Can a doctor prescribe cbd oil for ptsd

Cannabidiol in the Treatment of Post-Traumatic Stress Disorder: A Case Series

1 Rocky Vista University, Osteopathic Medical Student IV, Parker, CO.

Scott Shannon

2 Department of Psychiatry, University of Colorado Denver, Denver, CO.

Shannon Hughes

3 School of Social Work, Colorado State University College of Health and Human Sciences, Fort Collins, CO.

Nicole Lewis

4 Department of Naturopathic Medicine, Wholeness Center, Fort Collins, CO.

3 School of Social Work, Colorado State University College of Health and Human Sciences, Fort Collins, CO.

Address correspondence to: Scott Shannon, MD, FAACAP, 2620 East Prospect Road, #190, Fort Collins, CO 80525 [email protected]

This Open Access article is distributed under the terms of the Creative Commons License (, which permits unrestricted use, distribution, and reproduction in any medium, provided that the original work is properly cited.


Objectives: Cannabidiol (CBD) is a non-psychotomimetic cannabinoid compound that is found in plants of the genus Cannabis. Preclinical research has suggested that CBD may have a beneficial effect in rodent models of post-traumatic stress disorder (PTSD). This effect is believed to be due to the action of CBD on the endocannabinoid system. CBD has seen a recent surge in research regarding its potential value in a number of neuro-psychiatric conditions. This is the first study to date examining the clinical benefit of CBD for patients with PTSD.

Methods: This retrospective case series examines the effect of oral CBD administration on symptoms of PTSD in a series of 11 adult patients at an outpatient psychiatry clinic. CBD was given on an open-label, flexible dosing regimen to patients diagnosed with PTSD by a mental health professional. Patients also received routine psychiatric care, including concurrent treatment with psychiatric medications and psychotherapy. The length of the study was 8 weeks. PTSD symptom severity was assessed every 4 weeks by patient-completed PTSD Checklist for the DSM-5 (PCL-5) questionnaires.

Results: From the total sample of 11 patients, 91% (n = 10) experienced a decrease in PTSD symptom severity, as evidenced by a lower PCL-5 score at 8 weeks than at their initial baseline. The mean total PCL-5 score decreased 28%, from a mean baseline score of 51.82 down to 37.14, after eight consecutive weeks of treatment with CBD. CBD was generally well tolerated, and no patients discontinued treatment due to side effects.

Conclusions: Administration of oral CBD in addition to routine psychiatric care was associated with PTSD symptom reduction in adults with PTSD. CBD also appeared to offer relief in a subset of patients who reported frequent nightmares as a symptom of their PTSD. Additional clinical investigation, including double-blind, placebo-controlled trials, would be necessary to further substantiate the response to CBD that was observed in this study.


P ost-traumatic stress disorder (PTSD) is a relatively common psychiatric condition with a lifetime prevalence of 6.1% in the United States. 1 PTSD often presents in clusters of symptoms, including the re-experiencing of traumatic events through intrusive memories and nightmares, avoidance of certain distressing factors, and alterations in mood, level of arousal, and cognition. Psychotherapy is the established first-line treatment for PTSD, and various psychiatric medications are also typically employed. The development of additional treatment agents is important because current medications, including selective serotonin reuptake inhibitors, serotonin/norepinephrine reuptake inhibitors, antiadrenergic agents, and second-generation antipsychotics, have questionable efficacy and often carry significant undesirable side-effect profiles.

Although the pathophysiology of PTSD has not yet been definitively described, a number of factors are suspected to contribute to the development of this disorder. One hypothesis relates PTSD to dysregulated memory retrieval through the process of reconsolidation and impaired extinction of aversive memories. 2 The endogenous cannabinoid system has been shown to play an important role in the process of aversive memory extinction through the activity of central CB1 receptors. 3 Two cannabinoid receptors are known to exist in the human body: CB1 and CB2 receptors. CB1 receptors are located mainly in the brain and modulate neurotransmitter release in a manner that prevents excessive neuronal activity, thus calming and decreasing anxiety. CB1 receptors also have a role in reducing pain, inflammation, regulating movement and posture control, and regulating sensory perception, memory, and cognitive function.

