/docs/genetics/correlation/ Directory Listing

Annotated bibliography of files in the directory /docs/genetics/correlation/.
2009-01-012021-04-07 in progress certainty: log importance: 0


  • 1943-hazel.pdf

  • 1951-rae.pdf

  • 1955-dickerson.pdf

  • 1962-smith.pdf

  • 1968-vandenberg-progressinhumanbehaviorgenetics.pdf

  • 1972-breland.pdf

  • 1975-karlsson.pdf

  • 1976-castleberry.pdf

  • 1977-leamy.pdf

  • 1977-taubman-kinometricsdeterminantssocioeconomicsuccesswithinbetweenfamilies.pdf

  • 1978-nance-twinresearchparta-psychologymethodology.pdf

  • 1980-smith-2.pdf

  • 1980-smith.pdf

  • 1981-gedda-twinresearch3-partbintelligencepersonalitydevelopment.pdf

  • 1982-black.pdf

  • 1983-goddard.pdf

  • 1983-wilson.pdf

  • 1985-mackenzie.pdf

  • 1985-plomin-originsofindividualdifferencesinfancy-coloradoadoptionproject.pdf

  • 1987-defries.pdf

  • 1987-kendler.pdf

  • 1988-cheverud.pdf

  • 1988-hewitt.pdf

  • 1988-thompson.pdf

  • 1989-tambs.pdf

  • 1990-brooks.pdf

  • 1990-cardon.pdf

  • 1990-grove.pdf

  • ⁠, S. Ooki, K. Yamada, A. Asaka (1990-01-01):

    The present study deals with the relationship between blood uric acid level and human behavior. Subjects were 37 MZ and 7 DZ twins aged from 18 to 45 years. In males, blood uric acid level increased with age, while it decreased with age in females. Blood uric acid level was corrected and standardized using regression lines separately for males and females. The distribution of standardized uric acid level corresponded well with the theoretical curve of normal distribution. The intraclass correlation coefficient for standardized uric acid level was r = 0.370 (p < 0.05) for the 37 MZ twins, but not statistically-significant for the 7 DZ twins. These findings suggest that blood uric acid level is genetically controlled. By the analysis of 12 personality traits in YG (Yatabe-Guilford) character test, it was revealed that “General activity” was more controlled by genetically than environmentally. In the evaluation of the correlation between standardized uric acid level and the YG 12 personality traits, statistically-significant correlation was observed in “Lack of agreeableness” and “Rhathymia”. Since these two personality traits include the factor of “activity”, it is concluded that the plasma uric acid level and activity in a broader sense are under genetic control. This conclusion is consistent with the generally accepted view that persons with high uric acid level are more active and energetic than those with low level.

  • 1991-defries.pdf

  • 1991-thompson.pdf

  • 1992-kendler.pdf

  • 1992-mcgue.pdf

  • 1993-petrill.pdf

  • 1994-defries-naturenurtureduringmiddlechildhood.pdf

  • 1994-reed.pdf

  • 1995-kendler.pdf

  • ⁠, Madeline McCarren, Gail R. Janes, Jack Goldberg, Seth A. Eisen, William R. True, William G. Henderson (1995-01-01):

    This study examines the association between post-traumatic stress disorder (PTSD) and combat exposure with the socioeconomic status of 2210 male monozygotic veteran twin pairs in 1987. In the unadjusted analysis on individuals, modest correlations indicated that those with PTSD were more likely to have been divorced, and less likely to be currently employed or to achieve high status in income, education or occupation. In the crude analysis of veterans not suffering from PTSD, there were small positive correlations between combat level experienced and the likelihood of ever being married, ever being divorced, and the number of years employed at the current job. However, when we examined identical twins discordant for PTSD, and adjusted for pre-military and military service factors, only unemployment remained statistically-significant. Likewise, in combat-discordant twins, no statistically-significant effects on the socioeconomic indicators were seen. We conclude that PTSD and combat experience in Southeast Asia have not had a major impact on the socioeconomic status of veterans.

  • 1995-pickens.pdf

  • 1995-roff.pdf

  • 1995-wadsworth-2.pdf

  • 1995-wadsworth.pdf

  • 1996-billig.pdf

  • 1996-karjalainen.pdf

  • 1996-ritland.pdf

  • 1996-silberg.pdf

  • 1996-swan.pdf

  • 1997-almasy.pdf

  • 1997-gjone.pdf

  • 1997-lichtenstein.pdf

  • 1997-saudino.pdf

  • 1997-swan.pdf

  • 1998-lynchwalsh-geneticsquantitativetraits-ch21-geneticcorrelations.pdf

  • 1998-oconnor-2.pdf

  • 1998-oconnor.pdf

  • 1998-sullivan.pdf

  • 1999-chambers.pdf

  • 1999-neiderhiser.pdf

  • 2000-petrill.pdf

  • 2001-purcell.pdf

  • 2001-schmitz.pdf

  • 2002-degenhardt.pdf

  • 2002-madden.pdf

  • 2003-bulik.pdf

  • 2003-scherrer.pdf

  • 2004-kendler.pdf

  • 2004-nigg.pdf

  • 2004-pfefferbaum.pdf

  • 2005-johnson.pdf

  • 2005-plomin.pdf

  • 2006-johnson.pdf

  • 2006-saetre.pdf

  • 2007-harlaar.pdf

  • 2008-kruuk.pdf

  • 2008-schmitt.pdf

  • 2009-schizophreniaconsortium.pdf

  • 2010-lopez-leon.pdf

  • 2010-vance.pdf

  • 2010-wade.pdf

  • 2011-dochtermann.pdf

  • 2012-barnes.pdf

  • 2012-boisvert.pdf

  • 2012-deary.pdf

  • 2012-gottschling.pdf

  • 2012-ntzani.pdf

  • 2013-avinun.pdf

  • 2013-boivin.pdf

  • ⁠, Marian L. Hamshere, Kate Langley, Joanna Martin, Sharifah Shameem Agha, Evangelia Stergiakouli, Richard J.L. Anney, Jan Buitelaar, Stephen V. Faraone, Klaus-Peter Lesch, Benjamin M. Neale, Barbara Franke, Edmund Sonuga-Barke, Philip Asherson, Andrew Merwood, Jonna Kuntsi, Sarah E. Medland, Stephan Ripke, Hans-Christoph Steinhausen, Christine Freitag, Andreas Reif, Tobias J. Renner, Marcel Romanos, Jasmin Romanos, Andreas Warnke, Jobst Meyer, Haukur Palmason, Alejandro Arias Vasquez, Nanda Lambregts-Rommelse, Herbert Roeyers, Joseph Biederman, Alysa E. Doyle, Hakon Hakonarson, Aribert Rothenberger, Tobias Banaschewski, Robert D. Oades, James J. McGough, Lindsey Kent, Nigel Williams, Michael J. Owen, Peter Holmans, Michael C. O’Donovan, Anita Thapar (2013-08-01):

    Objective: Although attention deficit hyperactivity disorder (ADHD) is highly heritable, genome-wide association studies (GWAS) have not yet identified any common genetic variants that contribute to risk. There is evidence that aggression or conduct disorder in children with ADHD indexes higher genetic loading and clinical severity. The authors examine whether common genetic variants considered en masse as polygenic scores for ADHD are especially enriched in children with comorbid conduct disorder.

    Method: Polygenic scores derived from an ADHD GWAS meta-analysis were calculated in an independent ADHD sample (452 case subjects, 5,081 comparison subjects). Multivariate logistic regression analyses were employed to compare polygenic scores in the ADHD and comparison groups and test for higher scores in ADHD case subjects with comorbid conduct disorder relative to comparison subjects and relative to those without comorbid conduct disorder. Association with symptom scores was tested using linear regression.

    Results: Polygenic risk for ADHD, derived from the meta-analysis, was higher in the independent ADHD group than in the comparison group. Polygenic score was statistically-significantly higher in ADHD case subjects with conduct disorder relative to ADHD case subjects without conduct disorder. ADHD polygenic score showed statistically-significant association with comorbid conduct disorder symptoms. This relationship was explained by the aggression items.

    Conclusions: Common genetic variation is relevant to ADHD, especially in individuals with comorbid aggression. The findings suggest that the previously published ADHD GWAS meta-analysis contains weak but true associations with common variants, support for which falls below genome-wide statistical-significance levels. The findings also highlight the fact that aggression in ADHD indexes genetic as well as clinical severity.

  • 2013-ludeke.pdf

  • ⁠, Andrew M. McIntosh, Alan Gow, Michelle Luciano, Gail Davies, David C. Liewald, Sarah E. Harris, Janie Corley, Jeremy Hall, John M. Starr, David J. Porteous, Albert Tenesa, Peter M. Visscher, Ian J. Deary (2013-05-15):

    Background: Genome-wide association studies (GWAS) have shown a polygenic component to the risk of schizophrenia. The disorder is associated with impairments in general cognitive ability that also have a substantial genetic contribution. No study has determined whether cognitive impairments can be attributed to schizophrenia’s polygenic architecture using data from GWAS.

    Methods: Members of the Lothian Birth Cohort 1936 (LBC1936, n = 937) were assessed using the Moray House Test at age 11 and with the Moray House Test and a further cognitive battery at age 70. To create polygenic risk scores for schizophrenia, we obtained data from the latest GWAS of the Psychiatric GWAS Consortium on Schizophrenia. Schizophrenia polygenic risk profile scores were calculated using information from the Psychiatric GWAS Consortium on Schizophrenia GWAS.

    Results: In LBC1936, polygenic risk for schizophrenia was negatively associated with IQ at age 70 but not at age 11. Greater polygenic risk for schizophrenia was associated with more relative decline in IQ between these ages. These findings were maintained when the results of LBC1936 were combined with that of the independent Lothian Birth Cohort 1921 (n = 517) in a meta-analysis.

