Download the section in PDF
Approximately 3.4 million people in the United States have epilepsy (Epilepsy Foundation, 2014), and nearly 30% of those people are unresponsive to standard medications (Detyniecki & Hirsch, 2015). Symptomatic treatment of epilepsy is the most common strategy; however, antiepileptic drugs often have troubling side effects and fail in the treatment of temporal lobe epilepsy (Soltesz et al., 2015). It is understandable that parents of children who must wear crash helmets because of seizures uncontrolled by current pharmaceutical treatments would consider reaching for marijuana or a marijuana-based drug for their children. It may seem a rational choice when weighing the extensive body of historical (Felter & Lloyd, 1898/1983) and anecdotal clinical evidence for successful treatment with marijuana against the risk that a child faces every time he or she suffers a seizure. To date, there is a lack of quality clinical research evidence with sufficient sample sizes to support or negate marijuana’s traditional use in the treatment of seizures in people of any age. However, evidence is increasing that physiological states such as stress and pathophysiological conditions such as epilepsy modify the endocannabinoid signaling system (ECS).
In epilepsy, cannabinoid type 1 (CB1) receptors are markedly downregulated throughout the hippocampus in the acute phase shortly after the initiating insult, but they are upregulated in the chronic phase of the disorder (Soltesz et al., 2015). “The concurrent upregulation of CB1 receptors on GABAergic terminals and downregulation of CB1 receptors on glutaminergic axons that takes place in epilepsy may mechanistically contribute to seizures” (Soltesz et al., 2015, p. 272), but the importance of these biological processes is not well understood.
Studies have shown that the ECS plays an important role in modulating seizure activity, and deficiency or defect in the ECS is being studied as the possible cause for seizure. For example, one study published in the New England Journal of Medicine (Friedman & Devinsky, 2015) found lower levels of anandamide in cerebrospinal fluid in people with epilepsy than in healthy people serving as study controls. It is well documented that cannabinoids can provoke seizures, depending on the dosage, the content and ratio of the cannabidiol (CBD) and THC, and the underlying conditions in the patient. However, anti-seizure medications that are already on the market are known also to provoke seizures in some patients and to be associated with clinically significant drug-drug interactions (Friedman & Devinsky, 2015). Current evidence also suggests that, although THC has anti-convulsive effects, at higher doses it can be proconvulsive (Detyniecki & Hirsch, 2015). However, phase III randomized controlled trials with oral CBD (Epidiolex) support efficacy and adequate safety profiles for children with Dravet syndrome (fever-induced epilepsy) and Lennox-Gastaut syndrome (childhood epilepsy) at doses of 10 and 20 mg/kg/day (O’Connell, Gloss, & Devinsky, 2017).
In 2014, the Cochrane Collaboration (Gloss & Vickrey, 2014) published its review on cannabinoid use in epilepsy. The stated goal of the review was to evaluate the literature for human studies that explored the effect of CBD on seizure freedom for 12 months, or three times the longest usual seizure-free interval. The researchers rejected many of the studies they reviewed because they were not clinical trials. Four pioneering studies from 1980 to 1990 met all the inclusion criteria except the primary outcome. They were reviewed because they included adverse events, one of the secondary outcomes; however, the studies included inadequate numbers of participants for the drawing of conclusions. In one study, 15 patients with temporal lobe epilepsy, who experienced at least one generalized seizure weekly, received 200 mg to 300 mg of CBD daily or placebo for as long as 4.5 months. Investigators did observe that participants tolerated the CBD without toxicity. In the second study reviewed, 12 participants with uncontrolled seizures were treated with three capsules of sunflower oil (as placebo) or sunflower oil and 100 mg of CBD (300 mg daily) for the first week, followed by two capsules (200 mg daily) for 3 more weeks. There were no differences in seizure frequency between the two groups, although no details were given. The only side effect was mild drowsiness. In the third study, nine participants were randomized to groups receiving either 200 mg of CBD or placebo. Participants continued to take their regular medication plus CBD or placebo for 3 months. Two of four participants treated with CBD were seizure-free for the 3 months of treatment, and none of the five in the placebo group experienced improvement. No adverse effects were reported. In the fourth trial, 12 participants were treated with a single-blind placebo for 6 months, then a double-blind dose of 300 mg of CBD or placebo in a crossover trial lasting an additional 12 months. Ten patients in the trial did not experience changes in the frequency or character of seizures, but reported no adverse effects. The small sample size (48 total participants) and low quality of the study designs left the authors unable to draw conclusions from the review.
