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3. Genome-wide association meta-analysis of childhood and adolescent internalizing symptoms

Author

Jami, E. S. (Eshim S.), Hammerschlag, A. R. (Anke R.), Ip, H. F. (Hill F.), Allegrini, A. G. (Andrea G.), Benyamin, B. (Beben), Border, R. (Richard), Diemer, E. W. (Elizabeth W.), Jiang, C. (Chang), Karhunen, V. (Ville), Lu, Y. (Yi), Lu, Q. (Qing), Mallard, T. T. (Travis T.), Mishra, P. P. (Pashupati P.), Nolte, I. M. (Ilja M.), Palviainen, T. (Teemu), Peterson, R. E. (Roseann E.), Sallis, H. M. (Hannah M.), Shabalin, A. A. (Andrey A.), Tate, A. E. (Ashley E.), Thiering, E. (Elisabeth), Vilor-Tejedor, N. (Natalia), Wang, C. (Carol), Zhou, A. (Ang), Adkins, D. E. (Daniel E.), Alemany, S. (Silvia), Ask, H. (Helga), Chen, Q. (Qi), Corley, R. P. (Robin P.), Ehli, E. A. (Erik A.), Evans, L. M. (Luke M.), Havdahl, A. (Alexandra), Hagenbeek, F. A. (Fiona A.), Hakulinen, C. (Christian), Henders, A. K. (Anjali K.), Hottenga, J. J. (Jouke Jan), Korhonen, T. (Tellervo), Mamun, A. (Abdullah), Marrington, S. (Shelby), Neumann, A. (Alexander), Rimfeld, K. (Kaili), Rivadeneira, F. (Fernando), Silberg, J. L. (Judy L.), van Beijsterveldt, C. E. (Catharina E.), Vuoksimaa, E. (Eero), Whipp, A. M. (Alyce M.), Tong, X. (Xiaoran), Andreassen, O. A. (Ole A.), Boomsma, D. I. (Dorret, I), Brown, S. A. (Sandra A.), Burt, S. A. (S. Alexandra), Copeland, W. (William), Dick, D. M. (Danielle M.), Harden, K. P. (K. Paige), Harris, K. M. (Kathleen Mullan), Hartman, C. A. (Catharina A.), Heinrich, J. (Joachim), Hewitt, J. K. (John K.), Hopfer, C. (Christian), Hypponen, E. (Elina), Järvelin, M.-R. (Marjo-Riitta), Kaprio, J. (Jaakko), Keltikangas-Jarvinen, L. (Liisa), Klump, K. L. (Kelly L.), Krauter, K. (Kenneth), Kuja-Halkola, R. (Ralf), Larsson, H. (Henrik), Lehtimaki, T. (Terho), Lichtenstein, P. (Paul), Lundstrom, S. (Sebastian), Maes, H. H. (Hermine H.), Magnus, P. (Per), Munafo, M. R. (Marcus R.), Najman, J. M. (Jake M.), Njolstad, P. R. (Pal R.), Oldehinkel, A. J. (Albertine J.), Pennell, C. E. (Craig E.), Plomin, R. (Robert), Reichborn-Kjennerud, T. (Ted), Reynolds, C. (Chandra), Rose, R. J. (Richard J.), Smolen, A. (Andrew), Snieder, H. (Harold), Stallings, M. (Michael), Standl, M. (Marie), Sunyer, J. (Jordi), Tiemeier, H. (Henning), Wadsworth, S. J. (Sally J.), Wall, T. L. (Tamara L.), Whitehouse, A. J. (Andrew J. O.), Williams, G. M. (Gail M.), Ystrom, E. (Eivind), Nivard, M. G. (Michel G.), Bartels, M. (Meike), Middeldorp, C. M. (Christel M.), Jami, E. S. (Eshim S.), Hammerschlag, A. R. (Anke R.), Ip, H. F. (Hill F.), Allegrini, A. G. (Andrea G.), Benyamin, B. (Beben), Border, R. (Richard), Diemer, E. W. (Elizabeth W.), Jiang, C. (Chang), Karhunen, V. (Ville), Lu, Y. (Yi), Lu, Q. (Qing), Mallard, T. T. (Travis T.), Mishra, P. P. (Pashupati P.), Nolte, I. M. (Ilja M.), Palviainen, T. (Teemu), Peterson, R. E. (Roseann E.), Sallis, H. M. (Hannah M.), Shabalin, A. A. (Andrey A.), Tate, A. E. (Ashley E.), Thiering, E. (Elisabeth), Vilor-Tejedor, N. (Natalia), Wang, C. (Carol), Zhou, A. (Ang), Adkins, D. E. (Daniel E.), Alemany, S. (Silvia), Ask, H. (Helga), Chen, Q. (Qi), Corley, R. P. (Robin P.), Ehli, E. A. (Erik A.), Evans, L. M. (Luke M.), Havdahl, A. (Alexandra), Hagenbeek, F. A. (Fiona A.), Hakulinen, C. (Christian), Henders, A. K. (Anjali K.), Hottenga, J. J. (Jouke Jan), Korhonen, T. (Tellervo), Mamun, A. (Abdullah), Marrington, S. (Shelby), Neumann, A. (Alexander), Rimfeld, K. (Kaili), Rivadeneira, F. (Fernando), Silberg, J. L. (Judy L.), van Beijsterveldt, C. E. (Catharina E.), Vuoksimaa, E. (Eero), Whipp, A. M. (Alyce M.), Tong, X. (Xiaoran), Andreassen, O. A. (Ole A.), Boomsma, D. I. (Dorret, I), Brown, S. A. (Sandra A.), Burt, S. A. (S. Alexandra), Copeland, W. (William), Dick, D. M. (Danielle M.), Harden, K. P. (K. Paige), Harris, K. M. (Kathleen Mullan), Hartman, C. A. (Catharina A.), Heinrich, J. (Joachim), Hewitt, J. K. (John K.), Hopfer, C. (Christian), Hypponen, E. (Elina), Järvelin, M.-R. (Marjo-Riitta), Kaprio, J. (Jaakko), Keltikangas-Jarvinen, L. (Liisa), Klump, K. L. (Kelly L.), Krauter, K. (Kenneth), Kuja-Halkola, R. (Ralf), Larsson, H. (Henrik), Lehtimaki, T. (Terho), Lichtenstein, P. (Paul), Lundstrom, S. (Sebastian), Maes, H. H. (Hermine H.), Magnus, P. (Per), Munafo, M. R. (Marcus R.), Najman, J. M. (Jake M.), Njolstad, P. R. (Pal R.), Oldehinkel, A. J. (Albertine J.), Pennell, C. E. (Craig E.), Plomin, R. (Robert), Reichborn-Kjennerud, T. (Ted), Reynolds, C. (Chandra), Rose, R. J. (Richard J.), Smolen, A. (Andrew), Snieder, H. (Harold), Stallings, M. (Michael), Standl, M. (Marie), Sunyer, J. (Jordi), Tiemeier, H. (Henning), Wadsworth, S. J. (Sally J.), Wall, T. L. (Tamara L.), Whitehouse, A. J. (Andrew J. O.), Williams, G. M. (Gail M.), Ystrom, E. (Eivind), Nivard, M. G. (Michel G.), Bartels, M. (Meike), and Middeldorp, C. M. (Christel M.)

