About

Hilary Coon, PhD, is a Benning Endowed Presidential Professor with appointments in Psychiatry, Bioinformatics, Neurobiology, and Genetic Epidemiology at the Spencer Fox Eccles School of Medicine. She uses Utah's unique research resources to study genetic and environmental risks leading to complex psychiatric conditions, with a current focus on risks leading to suicide mortality. Her work leverages the world’s largest resource of genetic data from suicide deaths, including approximately 8,000 Utah suicides, linked to statewide data such as demographics, autopsy records, clinical data, environmental exposures, and genealogical information. Dr. Coon has established collaborations across scientific fields, creating an ecosystem of researchers dedicated to understanding the complex genetic, clinical, environmental, and social factors that contribute to suicide risk. Her research has led to recent discoveries of genetic risks associated with suicide and aims to translate these findings into strategies to prevent deaths, positioning Utah as a leader in this field. Her primary research interests include identifying genes associated with susceptibility to autism, suicide, and addiction to nicotine and alcohol, often through analyses of extended families in the Utah Population Data Base. She also studies intermediate traits, co-morbid conditions, protective mechanisms, and environmental exposures that influence disease risk, with additional interests in statistical methods for genetic data, cardiovascular genetics, obesity, lung disorders, and research ethics. Dr. Coon is a long-time member of the University of Utah Institutional Review Board.

Research topics

• Biology
• Genetics
• Psychology
• Medicine
• Computational biology
• Psychiatry
• Clinical psychology
• Medical emergency
• Evolutionary biology
• Developmental psychology
• Neuroscience
• Criminology

Selected publications

• 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

• Abstract 1245: Suicide Risk in Oncology: Sex and Cancer Type Differences in a Case-Control Study.

  Cancer Research · 2026-04-03

  article

  Abstract Background: Suicide risk among people with cancer may vary by sex and cancer site, reflecting different biological, psychosocial, and care-system pathways. We used statewide linked mortality and clinical data to examine whether cancer history and sex-specific cancer types differentially relate to pre-death suicidality and suicide mortality. Methods: We conducted a two-step study using population-level data from Utah linking suicide mortality, cancer, and electronic health records. First, we compared suicide decedents with versus without a prior cancer diagnosis (n=14,644) on suicidal ideation (SI), self-injurious behavior (SI), prior suicide attempts (SA), psychiatric and medical comorbidities. Second, we performed an age-and sex-matched case-control analysis of suicide decedents (cases; n=1,015) and living controls (n=9,173) to estimate adjusted odds of suicide death associated with any cancer history and specific cancer types, stratified by sex. Logistic regression models adjusted for prior suicidality, diagnosed mental and substance use disorders (SUD), and chronic medical morbidity. We also characterized the temporal sequencing of first-recorded encounter types (mental health, SUD, chronic medical, or cancer-related). Results: Among suicide decedents, those with any history of a cancer diagnosis had higher odds of pre-death SA (OR=1.27, 95% CI 1.09-1.49), SII (OR=1.34, 1.12-1.60), and SI (OR=1.29, 1.07-1.56) than decedents without cancer. Mental-health burden was substantially greater among female than male decedents (OR=7.90 vs 2.07). In case-control analyses, a history of any cancer was associated with lower overall odds of suicide death, but this aggregate effect masked heterogeneity by sex and cancer type. Among women, cervical cancer/dysplasia was over-represented in cases compared to controls (OR=1.53, 1.13-2.06), suggesting elevated risk in sex-specific, identity-salient cancers. Among men, prostate cancer was inversely associated with suicide death (OR=0.73, 0.59-0.91). First encounters for mental health and substance use were over-represented among cases of both sexes, while chronic-condition encounters suggest additional risk in men. Conclusions: In this study, any history of a cancer diagnosis was linked to greater pre-death suicidality but lower overall odds of suicide death, with important sex-and cancer-type specific differences. Patterns may support a dual-pathway model in which psychosocial/identity-related mechanisms may predominate among women with sex-specific cancers, whereas functional or disease-burden pathways may predominate among men with high-burden cancers. Tailored, sex-and cancer-type-specific suicide risk screening that leverages mental health and substance use encounter history may improve prevention in oncology settings. Citation Format: Brandy M. Byrwa-Hill, Eric T. Monson, Emily DiBlasi, Hilary Coon, Danli Chen, Michael J. Staley, Amanda V. Bakian. Suicide Risk in Oncology: Sex and Cancer Type Differences in a Case-Control Study [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 1245.

