanabe, M, Sakai, N, Rebato, E, Busjahn, A, Tyler, J, Hopper, JL, Ordonana, JR, Sanchez-Romera, JF, Colodro-Conde, L, Calais-Ferreira, L, Oliveira, VC, Ferreira, PH, Medda, E, Nistico, L, Toccaceli, V, Derom, CA, Vlietinck, RF, Loos, RJF, Siribaddana, SH, Hotopf, M, Sumathipala, A, Rijsdijk, F, Duncan, GE, Buchwald, D, Tynelius, P, Rasmussen, F, Tan, Q, Zhang, D, Pang, Z, Magnusson, PKE, Pedersen, NL, Aslan, AKD, Hwang, AE, Mack, TM, Krueger, RF, McGue, M, Pahlen, S, Brandt, I, Nilsen, TS, Harris, JR, Martin, NG, Medland, SE, Montgomery, GW, Willemsen, G, Bartels, M, van Beijsterveldt, CEM, Franz, CE, Kremen, WS, Lyons, MJ, Silberg, JL, Maes, HH, Kandler, C, Nelson, TL, Whitfield, KE, Corley, RP, Huibregtse, BM, Gatz, M, Butler, DA, Tarnoki, AD, Tarnoki, DL, Park, HA, Lee, J, Lee, SJ, Sung, J, Yokoyama, Y, Sorensen, TIA, Boomsma, D, and Kaprio, J

Abstract

We investigated the heritability of educational attainment and how it differed between birth cohorts and cultural-geographic regions. A classical twin design was applied to pooled data from 28 cohorts representing 16 countries and including 193,518 twins with information on educational attainment at 25 years of age or older. Genetic factors explained the major part of individual differences in educational attainment (heritability: a2 = 0.43; 0.41-0.44), but also environmental variation shared by co-twins was substantial (c2 = 0.31; 0.30-0.33). The proportions of educational variation explained by genetic and shared environmental factors did not differ between Europe, North America and Australia, and East Asia. When restricted to twins 30 years or older to confirm finalized education, the heritability was higher in the older cohorts born in 1900-1949 (a2 = 0.44; 0.41-0.46) than in the later cohorts born in 1950-1989 (a2 = 0.38; 0.36-0.40), with a corresponding lower influence of common environmental factors (c2 = 0.31; 0.29-0.33 and c2 = 0.34; 0.32-0.36, respectively). In conclusion, both genetic and environmental factors shared by co-twins have an important influence on individual differences in educational attainment. The effect of genetic factors on educational attainment has decreased from the cohorts born before to those born after the 1950s.

Published
2020

13. Genetic and environmental variation in educational attainment : an individual-based analysis of 28 twin cohorts

Author

Silventoinen, K., Jelenkovic, A., Sund, R., Latvala, A., Honda, C., Inui, F., Tomizawa, R., Watanabe, M., Sakai, N., Rebato, E., Busjahn, A., Tyler, J., Hopper, J. L., Ordoñana, J. R., Sánchez-Romera, J. F., Colodro-Conde, L., Calais-Ferreira, L., Oliveira, V. C., Ferreira, P. H., Medda, E., Nisticò, L., Toccaceli, V., Derom, C. A., Vlietinck, R. F., Loos, R. J. F., Siribaddana, S. H., Hotopf, M., Sumathipala, A., Rijsdijk, F., Duncan, G. E., Buchwald, D., Tynelius, P., Rasmussen, F., Tan, Q., Zhang, D., Pang, Z., Magnusson, P. K. E., Pedersen, N. L., Dahl Aslan, Anna K., Hwang, A. E., Mack, T. M., Krueger, R. F., McGue, M., Pahlen, S., Brandt, I., Nilsen, T. S., Harris, J. R., Martin, N. G., Medland, S. E., Montgomery, G. W., Willemsen, G., Bartels, M., van Beijsterveldt, C. E. M., Franz, C. E., Kremen, W. S., Lyons, M. J., Silberg, J. L., Maes, H. H., Kandler, C., Nelson, T. L., Whitfield, K. E., Corley, R. P., Huibregtse, B. M., Gatz, M., Butler, D. A., Tarnoki, A. D., Tarnoki, D. L., Park, H. A., Lee, J., Lee, S. J., Sung, J., Yokoyama, Y., Sørensen, T. I. A., Boomsma, D. I., Kaprio, J., Silventoinen, K., Jelenkovic, A., Sund, R., Latvala, A., Honda, C., Inui, F., Tomizawa, R., Watanabe, M., Sakai, N., Rebato, E., Busjahn, A., Tyler, J., Hopper, J. L., Ordoñana, J. R., Sánchez-Romera, J. F., Colodro-Conde, L., Calais-Ferreira, L., Oliveira, V. C., Ferreira, P. H., Medda, E., Nisticò, L., Toccaceli, V., Derom, C. A., Vlietinck, R. F., Loos, R. J. F., Siribaddana, S. H., Hotopf, M., Sumathipala, A., Rijsdijk, F., Duncan, G. E., Buchwald, D., Tynelius, P., Rasmussen, F., Tan, Q., Zhang, D., Pang, Z., Magnusson, P. K. E., Pedersen, N. L., Dahl Aslan, Anna K., Hwang, A. E., Mack, T. M., Krueger, R. F., McGue, M., Pahlen, S., Brandt, I., Nilsen, T. S., Harris, J. R., Martin, N. G., Medland, S. E., Montgomery, G. W., Willemsen, G., Bartels, M., van Beijsterveldt, C. E. M., Franz, C. E., Kremen, W. S., Lyons, M. J., Silberg, J. L., Maes, H. H., Kandler, C., Nelson, T. L., Whitfield, K. E., Corley, R. P., Huibregtse, B. M., Gatz, M., Butler, D. A., Tarnoki, A. D., Tarnoki, D. L., Park, H. A., Lee, J., Lee, S. J., Sung, J., Yokoyama, Y., Sørensen, T. I. A., Boomsma, D. I., and Kaprio, J.

Abstract

We investigated the heritability of educational attainment and how it differed between birth cohorts and cultural–geographic regions. A classical twin design was applied to pooled data from 28 cohorts representing 16 countries and including 193,518 twins with information on educational attainment at 25 years of age or older. Genetic factors explained the major part of individual differences in educational attainment (heritability: a2 = 0.43; 0.41–0.44), but also environmental variation shared by co-twins was substantial (c2 = 0.31; 0.30–0.33). The proportions of educational variation explained by genetic and shared environmental factors did not differ between Europe, North America and Australia, and East Asia. When restricted to twins 30 years or older to confirm finalized education, the heritability was higher in the older cohorts born in 1900–1949 (a2 = 0.44; 0.41–0.46) than in the later cohorts born in 1950–1989 (a2 = 0.38; 0.36–0.40), with a corresponding lower influence of common environmental factors (c2 = 0.31; 0.29–0.33 and c2 = 0.34; 0.32–0.36, respectively). In conclusion, both genetic and environmental factors shared by co-twins have an important influence on individual differences in educational attainment. The effect of genetic factors on educational attainment has decreased from the cohorts born before to those born after the 1950s.