An Israeli multicenter trial was conducted with 74 children (aged 1 to 18 years) with refractory epilepsy (resistant to more than seven drugs) who were treated with marijuana oil for at least 3 months and an average of 6 months. Patients were treated with sublingual marijuana oil extract of one of two strains: “Cheese pie” and “Avidekel,” both containing a CBD/THC ratio of 20:1, dissolved in olive oil, given three times daily. Daily dose ranged from 2 to 27 mg/kg/ day. The response to treatment was evaluated as a parental-reported change in the mean monthly seizure frequency. Of the 74 patients, 66 (89%) reported reduction in seizure frequency. The reduction was 75% to 100% in 13 patients (18%), 50% to 75% in 25 (34%), 25% to 50% in 9 (12%), and less than 25% in 19 (26%). Five (7%) patients reported aggravation of seizures, which led to discontinuation of use of the CBD (Tzadok et al., 2016).
Researchers suggest that future studies focus on the underlying mechanisms of alterations in the ECS in chronic epilepsy and other related pathological conditions, including autism, cell type-specific boosting of the ECS (for example, ECS-based gene therapy), physiological conditions that selectively control phasic or tonic ECS in vivo, and cannabinoid-based prophylaxis against epileptogenesis after various forms of brain injury (Soltesz et al., 2015).
Given the proven anticonvulsant effects from preclinical studies, and the lack of psychoactive properties, CBD is considered to be a promising alternative if not a candidate as a medication for epilepsy. Its safety record is strong to date but the long-term effects of CBD are unknown. Researching the long-term neuropsychological effects in the developing brains of children is particularly important.
Glaucoma treatment focuses on the continuous reduction of intraocular pressure (IOP). Because marijuana smoking and THC ingestion have been found to reduce IOP by 60% to 65%, oral and topical cannabinoids show promise for future use in glaucoma treatment. The concern with smoking is that the effects on IOP last only 3 to 4 hours and the amount of smoking necessary may be prohibitive (Green, 1998). In a 2001 study, eight participants were given either two drops (50 mL) of a 25-mg or 50-mg WIN55212-2 solution or placebo solution. WIN55212-2 is a synthetic and selective CB1 receptor agonist. These drops decreased intraocular pressure within 30 minutes of application in participants with resistant glaucoma (Porcella, Maxia, Gessa, & Pani, 2001). Studies continue to explore the relationship between the ECS and the pathophysiology of glaucoma as well as the long-term treatment of glaucoma with cannabinoids as hypotensive and neuroprotective agents for the eye (Cairns, Baldridge, & Kelly, 2016).
Although marijuana use has been thought to be associated with a broad range of psychiatric disorders, statistical analysis has shown marijuana use to be associated only with increased prevalence and incidence of alcohol and drug use disorders, including nicotine dependence (Blanco et al., 2016). However, marijuana use among people with anxiety or depression has been reported to be two to eight times higher than in the general population, with rates as high as 60% among people with panic symptoms (Bricker et al., 2007). Several studies suggest that marijuana, self-prescribed and smoked, or prescribed in pharmaceutical form, may be effective in treating symptoms related to anxiety, however, a 2015 review of the literature by Vorspan, Mehtelli, Dupuy, Bloch, and Lépine found that marijuana used in self-medication as a sedative can also be a “cause of anxiety disorders” (p. 4).