    Conclusions: Increased polygenic risk of schizophrenia is associated with lower cognitive ability at age 70 and greater relative decline in general cognitive ability between the ages of 11 and 70. Common genetic variants may underlie both cognitive aging and risk of schizophrenia. [Keywords: Aging, cognition, dementia, schizophrenia]

  • 2013-parkes.pdf

  • 2013-pettersson.pdf

  • ⁠, Frances Rice, Gema Lewis, Gordon T. Harold, Anita Thapar (2013-02-11):


    Parental depression is associated with disruptions in the parent–child relationship, exposure to stressful family life events, and offspring depressive symptoms. Evidence suggests that intergenerational transmission of depression involves environmental and inherited contributions. We sought to evaluate the role of passive gene–environment correlation (rGE) in relation to depression, family life events that were due to parental behavior, and parental positivity in a sample where children varied in genetic relatedness to their rearing parents. Our study included 865 families with children born through assisted conception (444 related to both parents, 210 related to the mother only, 175 related to the father only, and 36 related to neither parent). Consistent with previous studies, the intergenerational transmission of depressive symptoms was largely due to environmental factors, although parent and child gender influenced results. Maternal and paternal depressive symptoms were associated with reduced positivity and increased parentally imposed life events regardless of parent–child relatedness. Results of path analysis were consistent with passive rGE for both maternal and paternal positivity in that positivity partially mediated the link between maternal/paternal depression and child depression only in genetically related parent–child pairs. Results also suggested passive rGE involving parentally imposed life events for mothers and fathers although passive rGE effects were smaller than for positivity.

  • 2014-connolly.pdf

  • 2014-klahr.pdf

  • 2014-mosing.pdf

  • 2014-sariaslan-1.pdf

  • ⁠, Amir Sariaslan, Henrik Larsson, Brian D’Onofrio, Niklas Långström, Seena Fazel, Paul Lichtenstein (2014-07-22):

    People living in densely populated and socially disorganized areas have higher rates of psychiatric morbidity, but the potential causal status of such factors is uncertain. We used nationwide Swedish longitudinal registry data to identify all children born 1967–1989 (n = 2361585), including separate datasets for all cousins (n = 1 715 059) and siblings (n = 1667 894). The nature of the associations between population density and neighborhood deprivation and individual risk for a schizophrenia diagnosis was investigated while adjusting for unobserved familial risk factors (through cousin and sibling comparisons) and then compared with similar associations for depression. We generated familial pedigree structures using the Multi-Generation Registry and identified study participants with schizophrenia and depression using the National Patient Registry. Fixed-effects logistic regression models were used to study within-family estimates. Population density, measured as ln(population size/km2), at age 15 predicted subsequent schizophrenia in the population (OR = 1.10; 95% CI: 1.09; 1.11). Unobserved familial risk factors shared by cousins within extended families attenuated the association (1.06; 1.03; 1.10), and the link disappeared entirely within nuclear families (1.02; 0.97; 1.08). Similar results were found for neighborhood deprivation as predictor and for depression as outcome. Sensitivity tests demonstrated that timing and accumulation effects of the exposures (mean scores across birth, ages 1–5, 6–10, and 11–15 years) did not alter the findings. Excess risks of psychiatric morbidity, particularly schizophrenia, in densely populated and socioeconomically deprived Swedish neighborhoods appear, therefore, to result primarily from unobserved familial selection factors. Previous studies may have overemphasized the etiological importance of these environmental factors.

  • 2014-toro.pdf

  • 2014-turkheimer.pdf

  • 2015-agerbo.pdf

  • 2015-he.pdf

  • 2015-krapohl.pdf

  • 2015-pettersson.pdf

  • ⁠, Robert A. Power, Stacy Steinberg, Gyda Bjornsdottir, Cornelius A. Rietveld, Abdel Abdellaoui, Michel M. Nivard, Magnus Johannesson, Tessel E. Galesloot, Jouke J. Hottenga, Gonneke Willemsen, David Cesarini, Daniel J. Benjamin, Patrik K. E Magnusson, Fredrik Ullén, Henning Tiemeier, Albert Hofman, Frank J. A van Rooij, G. Bragi Walters, Engilbert Sigurdsson, Thorgeir E. Thorgeirsson, Andres Ingason, Agnar Helgason, Augustine Kong, Lambertus A. Kiemeney, Philipp Koellinger, Dorret I. Boomsma, Daniel Gudbjartsson, Hreinn Stefansson & Kari Stefansson (2015-06-08):

    We tested whether polygenic risk scores for schizophrenia and bipolar disorder would predict creativity. Higher scores were associated with artistic society membership or creative profession in both Icelandic (p = 5.2 × 10−6 and 3.8 × 10−6 for schizophrenia and bipolar disorder scores, respectively) and replication cohorts (p = 0.0021 and 0.00086). This could not be accounted for by increased relatedness between creative individuals and those with psychoses, indicating that creativity and psychosis share genetic roots.

  • 2015-zhu.pdf

  • 2016-adams.pdf

  • ⁠, Nicola Barban, Rick Jansen, Ronald de Vlaming, Ahmad Vaez, Jornt J. Mandemakers, Felix C. Tropf, Xia Shen, James F. Wilson, Daniel I. Chasman, Ilja M. Nolte, Vinicius Tragante, Sander W. van der Laan, John R. B. Perry, Augustine Kong, BIOS Consortium, Tarunveer S. Ahluwalia, Eva Albrecht, Laura YergesArmstrong, Gil Atzmon, Kirsi Auro, Kristin Ayers, Andrew Bakshi, Danny BenAvraham, Klaus Berger, Aviv Bergman, Lars Bertram, Lawrence F. Bielak, Gyda Bjornsdottir, Marc Jan Bonder, Linda Broer, Minh Bui, Caterina Barbieri, Alana Cavadino, Jorge E. Chavarro, Constance Turman, Maria Pina Concas, Heather J. Cordell, Gail Davies, Peter Eibich, Nicholas Eriksson, Tõnu Esko, Joel Eriksson, Fahimeh Falahi, Janine F. Felix, Mark Alan Fontana, Lude Franke, Ilaria Gandin, Audrey J. Gaskins, Christian Gieger, Erica P. Gunderson, Xiuqing Guo, Caroline Hayward, Chunyan He, Edith Hofer, Hongyan Huang, Peter K. Joshi, Stavroula Kanoni, Robert Karlsson, Stefan Kiechl, Annette Kifley, Alexander Kluttig, Peter Kraft, Vasiliki Lagou, Cecile Lecoeur, Jari Lahti, Ruifang LiGao, Penelope A. Lind, Tian Liu, Enes Makalic, Crysovalanto Mamasoula, Lindsay Matteson, Hamdi Mbarek, Patrick F. McArdle, George McMahon, S. Fleur W. Meddens, Evelin Mihailov, Mike Miller, Stacey A. Missmer, Claire Monnereau, Peter J. van der Most, Ronny Myhre, Mike A. Nalls, Teresa Nutile, Ioanna Panagiota Kalafati, Eleonora Porcu, Inga Prokopenko, Kumar B. Rajan, Janet RichEdwards, Cornelius A. Rietveld, Antonietta Robino, Lynda M. Rose, Rico Rueedi, Kathleen A. Ryan, Yasaman Saba, Daniel Schmidt, Jennifer A. Smith, Lisette Stolk, Elizabeth Streeten, Anke Tönjes, Gudmar Thorleifsson, Sheila Ulivi, Juho Wedenoja, Juergen Wellmann, Peter Willeit, Jie Yao, Loic Yengo, Jing Hua Zhao, Wei Zhao, Daria V. Zhernakova, Najaf Amin, Howard Andrews, Beverley Balkau, Nir Barzilai, Sven Bergmann, Ginevra Biino, Hans Bisgaard, Klaus Bønnelykke, Dorret I. Boomsma, Julie E. Buring, Harry Campbell, Stefania Cappellani, Marina Ciullo, Simon R. Cox, Francesco Cucca, Daniela Toniolo, George DaveySmith, Ian J. Deary, George Dedoussis, Panos Deloukas, Cornelia M. van Duijn, Eco J. C. de Geus, Johan G. Eriksson, Denis A. Evans, Jessica D. Faul, Cinzia Felicita Sala, Philippe Froguel, Paolo Gasparini, Giorgia Girotto, HansJörgen Grabe, Karin Halina Greiser, Patrick J. F. Groenen, Hugoline G. de Haan, Johannes Haerting, Tamara B. Harris, Andrew C. Heath, Kauko Heikkilä, Albert Hofman, Georg Homuth, Elizabeth G. Holliday, John Hopper, Elina Hyppönen, Bo Jacobsson, Vincent W. V. Jaddoe, Magnus Johannesson, Astanand Jugessur, Mika Kähönen, Eero Kajantie, Sharon L. R. Kardia, Bernard Keavney, Ivana Kolcic, Päivikki Koponen, Peter Kovacs, Florian Kronenberg, Zoltan Kutalik, Martina La Bianca, Genevieve Lachance, William G. Iacono, Sandra Lai, Terho Lehtimäki, David CLiewald, LifeLines Cohort Study, Cecilia M. Lindgren, Yongmei Liu, Robert Luben, Michael Lucht, Riitta Luoto, Per Magnus, Patrik K. E Magnusson, Nicholas G. Martin, Matt McGue, Ruth McQuillan, Sarah E. Medland, Christa Meisinger, Dan Mellström, Andres Metspalu, Michela Traglia, Lili Milani, Paul Mitchell, Grant W. Montgomery, Dennis MookKanamori, Renée de Mutsert, Ellen A. Nohr, Claes Ohlsson, Jørn Olsen, Ken K. Ong, Lavinia Paternoster, Alison Pattie, Brenda W. J. H. Penninx, Markus Perola, Patricia A. Peyser, Mario Pirastu, Ozren Polasek, Chris Power, Jaakko Kaprio, Leslie J. Raffel, Katri Räikkönen, Olli Raitakari, Paul M. Ridker, Susan M. Ring, Kathryn Roll, Igor Rudan, Daniela Ruggiero, Dan Rujescu, Veikko Salomaa, David Schlessinger, Helena Schmidt, Reinhold Schmidt, Nicole Schupf, Johannes Smit, Rossella Sorice, Tim D. Spector, John M. Starr, Doris Stöckl, Konstantin Strauch, Michael Stumvoll, Morris A. Swertz, Unnur Thorsteinsdottir, A. Roy Thurik, Nicholas J. Timpson, Joyce Y. Tung, André G. Uitterlinden, Simona Vaccargiu, Jorma Viikari, Veronique Vitart, Henry Völzke, Peter Vollenweider, Dragana Vuckovic, Johannes Waage, Gert G. Wagner, Jie Jin Wang, Nicholas J. Wareham, David R. Weir, Gonneke Willemsen, Johann Willeit, Alan F. Wright, Krina T. Zondervan, Kari Stefansson, Robert F. Krueger, James J. Lee, Daniel J. Benjamin, David Cesarini, Philipp D. Koellinger, Marcel den Hoed, Harold Snieder, Melinda C. Mills (2016-10-31):