Published
2020
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19. The relationship between ADHD and key cognitive phenotypes is not mediated by shared familial effects with IQ

Author

Wood, A. C., Rijsdijk, F., Johnson, K. A., Andreou, P., Albrecht, B., Arias-Vasquez, A., Buitelaar, J. K., McLoughlin, G., Rommelse, N. N. J., Sergeant, J. A., Sonuga-Barke, E. J. S., Uebel, H., van der Meere, J. J., Banaschewski, T., Gill, M., Manor, I., Miranda, A., Mulas, F., Oades, R. D., Roeyers, H., Rothenberger, A., Steinhausen, H. C., Faraone, S. V., Asherson, P., and Kuntsi, J.

Published
2011

24. Emotional over- and under-eating in early childhood are learned not inherited

Author

Herle, M, Fildes, A, Steinsbekk, S, Rijsdijk, F, and Llewellyn, CH

Subjects
Male, Genotyping Techniques, Science, Twins, Gestational Age, Feeding Behavior, Hyperphagia, Article, Risk Factors, Child, Preschool, Surveys and Questionnaires, Humans, Learning, Medicine, Female, Feeding and Eating Disorders of Childhood
Abstract

Emotional overeating (EOE) has been associated with increased obesity risk, while emotional undereating (EUE) may be protective. Interestingly, EOE and EUE tend to correlate positively, but it is unclear whether they reflect different aspects of the same underlying trait, or are distinct behaviours with different aetiologies. Data were from 2054 five-year-old children from the Gemini twin birth cohort, including parental ratings of child EOE and EUE using the Child Eating Behaviour Questionnaire. Genetic and environmental influences on variation and covariation in EUE and EOE were established using a bivariate Twin Model. Variation in both behaviours was largely explained by aspects of the environment completely shared by twin pairs (EOE: C = 90%, 95% CI: 89%-92%; EUE: C = 91%, 95% CI: 90%-92%). Genetic influence was low (EOE: A = 7%, 95% CI: 6%-9%; EUE: A = 7%, 95% CI: 6%-9%). EOE and EUE correlated positively (r = 0.43, p

Published
2017

30. Letter to the Editor

Author

ORMEL, J., RIJSDIJK, F. V., RIESE, H., SNIEDER, H., and ROSMALEN, J. G. M.

Published
2008

32. Proteome-based plasma biomarkers for Alzheimerʼs disease

Author

Hye, A., Lynham, S., Thambisetty, M., Causevic, M., Campbell, J., Byers, H. L., Hooper, C., Rijsdijk, F., Tabrizi, S. J., Banner, S., Shaw, C. E., Foy, C., Poppe, M., Archer, N., Hamilton, G., Powell, J., Brown, R. G., Sham, P., Ward, M., and Lovestone, S.

Published
2006

34. The CODATwins Project: The Current Status and Recent Findings of COllaborative Project of Development of Anthropometrical Measures in Twins

Author

Silventoinen, K., Jelenkovic, A., Yokoyama, Y., Sund, R., Sugawara, M., Tanaka, M., Matsumoto, S., Bogl, L. H., Freitas, D. L., Maia, J. A., Hjelmborg, J. v. B., Aaltonen, S., Piirtola, M., Latvala, A., Calais-Ferreira, L., Oliveira, V. C., Ferreira, P. H., Ji, F., Ning, F., Pang, Z., Ordonana, J. R., Sanchez-Romera, J. F., Colodro-Conde, L., Burt, S. A., Klump, K. L., Martin, N. G., Medland, S. E., Montgomery, G. W., Kandler, C., McAdams, T. A., Eley, T. C., Gregory, A. M., Saudino, K. J., Dubois, L., Boivin, M., Brendgen, M., Dionne, G., Vitaro, F., Tarnoki, A. D., Tarnoki, D. L., Haworth, C. M. A., Plomin, R., Oncel, S. Y., Aliev, F., Medda, E., Nistico, L., Toccaceli, V., Craig, J. M., Saffery, R., Siribaddana, S. H., Hotopf, M., Sumathipala, A., Rijsdijk, F., Jeong, H. -U., Spector, T., Mangino, M., Lachance, G., Gatz, M., Butler, D. A., Gao, W., Yu, C., Li, L., Bayasgalan, G., Narandalai, D., Harden, K. P., Tucker-Drob, E. M., Christensen, K., Skytthe, A., Kyvik, K. O., Derom, C. A., Vlietinck, R. F., Loos, R. J. F., Cozen, W., Hwang, A. E., Mack, T. M., He, M., Ding, X., Silberg, J. L., Maes, H. H., Cutler, T. L., Hopper, J. L., Magnusson, P. K. E., Pedersen, N. L., Dahl Aslan, A. K., Baker, L. A., Tuvblad, C., Bjerregaard-Andersen, M., Beck-Nielsen, H., Sodemann, M., Ullemar, V., Almqvist, C., Tan, Q., Zhang, D., Swan, G. E., Krasnow, R., Jang, K. L., Knafo-Noam, A., Mankuta, D., Abramson, L., Lichtenstein, P., Krueger, R. F., McGue, M., Pahlen, S., Tynelius, P., Rasmussen, F., Duncan, G. E., Buchwald, D., Corley, R. P., Huibregtse, B. M., Nelson, T. L., Whitfield, K. E., Franz, C. E., Kremen, W. S., Lyons, M. J., Ooki, S., Brandt, I., Nilsen, T. S., Harris, J. R., Sung, J., Park, H. A., Lee, J., Lee, S. J., Willemsen, G., Bartels, M., Van Beijsterveldt, C. E. M., Llewellyn, C. H., Fisher, A., Rebato, E., Busjahn, A., Tomizawa, R., Inui, F., Watanabe, M., Honda, C., Sakai, N., Hur, Y. -M., Sørensen, T. I. A., Boomsma, D. I., Kaprio, J., Silventoinen, K., Jelenkovic, A., Yokoyama, Y., Sund, R., Sugawara, M., Tanaka, M., Matsumoto, S., Bogl, L. H., Freitas, D. L., Maia, J. A., Hjelmborg, J. v. B., Aaltonen, S., Piirtola, M., Latvala, A., Calais-Ferreira, L., Oliveira, V. C., Ferreira, P. H., Ji, F., Ning, F., Pang, Z., Ordonana, J. R., Sanchez-Romera, J. F., Colodro-Conde, L., Burt, S. A., Klump, K. L., Martin, N. G., Medland, S. E., Montgomery, G. W., Kandler, C., McAdams, T. A., Eley, T. C., Gregory, A. M., Saudino, K. J., Dubois, L., Boivin, M., Brendgen, M., Dionne, G., Vitaro, F., Tarnoki, A. D., Tarnoki, D. L., Haworth, C. M. A., Plomin, R., Oncel, S. Y., Aliev, F., Medda, E., Nistico, L., Toccaceli, V., Craig, J. M., Saffery, R., Siribaddana, S. H., Hotopf, M., Sumathipala, A., Rijsdijk, F., Jeong, H. -U., Spector, T., Mangino, M., Lachance, G., Gatz, M., Butler, D. A., Gao, W., Yu, C., Li, L., Bayasgalan, G., Narandalai, D., Harden, K. P., Tucker-Drob, E. M., Christensen, K., Skytthe, A., Kyvik, K. O., Derom, C. A., Vlietinck, R. F., Loos, R. J. F., Cozen, W., Hwang, A. E., Mack, T. M., He, M., Ding, X., Silberg, J. L., Maes, H. H., Cutler, T. L., Hopper, J. L., Magnusson, P. K. E., Pedersen, N. L., Dahl Aslan, A. K., Baker, L. A., Tuvblad, C., Bjerregaard-Andersen, M., Beck-Nielsen, H., Sodemann, M., Ullemar, V., Almqvist, C., Tan, Q., Zhang, D., Swan, G. E., Krasnow, R., Jang, K. L., Knafo-Noam, A., Mankuta, D., Abramson, L., Lichtenstein, P., Krueger, R. F., McGue, M., Pahlen, S., Tynelius, P., Rasmussen, F., Duncan, G. E., Buchwald, D., Corley, R. P., Huibregtse, B. M., Nelson, T. L., Whitfield, K. E., Franz, C. E., Kremen, W. S., Lyons, M. J., Ooki, S., Brandt, I., Nilsen, T. S., Harris, J. R., Sung, J., Park, H. A., Lee, J., Lee, S. J., Willemsen, G., Bartels, M., Van Beijsterveldt, C. E. M., Llewellyn, C. H., Fisher, A., Rebato, E., Busjahn, A., Tomizawa, R., Inui, F., Watanabe, M., Honda, C., Sakai, N., Hur, Y. -M., Sørensen, T. I. A., Boomsma, D. I., and Kaprio, J.

