About

Cynthia Bulik, PhD, FAED, is a Distinguished Professor of Eating Disorders in the Department of Psychiatry and a professor of nutrition at the UNC Gillings School of Global Public Health. She is the founding director of the UNC Center of Excellence for Eating Disorders and co-director of the UNC Center for Psychiatric Genomics. Dr. Bulik is also a professor of medical epidemiology and biostatistics at Karolinska Institutet in Stockholm, Sweden, where she established the Centre for Eating Disorders Innovation. Her research encompasses treatment, laboratory, epidemiological, twin, and molecular genetic studies of eating disorders and weight regulation. She has held leadership roles in major consortia studying the genetics of eating disorders and is the Founder and Co-Chair of the Eating Disorders Working Group of the Psychiatric Genomics Consortium. She has authored over 800 scientific papers and 60 chapters on eating disorders, and has written several books including 'Crave: Why You Binge Eat and How to Stop' and 'Binge Control: A Compact Recovery Guide.' Dr. Bulik has received numerous awards for her lifetime achievements, including honors from the National Eating Disorders Association, the Academy for Eating Disorders, and the International Society of Psychiatric Genetics. Her academic career is complemented by her personal life, being happily married with three adult children and an accomplished ice dancer.

Research topics

• Psychology
• Biology
• Psychiatry
• Medicine
• Genetics
• Clinical psychology
• Bioinformatics
• Neuroscience
• Virology
• Medical emergency
• Geography
• Computational biology
• Environmental health
• Gerontology
• Pathology
• Immunology
• Cognitive science
• Internal medicine
• Evolutionary biology

Selected publications

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

  Archive ouverte UNIGE (University of Geneva) · 2026-02-10

  articleOpen access

  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.

  PublisherOA PDFDOI

• Associations Between Avoidant/Restrictive Food Intake Disorder Dimensions and Obsessive‐Compulsive Symptomatology

  European Eating Disorders Review · 2026-04-26

  articleOpen access

  OBJECTIVE: Although obsessive-compulsive disorder (OCD) commonly co-occurs with anorexia nervosa and bulimia nervosa, less is known about its relationship with avoidant/restrictive food intake disorder (ARFID) dimensions. Whether associations between ARFID dimensions and OCD differ by sex is also unclear. We examined associations between ARFID dimensions and OCD symptoms by sex, accounting for depression and anxiety. METHODS: Data from 3120 participants ages 15+ in the ARFID Genes and Environment (ARFID-GEN) study were analyzed. ARFID dimensions (i.e., sensory sensitivity; low appetite/lack of interest in food; and fear of aversive consequences), OCD symptoms, anxiety, and depression were assessed using validated self-report measures. We evaluated associations between ARFID dimensions and OCD symptoms using general linear models, adjusting for depression and anxiety. RESULTS: ARFID dimensions were significantly associated with OCD symptoms. After adjusting for depression and anxiety, these associations were attenuated but remained significant for all ARFID dimensions. Associations between ARFID dimensions and OCD symptoms varied by sex. CONCLUSION: The relation between ARFID symptomatology and OCD warrants further exploration across the developmental spectrum in which ARFID appears. Clinically, bidirectional screening may improve diagnostic clarity and be informative to tailor interventions appropriately. TRIAL REGISTRATION: ARFID-GEN is registered in clinicaltrials.gov (NCT05605067).

  PublisherDOI

• Suicidality phenotypes reflect both shared and distinct genetic factors

  medRxiv · 2026-05-19

  article

  ABSTRACT Suicidality phenotypes, including suicidal ideation (SI), non-fatal suicide attempt (SA), and suicide death (SD), are heritable and exhibit both shared and phenotype-specific genetic influences. Using genomic structural equation modelling, we estimated the shared genetic architecture across GWAS of SI (176,147 cases, 1,010,300 controls), SA (53,919 cases, 1,063,988 controls), and SD (7,584 cases, 652,070 controls) and conducted a multivariate GWAS of a latent suicidality factor capturing their shared liability. This analysis identified 36 genome-wide significant loci, including seven not previously reported in any suicidality GWAS. Follow-up analyses identified residual genetic variance specific to each phenotype, including three SD-specific genomic risk loci. Conditioning suicidality phenotypes on genetic liability to psychiatric disorders revealed significant residual genetic variance across SI, SA, SD, and the suicidality common factor. Together, these results suggest that suicidality reflects both shared genetic liability and phenotype-specific contributions.