    The genetic architecture of human reproductive behavior—age at first birth (AFB) and number of children ever born (NEB)—has a strong relationship with fitness, human development, infertility and risk of neuropsychiatric disorders. However, very few genetic loci have been identified, and the underlying mechanisms of AFB and NEB are poorly understood. We report a large genome-wide association study of both sexes including 251,151 individuals for AFB and 343,072 individuals for NEB. We identified 12 independent loci that are statistically-significantly associated with AFB and/or NEB in a SNP-based genome-wide association study and 4 additional loci associated in a gene-based effort. These loci harbor genes that are likely to have a role, either directly or by affecting non-local gene expression, in human reproduction and infertility, thereby increasing understanding of these complex traits.

  • ⁠, Daniel W. Belsky, Terrie E. Moffitt, David L. Corcoran, Benjamin Domingue, HonaLee Harrington, Sean Hogan, Renate Houts, Sandhya Ramrakha, Karen Sugden, Benjamin S. Williams, Richie Poulton, Avshalom Caspi (2016-06-01):

    A previous genome-wide association study (GWAS) of more than 100,000 individuals identified molecular-genetic predictors of educational attainment. We undertook in-depth life-course investigation of the polygenic score derived from this GWAS using the four-decade Dunedin Study (N = 918). There were five main findings. First, polygenic scores predicted adult economic outcomes even after accounting for educational attainments. Second, genes and environments were correlated: Children with higher polygenic scores were born into better-off homes. Third, children’s polygenic scores predicted their adult outcomes even when analyses accounted for their social-class origins; social-mobility analysis showed that children with higher polygenic scores were more upwardly mobile than children with lower scores. Fourth, polygenic scores predicted behavior across the life course, from early acquisition of speech and reading skills through geographic mobility and mate choice and on to financial planning for retirement. Fifth, polygenic-score associations were mediated by psychological characteristics, including intelligence, self-control, and interpersonal skill. Effect sizes were small. Factors connecting GWAS sequence with life outcomes may provide targets for interventions to promote population-wide positive development. [Keywords: genetics, behavior genetics, intelligence, personality, adult development]

  • 2016-benca.pdf

  • ⁠, Felix R. Day, Hannes Helgason, Daniel I. Chasman, Lynda M. Rose, Po-Ru Loh, Robert A. Scott, Agnar Helgason, Augustine Kong, Gisli Masson, Olafur Th Magnusson, Daniel Gudbjartsson, Unnur Thorsteinsdottir, Julie E. Buring, Paul M. Ridker, Patrick Sulem, Kari Stefansson, Ken K. Ong & John R. B. Perry (2016-04-18):

    The ages of puberty, first sexual intercourse and first birth signify the onset of reproductive ability, behavior and success, respectively. In a genome-wide association study of 125,667 UK Biobank participants, we identify 38 loci associated (p < 5 × 10−8) with age at first sexual intercourse. These findings were taken forward in 241,910 men and women from Iceland and 20,187 women from the Women’s Genome Health Study. Several of the identified loci also exhibit associations (p < 5 × 10−8) with other reproductive and behavioral traits, including age at first birth (variants in or near ESR1 and RBM6-SEMA3F), number of children (CADM2 and ESR1), irritable temperament (MSRA) and risk-taking propensity (CADM2). Mendelian randomization analyses infer causal influences of earlier puberty timing on earlier first sexual intercourse, earlier first birth and lower educational attainment. In turn, likely causal consequences of earlier first sexual intercourse include reproductive, educational, psychiatric and cardiometabolic outcomes.

  • 2016-gao.pdf

  • 2016-hodgson.pdf

  • 2016-horikoshi.pdf

  • 2016-hwang.pdf

  • ⁠, Craig L. Hyde, Michael W. Nagle, Chao Tian, Xing Chen, Sara A. Paciga, Jens R. Wendland, Joyce Y. Tung, David A. Hinds, Roy H. Perlis, Ashley R. Winslow (2016-08-01):

    Despite strong evidence supporting the heritability of major depressive disorder (MDD), previous genome-wide studies were unable to identify risk loci among individuals of European descent. We used self-report data from 75,607 individuals reporting clinical diagnosis of depression and 231,747 individuals reporting no history of depression through 23andMe and carried out meta-analysis of these results with published MDD genome-wide association study results. We identified five independent variants from four regions associated with self-report of clinical diagnosis or treatment for depression. Loci with a p value <1.0 × 10−5 in the meta-analysis were further analyzed in a replication data set (45,773 cases and 106,354 controls) from 23andMe. A total of 17 independent SNPs from 15 regions reached genome-wide statistical-significance after joint analysis over all three data sets. Some of these loci were also implicated in genome-wide association studies of related psychiatric traits. These studies provide evidence for large-scale consumer genomic data as a powerful and efficient complement to data collected from traditional means of ascertainment for neuropsychiatric disease genomics.

  • ⁠, Sira Karvinen (2016-04-22):

    Obesity and metabolic disorders have become a notable world-wide epidemic. The pathogenesis of metabolic diseases, such as metabolic syndrome and type 2 diabetes, has begun to negatively affect life expectancy of current generations. Low aerobic capacity has shown to be a strong predictor of mortality both in rodents and humans. Exercise is known to increase an individual’s aerobic capacity; interestingly, recent studies have suggested that genetic background may play a substantial role in the physical activity level of an individual. The purpose of this study was to investigate the role of genetic background and physical activity on skeletal muscle properties, metabolism and lifespan.

    The study consisted of three parts:

    1. a cross-sectional voluntary running intervention in high-capacity runner (HCR) and low-capacity runner (LCR) rats,
    2. a longitudinal voluntary running intervention in HCR and LCR rats, and
    3. a long-term follow-up study with physical activity discordant human twins.

    Our study showed that low intrinsic aerobic capacity is associated with fast muscular fatigue and slow metabolic recovery after maximal muscle contractions. At the whole-body level, low intrinsic aerobic capacity was linked to low body temperature, which may play a role in the onset of gaining extra weight and, thus, developing metabolic disorders. High intrinsic aerobic capacity in turn was associated with elevated SIRT3 protein level in skeletal muscle, which is possibly linked to increased lifespan. Nevertheless, vigorous physical activity commenced at adult age did not reduce mortality or increase lifespan in rodents. High long-term participation in vigorous leisure-time physical activity did predict statistically-significantly reduced mortality in dizygotic twins; however, there was no difference in the lifespan of monozygotic twins that are genetically identical. HCRs were more physically active both in control and voluntary running groups when compared to corresponding LCR groups. Also, the persistent discordances in participation of vigorous physical activity were statistically-significantly more common in dizygotic twin pairs than in monozygotic pairs stating that genes have an influence on the persistent voluntary participation in vigorous leisure-time physical activity.

    Our results indicated that genetic predisposition plays a substantial role in exercise participation, hence, genetic pleiotropy may partly explain the associations observed previously between high physical activity and mortality.

    1. Torvinen et al 2012,
    2. Karvinen et al 2012,
    3. Karvinen et al 2016, “Effects of intrinsic aerobic capacity, aging and voluntary running on skeletal muscle sirtuins and heat shock proteins”
    4. Karvinen et al 2016,
  • 2016-kendall.pdf

  • 2016-lee.pdf

  • 2016-lo.pdf

  • 2016-lonnberg.pdf

  • 2016-mosing.pdf

  • 2016-neumann.pdf

  • 2016-oconnor.pdf

  • 2016-okbay.pdf

  • ⁠, Sven Oskarsson, Peter Thisted Dinesen, Christopher T. Dawes, Magnus Johannesson, Patrik K. E. Magnusson (2016-04-27):

    One of the clearest results in previous studies on social trust is the robust positive relationship with educational attainment. The most common interpretation is that education has a causal effect on social trust. The theoretical argument and empirical results in this article suggest a different interpretation. We argue that common pre-adult factors such as cognitive abilities and personality traits rooted in genes and early-life family environment may confound the relationship between educational attainment and social trust. We provide new evidence on this question by utilizing the quasi-experiment of twinning. By looking at the relationship between education and social trust within monozygotic (MZ) twin pairs, we are able to avoid potential confounders rooted in genetic factors and common environmental influences because the monozygotic twins share both. The results suggest that when controlling for such familial factors the estimated effects of education on social trust are close to zero and far from reaching statistical-significance. Further analyses show that the relationship between education and social trust largely is driven by common genetic factors.