A review of the literature suggested that, as of 2009, frequent users of marijuana consistently had a high prevalence of anxiety disorders and people suffering from an anxiety disorder have often used marijuana. It was not clear from existing data if marijuana use increased the risk of developing long-lasting anxiety disorders (Crippa et al., 2009). Studies are needed to further understand and test the hypotheses regarding the relationship between anxiety and marijuana, taking into account neurobiological, environmental, and social influences.
One study found that social anxiety is positively associated with marijuana-related problems. Although no significant direct effect of social anxiety from marijuana use frequency was observed, a significant indirect effect on solitary marijuana use was found. This research suggests that social anxiety exerts its influence on marijuana use frequency indirectly via more frequent solitary use. Solitary marijuana use was related to more marijuana-related problems. This finding was congruent with the investigators’ previous work, which found that socially anxious marijuana users tended to avoid social situations when marijuana was unavailable. Socially anxious persons used marijuana prior to social events to manage anticipatory anxiety about the event and/or used marijuana following the social event to manage their anxiety associated with review of negative aspects of their behavior during the social event (Buckner, Ecker, & Dean, 2016).
A study of 149 male and female participants, aged 18 to 36, used various statistics to investigate the factors, such as social anxiety, norms, and expectancies, that might be related to craving marijuana. The craving was greatest when marijuana use was viewed as acceptable and expected to reduce tension. Cravings due to social anxiety were low when expectations were low. The study found that non-Caucasian participants reported greater tension-reduction expectancies than Caucasian participants. This study suggests the importance of considering social norms, expectancies, and social anxiety in understanding marijuana-related behaviors, given that craving is robustly related to marijuana use problems, such as relapse during an attempt to quit (Foster, Ecker, Zvolensky, & Buckner, 2015).
A meta-analysis included a total of 267 studies on marijuana use in anxiety. The results of 31 of those studies were re-analyzed using a random-effects meta-analysis with inverse variance weights. Analysis of the epidemiological data from this cohort representing 112,000 non-institutionalized members of the general population of 10 countries (the United States, Canada, Switzerland, Australia, France, Colombia, New Zealand, Netherlands, Germany, and the United Kingdom) found a small positive association between anxiety and either marijuana use (Odds ratio [OR] = 1.24, 95% confidence interval [CI], p = 0.006; n = 15 studies) or marijuana use disorders (OR = 1.68, 95% CI, p = 0.001; n = 13 studies) and between comorbid anxiety and depression and marijuana use (OR = 1.68, 95% CI, p = 0.004; n = 5 studies; Kedzior & Laeber, 2014).
A study conducted with 232 participants between the ages of 18 and 70 years who met the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) criteria for panic disorder tested an intervention that included cognitive-behavioral therapy (CBT; six sessions in 3 months followed by six follow-up 15- to 30-minute phone sessions) and marijuana use. Core panic symptoms were assessed using the Anxiety Sensitivity Index, social phobia by the social phobia subscale of the Fear Questionnaire, and depression by the 20-item Center for Epidemiological Studies Depression Scale. Recent marijuana use (smoking) was also recorded. Findings of the study suggested that monthly marijuana use combined with CBT did not significantly reduce anxiety, panic, or social phobia, but it was effective in persons with depression. The investigators noted significant comorbidity between anxiety and depression and suggested that the anxiety arm of the study may not have had sufficient power to detect the effect. The symptoms of persons with depression who smoked marijuana monthly showed no more improvement than the symptoms of persons who smoked less than monthly (Bricker et al., 2007).
Trauma and Stressor-Related Disorders
Rates of marijuana use have increased in the wake of major disasters. There are high rates of posttraumatic stress disorder (PTSD) in the United States, particularly in combat-exposed veterans, and marijuana use disorder is associated with PTSD (OR = 4.3). While some researchers hypothesize that individuals with PTSD might benefit from marijuana use, one review of the literature found that the known risks of marijuana use outweigh the unknown benefits for PTSD (Steenkamp, Blessing, Galatzer-Levy, Hollahan, & Anderson, 2017). Posttraumatic stress disorder symptom severity is positively associated with (a) use of marijuana to cope, (b) marijuana use problems, (c) severity of marijuana withdrawal, and (d) experiences of craving related to compulsivity and emotionality, with findings regarding withdrawal and emotion-related craving remaining significant after adjusting for covariates. (Boden, Babson, Vujanovic, Short, & Bonn-Miller, 2013, p. 277)
Although a range of psychotherapies have been employed with varying degrees of effectiveness, persons who suffer with PTSD may not seek care, and a recent meta-analysis of pharmacotherapy for PTSD found only small effects (Steenkamp et al., 2017).