Cannabidiol (CBD) is known to have multiple physiologic mechanisms of action, including 5-HT1A serotonergic agonism, adenosine and opioid receptor modulation, activation of the endogenous endocannabinoid system, antagonism at GPR55 receptors, and activation of transient receptor potential channels. 4,5 CBD’s activity at 5-HT1A receptors may drive its neuroprotective, antidepressive, and anxiolytic benefits, although the mechanism of action by which CBD decreases anxiety is still unclear. 6 CBD was shown to be helpful for decreasing anxiety through a simulated public speaking test at doses of 300–600 mg in single-dose studies. 7–9 Other studies suggest that lower doses of 10 mg/kg have a more anxiolytic effect than higher doses of 100 mg/kg in rats. 10

Of particular interest to this study is the effect of CBD on the endogenous cannabinoid system. CBD has minimal affinity for CB1 and CB2 receptors, 11 but it does indirectly cause activation of CB1 receptors by increasing the availability of endogenous endocannabinoids. Anandamide is an endogenous cannabinoid that acts as a partial agonist at CB1 receptors. It is metabolically deactivated by the enzyme fatty acid amide hydrolase (FAAH). CBD has been shown in some studies to inhibit FAAH, thus increasing the availability of anandamide and causing activation of the endocannabinoid system. 12 Studies in rodent models have shown that pharmacologic activation of the endocannabinoid system through CB1-receptor agonist agents leads to decreased behavioral response to aversive memories in rodent models through the inhibition of memory reconsolidation and enhanced extinction. 13–15 This early research suggests that agents such as CBD that cause indirect activation of the endocannabinoid system may have utility in the treatment of PTSD.

Current evidence regarding the use of CBD for PTSD in humans is minimal. One case report showed that administration of 12–37 mg of oral CBD daily was associated with a reduction in anxiety symptoms and sleep disturbances in a 10-year-old patient with PTSD due to sexual trauma. 16 Another study showed that 32 mg of inhaled CBD resulted in consolidation of aversive memory extinction and attenuation of explicit fearful responding in healthy human subjects. 17 See Bittencourt and Takahashi 18 for a recent comprehensive review of pre-clinical and clinical studies regarding the relationship of CBD to PTSD. To date, no clinical trial evaluating the effectiveness of CBD in reducing symptoms of PTSD in humans has been completed.

The hypothesis of this study was that patients with DSM-5-diagnosed PTSD who were administered CBD along with routine psychiatric care would show a decrease in PTSD-specific symptomatology. This hypothesis was based on prior rodent and limited human studies that suggest that (1) CBD may cause decreased response to and increased extinction of aversive memories, and that (2) CBD may have an anxiolytic effect, which, in turn, would have therapeutic value in patients with PTSD. To this end, we conducted a retrospective file review of adult patients with PTSD who were treated with CBD as part of standard psychiatric care in an outpatient clinic. The goal of this review was to examine the tolerability of CBD and its effectiveness in PTSD symptom reduction.

Materials and Methods

Design and procedures

This article describes a retrospective chart review of adult psychiatric patients with a diagnosis of PTSD who consented to treatment with CBD as augmentation to routine psychiatric treatment at an outpatient psychiatric clinic. All current patients with a diagnosis of PTSD were considered for treatment with CBD between February 2016 and May 2018. Patients were not excluded based on the presence of other psychiatric comorbidities (aside from an active thought disorder) or concurrent use of cannabis. The diagnosis of PTSD was established through clinical evaluation by a mental health professional (psychiatrist, psychiatric nurse practitioner, or physician assistant). Inclusion criteria for the present analysis required a cut-off score of 33 on the Post-Traumatic Stress Disorder Checklist for the DSM-5 (PCL-5) 19 and a minimum of two consecutive follow-up appointments after the initial intake appointment. The final sample consisted of 11 adult patients with a diagnosis of PTSD and who met inclusion criteria.

After the initial baseline assessment, PCL-5 assessments were completed by patients every 4 weeks to monitor changes in the severity of PTSD symptoms. In addition to CBD, patients also received routine treatment in the form of psychiatric medications, various psychotherapy modalities, and standard integrative treatments, as indicated for their diagnoses of PTSD and other psychiatric comorbidities. These integrative treatments often included dietary changes, herbal supplementation, neurofeedback, and intravenous infusions of vitamins and minerals.