  • 2016-pasaniuc.pdf

  • 2016-pickrell.pdf

  • 2016-rees.pdf

  • 2016-riglin.pdf

  • 2016-rimfeld.pdf

  • 2016-robinson.pdf

  • 2016-salvatore.pdf

  • 2016-shen.pdf

  • ⁠, D J. Smith, V. Escott-Price, G. Davies, M. E S. Bailey, L. Colodro-Conde, J. Ward, A. Vedernikov, R. Marioni, B. Cullen, D. Lyall, S. P Hagenaars, D. C M. Liewald, M. Luciano, C. R Gale, S. J Ritchie, C. Hayward, B. Nicholl, B. Bulik-Sullivan, M. Adams, B. Couvy-Duchesne, N. Graham, D. Mackay, J. Evans, B. H Smith, D. J Porteous, S. E Medland, N. G Martin, P. Holmans, A. M McIntosh, J. P Pell, I. J Deary, M. C O'Donovan, (2016):

    Neuroticism is a personality trait of fundamental importance for psychological well-being and public health. It is strongly associated with major depressive disorder (MDD) and several other psychiatric conditions. Although neuroticism is heritable, attempts to identify the alleles involved in previous studies have been limited by relatively small sample sizes. Here we report a combined meta-analysis of genome-wide association study (GWAS) of neuroticism that includes 91 370 participants from the UK Biobank cohort, 6659 participants from the Generation Scotland: Scottish Family Health Study (GS:SFHS) and 8687 participants from a QIMR (Queensland Institute of Medical Research) Berghofer Medical Research Institute (QIMR) cohort. All participants were assessed using the same neuroticism instrument, the Eysenck Personality Questionnaire-Revised (EPQ-R-S) Short Form’s Neuroticism scale. We found a single-nucleotide polymorphism-based heritability estimate for neuroticism of ~15% (s.e. = 0.7%). Meta-analysis identified nine novel loci associated with neuroticism. The strongest evidence for association was at a locus on chromosome 8 (P = 1.5 × 10−15) spanning 4 Mb and containing at least 36 genes. Other associated loci included interesting candidate genes on chromosome 1 (GRIK3 (glutamate receptor ionotropic kainate 3)), chromosome 4 (KLHL2 (Kelch-like protein 2)), chromosome 17 (CRHR1 (corticotropin-releasing hormone receptor 1) and MAPT (microtubule-associated protein Tau)) and on chromosome 18 (CELF4 (CUGBP elav-like family member 4)). We found no evidence for genetic differences in the common allelic architecture of neuroticism by sex. By comparing our findings with those of the Psychiatric Genetics Consortia, we identified a strong genetic correlation between neuroticism and MDD and a less strong but statistically-significant genetic correlation with schizophrenia, although not with bipolar disorder. Polygenic risk scores derived from the primary UK Biobank sample captured ~1% of the variance in neuroticism in the GS:SFHS and QIMR samples, although most of the genome-wide statistically-significant alleles identified within a UK Biobank-only GWAS of neuroticism were not independently replicated within these cohorts. The identification of nine novel neuroticism-associated loci will drive forward future work on the neurobiology of neuroticism and related phenotypes.

  • 2016-treur.pdf

  • 2016-tucker-drob.pdf

  • 2016-vanhulzen.pdf

  • 2016-vonberg.pdf

  • 2016-wang-2.pdf

  • 2016-wang.pdf

  • 2016-zheng-ldhub-49x49geneticcorrelation.csv

  • ⁠, Masato Akiyama, Yukinori Okada, Masahiro Kanai, Atsushi Takahashi, Yukihide Momozawa, Masashi Ikeda, Nakao Iwata, Shiro Ikegawa, Makoto Hirata, Koichi Matsuda, Motoki Iwasaki, Taiki Yamaji, Norie Sawada, Tsuyoshi Hachiya, Kozo Tanno, Atsushi Shimizu, Atsushi Hozawa, Naoko Minegishi, Shoichiro Tsugane, Masayuki Yamamoto, Michiaki Kubo Yoichiro Kamatani (2017-09-11):

    Obesity is a risk factor for a wide variety of health problems. In a genome-wide association study (GWAS) of body mass index (BMI) in Japanese people (n = 173,430), we found 85 loci statistically-significantly associated with obesity (p < 5.0 × 10−8), of which 51 were previously unknown. We conducted trans-ancestral meta-analyses by integrating these results with the results from a GWAS of Europeans and identified 61 additional new loci. In total, this study identifies 112 novel loci, doubling the number of previously known BMI-associated loci. By annotating associated variants with cell-type-specific regulatory marks, we found enrichment of variants in CD19+ cells. We also found statistically-significant genetic correlations between BMI and lymphocyte count (p = 6.46 × 10−5, rg = 0.18) and between BMI and multiple complex diseases. These findings provide genetic evidence that lymphocytes are relevant to body weight regulation and offer insights into the pathogenesis of obesity.

  • 2017-allardyce.pdf

  • 2017-aschard.pdf

  • 2017-bidwell.pdf

  • 2017-brikell.pdf

  • 2017-cesta.pdf

  • 2017-chester.pdf

  • 2017-cole-tables3.pdf

  • 2017-cole-tables4.pdf

  • 2017-coram.pdf

  • 2017-cortes.pdf

  • 2017-gustavson.pdf

  • 2017-hammerschlag.pdf

  • 2017-jermendy.pdf

  • 2017-jorgenson.pdf

  • 2017-kemp.pdf

  • 2017-king.pdf

  • 2017-klarin.pdf

  • 2017-lau.pdf

  • 2017-li.pdf

  • 2017-mann.pdf

  • 2017-peyrot.pdf

  • 2017-robinson.pdf

  • 2017-rosenstrom.pdf

  • 2017-rydell.pdf

  • 2017-schwartz.pdf

  • 2017-smeland.pdf

  • 2017-smoller.pdf

  • 2017-stein.pdf

  • 2017-tieman.pdf

  • 2017-tropf.pdf

  • 2017-veatch.pdf

  • 2017-verhulst.pdf

  • 2017-wang.pdf

  • ⁠, Yilan Xu, Daniel A. Briley, Jeffrey R. Brown, William G. Karnes, Brent W. Roberts (2017-01-08):

    Heterogeneity of household financial outcomes emerges from various individual and environmental factors, including personality, cognitive ability, and socioeconomic status (SES), among others. Using a genetically informative data set, we decompose the variation in financial management behavior into genetic, shared environmental and non-shared environmental factors. We find that about half of the variation in financial distress is genetically influenced, and personality and cognitive ability are associated with financial distress through genetic and within-family pathways. Moreover, the genetic influences of financial distress are highest at the extremes of SES, which in part can be explained by neuroticism and cognitive ability being more important predictors of financial distress at low and high levels of SES, respectively.

  • 2017-zhao.pdf

  • ⁠, Mona Ayoub, Daniel A. Briley, Andrew Grotzinger, Megan W. Patterson, Laura E. Engelhardt, Jennifer L. Tackett, K. Paige Harden,, Elliot M. Tucker-Drob (2018):

    Parenting is often conceptualized in terms of its effects on offspring. However, children may also play an active role in influencing the parenting they receive. Simple correlations between parenting and child outcomes may be due to parent-to-child causation, child-to-parent causation, or some combination of the two. We use a multirater, genetically informative, large sample (n = 1,411 twin sets) to gain traction on this issue as it relates to parental warmth and stress in the context of child Big Five personality. Considerable variance in parental warmth (27%) and stress (45%) was attributable to child genetic influences on parenting. Incorporating child Big Five personality into the model roughly explained half of this variance. This result is consistent with the hypothesis that parents mold their parenting in response to their child’s personality. Residual heritability of parenting is likely due to child characteristics beyond the Big Five.

  • ⁠, Danielle L. Boisvert, Eric J. Connolly, Jamie C. Vaske, Todd A. Armstrong,, Brian B. Boutwell (2018):

    During adolescence, many teens begin to experiment with substances and engage in delinquent behavior. The current study seeks to examine whether and to what extent genetic and environmental factors contribute to the association between substance use (i.e., marijuana and alcohol) and different forms of delinquent offending (i.e., violent and nonviolent) across males and females. Analyses were based on same-sex twins (n = 1,072) from the sibling subsample of the National Longitudinal Study of Adolescent to Adult Health (Add Health). The results revealed moderate to large genetic overlap between substance use and delinquent behavior for males. Much of the covariation between alcohol use and offending behavior for females was attributable to common environmental factors, while common genetic factors explained a large portion of the overlap between marijuana use and offending in males and females. The implications of these findings for sex differences in prevention and intervention efforts are discussed from a biosocial perspective.

  • 2018-colodroconde.pdf

  • 2018-domingue.pdf

  • 2018-gotby.pdf

  • 2018-gustavson.pdf

  • 2018-khramtsova.pdf

  • ⁠, Richard H. Lewis, Eric J. Connolly, Danielle L. Boisvert, Brian B. Boutwell (2018):

    A developed line of research has found that psychopathic personality traits and criminal behavior are correlated with one another. Although there is little question about the association between psychopathic personality traits and criminal behavior, what remains less clear is whether psychopathic traits exert a direct effect on criminal behavior. An alternative possibility is that previously unmeasured genetic and shared environmental factors account for much of the association between the two. Understanding the extent to which genetic and environmental factors influence the covariance between psychopathic personality traits and criminal behavior can further our understanding of individual differences in propensity to engage in antisocial behavior. The current study analyzes 872 twins (MZ twins = 352, DZ twins = 520) from the National Longitudinal Study of Adolescent to Adult Health (Add Health) to examine the magnitude of genetic and environmental effects on the covariation between psychopathic personality and criminal behavior. Results from bivariate behavioral genetic analyses revealed that the correlation between psychopathic personality traits and criminal behavior was accounted for by common additive genetic (58%) and nonshared environmental (42%) influences. Fixed-effect linear regression models, however, suggested that psychopathic personality traits were not statistically-significantly associated with criminal behavior once common genetic and environmental influences were taken into account.