Depressive and Bipolar Disorders
A recent survey measured the statistical association between the age at which people first used marijuana and depression in two ways. First, two statistics (linear regressions) used scores from three assessments – the 12-Item Short-Form Health Survey, the Mental Component Summary, and the Major Depression Inventory – as the dependent variables, with the age at first use of marijuana as the independent variable. Second, two regression analyses used age at marijuana first use as the independent variable (with lifetime nonusers as a reference), and poor mental health and major depression as the dependent variables. The results confirmed that marijuana first use at a young age is an important risk factor in the progression to other drug use. Mental health and depression were significantly predicted by age at marijuana first use. However, after controlling for the frequency of marijuana use and for the misuse of alcohol, cigarettes, and other drugs, the association with depression did not persist and the association with poor mental health was reduced. These results underscore the importance of preventing early marijuana users from progressing to other drugs. Among individuals whose first use of marijuana is early in life, these results suggest that the risks of mental health problems and depression are subsequently mediated by abusive consumption of marijuana or other substances. Early onset does not appear to be an indicator of later mental health problems per se, as long as it is not followed by harmful patterns of substance use.
Major depressive disorder is known to be more common in women. Conflicting reports exist concerning the relationship between gender and the prevalence of the use of marijuana to cope with emotional distress. Researchers conducted a secondary analysis of the results of a marijuana intervention trial involving 332 young adult women. Changes in depression symptoms (categorized as minimal, mild, and moderate or more severe depression) were assessed using Beck’s Depression Scale in relation to changes in marijuana use at 3 and 6 months after the baseline assessment. The purpose of the study was to examine reduction in marijuana use and its impact on depression symptoms. After controlling for alcohol, investigators found a significant relationship between reductions in marijuana use and reductions in depression symptoms among young women who reported at least some mild depression symptoms (Moitra, Anderson, & Stein, 2016).
Recently, the European Mania in Bipolar Longitudinal Evaluation of Medication study analyzed a sample of 1,922 adults who had experienced a manic/mixed episode of bipolar disorder. Participants’ data were organized into three groups: current use of marijuana (between 12-week and 24-month visits), no current but previous use (during first 12 weeks), and never use marijuana. The study found that people with bipolar disorder who stopped using marijuana during their manic/mixed episode had similar clinical and functional outcomes to those who had never used marijuana. People who continued to use marijuana had a higher risk of recurrence and poorer functioning, such as work impairment and not living with a partner.
Investigators surmised that the clinical implications of the findings were that a holistic management plan for bipolar patients should include psychoeducation and other treatments/interventions that focus on stopping use of marijuana, alcohol, and other drugs, as well as on improving adherence and preventing relapses (Zorrilla et al., 2015).