Published
2019

35. The CODATwins Project: The Current Status and Recent Findings of COllaborative Project of Development of Anthropometrical Measures in Twins

Author

Silventoinen, K, Jelenkovic, A, Yokoyama, Y, Sund, R, Sugawara, M, Tanaka, M, Matsumoto, S, Bogl, L H, Freitas, D L, Maia, J A, Hjelmborg, J V B, Aaltonen, S, Piirtola, M, Latvala, A, Calais-Ferreira, L, Oliveira, V C, Ferreira, P H, Ji, F, Ning, F, Pang, Z, Ordoñana, J R, Sánchez-Romera, J F, Colodro-Conde, L, Burt, S A, Klump, K L, Martin, N G, Medland, S E, Montgomery, G W, Kandler, C, McAdams, T A, Eley, T C, Gregory, A M, Saudino, K J, Dubois, L, Boivin, M, Brendgen, M, Dionne, G, Vitaro, F, Tarnoki, A D, Tarnoki, D L, Haworth, C M A, Plomin, R, Öncel, S Y, Aliev, F, Medda, E, Nisticò, L, Toccaceli, V, Craig, J M, Saffery, R, Siribaddana, S H, Hotopf, M, Sumathipala, A, Rijsdijk, F, Jeong, H-U, Spector, T, Mangino, M, Lachance, G, Gatz, M, Butler, D A, Gao, W, Yu, C, Li, L, Bayasgalan, G, Narandalai, D, Harden, K P, Tucker-Drob, E M, Christensen, K, Skytthe, A, Kyvik, K O, Derom, C A, Vlietinck, R F, Loos, R J F, Cozen, W, Hwang, A E, Mack, T M, He, M, Ding, X, Silberg, J L, Maes, H H, Cutler, T L, Hopper, J L, Magnusson, P K E, Pedersen, N L, Dahl Aslan, A K, Baker, L A, Tuvblad, C, Bjerregaard-Andersen, M, Beck-Nielsen, H, Sodemann, M, Ullemar, V, Almqvist, C, Tan, Q, Zhang, D, Swan, G E, Krasnow, R, Jang, K L, Knafo-Noam, A, Mankuta, D, Abramson, L, Lichtenstein, P, Krueger, R F, McGue, M, Pahlen, S, Tynelius, P, Rasmussen, F, Duncan, G E, Buchwald, D, Corley, R P, Huibregtse, B M, Nelson, T L, Whitfield, K E, Franz, C E, Kremen, W S, Lyons, M J, Ooki, S, Brandt, I, Nilsen, T S, Harris, J R, Sung, J, Park, H A, Lee, J, Lee, S J, Willemsen, Gonneke, Bartels, Meike, van Beijsterveldt, C.E.M., Llewellyn, C H, Fisher, A, Rebato, E, Busjahn, A, Tomizawa, R, Inui, F, Watanabe, M, Honda, C, Sakai, N, Hur, Y-M, Sørensen, T I A, Boomsma, D.I., Kaprio, J, Silventoinen, K, Jelenkovic, A, Yokoyama, Y, Sund, R, Sugawara, M, Tanaka, M, Matsumoto, S, Bogl, L H, Freitas, D L, Maia, J A, Hjelmborg, J V B, Aaltonen, S, Piirtola, M, Latvala, A, Calais-Ferreira, L, Oliveira, V C, Ferreira, P H, Ji, F, Ning, F, Pang, Z, Ordoñana, J R, Sánchez-Romera, J F, Colodro-Conde, L, Burt, S A, Klump, K L, Martin, N G, Medland, S E, Montgomery, G W, Kandler, C, McAdams, T A, Eley, T C, Gregory, A M, Saudino, K J, Dubois, L, Boivin, M, Brendgen, M, Dionne, G, Vitaro, F, Tarnoki, A D, Tarnoki, D L, Haworth, C M A, Plomin, R, Öncel, S Y, Aliev, F, Medda, E, Nisticò, L, Toccaceli, V, Craig, J M, Saffery, R, Siribaddana, S H, Hotopf, M, Sumathipala, A, Rijsdijk, F, Jeong, H-U, Spector, T, Mangino, M, Lachance, G, Gatz, M, Butler, D A, Gao, W, Yu, C, Li, L, Bayasgalan, G, Narandalai, D, Harden, K P, Tucker-Drob, E M, Christensen, K, Skytthe, A, Kyvik, K O, Derom, C A, Vlietinck, R F, Loos, R J F, Cozen, W, Hwang, A E, Mack, T M, He, M, Ding, X, Silberg, J L, Maes, H H, Cutler, T L, Hopper, J L, Magnusson, P K E, Pedersen, N L, Dahl Aslan, A K, Baker, L A, Tuvblad, C, Bjerregaard-Andersen, M, Beck-Nielsen, H, Sodemann, M, Ullemar, V, Almqvist, C, Tan, Q, Zhang, D, Swan, G E, Krasnow, R, Jang, K L, Knafo-Noam, A, Mankuta, D, Abramson, L, Lichtenstein, P, Krueger, R F, McGue, M, Pahlen, S, Tynelius, P, Rasmussen, F, Duncan, G E, Buchwald, D, Corley, R P, Huibregtse, B M, Nelson, T L, Whitfield, K E, Franz, C E, Kremen, W S, Lyons, M J, Ooki, S, Brandt, I, Nilsen, T S, Harris, J R, Sung, J, Park, H A, Lee, J, Lee, S J, Willemsen, Gonneke, Bartels, Meike, van Beijsterveldt, C.E.M., Llewellyn, C H, Fisher, A, Rebato, E, Busjahn, A, Tomizawa, R, Inui, F, Watanabe, M, Honda, C, Sakai, N, Hur, Y-M, Sørensen, T I A, Boomsma, D.I., and Kaprio, J

