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1. GWAS Meta-Analysis of Suicide Attempt: Identification of 12 Genome-Wide Significant Loci and Implication of Genetic Risks for Specific Health Factors.

Author

Docherty, Anna, Mullins, Niamh, Ashley-Koch, Allison, Qin, Xuejun, Coleman, Jonathan, Shabalin, Andrey, Kang, JooEun, Murnyak, Balasz, Wendt, Frank, Adams, Mark, Campos, Adrian, DiBlasi, Emily, Fullerton, Janice, Kranzler, Henry, Bakian, Amanda, Monson, Eric, Rentería, Miguel, Walss-Bass, Consuelo, Andreassen, Ole, Behera, Chittaranjan, Bulik, Cynthia, Edenberg, Howard, Kessler, Ronald, Mann, J, Nurnberger, John, Pistis, Giorgio, Streit, Fabian, Ursano, Robert, Polimanti, Renato, Dennis, Michelle, Garrett, Melanie, Hair, Lauren, Harvey, Philip, Hauser, Elizabeth, Hauser, Michael, Huffman, Jennifer, Jacobson, Daniel, Madduri, Ravi, McMahon, Benjamin, Oslin, David, Trafton, Jodie, Awasthi, Swapnil, Berrettini, Wade, Bohus, Martin, Chang, Xiao, Chen, Hsi-Chung, Chen, Wei, Christensen, Erik, Crow, Scott, Duriez, Philibert, Edwards, Alexis, Fernández-Aranda, Fernando, Galfalvy, Hanga, Gandal, Michael, Gorwood, Philip, Guo, Yiran, Hafferty, Jonathan, Hakonarson, Hakon, Halmi, Katherine, Hishimoto, Akitoyo, Jain, Sonia, Jamain, Stéphane, Jiménez-Murcia, Susana, Johnson, Craig, Kaplan, Allan, Kaye, Walter, Keel, Pamela, Kennedy, James, Kim, Minsoo, Klump, Kelly, Levey, Daniel, Li, Dong, Liao, Shih-Cheng, Lieb, Klaus, Lilenfeld, Lisa, Marshall, Christian, Mitchell, James, Okazaki, Satoshi, Otsuka, Ikuo, Pinto, Dalila, Powers, Abigail, Ramoz, Nicolas, Ripke, Stephan, Roepke, Stefan, Rozanov, Vsevolod, Scherer, Stephen, Schmahl, Christian, Sokolowski, Marcus, Starnawska, Anna, Strober, Michael, Su, Mei-Hsin, Thornton, Laura, Treasure, Janet, Ware, Erin, Watson, Hunna, Witt, Stephanie, Woodside, D, Yilmaz, Zeynep, Zillich, Lea, and Adolfsson, Rolf

Subjects
Biological Markers, Depressive Disorders, Genetics, Schizophrenia Spectrum and Other Psychotic Disorders, Self-Harm, Suicide, Humans, Genome-Wide Association Study, Suicide, Attempted, Depressive Disorder, Major, Risk Factors, Suicidal Ideation, Polymorphism, Single Nucleotide, Genetic Predisposition to Disease, Genetic Loci
Abstract

OBJECTIVE: Suicidal behavior is heritable and is a major cause of death worldwide. Two large-scale genome-wide association studies (GWASs) recently discovered and cross-validated genome-wide significant (GWS) loci for suicide attempt (SA). The present study leveraged the genetic cohorts from both studies to conduct the largest GWAS meta-analysis of SA to date. Multi-ancestry and admixture-specific meta-analyses were conducted within groups of significant African, East Asian, and European ancestry admixtures. METHODS: This study comprised 22 cohorts, including 43,871 SA cases and 915,025 ancestry-matched controls. Analytical methods across multi-ancestry and individual ancestry admixtures included inverse variance-weighted fixed-effects meta-analyses, followed by gene, gene-set, tissue-set, and drug-target enrichment, as well as summary-data-based Mendelian randomization with brain expression quantitative trait loci data, phenome-wide genetic correlation, and genetic causal proportion analyses. RESULTS: Multi-ancestry and European ancestry admixture GWAS meta-analyses identified 12 risk loci at p values

Published
2023

3. Common Genetic Variation and Age of Onset of Anorexia Nervosa.

Author

Watson, Hunna J, Thornton, Laura M, Yilmaz, Zeynep, Baker, Jessica H, Coleman, Jonathan RI, Adan, Roger AH, Alfredsson, Lars, Andreassen, Ole A, Ask, Helga, Berrettini, Wade H, Boehnke, Michael, Boehm, Ilka, Boni, Claudette, Buehren, Katharina, Bulant, Josef, Burghardt, Roland, Chang, Xiao, Cichon, Sven, Cone, Roger D, Courtet, Philippe, Crow, Scott, Crowley, James J, Danner, Unna N, de Zwaan, Martina, Dedoussis, George, DeSocio, Janiece E, Dick, Danielle M, Dikeos, Dimitris, Dina, Christian, Djurovic, Srdjan, Dmitrzak-Weglarz, Monika, Docampo-Martinez, Elisa, Duriez, Philibert, Egberts, Karin, Ehrlich, Stefan, Eriksson, Johan G, Escaramís, Geòrgia, Esko, Tõnu, Estivill, Xavier, Farmer, Anne, Fernández-Aranda, Fernando, Fichter, Manfred M, Föcker, Manuel, Foretova, Lenka, Forstner, Andreas J, Frei, Oleksandr, Gallinger, Steven, Giegling, Ina, Giuranna, Johanna, Gonidakis, Fragiskos, Gorwood, Philip, Gratacòs, Mònica, Guillaume, Sébastien, Guo, Yiran, Hakonarson, Hakon, Hauser, Joanna, Havdahl, Alexandra, Hebebrand, Johannes, Helder, Sietske G, Herms, Stefan, Herpertz-Dahlmann, Beate, Herzog, Wolfgang, Hinney, Anke, Hübel, Christopher, Hudson, James I, Imgart, Hartmut, Jamain, Stephanie, Janout, Vladimir, Jiménez-Murcia, Susana, Jones, Ian R, Julià, Antonio, Kalsi, Gursharan, Kaminská, Deborah, Kaprio, Jaakko, Karhunen, Leila, Kas, Martien JH, Keel, Pamela K, Kennedy, James L, Keski-Rahkonen, Anna, Kiezebrink, Kirsty, Klareskog, Lars, Klump, Kelly L, Knudsen, Gun Peggy S, La Via, Maria C, Le Hellard, Stephanie, Leboyer, Marion, Li, Dong, Lilenfeld, Lisa, Lin, Bochao, Lissowska, Jolanta, Luykx, Jurjen, Magistretti, Pierre, Maj, Mario, Marsal, Sara, Marshall, Christian R, Mattingsdal, Morten, Meulenbelt, Ingrid, Micali, Nadia, Mitchell, Karen S, and Monteleone, Alessio Maria

