Cynthia Bulik

Cynthia Bulik

Professor
E-postadress: cynthia.bulik@ki.se
Telefon: +46852482419
Besöksadress: Nobels väg 12a, 17165 Solna
Postadress: C8 Medicinsk epidemiologi och biostatistik, C8 MEB Bulik, 171 77 Stockholm
Del av:

Om mig

  • Jag är legitimerad psykolog och har bedrivit forskning och behandling inom området ätstörningar sedan 1984. Jag har undersökt ätstörningar på många olika sätt, från djurmodeller till kliniska prövningar, men mitt största bidrag till forskningen har skett genom metoder inom genetisk epidemiologi – bland annat med familj-, tvilling- och molekylärgenetisk design. Jag har grundat University of North Carolina Center of Excellence for Eating Disorders och fortsätter mitt arbete som dess chef. Dessutom leder jag ett centrum vid Karolinska Institutet med fokus på att vidareutveckla forskningen i genetisk epidemiologi inom ätstörningar (CEDI). Tillsammans med min forskargrupp hoppas jag knäcka den genetiska koden för ätstörningar för att öka förståelsen av den underliggande neurobiologin bakom dessa sjukdomar för att förbättra både förebyggande och behandling.

    NUVARANDE POSITION OCH UPPDRAG

    • Professor, Institutionen för Medicinsk Epidemiologi och Biostatistik, Karolinska Institutet, Stockholm, Sverige
    • Distinguished Professor of Eating Disorders, Department of Psychiatry, University of North Carolina at Chapel Hill, USA
    • Grundare och chef, Center of Excellence for Eating Disorders, University of North Carolina at Chapel Hill, USA
    • Professor, Department of Nutrition, Gillings School of Global Public Health, UNC Chapel Hill
    • Adjungerad Professor, Folkehelseinstituttet, Oslo, Norge
    • Co-Director UNC Center for Psychiatric Genomics, University of North Carolina at Chapel Hill, USA

      UTBILDNING
      University of Notre Dame, Notre Dame, Indiana: B.A. – Psykologi
      University of California at Berkeley, Kalifornien: M.A. – Psykologi (Klinisk inriktning)
      University of California at Berkeley, Kalifornia: Ph.D. – Psykologi (Klinisk inriktning)
      University of Pittsburgh, Dept. of Psychiatry, NIMH: (Post-doc) – Forskning inom psykiatri
      University of Pittsburgh, Dept. of Psychiatry, MacArthur: (Post-doc) – Forskning inom psykiatri

Forskningsbeskrivning

  • Min forskning är mer utförligt beskriven på den engelska profilsidan, så byt språk om du är intresserad av att läsa mer.

    SAMMANFATTNING

    • Ökat förståelsen av riskfaktorer för ätstörningar genom att visa hur genetiska faktorer påverkar risken för anorexia nervosa, bulimia nervosa, och hetsätningsstörning och fört vetenskapen från familjestudier till tvillingstudier, genom linkage- och kandidatgen-studier, till studier av hela genomet s.k. genom-wide association-studies (GWAS).
    • Undersökt effekterna av graviditet på utfall för mor och barn hos kvinnor med ätstörningar.
    • Utvecklat och spridit interventionsmetoder som har förbättrat behandlingen av anorexia nervosa, bulimi nervosa och hetsätningstörning.
    • Breddat förståelsen av annan sjuklighet vid ätstörningar genom att utforska biologin och mekanismerna bakom ångest, depression, autism, och missbruksstörningar.

      AKTUELLA FORSKNINGSPROJEKT

      CEDI - Centre for Eating Disorders Innovation - ett centra för ätstörningsforskning där vi vill studera den roll som både genetik och miljö spelar för risken och utvecklingen av ätstörningar.

      ANGI - Anorexia Nervosa Genetics Initiative - är den största genetiska undersökningen av ätstörningar som hittills genomförts. Forskare i USA, Sverige, Australien och Danmark kommer att samla klinisk information och blodprover från över 13 000 personer med anorexia nervosa och personer utan ätstörningar. ANGI är en global satsning för att upptäcka genetiska variationer som bidrar till denna potentiellt livshotande sjukdom. Målet med studien är att använda vår kunskap om orsakerna till ätstörningar i arbetet mot ökad förståelse och slutligen ett botemedel. Studien har också en svensk hemsida.

