Pharmacology & Addiction

While lawmakers are moving to legalize the recreational use of marijuana in many states, psychological science is demonstrating its serious risks to the mental health of youth and adults.

The use of marijuana has been identified in numerous other international studies as a major cause of psychosis, violence, and crime. Three meta-analyses have concluded that cannabis use is associated with a three-fold increased risk of developing psychosis, primarily with paranoid symptoms that can be associated with the risk of violent reactions (Moore T.H., et al., 2007).

As a psychiatrist, I have seen increased numbers of young adults who have developed psychotic illness without the usual psychological risk factors. Instead, their histories often revealed one strikingly common factor—daily use of cannabis.

Now, whenever I see a young adult patient who has psychotic symptoms, the leading risk factor I explore is the person’s history of marijuana use.

In the important new book Tell Your Children the Truth About Marijuana, Mental Illness, and Violence (Free Press, 2019) Alex Berensen, former New York Times reporter and award-winning novelist, has made a major contribution to marriages, families, the mental health field, and the larger culture. Parents, educators, and health professionals should be aware of the studies of severe psychiatric illness, violent behavior, and crime related to marijuana use that he cites.

A 2018 study of people with psychosis in Switzerland found that almost half of the cannabis users became violent over a three-year period; their risk of violence was four times that of psychotic people who did not use cannabis.

The psychological dynamic at work in paranoid thinking leads people to believe that others plan to harm them. Under this cognitive distortion/delusion, paranoid persons commit violent acts to protect themselves from others whom they believe are a threat to them. In fact, the most dangerous psychiatric patients are those who are paranoid.

A 2012 study of 12,000 high school students across the United States showed that those who used cannabis were more than three times as likely to become violent as those who didn’t, surpassing the risk of alcohol use.

Studies of children who have died from abuse and neglect consistently show that the adults responsible for their deaths use marijuana far more frequently than alcohol or other drugs—and far, far more than the general population.

All four states that legalized cannabis in 2014 and 2015—Alaska, Colorado, Oregon, and Washington—have seen a sharp rise in murders and aggravated assaults since legalization. Combined, the four states saw a 35 percent increase in murders and a 25 percent increase in assaults between 2013 and 2017, far outpacing the national trend.

A 2010 study of 3,801 participants in Australia demonstrated that using cannabis beginning at age 15 raised the risk of hallucinations by almost three times at age 21.

A 2018 study of 5,300 participants in England revealed that teenage cannabis use roughly tripled the risk of psychotic symptoms.

A 2018 Finnish study with 6,534 participants showed that using cannabis more than five times raised the risk of psychotic disorders almost sevenfold.

The number of people showing up at hospitals with psychosis has soared since 2006, alongside marijuana use. By 2014, the most recent year for which data is available, 11 percent of Americans who showed up in emergency rooms with a psychotic disorder also had a secondary diagnosis of marijuana abuse.

Berenson states that the casual use of cannabis has risen only moderately in the last decade, but heavy use has soared—almost tripling. Through the mid-1970s, most marijuana consumed in the United States contained less than 2 percent tetrahydrocannabinol, or THC. Today’s users wouldn’t even recognize that drug as marijuana. Marijuana sold at legal dispensaries now routinely contains 25 percent THC.

A major international 2019 study of first-episode psychosis at 11 European sites and Brazil reported in The Lancet that daily cannabis use was associated with increased psychotic disorder, increasing to nearly five-times increased odds for daily use of high-potency types of cannabis.

In the three sites with the greatest consumption of high-potency cannabis, daily use of high-potency cannabis was associated with the greatest increase in the odds for psychotic disorder compared with never having used: four times greater in Paris, five times greater in London, and more than nine times greater in Amsterdam.

In addition, a large meta-analysis from McGill University published in the Journal of the American Medical Association concluded that marijuana consumption in adolescence is associated with increased risk of developing major depression in young adulthood and suicidal thoughts in young adulthood.

As a result of its widespread use, today cannabis may be the greatest threat to the mental health of youth and young adults and to the physical health of those victimized by the violence arising from paranoid thinking.

Cannabis users often state that it helps them to relax after a stressful day which, of course, is cited also as a benefit of alcohol use. Its use early in the day is an unconscious attempt to diminish the anxiety that arises from insecurity, loneliness, or excessive anger. Its effects are powerful making the drug difficult to give up.