Subjects
Age of onset, Anorexia nervosa, Early-onset, GWAS, Genetic risk score, Genetics, Menarche, Mendelian randomization, Puberty, Mental Health, Human Genome, Eating Disorders, Anorexia, Brain Disorders, Pediatric, Prevention, Aetiology, 2.1 Biological and endogenous factors
Abstract

BackgroundGenetics and biology may influence the age of onset of anorexia nervosa (AN). The aims of this study were to determine whether common genetic variation contributes to age of onset of AN and to investigate the genetic associations between age of onset of AN and age at menarche.MethodsA secondary analysis of the Psychiatric Genomics Consortium genome-wide association study (GWAS) of AN was performed, which included 9335 cases and 31,981 screened controls, all from European ancestries. We conducted GWASs of age of onset, early-onset AN (

Published
2022

5. Genome-wide Association Meta-analysis of Childhood and Adolescent Internalizing Symptoms

Author

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

Subjects
Biological Psychology, Psychology, Serious Mental Illness, Brain Disorders, Pediatric, Human Genome, Genetics, Behavioral and Social Science, Depression, Mental Health, Mental Illness, 2.1 Biological and endogenous factors, 2.3 Psychological, social and economic factors, Mental health, Adolescent, Adult, Aggression, Anxiety, Attention Deficit Disorder with Hyperactivity, Autistic Disorder, Bipolar Disorder, Child, Child, Preschool, Genome-Wide Association Study, Humans, Loneliness, Polymorphism, Single Nucleotide, Schizophrenia, Sleep Initiation and Maintenance Disorders, depression, anxiety, repeated measures, genetic epidemiology, molecular genetics, Medical and Health Sciences, Psychology and Cognitive Sciences, Developmental & Child Psychology, Clinical sciences, Paediatrics, Applied and developmental psychology
Abstract

ObjectiveTo investigate the genetic architecture of internalizing symptoms in childhood and adolescence.MethodIn 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.ResultsThe 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.ConclusionGenetic 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

10. Dissecting the Shared Genetic Architecture of Suicide Attempt, Psychiatric Disorders, and Known Risk Factors.

Author

Mullins, Niamh, Kang, JooEun, Campos, Adrian I, Coleman, Jonathan RI, Edwards, Alexis C, Galfalvy, Hanga, Levey, Daniel F, Lori, Adriana, Shabalin, Andrey, Starnawska, Anna, Su, Mei-Hsin, Watson, Hunna J, Adams, Mark, Awasthi, Swapnil, Gandal, Michael, Hafferty, Jonathan D, Hishimoto, Akitoyo, Kim, Minsoo, Okazaki, Satoshi, Otsuka, Ikuo, Ripke, Stephan, Ware, Erin B, Bergen, Andrew W, Berrettini, Wade H, Bohus, Martin, Brandt, Harry, Chang, Xiao, Chen, Wei J, Chen, Hsi-Chung, Crawford, Steven, Crow, Scott, DiBlasi, Emily, Duriez, Philibert, Fernández-Aranda, Fernando, Fichter, Manfred M, Gallinger, Steven, Glatt, Stephen J, Gorwood, Philip, Guo, Yiran, Hakonarson, Hakon, Halmi, Katherine A, Hwu, Hai-Gwo, Jain, Sonia, Jamain, Stéphane, Jiménez-Murcia, Susana, Johnson, Craig, Kaplan, Allan S, Kaye, Walter H, Keel, Pamela K, Kennedy, James L, Klump, Kelly L, Li, Dong, Liao, Shih-Cheng, Lieb, Klaus, Lilenfeld, Lisa, Liu, Chih-Min, Magistretti, Pierre J, Marshall, Christian R, Mitchell, James E, Monson, Eric T, Myers, Richard M, Pinto, Dalila, Powers, Abigail, Ramoz, Nicolas, Roepke, Stefan, Rozanov, Vsevolod, Scherer, Stephen W, Schmahl, Christian, Sokolowski, Marcus, Strober, Michael, Thornton, Laura M, Treasure, Janet, Tsuang, Ming T, Witt, Stephanie H, Woodside, D Blake, Yilmaz, Zeynep, Zillich, Lea, Adolfsson, Rolf, Agartz, Ingrid, Air, Tracy M, Alda, Martin, Alfredsson, Lars, Andreassen, Ole A, Anjorin, Adebayo, Appadurai, Vivek, Soler Artigas, María, Van der Auwera, Sandra, Azevedo, M Helena, Bass, Nicholas, Bau, Claiton HD, Baune, Bernhard T, Bellivier, Frank, Berger, Klaus, Biernacka, Joanna M, Bigdeli, Tim B, Binder, Elisabeth B, Boehnke, Michael, Boks, Marco P, Bosch, Rosa, and Braff, David L

Subjects
Major Depressive Disorder Working Group of the Psychiatric Genomics Consortium, Bipolar Disorder Working Group of the Psychiatric Genomics Consortium, Eating Disorders Working Group of the Psychiatric Genomics Consortium, German Borderline Genomics Consortium, MVP Suicide Exemplar Workgroup, VA Million Veteran Program, Humans, Risk Factors, Suicide, Attempted, Mental Disorders, Depressive Disorder, Major, Polymorphism, Single Nucleotide, Genome-Wide Association Study, Genetic correlation, Genome-wide association study, Pleiotropy, Polygenicity, Suicide, Suicide attempt, Human Genome, Behavioral and Social Science, Mental Health, Prevention, Genetics, Brain Disorders, Aetiology, 2.1 Biological and endogenous factors, Mental health, Good Health and Well Being, Biological Sciences, Medical and Health Sciences, Psychology and Cognitive Sciences, Psychiatry
Abstract