Schizophrenia and Other Psychoses
One of the primary concerns cited in the controversy over decriminalization and legalization of marijuana is its causal relationship with psychosis. Debate is ongoing concerning whether ingesting or smoking marijuana increases the risk for psychosis or, conversely, whether marijuana use contributes to the alleviation of symptoms associated with schizophrenia. Marijuana, while not seeming to cause any basic structural changes in the brain, does appear to make changes in areas of the brain responsible for memory and emotion. Whether these changes are transitory or permanent and whether they contribute to the pathophysiology of schizophrenia are unknown. Many studies now show a robust and consistent association between marijuana consumption and the development of psychosis, but this may not be the case for schizophrenia specifically. Two primary kinds of data inform this issue: studies done with people with schizophrenia and studies of first-episode psychosis. Evidence suggests that the use of marijuana does not in itself cause a psychotic disorder. Rather, the evidence suggests that both early and heavy use of marijuana are more likely in individuals with a vulnerability to psychosis (Ksir & Hart, 2016). Longitudinal studies show a consistent association between adolescent initiation of marijuana use, in a dose-dependent fashion, and the emergence of psychotic symptoms and their severity, along with functional impairment and worse outcomes (Bagot, Milin, & Kaminer, 2015). A study of 64 participants who were followed for 5 years demonstrated that continued marijuana use with subclinical depression symptoms is associated with poorer clinical outcome, and may be a predictor of negative outcomes in persons experiencing their first episode of psychosis (González-Ortega et al., 2015). Another study found a dose-dependent association between change in marijuana use (from intermittent to continual use) and relapse of psychosis that is not thought to be the result of self-medication or genetic or environmental variables (Schoeler et al., 2016). Such findings are helpful for healthcare professionals, who can test them in practice. For example, a person considering the benefits and risks of marijuana use might be told that a study by Schoeler and colleagues in 2016 found that when users who had experienced psychosis changed from intermittent or occasional use to more continual use, such as smoking marijuana every day, they had a statistically greater risk of psychosis relapse.
According to a Cochrane review (McLoughlin et al., 2014), the evidence from research is unclear concerning a possible relationship between marijuana and schizophrenia. For some people with schizophrenia, positive symptoms are worse when they use marijuana. “For many, however, using marijuana seems only to have the expected mild soporific effects that probably compound negative symptoms” (McLoughlin et al., 2014, p. 41) such as blunted affect, anhedonia, and asociality. Upon reinspection with lead investigators of the studies covered in the Cochrane review on marijuana and schizophrenia, researchers concluded that there was as yet no evidence to demonstrate that one type of adjunct psychological therapy or one type of drug therapy was more effective than another and that there was also insufficient evidence to show that CBD had an antipsychotic effect (Pushpa-Rajah et al., 2015). Alcohol use is known to confound data in studies on psychosis risk related to marijuana use (Auther et al. 2015), as could any substance, such as stimulants. Research also differentiates the amount of marijuana use in self-care as a factor in research outcomes. For example, “heavy” marijuana consumption (defined as smoking more than three marijuana cigarettes per day) seems to impair verbal memory in first-psychotic-episode patients. Heavy users also perform worse than medium users in other neurocognitive tasks. Medium users (one to three “joints” or marijuana cigarettes per day) did not show any greater risk than nonusers. Based on these results, investigators inferred the existence of a dose-related effect of marijuana consumption (Núñez et al., 2015).
Multiple Sclerosis and Spasticity
Data from more than 40 clinical trials of marijuana and cannabinoids have been published. Beyond the two indications for which dronabinol and nabilone are already approved by the FDA, the strongest evidence exists for the use of marijuana and cannabinoids as phytotherapies for chronic pain, neuropathic pain, and spasticity associated with multiple sclerosis. As of March 2015, there had been six trials (n = 325 patients) that examined chronic pain, six trials (n = 396 patients) that investigated neuropathic pain, and 12 trials (n = 1,600 patients) that focused on multiple sclerosis. Several of these trials had positive results, suggesting that marijuana or cannabinoids may be effective therapies. In 2014, the American Academy of Neurology published evidence-based guidelines that recommended an oral marijuana extract containing both THC and CBD (not yet available in the United States as an FDA-approved medication) as having the highest level of empirical support as a treatment for spasticity and pain associated with multiple sclerosis. Synthetic oral THC and Sativex© (THC and CBD) oromucosal spray followed with “effective” ratings (Yadav et al., 2014). One systematic review of the literature suggests a clear role for marijuana preparations in symptom management of movement disorders that are known to worsen in people who are anxious. The review found that marijuana in various formulations is effective in reducing symptoms, especially hyperkinetic symptoms, or the anxiety that aggravates symptoms in some conditions (Koppel, 2015).