Abstract

The COllaborative project of Development of Anthropometrical measures in Twins (CODATwins) project is a large international collaborative effort to analyze individual-level phenotype data from twins in multiple cohorts from different environments. The main objective is to study factors that modify genetic and environmental variation of height, body mass index (BMI, kg/m2) and size at birth, and additionally to address other research questions such as long-term consequences of birth size. The project started in 2013 and is open to all twin projects in the world having height and weight measures on twins with information on zygosity. Thus far, 54 twin projects from 24 countries have provided individual-level data. The CODATwins database includes 489,981 twin individuals (228,635 complete twin pairs). Since many twin cohorts have collected longitudinal data, there is a total of 1,049,785 height and weight observations. For many cohorts, we also have information on birth weight and length, own smoking behavior and own or parental education. We found that the heritability estimates of height and BMI systematically changed from infancy to old age. Remarkably, only minor differences in the heritability estimates were found across cultural-geographic regions, measurement time and birth cohort for height and BMI. In addition to genetic epidemiological studies, we looked at associations of height and BMI with education, birth weight and smoking status. Within-family analyses examined differences within same-sex and opposite-sex dizygotic twins in birth size and later development. The CODATwins project demonstrates the feasibility and value of international collaboration to address gene-by-exposure interactions that require large sample sizes and address the effects of different exposures across time, geographical regions and socioeconomic status.

Published
2019
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36. Protocol for establishing a child and adolescent twin register for mental health research and capacity building in Sri Lanka and other low and middle-income countries in South Asia

Author

Jayaweera, K, Craig, JM, Zavos, HMS, Abeysinghe, N, De Alwis, S, Andras, A, Dissanayake, L, Dziedzic, K, Fernando, B, Glozier, N, Hewamalage, A, Ives, J, Jordan, KP, Kodituwakku, G, Mallen, C, Rahman, O, Zafar, S, Saxena, A, Rijsdijk, F, Saffery, R, Simonoff, E, Yusuf, R, Sumathipala, A, Ahmad, A, Jayathilake, A, Nagahawatte, A, Bhan, A, Wickramatilake, C, Ponnamperuma, G, Selvarathnam, L, Udagama, P, Chonnachtaigh, SU, Blackburn, S, Shepherd, T, Helliwell, T, Samaraweera, S, Makuloluwa, T, Balhara, Y, Cooray, R, Jayaweera, K, Craig, JM, Zavos, HMS, Abeysinghe, N, De Alwis, S, Andras, A, Dissanayake, L, Dziedzic, K, Fernando, B, Glozier, N, Hewamalage, A, Ives, J, Jordan, KP, Kodituwakku, G, Mallen, C, Rahman, O, Zafar, S, Saxena, A, Rijsdijk, F, Saffery, R, Simonoff, E, Yusuf, R, Sumathipala, A, Ahmad, A, Jayathilake, A, Nagahawatte, A, Bhan, A, Wickramatilake, C, Ponnamperuma, G, Selvarathnam, L, Udagama, P, Chonnachtaigh, SU, Blackburn, S, Shepherd, T, Helliwell, T, Samaraweera, S, Makuloluwa, T, Balhara, Y, and Cooray, R

Abstract

INTRODUCTION: Worldwide, 10%-20% of children and adolescents experience mental health conditions. However, most such disorders remain undiagnosed until adolescence or adulthood. Little is known about the factors that influence mental health in children and adolescents, especially in low and middle-income countries (LMIC), where environmental threats, such as poverty and war, may affect optimal neurodevelopment. Cohort studies provide important information on risks and resilience across the life course by enabling tracking of the effects of early life environment on health during childhood and beyond. Large birth cohort studies, including twin cohorts that can be aetiologically informative, have been conducted within high-income countries but are not generalisable to LMIC. There are limited longitudinal birth cohort studies in LMIC. METHODS: We sought to enhance the volume of impactful research in Sri Lanka by establishing a Centre of Excellence for cohort studies. The aim is to establish a register of infant, child and adolescent twins, including mothers pregnant with twins, starting in the districts of Colombo (Western Province) and Vavuniya (Northern Province). We will gain consent from twins or parents for future research projects. This register will provide the platform to investigate the aetiology of mental illness and the impact of challenges to early brain development on future mental health. Using this register, we will be able to conduct research that will (1) expand existing research capacity on child and adolescent mental health and twin methods; (2) further consolidate existing partnerships and (3) establish new collaborations. The initiative is underpinned by three pillars: high-quality research, ethics, and patient and public involvement and engagement (PPIE). ETHICS AND DISSEMINATION: Ethical approval for this study was obtained from the Ethics Review Committee of Sri Lanka Medical Association and Keele University's Ethical Review Panel. In addition t

Published
2019

41. The CODATwins Project: The Current Status and Recent Findings of COllaborative Project of Development of Anthropometrical Measures in Twins