BackgroundSuicide is a leading cause of death worldwide, and nonfatal suicide attempts, which occur far more frequently, are a major source of disability and social and economic burden. Both have substantial genetic etiology, which is partially shared and partially distinct from that of related psychiatric disorders.MethodsWe conducted a genome-wide association study (GWAS) of 29,782 suicide attempt (SA) cases and 519,961 controls in the International Suicide Genetics Consortium (ISGC). The GWAS of SA was conditioned on psychiatric disorders using GWAS summary statistics via multitrait-based conditional and joint analysis, to remove genetic effects on SA mediated by psychiatric disorders. We investigated the shared and divergent genetic architectures of SA, psychiatric disorders, and other known risk factors.ResultsTwo loci reached genome-wide significance for SA: the major histocompatibility complex and an intergenic locus on chromosome 7, the latter of which remained associated with SA after conditioning on psychiatric disorders and replicated in an independent cohort from the Million Veteran Program. This locus has been implicated in risk-taking behavior, smoking, and insomnia. SA showed strong genetic correlation with psychiatric disorders, particularly major depression, and also with smoking, pain, risk-taking behavior, sleep disturbances, lower educational attainment, reproductive traits, lower socioeconomic status, and poorer general health. After conditioning on psychiatric disorders, the genetic correlations between SA and psychiatric disorders decreased, whereas those with nonpsychiatric traits remained largely unchanged.ConclusionsOur results identify a risk locus that contributes more strongly to SA than other phenotypes and suggest a shared underlying biology between SA and known risk factors that is not mediated by psychiatric disorders.

Published
2022

12. Open science practices for eating disorders research

Author

Burke, Natasha L, Frank, Guido KW, Hilbert, Anja, Hildebrandt, Thomas, Klump, Kelly L, Thomas, Jennifer J, Wade, Tracey D, Walsh, B Timothy, Wang, Shirley B, and Weissman, Ruth Striegel

Subjects
Mental Health, Feeding and Eating Disorders, Humans, clinical trial preregistration, data sharing, eating disorder, material sharing, open access, open science, registered report, replication, reproducibility, transparency, Medical and Health Sciences, Psychology and Cognitive Sciences, Clinical Psychology
Abstract

This editorial seeks to encourage the increased application of three open science practices in eating disorders research: Preregistration, Registered Reports, and the sharing of materials, data, and code. For each of these practices, we introduce updated International Journal of Eating Disorders author and reviewer guidance. Updates include the introduction of open science badges; specific instructions about how to improve transparency; and the introduction of Registered Reports of systematic or meta-analytical reviews. The editorial also seeks to encourage the study of open science practices. Open science practices pose considerable time and other resource burdens. Therefore, research is needed to help determine the value of these added burdens and to identify efficient strategies for implementing open science practices.

Published
2021

16. Shared genetic risk between eating disorder‐ and substance‐use‐related phenotypes: Evidence from genome‐wide association studies

Author

Munn‐Chernoff, Melissa A, Johnson, Emma C, Chou, Yi‐Ling, Coleman, Jonathan RI, Thornton, Laura M, Walters, Raymond K, Yilmaz, Zeynep, Baker, Jessica H, Hübel, Christopher, Gordon, Scott, Medland, Sarah E, Watson, Hunna J, Gaspar, Héléna A, Bryois, Julien, Hinney, Anke, Leppä, Virpi M, Mattheisen, Manuel, Ripke, Stephan, Yao, Shuyang, Giusti‐Rodríguez, Paola, Hanscombe, Ken B, Adan, Roger AH, Alfredsson, Lars, Ando, Tetsuya, Andreassen, Ole A, Berrettini, Wade H, Boehm, Ilka, Boni, Claudette, Perica, Vesna Boraska, Buehren, Katharina, Burghardt, Roland, Cassina, Matteo, Cichon, Sven, Clementi, Maurizio, Cone, Roger D, Courtet, Philippe, Crow, Scott, Crowley, James J, Danner, Unna N, Davis, Oliver SP, de Zwaan, Martina, Dedoussis, George, Degortes, Daniela, DeSocio, Janiece E, Dick, Danielle M, Dikeos, Dimitris, Dina, Christian, Dmitrzak‐Weglarz, Monika, Docampo, Elisa, Duncan, Laramie E, Egberts, Karin, Ehrlich, Stefan, Escaramís, Geòrgia, Esko, Tõnu, Estivill, Xavier, Farmer, Anne, Favaro, Angela, Fernández‐Aranda, Fernando, Fichter, Manfred M, Fischer, Krista, Föcker, Manuel, Foretova, Lenka, Forstner, Andreas J, Forzan, Monica, Franklin, Christopher S, Gallinger, Steven, Giegling, Ina, Giuranna, Johanna, Gonidakis, Fragiskos, Gorwood, Philip, Mayora, Monica Gratacos, Guillaume, Sébastien, Guo, Yiran, Hakonarson, Hakon, Hatzikotoulas, Konstantinos, Hauser, Joanna, Hebebrand, Johannes, Helder, Sietske G, Herms, Stefan, Herpertz‐Dahlmann, Beate, Herzog, Wolfgang, Huckins, Laura M, Hudson, James I, Imgart, Hartmut, Inoko, Hidetoshi, Janout, Vladimir, Jiménez‐Murcia, Susana, Julià, Antonio, Kalsi, Gursharan, Kaminská, Deborah, Karhunen, Leila, Karwautz, Andreas, Kas, Martien JH, Kennedy, James L, Keski‐Rahkonen, Anna, Kiezebrink, Kirsty, Kim, Youl‐Ri, Klump, Kelly L, Knudsen, Gun Peggy S, and La Via, Maria C

Subjects
Biomedical and Clinical Sciences, Biological Psychology, Epidemiology, Health Sciences, Psychology, Pharmacology and Pharmaceutical Sciences, Nutrition, Brain Disorders, Alcoholism, Alcohol Use and Health, Mental Health, Eating Disorders, Substance Misuse, Genetics, Tobacco Smoke and Health, Tobacco, Human Genome, Drug Abuse (NIDA only), Prevention, Clinical Research, 2.1 Biological and endogenous factors, 2.3 Psychological, social and economic factors, Aetiology, Mental health, Good Health and Well Being, Alcoholism, Depressive Disorder, Major, Feeding and Eating Disorders, Genome-Wide Association Study, Humans, Linkage Disequilibrium, Phenotype, Polymorphism, Single Nucleotide, Risk Factors, Schizophrenia, Substance-Related Disorders, Tobacco Use Disorder, eating disorders, genetic correlation, substance use, Medical and Health Sciences, Psychology and Cognitive Sciences, Substance Abuse, Biomedical and clinical sciences, Health sciences
Abstract