Abstract

Objective: To investigate the genetic architecture of internalizing symptoms in childhood and adolescence. Method: In 22 cohorts, multiple univariate genome-wide association studies (GWASs) were performed using repeated assessments of internalizing symptoms, in a total of 64,561 children and adolescents between 3 and 18 years of age. Results were aggregated in meta-analyses that accounted for sample overlap, first using all available data, and then using subsets of measurements grouped by rater, age, and instrument. Results: The meta-analysis of overall internalizing symptoms (INToverall) detected no genome-wide significant hits and showed low single nucleotide polymorphism (SNP) heritability (1.66%, 95% CI = 0.84–2.48%, neffective = 132,260). Stratified analyses indicated rater-based heterogeneity in genetic effects, with self-reported internalizing symptoms showing the highest heritability (5.63%, 95% CI = 3.08%–8.18%). The contribution of additive genetic effects on internalizing symptoms appeared to be stable over age, with overlapping estimates of SNP heritability from early childhood to adolescence. Genetic correlations were observed with adult anxiety, depression, and the well-being spectrum (|rg| < 0.70), as well as with insomnia, loneliness, attention-deficit/hyperactivity disorder, autism, and childhood aggression (range |rg| = 0.42–0.60), whereas there were no robust associations with schizophrenia, bipolar disorder, obsessive-compulsive disorder, or anorexia nervosa. Conclusion: Genetic correlations indicate that childhood and adolescent internalizing symptoms share substantial genetic vulnerabilities with adult internalizing disorders and other childhood psychiatric traits, which could partially explain both the persistence of internalizing symptoms over time and the high comorbidity among childhood psychiatric traits. Reducing phenotypic heterogeneity in childhood samples will be key in paving the way to future GWAS success.

Published
2022

4. Genetic associations between childhood psychopathology and adult depression and associated traits in 42 998 individuals:a meta-analysis

Author

Akingbuwa, W. A. (Wonuola A.), Hammerschlag, A. R. (Anke R.), Jami, E. S. (Eshim S.), Allegrini, A. G. (Andrea G.), Karhunen, V. (Ville), Sallis, H. (Hannah), Ask, H. (Helga), Askeland, R. B. (Ragna B.), Baselmans, B. (Bart), Diemer, E. (Elizabeth), Hagenbeek, F. A. (Fiona A.), Havdahl, A. (Alexandra), Hottenga, J.-J. (Jouke-Jan), Mbarek, H. (Hamdi), Rivadeneira, F. (Fernando), Tesli, M. (Martin), van Beijsterveldt, C. (Catharina), Breen, G. (Gerome), Lewis, C. M. (Cathryn M.), Thapar, A. (Anita), Boomsma, D. I. (Dorret I.), Kuja-Halkola, R. (Ralf), Reichborn-Kjennerud, T. (Ted), Magnus, P. (Per), Rimfeld, K. (Kaili), Ystrom, E. (Eivind), Järvelin, M.-R. (Marjo-Riitta), Lichtenstein, P. (Paul), Lundstrom, S. (Sebastian), Munafo, M. R. (Marcus R.), Plomin, R. (Robert), Tiemeier, H. (Henning), Nivard, M. G. (Michel G.), Bartels, M. (Meike), Middeldorp, C. M. (Christel M.), Akingbuwa, W. A. (Wonuola A.), Hammerschlag, A. R. (Anke R.), Jami, E. S. (Eshim S.), Allegrini, A. G. (Andrea G.), Karhunen, V. (Ville), Sallis, H. (Hannah), Ask, H. (Helga), Askeland, R. B. (Ragna B.), Baselmans, B. (Bart), Diemer, E. (Elizabeth), Hagenbeek, F. A. (Fiona A.), Havdahl, A. (Alexandra), Hottenga, J.-J. (Jouke-Jan), Mbarek, H. (Hamdi), Rivadeneira, F. (Fernando), Tesli, M. (Martin), van Beijsterveldt, C. (Catharina), Breen, G. (Gerome), Lewis, C. M. (Cathryn M.), Thapar, A. (Anita), Boomsma, D. I. (Dorret I.), Kuja-Halkola, R. (Ralf), Reichborn-Kjennerud, T. (Ted), Magnus, P. (Per), Rimfeld, K. (Kaili), Ystrom, E. (Eivind), Järvelin, M.-R. (Marjo-Riitta), Lichtenstein, P. (Paul), Lundstrom, S. (Sebastian), Munafo, M. R. (Marcus R.), Plomin, R. (Robert), Tiemeier, H. (Henning), Nivard, M. G. (Michel G.), Bartels, M. (Meike), and Middeldorp, C. M. (Christel M.)