Cancer and Pain Management
Cannabinoids have known antineoplastic and antitumor effects (Ramer & Hinz, 2008, as cited in Kendall & Alexander, 2017). Marijuana use is not a new subject for healthcare professionals who care for people being treated for cancer and the discomfort related to the disease and treatments. Nor is it new to those who care for people being treated for chronic and intractable non-cancer pain. According to Donald Abrams (2016, p. 404), who has been an oncologist for 35 years and has advised patients about the use of marijuana for some time, “We recommend a self-titrated dosing regimen for the patient as the safest option, rather than attempting to prescribe an actual dose.” Dr. Abrams expresses caution in recommending marijuana to older adults because of the plant’s ability to lower blood pressure and raise the heart rate. Older adults can experience postural hypotension, leading to falls. He remarks that he has found that his patients generally tolerate the mild euphoria that they feel as an effect of marijuana. Dr. Abrams (2016, p. 404) notes that, “If I have a single medicine that I can recommend to assist with nausea, anorexia, insomnia, depression, and pain rather than prescribing five or six pharmaceuticals that may interact with each other or the patient’s chemotherapy, I consider it an attractive option for my patients.” This experienced physician takes a pragmatic approach. He understands that a person who has been told to eat only a quarter of a marijuana cookie might then consume the rest of the cookie if his or her pain is not relieved quickly. However, the person may then suffer discomfort from the psychoactive effects of the plant. Helping a person who has had an experience such as this could be compared to guiding the behavior of someone who has been overeating or over-exercising to a level of discomfort or injury. Self-care is a vital part of a person’s healing process. It is a time when a person learns about his or her own body’s needs in new ways. Nurse-scientist Dorothea Orem wrote, “Self-care is not the performance of this act or that act. Self-care requires the seeing of relationships among factors, for example, diet, activity, and insulin in the management of a diabetic condition. It requires the making of adjustments in care actions on a day-to-day basis or more frequently. It requires the incorporation of self-care into the pattern of daily living” (Orem, Renpenning & Taylor, 2003, p. 213). Marijuana self-care compels a period of time spent adapting to its effects and titrating to the right dose as the person incorporates the plant into his or her lifestyle.
Marijuana has also been used extensively by people who suffer from nausea and vomiting during chemotherapy treatment. Cotter (2009) conducted a systematic literature review to evaluate the efficacy of smoked marijuana and THC as treatment for chemotherapy-induced nausea and vomiting (CINV), a well-documented concern. A synthesis of the data in the review shows that marijuana and synthetic oral THC are more effective than placebo in treating CINV from unnamed chemotherapeutic drugs with a high emetic potential. When using traditional oral antiemetics or drugs of a moderate to high potential for CINV, smoked marijuana and oral THC were found to be equally effective. Oral THC and smoked marijuana have similar efficacy, but with smoked marijuana having the additional risk related to inhalation of smoke (Cotter, 2009).
Whiting and colleagues (2015) published a systematic review considering 28 studies involving a total of 2,454 participants and preparations including inhaled marijuana, dronabinol, nabilone, and Sativex©, among others. Twelve of the studies investigated neuropathic pain, and three looked at patients with cancer pain. The studies generally showed improvement in pain measures, with an overall OR of 1.41 (95% CI: 0.99 to 2.00) for improvement in pain with the use of cannabinoids compared with placebo. An earlier systematic review (Lynch & Campbell, 2011) of 18 randomized controlled trials of cannabinoids in 766 participants with chronic noncancer pain found that 15 of the studies reported a significant analgesic effect for the cannabinoids compared with placebo, and a number of the studies also noted improvements in sleep.
