Cannabis & Post-Traumatic Stress Disorder (PTSD)
Ten years ago when I first investigated links between cannabis use and PTSD there were no published human studies investigating this question. For this case a Medline search for cannabi* and ‘traumatic’ generated 100x studies (including those relating to traumatic brain injury).
Association with cannabis use
Cornelius et al[i], studying interactions between PTSD and cannabis use, reported “PTSD is directly associated with the presence of a CUD (cannabis use disorder) and with peer deviance, that higher peer deviance is associated with the presence of a CUD, and that PTSD mediated the association between peer deviance and CUD… These findings suggest that PTSD contributes to the etiology of CUD among teenagers”
Saban et al[ii] found “significant associations were found between PTSD and all substance use, between depression, alcohol, cannabis and inhalant use, and between anxiety and cannabis use.” Clark et al[iii] found PTSD to be a common diagnosis among a group of alcoholic adolescents, who also showed high rates of cannabis and hallucinogen use, considering the relationship to reflect a comorbid disorder
Theoretical & Animal Studies
Reviewing animal studies, Abush & Akirav[iv] reported these provided “preclinical support for the suggestion that targeting the endocannabinoid system may aid in the treatment of disorders associated with impaired extinction-like processes, such as post-traumatic stress disorder.” Kamprath et al[v] proposed “CB1 proteins (as) a potential therapeutic target to accompany habituation-based therapies of post-traumatic symptoms.” Hill & Gorzalka[vi] reviewed the “endocannabinoid system in the etiology and treatment of mood and anxiety disorders, such as depression, anxiety and post-traumatic stress disorder” and concluded “Collectively, both clinical and preclinical data argue that cannabinoid receptor signalling may be a realistic target in the development of a novel class of agent for the pharmacotherapy of mood and anxiety disorders.”
Ursano et al[vii] noted “PTSD is a "forgetting" disorder… cannabinoids are bringing new perspectives to understanding brain function in PTSD” Lehner et al[viii] postulated “Behavioural therapy of phobias and PTSD can be facilitated by … ligands stimulating endogenous cannabinoid system and by gluocorticosteroids.” In a genetic study of the cannabinoid receptor gene CNR1, Lu et al[ix] suggested “the CNR1 gene may be a risk factor for ADHD and possibly PTSD” Chwattal et al[x] found “the eCB (endocannabinoid) system can be modulated to enhance emotional learning, and suggest that eCB modulators may be therapeutically useful as adjuncts for exposure-based psychotherapies such as those used to treat Post-Traumatic Stress Disorder and other anxiety disorders.”
In an inpatient setting, Van Zyl et al[xi] noted “We did not find significant clinical differentiating factors between subjects with and without PTSD; however subjects with PTSD were more likely to use cannabis.” Guillem et al[xii] studying cannabis users in an outpatient setting, found “The prevalence of anxiety disorders in the last 12 months was social phobia (29%); generalised anxiety disorder (17%); panic disorder with or without agoraphobia (16%); obsessive compulsive disorder (12%); agoraphobia without panic disorder (9%) and post-traumatic stress disorder (5%)”
In a study of HIV+ incarcerated women, Lewis[xiii] reported “Women with lifetime PTSD were also more likely to have had outpatient psychiatric treatment, treatment with psychiatric medications, suicide attempts, lifetime cannabis abuse/dependence, lifetime major depression, and antisocial personality disorder.”
Particular patient groups
In a study of Swiss citizens caught in the 2004 Tsunami, Vetter et al[xiv] reported “In women PTSD symptoms and degree of exposure enlarged the odds of increased alcohol, pharmaceuticals and cannabis use significantly. In men the relationship was more specific: PTSD symptoms and degree of exposure only enlarged the odds of increased pharmaceutical consumption significantly. Increases in alcohol, cannabis and tobacco use were only significantly associated with the degree of PTSD symptoms.”
In a study of Israeli youths personally affected by terrorist attacks, Schiff et al[xv] found “Close physical exposure to acts of terrorism predicted higher levels of alcohol consumption (including binge drinking among drinkers) and cannabis use. These relationships remained even after we controlled for posttraumatic stress and depressive symptoms.”
In a study of Nigerian army veterans, Okulate & Jones[xvi] noted “PTSD was significantly associated with long duration of stay in the mission area, current alcohol use, lifetime use of an alcohol/gunpowder mixture, and lifetime cannabis use.” In a twin study of Vietnam veterans, Koenen et al[xvii] reported “combat exposure, adjusted for C-PTSD, was significantly associated with increased risk for alcohol and cannabis dependence and that C-PTSD mediated the association between combat exposure and both major depression and tobacco dependence.” DeFazio et al[xviii] studied Vietnam veterans, finding a higher incidence of PTSD symptoms among combat, compared to non-combat groups, the relationship to cannabis use is unclear, but may reflect a coping strategy, where the use of marijuana by US troops during combat has been widely-documented, and upon return to civilian life.