  PublisherDOI

• Reward responses to food stimuli across sensory modalities: Hunger modulates wanting differentially for pictures and odors

  Appetite · 2026-04-03

  articleOpen access

  Food reward responses are guided both by hunger as a homeostatic need state and by the perceptual evaluation of food cues. Whether interactions between the two vary depending on the sensory modality through which food cues are presented, however, remains unclear. In a preregistered within-subject study, we tested whether modulations of food reward valuation by hunger are more pronounced for food odors compared to food pictures. Participants (N = 43) rated visual and olfactory presentations of food, non-food, and disgusting stimuli in both fasted and sated states across the separable reward dimensions of liking and wanting. Our results showed that hunger selectively increased wanting for food cues (p < 0.001) while food liking was not significantly affected (p = 0.063). Contrary to our hypothesis, this hunger-induced increase in wanting was less pronounced for food odors than for food pictures (p < 0.001). Liking and wanting ratings of non-food stimuli were largely unaffected, regardless of state (p = 1.00; p = 0.208). Overall, our findings indicate that hunger selectively modulates motivational rather than hedonic components of food reward in a modality-dependent manner. The present study establishes a methodological framework for examining how metabolic state and perceptual factors jointly shape food reward evaluation, highlighting the importance of multi-modal approaches for understanding both normative appetite regulation and maladaptive eating behaviors.

  PublisherDOI

• Polygenicity at the pathway level for anorexia nervosa

  medRxiv · 2025-10-09 · 2 citations

  preprintOpen access

  Genome-wide association studies of common disorders reveal polygenic architectures. While these variants may converge into biologically relevant pathways, how polygenicity aggregates across pathways remains unknown. We studied polygenicity at the pathway level in anorexia nervosa (AN) - a psychiatric disorder with multi-systemic clinical manifestations. We constructed pathway-based polygenic risk scores (pathway PRS) to model genetic risk at the pathway level for 3,687 individuals with AN and 11,257 controls. We identified 497 AN-associated pathways after Bonferroni correction, including pathways involved in the brain, metabolism, immunity/stress, and reproduction/development. A strong positive correlation was observed between number of pathways ranking at top 10% and AN case proportion (r = 0.74, P = 7.98x10 -21 ). The positive correlation between pathway count and AN risk was also observed when restricted to individuals with low overall genetic risk of AN. Pathways ranking at top 10% among cases were more diverse than those in controls. Higher AN risk was observed for pathway aggregation within function (e.g., brain or metabolism) and across functions (e.g., brain + metabolism). Individuals at top 10% risk of brain-brain and brain-metabolism pathway pairs had the highest average AN risk compared to other pathway pairs (e.g., brain-immune, metabolism-metabolism). Further, pathway PRS provided higher prediction power of AN than overall genome-wide PRS and contributed to the genetic liability of AN among AN cases with low overall genetic risk. Together, our results demonstrate that polygenicity exists at the pathway level, opening new avenues for disease prediction and identification of actionable targets.

