About

Anna R. Docherty, PhD, is an Assistant Professor in the Department of Psychiatry at the University of Utah. Her research focuses on identifying the genetic basics of suicide, leveraging new computational techniques to analyze millions of DNA variants in Utah suicide death samples. Her work aims to validate genetic risk scores for suicide that predict case-control status in the lab, with the goal of reducing stigma, increasing education, and enabling better prediction and prevention strategies for suicide. Her research also explores how the genetics of suicide overlap with genetic risks for other medical conditions and how genetic risk interacts with environmental factors to influence individual risk.

Research topics

• Biology
• Genetics
• Psychology
• Medicine
• Psychiatry
• Clinical psychology
• Computer Science
• Computational biology
• Medical emergency
• Evolutionary biology
• Environmental health
• Criminology
• Internal medicine

Selected publications

• Negative symptoms in the Hierarchical Taxonomy of Psychopathology: Nosology, etiology, and pathophysiology

  Schizophrenia Research · 2026-05-20

  articleOpen access

  This review examines negative symptoms in the context of the Hierarchical Taxonomy of Psychopathology (HiTOP) model of psychopathology. The HiTOP model was developed as an alternative to traditional psychiatric diagnoses-improving reliability, parsing heterogeneity, and accounting for patterns of comorbidity--thus advancing the ability of researchers and clinicians to understand negative symptoms. In the current HiTOP model, negative symptoms are components of the psychoticism (thought disorder) spectrum alongside positive symptoms and disorganization, though recent HiTOP consortium publications suggest it may be more closely associated with the detachment spectrum. The primary objective of this review is to determine which placement is correct and the implications of this placement for HiTOP and negative symptoms research. In particular, factor analytic research that has emerged since the initial publication of the HiTOP model suggests that negative symptoms can be fully accounted for by the detachment spectrum, alongside personality traits and disorders related to detachment (avoidant, schizoid, extraversion, etc.). In addition, the etiological, developmental, neurobehavioral, and treatment research literatures are reviewed from the perspective of how existing evidence may fit this revised conceptualization of negative symptoms and psychosis. Overall, these research areas provide support for distinctions between psychoticism and detachment in the HiTOP model. Finally, recommendations are offered regarding how the HiTOP model may be further advanced and how researchers and clinicians may benefit from this approach to understanding negative symptoms.

  PublisherDOI

• The Psychiatric Genomics Consortium: discoveries and directions

  UNC Libraries · 2026-02-10

  articleOpen access
  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

• Mapping the genetic landscape across 14 psychiatric disorders

  JuSER Publikationsportal · 2026-01-01

  articleOpen access
  PublisherDOI

• Pathways from Polygenic Risk to Suicidality: Effects of Alcohol Use Disorder and Childhood Adversity

  medRxiv · 2026-02-12

  articleOpen access

  Abstract Background The prevalences of suicidal ideation (SI) and suicide attempt (SA) are influenced by genetic, behavioral, and environmental factors. Alcohol use disorder (AUD) and adverse childhood experiences (ACEs) may mediate or moderate genetic liability for suicidality. Methods Using data from 10,275 participants (43.8% female; 47.2% African-like genetic ancestry [AFR], 52.8% European-like genetic ancestry [EUR]), we tested whether polygenic scores (PGS) for SI and SA predicted lifetime SI or SA. We also evaluated whether alcohol use disorder (AUD) mediated these associations and whether adverse childhood experiences (ACEs) moderated the direct and indirect pathways. Results Although there were significant direct associations of the SA PGS with SA (AFR: b = 0.36, SE = 0.01; EUR: b = 0.17, SE = 0.01; both p s < 2e-16), the SI PGS did not predict SI (p > 0.55). AUD mediated SA genetic risk (average causal mediation effect (ACME): AFR = 0.01, 95% CI [0.01-0.01]; EUR = 0.02, 95% CI [0.01-0.02]; both p s < 2e-16). Moderation analyses indicated that indirect effects were attenuated by ACEs score (ΔACME: AFR = 0.02, p < 2e-16; EUR = 0.01, p = 0.03). There was neither mediation nor moderated mediation for SI. Conclusions Genetic liability to SA operates partly through AUD, particularly among individuals with lower childhood adversity. Under higher adversity, alternative pathways to SA likely predominate. These findings highlight the need to consider distinct etiological pathways to the development of suicidality and the relevance of AUD as a modifiable target for suicide prevention among individuals at high genetic liability.

  PublisherOA PDFDOI

• Independent and interactive effects of wet bulb globe temperature and air pollution exposures on suicide mortality

  Environment International · 2026-02-21

  articleOpen access

  BACKGROUND: ) on suicide mortality. METHODS: on suicide. For exposure windows, we considered single days preceding suicide (lag 0 to 6) and their averages across preceding days (lag 0-1, 0-3, and 0-6). Analyses were stratified by season. RESULTS: levels. CONCLUSIONS: on suicide in the warm season, emphasizing the need for considering the combined effects of heat stress and air pollution in suicide prevention strategies.