Eating disorders and substance use disorders frequently co-occur. Twin studies reveal shared genetic variance between liabilities to eating disorders and substance use, with the strongest associations between symptoms of bulimia nervosa and problem alcohol use (genetic correlation [rg ], twin-based = 0.23-0.53). We estimated the genetic correlation between eating disorder and substance use and disorder phenotypes using data from genome-wide association studies (GWAS). Four eating disorder phenotypes (anorexia nervosa [AN], AN with binge eating, AN without binge eating, and a bulimia nervosa factor score), and eight substance-use-related phenotypes (drinks per week, alcohol use disorder [AUD], smoking initiation, current smoking, cigarettes per day, nicotine dependence, cannabis initiation, and cannabis use disorder) from eight studies were included. Significant genetic correlations were adjusted for variants associated with major depressive disorder and schizophrenia. Total study sample sizes per phenotype ranged from ~2400 to ~537 000 individuals. We used linkage disequilibrium score regression to calculate single nucleotide polymorphism-based genetic correlations between eating disorder- and substance-use-related phenotypes. Significant positive genetic associations emerged between AUD and AN (rg = 0.18; false discovery rate q = 0.0006), cannabis initiation and AN (rg = 0.23; q < 0.0001), and cannabis initiation and AN with binge eating (rg = 0.27; q = 0.0016). Conversely, significant negative genetic correlations were observed between three nondiagnostic smoking phenotypes (smoking initiation, current smoking, and cigarettes per day) and AN without binge eating (rgs = -0.19 to -0.23; qs < 0.04). The genetic correlation between AUD and AN was no longer significant after co-varying for major depressive disorder loci. The patterns of association between eating disorder- and substance-use-related phenotypes highlights the potentially complex and substance-specific relationships among these behaviors.

Published
2021

19. IJED support for eating disorders research in the time of COVID‐19

Author

Weissman, Ruth S, Klump, Kelly L, Wade, Tracey, Thomas, Jennifer J, Frank, Guido, and Waller, Glenn

Subjects
Betacoronavirus, Biomedical Research, COVID-19, Coronavirus Infections, Feeding and Eating Disorders, Humans, Pandemics, Periodicals as Topic, Pneumonia, Viral, Publishing, SARS-CoV-2, coronavirus, eating disorders, registered report, scientific research, scientific review, Medical and Health Sciences, Psychology and Cognitive Sciences, Clinical Psychology
Abstract

This editorial reports on an anonymous survey question posed to eating disorders researchers about changes the International Journal of Eating Disorders (IJED) should implement to support the eating disorders research community affected by COVID-19. The editorial accompanies an IJED article that details responses to the larger survey focusing more broadly on COVID-19-related research disruptions. Survey invitations were sent to editorial board members of eating disorders journals, members of eating disorder scientific organizations (e.g., Eating Disorders Research Society), and individuals who provided at least three IJED reviews in the prior 12 months. We reviewed the responses of 187 participants and identified three categories of changes that: (a) had already been implemented by the journal, (b) cannot be implemented because they fall outside the scope of IJED, or (c) will be implemented in coming weeks or months. The latter category includes publishing topical COVID-19 papers, making some COVID-19-related content available open access, revising statistical guidelines, and issuing author guidance on reporting protocol changes caused by COVID-19-related disruptions. IJED recognizes the disruptive impacts that COVID-19 has on all activities in our field, including clinical work, teaching, and advocacy, and is committed to supporting authors during this difficult time while striving to publish high-quality research.

Published
2020

20. Genetic and environmental influences on human height from infancy through adulthood at different levels of parental education

Author

Jelenkovic, Aline, Sund, Reijo, Yokoyama, Yoshie, Latvala, Antti, Sugawara, Masumi, Tanaka, Mami, Matsumoto, Satoko, Freitas, Duarte L, Maia, José Antonio, Knafo-Noam, Ariel, Mankuta, David, Abramson, Lior, Ji, Fuling, Ning, Feng, Pang, Zengchang, Rebato, Esther, Saudino, Kimberly J, Cutler, Tessa L, Hopper, John L, Ullemar, Vilhelmina, Almqvist, Catarina, Magnusson, Patrik KE, Cozen, Wendy, Hwang, Amie E, Mack, Thomas M, Nelson, Tracy L, Whitfield, Keith E, Sung, Joohon, Kim, Jina, Lee, Jooyeon, Lee, Sooji, Llewellyn, Clare H, Fisher, Abigail, Medda, Emanuela, Nisticò, Lorenza, Toccaceli, Virgilia, Baker, Laura A, Tuvblad, Catherine, Corley, Robin P, Huibregtse, Brooke M, Derom, Catherine A, Vlietinck, Robert F, Loos, Ruth JF, Burt, S Alexandra, Klump, Kelly L, Silberg, Judy L, Maes, Hermine H, Krueger, Robert F, McGue, Matt, Pahlen, Shandell, Gatz, Margaret, Butler, David A, Harris, Jennifer R, Brandt, Ingunn, Nilsen, Thomas S, Harden, K Paige, Tucker-Drob, Elliot M, Franz, Carol E, Kremen, William S, Lyons, Michael J, Lichtenstein, Paul, Bartels, Meike, Beijsterveldt, Catharina EM van, Willemsen, Gonneke, Öncel, Sevgi Y, Aliev, Fazil, Jeong, Hoe-Uk, Hur, Yoon-Mi, Turkheimer, Eric, Boomsma, Dorret I, Sørensen, Thorkild IA, Kaprio, Jaakko, and Silventoinen, Karri

Subjects
Biological Psychology, Health Sciences, Psychology, Pediatric, Nutrition, Genetics, Prevention, 2.1 Biological and endogenous factors, Aetiology, Quality Education, Adolescent, Adult, Body Height, Child, Child, Preschool, Environment, Female, Gene-Environment Interaction, Genetic Background, Humans, Infant, Infant, Newborn, Male, Parenting, Parents, Quantitative Trait Loci, Quantitative Trait, Heritable, Young Adult
Abstract

Genetic factors explain a major proportion of human height variation, but differences in mean stature have also been found between socio-economic categories suggesting a possible effect of environment. By utilizing a classical twin design which allows decomposing the variation of height into genetic and environmental components, we tested the hypothesis that environmental variation in height is greater in offspring of lower educated parents. Twin data from 29 cohorts including 65,978 complete twin pairs with information on height at ages 1 to 69 years and on parental education were pooled allowing the analyses at different ages and in three geographic-cultural regions (Europe, North America and Australia, and East Asia). Parental education mostly showed a positive association with offspring height, with significant associations in mid-childhood and from adolescence onwards. In variance decomposition modeling, the genetic and environmental variance components of height did not show a consistent relation to parental education. A random-effects meta-regression analysis of the aggregate-level data showed a trend towards greater shared environmental variation of height in low parental education families. In conclusion, in our very large dataset from twin cohorts around the globe, these results provide only weak evidence for the study hypothesis.