  • 2018-magnusson.pdf

  • 2018-malanchini.pdf

  • ⁠, Joseph L. Nedelec, Ian A. Silver (2018):

    A key assumption underlying various components of criminological thought is the criminogenic effect of involvement with the criminal justice system. Prior assessments of this effect, however, have been mixed and all are subject to potential genetic confounding. In the current study, we employ twin difference scores using both monozygotic and dizygotic twins to isolate the effect of involvement with the criminal justice system on future criminal behavior. The findings illustrate null associations between a variety of interactions of the criminal justice system and subsequent criminal offending. The study illustrates the continued ineffectiveness of the standard social science methodological approach to assessing criminology’s main assumptions.

  • 2018-ni.pdf

  • 2018-pasman.pdf

  • 2018-patterson.pdf

  • 2018-pingault.pdf

  • 2018-razaz.pdf

  • 2018-ronald.pdf

  • 2018-south.pdf

  • 2018-teeuw.pdf

  • ⁠, Patrick Turley, Raymond K. Walters, Omeed Maghzian, Aysu Okbay, James J. Lee, Mark Alan Fontana, Tuan Anh Nguyen-Viet, Robbee Wedow, Meghan Zacher, Nicholas A. Furlotte, 23andMe Research Team, Social Science Genetic Association Consortium, Patrik Magnusson, Sven Oskarsson, Magnus Johannesson, Peter M. Visscher, David Laibson, David Cesarini, Benjamin M. Neale, Daniel J. Benjamin (2017-10-23):

    We introduce multi-trait analysis of GWAS (MTAG), a method for joint analysis of summary statistics from genome-wide association studies (GWAS) of different traits, possibly from overlapping samples. We apply MTAG to summary statistics for depressive symptoms (Neff = 354,862), neuroticism (n = 168,105), and subjective well-being (n = 388,538). As compared to the 32, 9, and 13 genome-wide statistically-significant loci identified in the single-trait GWAS (most of which are themselves novel), MTAG increases the number of associated loci to 64, 37, and 49, respectively. Moreover, association statistics from MTAG yield more informative bioinformatics analyses and increase the variance explained by polygenic scores by approximately 25%, matching theoretical expectations.

  • 2018-verbanck.pdf

  • 2018-walters.pdf

  • ⁠, Aaron C. Weinschenk, Christopher T. Dawes (2018):

    Political scientists have long been interested in the determinants of political knowledge. In many studies, education is the strongest predictor of political knowledge. However, some studies have found that education has no effect on knowledge once confounding variables are taken into account. In addition, some recent work suggests that education remains the strongest predictor of knowledge even after accounting for confounders like personality traits and intelligence. We provide new evidence on the effect of education on political knowledge by utilizing the co-twin control design. By looking at the relationship between education and knowledge within monozygotic twin pairs, we are able to circumvent sources of confounding of the relationship due to genetic factors and early-life family environment because monozygotic twins share both. We find that the relationship between education and political knowledge is highly confounded by genes and/or familial environment. The results from a naive model that does not take into account unobserved family factors indicate that education has a positive and statistically-significant effect on political knowledge. However, in a twin fixed-effects model that accounts for confounding due to genetic factors and familial socialization, we find that the effect of education on political knowledge drops substantially and is not statistically-significant at conventional levels.

  • 2018-wiklund.pdf

  • 2018-yilmaz.pdf

  • 2018-zanetti.pdf

  • 2019-baselmans.pdf

  • 2019-belsky-2.pdf

  • 2019-conroybeam.pdf

  • ⁠, Malin Ericsson, Nancy L. Pedersen, Anna L. V Johansson, Stefan Fors, Anna K. Dahl Aslan (2019):

    Background: Despite advances in life expectancy, low socioeconomic status is associated with a shorter lifespan. This study was conducted to investigate socioeconomic differences in mortality by comparing preventable with non-preventable causes of death in 39 506 participants from the Swedish Twin Registry born before 1935.

    Methods: Childhood social class, own education, own social class and social mobility were used as separate indicators of socioeconomic status. These data were linked to the Swedish Cause of Death Register. Cause of death was categorized as preventable or non-preventable mortality according to indicators presented in the Avoidable Mortality in the European Union (AMIEHS) atlas. Using Cox proportional hazard models, we tested the association between the socioeconomic measures and all-cause mortality, preventable mortality and non-preventable mortality. Additional co-twin control analyses indicated whether the associations reflected genetic confounding.

    Results: The social gradient for mortality was most prominent for the adult socioeconomic measures. There was a social gradient in both preventable mortality and non-preventable mortality, but with an indication of a moderately stronger effect in preventable causes of death. In analyses of social mobility, those who experienced life-time low socioeconomic status (SES) or downward social mobility had an increased mortality risk compared with those with life-time high SES and upward social mobility. Adjustments for genetic confounding did not change the observed associations for education, social class or social mobility and mortality. In the co-twin control analyses of reared-apart twins, the association between childhood social class and mortality weakened, indicating possible genetic influences on this association.

    Conclusions: Our results indicate that there is an association between low adult socioeconomic status and increased mortality independent of genetic endowment. Thus, we do not find support for indirect social selection as the basis for mortality inequalities in Sweden. [Keywords: mortality, socioeconomic status, social mobility, social gradient, social selection, co-twin control]

    Key Messages:

    • Mortality followed a social gradient with higher mortality for lower socioeconomic groups, independent of preventability, in a large Swedish twin study linked to register-based mortality data.
    • There was a similar gradient in both preventable and non-preventable mortality, with an indication of a moderately stronger effect in preventable causes of death, and the adult socioeconomic indicator was more important compared with the childhood measure.
    • The impact of socioeconomic factors was stronger in premature mortality (<70 years of age), but the social gradient was present also in late-life mortality.
    • Familial confounding could not explain the observed associations between adult socioeconomic circumstances and mortality inequalities, indicating that socioeconomic status in itself may have an effect on mortality.
  • 2019-gurdasani.pdf

  • 2019-harden.pdf

  • 2019-heiland.pdf

  • 2019-hufer.pdf

  • ⁠, Christian Kandler, Trine Waaktaar, René Mõttus, Rainer Riemann, Svenn Torgersen, Cornelia Wrzus (2019):

    In two studies, we examined the genetic and environmental sources of the unfolding of personality trait differences from childhood to emerging adulthood. Using self–reports from over 3000 representative German twin pairs of three birth cohorts, we could replicate previous findings on the primary role of genetic sources accounting for the unfolding of inter–individual differences in personality traits and stabilizing trait differences during adolescence. More specifically, the genetic variance increased between early (ages 10–12 years) and late (ages 16–18 years) adolescence and stabilized between late adolescence and young adulthood (ages 21–25 years). This trend could be confirmed in a second three–wave longitudinal study of adolescents’ personality self–reports and parent ratings from about 1400 Norwegian twin families (average ages between 15 and 20 years). Moreover, the longitudinal study provided evidence for increasing genetic differences being primarily due to accumulation of novel genetic influences instead of an amplification of initial genetic variation. This is in line with cumulative interaction effects between twins’ correlated genetic makeups and environmental circumstances shared by adolescent twins reared together. In other words, nature × nurture interactions rather than transactions can account for increases in genetic variance and thus personality variance during adolescence. © 2019 European Association of Personality Psychology

  • 2019-karlsson.pdf

  • 2019-kim.pdf

  • ⁠, Rachel A. Knoblach, Joseph A. Schwartz, Marianna McBride,, Kevin M. Beaver (2019):

    An extensive body of research has examined the role that genetic influences play in the development of antisocial behavior. Even so, there remains much that is unknown regarding the intersections among antisocial behavior, environments, and genetic influences. The current study is designed to shed some light on this issue by examining whether gene–environment correlations are present in the lives of adopted adolescents. More specifically, this article seeks to contribute to scholarship efforts aimed at understanding whether biological parents’ antisocial behavioral phenotypes—behaviors often attributed to an increased likelihood of receiving a genetic propensity for antisocial behaviors—predict variation in environments that are experienced by their adopted-away offspring. To do so, the biological parents of adoptees were assessed and used to identify ways in which children elicit certain responses from their adoptive parents based, in part, on their genotype. Correlational analyses were calculated on a sample of adoptees (the final analytic sample ranged between n = 229 and n = 293) drawn from the National Longitudinal Study of Adolescent to Adult Health (Add Health). The results of the study revealed very little evidence of gene–environment correlations. The implications of these findings are considered.

  • 2019-liu.pdf

  • ⁠, Cross-Disorder Group of the Psychiatric Genomics Consortium (PGC) (2019-12-12):

    • Three groups of highly genetically-related disorders among 8 psychiatric disorders
    • Identified 109 pleiotropic loci affecting more than one disorder
    • Pleiotropic genes show heightened expression beginning in 2nd prenatal trimester
    • Pleiotropic genes play prominent roles in neurodevelopmental processes

    Genetic influences on psychiatric disorders transcend diagnostic boundaries, suggesting substantial pleiotropy of contributing loci. However, the nature and mechanisms of these pleiotropic effects remain unclear. We performed analyses of 232,964 cases and 494,162 controls from genome-wide studies of anorexia nervosa, attention-deficit/hyperactivity disorder, autism spectrum disorder, bipolar disorder, major depression, obsessive-compulsive disorder, schizophrenia, and Tourette syndrome. Genetic correlation analyses revealed a meaningful structure within the eight disorders, identifying three groups of inter-related disorders. Meta-analysis across these eight disorders detected 109 loci associated with at least two psychiatric disorders, including 23 loci with pleiotropic effects on four or more disorders and 11 loci with antagonistic effects on multiple disorders. The pleiotropic loci are located within genes that show heightened expression in the brain throughout the lifespan, beginning prenatally in the second trimester, and play prominent roles in neurodevelopmental processes. These findings have important implications for psychiatric nosology, drug development, and risk prediction.

