Elucidating the Neurobiologic Etiology of Comorbid PTSD and Substance Use Disorders

Early childhood maltreatment and other traumatic event experiences (“trauma”) are common among youth, including those with substance use problems including substance use disorders (SUD). Particularly, interpersonal violence is associated with high rates of comorbidity between posttraumatic stress di...

Full description

Bibliographic Details
Main Authors: Jesse D. Hinckley, Carla Kmett Danielson
Format: Article
Language:English
Published: MDPI AG 2022-08-01
Series:Brain Sciences
Subjects:
Online Access:https://www.mdpi.com/2076-3425/12/9/1166
_version_ 1797490524045705216
author Jesse D. Hinckley
Carla Kmett Danielson
author_facet Jesse D. Hinckley
Carla Kmett Danielson
author_sort Jesse D. Hinckley
collection DOAJ
description Early childhood maltreatment and other traumatic event experiences (“trauma”) are common among youth, including those with substance use problems including substance use disorders (SUD). Particularly, interpersonal violence is associated with high rates of comorbidity between posttraumatic stress disorder (PTSD) and SUD, and these comorbid disorders exhibit high levels of overlapping symptomatology. Theoretical models proposed to explain the bidirectional relationship between PTSD and SUD include the self-medication hypothesis and susceptibility hypothesis. In this article, we explore neurobiologic changes associated with trauma, PTSD, and SUD that underly dysregulated stress response. Examining lessons learned from recent translational and clinical research, we propose that further elucidating the neurobiologic etiology of comorbid PTSD and SUD will require a collaborative, interdisciplinary approach, including the integration of preclinical and clinical studies, exploration of biologic markers in clinical studies, and accumulation of larger studies and longitudinal studies with the power to study PTSD and SUD. Such research can transform the field and ultimately reduce high rates and costly impairment of co-occurring PTSD and SUD across the lifespan.
first_indexed 2024-03-10T00:34:12Z
format Article
id doaj.art-288a109b632945e1b0d73e33fa6dba77
institution Directory Open Access Journal
issn 2076-3425
language English
last_indexed 2024-03-10T00:34:12Z
publishDate 2022-08-01
publisher MDPI AG
record_format Article
series Brain Sciences
spelling doaj.art-288a109b632945e1b0d73e33fa6dba772023-11-23T15:20:19ZengMDPI AGBrain Sciences2076-34252022-08-01129116610.3390/brainsci12091166Elucidating the Neurobiologic Etiology of Comorbid PTSD and Substance Use DisordersJesse D. Hinckley0Carla Kmett Danielson1Division of Addiction Science, Treatment & Prevention, Department of Psychiatry, University of Colorado School of Medicine, 1890 N Revere Court, MS-F570, Aurora, CO 80045, USANational Crime Victims Research & Treatment Center, Department of Psychiatry & Behavioral Sciences, Medical University of South Carolina, 67 President Street, MSC 861, Charleston, SC 29425, USAEarly childhood maltreatment and other traumatic event experiences (“trauma”) are common among youth, including those with substance use problems including substance use disorders (SUD). Particularly, interpersonal violence is associated with high rates of comorbidity between posttraumatic stress disorder (PTSD) and SUD, and these comorbid disorders exhibit high levels of overlapping symptomatology. Theoretical models proposed to explain the bidirectional relationship between PTSD and SUD include the self-medication hypothesis and susceptibility hypothesis. In this article, we explore neurobiologic changes associated with trauma, PTSD, and SUD that underly dysregulated stress response. Examining lessons learned from recent translational and clinical research, we propose that further elucidating the neurobiologic etiology of comorbid PTSD and SUD will require a collaborative, interdisciplinary approach, including the integration of preclinical and clinical studies, exploration of biologic markers in clinical studies, and accumulation of larger studies and longitudinal studies with the power to study PTSD and SUD. Such research can transform the field and ultimately reduce high rates and costly impairment of co-occurring PTSD and SUD across the lifespan.https://www.mdpi.com/2076-3425/12/9/1166PTSDsubstance use disordersadolescenceamygdalaprefrontal cortexmesolimbic dopamine system
spellingShingle Jesse D. Hinckley
Carla Kmett Danielson
Elucidating the Neurobiologic Etiology of Comorbid PTSD and Substance Use Disorders
Brain Sciences
PTSD
substance use disorders
adolescence
amygdala
prefrontal cortex
mesolimbic dopamine system
title Elucidating the Neurobiologic Etiology of Comorbid PTSD and Substance Use Disorders
title_full Elucidating the Neurobiologic Etiology of Comorbid PTSD and Substance Use Disorders
title_fullStr Elucidating the Neurobiologic Etiology of Comorbid PTSD and Substance Use Disorders
title_full_unstemmed Elucidating the Neurobiologic Etiology of Comorbid PTSD and Substance Use Disorders
title_short Elucidating the Neurobiologic Etiology of Comorbid PTSD and Substance Use Disorders
title_sort elucidating the neurobiologic etiology of comorbid ptsd and substance use disorders
topic PTSD
substance use disorders
adolescence
amygdala
prefrontal cortex
mesolimbic dopamine system
url https://www.mdpi.com/2076-3425/12/9/1166
work_keys_str_mv AT jessedhinckley elucidatingtheneurobiologicetiologyofcomorbidptsdandsubstanceusedisorders
AT carlakmettdanielson elucidatingtheneurobiologicetiologyofcomorbidptsdandsubstanceusedisorders