Published
2020

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

Author

Silventoinen, Karri, Li, Weilong, Jelenkovic, Aline, Sund, Reijo, Yokoyama, Yoshie, Aaltonen, Sari, Piirtola, Maarit, Sugawara, Masumi, Tanaka, Mami, Matsumoto, Satoko, Baker, Laura A., Tuvblad, Catherine, Tynelius, Per, Rasmussen, Finn, Craig, Jeffrey M., Saffery, Richard, Willemsen, Gonneke, Bartels, Meike, van Beijsterveldt, Catharina E. M., Martin, Nicholas G., Medland, Sarah E., Montgomery, Grant W., Lichtenstein, Paul, Krueger, Robert F., McGue, Matt, Pahlen, Shandell, Christensen, Kaare, Skytthe, Axel, Kyvik, Kirsten O., Saudino, Kimberly J., Dubois, Lise, Boivin, Michel, Brendgen, Mara, Dionne, Ginette, Vitaro, Frank, Ullemar, Vilhelmina, Almqvist, Catarina, Magnusson, Patrik K. E., Corley, Robin P., Huibregtse, Brooke M., Knafo-Noam, Ariel, Mankuta, David, Abramson, Lior, Haworth, Claire M. A., Plomin, Robert, Bjerregaard-Andersen, Morten, Beck-Nielsen, Henning, Sodemann, Morten, Duncan, Glen E., Buchwald, Dedra, Burt, S. Alexandra, Klump, Kelly L., Llewellyn, Clare H., Fisher, Abigail, Boomsma, Dorret I., Sørensen, Thorkild I. A., and Kaprio, Jaakko

Published
2022
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23. Genome-wide association study identifies eight risk loci and implicates metabo-psychiatric origins for anorexia nervosa

Author

Watson, Hunna J, Yilmaz, Zeynep, Thornton, Laura M, Hübel, Christopher, Coleman, Jonathan RI, Gaspar, Héléna A, Bryois, Julien, Hinney, Anke, Leppä, Virpi M, Mattheisen, Manuel, Medland, Sarah E, Ripke, Stephan, Yao, Shuyang, Giusti-Rodríguez, Paola, Hanscombe, Ken B, Purves, Kirstin L, Adan, Roger AH, Alfredsson, Lars, Ando, Tetsuya, Andreassen, Ole A, Baker, Jessica H, Berrettini, Wade H, Boehm, Ilka, Boni, Claudette, Perica, Vesna Boraska, Buehren, Katharina, Burghardt, Roland, Cassina, Matteo, Cichon, Sven, Clementi, Maurizio, Cone, Roger D, Courtet, Philippe, Crow, Scott, Crowley, James J, Danner, Unna N, Davis, Oliver SP, de Zwaan, Martina, Dedoussis, George, Degortes, Daniela, DeSocio, Janiece E, Dick, Danielle M, Dikeos, Dimitris, Dina, Christian, Dmitrzak-Weglarz, Monika, Docampo, Elisa, Duncan, Laramie E, Egberts, Karin, Ehrlich, Stefan, Escaramís, Geòrgia, Esko, Tõnu, Estivill, Xavier, Farmer, Anne, Favaro, Angela, Fernández-Aranda, Fernando, Fichter, Manfred M, Fischer, Krista, Föcker, Manuel, Foretova, Lenka, Forstner, Andreas J, Forzan, Monica, Franklin, Christopher S, Gallinger, Steven, Giegling, Ina, Giuranna, Johanna, Gonidakis, Fragiskos, Gorwood, Philip, Mayora, Monica Gratacos, Guillaume, Sébastien, Guo, Yiran, Hakonarson, Hakon, Hatzikotoulas, Konstantinos, Hauser, Joanna, Hebebrand, Johannes, Helder, Sietske G, Herms, Stefan, Herpertz-Dahlmann, Beate, Herzog, Wolfgang, Huckins, Laura M, Hudson, James I, Imgart, Hartmut, Inoko, Hidetoshi, Janout, Vladimir, Jiménez-Murcia, Susana, Julià, Antonio, Kalsi, Gursharan, Kaminská, Deborah, Kaprio, Jaakko, Karhunen, Leila, Karwautz, Andreas, Kas, Martien JH, Kennedy, James L, Keski-Rahkonen, Anna, Kiezebrink, Kirsty, Kim, Youl-Ri, Klareskog, Lars, Klump, Kelly L, Knudsen, Gun Peggy S, La Via, Maria C, Le Hellard, Stephanie, and Levitan, Robert D

Subjects
Biological Sciences, Genetics, Anorexia, Serious Mental Illness, Nutrition, Prevention, Mental Health, Clinical Research, Human Genome, Brain Disorders, Pediatric, Eating Disorders, Mental health, Adult, Anorexia Nervosa, Body Mass Index, Case-Control Studies, Female, Genetic Predisposition to Disease, Genome-Wide Association Study, Genomics, Humans, Male, Mental Disorders, Metabolic Diseases, Phenotype, Prognosis, Quantitative Trait Loci, Anorexia Nervosa Genetics Initiative, Eating Disorders Working Group of the Psychiatric Genomics Consortium, Medical and Health Sciences, Developmental Biology, Agricultural biotechnology, Bioinformatics and computational biology
Abstract

Characterized primarily by a low body-mass index, anorexia nervosa is a complex and serious illness1, affecting 0.9-4% of women and 0.3% of men2-4, with twin-based heritability estimates of 50-60%5. Mortality rates are higher than those in other psychiatric disorders6, and outcomes are unacceptably poor7. Here we combine data from the Anorexia Nervosa Genetics Initiative (ANGI)8,9 and the Eating Disorders Working Group of the Psychiatric Genomics Consortium (PGC-ED) and conduct a genome-wide association study of 16,992 cases of anorexia nervosa and 55,525 controls, identifying eight significant loci. The genetic architecture of anorexia nervosa mirrors its clinical presentation, showing significant genetic correlations with psychiatric disorders, physical activity, and metabolic (including glycemic), lipid and anthropometric traits, independent of the effects of common variants associated with body-mass index. These results further encourage a reconceptualization of anorexia nervosa as a metabo-psychiatric disorder. Elucidating the metabolic component is a critical direction for future research, and paying attention to both psychiatric and metabolic components may be key to improving outcomes.