      CREAT - Comprehensive Risk Evaluation for Anorexia nervosa in Twins – en forskningsstudie med diskordanta enäggstvillingar med anorexia nervosa.

      Binge eating disorder: Ett projekt gemensamt för KI och University of North Carolina som stöds av Shire Pharmaceuticals Inc., där vi studierar sjukdomens epidemiologi, klinisk riktning, nyttjandemönster inom sjukvården, och utfall av hetsätningsstörning (BED) genom data i det svenska kvalitetsregistret för ätstörningar, RIKSÄT och Stepwise och de svenska befolkningsregistren.

      MEDARBETARE VID UNIVERSITY OF NORTH CAROLINA

      Laura Thornton, Ph.D.
      Jessica Baker, Ph.D.
      Melissa Munn-Chernoff, Ph.D.
      Hunna Watson, Ph.D.

      MEDARBETARE VID KAROLINSKA INSTITUTET
      Anna Hedman, Ph.D., post doc
      Ida Nilsson, Ph.D., post doc
      Shuyang Yao, Ph.D., post doc
      Afrouz Abbaspour, Ph.D., post doc

Utvalda publikationer

  • Article: JOURNAL OF PSYCHIATRIC RESEARCH. 2015;65:16-22
    Zerwas S; Larsen JT; Petersen L; Thornton LM; Mortensen PB; Bulik CM
  • Article: MOLECULAR PSYCHIATRY. 2014;19(10):1085-1094
    Boraska V; Franklin CS; Floyd JAB; Thornton LM; Huckins LM; Southam L; Rayner NW; Tachmazidou I; Klump KL; Treasure J; Lewis CM; Schmidt U; Tozzi F; Kiezebrink K; Hebebrand J; Gorwood P; Adan RAH; Kas MJH; Favaro A; Santonastaso P; Fernandez-Aranda F; Gratacos M; Rybakowski F; Dmitrzak-Weglarz M; Kaprio J; Keski-Rahkonen A; Raevuori A; Van Furth EF; 't Landt MCTS-O; Hudson JI; Reichborn-Kjennerud T; Knudsen GPS; Monteleone P; Kaplan AS; Karwautz A; Hakonarson H; Berrettini WH; Guo Y; Li D; Schork NJ; Komaki G; Ando T; Inoko H; Esko T; Fischer K; Maennik K; Metspalu A; Baker JH; Cone RD; Dackor J; DeSocio JE; Hilliard CE; O'Toole JK; Pantel J; Szatkiewicz JP; Taico C; Zerwas S; Trace SE; Davis OSP; Helder S; Buehren K; Burghardt R; de Zwaan M; Egberts K; Ehrlich S; Herpertz-Dahlmann B; Herzog W; Imgart H; Scherag A; Scherag S; Zipfel S; Boni C; Ramoz N; Versini A; Brandys MK; Danner UN; de Kovel C; Hendriks J; Koeleman BPC; Ophoff RA; Strengman E; van Elburg AA; Bruson A; Clementi M; Degortes D; Forzan M; Tenconi E; Docampo E; Escaramis G; Jimenez-Murcia S; Lissowska J; Rajewski A; Szeszenia-Dabrowska N; Slopien A; Hauser J; Karhunen L; Meulenbelt I; Slagboom PE; Tortorella A; Maj M; Dedoussis G; Dikeos D; Gonidakis F; Tziouvas K; Tsitsika A; Papezova H; Slachtova L; Martaskova D; Kennedy JL; Levitan RD; Yilmaz Z; Huemer J; Koubek D; Merl E; Wagner G; Lichtenstein P; Breen G; Cohen-Woods S; Farmer A; McGuffin P; Cichon S; Giegling I; Herms S; Rujescu D; Schreiber S; Wichmann H-E; Dina C; Sladek R; Gambaro G; Soranzo N; Julia A; Marsal S; Rabionet R; Gaborieau V; Dick DM; Palotie A; Ripatti S; Widen E; Andreassen OA; Espeseth T; Lundervold A; Reinvang I; Steen VM; Le Hellard S; Mattingsdal M; Ntalla I; Bencko V; Foretova L; Janout V; Navratilova M; Gallinger S; Pinto D; Scherer SW; Aschauer H; Carlberg L; Schosser A; Alfredsson L; Ding B; Klareskog L; Padyukov L; Courtet P; Guillaume S; Jaussent I; Finan C; Kalsi G; Roberts M; Logan DW; Peltonen L; Ritchie GRS; Barrett JC; Estivill X; Hinney A; Sullivan PF; Collier DA; Zeggini E; Bulik CM
  • Article: NORSK EPIDEMIOLOGI. 2014;24(1-2):51-62
    Watson HJ; Torgersen L; Zerwas S; Reichborn-Kjennerud T; Knoph C; Stoltenberg C; Siega-Riz AM; Von Holle A; Hamer RM; Meltzer H; Ferguson EH; Haugen M; Magnus P; Kuhns R; Bulik CM
  • Article: BIOLOGICAL PSYCHIATRY. 2010;67(1):71-77
    Bulik CM; Thornton LM; Root TL; Pisetsky EM; Lichtenstein P; Pedersen NL
  • Article: ARCHIVES OF GENERAL PSYCHIATRY. 2006;63(3):305-312
    Bulik CM; Sullivan PF; Tozzi F; Furberg H; Lichtenstein P; Pedersen NL