Four patients received CBD as an oral capsule only. One patient only received CBD in the form of an oral liquid spray. Fifty-five percent (n = 6) of patients received both forms of CBD either concurrently or sequentially over the course of the study. The form of CBD (capsule vs. liquid spray) was determined by provider and patient preference. The CBD products used in this study were supplied by CV Sciences. Capsules were demonstrated by high-performance liquid chromatography with ultraviolet detection (HPLC-UV) to contain 22–28 mg of CBD per capsule. Patients were instructed to take whole capsules, which were assumed to contain 25 mg of CBD for dosing purposes. Patients were instructed to take liquid CBD as a specified number of sprays from a spray bottle. The liquid product used in this article was demonstrated by HPLC-UV to contain between 425 and 575 mg of CBD in total per bottle, equating to about 1.5 mg of CBD per spray.

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Patients were instructed to take CBD once or twice per day based on severity of symptoms. The median starting oral capsular dose was 25 mg per day (range: 25–100). The median dose of liquid CBD given throughout the study was 9 mg per day (range: 1–16). The mean total starting dose of CBD (liquid or capsular or both) was 33.18 mg (standard deviation [SD] = 23.34). The mean total dose of CBD prescribed at the 8-week follow-up appointment at the conclusion of the study period was 48.64 mg (range: 2–100). The dose of CBD was adjusted at each 4-week appointment based on the patient’s presentation and experience. Most patients received an increase in the dose of CBD because treatment was provided to maximize PTSD symptom reduction, which seemed to be directly correlated with dose. These doses are much lower than the doses used in the previous clinical literature for multiple reasons. The first is that lower doses appear to elicit an adequate clinical response in our experience. Second, the current retail cost of CBD would make the use of 600 mg per day cost-prohibitive. Finally, doses for the liquid spray route of administration are typically lower than that of capsules and are usually measured as single milligrams of CBD per spray, thus rendering higher doses impractical for patients relying on liquid CBD.

Informed consent was obtained for each patient at their intake appointment. Appointments every 4 weeks included clinical evaluation and documentation of patients’ PTSD symptomatology through PCL-5 questionnaires. Concurrent psychiatric medications were held constant or changed according to routine clinical practice, whereas CBD was often intentionally used as a method of decreasing or avoiding the use of psychiatric medications. CBD was added to care, dropped from care, or refused as per individual patient and practitioner preference. The Western Institutional Review Board approved a retrospective analysis of the charts of patients with a diagnosis of PTSD who received CBD as part of their treatment program.


Wholeness Center is a large mental health clinic with a focus on integrative medicine and psychiatry. Practitioners from a range of disciplines (psychiatry, naturopathy, acupuncture, neurofeedback, yoga, etc.) work together in a collaborative and cross-disciplinary environment. Based on existing research and patient experience, CBD had been widely incorporated into clinical care a few years before this study.


Characteristics of the study sample are presented in Table 1 . The average age of the population in this study was 39.91 (range: 22–69, n = 11). The majority (73%, n = 8) of patients were female. On average, patients were concurrently taking three psychiatric medications, including antidepressants, mood stabilizers, anxiolytics, and stimulants. One patient used cannabis daily throughout the study. Overall, 73% (n = 8) of patients were concurrently receiving psychotherapy as part of their overall care. Patients had on average 1.8 comorbid psychiatric conditions in addition to their PTSD diagnosis, including anxiety, mood, personality, and sleep disorders.

Table 1.

Characteristics of the Patient Population and Concurrent Treatments Received

The Use of Medicinal Marijuana for Posttraumatic Stress Disorder: A Review of the Current Literature

Corresponding author: Stephanie Yarnell, MD, PhD, Department of Psychiatry, Yale University, 300 George St, Ste 901, New Haven, CT 06510 ([email protected]).



Medicinal marijuana has already been legalized in over 23 states with more considering legalization. Despite the trend toward legalization, to date, there has been no systematic review of the existing literature for the efficacy of medicinal marijuana for many of the conditions for which it is proposed to treat. This study seeks to understand the current literature regarding the use of medicinal marijuana in the treatment of posttraumatic stress disorder (PTSD).

Data Sources:

PubMed and PsycINFO databases were searched until April 2014 for articles outlining outcomes of case files, control studies, and observational studies regarding the efficacy of medicinal marijuana in treating PTSD. Various combinations of the following search terms were used: marijuana, medicinal marijuana, cannabis, cannabinoid, PTSD, efficacy, trial, and neurobiology.

Study Selection:

Full text of each article was reviewed, and those directly addressing the question of efficacy of medicinal marijuana on PTSD symptomatology were included. Data were extracted from a total of 46 articles.