Published
2019

39. Genetic association study of childhood aggression across raters, instruments, and age

Author

Ip, Hill F., van der Laan, Camiel M., Krapohl, Eva M. L., Brikell, Isabell, Sánchez-Mora, Cristina, Nolte, Ilja M., St Pourcain, Beate, Bolhuis, Koen, Palviainen, Teemu, Zafarmand, Hadi, Colodro-Conde, Lucía, Gordon, Scott, Zayats, Tetyana, Aliev, Fazil, Jiang, Chang, Wang, Carol A., Saunders, Gretchen, Karhunen, Ville, Hammerschlag, Anke R., Adkins, Daniel E., Border, Richard, Peterson, Roseann E., Prinz, Joseph A., Thiering, Elisabeth, Seppälä, Ilkka, Vilor-Tejedor, Natàlia, Ahluwalia, Tarunveer S., Day, Felix R., Hottenga, Jouke-Jan, Allegrini, Andrea G., Rimfeld, Kaili, Chen, Qi, Lu, Yi, Martin, Joanna, Soler Artigas, María, Rovira, Paula, Bosch, Rosa, Español, Gemma, Ramos Quiroga, Josep Antoni, Neumann, Alexander, Ensink, Judith, Grasby, Katrina, Morosoli, José J., Tong, Xiaoran, Marrington, Shelby, Middeldorp, Christel, Scott, James G., Vinkhuyzen, Anna, Shabalin, Andrey A., Corley, Robin, Evans, Luke M., Sugden, Karen, Alemany, Silvia, Sass, Lærke, Vinding, Rebecca, Ruth, Kate, Tyrrell, Jess, Davies, Gareth E., Ehli, Erik A., Hagenbeek, Fiona A., De Zeeuw, Eveline, Van Beijsterveldt, Toos C.E.M., Larsson, Henrik, Snieder, Harold, Verhulst, Frank C., Amin, Najaf, Whipp, Alyce M., Korhonen, Tellervo, Vuoksimaa, Eero, Rose, Richard J., Uitterlinden, André G., Heath, Andrew C., Madden, Pamela, Haavik, Jan, Harris, Jennifer R., Helgeland, Øyvind, Johansson, Stefan, Knudsen, Gun Peggy S., Njolstad, Pal Rasmus, Lu, Qing, Rodriguez, Alina, Henders, Anjali K., Mamun, Abdullah, Najman, Jackob M., Brown, Sandy, Hopfer, Christian, Krauter, Kenneth, Reynolds, Chandra, Smolen, Andrew, Stallings, Michael, Wadsworth, Sally, Wall, Tamara L., Silberg, Judy L., Miller, Allison, Keltikangas-Järvinen, Liisa, Hakulinen, Christian, Pulkki-Råback, Laura, Havdahl, Alexandra, Magnus, Per, Raitakari, Olli T., Perry, John R. B., Llop, Sabrina, Lopez-Espinosa, Maria-Jose, Bønnelykke, Klaus, Bisgaard, Hans, Sunyer, Jordi, Lehtimäki, Terho, Arseneault, Louise, Standl, Marie, Heinrich, Joachim, Boden, Joseph, Pearson, John, Horwood, L. John, Kennedy, Martin, Poulton, Richie, Eaves, Lindon J., Maes, Hermine H., Hewitt, John, Copeland, William E., Costello, Elizabeth J., Williams, Gail M., Wray, Naomi, Järvelin, Marjo-Riitta, McGue, Matt, Iacono, William, Caspi, Avshalom, Moffitt, Terrie E., Whitehouse, Andrew, Pennell, Craig E., Klump, Kelly L., Burt, S. Alexandra, Dick, Danielle M., Reichborn-Kjennerud, Ted, Martin, Nicholas G., Medland, Sarah E., Vrijkotte, Tanja, Kaprio, Jaakko, Tiemeier, Henning, Davey Smith, George, Hartman, Catharina A., Oldehinkel, Albertine J., Casas, Miquel, Ribasés, Marta, Lichtenstein, Paul, Lundström, Sebastian, Plomin, Robert, Bartels, Meike, Nivard, Michel G., and Boomsma, Dorret I.

Published
2021
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41. Parent Depressive Symptomatology Moderates the Etiology of Externalizing Behavior in Childhood: An Examination of Gene-Environment Interaction Effects

Author

Clark, D. Angus, Klump, Kelly L., and Burt, S. Alexandra

Abstract

Parent depressive symptomatology is robust risk factor for externalizing behavior in childhood (Goodman et al., 2011). Although the precise mechanisms underlying this association have yet to be fully illuminated, there is some evidence that parent depression can impact externalizing behavior via both genetic and environmental pathways. In the current study, we investigated the extent to which genetic and environmental influences on externalizing behavior are moderated by parent depressive symptoms (i.e., genotype-environment interaction) in a sample of 2,060, 6- to 11-year-old twins. Results suggest that genetic influences explain more variance in externalizing behavior as maternal depressive symptoms increase, whereas shared environmental effects decrease. These findings were specific to maternal depressive symptoms, however, and did not extend to not paternal depressive symptoms. Findings are critical for understanding the role of parental depression as a risk factor for problematic child behavior, and informing programs that seek to minimize the impact of this risk factor.

Published
2018
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43. Associations Between Attention-Deficit/Hyperactivity Disorder and Various Eating Disorders: A Swedish Nationwide Population Study Using Multiple Genetically Informative Approaches