  • 2019-ross.pdf

  • 2019-schoeler.pdf

  • 2019-smeland.pdf

  • 2019-suzuki.pdf

  • 2019-trzaskowski.pdf

  • 2019-vanrheenen.pdf

  • 2019-watson.pdf

  • ⁠, Aaron C. Weinschenk, Christopher T. Dawes, Christian Kandler, Edward Bell, Rainer Riemann (2019):

    We investigate the link between genes, psychological traits, and political engagement using a new data set containing information on a large sample of young German twins. The TwinLife Study enables us to examine the predominant model of personality, the Big Five framework, as well as traits that fall outside the Big Five, such as cognitive ability, providing a more comprehensive understanding of the underpinnings of political engagement. Our results support previous work showing genetic overlap between some psychological traits and political engagement. More specifically, we find that cognitive ability and openness to experience are correlated with political engagement and that common genes can explain most of the relationship between these psychological traits and political engagement. Relationships between genes, psychological traits, and political engagement exist even at a fairly young age, which is an important finding given that previous work has relied heavily on older samples to study the link between genes, psychological traits, and political engagement.

  • 2019-wojcik.pdf

  • ⁠, Lene Aarøe, Vivek Appadurai, Kasper M. Hansen, Andrew J. Schork, Thomas Werge, Ole Mors, Anders D. Børglum, David M. Hougaard, Merete Nordentoft, Preben B. Mortensen, Wesley Kurt Thompson, Alfonso Buil, Esben Agerbo, Michael Bang Petersen (2020-11-09):

    Although the genetic influence on voter turnout is substantial (typically 40–50%), the underlying mechanisms remain unclear. Across the social sciences, research suggests that ‘resources for politics’ (as indexed notably by educational attainment and intelligence test performance) constitute a central cluster of factors that predict electoral participation. Educational attainment and intelligence test performance are heritable. This suggests that the genotypes that enhance these phenotypes could positively predict turnout. To test this, we conduct a genome-wide complex trait analysis of individual-level turnout. We use two samples from the Danish iPSYCH case-cohort study, including a nationally representative sample as well as a sample of individuals who are particularly vulnerable to political alienation due to psychiatric conditions (n = 13,884 and n = 33,062, respectively). Using validated individual-level turnout data from the administrative records at the polling station, genetic correlations and Mendelian randomization, we show that there is a substantial genetic overlap between voter turnout and both educational attainment and intelligence test performance.

  • ⁠, Enda M. Byrne, Zhihong Zhu, Ting Qi, Nathan G. Skene, Julien Bryois, Antonio F. Pardinas, Eli Stahl, Jordan W. Smoller, Marcella Rietschel, Michael J. Owen, James T. R. Walters, Michael C. O’Donovan, John G. McGrath, Jens Hjerling-Leffler, Patrick F. Sullivan, Michael E. Goddard, Peter M. Visscher, Jian Yang, Naomi R. Wray (2020-05-12):

    Substantial genetic liability is shared across psychiatric disorders but less is known about risk variants that are specific to a given disorder. We used multi-trait conditional and joint analysis (mtCOJO) to adjust GWAS summary statistics of one disorder for the effects of genetically correlated traits to identify putative disorder-specific SNP associations. We applied mtCOJO to summary statistics for five psychiatric disorders from the Psychiatric Genomics Consortium—schizophrenia (SCZ), bipolar disorder (BIP), major depression (MD), attention-deficit hyperactivity disorder (ADHD) and autism (AUT). Most genome-wide statistically-significant variants for these disorders had evidence of pleiotropy (i.e., impact on multiple psychiatric disorders) and hence have reduced mtCOJO conditional effect sizes. However, subsets of genome-wide statistically-significant variants had larger conditional effect sizes consistent with disorder-specific effects: 15 of 130 genome-wide statistically-significant variants for schizophrenia, 5 of 40 for major depression, 3 of 11 for ADHD and 1 of 2 for autism. We show that decreased expression of VPS29 in the brain may increase risk to SCZ only and increased expression of CSE1L is associated with SCZ and MD, but not with BIP. Likewise, decreased expression of PCDHA7 in the brain is linked to increased risk of MD but decreased risk of SCZ and BIP.

  • ⁠, Karmel W. Choi, Murray B. Stein, Kristen M. Nishimi, Tian Ge, Jonathan R.I. Coleman, Chia-Yen Chen, Andrew Ratanatharathorn, Amanda B. Zheutlin, Erin C. Dunn, 23andMe Research Team, Major Depressive Disorder Working Group of the Psychiatric Genomics Consortium, Gerome Breen, Karestan C. Koenen, Jordan W. Smoller (2020-08-14):

    Objective:: Efforts to prevent depression, the leading cause of disability worldwide, have focused on a limited number of candidate factors. Using phenotypic and genomic data from over 100,000 UK Biobank participants, the authors sought to systematically screen and validate a wide range of potential modifiable factors for depression.

    Methods:: Baseline data were extracted for 106 modifiable factors, including lifestyle (e.g., exercise, sleep, media, diet), social (e.g., support, engagement), and environmental (e.g., green space, pollution) variables. Incident depression was defined as minimal depressive symptoms at baseline and clinically-significant depression at follow-up. At-risk individuals for incident depression were identified by polygenic risk scores or by reported traumatic life events. An exposure-wide association scan was conducted to identify factors associated with incident depression in the full sample and among at-risk individuals. Two-sample Mendelian randomization was then used to validate potentially causal relationships between identified factors and depression.

    Results:: Numerous factors across social, sleep, media, dietary, and exercise-related domains were prospectively associated with depression, even among at-risk individuals. However, only a subset of factors was supported by Mendelian randomization evidence, including confiding in others (odds ratio = 0.76, 95% CI = 0.67, 0.86), television watching time (odds ratio = 1.09, 95% CI = 1.05–1.13), and daytime napping (odds ratio = 1.34, 95% CI = 1.17–1.53).

    Conclusions:: Using a two-stage approach, this study validates several actionable targets for preventing depression. It also demonstrates that not all factors associated with depression in observational research may translate into robust targets for prevention. A large-scale exposure-wide approach combined with genetically informed methods for causal inference may help prioritize strategies for multimodal prevention in psychiatry.

  • ⁠, Nathan A. Gillespie, Kenneth S. Kendler (2020-11-04):

    When evaluating efforts to reduce cannabis use as a means of preventing schizophrenia, the proportion of this association that is causal is critical. Given the high heritability of schizophrenia, we reviewed reports that relied on 4 genetic methods (Table) capable of addressing the nature of the cannabis-schizophrenia association. We evaluated 3 hypotheses: (1) it is entirely causal, (2) it is partly causal and partly confounded by genetic/familial effects and/or reverse causation, or (3) it is entirely noncausal. (We are unable to review the literature regarding short-term psychiatric effects of cannabis administration.)

    Confounding here refers to genetic risks that increase the probability of both using/misusing cannabis and schizophrenia, thereby explaining at least part of the association. In this example, reverse causality refers to a theoretical underlying mechanism in which schizophrenia liability or symptoms increase the risk of using cannabis. The first 2 methods are natural experiments, discordant relative design, and Mendelian randomization, that directly evaluate each hypothesis. The 2 other methods, linkage disequilibrium score regression (LDSR) and polygenic risks scores (PRSs), measure genetic associations, which, although less definitive, provide evidence of correlated genetic risks that undermine the plausibility of hypothesis 1.

    …As summarized in the Table, when triangulating across 4 genetically informative methods, the findings, with considerable but not complete consistency, argue against hypothesis 1. Although the number of available studies is modest, there is relatively reliable evidence across multiple methods that the cannabis-schizophrenia association stems partly from shared familial/genetic risk factors and/or reverse causation. We also have good evidence against hypothesis 3, ie, familial/genetic risk factors explaining all of the association. The 1 study that directly estimated the degree of familial confounding 4 suggests that it is substantial and accounts for more than half of the observed association. Results from LDSR and PRS methods suggest more modest degrees of confounding while raising the possibility of reverse causation. A prudent conclusion is that the observed cannabis-schizophrenia association in the general population may arise from some potential causal effect of cannabis on the risk of schizophrenia, while an appreciable proportion of the association is not causal. When based on associations observed in the population (ie, without control for confounders), claims made about the changes in risk for schizophrenia stemming from changing levels of cannabis use are very likely to be exaggerated and potentially substantially so.

  • ⁠, S. Gulsuner, D. J. Stein, E. S. Susser, G. Sibeko, A. Pretorius, T. Walsh, L. Majara, M. M. Mndini, S. G. Mqulwana, O. A. Ntola, S. Casadei, L. L. Ngqengelele, V. Korchina, C. van der Merwe, M. Malan, K. M. Fader, M. Feng, E. Willoughby, D. Muzny, A. Baldinger, H. F. Andrews, R. C. Gur, R. A. Gibbs, Z. Zingela, M. Nagdee, R. S. Ramesar, M.-C. King, J. M. McClellan (2020-01-31):

    Africa, the ancestral home of all modern humans, is the most informative continent for understanding the human genome and its contribution to complex disease. To better understand the genetics of schizophrenia, we studied the illness in the Xhosa population of South Africa, recruiting 909 cases and 917 age-matched, gender-matched, and residence-matched controls. Individuals with schizophrenia were statistically-significantly more likely than controls to harbor private, severely damaging mutations in genes that are critical to synaptic function, including neural circuitry mediated by the neurotransmitters glutamine, γ-aminobutyric acid, and dopamine. Schizophrenia is genetically highly heterogeneous, involving severe ultra-rare mutations in genes that are critical to synaptic plasticity. The depth of genetic variation in Africa revealed this relationship with a moderate sample size and informed our understanding of the genetics of schizophrenia worldwide.