  PublisherOA PDFDOI

• Contrasting Risk Profiles for Suicide Attempt and Suicide Using Danish Registers and Genetic Data

  JAMA Psychiatry · 2025-10-21 · 1 citations

  articleOpen access

  Importance: Not all individuals who die by suicide have a history of nonfatal suicide attempt (SA); however, little is known about the extent to which the genetic and environmental etiologies of SA and suicide are shared or distinct. Objective: To examine shared and distinct risk factors for SA and suicide, focusing on clinically diagnosed health conditions and genetic factors. Design, Setting, and Participants: For health conditions, a nested case-control study was performed using data from the Danish registers. For genetic factors, a case-control analysis framework was used, with individual genotypes retrieved from the iPSYCH2015 dataset, which was nested within the entire Danish population. Individuals older than 10 years were included to minimize the risk of misclassification for SA and suicide. Data were analyzed from January 2024 to April 2025. Exposures: Twenty-eight health conditions and 35 polygenic scores (PGSs) for complex traits. Main Outcomes and Measures: The primary outcomes were SA, suicide, and cumulative SA burden. Associations between health conditions and the risk of SA and suicide were assessed using conditional logistic regression. PGSs for complex traits were calculated using LDpred2-auto, and their associations with SA and suicide were evaluated via logistic regression. To assess whether effect sizes differed significantly between SA and suicide, bayesian model-based classification and Cochran Q test were applied. Results: A total of 81 713 cases of SA (50 512 [61.8%] female; mean [SD] age, 32.3 [14.9] years), with 408 490 age-matched controls (252 525 [61.8%] female; mean [SD] age, 32.3 [14.9] years), and 9362 cases of suicide (2360 [25.2%] female; mean [SD] age, 45.1 [14.6] years), along with 46 749 matched controls (11 796 [25.2%] female; mean [SD] age, 45.1 [14.6] years) who were alive at the date of the case's death, were included in the health conditions analysis. The PGS analysis included 8221 cases of SA (5944 [72.3%] female; mean [SD] age, 19.7 [4.4] years) and 225 cases of suicide (80 [35.6%] female; mean [SD] age, 24.6 [5.0] years). Chronic diseases (eg, dyslipidemia or hearing problems) showed stronger associations with SA, while severe conditions (eg, cancer) were more strongly associated with suicide. Suicide was influenced only by PGSs for mental disorders, whereas SA was associated with both psychiatric and broader health-related genetic risk factors. Notably, dose-response associations were observed for most health conditions and PGSs in relation to cumulative SA burden. Conclusions and Relevance: A broad range of health conditions and genetic factors were associated with increased risk of both outcomes; however, their shared and distinct risk factors suggest that SA and death by suicide are not solely differentiated by liability severity.

  PublisherOA PDFDOI

• Polygenic Scores and Environmental Factors in Psychiatric Disorders: Gene–Environment Interaction Analyses Using the iPSYCH Study

  Research Square · 2025-12-05

  preprintOpen access

  Background: Psychiatric disorders represent a significant global health burden with complex etiologies involving both genetic and environmental factors. However, while the main effects of genetic and environmental factors are frequently studied, their interplay in shaping psychiatric disorder risk remains poorly understood. This study investigates the interaction between polygenic scores (PGS) as proxies for genetic risk and environmental factors in the risk of psychiatric disorders. Method: This study utilized the iPSYCH case-cohort sample (n = 141,265). Environmental factors, including region, urbanicity, parental socioeconomic status, parental age, parental psychiatric history and early-life exposures: autoimmune disease, brain injury, and central nervous system (CNS) infections, were obtained from Danish nationwide registers. Logistic regression was used to examine the effects of targeted disorder-specific PGSs, environmental factors and their interactions on psychiatric disorders. Analyses were adjusted for age, sex and ancestral principal components to account for population stratification. Results: Both PGS and environmental factors were associated with psychiatric disorders. We found limited evidence of gene-environment interactions across the investigated psychiatric disorders. Most interaction terms were small and not statistically significant, but a few remained significant. These included a smaller PGS association with attention deficit hyperactivity disorder in Southern Denmark compared with the Capital Region, a reduced PGS association with bipolar disorder in the medium and lowest parental income groups compared with the highest income group, and a weaker PGS association with major depressive disorder in individuals with parental psychiatric history compared with those without such history. In contrast, a larger PGS association with schizophrenia was observed in the paternal age group 31-35 years compared with the 26-30 years reference group, and a stronger PGS association with anorexia nervosa in North Denmark compared with the Capital Region. Conclusion: Genetic liability for psychiatric disorders, captured through PGS, was associated with mental disorder risk across environmental contexts. Only a few gene-environment interactions were significant, and these were modest and mental disorder-specific. Overall, the findings highlight the difficulty of detecting robust gene-environment interactions and the need for studies of sufficient scale and statistical power to identify subtle gene-environment effects and improve understanding of psychiatric disorder etiology.