Author

Adan, Roger, Ando, Tetsuya, Baker, Jessica, Bergen, Andrew, Berrettini, Wade, Birgegård, Andreas, Boni, Claudette, Boraska Perica, Vesna, Brandt, Harry, Burghardt, Roland, Cassina, Matteo, Cesta, Carolyn, Clementi, Maurizio, Coleman, Joni, Cone, Roger, Courtet, Philippe, Crawford, Steven, Crow, Scott, Crowley, James, Danner, Unna, Davis, Oliver, de Zwaan, Martina, Dedoussis, George, Degortes, Daniela, DeSocio, Janiece, Dick, Danielle, Dikeos, Dimitris, Dmitrzak-Weglarz, Monika, Docampo, Elisa, Egberts, Karin, Ehrlich, Stefan, Escaramís, Geòrgia, Esko, Tõnu, Estivill, Xavier, Favaro, Angela, Fernández-Aranda, Fernando, Fichter, Manfred, Finan, Chris, Fischer, Krista, Föcker, Manuel, Foretova, Lenka, Forzan, Monica, Franklin, Christopher, Gaspar, Héléna, Gonidakis, Fragiskos, Gorwood, Philip, Gratacos, Monica, Guillaume, Sébastien, Guo, Yiran, Hakonarson, Hakon, Halmi, Katherine, Hatzikotoulas, Konstantinos, Hauser, Joanna, Hebebrand, Johannes, Helder, Sietske, Hendriks, Judith, Herpertz-Dahlmann, Beate, Herzog, Wolfgang, Hilliard, Christopher, Hinney, Anke, Huckins, Laura, Hudson, James, Huemer, Julia, Imgart, Hartmut, Inoko, Hidetoshi, Jiménez-Murcia, Susana, Johnson, Craig, Jordan, Jenny, Juréus, Anders, Kalsi, Gursharan, Kaminska, Debora, Kaplan, Allan, Kaprio, Jaakko, Karhunen, Leila, Karwautz, Andreas, Kas, Martien, Kaye, Walter, Kennedy, James, Kennedy, Martin, Keski-Rahkonen, Anna, Kiezebrink, Kirsty, Kim, Youl-Ri, Klump, Kelly, Knudsen, Gun Peggy, Koeleman, Bobby, Koubek, Doris, La Via, Maria, Landén, Mikael, Levitan, Robert, Li, Dong, Lichtenstein, Paul, Lilenfeld, Lisa, Lissowska, Jolanta, Magistretti, Pierre, Maj, Mario, Mannik, Katrin, Martin, Nicholas, McDevitt, Sara, McGuffin, Peter, Merl, Elisabeth, Metspalu, Andres, Meulenbelt, Ingrid, Micali, Nadia, Mitchell, James, Mitchell, Karen, Monteleone, Palmiero, Monteleone, Alessio Maria, Mortensen, Preben, Munn-Chernoff, Melissa, Nacmias, Benedetta, Nilsson, Ida, Norring, Claes, Ntalla, Ioanna, O’Toole, Julie, Pantel, Jacques, Papezova, Hana, Parker, Richard, Rabionet, Raquel, Raevuori, Anu, Rajewski, Andrzej, Ramoz, Nicolas, Rayner, N. William, Reichborn-Kjennerud, Ted, Ricca, Valdo, Ripke, Stephan, Ritschel, Franziska, Roberts, Marion, Rotondo, Alessandro, Rybakowski, Filip, Santonastaso, Paolo, Scherag, André, Schmidt, Ulrike, Schork, Nicholas, Schosser, Alexandra, Seitz, Jochen, Slachtova, Lenka, Slagboom, P. Eline, Slof-Op’t Landt, Margarita, Slopien, Agnieszka, Smith, Tosha, Sorbi, Sandro, Strengman, Eric, Strober, Michael, Sullivan, Patrick, Szatkiewicz, Jin, Szeszenia-Dabrowska, Neonila, Tachmazidou, Ioanna, Tenconi, Elena, Thornton, Laura, Tortorella, Alfonso, Tozzi, Federica, Treasure, Janet, Tsitsika, Artemis, Tziouvas, Konstantinos, van Elburg, Annemarie, van Furth, Eric, Wade, Tracey, Wagner, Gudrun, Walton, Esther, Watson, Hunna, Woodside, D. Blake, Yao, Shuyang, Yilmaz, Zeynep, Zeggini, Eleftheria, Zerwas, Stephanie, Zipfel, Stephan, Alfredsson, Lars, Andreassen, Ole, Aschauer, Harald, Barrett, Jeffrey, Bencko, Vladimir, Carlberg, Laura, Cichon, Sven, Cohen-Woods, Sarah, Dina, Christian, Ding, Bo, Espeseth, Thomas, Floyd, James, Gallinger, Steven, Gambaro, Giovanni, Giegling, Ina, Herms, Stefan, Janout, Vladimir, Julià, Antonio, Klareskog, Lars, Le Hellard, Stephanie, Leboyer, Marion, Lundervold, Astri, Marsal, Sara, Mattingsdal, Morten, Navratilova, Marie, Ophoff, Roel, Palotie, Aarno, Pinto, Dalila, Ripatti, Samuli, Rujescu, Dan, Scherer, Stephen, Scott, Laura, Sladek, Robert, Soranzo, Nicole, Southam, Lorraine, Steen, Vidar, Wichmann, H-Erich, Widen, Elisabeth, Breen, Gerome, Bulik, Cynthia, Kuja-Halkola, Ralf, Martin, Joanna, Lu, Yi, Hübel, Christopher, Almqvist, Catarina, Thornton, Laura M., Magnusson, Patrik K., Bulik, Cynthia M., and Larsson, Henrik

Published
2019
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47. Characterization of genetic variation in the VGLL4 gene in anorexia nervosa

Author

Clarke, Toni-Kim, Crist, Richard C, Doyle, Glenn A, Weiss, Amy RD, Brandt, Harry, Crawford, Steve, Crow, Scott, Fichter, Manfred M, Halmi, Katherine A, Johnson, Craig, Kaplan, Allan S, La Via, Maria, Mitchell, James E, Strober, Michael, Rotondo, Alessandro, Treasure, Janet, Woodside, D Blake, Keel, Pamela, Klump, Kelly L, Lilenfeld, Lisa, Plotnicov, Katherine, Magistretti, Pierre J, Bergen, Andrew W, Kaye, Walter H, Schork, Nicholas J, and Berrettini, Wade H

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Clinical Sciences, Neurosciences, Adult, Anorexia Nervosa, DNA Mutational Analysis, Female, Genetic Predisposition to Disease, Genetic Variation, Humans, Polymorphism, Single Nucleotide, Transcription Factors, Psychiatry, Clinical sciences
Published
2014

48. The role of leptin, melanocortin, and neurotrophin system genes on body weight in anorexia nervosa and bulimia nervosa

Author

Yilmaz, Zeynep, Kaplan, Allan S, Tiwari, Arun K, Levitan, Robert D, Piran, Sara, Bergen, Andrew W, Kaye, Walter H, Hakonarson, Hakon, Wang, Kai, Berrettini, Wade H, Brandt, Harry A, Bulik, Cynthia M, Crawford, Steven, Crow, Scott, Fichter, Manfred M, Halmi, Katherine A, Johnson, Craig L, Keel, Pamela K, Klump, Kelly L, Magistretti, Pierre, Mitchell, James E, Strober, Michael, Thornton, Laura M, Treasure, Janet, Woodside, D Blake, Knight, Joanne, and Kennedy, James L