Abstract

Importance: Adult mood disorders are often preceded by behavioral and emotional problems in childhood. It is yet unclear what explains the associations between childhood psychopathology and adult traits. Objective: To investigate whether genetic risk for adult mood disorders and associated traits is associated with childhood disorders. Design, Setting, and Participants: This meta-analysis examined data from 7 ongoing longitudinal birth and childhood cohorts from the UK, the Netherlands, Sweden, Norway, and Finland. Starting points of data collection ranged from July 1985 to April 2002. Participants were repeatedly assessed for childhood psychopathology from ages 6 to 17 years. Data analysis occurred from September 2017 to May 2019. Exposures: Individual polygenic scores (PGS) were constructed in children based on genome-wide association studies of adult major depression, bipolar disorder, subjective well-being, neuroticism, insomnia, educational attainment, and body mass index (BMI). Main Outcomes and Measures: Regression meta-analyses were used to test associations between PGS and attention-deficit/hyperactivity disorder (ADHD) symptoms and internalizing and social problems measured repeatedly across childhood and adolescence and whether these associations depended on childhood phenotype, age, and rater. Results: The sample included 42 998 participants aged 6 to 17 years. Male participants varied from 43.0% (1040 of 2417 participants) to 53.1% (2434 of 4583 participants) by age and across all cohorts. The PGS of adult major depression, neuroticism, BMI, and insomnia were positively associated with childhood psychopathology (β estimate range, 0.023–0.042 [95% CI, 0.017–0.049]), while associations with PGS of subjective well-being and educational attainment were negative (β, −0.026 to −0.046 [95% CI, −0.020 to −0.057]). There was no moderation of age, type of childhood phenotype, or rater with the associations. The exceptions were stronger associations betwe

Published
2020

7. Collaborative meta-analysis finds no evidence of a strong interaction between stress and 5-HTTLPR genotype contributing to the development of depression

Author

Culverhouse, R. C., Saccone, N. L., Horton, A. C., Ma, Y., Anstey, K. J., Banaschewski, T., Burmeister, M., Cohen-Woods, S., Etain, B., Fisher, H. L., Goldman, N., Guillaume, S., Horwood, J., Juhasz, G., Lester, K. J., Mandelli, L., Middeldorp, C. M., Olie, E., Villafuerte, S., Air, T. M., Araya, R., Bowes, L., Burns, R., Byrne, E. M., Coffey, C., Coventry, W. L., Gawronski, K. A. B., Glei, D., Hatzimanolis, A., Hottenga, J-J, Jaussent, I., Jawahar, C., Jennen-Steinmetz, C., Kramer, J. R., Lajnef, M., Little, K., zu Schwabedissen, H. M., Nauck, M., Nederhof, E., Petschner, P., Peyrot, W. J., Schwahn, C., Sinnamon, G., Stacey, D., Tian, Y., Toben, C., Van der Auwera, S., Wainwright, N., Wang, J-C, Willemsen, G., Anderson, I. M., Arolt, V., Åslund, Cecilia, Bagdy, G., Baune, B. T., Bellivier, F., Boomsma, D. I., Courtet, P., Dannlowski, U., de Geus, E. J. C., Deakin, J. F. W., Easteal, S., Eley, T., Fergusson, D. M., Goate, A. M., Gonda, X., Grabe, H. J., Holzman, C., Johnson, E. O., Kennedy, M., Laucht, M., Martin, N. G., Munafo, M. R., Nillson, Kent W., Oldehinkel, A. J., Olsson, C. A., Ormel, J., Otte, C., Patton, G. C., Penninx, B. W. J. H., Ritchie, K., Sarchiapone, M., Scheid, J. M., Serretti, A., Smit, J. H., Stefanis, N. C., Surtees, P. G., Voelzke, H., Weinstein, M., Whooley, M., Nurnberger, J. I., Jr., Breslau, N., Bierut, L. J., Culverhouse, R. C., Saccone, N. L., Horton, A. C., Ma, Y., Anstey, K. J., Banaschewski, T., Burmeister, M., Cohen-Woods, S., Etain, B., Fisher, H. L., Goldman, N., Guillaume, S., Horwood, J., Juhasz, G., Lester, K. J., Mandelli, L., Middeldorp, C. M., Olie, E., Villafuerte, S., Air, T. M., Araya, R., Bowes, L., Burns, R., Byrne, E. M., Coffey, C., Coventry, W. L., Gawronski, K. A. B., Glei, D., Hatzimanolis, A., Hottenga, J-J, Jaussent, I., Jawahar, C., Jennen-Steinmetz, C., Kramer, J. R., Lajnef, M., Little, K., zu Schwabedissen, H. M., Nauck, M., Nederhof, E., Petschner, P., Peyrot, W. J., Schwahn, C., Sinnamon, G., Stacey, D., Tian, Y., Toben, C., Van der Auwera, S., Wainwright, N., Wang, J-C, Willemsen, G., Anderson, I. M., Arolt, V., Åslund, Cecilia, Bagdy, G., Baune, B. T., Bellivier, F., Boomsma, D. I., Courtet, P., Dannlowski, U., de Geus, E. J. C., Deakin, J. F. W., Easteal, S., Eley, T., Fergusson, D. M., Goate, A. M., Gonda, X., Grabe, H. J., Holzman, C., Johnson, E. O., Kennedy, M., Laucht, M., Martin, N. G., Munafo, M. R., Nillson, Kent W., Oldehinkel, A. J., Olsson, C. A., Ormel, J., Otte, C., Patton, G. C., Penninx, B. W. J. H., Ritchie, K., Sarchiapone, M., Scheid, J. M., Serretti, A., Smit, J. H., Stefanis, N. C., Surtees, P. G., Voelzke, H., Weinstein, M., Whooley, M., Nurnberger, J. I., Jr., Breslau, N., and Bierut, L. J.