  PublisherOA PDFDOI

• Co‐Occurring Weight‐ and/or Shape‐Motivated Restriction in 5747 Adults With Probable Avoidant/Restrictive Food Intake Disorder

  UNC Libraries · 2025-12-11

  articleOpen access

  OBJECTIVE: According to DSM-5-TR, avoidant/restrictive food intake disorder (ARFID) cannot be diagnosed alongside anorexia nervosa (AN), bulimia nervosa (BN), or any other body image disturbance. This does not accurately reflect real-world symptomatology and recent research, indicating the potential need to revise DSM-5-TR Criteria. We investigated the co-occurrence of weight- and/or shape-motivated restriction (WSR) in adults who screened positive for ARFID, providing evidence to inform such changes. METHOD: The sample comprised 5747 adults who consented to participate in the ARFID-Genes and Environment (ARFID-GEN) research study, screened positive for ARFID on the NIAS and PARDI-AR-Q, and completed the EDE-Q. We placed our participants into four groups: groups one and two screened positive for AN (ARFID-AN; n&thinsp;=&thinsp;147) or BN (ARFID-BN; n&thinsp;=&thinsp;193), group three endorsed WSR without meeting AN or BN criteria (ARFID-WSR; n&thinsp;=&thinsp;2159), and group four endorsed ARFID symptoms only (ARFID-nWSR; n&thinsp;=&thinsp;3248). We used generalized linear models to test group differences on the NIAS, PARDI-AR-Q, and EDE-Q. RESULTS: Where significant differences were present, ARFID-nWSR demonstrated lower scores than all other groups across ARFID dimensions on the NIAS and PARDI-AR-Q, and lower odds of meeting DSM-5-TR Criteria A1 to A3 (i.e., weight loss; nutritional deficiencies; dependence on nutritional supplements). DISCUSSION: These findings indicate a mixed phenotype with features of both ARFID and WSR associated with more severe&nbsp;ARFID symptomatology. The DSM-5-TR Criteria may not capture complex real-world symptomatology in adults with probable ARFID, potentially precluding those with the most severe symptoms from receiving accurate diagnoses and appropriate care.

  PublisherDOI

• Co‐Occurring Weight‐ and/or Shape‐Motivated Restriction in 5747 Adults With Probable Avoidant/Restrictive Food Intake Disorder

  International Journal of Eating Disorders · 2025-12-04

  articleOpen access

  OBJECTIVE: According to DSM-5-TR, avoidant/restrictive food intake disorder (ARFID) cannot be diagnosed alongside anorexia nervosa (AN), bulimia nervosa (BN), or any other body image disturbance. This does not accurately reflect real-world symptomatology and recent research, indicating the potential need to revise DSM-5-TR Criteria. We investigated the co-occurrence of weight- and/or shape-motivated restriction (WSR) in adults who screened positive for ARFID, providing evidence to inform such changes. METHOD: The sample comprised 5747 adults who consented to participate in the ARFID-Genes and Environment (ARFID-GEN) research study, screened positive for ARFID on the NIAS and PARDI-AR-Q, and completed the EDE-Q. We placed our participants into four groups: groups one and two screened positive for AN (ARFID-AN; n = 147) or BN (ARFID-BN; n = 193), group three endorsed WSR without meeting AN or BN criteria (ARFID-WSR; n = 2159), and group four endorsed ARFID symptoms only (ARFID-nWSR; n = 3248). We used generalized linear models to test group differences on the NIAS, PARDI-AR-Q, and EDE-Q. RESULTS: Where significant differences were present, ARFID-nWSR demonstrated lower scores than all other groups across ARFID dimensions on the NIAS and PARDI-AR-Q, and lower odds of meeting DSM-5-TR Criteria A1 to A3 (i.e., weight loss; nutritional deficiencies; dependence on nutritional supplements). DISCUSSION: These findings indicate a mixed phenotype with features of both ARFID and WSR associated with more severe ARFID symptomatology. The DSM-5-TR Criteria may not capture complex real-world symptomatology in adults with probable ARFID, potentially precluding those with the most severe symptoms from receiving accurate diagnoses and appropriate care.