Author

Silventoinen, K., primary, Jelenkovic, A., additional, Yokoyama, Y., additional, Sund, R., additional, Sugawara, M., additional, Tanaka, M., additional, Matsumoto, S., additional, Bogl, L. H., additional, Freitas, D. L., additional, Maia, J. A., additional, Hjelmborg, J. v. B., additional, Aaltonen, S., additional, Piirtola, M., additional, Latvala, A., additional, Calais-Ferreira, L., additional, Oliveira, V. C., additional, Ferreira, P. H., additional, Ji, F., additional, Ning, F., additional, Pang, Z., additional, Ordoñana, J. R., additional, Sánchez-Romera, J. F., additional, Colodro-Conde, L., additional, Burt, S. A., additional, Klump, K. L., additional, Martin, N. G., additional, Medland, S. E., additional, Montgomery, G. W., additional, Kandler, C., additional, McAdams, T. A., additional, Eley, T. C., additional, Gregory, A. M., additional, Saudino, K. J., additional, Dubois, L., additional, Boivin, M., additional, Brendgen, M., additional, Dionne, G., additional, Vitaro, F., additional, Tarnoki, A. D., additional, Tarnoki, D. L., additional, Haworth, C. M. A., additional, Plomin, R., additional, Öncel, S. Y., additional, Aliev, F., additional, Medda, E., additional, Nisticò, L., additional, Toccaceli, V., additional, Craig, J. M., additional, Saffery, R., additional, Siribaddana, S. H., additional, Hotopf, M., additional, Sumathipala, A., additional, Rijsdijk, F., additional, Jeong, H.-U., additional, Spector, T., additional, Mangino, M., additional, Lachance, G., additional, Gatz, M., additional, Butler, D. A., additional, Gao, W., additional, Yu, C., additional, Li, L., additional, Bayasgalan, G., additional, Narandalai, D., additional, Harden, K. P., additional, Tucker-Drob, E. M., additional, Christensen, K., additional, Skytthe, A., additional, Kyvik, K. O., additional, Derom, C. A., additional, Vlietinck, R. F., additional, Loos, R. J. F., additional, Cozen, W., additional, Hwang, A. E., additional, Mack, T. M., additional, He, M., additional, Ding, X., additional, Silberg, J. L., additional, Maes, H. H., additional, Cutler, T. L., additional, Hopper, J. L., additional, Magnusson, P. K. E., additional, Pedersen, N. L., additional, Dahl Aslan, A. K., additional, Baker, L. A., additional, Tuvblad, C., additional, Bjerregaard-Andersen, M., additional, Beck-Nielsen, H., additional, Sodemann, M., additional, Ullemar, V., additional, Almqvist, C., additional, Tan, Q., additional, Zhang, D., additional, Swan, G. E., additional, Krasnow, R., additional, Jang, K. L., additional, Knafo-Noam, A., additional, Mankuta, D., additional, Abramson, L., additional, Lichtenstein, P., additional, Krueger, R. F., additional, McGue, M., additional, Pahlen, S., additional, Tynelius, P., additional, Rasmussen, F., additional, Duncan, G. E., additional, Buchwald, D., additional, Corley, R. P., additional, Huibregtse, B. M., additional, Nelson, T. L., additional, Whitfield, K. E., additional, Franz, C. E., additional, Kremen, W. S., additional, Lyons, M. J., additional, Ooki, S., additional, Brandt, I., additional, Nilsen, T. S., additional, Harris, J. R., additional, Sung, J., additional, Park, H. A., additional, Lee, J., additional, Lee, S. J., additional, Willemsen, G., additional, Bartels, M., additional, van Beijsterveldt, C. E. M., additional, Llewellyn, C. H., additional, Fisher, A., additional, Rebato, E., additional, Busjahn, A., additional, Tomizawa, R., additional, Inui, F., additional, Watanabe, M., additional, Honda, C., additional, Sakai, N., additional, Hur, Y.-M., additional, Sørensen, T. I. A., additional, Boomsma, D. I., additional, and Kaprio, J., additional

Published
2019
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42. Concurrent and longitudinal contribution of exposure to bullying in childhood to mental health: the role of vulnerability and resilience

Author

Singham, T., Viding, E., Schoeler, T., Arseneault, L., Ronald, Angelica, Cecil, C.M., McCrory, E., Rijsdijk, F., and Pingault, J.B.

Subjects
psyc
Abstract

Importance: Exposure to bullying is associated with poor mental health. However, the degree to which observed associations reflect direct detrimental contributions of exposure to bullying to mental health remains uncertain, as noncausal relationships may arise from genetic and environmental confounding (eg, preexisting vulnerabilities). Determining to what extent exposure to bullying contributes to mental health is an important concern, with implications for primary and secondary interventions.\ud \ud Objective: To characterize the concurrent and longitudinal contribution of exposure to bullying to mental health in childhood and adolescence using a twin differences design to strengthen causal inference.\ud \ud Design, Setting, and Participants: Participants were drawn from the Twins Early Development Study, a population-based cohort recruited from population records of births in England and Wales between January 1, 1994, and December 31, 1996. Data collection took place when the participants were between 11 and 16 years of age from December 1, 2005, to January 31, 2013. Data analysis was conducted from January 1, 2016, to June 20, 2017.\ud \ud Exposures: Participants completed the Multidimensional Peer-Victimization Scale at 11 and 14 years of age.\ud \ud Main Outcomes and Measures: Mental health assessments at 11 and 16 years of age included anxiety, depression, hyperactivity and impulsivity, inattention, conduct problems, and psychotic-like experiences (eg, paranoid thoughts or cognitive disorganization).\ud \ud Results: The 11 108 twins included in the final sample (5894 girls and 5214 boys) were a mean age of 11.3 years at the first assessment and 16.3 years at the last assessment. The most stringent twin differences estimates (monozygotic) were consistent with causal contribution of exposure to bullying at 11 years to concurrent anxiety, depression, hyperactivity and impulsivity, inattention, and conduct problems. Effects decreased over time; that is, substantial concurrent contributions to anxiety (β = 0.27; 95% CI, 0.22-0.33) persisted for 2 years (β = 0.12; 95% CI, 0.04-0.20) but not 5 years. Direct contributions to paranoid thoughts and cognitive disorganization persisted for 5 years.\ud \ud Conclusions and Relevance: This study is the largest to date to characterize the contribution of exposure to bullying in childhood to mental health using a twin differences design and multi-informant, multiscale data. Stringent evidence of the direct detrimental contribution of exposure to bullying in childhood to mental health is provided. Findings also suggest that childhood exposure to bullying may partly be viewed as a symptom of preexisting vulnerabilities. Finally, the dissipation of effects over time for many outcomes highlights the potential for resilience in children who were bullied. In addition to programs that aim to reduce exposure to bullying, interventions may benefit from addressing preexisting vulnerabilities and focus on resilience.