When I expressed a concern to a young adult patient that his daily use of marijuana may have played a role in his several recent and long psychiatric hospitalizations for psychosis, he responded with an expression of total disbelief that his weed could be harming him. He had always felt that it had helped him to cope with stress, and it was a source of pleasure for him.

He asked me with a very sad and troubled expression on his face whether if I was asking him to stop smoking weed daily.

My response was that we had to talk further about the findings that cannabis could cause paranoid thinking. Then I shared with him a composite description of several young adult patients in which their paranoid thinking ceased after the use of anti-psychotic medication and cessation from cannabis use.

While marijuana initially reduces anxiety in its regular users, it also can lead to social withdrawal. As with other drugs, alcohol and pornography use, it can also lead to a person becoming a prisoner within himself, and to the undermining healthy self-giving in relationships.

The American Academy of Child and Adolescent Psychiatry has cited the following signs that parents should consider in regard to marijuana use by a child:

§ worsening of underlying mental health conditions including mood changes and suicidal ideation

§ excessive time in solitary activities such as excessive video-gaming, especially violent video-gaming.

Cannabis, like opioids, alcohol, and pornography, is used to diminish or cover-up the emotional pain of anxiety, sadness and loneliness, mistrust of others, strong anger, insecurity, hopelessness, or trauma. As with substance abuse or pornography, it also can be a manifestation of strong selfishness and an obsession with comfort-seeking behaviors.

These psychological conflicts can be addressed by the use of forgiveness therapy, which reduces the anger associated with all psychological conflicts and facilitates their resolution. In addition, growth in virtues can reduce the painful feelings and the obsession with self and pleasure.

When paranoid thinking is the result of the use of marijuana, the first intervention needs to be the cessation of the drug and initiation of antipsychotic medication. However, the cultural attempts to normalize the use of a dangerous drug and the dependence upon it often combine to produce a strong denial in patients, family members, and even mental health professionals that the use of cannabis could be a cause of paranoid thinking, excessive anger, and violent behavior.

In marriages or cohabiting relationships, when paranoid thinking is intense, separation should be strongly considered for protection from possible severe anger. Reconciliation should depend upon the cessation of marijuana use, clear urine screening, and the use of antipsychotic medication.

Participation in a 12-step recovery program is also an important part of the treatment plan.

If a person is able to maintain a prolonged period of sobriety and a resolution of paranoid thinking, a trial off medication should be considered.

Also, being raised in a family with faith, regular church attendance, and prayer has been shown to have benefits, in a 2018 Harvard School of Public Health study of 5,000 youth followed into adulthood.

Such faith-based practices are associated with lower probabilities of marijuana use, greater life satisfaction, and character strengths, compared with those who have no church attendance. The authors of this study, Chen and Vanderweele, wrote that,

“Although decisions about religion are not shaped principally by health, encouraging service attendance and private practices (prayer) in adolescents who already hold religious beliefs may be meaningful avenues of development and support, possibly leading to better health and well-being.”

Many years of clinical experience support the recommendations in Berenson’s book to address the epidemic of marijuana-induced psychosis. It strongly indicates the importance of fighting the drug’s legalization.

A major challenge to an effective treatment plan is the cultural attempt to normalize the use of marijuana as a recreational drug. Such an agenda about this dangerous drug is a manifestation of severe denial and, ultimately, delusional thinking of influential and powerful segments of the culture. It is a denial of the scientific studies that show the negative effects of marijuana use.

In the past, the tobacco industry reaped enormous profits while denying the harm of cigarettes. History must not repeat itself, this time with a powerful cannabis lobby that also stands to make enormous financial gain.

In fact, the tobacco industry has an interest in marijuana, according to the New York Times. The maker of Marlboro and other cigarettes paid $1.8 billion for almost half of Cronos Group, a cannabis company in Toronto.

In August 2014, Constellation Brands, which owns Corona and other beers, paid $4 billion for a major stake in Canopy Growth, another Canadian marijuana company. That month, Molson Coors, another brewer, formed a joint venture with a cannabis company in Quebec.