  PublisherOA PDFDOI

• Maternal Gestational Low‐Grade Inflammation and the Risk of Anorexia Nervosa in Daughters

  International Journal of Eating Disorders · 2025-10-24

  articleOpen access

  OBJECTIVE: Prenatal exposures have been suggested to have a programming effect on neural and metabolic development, which may affect the risk of eating disorders. We investigated the association between prospectively measured maternal gestational high-sensitivity C-reactive protein (hs-CRP), an established inflammatory biomarker, and subsequent risk of AN in daughters. METHOD: This nested case-control study with sibling-comparison design used systematic sampling from a register-based cohort including all eating disorder patients in Finland born 1991-2000 and diagnosed in specialized health care. Final sample included 150 full triads of females with severe AN (ICD-10 code F50.0), age- and sex-matched population controls, and biological sister controls (total N = 450). RESULTS: Mean gestational hs-CRP values were 4.10 mg/L (SD 5.22), 4.83 mg/L (SD 4.88), and 5.53 mg/L (SD 10.36), for individuals with AN, population controls, and sister controls, respectively. Higher hs-CRP was associated with decreased risk for AN when compared to sister controls (adjusted OR 0.68, 95% Cl 0.48-0.97, p = 0.03). Analyzing hs-CRP in tertiles, maternal hs-CRP in the highest tertile (≥ 5.13 mg/L) versus lowest tertile (≤ 1.94 mg/L) was associated with decreased risk for AN compared to sisters (adjusted OR 0.35, 95% Cl 0.15-0.80, p = 0.01), and to all controls combined (adjusted OR 0.52, 95% Cl 0.29-0.93, p = 0.03). DISCUSSION: We found no evidence that higher gestational CRP would increase the later risk of AN. On the contrary, lower maternal low-grade inflammation early in pregnancy was associated with an increased risk of AN in daughters.

  PublisherOA PDFDOI

Recent grants

• NIH Grant R01MH080065

  NIH · $3.2M · 2014

• NIH Grant R01HD047186

  NIH · $1.4M · 2008

• NIH Grant R01MH082732

  NIH · $919k · 2011

• NIH Grant R21MH070781

  NIH · $359k · 2008

• Enhancing Treatment for Adult Anorexia Nervosa with a Couple-Based Approach

  NIH · $3.1M · 2012–2018

Frequent coauthors

• Hunna J. Watson

  University of North Carolina at Chapel Hill

  378 shared

• Gerome Breen

  NIHR Biomedical Research Centre at The Royal Marsden and the ICR

  326 shared

• Christopher Hübel

  King's College London

  316 shared

• Nadia Micali

  University College London

  246 shared

• Laura M. Thornton

  University of North Carolina at Chapel Hill

  239 shared

• Walter H. Kaye

  University of California, San Diego

  235 shared

• Katherine A. Halmi

  225 shared

• Zeynep Yılmaz

  206 shared

Awards & honors

• Most Valued Colleague Award 2025, Psychiatric Genomics Conso…
• Ming Tsuang Lifetime Achievement Award 2023, International S…
• Lifetime Achievement Award 2022, Academy for Eating Disorder…
• Honorary Professor 2020, Department of Psychological Medicin…
• Erskine Fellowship 2016, University of Canterbury, Christchu…