Analysis revealed that most reports are correlational and observational in basis with a notable lack of randomized, controlled studies. Many of the published studies suggest a decrease in PTSD symptoms with marijuana use. Though the directionality of cannabis use and PTSD could not be fully differentiated at this time, there appears to also be a correlation between PTSD and problematic cannabis use. Despite this finding, there is a growing amount of neurobiological evidence and animal studies suggesting potential neurologically based reasons for the reported efficacy.


Posttraumatic stress disorder is 1 of the approved conditions for medicinal marijuana in some states. While the literature to date is suggestive of a potential decrease in PTSD symptomatology with the use of medicinal marijuana, there is a notable lack of large-scale trials, making any final conclusions difficult to confirm at this time.

Clinical Points

■ Posttraumatic stress disorder (PTSD) is one of the approved conditions for medical marijuana in some states.

■ Current literature is suggestive of a potential decrease in PTSD symptomatology with medical marijuana, but also suggests a correlation with problematic cannabis use, though directionality is not established at this time.

■ Neurobiological studies in both humans and animal models are providing further insights into the reported efficacy of medical marijuana for PTSD.

■ Lack of large-scale randomized controlled trials makes any final conclusions difficult.

Cannabis is currently the most widely used illicit substance, with approximately 18.1 million people reporting use within a 1-month period in 2011 within the United States alone. 1 The rapidly changing legal environment surrounding cannabis, both for medicinal and recreational use, is becoming increasingly relevant to patient care. While still illegal under federal law, at least 23 states have approved marijuana for medical use, and recreational use is now legal in Colorado and Washington. The approval of marijuana as a purported medication is unique, as it is done under state authority, either by ballot or by state legislature approval, without approval of the US Food and Drug Administration (FDA). Whereas the FDA requires multiple rigorous clinical trials evaluating safety and efficacy prior to the approval of a drug for a specific indication, there are no standard requirements for state approval of indications for medical marijuana. In at least 8 states, 1 of the indications for medical marijuana is posttraumatic stress disorder (PTSD). 2 The current circumstances create an awkward situation in which researchers must evaluate the safety and efficacy of medical marijuana after its approval for various indications, including PTSD.


Despite claims of medical use, marijuana remains illegal. Currently, in the United States marijuana remains listed as a Schedule I drug, meaning that there is a high abuse potential and no accepted medical use. Despite this, there are a growing number of claims that marijuana, particularly in the smoked form, has medical benefits. Indeed, early National Institutes of Health (NIH)–sponsored studies supported the claim that marijuana decreased nausea and vomiting in chemotherapy patients, resulting in FDA approval of a synthetic form of oral cannabis. Later, FDA approval for synthetic cannabis was extended to AIDS wasting syndrome. 3 This approval resulted in a multitude of claims of the benefits of marijuana for other potential conditions, leading to 2 large government-sponsored studies into the use of medical marijuana. 4 , 5 While both of these studies set out to finalize views on the matter, both ultimately found that there were simply too few scientific studies to determine the utility of medical marijuana; however, both concluded further research on the matter was justified. 3 This article seeks to review the existent literature to help determine the current state of such studies in regard to the use of medicinal marijuana in the treatment of PTSD.


Potential studies for inclusion were identified by querying PubMed and PsycINFO for various combinations of the terms marijuana, medicinal marijuana, cannabis, cannabinoid, PTSD, efficacy, trial, and neurobiology up to April 2014. Duplicate studies were removed from inclusion. Articles adopting descriptive, observational, analytic, and experimental studies of both human and animal trials were considered for establishing proposed neurobiological basis. As such, animal studies, case studies, qualitative articles, reviews, and commentaries were reviewed. Given the limited number of studies on this topic, all were considered for inclusion. Full text of each article was reviewed, and those directly addressing the question of efficacy of medicinal marijuana on PTSD symptomatology were included. Data were extracted from a total of 46 articles.


Who Uses Medicinal Marijuana?