  PublisherDOI

• Mapping the genetic landscape across 14 psychiatric disorders

  JuSER Publikationsportal · 2026-01-01

  articleOpen access
  PublisherDOI

• 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 access

  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

• Deleterious coding variation associated with autism is shared across ancestries

  Nature Medicine · 2026-03-30

  articleOpen access

  The past decade has seen remarkable progress in identifying genes that, when impacted by deleterious coding variation, confer high likelihood for autism spectrum disorder (ASD), intellectual disability and other associated developmental disorders. However, most underlying gene discovery efforts have focused on individuals of European ancestry, limiting insights into genetic liability across diverse populations. To help address this, the Genomics of Autism in Latin American Ancestries (GALA) Consortium was formed, presenting here the largest sequencing study of autism in Latin American individuals (n > 15,000, including 4,717 participants with an ASD diagnosis). We identified 35 genome-wide significant (false discovery rate < 0.05) autism-associated genes, with substantial overlap with findings from European cohorts, and highly constrained genes showing consistent signal across populations. The results provide support for emerging (for example, MARK2, YWHAG, PACS1, RERE, SPEN, GSE1, GLS, TNPO3 and ANKRD17) and established autism genes and for the utility of genetic testing approaches for deleterious variants in individuals from diverse backgrounds; the results also demonstrate the ongoing need for more inclusive genetic research and testing. We conclude that the biology of autism is consistent across populations, with no detectable influence of ancestry.

  PublisherOA PDFDOI

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

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

  articleOpen access1st authorCorresponding

  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.

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• Distinguishing clinical and genetic risk factors for suicidal ideation and behavior in a diverse hospital population

  Translational Psychiatry · 2025-02-20 · 7 citations

  articleOpen access

  Suicidal ideation (SI) and behavior (SB) are major public health concerns, but risk factors for their development and progression are poorly understood. We used ICD codes and a natural language processing algorithm to identify individuals in a hospital biobank with SI-only, SB, and controls without either. We compared the profiles of SB and SI-only patients to controls, and each other, using phenome-wide association studies (PheWAS) and polygenic risk scores (PRS). PheWAS identified many risk factors for SB and SI-only, plus specific psychiatric disorders which may be involved in progression from SI-only to SB. PRS for suicide attempt were only associated with SB, and even after accounting for psychiatric disorder PRS. SI PRS were only associated with SI-only, although not after accounting for psychiatric disorder PRS. These findings advance understanding of distinct genetic and clinical risk factors for SB and SI-only, which will aid in early detection and intervention efforts.