  PublisherDOI

• Clinical and Genetic Evaluation of Suicide Death with and without Interpersonal Trauma Exposure

  medRxiv · 2026-04-16

  articleOpen access

  Abstract Importance Suicide is a leading cause of death in the United States with risk strongly influenced by Interpersonal trauma, contributing to treatment resistance and clinical complexity. Objective To assess clinical and genetic factors in individuals who died from suicide, with and without interpersonal trauma exposure. Design Individuals who died from suicide with and without trauma were compared in a retrospective case-case design. Prevalence of 19 broad clinical categories was assessed between groups. Results directed selection of 42 clinical subcategories, and 40 polygenic scores (PGS) for further assessment. Multivariable logistic regression models, adjusted for critical covariates and multiple tests, were formulated. Models were also stratified by age group (<26yo and ≥26yo), sex, and age/sex. Setting A population-based evaluation of comorbidity and polygenic scoring in two suicide death subgroups. Participants A total of 8 738 Utah Suicide Mortality Research Study individuals (23.9% female, average age = 42.6 yo) who died from suicide were evaluated, divided into trauma ( N = 1 091) and non-trauma exposed ( N = 7 647) individuals. A subset of unrelated European genotyped individuals was also assessed in PGS analyses (Trauma N = 491; Non-trauma N = 3 233). Exposures “Trauma” is here defined as interpersonal trauma exposure, including abuse, assault, and neglect from International Classification of Disease coding. Main Outcomes and Measures Prevalence of comorbid clinical sub/categories and PGS enrichment in trauma versus non-trauma exposed suicide deaths. Results Overall, trauma-exposed individuals died from suicide earlier (mean age of 38.1 yo versus 43.3 yo; P <0.0001) and were disproportionately female (38% versus 21%, OR = 3.3, CI = 2.9-3.8). Prevalence of asphyxiation and overdose methods, prior suicidality, psychiatric diagnoses, and substance use (OR range = 1.3-3.7) were elevated in trauma exposed individuals who died from suicide. Genetic PGS were also elevated in trauma-exposed individuals who died from suicide for depression, bipolar disorder, cannabis use, PTSD, insomnia, and schizophrenia (OR range = 1.1-1.4) with ADHD and opioid use showing uniquely elevated PGS in trauma exposed males (OR range = 1.2-1.4). Conclusions and Relevance Results demonstrated multiple convergent lines of age- and sex-specific evidence differentiating trauma-exposed from non-trauma exposed suicide death. Such findings suggest unique biological backgrounds and may refine identification and treatment of this high-risk group.

  PublisherOA PDFDOI

• Genetic risk of chronic pain conditions associated with risk of suicide death through an integrative analysis of EHR and genomics data

  Translational Psychiatry · 2026-02-16

  articleOpen accessSenior author

  Abstract Chronic pain represents heritable conditions linked to suicide death. It has been suggested that a shared genetic predisposition may contribute to this relationship, but there has not yet been a comprehensive assessment of genetic and clinical overlaps of different types of chronic pain with suicide death. Here, we integrated whole-genome sequencing and electronic health records from 986 unrelated individuals of European ancestry who died by suicide in the Utah Suicide Mortality Research Study and 415 ancestrally-matched population controls selected for absence of disease. Polygenic scores (PGSs) for seven distinct types of chronic pain were calculated and tested in the suicide cohort. We observed significant positive associations of PGSs for multisite chronic pain (PGS MCP ) and chronic widespread pain (PGS CWP ) with suicide mortality. Sex-stratified analyses showed elevations in both males and females. Pain diagnosis-stratified analyses revealed associations with suicide death regardless of chronic pain diagnoses. Follow-up tests of PGSs for more specific pain conditions showed additional associations with suicide death for: 1) monoarticular arthritis, 2) back pain, and 3) chronic inflammatory demyelinating polyneuropathy across all suicide death individuals, and 4) irritable bowel syndrome within males only. In a multiple logistic regression test of all chronic pain PGSs associating suicide death status, four types of pain remained uniquely associated with suicide death, highlighting distinct subgroups within suicide death: some attributed to MCP and CWP, and others associated with monoarticular arthritis or chronic inflammatory demyelinating polyneuropathy. This cohort study reports associations between suicide death and PGSs from various pain conditions, regardless of sex or chronic pain diagnosis, suggesting that combining genetic and clinical risk factors may better identify genetic overlap, causal directions, and/or specific gene pathways.

