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

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 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
    Schizophrenia (SCZ) and anorexia nervosa (AN) are severe psychiatric disorders with insufficient treatments and an unexpectedly high genetic correlation. To further investigate this genetic relationship and the clinical impact of shared genes, we aim to:1) Use conjunctional FDR to identify shared genomic risk loci for SCZ and AN using data from the Psychiatric Genomics Consortium (94 390 total cases)2) Quantify the impact of AN and SCZ-AN genomic risk on the clinical presentation and outcome of SCZ in 10 827 cases from the Swedish Schizophrenia Study (S3
    PI: Sullivan)3) Quantify the impact of SCZ and SCZ-AN genomic risk on the clinical presentation and outcome of AN in 6187 cases from the Eating Disorder Genetics Initiative (EDGI
    PI: Bulik)4) Define relationships between SCZ-AN genomic risk and other medical outcomes by conducting a PheWAS in individuals without either disorder from S3 and EDGI (N=18 532) and the UK Biobank (N=400k)  The project involves 5 years of international and local collaboration with clinical and basic researchers specializing in SCZ (PI Bergen-KI
    Prof. Sullivan-KI/UNC) or AN (Dr. Baker-UNC
    Prof. Bulik-KI/UNC
    Dr. Birgegard-KI).Successful completion of these aims will identify genetic risk loci for SCZ-AN, the ways these loci modify clinical features of SCZ and AN, and their impact on risk for other medical problems. These results can be leveraged to improve outcomes for two difficult to treat and deadly psychiatric illnesses.
  • 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.
  • 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
    18 September 2017 - 31 August 2021
  • Southern and Eastern Norway Regional Health Authority
    1 January 2017 - 31 December 2021
  • National Institute of Mental Health
    11 June 2012 - 28 February 2018
  • National Institute of Mental Health
    8 April 2011 - 31 January 2014
  • A Genomewide association study of anorexia nervosa.
    Wellcome Trust Ltd
    1 August 2009 - 31 July 2012
  • National Institute of Mental Health
    6 June 2008 - 28 February 2012
  • National Institute of Mental Health
    1 April 2008 - 31 March 2014
  • National Institute of Mental Health
    28 September 2007 - 31 July 2011
  • National Institute of Mental Health
    17 July 2007 - 30 June 2018
  • National Institute of Mental Health
    27 September 2005 - 29 February 2008
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development
    4 February 2005 - 31 December 2008
  • National Institute of Mental Health
    1 April 2001 - 31 March 2006
  • National Institute of Mental Health
    15 July 1998 - 30 June 2002
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Anställningar

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

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