Artiklar

Alla övriga publikationer

Forskningsbidrag

  • Swedish Research Council
    1 December 2025 - 31 December 2029
    This project targets tertiary prevention in psychiatry: identifying, early in the course of care, individuals most likely to develop severe, persistent illness and tailoring care accordingly. We focus on major depressive disorder (MDD), anorexia nervosa (AN), and bulimia nervosa (BN)—disorders with high female predominance and major contributions to disability among Swedish women. Using Sweden’s exceptional national health registers, we will construct large, richly phenotyped cohorts spanning four decades and apply modern machine learning to detect reproducible, data-driven patterns of long-term outcomes (Aim 1), identify early predictors of poor trajectories including clinical, social, developmental, and genomic factors (Aim 2), and use causal inference to determine which treatments are associated with better outcomes in those at highest risk (Aim 3). Analyses will emphasize replication, generalizability, and clinical relevance, with a focus on sex differences. Preliminary results demonstrate feasibility and identify clinically actionable subgroups, including those at elevated risk for suicide or diagnostic crossover. Successful completion will yield robust, generalizable predictive models to guide personalized, proactive psychiatric care and inform scalable tertiary prevention strategies. Findings will be directly relevant to Swedish healthcare and may serve as a model internationally.
  • Swedish Research Council
    1 January 2025 - 31 December 2027
    Anorexia nervosa and bulimia nervosa are serious eating disorders (EDs) with significant morbidity and mortality. Recent genetic research has led to a reconceptualization of anorexia nervosa not only as a psychiatric disorder, but also a condition with metabolic underpinnings—evidence of which has been observed as early as age two, long before the onset of the ED. Metabolites measured in neonatal blood could serve as very early markers of ED risk, unconfounded by state or scar factors related to prolonged starvation. We propose to comprehensively analyze neonatal biomarkers (metabolic, immune, and neurotrophic), epidemiological factors, and genetics to understand ED risk and develop risk prediction models of diagnostic stability, somatic and psychiatric comorbidity, illness course and severity, and psychotropic medication response. Successful completion of our aims will have important implications for prediction of ED type, course, severity, and outcome informed by biology at birth to aid in early identification of individuals at risk to inform precision prevention, while extending the knowledge about the etiology of EDs.
  • Swedish Research Council for Health Working Life and Welfare
    10 December 2024 - 30 November 2025
  • National Institute of Mental Health
    13 May 2024 - 28 February 2029
    PROJECT SUMMARY We propose the Eating Disorders Genetics Initiative 2 (EDGI2), a new collaborative R01 in response to PAR- 23-050 Clinical Studies of Mental Illness. Its single-site predecessors, EDGI1 (R01 MH120170) and ARFID-GEN (R56 MH129437) have been resoundingly successful. We now unite the four original EDGI1 sites with exceptionally productive global new sites to advance genomic discovery across all major eating disorders (EDs) to identify biologically, clinically, culturally, and therapeutically meaningful and actionable insights. Aim 1: EDGI2 extends our core business by increasing sample size, diversity, and ED phenotypes. Using our comprehensive harmonized online assessment battery, we will phenotype and bio-sample 20,000 new participants with anorexia nervosa (AN), bulimia nervosa (BN), binge-eating disorder (BED), avoidant/restrictive food intake disorder (ARFID), and controls. EDGI2 emphasizes co-production—with representatives from minoritized and marginalized communities, we will ascertain 30% of samples from underrepresented groups. We will also over- sample individuals with severe and enduring AN (SE-AN), whose DNA may be enriched for causative alleles. Aim 2: We will apply statistical genetic analyses to explicate heterogeneity and biology of EDs by: conducting standard GWAS analyses on diagnoses, trans-diagnostic behaviors, and continuous phenotypes including polygenic risk score (PRS), and rare variant CNV analyses
    identifying clinically meaningfully patient subsets