In a study of childhood abuse Reigstad et al[xix] reported “Self-reports of abuse were associated with referral for depression, symptoms of depression and suicidal risk” Houston et al[xx] found no relationship between early-onset cannabis use or childhood sexual trauma and subsequent depression or psychosis. In a study of female drug clinic patients with histories of post-traumatic stress disorder following physical or sexual abuse, Gil-Revas et al[xxi] reported “Sexual and physical abuse are associated with higher levels of posttraumatic stress disorder (PTSD) symptomatology. Moreover, women are more likely than men to possess an array of psychological factors that predict relapse to drug use after treatment, including low self-esteem, depression, anxiety, and suicidal behavior, among others. But contrary to expectation, PTSD is not associated with relapse to drug use, nor are women more likely than men to relapse within a six-month posttreatment interval.””.
Harley et al[xxii] reported “the presence of both childhood trauma and early cannabis use significantly increased the risk for psychotic symptoms beyond the risk posed by either risk factor alone, indicating that there was a greater than additive interaction between childhood trauma and cannabis use
Vauth & Nyberg[xxiii] reported that among schizophrenics with undiagnosed PTSD “Risk for development of alcohol misuse, cannabis misuse or benzodiazepine misuse and depression may be higher” Corstophine et al[xxiv], studying eating disorders, reported “Childhood sexual abuse was particularly important, and was associated with self-cutting, alcohol abuse, and substance abuse (amphetamines, cocaine, cannabis and 'other substances', including ketamine and benzodiazepines).”
Fraser[xxv] reports a clinical trial of Nabilone, a synthetic cannabinoid on PTSD patients, finding “The majority of patients (72%) receiving nabilone experienced either cessation of nightmares or a significant reduction in nightmare intensity. Subjective improvement in sleep time, the quality of sleep, and the reduction of daytime flashbacks and nightsweats were also noted by some patients. The results of this study indicate the potential benefits of nabilone, a synthetic cannabinoid, in patients with PTSD experiencing poor control of nightmares with standard pharmacotherapy”
Reggio[xxvi] concluded “Cannabinoid agonists have been suggested to have potential therapeutic uses as appetite stimulants, analgesics, anti-emetics, anti-diarrheals, anti-spasmodics, tumor anti-proliferative agents, anti-glaucoma agents and as agents for the treatment of diseases associated with inappropriate retention of aversive memories such as post-traumatic stress disorders and phobias.” Bucherelli et al[xxvii] observed “cannabinoids are involved in both consolidation and reactivation” and suggested “The lability of retrieved memory affords opportunities to treat disorders such as phobias, post-traumatic stress, or chronic pain, and these results help searching for appropriate therapeutic targets.”
Cannabis & PTSD Summary
There is now significant evidence of an association between post-traumatic stress disorder and cannabis use (as with use of alcohol and other drugs) by way of self-medication. Basic research in animal models and receptor studies suggests a role for endocannabinoids in the encoding, storage and retrieval of painful memories.
Clinical trials of cannabinoids with similar activity to THC on PTSD patients has resulted in symptomatic relief (fewer/less severe nightmares). In PTSD patients cannabis use appears in many cases to reflect a coping mechanism.
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[xiii] Lewis CF.  Post-traumatic stress disorder in HIV-positive incarcerated women. J Am Acad Psychiatry Law. 33(4):455-64.
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[xviii] DeFazio VJ, Rustin S, Diamond A (1975) Symptom development in Vietnam era veterans. Am J Orthopsychiatry 45(1):158-63
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[xxi] Gil-Rivas V, Fiorentine R, Anglin MD (1996) Sexual abuse, physical abuse, and posttraumatic stress disorder among women participating in outpatient drug abuse treatment. J Psychoactive Drugs 28(1):95-102
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[xxiii] Vauth R, Nyberg E.  [Untreated PTSD in schizophrenia - unrecognized risk factor for recovery and course of illness?].[Article in German] Fortschr Neurol Psychiatr. 75(8):463-72.
[xxv] Fraser GA.  The use of a synthetic cannabinoid in the management of treatment-resistant nightmares in posttraumatic stress disorder (PTSD). CNS Neurosci Ther. 15(1):84-8.
[xxvi] Reggio PH.  Pharmacophores for ligand recognition and activation/inactivation of the cannabinoid receptors. Curr Pharm Des. 9(20):1607-33.
[xxvii] Bucherelli C, Baldi E, Mariottini C, Passani MB, Blandina P.  Aversive memory reactivation engages in the amygdala only some neurotransmitters involved in consolidation. Learn Mem. 13(4):426-30.