  • ⁠, Huijuan Li, Chuyi Zhang, Xin Cai, Lu Wang, Fang Luo, Yina Ma, Ming Li, Xiao Xiao (2020-03-05):

    Creativity represents one of the most important and partially heritable human characteristics, yet little is known about its genetic basis. Epidemiological studies reveal associations between creativity and psychiatric disorders as well as multiple personality and behavioral traits. To test whether creativity and these disorders or traits share genetic basis, we performed genome-wide association studies (GWAS) followed by polygenic risk score (PRS) analyses. Two cohorts of Han Chinese subjects (4,834 individuals in total) aged 18–45 were recruited for creativity measurement using typical performance test. After exclusion of the outliers with statistically-significantly deviated creativity scores and low-quality genotyping results, 4,664 participants were proceeded for GWAS. We conducted PRS analyses using both the classical pruning and thresholding (P+T) method and the LDpred method. The extent of polygenic risk was estimated through linear regression adjusting for the top 3 genotyping principal components. R2 was used as a measurement of the explained variance. PRS analyses demonstrated statistically-significantly positive genetic overlap, respectively, between creativity with schizophrenia ((P+T) method: R2(max) ~ .196%, p = 0.00245; LDpred method: R2(max) ~ .226%, p = 0.00114), depression ((P+T) method: R2(max) ~ .178%, p = 0.00389; LDpred method: R2(max) ~ .093%, p = 0.03675), general risk tolerance ((P+T) method: R2(max) ~ .177%, p = 0.00399; LDpred method: R2(max) ~ .305%, p = 0.00016), and risky behaviors ((P+T) method: R2(max) ~ .187%, p = 0.00307; LDpred method: R2(max) ~ .155%, p = 0.00715). Our results suggest that human creativity is probably a polygenic trait affected by numerous variations with tiny effects. Genetic variations that predispose to psychiatric disorders and risky behaviors may underlie part of the genetic basis of creativity, confirming the epidemiological associations between creativity and these traits.

  • ⁠, Claire L. Morrison, Soo Hyun Rhee, Harry R. Smolker, Robin P. Corley, John K. Hewitt, Naomi P. Friedman (2020-09-21):

    Although stress is frequently considered an environmental factor, dependent stressful life events (SLEs)—-stressors that result from one’s actions or behaviors—-may in fact be evoked by a genetic liability. It has been suggested that dependent SLEs may be partially caused by poor executive function (EFs), higher-level cognitive abilities that enable individuals to implement goal-directed behavior. We investigated the possibility of genetic and environmental overlap between SLEs and EFs in a longitudinal twin study. We found high genetic stability in the number of dependent SLEs from age 23 to age 29, suggesting that the number of dependent stressors show persistence across time due to their genetic etiology. In addition, there was a nominally statistically-significant negative genetic correlation between a Common EF latent factor and dependent SLEs at age 23. The genetic stability of dependent SLEs and association with Common EF provides insight into how some behaviors may lead to persistent stress. [Keywords: dependent stress, independent stress, executive control, genetic correlation, behavior genetics, twins]

  • ⁠, Joseph L. Nedelec, Brian B. Boutwell, Kalliopi Theocharidou (2020-09-22):

    In societies where military service is voluntary multiple factors are likely to affect the decision to enlist. Past research has produced evidence that a handful of personality and social factors seem to predict service in the military. However, recent quantitative genetic research has illustrated that enlistment in the military appears to be partially heritable and thus past research is potentially subject to genetic confounding. To assess the extent to which genetic confounding exists, the current study examined a wide range of individual-level factors using a subsample of twins (n = 1,232) from the restricted-use version of the National Longitudinal Study of Adolescent to Adult Health. The results of a series of longitudinal twin comparison models, which control for the latent sources of influence that cluster within families (i.e., shared genetic and family factors), illustrated generally null findings. However, individuals with higher scores on measures of extraversion and the general factor of personality were more likely to enlist in the military, after correction for familial confounding. Nonetheless, the overall results suggest that familial confounding should be a methodological concern in this area of research, and future work is encouraged to employ genetically informed methodologies in assessments of predictors of military enlistment. [Keywords: military enlistment, genetic confounding, twin comparison, Add Health]

  • ⁠, Zheng Ning (2020-06-29):

    Genetic correlation is a central parameter for understanding shared genetic architecture between complex traits. By using summary statistics from genome-wide association studies (GWAS), linkage disequilibrium score regression (LDSC) was developed for unbiased estimation of genetic correlations. Although easy to use, LDSC only partially utilizes LD information. By fully accounting for LD across the genome, we develop a high-definition likelihood (HDL) method to improve precision in genetic correlation estimation. Compared to LDSC, HDL reduces the variance of genetic correlation estimates by about 60%, equivalent to a 2.5-fold increase in sample size. We apply HDL and LDSC to estimate 435 genetic correlations among 30 behavioral and disease-related phenotypes measured in the UK Biobank (UKBB). In addition to 154 statistically-significant genetic correlations observed for both methods, HDL identified another 57 statistically-significant genetic correlations, compared to only another 2 statistically-significant genetic correlations identified by LDSC. HDL brings more power to genomic analyses and better reveals the underlying connections across human complex traits.

  • ⁠, Samantha Perlstein, Rebecca Waller (2020-11-29):

    Objective: A key principle of individual differences research is that biological and environmental factors jointly influence personality and psychopathology. Genes and environments interact to influence the emergence and stability of both normal and abnormal behavior (i.e., genetic predisposition, X, is exacerbated or buffered under environmental conditions, Y, or vice versa), including by shaping the neural circuits underpinning behavior. The interplay of genes and environments is also reflected in various ways in which they are correlated (i.e., rGE). That is, the same genetic factors that give rise to personality or psychopathology also shape that person’s environment.

    Methods: In this review, we outline passive, evocative, and active rGE processes and review the findings of studies that have addressed rGE in relation to understanding individual differences in personality and psychopathology across development.

    Results: Throughout, we evaluate the question of whether it is possible, not only to differentiate the person from their problems, but also to differentiate the person from their problems and their environment.

    Conclusions: We provide recommendations for future research to model rGE and better inform our ability to study personality and psychopathology, while separating the influence of the environment.

  • ⁠, Patrick D. Quinn, Sandra M. Meier, Brian M. D'Onofrio (2020-04-02):

    In the context of continued uncertainty regarding the long-term mental health effects of prenatal exposure to maternal smoking during pregnancy, we read with great interest the recently published meta-analysis of smoking and schizophrenia by Hunter and colleagues. Although the meta-analysis found that “exposure to prenatal smoke increased the risk of schizophrenia by 29%” (p. 3), the authors noted that “familial confounding may explain some of the observed association” (p. 8). We agree with the importance of this alternative hypothesis. In fact, we were surprised that the review did not consider the results of sibling comparison studies that have directly addressed it, particularly given that the review had the opportunity to do so using data from articles included in the meta-analysis.

    …The two studies of interest represented over 60% of the weighted sample. They yielded covariate-adjusted hazard ratios of 1.33 (95% confidence interval [CI], 1.23–1.45) and 1.13 (95% CI, 1.05–1.23). However, their sibling comparison results, which were excluded from the review, were weaker and not statistically-significant (hazard ratios, 1.21 [95% CI, 0.96–1.52] and 1.09 [0.84–1.42], respectively). These results suggest that familial confounding, rather than a true casual effect, explains much of the observed associations. The weaker associations from the sibling comparisons may thus dampen enthusiasm regarding a potentially meaningful role of exposure to maternal smoking during pregnancy in offspring schizophrenia. An approximately 10%–20% relative difference in rates of what is a rare outcome would suggest that modifying maternal smoking would have only a limited impact on the incidence of offspring schizophrenia.

  • ⁠, Tom Rosenström, Fartein Ask Torvik, Eivind Ystrom, Steven H. Aggen, Nathan A. Gillespie, Robert F. Krueger, Nikolai Olavi Czajkowski, Kenneth S. Kendler, Ted Reichborn-Kjennerud (2020-06-25):

    Antisocial (ASPD) and borderline (BPD) personality disorders (PDs) are associated with increased risk for substance use. They are “specific” risk factors among PDs in that they withstand adjusting for the other PDs, whereas the reverse does not hold. Specificity is a classic sign of causation. This empirical work addresses 3 further problems that can undermine causal inferences in personality and substance-use research: hierarchical nature of etiologic factors in psychiatry, imperfectly operationalized PD criteria, and possible genetic or environmental confounding, as seen in lack of “etiologic continuity.” We used exploratory structural equation bifactor modeling and biometric models to mitigate these problems. The participants were Norwegian adult twins of ages 19–36 years (n = 2,801). Criteria for Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM–5), PDs were assessed using a structured interview. General substance-use risk was indicated by World Health Organization Composite International Diagnostic Interviewed alcohol use disorder and illicit drug use, and by self-reported regular smoking. A general risk factor for all criteria of both ASPD and BPD was the strongest individual correlate of general substance use and showed etiologic continuity, though just 3 specific PD criteria could predict substance use to the same extent. The findings indicate that a broad latent factor for both ASPD and BPD may be a specific and a genetically and environmentally unconfounded risk factor for substance use. Substance-use treatment research might benefit from attending to transdiagnostic models of ASPD, BPD, and related behavioral disinhibition.