    and intensively evaluating our proposal that AN is a metabo-psychiatric disorders using LDSC, PRSet, pheWAS, and Mendelian randomization to clarify direction of causation. Aim 3: We will evaluate the relative roles of genetic and environmental risk and resilience factors to inform risk prediction by phenotypically characterizing cases and controls with high and low PRS for EDs and then by genotypically characterizing those with severe ED phenotypes. We will characterize distinct genetic or molecular groupings/patterns across cases and controls and phenotypically characterize identified molecular subtypes. Aim 4: To determine where in the body EDs “live”, we will identify brain cell types and anatomical regions implicated by genomic studies of EDs
    predict genetically regulated gene expression (GREx) in brain, gut, adipose, and other ED-relevant tissues
    use snRNAseq atlases to sharpen preliminary GTEx and TWAS analyses to identify brain cell types strongly implicated by the genomics of each ED
    expand to relevant non-brain cell types (e.g., adipose, muscle, liver, salivary)
    and use dynamic GREx to model gene expression in ED-relevant contexts (e.g., sex, BMI, stress) enabling precise and personalized modelling of gene expression. Aim 5: EDGI2 will culminate in a Translational Summit uniting forward-thinking stakeholders from multiple sectors to develop a translational roadmap for evidence-based ED prevention and treatment. EDGI2 will yield critical knowledge about genetic and environmental risk for EDs, reveal mechanisms that potentiate or protect against genetic risk, and transition ED genetics from discovery to clinical translation.
  • Swedish Research Council
    1 January 2023 - 31 December 2026
    Human food consumption habits pose a fundamental problem for public health and environmental sustainability, but the complex interactions between homeostatic needs and the desire to eat remain poorly understood. This project aims to delineate the mechanisms by which metabolic states (hunger/satiety) regulate reward attribution to sensory food stimuli, making it difficult to resist flavorful meals when we are hungry and to continue eating when we are full. Study 1 will behaviorally assess the specificity of metabolic modulation to the olfactory modality and the food content of the anticipatory reward stimulus, and probe implicit effects on reward-seeking behavior with the help of a novel ecologically relevant adaption of the incentive delay paradigm. Study 2 will use multivariate fMRI analyses to identify differences in perceptual stimulus encoding during hunger and satiety, and determine invigorating effects of anticipatory food reward on sensory-striatal connectivity. We will then seek to understand the impact of dysregulation in this circuitry for disturbed eating behavior
    the final two studies will, on a behavioral and neuroanatomical level, pinpoint the stages of anticipatory reward regulation where eating disorder patients show deficits relative to controls. Taken together, this project will answer fundamental questions about human food intake regulation, and provide a starting point for development of intervention strategies for dysregulated food consumption behavior.
  • Swedish Research Council for Health Working Life and Welfare
    1 November 2022 - 30 September 2026
    Research problem and specific questions. Avoidant/restrictive food intake disorder is a serious, taxing, and potentially life-threatening condition that affects 1-5% of the population. First recognized in 2013, we know little about causes, course, maintenance factors, and outcome
    however, nutritional, medical, and psychosocial consequences are severe. We propose establishing a re-contactable, longitudinal cohort (ARFID InitiativE Sweden: ARIES) to study genetic and environmental contributors to ARFID through a developmental lens. ARIES will include rich phenotyping, DNA samples, and stool samples in a national data- and biorepository linkable to Swedish population health and quality registers to answer fundamental questions about this pernicious, life-impairing, and understudied condition. Data and method. We will first form a community-based Parent Advisory Committee (PAC) to guide our assessment domains and then recruit 500 children ages 4-9 with ARFID and 500 age and gender matched controls
    collect parental report via online questionnaires on development, feeding history, food preferences, behavior, mood, feeding-related adverse events, and other domains suggested by the PAC
    and create a biobank of saliva (for DNA) and stool (for intestinal microbiota and microbiome). Plan for project realisation. We will launch a national recruitment campaign using our country-wide collaborations with eating disorders clinicians and pediatricians and our social media channels to reach parents of children with ARFID. After an online eligibility screen, parents will complete questionnaires
    submit saliva samples for their children