Published
2017

44. Effects of risk for bipolar disorder on brain function: A twin and family study.

Author

Sugihara, G, Kane, F, Picchioni, MM, Chaddock, CA, Kravariti, E, Kalidindi, S, Rijsdijk, F, Toulopoulou, T, Curtis, VA, McDonald, C, Murray, RM, McGuire, P, Sugihara, G, Kane, F, Picchioni, MM, Chaddock, CA, Kravariti, E, Kalidindi, S, Rijsdijk, F, Toulopoulou, T, Curtis, VA, McDonald, C, Murray, RM, and McGuire, P

Abstract

Bipolar disorder (BPD) is associated with altered regional brain function during the performance of cognitive tasks. The relative contribution of genetic and environmental risk factors for BPD to these changes has not yet been quantified. We sought to address this issue in a functional neuroimaging study of people who varied in their risk for BPD. Functional magnetic resonance imaging was used to study 124 subjects (29 twin and 9 sibling pairs with at least one member with BPD, and 24 healthy twin pairs) performing a working memory task. We assessed the influence of risk for BPD on regional brain function during the task in a two stage process. Firstly, we identified areas where there were group differences in activation. Secondly, we estimated the heritability and phenotypic correlation of activation and BPD using genetic modeling. BPD was associated with increased activation in the anterior cingulate, orbitofrontal, medial prefrontal, and left precentral cortices, and in the precuneus. Within these regions, activation in the orbitofrontal cortex rendered the most significant heritability estimate (h2=0.40), and was significantly correlated with BPD phenotype (rph=0.29). A moderate proportion of the genetic influences (rg=0.69) acting on both BPD and on the degree of orbitofrontal activation were shared. These findings suggest that genetic factors that confer vulnerability to BPD alter brain function in BPD.

Published
2017

45. Cannabis and Depression: A Twin Model Approach to Co-morbidity

Author

Smolkina, M, Morley, KI, Rijsdijk, F, Agrawal, A, Bergin, JE, Nelson, EC, Statham, D, Martin, NG, Lynskey, MT, Smolkina, M, Morley, KI, Rijsdijk, F, Agrawal, A, Bergin, JE, Nelson, EC, Statham, D, Martin, NG, and Lynskey, MT

Abstract

Cannabis use disorder (CUD) co-occurs with major depressive disorder (MDD) more frequently than would be expected by chance. However, studies to date have not produced a clear understanding of the mechanisms underlying this co-morbidity. Genetically informative studies can add valuable insight to this problem, as they allow the evaluation of competing models of co-morbidity. This study uses data from the Australian Twin Registry to compare 13 co-morbidity twin models initially proposed by Neale and Kendler (Am J Hum Genet 57:935-953, 1995). The analysis sample comprised 2410 male and female monozygotic and dizygotic twins (average age 32) who were assessed on CUD and MDD using the SSAGA-OZ interview. Data were analyzed in OpenMx. Of the 13 different co-morbidity models, two fit equally well: CUD causes MDD and Random Multiformity of CUD. Both fit substantially better than the Correlated Liabilities model. Although the current study cannot differentiate between them statistically, these models, in combination, suggest that CUD risk factors may causally influence the risk to develop MDD, but only when risk for CUD is high.

Published
2017

46. Does the sex of one's co-twin affect height and BMI in adulthood? A study of dizygotic adult twins from 31 cohorts

Author

Bogl, LH, Jelenkovic, A, Vuoksimaa, E, Ahrenfeldt, L, Pietilainen, KH, Stazi, MA, Fagnani, C, D'Ippolito, C, Hur, Y-M, Jeong, H-U, Silberg, JL, Eaves, LJ, Maes, HH, Bayasgalan, G, Narandalai, D, Cutler, TL, Kandler, C, Jang, KL, Christensen, K, Skytthe, A, Kyvik, KO, Cozen, W, Hwang, AE, Mack, TM, Derom, CA, Vlietinck, RF, Nelson, TL, Whitfield, KE, Corley, RP, Huibregtse, BM, McAdams, TA, Eley, TC, Gregory, AM, Krueger, RF, Mcgue, M, Pahlen, S, Willemsen, G, Bartels, M, van Beijsterveldt, TCEM, Pang, Z, Tan, Q, Zhang, D, Martin, NG, Medland, SE, Montgomery, GW, Hjelmborg, JVB, Rebato, E, Swan, GE, Krasnow, R, Busjahn, A, Lichtenstein, P, Oncel, SY, Aliev, F, Baker, LA, Tuvblad, C, Siribaddana, SH, Hotopf, M, Sumathipala, A, Rijsdijk, F, Magnusson, PKE, Pedersen, NL, Aslan, AKD, Ordonana, JR, Sanchez-Romera, JF, Colodro-Conde, L, Duncan, GE, Buchwald, D, Tarnoki, AD, Tarnoki, DL, Yokoyama, Y, Hopper, JL, Loos, RJF, Boomsma, DI, Sorensen, TIA, Silventoinen, K, Kaprio, J, Bogl, LH, Jelenkovic, A, Vuoksimaa, E, Ahrenfeldt, L, Pietilainen, KH, Stazi, MA, Fagnani, C, D'Ippolito, C, Hur, Y-M, Jeong, H-U, Silberg, JL, Eaves, LJ, Maes, HH, Bayasgalan, G, Narandalai, D, Cutler, TL, Kandler, C, Jang, KL, Christensen, K, Skytthe, A, Kyvik, KO, Cozen, W, Hwang, AE, Mack, TM, Derom, CA, Vlietinck, RF, Nelson, TL, Whitfield, KE, Corley, RP, Huibregtse, BM, McAdams, TA, Eley, TC, Gregory, AM, Krueger, RF, Mcgue, M, Pahlen, S, Willemsen, G, Bartels, M, van Beijsterveldt, TCEM, Pang, Z, Tan, Q, Zhang, D, Martin, NG, Medland, SE, Montgomery, GW, Hjelmborg, JVB, Rebato, E, Swan, GE, Krasnow, R, Busjahn, A, Lichtenstein, P, Oncel, SY, Aliev, F, Baker, LA, Tuvblad, C, Siribaddana, SH, Hotopf, M, Sumathipala, A, Rijsdijk, F, Magnusson, PKE, Pedersen, NL, Aslan, AKD, Ordonana, JR, Sanchez-Romera, JF, Colodro-Conde, L, Duncan, GE, Buchwald, D, Tarnoki, AD, Tarnoki, DL, Yokoyama, Y, Hopper, JL, Loos, RJF, Boomsma, DI, Sorensen, TIA, Silventoinen, K, and Kaprio, J

Abstract

BACKGROUND: The comparison of traits in twins from opposite-sex (OS) and same-sex (SS) dizygotic twin pairs is considered a proxy measure of prenatal hormone exposure. To examine possible prenatal hormonal influences on anthropometric traits, we compared mean height, body mass index (BMI), and the prevalence of being overweight or obese between men and women from OS and SS dizygotic twin pairs. METHODS: The data were derived from the COllaborative project of Development of Anthropometrical measures in Twins (CODATwins) database, and included 68,494 SS and 53,808 OS dizygotic twin individuals above the age of 20 years from 31 twin cohorts representing 19 countries. Zygosity was determined by questionnaires or DNA genotyping depending on the study. Multiple regression and logistic regression models adjusted for cohort, age, and birth year with the twin type as a predictor were carried out to compare height and BMI in twins from OS pairs with those from SS pairs and to calculate the adjusted odds ratios and 95% confidence intervals for being overweight or obese. RESULTS: OS females were, on average, 0.31 cm (95% confidence interval (CI) 0.20, 0.41) taller than SS females. OS males were also, on average, taller than SS males, but this difference was only 0.14 cm (95% CI 0.02, 0.27). Mean BMI and the prevalence of overweight or obesity did not differ between males and females from SS and OS twin pairs. The statistically significant differences between OS and SS twins for height were small and appeared to reflect our large sample size rather than meaningful differences of public health relevance. CONCLUSIONS: We found no evidence to support the hypothesis that prenatal hormonal exposure or postnatal socialization (i.e., having grown up with a twin of the opposite sex) has a major impact on height and BMI in adulthood.