Despite the lack of established medical use, marijuana is currently used for a number of conditions. Most commonly, medical marijuana users were found to be male, white, between 25 and 44 years of age, and employed. 6 Reportedly, the most commonly cited primary uses for medical marijuana were pain, ranging between 82.6% and 92.2% of subjects, followed by muscle spasm (21%–41.3%). 6 , 7 Other reported primary uses included headaches, anxiety, insomnia, relaxation, poor appetite, nausea, and vomiting. 6 Interestingly, in states that allow for use of medical marijuana for traumatic intrusions and PTSD, this was listed as the primary indication in 38.5% of registered users. 7

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Studies Evaluating Use in PTSD

To date, there has been little research investigating the relationship between marijuana use and PTSD. Existing studies have mostly focused on the tendency of individuals who suffer PTSD symptoms to self-medicate with marijuana. Undoubtedly, marijuana has long been reported as a coping mechanism for individuals with heightened PTSD symptoms. 8 – 10 It has been suggested that individuals with less perceived ability to withstand emotional distress were more likely to attempt to self-soothe with marijuana in response to distressing emotions related to trauma. Additionally, those with more symptomatology associated with PTSD were suggested to be more likely to use marijuana with the explicit purpose of coping. 11 Bonn-Miller et al 8 suggested that patients with more severe PTSD symptoms may be more motivated to use cannabis. In their study, marijuana use positively correlated with PTSD symptoms and, according to self-reports, cannabis was used with intent to cope with these PTSD symptoms. 8 Indeed, the mere fact that an individual carries a diagnosis of PTSD significantly increases his or her chance of using marijuana at some point in life, 12 a relationship that also holds true even among teenagers. 13 , 14

Cannabis use has been associated with a decrease in symptomatology, but may also be associated with higher risk of cannabis use disorder. Greer et al 15 reported a 75% reduction in Clinician Administered Posttraumatic Scale for DSM-IV (CAPS) scores through use of medical marijuana, and cannabis has been reported to be particularly helpful among persons with severe traumatic intrusions, 16 commonly referred to as flashbacks, as well as for managing hyperarousal symptoms. 17 Many people suffering from PTSD often have interrupted sleep, with many seeking medical marijuana as a means of helping them treat their sleep issues; however, while marijuana may help with sleep in the short term, it may also interfere with long-term sleep structure. 18 , 19 Cannabis has also been shown to have anxiolytic and anxiogenic properties depending on the primary cannabinoid. 20 The perceived sense of anxiolytic relief from cannabis may drive the high prevalence rates and co-occurrence between PTSD and cannabis use, 17 , 21 , 22 though arguments do exist that anxiety (including PTSD) and depression are associated with problematic cannabis use patterns and dependence. 12 , 23 – 27 Several studies have shown an increased chance of cannabis use disorders among adults suffering from, in particular, PTSD. 12 , 23 , 28 , 29 Boden et al 30 explained this phenomenon by suggesting “(a) the experience of PTSD predisposes affected individuals to use cannabis to cope with negative internal states, (b) discontinuation of cannabis use (even temporarily) paradoxically leads to greater PTSD symptomatology, via withdrawal, resulting in (c) heightened craving for cannabis, and (d) greater cannabis use problems as well as relapse to cannabis use to cope with increased negative internal states.” (p282) Further, increasing rates of cannabis use disorder diagnoses have been documented among military veterans, 22 , 23 especially those who endorse high rates of trauma exposure and PTSD. 31 – 35 With the large number of young men and women returning from war with traumatic experiences, veterans appear to be at particular risk for potential cannabis use disorders as a result. Therefore, determining the true causal relationship has never been more important.

Proposed Neurobiological Mechanisms

Marijuana is not just a single drug; it is a mixture of leaves from the Cannabis sativa plant and contains more than 400 chemicals with over 60 of these referenced as cannabinoids. Perhaps the most well-known and well-studied, delta-9-tetrahydrocannabinol (THC), is the main psychoactive cannabinoid. While ingested in a number of forms, once in the body, THC interacts with the cannabinoid receptors. There are 2 main cannabinoid receptors. Cannabinoid receptor 2 (CB2) is thought to exist primarily external to the central nervous system (CNS). CB2 is thought to exert its main effects on the immune and reproductive systems 3 , 36 , 37 and is thought responsible for the reported alleviating effects of cannabis on autoimmune dysfunction and potentiation of inflammatory reactions. 37 Given the limited neurologic interaction of CB2, this article will focus on cannabinoid receptor 1 (CB1), which is believed to be responsible for most, if not all, of the psychoactive effects of THC. 3 , 37