    and provide a stool sample. Families will enroll in ARIES, agreeing to regular follow-ups. In addition to baseline research aims, ARIES will enable identification of predictors of transient versus enduring illness course, impact of puberty on ARFID symptoms, and impact of ARFID on educational achievement. Linking ARIES with population registers will allow research questions about ARFID comorbidity and healthcare utilization. Relevance. No evidence-based treatment for ARFID and no national guidelines exist. Parents desperately seek guidance on managing ARFID and fear for their child’s long-term well-being. ARIES will be the foundation for understanding ARFID, identifying factors related to onset, maintenance, and outcome, and be a national and international resource for essential research.
  • National Institute of Mental Health
    16 August 2022 - 31 July 2025
  • Swedish Research Council
    1 December 2021 - 30 November 2025
  • National Institute of Mental Health
    14 April 2021 - 28 February 2026
    Project Summary Now in its 13th year, the Psychiatric Genomics Consortium is perhaps the most innovative and productive experiment in the history of psychiatry. The PGC unified the field and attracted a cadre of outstanding scientists (802 investigators from 157 institutions in 41 countries). PGC work has led to identification of ~500 genetic loci in the 11 psychiatric disorders we study. Our work has led to 320 papers, many in high-profile journals (Nature 3, Cell 5, Science 2, Nat Genet 27, Nat Neurosci 9, Mol Psych 37, Biol Psych 25). As summary statistics are freely available, psychiatric disorders often feature prominently in papers by non-PGC investigators. To advance discovery and impact, we propose to continue the work of the PGC across 11 disorder groups. Considerable new data are coming in the next five years. We thus can rapidly and efficiently increase our knowledge of the fundamental basis of major psychiatric disorders. Aim 1: we will continue to advance genetic discovery for severe psychiatric disorders in all working groups, systematically interface with large biobank studies to ensure maximal comparability, and aggressively promote new studies of individuals with psychiatric disorders from diverse ancestries to increase discovery and improve fine-mapping. Aim 2: most studies analyze common variation (Aim 1), rare CNV (Aim 2), and rare exome/genome resequencing results (via collaboration) in isolation: we will apply an integrative framework to rigorously evaluate the contributions of all measured types of genetic variation on risk for psychiatric disorders. Aim 3: we will move beyond classical case-control definitions to a more biologically-based and nuanced understanding by enabling large trans-diagnostic studies, convene trans-disciplinary teams to use genetics to address unresolved questions about the nature of psychiatric disorders, and to promote large studies of the severest cases seen in psychiatric practice (leveraging the global reach of PGC investigators). Aim 4: we will work to maximize the impact of our work via translational efforts: close collaborations with neuroscience consortia to understand the biological implications of our findings
    work to identify modifiable causal risk factors
    and work to robustly predict clinical outcomes and identify patient subsets. Aim 5: we will increase impact of our work by extending and formalizing outreach to different communities (including pharma and biotech), via digital media (Twitter, Facebook, Wikipedia), and by developing, distributing, and updating resources/educational material for patients, families, and medical professionals. We will convene a Scientific Advisory Board to ensure we respond positively to those invested in our results Successful completion of this body of work will greatly advance knowledge of the genetic basis of psychiatric disorders with potentially major nosological and treatment implications. These goals are consistent with a core mission of the NIMH, and the central idea of the PGC: to convert the family history risk factor into biologically, clinically, and therapeutically meaningful insights.
  • Southern and Eastern Norway Regional Health Authority
    1 January 2020