Published
2017

47. The relationship between ADHD and key cognitive phenotypes is not mediated by shared familial effects with IQ

Author

Wood, A. C., Rijsdijk, F., Johnson, K. A., Andreou, P., Albrecht, B., Arias-Vasquez, A., Buitelaar, J. K., McLoughlin, G., Rommelse, N. N. J., Sergeant, J. A., Sonuga-Barke, E. J. S., Uebel, H., van der Meere, J. J., Banaschewski, T., Gill, M., Manor, I., Miranda, A., Mulas, F., Oades, R. D., Roeyers, H., Rothenberger, A., Steinhausen, H. C., Faraone, S. V., Asherson, P., Kuntsi, J., Wood, A. C., Rijsdijk, F., Johnson, K. A., Andreou, P., Albrecht, B., Arias-Vasquez, A., Buitelaar, J. K., McLoughlin, G., Rommelse, N. N. J., Sergeant, J. A., Sonuga-Barke, E. J. S., Uebel, H., van der Meere, J. J., Banaschewski, T., Gill, M., Manor, I., Miranda, A., Mulas, F., Oades, R. D., Roeyers, H., Rothenberger, A., Steinhausen, H. C., Faraone, S. V., Asherson, P., and Kuntsi, J.

Abstract

Background Twin and sibling studies have identified specific cognitive phenotypes that may mediate the association between genes and the clinical symptoms of attention deficit hyperactivity disorder (ADHD). ADHD is also associated with lower IQ scores. We aimed to investigate whether the familial association between measures of cognitive performance and the clinical diagnosis of ADHD is mediated through shared familial influences with IQ. Method Multivariate familial models were run on data from 1265 individuals aged 6-18 years, comprising 920 participants from ADHD sibling pairs and 345 control participants. Cognitive assessments included a four-choice reaction time (RT) task, a go/no-go task, a choice-delay task and an IQ assessment. The analyses focused on the cognitive variables of mean RT (MRT), RT variability (RTV), commission errors (CE), omission errors (OE) and choice impulsivity (CI). Results Significant familial association (rF) was confirmed between cognitive performance and both ADHD (rF=0.41-0.71) and IQ (rF=−0.25 to −0.49). The association between ADHD and cognitive performance was largely independent (80-87%) of any contribution from etiological factors shared with IQ. The exception was for CI, where 49% of the overlap could be accounted for by the familial variance underlying IQ. Conclusions The aetiological factors underlying lower IQ in ADHD seem to be distinct from those between ADHD and RT/error measures. This suggests that lower IQ does not account for the key cognitive impairments observed in ADHD. The results have implications for molecular genetic studies designed to identify genes involved in ADHD

Published
2017

48. Differences in genetic and environmental variation in adult BMI by sex, age, time period, and region : An individual-based pooled analysis of 40 twin cohorts

Author

Silventoinen, K., Jelenkovic, A., Sund, R., Yokoyama, Y., Hur, Y. -M, Cozen, W., Hwang, A. E., Mack, T. M., Honda, C., Inui, F., Iwatani, Y., Watanabe, M., Tomizawa, R., Pietilainen, K. H., Rissanen, A., Siribaddana, S. H., Hotopf, M., Sumathipala, A., Rijsdijk, F., Tan, Q., Zhang, D., Pang, Z., Piirtola, M., Aaltonen, S., Oncel, S. Y., Aliev, F., Rebato, E., Hjelmborg, J. B., Christensen, K., Skytthe, A., Kyvik, K. O., Silberg, J. L., Eaves, L. J., Cutler, T. L., Ordonana, J. R., Sanchez-Romera, J. F., Colodro-Conde, L., Song, Y. -M, Yang, S., Lee, K., Franz, C. E., Kremen, W. S., Lyons, M. J., Busjahn, A., Nelson, T. L., Whitfield, K. E., Kandler, C., Jang, K. L., Gatz, M., Butler, D. A., Stazi, M. A., Fagnani, C., D'Ippolito, C., Duncan, G. E., Buchwald, D., Martin, N. G., Medland, S. E., Montgomery, G. W., Jeong, H. -U, Swan, G. E., Krasnow, R., Magnusson, P. K. E., Pedersen, N. L., Dahl Aslan, Anna K., McAdams, T. A., Eley, T. C., Gregory, A. M., Tynelius, P., Baker, L. A., Tuvblad, C., Bayasgalan, G., Narandalai, D., Spector, T. D., Mangino, M., Lachance, G., Burt, S. A., Klump, K. L., Harris, J. R., Brandt, I., Nilsen, T. S., Krueger, R. F., McGue, M., Pahlen, S., Corley, R. P., Huibregtse, B. M., Bartels, M., Van Beijsterveldt, C. E. M., Willemsen, G., Goldberg, J. H., Rasmussen, F., Tarnoki, A. D., Tarnoki, D. L., Derom, C. A., Vlietinck, R. F., Loos, R. J. F., Hopper, J. L., Sung, J., Maes, H. H., Turkheimer, E., Boomsma, D. I., Sørensen, T. I. A., Kaprio, J., Silventoinen, K., Jelenkovic, A., Sund, R., Yokoyama, Y., Hur, Y. -M, Cozen, W., Hwang, A. E., Mack, T. M., Honda, C., Inui, F., Iwatani, Y., Watanabe, M., Tomizawa, R., Pietilainen, K. H., Rissanen, A., Siribaddana, S. H., Hotopf, M., Sumathipala, A., Rijsdijk, F., Tan, Q., Zhang, D., Pang, Z., Piirtola, M., Aaltonen, S., Oncel, S. Y., Aliev, F., Rebato, E., Hjelmborg, J. B., Christensen, K., Skytthe, A., Kyvik, K. O., Silberg, J. L., Eaves, L. J., Cutler, T. L., Ordonana, J. R., Sanchez-Romera, J. F., Colodro-Conde, L., Song, Y. -M, Yang, S., Lee, K., Franz, C. E., Kremen, W. S., Lyons, M. J., Busjahn, A., Nelson, T. L., Whitfield, K. E., Kandler, C., Jang, K. L., Gatz, M., Butler, D. A., Stazi, M. A., Fagnani, C., D'Ippolito, C., Duncan, G. E., Buchwald, D., Martin, N. G., Medland, S. E., Montgomery, G. W., Jeong, H. -U, Swan, G. E., Krasnow, R., Magnusson, P. K. E., Pedersen, N. L., Dahl Aslan, Anna K., McAdams, T. A., Eley, T. C., Gregory, A. M., Tynelius, P., Baker, L. A., Tuvblad, C., Bayasgalan, G., Narandalai, D., Spector, T. D., Mangino, M., Lachance, G., Burt, S. A., Klump, K. L., Harris, J. R., Brandt, I., Nilsen, T. S., Krueger, R. F., McGue, M., Pahlen, S., Corley, R. P., Huibregtse, B. M., Bartels, M., Van Beijsterveldt, C. E. M., Willemsen, G., Goldberg, J. H., Rasmussen, F., Tarnoki, A. D., Tarnoki, D. L., Derom, C. A., Vlietinck, R. F., Loos, R. J. F., Hopper, J. L., Sung, J., Maes, H. H., Turkheimer, E., Boomsma, D. I., Sørensen, T. I. A., and Kaprio, J.