Purportedly the most abundant receptor in the brain, the actual density of CB1 receptors varies. Brain regions with the highest concentrations of CB1 receptors are in areas primarily involved in memory formation (hippocampus), motor coordination (the cerebellum), and emotionality (prefrontal cortex). 37 This distribution correlates well with reported effects of THC on human behavior: modulation of pain, regulation of appetite, regulation of pleasure, memory formation, concentration, sensory and time perception, and coordination of movement and motor function, as well as abuse and addictive potential. 3 , 37 , 38 An example of such an effect on human behaviors is the reported correlation between cannabis and decreased hyperarousal states. The modulation of the “fight or flight” response occurs largely in the amygdala; animal studies have demonstrated that electrical stimulation of various regions of the amygdala can send the animal into states of terror or surreal calm. There is a heavy concentration of CB1 receptors and endocannabinoids in the amygdala, which may help explain why low-dose cannabinoid stimulation is generally felt as calming. 39 Indeed, transgenic mouse models have shown that CB1 overexpression decreases excessive excitatory neurotransmission in these brain areas, which may explain the decreased arousal symptoms, as well as reduction of anxiety associated with cannabis use. 40 Given that hypervigilance and hyperarousal are symptoms of PTSD, this correlation may help explain, at least in part, the proposed benefit of cannabis for patients with PTSD. 17 , 23

One commonly reported side effect of chronic cannabis abuse is impairment in short-term memory. At first this may sound unwanted, but at times, it may be desirable to forget negative traumatic events and so may be potentially useful in treatment of PTSD. 3 Animal experiments have demonstrated that it took cannabinoid-deficient CB1 knock-out mice significantly longer to forget an association with painful foot shocks and bell ringing than wild-type controls, but both groups continued to make positive associations, suggesting THC may facilitate the extinction of negative memory without affecting positive memory formation. 41 – 43 Reciprocally, when the endocannabinoid system was activated through slowing of breakdown of endogenous cannabinoids, animal models demonstrated the ability to dissociate negative associations faster than in their normal state, leading to proposed involvement of the endocannabinoid system in the extinction of aversive memory. 43 Indeed, it may be this trait of cannabis that drives persons with PTSD to seek out and, at times, abuse cannabis. 16 However, this correlation has not yet been investigated in a well-structured clinical setting. 16 , 37 , 43

External stimulation of CB1 may not fully explain extinction of aversive memories. While CB1 knockout mice may require more time to forget adverse memories, so do mice with blockade of the endocannabinoid system. 41 , 42 Indeed administering THC on a chronic basis reduces the number of available cannabinoid receptors by 20%–60%, which effectively leaves the body’s natural endocannabinoids with fewer sites to activate, which may reduce their overall impact. 44 Some have attempted to reconcile this incongruity by suggesting the extinction response is due to fatty acid amide hydrolase, the enzyme that degrades endocannabinoids. 45 Clearly, more studies are needed on this matter. Another argument against mere stimulation of CB1 focused on the exclusive use of classical conditioning in the extinction studies, as this is seen as far removed from the experiences that result in PTSD in which the stressor is often seen as being of “human design.” 44 Indeed, as critics of medical marijuana have observed, no amount of numbing of PTSD is likely to help veterans process the deep grief and pain of having participated in the human tragedy of war. 44 , 46


In summary, cannabis is the most widely used illicit substance in the United States. With a growing number of states seeking to legalize marijuana for medicinal purposes, there is a need for a better understanding regarding the mechanism of action and efficacy of cannabis for the conditions for which it is prescribed. This article sought to review the existing literature regarding the use of cannabis for PTSD. To date, there is no large-scale, randomized, controlled study investigating efficacy of marijuana and PTSD symptomatology; however, the literature that exists suggests that it may have an effect on decreasing PTSD symptoms, and the neurobiological and animal studies seem to suggest potential underlying mechanisms consistent with these findings. However, PTSD may also be related to problematic, pathological use of cannabis. Additionally, the overall literature may be limited by publication bias, and the lack of standardized, large-scale controlled trials at this time makes any final conclusions on the efficacy uncertain. As the number of people seeking medical marijuana as well as those self-medicating for PTSD continues to rise, there is a clear need for more research trials and monitoring of the long-term effects of using cannabis for the treatment of PTSD and other medical conditions. Until then, given the limited evidence, physicians need to use their own clinical judgment when weighing the potential risks and benefits for a particular patient.

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Potential conflicts of interest:

The author has no connection with tobacco, alcohol, pharmaceutical, or gaming industries or any entity funded by one of these organizations.



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