About

Alex Bennion, DO, is an Assistant Professor (Clinical) in the Department of Psychiatry at the University of Utah. He earned his medical degree at Des Moines University and completed his Adult Psychiatry residency at the University of Utah Spencer Fox Eccles School of Medicine, during which he was awarded the professionalism award. His clinical interests include psychiatric care for college-aged individuals, depressive disorders, anxiety disorders, treatment-resistant disorders, psychotherapies, medical education, and medical ethics. Dr. Bennion is board-certified in Psychiatry by the American Board of Psychiatry & Neurology and is actively involved in outpatient psychiatric care at the University of Utah Huntsman Mental Health Institute and the Madsen Student Health Center. He was born and raised in Salt Lake City, Utah, and has a strong desire to improve mental healthcare within his community. He views mental health care as a partnership with his patients, values high standards of patient care, and mentors medical students and residents to instill these values.

Research topics

• Medicine
• Computer Science
• Biology
• Ophthalmology
• Bioinformatics
• World Wide Web
• Psychology
• Psychiatry
• Multimedia
• Medical education
• Genetics
• Optometry
• Internet privacy
• Applied psychology

Selected publications

• 508. Leveraging Technology for Youth Suicide Crisis Intervention Through a Smartphone App

  Biological Psychiatry · 2023

  • Computer Science
  • Psychology
  • Psychiatry
  PublisherDOI

• Author Correction: Macular retinal thickness differs markedly in age-related macular degeneration driven by risk polymorphisms on chromosomes 1 and 10

  Scientific Reports · 2021 · 1 citations

  • Ophthalmology
  • Medicine
  • Optometry

  An amendment to this paper has been published and can be accessed via a link at the top of the paper.

  PublisherOA PDFDOI

• Macular retinal thickness differs markedly in age-related macular degeneration driven by risk polymorphisms on chromosomes 1 and 10

  Scientific Reports · 2020 · 30 citations

  • Ophthalmology
  • Medicine
  • Bioinformatics

  The two most common genetic contributors to age-related macular degeneration (AMD), a leading cause of irreversible vision loss worldwide, are variants associated with CFH-CFHR5 on chromosome 1 (Chr1) and ARMS2/HTRA1 on chromosome 10 (Chr10). We sought to determine if risk and protective variants associated with these two loci drive differences in macular retinal thickness prior and subsequent to the onset of clinically observable signs of AMD. We considered 299 individuals (547 eyes) homozygous for risk variants or haplotypes on Chr1 or Chr10 exclusively (Chr1-risk and Chr10-risk, respectively) or homozygous for a neutral haplotype (Chr1-neu), for the protective I62 tagged haplotype (Chr1-prot-I62) or for the protection conferring CFHR1/3 deletion haplotype (Chr1-prot-del) on Chr1 without any risk alleles on Chr10. Among eyes with no clinically observable signs of AMD, the deletion of CFHR1/3, which is strongly protective against this disease, is associated with significantly thicker retinas in the perifovea. When controlling for age, Chr10-risk eyes with early or intermediate AMD have thinner retinas as compared to eyes from the Chr1-risk group with similar disease severity. Our analysis indicates that this difference likely results from distinct biological and disease initiation and progression events associated with Chr1- and Chr10-directed AMD.

  PublisherOA PDFDOI

Frequent coauthors

• Jill L. Hageman

  University of Utah

  2 shared

• Gregory S. Hageman

  University of Utah

  2 shared

• Burt T. Richards

  University of Utah

  2 shared

• Moussa A. Zouache

  University of Utah

  2 shared

• Christian Pappas

  St George Hospital

  2 shared

• Melinda Westlund Schreiner

  University of Utah

  1 shared

• Scott A. Langenecker

  The Ohio State University

  1 shared

• Daniel Feldman

  University of Utah

  1 shared

Awards & honors

• professionalism award