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...
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Format: | Article |
Language: | English |
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MDPI AG
2022-08-01
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Series: | Brain Sciences |
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Online Access: | https://www.mdpi.com/2076-3425/12/9/1166 |
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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 |