  • 2020-ruish.pdf

  • 2020-sakaue.pdf

  • ⁠, Theresia M. Schnurr, Bente M. Stallknecht, Thorkild I.A. Sørensen, Tuomas O. Kilpeläinen, Torben Hansen (2020-12-22):

    Observational, cross-sectional and longitudinal studies showed that physical activity and sedentary behaviour are associated with adiposity-related traits, apparently in a bidirectional manner. Physical activity is also suggested to suppress the genetic risk of adiposity.

    Since phenotypic associations with genetic variants are not subject to reverse causation or confounding, they may be used as tools to shed light on cause and effect in this complex interdependency. We review the evidence for shared genetics of physical activity and adiposity-related traits and for gene-by-physical activity interactions on adiposity-related traits in human studies. We outline limitations, challenges and opportunities in studying and understanding of these relationships.

    In summary, physical activity and sedentary behaviour are genetically correlated with body mass index and fat percentage but may not be correlated with lean body mass. Mendelian randomisation analyses show that physical activity and sedentary behaviour have bidirectional relationships with adiposity. Several studies suggest that physical activity suppresses genetic risk of adiposity. No studies have yet tested whether adiposity enhances genetic predisposition to sedentariness.

    The complexity of the comprehensive causal model makes the assessment of the single or combined components challenging. Substantial progress in this field may need long-term intervention studies. [Keywords: adiposity, genetic determinants, physical activity, sedentary behaviour]

  • ⁠, Jakob Skov, Daniel Eriksson, Ralf Kuja-Halkola, Jonas Höijer, Soffia Gudbjörnsdottir, Ann-Marie Svensson, Patrik K. E. Magnusson, Jonas F. Ludvigsson, Olle Kämpe, Sophie Bensing (2020-05-01):

    Objective: Co-aggregation of autoimmune diseases is common, suggesting partly shared etiologies. Genetic factors are believed to be important, but objective measures of environmental vs heritable influences on co-aggregation are absent. With a novel approach to twin studies, we aimed at estimating heritability and genetic overlap in seven organ-specific autoimmune diseases.

    Design: Prospective twin cohort study.

    Methods: We used a cohort of 110 814 twins to examine co-aggregation and heritability of Hashimoto’s thyroiditis, atrophic gastritis, celiac disease, Graves’ disease, type 1 diabetes, vitiligo and Addison’s disease. Hazard ratios (HR) were calculated for twins developing the same or different disease as compared to their co-twin. The differences between monozygotic and dizygotic twin pairs were used to estimate the genetic influence on co-aggregation. Heritability for individual disorders was calculated using structural equational modeling adjusting for censoring and truncation of data.

    Results: Co-aggregation was more pronounced in monozygotic twins (median HR: 3.2, range: 2.2–9.2) than in dizygotic twins (median HR: 2.4, range: 1.1–10.0). Heritability was moderate for atrophic gastritis (0.38, 95% CI: 0.23–0.53) but high for all other diseases, ranging from 0.60 (95% CI: 0.49–0.71) for Graves’ disease to 0.97 (95% CI: 0.91–1.00) for Addison’s disease.

    Conclusions: Overall, co-aggregation was more pronounced in monozygotic than in dizygotic twins, suggesting that disease overlap is largely attributable to genetic factors. Co-aggregation was common, and twins faced up to a 10-fold risk of developing diseases not present in their co-twin. Our results validate and refine previous heritability estimates based on smaller twin cohorts.

  • ⁠, Yusuke Takahashi, Christopher R. Pease, Jean-Baptiste Pingault, Essi Viding (2020-05-17):

    Background: This study examined the genetic and environmental influences underlying baseline level and developmental course of callous-unemotional (CU) traits across childhood and adolescence.

    Methods: The data on 8,958 twin pairs (3,108 MZ twin pairs and 5,850 DZ twin pairs) from the Twins Early Development Study were analysed. CU traits were assessed at ages 7, 9, 12 and 16 by mothers and analysed using a biometric latent growth model.

    Results: Individual differences in the baseline level of CU traits were highly heritable (76.5%), while the heritability of the developmental course of CU traits was moderate (43.6%). The genetic influences on baseline level and developmental course of CU traits were mostly non-overlapping. Nonshared environment made a modest contribution to the baseline level of CU traits (21.7%). Nonshared environmental influences on the developmental course of CU traits were moderate (43.2%), with nearly half of them being the same as those influencing the baseline level and just over half being specific. Shared environmental effects did not contribute to systematic change across childhood and adolescence but were rather age-specific.

    Conclusions: Our findings demonstrate that rather than only being conceptualized as factors of stability, genes also play a dynamic role in explaining systematic change in CU traits. Genetic effects for the initial risk and subsequent development of CU traits are not the same. In addition to genetic factors, nonshared environmental influences play an important role in explaining why some children will increase or maintain their CU traits over time, whereas other will desist. New genetic and environmental influences with age suggest that repeated, age-tailored interventions may be required throughout development to make a lasting difference in the presentation of CU traits and associated outcomes.

  • ⁠, Hang Zhou, Julia M. Sealock, Sandra Sanchez-Roige, Toni-Kim Clarke, Daniel F. Levey, Zhongshan Cheng, Boyang Li, Renato Polimanti, Rachel L. Kember, Rachel Vickers Smith, Johan H. Thygesen, Marsha Y. Morgan, Stephen R. Atkinson, Mark R. Thursz, Mette Nyegaard, Manuel Mattheisen, Anders D. Borglum, Emma C. Johnson, Amy C. Justice, Abraham A. Palmer, Andrew McQuillin, Lea K. Davis, Howard J. Edenberg, Arpana Agrawal, Henry R. Kranzler, Joel Gelernter (2020-05-25):

    Problematic alcohol use (PAU) is a leading cause of death and disability worldwide. Although genome-wide association studies have identified PAU risk genes, the genetic architecture of this trait is not fully understood. We conducted a proxy-phenotype meta-analysis of PAU, combining alcohol use disorder and problematic drinking, in 435,563 European-ancestry individuals. We identified 29 independent risk variants, 19 of them novel. PAU was genetically correlated with 138 phenotypes, including substance use and psychiatric traits. Phenome-wide polygenic risk score analysis in an independent biobank sample (BioVU, n = 67,589) confirmed the genetic correlations between PAU and substance use and psychiatric disorders. Genetic heritability of PAU was enriched in brain and in conserved and regulatory genomic regions. Mendelian randomization suggested causal effects on liability to PAU of substance use, psychiatric status, risk-taking behavior and cognitive performance. In summary, this large PAU meta-analysis identified novel risk loci and revealed genetic relationships with numerous other traits.

  • ⁠, Zlatan Krizan, Garrett Hisler, Robert F. Krueger, Matt McGue (2021-02-01):


    • Examined genetic background and environmental experiences as reasons for ties between personality and sleep quality.
    • Among 734 twin-pairs genetic factors accounted for the majority of associations between sleep quality and traits.
    • Non-shared environmental experiences also contributed to linkages of sleep quality with some traits.
    • Genetic influences that tied traits to sleep quality were somewhat unique across traits.

    Despite consistent links between personality traits and poor sleep, little is known about genetic and environmental influences that may produce them. This study examined how much genetic background and environmental experiences contributed to phenotypic linkages between personality and subjective sleep quality.

    734 twin pairs from the Minnesota Study of Twin Aging and Development rated their sleep quality and provided personality reports. Bi-variate analyses revealed that genetic factors accounted for the majority of observed associations between subjective sleep quality and traits, but also that non-shared environmental experience played a role that varied across traits.

    The findings strongly implicate genotype in tying subjective sleep quality to personality variation, alongside non-shared environmental influences, and suggest indicate influences unique to individual traits.

  • ⁠, Lauren M. O'Reilly, Erik Pettersson, Patrick D. Quinn, E. David Klonsky, Jessie R. Baldwin, Sebastian Lundström, Henrik Larsson, Paul Lichtenstein, Brian M. D'Onofrio (2021-01-18):

    Purpose: The aim of the study was to investigate the magnitude of an independent association between bullying victimization and self-harm and suicide attempt in adolescence after adjusting for unmeasured and measured confounding factors.

    Methods: Using the Child and Adolescent Twin Study in Sweden, we examined twins born between 1994 and 1999 (n = 13,852). Twins self-reported bullying victimization at age 15 years and self-harm and suicide attempt at age 18 years. We created a factor score of 13 bullying items, on which self-harm and suicide attempt items were regressed in three models: (1) among unrelated individuals; (2) among co-twins, in which a twin exposed to more bullying was compared with his/her co-twin who was exposed to less; and (3) among co-twins while adjusting for indicators of childhood psychopathology.

    Results: Among unrelated individuals, a one standard deviation increase in bullying victimization was associated with increased odds for self-harm (odds ratio [OR], 1.29 [95% confidence interval, 1.23–1.36]) and suicide attempt (OR, 1.68 [1.53–1.85]). Among co-twins, the odds attenuated for self-harm (OR, 1.19 [1.09–1.30]) and suicide attempt (OR, 1.39 [1.17–1.66]). Finally, when accounting for childhood psychopathology, there was a 14% (1.04–1.25) and 25% (1.03–1.52) relative increase in odds of self-harm and suicide attempt, respectively.

    Conclusions: The results suggest that bullying victimization was uniquely associated with self-harm and suicide attempt over and above the confounding because of unmeasured and measured factors (i.e., familial vulnerability and pre-existing psychopathy). However, magnitudes were small, suggesting that additional interventions and screenings are needed to address suicidality apart from bullying interventions. [Keywords: bullying victimization, suicide attempt, self-harm, co-twin]