    High activity in the PaGE-project in 2024<br/><br/>PhD-student Laura Hegemann spent 3 months at Rutgers University and the Broad Institute of Harvard and MIT in the US. The stay had great value for the learning and career development of the student, and for the collaborative network of our research group. <br/><br/>By visiting the LifeSPAN Autism Lab at Rutgers University, the PhD candidate was be able to receive world-leading training in approaches to studying screening, diagnosis, and wellbeing in autism. Additionally, she received expert advice and consultation on approaches to enhance user involvement in research projects, which is an important focus in the PaGE research group at Lovisenberg hospital. <br/><br/>The visit at the Broad Institute at Harvard University and MIT provided the PhD candidate and the research group with an advanced understanding of the genetics of neurodiversity and important methods development to advance the research field, which was shared with the research group at Lovisenberg hospital. <br/><br/>The research stay has led to strengthened collaboration between the PaGE group and the research environments at Rutgers University and the Broad Institute.Forskningsopphold i utlandetIn 2024, the first doctoral student in the project successfully defended the PhD and published 3 articles, the second doctoral student submitted the first article and completed all PhD courses. The research group has also published a range of articles in recognized international journals.*Milestones achieved in 2024 for PhD student 1 Laura Hegemann*<br/><br/>The candidate successfully defended the dissertation "Etiology of Neurodevelopmental Traits: Measurement, Specificity, and Within-Family Transmission", including 3 lead-authored publications:<br/><br/>In the 1st paper, published in Autism, we examine the Social Communication Questionnaire (SCQ) in a general population sample, assessing the factor structure and measurement invariance across birth sex and autism diagnostic status. This work contributes valuable knowledge on how the SCQ performs in general population samples. <br/><br/>The 2nd paper, published in Molecular Autism, we explore the genetic and phenotypic structure of neurodevelopmental traits in preschool-aged children from the general population. We did not find support for a single general factor of liability across all early neurodevelopmental traits. Instead, genetic factors are associated with more specific areas of neurodevelopment. While there is evidence of shared genetic factors in social and communication traits, the study also reports increased heterogeneity in other areas, such as motor development. The study opens avenues for research into the distinct genetic mechanisms underlying various neurodevelopmental traits.<br/><br/>In the 3rd paper, published in Journal of Child Psychology and Psychiatry, we investigate genetic effects on children’s neurodevelopment at age 3 years by assessing the contributions of both direct genetic effects of inherited variants and indirect genetic effects from parental variants not inherited by the child. We find that direct genetic effects contribute to early neurodevelopment traits, with differing levels of importance across the areas of neurodevelopment. In addition, we find evidence of indirect genetic effects on inattention, hyperactivity, and restrictive and repetitive behaviors and interests, contrasting with evidence of direct effects only for social communication traits, language, and motor development. This advances our understanding of the complexity in genetic processes influencing neurodevelopment. <br/><br/>* Milestones achieved in 2024 for PhD student 2 Meseret Mamo Bazezew*<br/><br/>The candidate completed the required PhD courses and seminars at the Department of Psychology at the University of Oslo. In addition, the candidate has completed several elective courses. <br/><br/>The candidate presented a poster at the international Behavior Genetics Association (BGA) conference in London. The candidate also completed and submitted the first PhD paper, entitled “The Reporting and Handling of Missing Data in Genetic Epidemiological Studies of Mental Health in Children and Adolescence: A Systematic Review” for publication. Further, she prepared the analysis plan and preregistration for the second PhD paper. <br/><br/>As a member of the Open and Reproducible Science Working Group, the candidate is contributing to the development of guidelines for analysis plans and preregistration for the entire research group, and to organizing events for researchers at Lovisenberg and collaborative partners to enhance research transparency. The candidate has also organized and hosted the PaGE group's weekly scientific meetings with the PsychGen Centre at the Norwegian Institute of Public Health.<br/><br/>* Milestones achieved in 2024 for the career fellow Alexandra Havdahl*<br/>The fellow led the research group, supervised the two PhD students, and contributed to publications. <br/><br/>The project group contributed to 16 articles published in 2024.<br/>
  • National Institute of Mental Health
    23 September 2019 - 31 July 2024
  • National Institute of Mental Health