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Clinical Research, Genetics, Eating Disorders, Anorexia, Nutrition, Brain Disorders, Serious Mental Illness, Mental Health, Obesity, 2.1 Biological and endogenous factors, Aetiology, Adult, Agouti-Related Protein, Anorexia Nervosa, Body Mass Index, Body Weight, Bulimia Nervosa, Case-Control Studies, Female, Genotyping Techniques, Humans, Leptin, Melanocortins, Membrane Glycoproteins, Middle Aged, Nerve Growth Factors, Polymorphism, Single Nucleotide, Protein Kinases, Protein-Tyrosine Kinases, Receptor, trkB, Anorexia nervosa, Bulimia nervosa, Candidate gene association, Body weight, Neurotrophins, Medical and Health Sciences, Psychology and Cognitive Sciences, Psychiatry, Clinical sciences, Clinical and health psychology
Abstract

ObjectiveAlthough low weight is a key factor contributing to the high mortality in anorexia nervosa (AN), it is unclear how AN patients sustain low weight compared with bulimia nervosa (BN) patients with similar psychopathology. Studies of genes involved in appetite and weight regulation in eating disorders have yielded variable findings, in part due to small sample size and clinical heterogeneity. This study: (1) assessed the role of leptin, melanocortin, and neurotrophin genetic variants in conferring risk for AN and BN; and (2) explored the involvement of these genes in body mass index (BMI) variations within AN and BN.MethodOur sample consisted of 745 individuals with AN without a history of BN, 245 individuals with BN without a history of AN, and 321 controls. We genotyped 20 markers with known or putative function among genes selected from leptin, melanocortin, and neurotrophin systems.ResultsThere were no significant differences in allele frequencies among individuals with AN, BN, and controls. AGRP rs13338499 polymorphism was associated with lowest illness-related BMI in those with AN (p = 0.0013), and NTRK2 rs1042571 was associated with highest BMI in those with BN (p = 0.0018).DiscussionTo our knowledge, this is the first study to address the issue of clinical heterogeneity in eating disorder genetic research and to explore the role of known or putatively functional markers in genes regulating appetite and weight in individuals with AN and BN. If replicated, our results may serve as an important first step toward gaining a better understanding of weight regulation in eating disorders.

Published
2014

49. Primary Amenorrhea in Anorexia Nervosa: Impact on Characteristic Masculine and Feminine Traits

Author

Baker, Jessica H, Sisk, Cheryl L, Thornton, Laura M, Brandt, Harry, Crawford, Steven, Fichter, Manfred M, Halmi, Katherine A, Johnson, Craig, Jones, Ian, Kaplan, Allan S, Mitchell, James E, Strober, Michael, Treasure, Janet, Woodside, D Blake, Berrettini, Wade H, Kaye, Walter H, Bulik, Cynthia M, and Klump, Kelly L

Subjects
Contraception/Reproduction, Mental Health, Brain Disorders, Eating Disorders, Nutrition, Anorexia, Adolescent, Adult, Amenorrhea, Anorexia Nervosa, Female, Femininity, Humans, Masculinity, Personality, Personality Inventory, organizational effects, sex differences, amenorrhea, pubertal timing, anorexia nervosa, Clinical Sciences, Psychology, Clinical Psychology
Abstract

Animal studies indicate that gonadal hormones at puberty have an effect on the development of masculine and feminine traits. However, it is unknown whether similar processes occur in humans. We examined whether women with anorexia nervosa (AN), who often experience primary amenorrhea, exhibit attenuated feminization in their psychological characteristics in adulthood due to the decrease/absence of gonadal hormones at puberty. Women with AN were compared on a number of psychological characteristics using general linear models on the basis of the presence/absence of primary amenorrhea. Although women with primary amenorrhea exhibited lower anxiety scores than those without primary amenorrhea, in general, results did not provide evidence of attenuated feminization in women with AN with primary amenorrhea. Future research should utilize novel techniques and direct hormone measurement to explore the effects of pubertal gonadal hormones on masculine and feminine traits.

Published
2014

50. Changes in affect longitudinally mediate associations between emotion regulation strategy use and disordered eating.

Author

Mikhail, Megan E., Burt, S. Alexandra, Neale, Michael C., Keel, Pamela K., Katzman, Debra K., and Klump, Kelly L.

Subjects
EMOTION regulation, BULIMIA, RESEARCH funding, QUESTIONNAIRES, POSITIVE psychology, PSYCHOLOGICAL adaptation, STRUCTURAL equation modeling, DESCRIPTIVE statistics, EATING disorders, FOOD habits, AFFECT (Psychology), FOOD diaries
Abstract

Background: Trait‐level emotion regulation (ER) difficulties are associated with eating disorders (EDs) transdiagnostically. However, little research has examined whether within‐person fluctuations in ER longitudinally predict ED behaviors in daily life or the mechanisms of ER effects. Investigating daily ER could help us better understand why people experience ED behaviors at a given time. We examined whether day‐to‐day changes in adaptive (e.g., cognitive reappraisal) and maladaptive (e.g., rumination) ER longitudinally predicted core ED behaviors (binge eating, purging, dieting) and whether changes in affect mediated effects. Method: Female participants (N = 688) ages 15–30 from the Michigan State University Twin Registry reported their adaptive and maladaptive ER use, negative affect (NA), positive affect (PA), binge eating, purging, and dieting on 49 consecutive days. Using structural equation modeling, we examined whether within‐person fluctuations in ER predicted same‐ and next‐day ED behaviors and whether changes in affect mediated longitudinal ER effects. Results: Greater maladaptive ER predicted increased likelihood of same‐day binge eating and next‐day binge eating and purging. The association between maladaptive ER and next‐day binge eating and purging was mediated by increased next‐day NA. In contrast, dieting was more closely related to changes in PA. Adaptive ER did not predict reduced likelihood of any ED behavior. Conclusions: Maladaptive ER may longitudinally increase risk for binge eating and purging by amplifying NA. Interventions focused on decreasing maladaptive ER and subsequent NA might help disrupt binge eating‐purging cycles. Conversely, results add to evidence that PA fluctuations may play a unique role in maintaining restrictive behaviors. Public Significance: Little is known about how daily changes in emotion regulation may impact disordered eating. We found that maladaptive emotion regulation (e.g., rumination) was associated with a higher likelihood of binge eating and purging on the next day because it predicted increased next‐day negative affect. In contrast, dieting was more closely tied to fluctuations in positive affect. Targeting daily emotion regulation and affective processes may help disrupt cycles of disordered eating. [ABSTRACT FROM AUTHOR]

Published
2024
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