Abstract

The hypothesis that the S allele of the 5-HTTLPR serotonin transporter promoter region is associated with increased risk of depression, but only in individuals exposed to stressful situations, has generated much interest, research and controversy since first proposed in 2003. Multiple meta-analyses combining results from heterogeneous analyses have not settled the issue. To determine the magnitude of the interaction and the conditions under which it might be observed, we performed new analyses on 31 data sets containing 38 802 European ancestry subjects genotyped for 5-HTTLPR and assessed for depression and childhood maltreatment or other stressful life events, and meta-analysed the results. Analyses targeted two stressors (narrow, broad) and two depression outcomes (current, lifetime). All groups that published on this topic prior to the initiation of our study and met the assessment and sample size criteria were invited to participate. Additional groups, identified by consortium members or self-identified in response to our protocol (published prior to the start of analysis) with qualifying unpublished data, were also invited to participate. A uniform data analysis script implementing the protocol was executed by each of the consortium members. Our findings do not support the interaction hypothesis. We found no subgroups or variable definitions for which an interaction between stress and 5-HTTLPR genotype was statistically significant. In contrast, our findings for the main effects of life stressors (strong risk factor) and 5-HTTLPR genotype (no impact on risk) are strikingly consistent across our contributing studies, the original study reporting the interaction and subsequent meta-analyses. Our conclusion is that if an interaction exists in which the S allele of 5-HTTLPR increases risk of depression only in stressed individuals, then it is not broadly generalisable, but must be of modest effect size and only observable in limited situations.

Published
2018
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11. Genome-wide association study of lifetime cannabis use based on a large meta-analytic sample of 32330 subjects from the International Cannabis Consortium

Author

University of Helsinki, Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Clinicum, Stringer, S., Minica, C. C., Verweij, K. J. H., Mbarek, H., Bernard, M., Derringer, J., van Eijk, K. R., Isen, J. D., Loukola, A., Maciejewski, D. F., Mihailov, E., van der Most, P. J., Sanchez-Mora, C., Roos, L., Sherva, R., Walters, R., Ware, J. J., Abdellaoui, A., Bigdeli, T. B., Branje, S. J. T., Brown, S. A., Bruinenberg, M., Casas, M., Esko, T., Garcia-Martinez, I., Gordon, S. D., Harris, J. M., Hartman, C. A., Henders, A. K., Heath, A. C., Hickie, I. B., Hickman, M., Hopfer, C. J., Hottenga, J. J., Huizink, A. C., Irons, D. E., Kahn, R. S., Korhonen, T., Kranzler, H. R., Krauter, K., van Lier, P. A. C., Lubke, G. H., Madden, P. A. F., Magi, R., McGue, M. K., Medland, S. E., Meeus, W. H. J., Miller, M. B., Montgomery, G. W., Nivard, M. G., Nolte, I. M., Oldehinkel, A. J., Pausova, Z., Qaiser, B., Quaye, L., Ramos-Quiroga, J. A., Richarte, V., Rose, R. J., Shin, J., Stallings, M. C., Stiby, A. I., Wall, T. L., Wright, M. J., Koot, H. M., Paus, T., Hewitt, J. K., Ribases, M., Kaprio, J., Boks, M. P., Snieder, H., Spector, T., Munafo, M. R., Metspalu, A., Gelernter, J., Boomsma, D. I., Iacono, W. G., Martin, N. G., Gillespie, N. A., Derks, E. M., Vink, J. M., University of Helsinki, Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Clinicum, Stringer, S., Minica, C. C., Verweij, K. J. H., Mbarek, H., Bernard, M., Derringer, J., van Eijk, K. R., Isen, J. D., Loukola, A., Maciejewski, D. F., Mihailov, E., van der Most, P. J., Sanchez-Mora, C., Roos, L., Sherva, R., Walters, R., Ware, J. J., Abdellaoui, A., Bigdeli, T. B., Branje, S. J. T., Brown, S. A., Bruinenberg, M., Casas, M., Esko, T., Garcia-Martinez, I., Gordon, S. D., Harris, J. M., Hartman, C. A., Henders, A. K., Heath, A. C., Hickie, I. B., Hickman, M., Hopfer, C. J., Hottenga, J. J., Huizink, A. C., Irons, D. E., Kahn, R. S., Korhonen, T., Kranzler, H. R., Krauter, K., van Lier, P. A. C., Lubke, G. H., Madden, P. A. F., Magi, R., McGue, M. K., Medland, S. E., Meeus, W. H. J., Miller, M. B., Montgomery, G. W., Nivard, M. G., Nolte, I. M., Oldehinkel, A. J., Pausova, Z., Qaiser, B., Quaye, L., Ramos-Quiroga, J. A., Richarte, V., Rose, R. J., Shin, J., Stallings, M. C., Stiby, A. I., Wall, T. L., Wright, M. J., Koot, H. M., Paus, T., Hewitt, J. K., Ribases, M., Kaprio, J., Boks, M. P., Snieder, H., Spector, T., Munafo, M. R., Metspalu, A., Gelernter, J., Boomsma, D. I., Iacono, W. G., Martin, N. G., Gillespie, N. A., Derks, E. M., and Vink, J. M.