  PublisherOA PDFDOI

• Intragenic deletions from whole genome sequencing of 1054 suicide deaths

  medRxiv · 2025-03-06 · 1 citations

  preprintOpen accessSenior authorCorresponding

  Suicide is an urgent public health crisis that claimed over 48,000 lives in the US in 2022. The importance of genetics in suicide risk has been established by classical twin and family studies, and confirmed with recent large genome-wide association studies (GWAS). While the GWAS are beginning to reveal genetic risk due to common variants each with small effect on liability, these results explain only a fraction of the genetic risk. As with other complex health conditions, some of this unexplained risk is likely due to rarer variants with larger effect on liability. Using whole genome sequencing (WGS) data from 1,054 population-ascertained Utah suicide deaths, we investigated intragenic deletions as a class of genomic variation highly likely to disrupt gene function. To minimize the chance of false positive results, studied deletions were limited to those found in three large publicly-available control datasets (1000 Genomes, GnomAD, and Centers for Common Disease Genomics). Additional internal replication also required deletions to occur at least twice in WGS from an initial cohort of 670 suicide deaths then again in a second cohort of 384 suicide deaths. All results meeting these filters were manually validated. There were 11 validated deletions with at least 2-fold increase in frequency over occurrence in controls (range 2.28 to 4.46). These results implicated genes associated with risk of mental health conditions (MPST, IL4R, CDH13), epilepsy (CLCA4), intellectual disability (ZNF44), neuronal function (OSBPL2), metabolic function (FBOX36), lipid metabolism (TM9SF3), immune related functions (PIPOX, IL4R), and transcriptional repression (ZHX3). SNPs in genes implicated by the deletions have also been associated with mental health conditions, neuronal function, immune response, and other critical biological pathways including neuroinflammation and cellular response to stress. Demographic and clinical associations of suicide deaths with specific genetic deletions, highlight the prevalence of mood, anxiety and bipolar disorders and variations in age at suicide death among affected individuals. This work is the largest genome-wide analyses of WGS variation in suicide deaths to date. Pending replication, results will guide future functional studies with the eventual goals of increased understanding of mechanisms leading to risk.

  PublisherOA PDFDOI

• Inherited genetic risk in stillbirth: A shared genomic segments analysis of high-risk pedigrees

  Human Genetics and Genomics Advances · 2025-11-14

  articleOpen access

  Stillbirth is a devastating adverse pregnancy outcome affecting 2 million pregnancies worldwide. Although an etiology may be found in some stillbirths, one-third remain unexplained. Stillbirth clusters in families and few underlying inherited genes associated with stillbirth are known. Well-characterized family-based studies may aid in identifying genetic contributors to unexplained stillbirth. Using the Utah Population Database, we defined pedigrees with high familial risk of stillbirth. Comprehensive phenotyping with review of primary medical records was conducted to identify stillbirth cases without identifiable causes. We generated whole-genome sequencing in seven stillborn placentas from three pedigrees. We performed shared genomic segments analysis to identify evidence for segregating haplotypes shared by the stillbirths to provide evidence for inherited risk. A region at 15q26.3 was identified in two independent pedigrees with genome-wide significance in both (a 1.2 Mb segment shared by two stillbirths in pedigree A, and a 1.8 Mb segment shared by two stillbirths in pedigree B). Four other regions reached genome-wide significance in single pedigrees at 16p13.13-p13.12, 9p13.3-p13.1, and 6p22.2-p22.1 (shared by the same two stillbirths in pedigree B), and a 0.8 Mb segment at 14q.32.2 shared by three stillbirths in pedigree C. The identified regions are implicated in in utero and postnatal development, pregnancy loss, and infertility. We identified evidence for inherited risk loci in stillbirth placental genes that are implicated in in utero and postnatal development, pregnancy loss, and infertility. Identification of inherited genes in stillbirth risk may provide therapeutic targets for prevention and treatment to improve pregnancy outcomes.

  PublisherDOI

Recent grants

• NIH Grant R01MH069359

  NIH · $2.1M · 2011

• Prediction of suicide death using EHR and polygenic risk scores

  NIH · $4.2M · 2020–2030

• Genetic risk discovery using WGS from a population-based resource of 10,000 suicide deaths with DNA

  NIH · $2.7M · 2026–2030

• NIH Grant R29MH052055

  NIH · $523k · 2002

• NIH Grant P01HD035476

  NIH · $6.6M · 2002

Frequent coauthors

• Anna R. Docherty

  150 shared

• Amanda V. Bakian

  Huntsman Cancer Institute

  107 shared

• Michael A. Province

  Washington University in St. Louis

  104 shared

• Donna K. Arnett

  University of Charleston

  103 shared

• Richard H. Myers

  Boston University

  93 shared

• Andrey A. Shabalin

  89 shared

• Emily DiBlasi

  Huntsman Cancer Institute

  84 shared

• Brooks Keeshin

  80 shared

Awards & honors

• Benning Endowed Presidential Professor