Abstract

Background: Genes and the environment contribute to variation in adult body mass index [BMI (in kg/m2)], but factors modifying these variance components are poorly understood. Objective: We analyzed genetic and environmental variation in BMI between men and women from young adulthood to old age from the 1940s to the 2000s and between cultural-geographic regions representing high (North America and Australia), moderate (Europe), and low (East Asia) prevalence of obesity. Design: We used genetic structural equation modeling to analyze BMI in twins ≥20 y of age from 40 cohorts representing 20 countries (140,379 complete twin pairs). Results: The heritability of BMI decreased from 0.77 (95% CI: 0.77, 0.78) and 0.75 (95% CI: 0.74, 0.75) in men and women 20-29 y of age to 0.57 (95% CI: 0.54, 0.60) and 0.59 (95% CI: 0.53, 0.65) in men 70-79 y of age and women 80 y of age, respectively. The relative influence of unique environmental factors correspondingly increased. Differences in the sets of genes affecting BMI in men and women increased from 20-29 to 60-69 y of age. Mean BMI and variances in BMI increased from the 1940s to the 2000s and were greatest in North America and Australia, followed by Europe and East Asia. However, heritability estimates were largely similar over measurement years and between regions. There was no evidence of environmental factors shared by co-twins affecting BMI. Conclusions: The heritability of BMI decreased and differences in the sets of genes affecting BMI in men and women increased from young adulthood to old age. The heritability of BMI was largely similar between cultural-geographic regions and measurement years, despite large differences in mean BMI and variances in BMI. Our results show a strong influence of genetic factors on BMI, especially in early adulthood, regardless of the obesity level in the population.

Published
2017
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49. Genetic analysis of reaction time variability: room for improvement?

Author

Kuntsi, J., Frazier-Wood, A. C., Banaschewski, T., Gill, M., Miranda, A., Oades, R. D., Roeyers, H., Rothenberger, A., Steinhausen, H.-C, van der Meere, J. J., Faraone, S. V., Asherson, P., Rijsdijk, F., Kuntsi, J., Frazier-Wood, A. C., Banaschewski, T., Gill, M., Miranda, A., Oades, R. D., Roeyers, H., Rothenberger, A., Steinhausen, H.-C, van der Meere, J. J., Faraone, S. V., Asherson, P., and Rijsdijk, F.

Abstract

Background Increased reaction time variability (RTV) on cognitive tasks requiring a speeded response is characteristic of several psychiatric disorders. In attention deficit hyperactivity disorder (ADHD), the association with RTV is strong phenotypically and genetically, yet high RTV is not a stable impairment but shows ADHD-sensitive improvement under certain conditions, such as those with rewards. The state regulation theory proposed that the RTV difference score, which captures change from baseline to a rewarded or fast condition, specifically measures ‘state regulation'. By contrast, the interpretation of RTV baseline (slow, unrewarded) scores is debated. We aimed to investigate directly the degree of phenotypic and etiological overlap between RTV baseline and RTV difference scores. Method We conducted genetic model fitting analyses on go/no-go and fast task RTV data, across task conditions manipulating rewards and event rate, from a population-based twin sample (n=1314) and an ADHD and control sibling-pair sample (n=1265). Results Phenotypic and genetic/familial correlations were consistently high (0.72-0.98) between RTV baseline and difference scores, across tasks, manipulations and samples. By contrast, correlations were low between RTV in the manipulated condition and difference scores. A comparison across two different go/no-go task RTV difference scores (slow-fast/slow-incentive) showed high phenotypic and genetic/familial overlap (r=0.75-0.83). Conclusions Our finding that RTV difference scores measure largely the same etiological process as RTV under baseline condition supports theories emphasizing the malleability of the observed high RTV. Given the statistical shortcomings of difference scores, we recommend the use of RTV baseline scores for most analyses, including genetic analyses

Published
2017

50. Modifiable arousal in ADHD and its etiological association with fluctuating reaction times

Author

James, S.-N., Cheung, Celeste, Rijsdijk, F., Asherson, P., and Kuntsi, J.

Subjects
psyc, mental disorders, behavioral disciplines and activities
Abstract

BACKGROUND: Cognitive theories of attention-deficit/hyperactivity disorder (ADHD) propose that high within-subject fluctuations of cognitive performance in ADHD, particularly reaction time (RT) variability (RTV), may reflect arousal dysregulation. Yet, direct evidence of arousal dysregulation and how it may account for fluctuating reaction times in ADHD is limited. We used skin conductance (SC) as a measure of peripheral arousal and aimed to investigate its phenotypic and familial association with RTV in a large sample of ADHD and control sibling pairs.\ud METHODS: 292 adolescents and young adults, consisting of 73 participants with ADHD and their 75 siblings, as well as 72 controls and their 72 siblings, completed the baseline (slow, unrewarded) and fast-incentive conditions of a RT task, whilst SC was simultaneously recorded.\ud RESULTS: A significant group by condition interaction emerged for SC level (SCL). Participants with ADHD had decreased SCL, compared to controls, in the baseline but not fast-incentive condition. Baseline SCL was negatively associated with RTV and multivariate model fitting demonstrated that the covariance of SCL with RTV, and of SCL with ADHD, was mostly explained by shared familial effects.\ud CPNCLUSIONS: ADHD is associated with decreased, but modifiable, tonic peripheral arousal. A shared familial etiology underlies the relationship between arousal and RTV, and between arousal and ADHD. Given the malleability of SCL, if our findings are replicated, it warrants further exploration as a potential treatment target for ADHD.

Published
2016

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