In an interview, Berensen claimed that George Soros was reported to be the largest backer of the Drug Policy Alliance, a major supporter of the legalization of marijuana.

In the report The Health Effects of Cannabis and Cannabinoids: The Current State of Evidence and Recommendations for Research, an expert, ad hoc committee of the National Academies of Sciences, Engineering, and Medicine presents nearly 100 conclusions related to the health effects of cannabis and cannabinoid use.

The committee developed standard language to categorize the weight of the evidence regarding whether cannabis or cannabinoids used for therapeutic purposes are an effective or ineffective treatment for certain prioritized health conditions, or whether cannabis or cannabinoids used primarily for recreational purposes are statistically associated with certain prioritized health conditions. The box on the next page describes these categories and the general parameters for the types of evidence supporting each category.

The numbers in parentheses after each conclusion correspond to chapter conclusion numbers. Each blue header below links to the corresponding chapter in the report, providing much more detail regarding the committee’s findings and conclusions. To read the full report, please visit nationalacademies.org/CannabisHealthEffects.

CONCLUSIONS FOR: THERAPEUTIC EFFECTS

There is conclusive or substantial evidence that cannabis or cannabinoids are effective:

● For the treatment for chronic pain in adults (cannabis) (4-1)

● Antiemetics in the treatment of chemotherapy-induced nausea and vomiting (oral cannabinoids) (4-3)

● For improving patient-reported multiple sclerosis spasticity symptoms (oral cannabinoids) (4-7a)

There is moderate evidence that cannabis or cannabinoids are effective for:

● Improving short-term sleep outcomes in individuals with sleep disturbance associated with obstructive sleep apnea syndrome, fibromyalgia, chronic pain, and multiple sclerosis (cannabinoids, primarily nabiximols) (4-19)

There is limited evidence that cannabis or cannabinoids are effective for:

● Increasing appetite and decreasing weight loss associated with HIV/AIDS (cannabis and oral cannabinoids) (4-4a)

● Improving clinician-measured multiple sclerosis spasticity symptoms (oral cannabinoids) (4-7a)

● Improving symptoms of Tourette syndrome (THC capsules) (4-8)

● Improving anxiety symptoms, as assessed by a public speaking test, in individuals with social anxiety disorders (cannabidiol) (4-17)

● Improving symptoms of posttraumatic stress disorder (nabilone; one single, small fair-quality trial) (4-20)

There is limited evidence of a statistical association between cannabinoids and:

● Better outcomes (i.e., mortality, disability) after a traumatic brain injury or intracranial hemorrhage (4-15)

There is limited evidence that cannabis or cannabinoids are ineffective for:

● Improving symptoms associated with dementia (cannabinoids) (4-13)

● Improving intraocular pressure associated with glaucoma (cannabinoids) (4-14)

● Reducing depressive symptoms in individuals with chronic pain or multiple sclerosis (nabiximols, dronabinol, and nabilone) (4-18)

There is no or insufficient evidence to support or refute the conclusion that cannabis or cannabinoids are an effective treatment for:

● Cancers, including glioma (cannabinoids) (4-2)

● Cancer-associated anorexia cachexia syndrome and anorexia nervosa (cannabinoids) (4-4b)

● Symptoms of irritable bowel syndrome (dronabinol) (4-5)

● Epilepsy (cannabinoids) (4-6)

● Spasticity in patients with paralysis due to spinal cord injury (cannabinoids) (4-7b)

● Symptoms associated with amyotrophic lateral sclerosis (cannabinoids) (4-9)

● Chorea and certain neuropsychiatric symptoms associated with Huntington’s disease (oral cannabinoids) (4-10)

● Motor system symptoms associated with Parkinson’s disease or the levodopa-induced dyskinesia (cannabinoids) (4-11)

● Dystonia (nabilone and dronabinol) (4-12)

● Achieving abstinence in the use of addictive substances (cannabinoids) (4-16)

● Mental health outcomes in individuals with schizophrenia or schizophreniform psychosis (cannabidiol) (4-21)

CONCLUSIONS FOR: CANCER

There is moderate evidence of no statistical association between cannabis use and:

· Incidence of lung cancer (cannabis smoking) (5-1)

· Incidence of head and neck cancers (5-2)

There is limited evidence of a statistical association between cannabis smoking and:

· Non-seminoma-type testicular germ cell tumors (current, frequent, or chronic cannabis smoking) (5-3)

There is no or insufficient evidence to support or refute a statistical association between cannabis use and:

· Incidence of esophageal cancer (cannabis smoking) (5-4)

· Incidence of prostate cancer, cervical cancer, malignant gliomas, non-Hodgkin lymphoma, penile cancer, anal cancer, Kaposi’s sarcoma, or bladder cancer (5-5)

· Subsequent risk of developing acute myeloid leukemia/acute non-lymphoblastic leukemia, acute lymphoblastic leukemia, rhabdomyosarcoma, astrocytoma, or neuroblastoma in offspring (parental cannabis use) (5-6)

CONCLUSIONS FOR: CARDIOMETABOLIC RISK

There is limited evidence of a statistical association between cannabis use and:

· The triggering of acute myocardial infarction (cannabis smoking) (6-1a)

· Ischemic stroke or subarachnoid hemorrhage (6-2)

· Decreased risk of metabolic syndrome and diabetes (6-3a)

· Increased risk of prediabetes (6-3b)

There is no evidence to support or refute a statistical association between chronic effects of cannabis use and:

· The increased risk of acute myocardial infarction (6-1b)

CONCLUSIONS FOR: RESPIRATORY DISEASE

There is substantial evidence of a statistical association between cannabis smoking and:

· Worse respiratory symptoms and more frequent chronic bronchitis episodes (long-term cannabis smoking) (7-3a)

· There is moderate evidence of a statistical association between cannabis smoking and:

· Improved airway dynamics with acute use, but not with chronic use (7-1a)

· Higher forced vital capacity (FVC) (7-1b)

There is moderate evidence of a statistical association between the cessation of cannabis smoking and:

· Improvements in respiratory symptoms (7-3b)

There is limited evidence of a statistical association between cannabis smoking and:

· An increased risk of developing chronic obstructive pulmonary disease (COPD) when controlled for tobacco use (occasional cannabis smoking) (7-2a)

CONCLUSIONS FOR: IMMUNITY

There is limited evidence of a statistical association between cannabis smoking and:

· A decrease in the production of several inflammatory cytokines in healthy individuals (8-1a)

There is limited evidence of no statistical association between cannabis use and:

· The progression of liver fibrosis or hepatic disease in individuals with viral Hepatitis C (HCV) (daily cannabis use) (8-3)

There is no or insufficient evidence to support or refute a statistical association between cannabis use and:

· Other adverse immune cell responses in healthy individuals (cannabis smoking) (8-1b)

· Adverse effects on immune status in individuals with HIV (cannabis or dronabinol use) (8-2)

· Increased incidence of oral human papilloma virus (HPV) (regular cannabis use) (8-4)

CONCLUSIONS FOR: INJURY AND DEATH

There is substantial evidence of a statistical association between cannabis use and:

· Increased risk of motor vehicle crashes (9-3)

There is moderate evidence of a statistical association between cannabis use and:

· Increased risk of overdose injuries, including respiratory distress, among pediatric populations in U.S. states where cannabis is legal (9-4b)

There is no or insufficient evidence to support or refute a statistical association between cannabis use and:

· All-cause mortality (self-reported cannabis use) (9-1)

· Occupational accidents or injuries (general, non-medical cannabis use) (9-2)

· Death due to cannabis overdose (9-4a)

CONCLUSIONS FOR: PRENATAL, PERINATAL, AND NEONATAL EXPOSURE

There is substantial evidence of a statistical association between maternal cannabis smoking and:

· Lower birth weight of the offspring (10-2)

There is limited evidence of a statistical association between maternal cannabis smoking and:

· Pregnancy complications for the mother (10-1)

· Admission of the infant to the neonatal intensive care unit (NICU) (10-3)

There is insufficient evidence to support or refute a statistical association between maternal cannabis smoking and:

· Later outcomes in the offspring (e.g., sudden infant death syndrome, cognition/academic achievement, and later substance use) (10-4)

There is substantial evidence of a statistical association between cannabis use and:

· The development of schizophrenia or other psychoses, with the highest risk among the most frequent users (12-1)

There is moderate evidence of a statistical association between cannabis use and:

· Better cognitive performance among individuals with psychotic disorders and a history of cannabis use (12-2a)

· Increased symptoms of mania and hypomania in individuals diagnosed with bipolar disorders (regular cannabis use) (12-4)

· A small increased risk for the development of depressive disorders (12-5)

· Increased incidence of suicidal ideation and suicide attempts with a higher incidence among heavier users (12-7a)

· Increased incidence of suicide completion (12-7b)

· Increased incidence of social anxiety disorder (regular cannabis use) (12-8b)

There is moderate evidence of no statistical association between cannabis use and:

· Worsening of negative symptoms of schizophrenia (e.g., blunted affect) among individuals with psychotic disorders (12-2c)

There is limited evidence of a statistical association between cannabis use and:

· An increase in positive symptoms of schizophrenia (e.g., hallucinations) among individuals with psychotic disorders (12-2b)

· The likelihood of developing bipolar disorder, particularly among regular or daily users (12-3)

· The development of any type of anxiety disorder, except social anxiety disorder (12-8a)

· Increased symptoms of anxiety (near daily cannabis use) (12-9)

· Increased severity of posttraumatic stress disorder symptoms among individuals with posttraumatic stress disorder (12-11)

There is no evidence to support or refute a statistical association between cannabis use and:

· Changes in the course or symptoms of depressive disorders (12-6)

· The development of posttraumatic stress disorder (12-10)

CONCLUSIONS FOR: PROBLEM CANNABIS USE

There is substantial evidence that:

· Stimulant treatment of attention deficit hyperactivity disorder (ADHD) during adolescence is not a risk factor for the development of problem cannabis use (13-2e)

· Being male and smoking cigarettes are risk factors for the progression of cannabis use to problem cannabis use (13-2i)

· Initiating cannabis use at an earlier age is a risk factor for the development of problem cannabis use (13-2j)

There is substantial evidence of a statistical association between:

· Increases in cannabis use frequency and the progression to developing problem cannabis use (13-1)

· Being male and the severity of problem cannabis use, but the recurrence of problem cannabis use does not differ between males and females (13-3b)

There is moderate evidence that:

· Anxiety, personality disorders, and bipolar disorders are not risk factors for the development of problem cannabis use (13-2b)

· Major depressive disorder is a risk factor for the development of problem cannabis use (13-2c)

· Adolescent ADHD is not a risk factor for the development of problem cannabis use (13-2d)

· Being male is a risk factor for the development of problem cannabis use (13-2f)

· Exposure to the combined use of abused drugs is a risk factor for the development of problem cannabis use (13-2g)

· Neither alcohol nor nicotine dependence alone are risk factors for the progression from cannabis use to problem cannabis use (13-2h)

· During adolescence the frequency of cannabis use, oppositional behaviors, a younger age of first alcohol use, nicotine use, parental substance use, poor school performance, antisocial behaviors, and childhood sexual abuse are risk factors for the development of problem cannabis use (13-2k)

There is moderate evidence of a statistical association between:

· A persistence of problem cannabis use and a history of psychiatric treatment (13-3a)

· Problem cannabis use and increased severity of posttraumatic stress disorder symptoms (13-3c)

There is limited evidence that:

· Childhood anxiety and childhood depression are risk factors for the development of problem cannabis use (13-2a)

There is limited evidence of a statistical association between cannabis use and:

· Changes in the rates and use patterns of other licit and illicit substances (14-2)

CONCLUSIONS FOR: CHALLENGES AND BARRIERS IN
CONDUCTING CANNABIS AND CANNABINOID RESEARCH

There are several challenges and barriers in conducting cannabis and cannabinoid research, including:

· There are specific regulatory barriers, including the classification of cannabis as a Schedule I substance, that impede the advancement of cannabis and cannabinoid research (15-1)

· It is often difficult for researchers to gain access to the quantity, quality, and type of cannabis product necessary to address specific research questions on the health effects of cannabis use (15-2)

· A diverse network of funders is needed to support cannabis and cannabinoid research that explores the beneficial and harmful effects of cannabis use (15-3)

· To develop conclusive evidence for the effects of cannabis use for short- and long-term health outcomes, improvements and standardization in research methodology (including those used in controlled trials and observational studies) are needed (15-4)

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