Neuropathic pain is also a concern in the care of cancer patients. A systematic review was conducted of the randomized controlled trials involving marijuana and cannabinoids for the treatment of chronic nonmalignant neuropathic pain. Analysis of the 13 included studies showed that cannabinoids may provide effective analgesia in chronic neuropathic pain that is unresponsive to other treatment (Boychuk, Goddard, Maurio, & Orellana, 2015). Another systematic review of six randomized, double-blind, placebo-controlled trials of cannabinoids (five specifically addressing neuropathic pain) found evidence for the use of low-dose medicinal marijuana in refractory neuropathic pain in conjunction with traditional analgesics (Deshpande, Mailis-Gagnon, Zoheiry, & Lakha, 2015). A randomized controlled trial of Sativex© in 359 cancer patients with poorly controlled pain despite a stable opioid regimen found that the sublingual preparation (4, 10, or 16 sprays daily for 5 weeks) reduced both pain and sleep disruption (Portenoy et al., 2012). A pharmacokinetic interaction study of vaporized marijuana in 21 patients with chronic – mostly non-cancer – pain taking sustained-release morphine or sustained-release oxycodone showed no significant effect on plasma levels of the opiates but did suggest enhanced analgesia. The investigators added anecdotal evidence for the decreasing need for opiates when patients began taking marijuana (Abrams, 2016).
In a randomized placebo-controlled trial, Sativex© did not show a statistically significant improvement in symptoms in those with intractable diabetic peripheral neuropathy pain. Participants were divided into those with and without a history of depression because people with depression have higher baseline pain scores. This study had a large placebo effect, possibly accounting for the failure to show differences between experimental and control groups (Selvarajah, Ghandi, Emery, & Tesgaye, 2010).
A systematic review performed by Fitzcharles, Baerwald, Ablin, and Hauser in 2016 concluded that the finding that cannabinoids are superior to placebo in reducing chronic pain was valid only for neuropathic pain. The evidence for efficacy of cannabinoids reducing pain in people diagnosed with fibromyalgia syndrome (FMS) is inconsistent. However, many people with FMS do seem to think that marijuana is effective. In a study conducted by the U.S. National Pain Foundation, more than 1,339 people with FMS rated marijuana more effective than FDA-approved duloxetine, milnacipran, and pregabalin. The survey showed that only 8% of duloxetine users, 10% of pregabalin users, and 10% of milnacipran users found the prescribed medication to be “very effective,” while 60% of duloxetine users, 61% of pregabalin users, and 68% of milnacipran users replied that the medications “do not help at all.” In contrast, 62% of marijuana users rated the plant “very effective.” Only 5% said that marijuana did not help at all (Fitzcharles et al., 2016).
MRSA and Antibacterial Action
Methicillin-resistant Staphylococcus aureus (MRSA) is an antibiotic-resistant gram-positive bacteria. Studies show that about one in three people in the United States carry S. aureus in their noses, usually without any signs of illness, and two in 100 people carry MRSA (Centers for Disease Control and Prevention, 2017). Terpenoids are aromatic compounds found in the essential oil molecules of plants that can act as a part of the broader immune response of a plant; they may be a protectant for a plant against a predator or an attractant for pollinators. Current research on the terpenoids in marijuana, such as alpha-pinene and limonene, could be explored to see if they, like the alpha-pinene in Sideritis erythrantha essential oil, are effective against MRSA and other antibiotic-resistant bacterial strains (Köse, Deniz, Sarikürkçü, Aktaş, & Yavuz, 2010). Pure CBD powerfully inhibits MRSA (minimum inhibitory concentration 0.5 to 2 mg/mL; Appendino et al., 2008). The ability of monoterpenoids to enhance skin permeability and entry of other drugs may further increase antibiotic benefits (Russo, 2011).
A study tested hemp seed oil, as well as its emulsion, against the growth of selected bacteria using disk diffusion and broth microdilution methods. The antibacterial effect of hemp seed oil was documented against Micrococcus luteus, Staphylococcus aureus, and Salmonella. Oil quality depends on seed origin and extraction method. The formulated emulsions did not exhibit the anticipated antibacterial activity. However, unrefined cold-pressed hemp seed oil did show activity (Mikulcová, Kašpárková, Humpoliček, & Buňková, 2017).
Download the section in PDF