Abstract

Cannabis is the most widely produced and consumed illicit psychoactive substance worldwide. Occasional cannabis use can progress to frequent use, abuse and dependence with all known adverse physical, psychological and social consequences. Individual differences in cannabis initiation are heritable (40-48%). The International Cannabis Consortium was established with the aim to identify genetic risk variants of cannabis use. We conducted a meta-analysis of genome-wide association data of 13 cohorts (N = 32 330) and four replication samples (N = 5627). In addition, we performed a gene-based test of association, estimated single-nucleotide polymorphism (SNP)-based heritability and explored the genetic correlation between lifetime cannabis use and cigarette use using LD score regression. No individual SNPs reached genome-wide significance. Nonetheless, gene-based tests identified four genes significantly associated with lifetime cannabis use: NCAM1, CADM2, SCOC and KCNT2. Previous studies reported associations of NCAM1 with cigarette smoking and other substance use, and those of CADM2 with body mass index, processing speed and autism disorders, which are phenotypes previously reported to be associated with cannabis use.

Published
2016

12. Genome-wide association study of lifetime cannabis use based on a large meta-analytic sample of 32330 subjects from the International Cannabis Consortium

Author

Stringer, S., Minica, C. C., Verweij, K. J. H., Mbarek, H., Bernard, M., Derringer, J., van Eijk, K. R., Isen, J. D., Loukola, A., Maciejewski, D. F., Mihailov, E., van der Most, P. J., Sanchez-Mora, C., Roos, L., Sherva, R., Walters, R., Ware, J. J., Abdellaoui, A., Bigdeli, T. B., Branje, S. J. T., Brown, S. A., Bruinenberg, M., Casas, M., Esko, T., Garcia-Martinez, I., Gordon, S. D., Harris, J. M., Hartman, C. A., Henders, A. K., Heath, A. C., Hickie, I. B., Hickman, M., Hopfer, C. J., Hottenga, J. J., Huizink, A. C., Irons, D. E., Kahn, R. S., Korhonen, T., Kranzler, H. R., Krauter, K., van Lier, P. A. C., Lubke, G. H., Madden, P. A. F., Magi, R., McGue, M. K., Medland, S. E., Meeus, W. H. J., Miller, M. B., Montgomery, G. W., Nivard, M. G., Nolte, I. M., Oldehinkel, A. J., Pausova, Z., Qaiser, B., Quaye, L., Ramos-Quiroga, J. A., Richarte, V., Rose, R. J., Shin, J., Stallings, M. C., Stiby, A. I., Wall, T. L., Wright, M. J., Koot, H. M., Paus, T., Hewitt, J. K., Ribases, M., Kaprio, J., Boks, M. P., Snieder, H., Spector, T., Munafo, M. R., Metspalu, A., Gelernter, J., Boomsma, D. I., Iacono, W. G., Martin, N. G., Gillespie, N. A., Derks, E. M., Vink, J. M., Stringer, S., Minica, C. C., Verweij, K. J. H., Mbarek, H., Bernard, M., Derringer, J., van Eijk, K. R., Isen, J. D., Loukola, A., Maciejewski, D. F., Mihailov, E., van der Most, P. J., Sanchez-Mora, C., Roos, L., Sherva, R., Walters, R., Ware, J. J., Abdellaoui, A., Bigdeli, T. B., Branje, S. J. T., Brown, S. A., Bruinenberg, M., Casas, M., Esko, T., Garcia-Martinez, I., Gordon, S. D., Harris, J. M., Hartman, C. A., Henders, A. K., Heath, A. C., Hickie, I. B., Hickman, M., Hopfer, C. J., Hottenga, J. J., Huizink, A. C., Irons, D. E., Kahn, R. S., Korhonen, T., Kranzler, H. R., Krauter, K., van Lier, P. A. C., Lubke, G. H., Madden, P. A. F., Magi, R., McGue, M. K., Medland, S. E., Meeus, W. H. J., Miller, M. B., Montgomery, G. W., Nivard, M. G., Nolte, I. M., Oldehinkel, A. J., Pausova, Z., Qaiser, B., Quaye, L., Ramos-Quiroga, J. A., Richarte, V., Rose, R. J., Shin, J., Stallings, M. C., Stiby, A. I., Wall, T. L., Wright, M. J., Koot, H. M., Paus, T., Hewitt, J. K., Ribases, M., Kaprio, J., Boks, M. P., Snieder, H., Spector, T., Munafo, M. R., Metspalu, A., Gelernter, J., Boomsma, D. I., Iacono, W. G., Martin, N. G., Gillespie, N. A., Derks, E. M., and Vink, J. M.