  PublisherOA PDFDOI

• Genetic Liabilities to Neuropsychiatric Conditions in Suicide Deaths With No Prior Suicidality

  JAMA Network Open · 2025-10-20 · 1 citations

  articleOpen access

  Importance: Although suicide attempt is the most robust estimator of suicide death, few individuals who attempt it go on to die by suicide (<10%), and approximately 50% of suicide deaths occur in the absence of evidence of prior attempts. The risks are particularly poorly understood in this group. Objective: To study underlying polygenic liabilities among suicide deaths without evidence of prior nonfatal suicidality (SD-N) compared with suicide deaths with prior suicidality (SD-S), testing prior results showing significantly lower clinical risks of neuropsychiatric traits in SD-N vs SD-S. Design, Setting, and Participants: In this cohort study, polygenic scores (PGS) were computed using summary statistics from 12 published source studies, then compared across SD-N and SD-S groups taken from the Utah Suicide Mortality Research Study (cases accrued between December 1998 and October 2022). PGS from the suicide death cohorts were also compared to unselected population controls. Evidence of prior suicidality was determined from diagnoses and clinical notes. Main Outcomes and Measures: Cohort differences in PGS reflecting neuropsychiatric conditions were tested using analysis of covariance, adjusting for sex, age, and genetic ancestry, followed by additional analyses within sex and within subgroups defined by age at death (50 years or younger vs older than 50 years). PGS spanned 12 neuropsychiatric conditions. Data were analyzed between July 2024 and July 2025. Results: The SD-N cohort (n = 1337) had significantly more male suicide deaths (1105 [82.65%] vs 974 [67.95%]), with an older mean (SD) age at death (47.5 [18.9] vs 41.4 [15.6] years) than the SD-S cohort (n = 1432). The control cohort (n = 19 499) had significantly fewer males (8597 [44.09%]) than both suicide death subsets. Genetic ancestry was similar across the SD-N and SD-S groups (96.77% and 96.81% European ancestry), and control (97.38% European ancestry) groups. Socioeconomic status was not significantly different across suicide cohorts adjusted for age and sex (occupation ranking SD-N mean [SD], 57.16 [24.54]; SD-S mean [SD], 54.72 [25.29]; t = 1.30; P = .70; maximum education SD-N mean [SD], 2.70 [1.12]; SD-S mean [SD], 2.67 [1.13]; Fisher exact test P = .38). Comparing SD-N to SD-S revealed significantly lower (false discovery rate P < .05) PGS in the SD-N group for major depressive disorder (adjusted mean difference, 0.085 [95% CI, 0.018-0.152]; P = .01), depressed affect (adjusted mean difference, 0.081 [95% CI, 0.012-0.149]; P = .02), anxiety (adjusted mean difference, 0.091 [95% CI, 0.021-0.161]; P = .01), neuroticism (adjusted mean difference, 0.102 [95% CI, 0.033-0.171]; P = .004), and Alzheimer disease (adjusted mean difference, 0.090 [95% CI, 0.021-0.1658]; P = .01), and lower (false discovery rate P < .10) PGS in SD-N for posttraumatic stress disorder (adjusted mean difference, 0.070 [95% CI, 0.001-0.139]; P = .04). Of note, SD-N PGS were not significantly different from controls for depressed affect (adjusted mean difference, 0.037 [95% CI, -0.019 to 0.093]), neuroticism (adjusted mean difference, -0.001 [95% CI, -0.057 to 0.055]), or Alzheimer disease (adjusted mean difference, -0.027 [95% CI, -0.083 to 0.029]). Conclusions and Relevance: In this cohort study, SD-N showed significantly different genetic liabilities to neuropsychiatric conditions from SD-S. Results have implications for future suicide research and prevention for persons at risk of mortality.

  PublisherOA PDFDOI

• ACCELERATING THE GENOMICS OF SUICIDE AND SUICIDAL BEHAVIORS: UPDATES FROM THE SUICIDE WORKING GROUP OF THE PSYCHIATRIC GENOMICS CONSORTIUM

  European Neuropsychopharmacology · 2025-10-01

  article1st authorCorresponding
  PublisherDOI

Recent grants

• Modeling Dimensionality and Genetic Heterogeneity in Schizophrenia

  NIH · $675k · 2016–2020

• NIH Grant F31MH092081

  NIH · $60k · 2012

• Genome-Wide Association Analysis of Suicide Death

  NIH · $3.2M · 2020–2026

Frequent coauthors

• Hilary Coon

  Huntsman Cancer Institute

  150 shared

• Andrey A. Shabalin

  146 shared

• Emily DiBlasi

  Huntsman Cancer Institute

  102 shared

• Amanda V. Bakian

  Huntsman Cancer Institute

  97 shared

• Tim B. Bigdeli

  SUNY Downstate Health Sciences University

  93 shared

• Brooks Keeshin

  82 shared

• Eric T. Monson

  80 shared

• Kenneth S. Kendler

  Icahn School of Medicine at Mount Sinai

  76 shared

Education

• Ph.D.

  University of Missouri Columbia

  2013