    11 September 2019 - 30 June 2025
  • Southern and Eastern Norway Regional Health Authority
    1 January 2019
    Further outputs from the MoBa-Eat project in 2024<br/><br/>NOForskningsopphold i utlandetIn 2024, MoBa-Eat researchers have continued to work on analyses to answer the core questions of the project: how and why do eating disorders develop early in life, and what are the role of familial risk transmission processes?In 2024 we have written several papers which are submitted or ready for submission. <br/><br/>In one study, we estimated the prevalence of avoidant/restrictive food intake in a general population sample, examined developmental characteristics across childhood, and investigated its genetic architecture using genome-wide association analysis. In data from 35 5751 children in MoBa, we identified children with avoidant/restrictive food intake (ARFI-Broad), separating between children with persistent (present at both ages 3 and 8), transient (only at age 3), and emergent (only at age 8) symptoms. Relevant register-based diagnostic codes were used as indicators of clinical significance to identify children with more severe problems (ARFI-Clinical). We found that prevalence of persistent avoidant/restrictive eating was 6%, while 18% had transient and 8% emergent symptoms. Children with persistent avoidant/restrictive eating exhibited more developmental difficulties across multiple domains from infancy to adolescence. We identified significant genome-wide heritability and a potential genetic variant association for avoidant/restrictive eating. Our findings point to substantial prevalence of avoidant and restrictive food intake and elevated risk for other developmental difficulties in affected children, the need for broad support interventions, and advance understanding of genetic influences on avoidant and restrictive eating.<br/><br/>In another study, we examined eating problems among adolescent boys and girls before and during the Covid-19 Pandemic. Based on a preregistered analysis plan, we used cross-sectional data collected from 22,706 14-16-year-olds over 6 years (55% during the pandemic) in the Norwegian Mother, Father, and Child Cohort. We used measurement invariance analyses to compare the level of eating restraint and body concern before and during the pandemic, and multi-group structural equation models to estimate pre-pandemic and pandemic patterns of associations. We found there was a general increase in eating problems among 14-16-year-olds over time. Adjusting for this trend, the pandemic appeared to exacerbate problems among girls. Although the mechanisms are unclear, our results point to factors susceptible to change that could have been intensified during the pandemic (e.g., screen time, mental distress). Our results highlight the importance of recognizing sex-specific differences in eating problems.<br/><br/>In a third study, we investigated associations between genetic liability to eating disorders indexed by polygenic scores (PGSs), exposure to childhood maltreatment, and lifetime risk of anorexia nervosa, bulimia nervosa, binge-eating disorder, purging disorder, and binge-eating spectrum disorder. The lifetime prevalence of eating disorders ranged from 0.52% (purging disorder) to 11.72% (binge-eating spectrum disorder). All forms of childhood maltreatment were robustly associated with elevated risk of eating disorders. Eating disorder PGSs also predicted a higher risk of eating disorders. We did not find consistent evidence of statistically significant interaction effects between childhood maltreatment and eating disorder PGSs. Our findings highlight substantial associations between both childhood maltreatment and genetic risk for eating disorders in mothers.<br/><br/>A fourth study on parental BMI and offspring childhood body size and eating behaviour is under review. <br/><br/>The MoBa-Eat team has also contributed as co-authors on several other publications.<br/>
  • National Institute of Mental Health
    23 August 2018 - 30 June 2022
  • National Institute of Mental Health
    18 September 2017 - 31 August 2021
  • Medical Research Council
    14 September 2017 - 31 October 2019
  • Swedish Research Council
    1 January 2017 - 31 July 2017
  • Southern and Eastern Norway Regional Health Authority
    1 January 2017 - 31 December 2021
  • Swedish Research Council
    1 January 2014 - 31 December 2023
  • National Institute of Mental Health
    11 June 2012 - 28 February 2018
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Anställningar

  • Professor, Medicinsk epidemiologi och biostatistik, Karolinska Institutet, 2014-

Handledning

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