Abstract

Cannabis is the most widely produced and consumed illicit psychoactive substance worldwide. Occasional cannabis use can progress to frequent use, abuse and dependence with all known adverse physical, psychological and social consequences. Individual differences in cannabis initiation are heritable (40–48%). The International Cannabis Consortium was established with the aim to identify genetic risk variants of cannabis use. We conducted a meta-analysis of genome-wide association data of 13 cohorts (N=32 330) and four replication samples (N=5627). In addition, we performed a gene-based test of association, estimated single-nucleotide polymorphism (SNP)-based heritability and explored the genetic correlation between lifetime cannabis use and cigarette use using LD score regression. No individual SNPs reached genome-wide significance. Nonetheless, gene-based tests identified four genes significantly associated with lifetime cannabis use: NCAM1, CADM2, SCOC and KCNT2. Previous studies reported associations of NCAM1 with cigarette smoking and other substance use, and those of CADM2 with body mass index, processing speed and autism disorders, which are phenotypes previously reported to be associated with cannabis use. Furthermore, we showed that, combined across the genome, all common SNPs explained 13–20% (P<0.001) of the liability of lifetime cannabis use. Finally, there was a strong genetic correlation (rg=0.83; P=1.85 × 10−8) between lifetime cannabis use and lifetime cigarette smoking implying that the SNP effect sizes of the two traits are highly correlated. This is the largest meta-analysis of cannabis GWA studies to date, revealing important new insights into the genetic pathways of lifetime cannabis use. Future functional studies should explore the impact of the identified genes on the biological mechanisms of cannabis use.

Published
2016

29. Book reviews

Author

Munafo, M. R., primary, Gudmundsdottir, Hafrun, additional, Parrott, Andy, additional, and De Ridder, Denise T.D., additional

Published
1998
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30. Genome-wide association study of lifetime cannabis use based on a large meta-analytic sample of 32 330 subjects from the International Cannabis Consortium

Author

Stringer, S, Minică, C C, Verweij, K J H, Mbarek, H, Bernard, M, Derringer, J, van Eijk, K R, Isen, J D, Loukola, A, Maciejewski, D F, Mihailov, E, van der Most, P J, Sánchez-Mora, C, Roos, L, Sherva, R, Walters, R, Ware, J J, Abdellaoui, A, Bigdeli, T B, Branje, S J T, Brown, S A, Bruinenberg, M, Casas, M, Esko, T, Garcia-Martinez, I, Gordon, S D, Harris, J M, Hartman, C A, Henders, A K, Heath, A C, Hickie, I B, Hickman, M, Hopfer, C J, Hottenga, J J, Huizink, A C, Irons, D E, Kahn, R S, Korhonen, T, Kranzler, H R, Krauter, K, van Lier, P A C, Lubke, G H, Madden, P A F, Mägi, R, McGue, M K, Medland, S E, Meeus, W H J, Miller, M B, Montgomery, G W, Nivard, M G, Nolte, I M, Oldehinkel, A J, Pausova, Z, Qaiser, B, Quaye, L, Ramos-Quiroga, J A, Richarte, V, Rose, R J, Shin, J, Stallings, M C, Stiby, A I, Wall, T L, Wright, M J, Koot, H M, Paus, T, Hewitt, J K, Ribasés, M, Kaprio, J, Boks, M P, Snieder, H, Spector, T, Munafò, M R, Metspalu, A, Gelernter, J, Boomsma, D I, Iacono, W G, Martin, N G, Gillespie, N A, Derks, E M, and Vink, J M

Abstract

Cannabis is the most widely produced and consumed illicit psychoactive substance worldwide. Occasional cannabis use can progress to frequent use, abuse and dependence with all known adverse physical, psychological and social consequences. Individual differences in cannabis initiation are heritable (40–48%). The International Cannabis Consortium was established with the aim to identify genetic risk variants of cannabis use. We conducted a meta-analysis of genome-wide association data of 13 cohorts (N=32 330) and four replication samples (N=5627). In addition, we performed a gene-based test of association, estimated single-nucleotide polymorphism (SNP)-based heritability and explored the genetic correlation between lifetime cannabis use and cigarette use using LD score regression. No individual SNPs reached genome-wide significance. Nonetheless, gene-based tests identified four genes significantly associated with lifetime cannabis use: NCAM1, CADM2, SCOC and KCNT2. Previous studies reported associations of NCAM1 with cigarette smoking and other substance use, and those of CADM2 with body mass index, processing speed and autism disorders, which are phenotypes previously reported to be associated with cannabis use. Furthermore, we showed that, combined across the genome, all common SNPs explained 13–20% (P<0.001) of the liability of lifetime cannabis use. Finally, there was a strong genetic correlation (rg=0.83; P=1.85 × 10−8) between lifetime cannabis use and lifetime cigarette smoking implying that the SNP effect sizes of the two traits are highly correlated. This is the largest meta-analysis of cannabis GWA studies to date, revealing important new insights into the genetic pathways of lifetime cannabis use. Future functional studies should explore the impact of the identified genes on the biological mechanisms of cannabis use.

Published
2016
Full Text
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31. Genetic Polymorphisms and Personality in Healthy Adults: A systematic review and meta-analysis.

Author

Munafo, M R, Clark, T G, Moore, L R, Payne, E, Walton, R, and Flint, J

Subjects
*META-analysis, *GENETIC polymorphisms, *PERSONALITY, *MULTIVARIATE analysis
Abstract

A meta-analysis was conducted on studies reporting data on associations between candidate genes and human personality. Studies reporting data for psychiatric populations (including organic disease and substance abuse) were excluded. A total of 46 studies contributed to the analysis. Pooled data using a fixed-effects model suggested significant associations between the 5HTT LPR, DRD4 c>t, DRD4 length, DRD2 A1/A2, DRD3 A1/A2 polymorphisms and personality traits. A multivariate analysis using a mixed-effects model and including age, sex and predominant ethnicity as covariates was applied to the analyses of 5HTT LPR and DRD4 length polymorphism data. Only the association between the 5HTT LPR polymorphism and avoidance traits remained significant (P = 0.038). However, sensitivity analyses excluding data from studies reporting allele frequencies not in Hardy-Weinberg equilibrium and unpublished data resulted in this association no longer being significant. Implications for the design of future association studies of human personality are discussed, including the likely sample sizes that will be required to achieve sufficient power and the potential role of moderating variables such as sex. [ABSTRACT FROM AUTHOR]

Published
2003

32. Perioperative anxiety and postoperative pain.

Author

MUNAFO', M. R.

Subjects
*POSTOPERATIVE pain, *ANXIETY, *PSYCHOLOGY
Abstract

Focuses on a study which determined the relationship between perioperative anxiety and postoperative pain in medical practice. Components of anxiety; Relationship between coping behavior and pain response; Perioperative information as an intervention.

Published
1998
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34. An interactive training programme to treat body image disturbance

Author

Gledhill, L. J., Cornelissen, K. K., Cornelissen, P. L., Penton-Voak, I. P., Munafo, M. R., Tovée, Martin J., Gledhill, L. J., Cornelissen, K. K., Cornelissen, P. L., Penton-Voak, I. P., Munafo, M. R., and Tovée, Martin J.

Abstract

Objectives: Anorexia nervosa (AN) is a life-threatening mental health condition. A core feature is a disturbance of body image, such that sufferers see themselves as fatter than they actually are. Design: We tested the effectiveness of a novel training program to recalibrate our participants’ perception of body size. Methods: In a novel adaptation of a cognitive bias training program, participants judged the body size of a series of female bodies and were given feedback to improve their accuracy over 4 daily training sessions. In Study 1, we recruited young women with high concerns about their body size for a randomised controlled study. In Study 2, we then applied the training program to a case series of women with atypical AN. Results: In Study 1, the training program significantly improved the body size judgements of women with high body concerns compared to controls. We also found evidence of improved body image and reduced eating concerns in this group. In Study 2, the program again recalibrated the body size judgements of women with atypical AN. We also saw evidence of a clinically meaningful reduction in their body size and eating disordered concerns. Conclusions: This training has the potential to be a valuable treatment used together with more traditional talking therapies.

35. Book reviews.

Author

MUNAFO', M. R.

Subjects
PAIN Management Psychotherapy: A Practical Guide (Book)
Abstract

Reviews the book `Pain management psychotherapy: a practical guide,' by Bruce N. Eimer and Arthur Freeman.

Published
1998
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36. Interventions for smoking cessation in hospitalised patients.

Author

Rigotti NA, Munafo MR, and Stead LF

Subjects
Humans, Patient Education as Topic, Randomized Controlled Trials as Topic, Sensitivity and Specificity, Smoking Prevention, Hospitalization, Smoking Cessation methods
Abstract

Background: An admission to hospital provides an opportunity to help people stop smoking. Individuals may be more open to help at a time of perceived vulnerability, and may find it easier to quit in an environment where smoking is restricted or prohibited. Initiating smoking cessation services during hospitalisation may help more people to make and sustain a quit attempt., Objectives: To determine the effectiveness of interventions for smoking cessation that are initiated for hospitalised patients., Search Strategy: We searched the Cochrane Tobacco Addiction Group register which includes papers identified from CENTRAL, MEDLINE, EMBASE and PSYCINFO in January 2007, and CINAHL in August 2006 for studies of interventions for smoking cessation in hospitalised patients, using terms including (hospital and patient*) or hospitali* or inpatient* or admission* or admitted., Selection Criteria: Randomized and quasi-randomized trials of behavioural, pharmacological or multicomponent interventions to help patients stop smoking, conducted with hospitalised patients who were current smokers or recent quitters (defined as having quit more than one month before hospital admission). The intervention had to start in the hospital but could continue after hospital discharge. We excluded studies of patients admitted for psychiatric disorders or substance abuse, studies that did not report abstinence rates and studies with follow up of less than six months., Data Collection and Analysis: Two authors extracted data independently for each paper, with disagreements resolved by consensus., Main Results: Thirty-three trials met the inclusion criteria. Intensive counselling interventions that began during the hospital stay and continued with supportive contacts for at least one month after discharge increased smoking cessation rates after discharge (Odds Ratio (OR) 1.65, 95% confidence interval (CI) 1.44 to 1.90; 17 trials). No statistically significant benefit was found for less intensive counselling interventions. The one study that tested a single brief (<=15 minutes) in-hospital intervention did not find it to be effective (OR 1.16, 95% CI 0.80 to 1.67). Counselling of longer duration during the hospital stay was not associated with a higher quit rate (OR 1.08, 95% CI 0.89 to 1.29, eight trials). Even counselling that began in the hospital but had less than one month of supportive contact after discharge did not show significant benefit (OR 1.09, 95% CI 0.91 to 1.31, six trials). Adding nicotine replacement therapy (NRT) did not produce a statistically significant increase in cessation over what was achieved by intensive counselling alone (OR 1.47, 95% CI 0.92 to 2.35, five studies). The one study that tested the effect of adding bupropion to intensive counselling had a similar nonsignificant effect (OR 1.56, 95% CI 0.79 to 3.06). A similar pattern of results was observed in smokers admitted to hospital because of cardiovascular disease (CVD). In this subgroup, intensive intervention with follow-up support increased the odds of smoking cessation (OR 1.81, 95% CI 1.54 to 2.15, 11 trials), but less intensive interventions did not. One trial of intensive intervention including counselling and pharmacotherapy for smokers admitted with CVD assessed clinical and health care utilization endpoints, and found significant reductions in all-cause mortality and hospital readmission rates over a two-year follow-up period., Authors' Conclusions: High intensity behavioural interventions that begin during a hospital stay and include at least one month of supportive contact after discharge promote smoking cessation among hospitalised patients. These interventions are effective regardless of the patient's admitting diagnosis. lnterventions of lower intensity or shorter duration have not been shown to be effective in this setting. There is insufficient direct evidence to conclude that adding NRT or bupropion to intensive counselling increases cessation rates over what is achieved by counselling alone, but the evidence of benefit for NRT has strengthened in this update and the point estimates are compatible with research in other settings showing that NRT and bupropion are effective.

Published
2007
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37. Interventions for smoking cessation in hospitalised patients.

Author

Rigotti NA, Munafo MR, Murphy MF, and Stead LF

Subjects
Humans, Patient Education as Topic, Randomized Controlled Trials as Topic, Sensitivity and Specificity, Smoking Prevention, Hospitalization, Smoking Cessation methods
Abstract

Background: An admission to hospital provides an opportunity to help people stop smoking. Individuals may be more open to help at a time of perceived vulnerability, and may find it easier to quit in an environment where smoking is restricted or prohibited. Providing smoking cessation services during hospitalisation may help more people to attempt and sustain a quit attempt., Objectives: To determine the effectiveness of interventions for smoking cessation in hospitalised patients., Search Strategy: We searched the Cochrane Tobacco Addiction Group register, CINAHL and the Smoking and Health database in March 2002 for studies of interventions for smoking cessation in hospitalised patients, using terms including (hospital and patient*) or hospitali* or inpatient* or admission* or admitted., Selection Criteria: Randomised and quasi-randomised trials of behavioural, pharmacological or multicomponent interventions to help patients stop smoking conducted with hospitalised patients who were current smokers or recent quitters. We excluded studies of patients admitted for psychiatric disorders or substance abuse, those that did not report abstinence rates and those with follow-up of less than six months., Data Collection and Analysis: Two authors extracted data independently for each paper, with disagreements resolved by consensus., Main Results: Seventeen trials met the inclusion criteria. Intensive intervention (inpatient contact plus follow-up for at least one month) was associated with a significantly higher quit rate compared to control (Peto Odds Ratio 1.82, 95% CI 1.49-2.22, six trials). Interventions with less than a month of follow-up did not show evidence of significant benefit (Peto Odds Ratio 1.09, 95% CI 0.91-1.31, seven trials). There was no evidence to judge the effect of very brief (<20 minutes) interventions delivered only during the hospital stay. Longer interventions delivered only during the hospital stay were not significantly associated with a higher quit rate (Peto Odds Ratio 1.07, 95% CI 0.79-1.44, three trials). Although the interventions increased quit rates irrespective of whether nicotine replacement therapy (NRT) was used, the results for NRT were compatible with other data indicating that it increases quit rates. There was no strong evidence that clinical diagnosis affected the likelihood of quitting., Reviewer's Conclusions: High intensity behavioural interventions that include at least one month of follow-up contact are effective in promoting smoking cessation in hospitalised patients. The findings of the review were compatible with research in other settings showing that NRT increases quit rates.

Published
2003
Full Text
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38. Interventions for smoking cessation in hospitalised patients.

Author

Rigotti NA, Munafo MR, Murphy MF, and Stead LF

Subjects
Humans, Patient Education as Topic, Randomized Controlled Trials as Topic, Sensitivity and Specificity, Smoking Prevention, Hospitalization, Smoking Cessation methods
Abstract

Background: An admission to hospital provides an opportunity to help people stop smoking. Individuals may be more open to help at a time of perceived vulnerability, and may find it easier to quit in an environment where smoking is restricted or prohibited. Providing smoking cessation services during hospitalisation may help more people to attempt and sustain a quit attempt., Objectives: To determine the effectiveness of interventions for smoking cessation in hospitalised patients., Search Strategy: We searched the Cochrane Tobacco Addiction Group register, CINAHL and the Smoking and Health database for studies of interventions for smoking cessation in hospitalised patients., Selection Criteria: Randomised and quasi-randomised trials of behavioural, pharmacological or multicomponent interventions to help patients stop smoking conducted with hospitalised patients who were current smokers or recent quitters. We excluded studies of patients admitted for psychiatric disorders or substance abuse, those that did not report abstinence rates and those with follow-up of less than six months., Data Collection and Analysis: Two authors extracted data independently for each paper, with disagreements resolved by consensus., Main Results: Intensive intervention (inpatient contact plus follow-up for at least one month) was associated with a significantly higher quit rate compared to control (Peto Odds Ratio 1.82, 95% CI 1.49-2.22). There was insufficient evidence to judge the effect of interventions delivered only during the hospital stay. Although the interventions increased quit rates irrespective of whether nicotine replacement therapy was used, the results for nicotine replacement therapy (NRT) were compatible with other data indicating that it increases quit rates. There was no strong evidence that clinical diagnosis affected the likelihood of quitting., Reviewer's Conclusions: High intensity behavioural interventions that include at least one month of follow-up contact are effective in promoting smoking cessation in hospitalised patients. The findings of the review were compatible with research in other settings showing that NRT increases quit rates.

Published
2001
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