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On Marijuana Part II: The Health Effects of Marijuana

By Jeremy Hausotter

Jan. 1, 2021

Table of Contents


1. The Pharmacological Properties of Cannabis

1.1. Cannabis and the FDA

1.2. THC and the Brain

2. The Negative Health Consequences of Marijuana Usage

2.1. Cannabis Mythmaking: Yesterday and Today

2.2. Cannabis and Teenagers

2.3. Marijuana and Academic Performance

2.4. Cannabis and Violence

2.5. Cannabis, Psychosis, and Schizophrenia

2.6. Cannabis and Addiction

2.7. Cannabis and Driving

2.8. Heart Attack and Strokes

2.9. Respiratory Problems

3. Medical Marijuana

3.1. Marijuana and Cancer
     3.2. Marijuana and Anorexia
     3.3. Marijuana as an Ineffective Treatment for Several Maladies
     3.4. Marijuana and Drug Usage
     3.5. Problematic Usage of Marijuana
     3.6. Marijuana and Anxiety
     3.7. Marijuana and Depression
     3.8. Marijuana and PTSD
     3.9. Marijuana and Schizophrenia
     3.10. Marijuana and Bipolar Disorders
     3.11. Marijuana and Suicide
     3.12. Marijuana and Pregnancy
4. Correlation and Causation



Note to the Reader:

As of January 2023, I have published this essay as part of my book The Opium of Happiness. This text is a thorough revision of the essays on this site while adding over 100 pages not found on the website. Several of the Church documents used in this research can be found as appendices in the book.


Today when one hears the terms “health” or “medicine” and “marijuana”, he or she would probably hold the belief that marijuana is a medicinally significant substance or at least assume a positive outlook towards the plant’s medical potentialities.[2] After all, there is an ever growing chorus of cannabis advocates arguing that marijuana has many health benefits and can improve symptoms for a myriad amount of maladies. My task here is to develop further some of the medical justification contained within the Pontifical Council for Health Pastoral Care’s Church: Drugs and Drug Addiction, (hereafter CDDA) which condemned marijuana usage outside of any therapeutic or medical purposes.

CDDA gives a detailed list of the health effects of cannabis usage but what is not given is the various medical studies supporting its statements. CDDA cites few sources from medical and psychological studies. The goal of Part II is hence providing a deeper engagement of the question of marijuana’s effects on man. While CDDA was written with the latest knowledge of the medical expertise at the time, it was written twenty years ago now and since then there has been several new studies that further defend some of the claims it made.

In addition to defending CDDA, a second purpose here is to help bring balance to the public discourse concerning the health effects of marijuana. As the authors of CDDA observed, several marijuana proponents argue for the safely of the drug in misleading ways in order to trivialize it and make it appear harmless.[3]

Part II is divided into four parts. The first of which examines some of the basic pharmacological facts about marijuana. The second reports on the ill-effects of marijuana. The third part exposes many of the fraudulent claims concerning the medicinal benefits of cannabis. Lastly, this part considers the question concerning correlation and causation in statistics.

1. The Pharmacological Properties of Cannabis

1.1. Cannabis and the FDA

A first point of confusion that must be clarified is that there are many marijuana products. In fact one regularly sees hemp products in grocery stores now which makes it all the more confusing. The two most commonly known compounds in marijuana are cannabidiol (CBD) and delta-9-tetrahydrocannabinol (THC). THC is responsible for cannabis users getting high while CBD is generally identified as medically significant. One immediate problem to note is that a lot of consumed marijuana has low levels of CBD and high levels of THC of 25% or more depending on the type of product.[4]

The kind of marijuana used by drug addicts and sold in pot shops is different from what is sold in the grocery store. By law the FDA oversees the regulation of marijuana products and synthesized cannabis chemicals and the current regulations on cannabis prevent any THC concentration of 0.3% dry weight.[5] The hemp products in grocery stores contain little to no THC.

Currently the FDA recognizes only four drugs based on cannabis. Epidiolex is based upon CBD and is used to treat seizures associated with both Lennox-Gastaut and Dravet syndromes, and seizures associated with tuberous sclerosis complex.[6] This is the only CBD-based drug the FDA has approved for treatments. There are no other FDA approved drugs based on or contain CBD. Epidiolex is also the only cannabis-derived drug that is FDA approved. A second important point that can be made is that one does not need to consume marijuana in order to treat seizures. One can avoid the high of THC since this is a CBD based drug, meaning that it is illicit to seek out marijuana for a treatment that already exists without the negative effects of marijuana itself.

The FDA approved three other drugs that are based upon THC but are synthetic. These are Marinol and Syndros which are used to treat anorexia associated with weight loss in AIDS patients and Cesamet which is used to prevent nausea and vomiting caused by cancer medication. As was argued concerning Epidiolox it is immoral to use marijuana to treat an illness when there is already a cannabis-based alternative that is a proven effective treatment since marijuana itself is a dangerous drug (which yet requires further demonstration).

Besides these drugs there are no other FDA approved cannabis medications. Concerning marijuana itself the FDA states:

FDA is aware that unapproved cannabis or cannabis-derived products are being used for the treatment of a number of medical conditions including, for example, AIDS wasting, epilepsy, neuropathic pain, spasticity associated with multiple sclerosis, and cancer and chemotherapy-induced nausea.

To date, FDA has not approved a marketing application for cannabis for the treatment of any disease or condition and thus has not determined that cannabis is safe and effective for any particular disease or condition.[7]

1.2. THC and the Brain[8]

The chemical structure of THC is similar to anandamide which is a neurotransmitter and affects the parts of the brain responsible for pleasure, memory, thinking, concentration, movement, coordination, sense perception, and time perception.[9] Due to THC’s similarity with anandamide it can attach to neurons and activate them as anandamide does in the manners above.

THC for example is capable of disrupting the hippocampus’ functionality and orbitofrontal cortex. These parts of the brain enable the formation of new memories and the ability to shift attentional focus; and so, since THC alters these parts of the brain cannabis usage can affect a person’s memory, impair thinking, ability to learn, and performance of complicated tasks.[10]

THC also alters the functioning of the basal ganglia and cerebellum, the parts of the brain responsible for regulating balance, posture, coordination, and reaction time.[11] This means that marijuana users cannot safely operate machinery or drive motorized vehicles, and have problems performing physical activities such as sports.

THC also activates the brain’s reward center, releasing dopamine. It is this effect that marijuana users seek when desiring to get high. This is also what makes marijuana potentially addictive and in part a psychostimulant.

2. The Negative Health Consequences of Marijuana Usage

2.1. Cannabis Mythmaking: Yesterday and Today

In the 1960’s and 1970’s marijuana gained popularity within American society and was favorably praised in films and the media. There was a strong push for its legalization, only it did not happen. Parents vocalized their disapproval of marijuana and created groups which brought public pressure down upon the newspapers and filmmakers such that the legalization movement effectively died for twenty years until a new marketing strategy by marijuana advocates started the medical marijuana advertisement campaign.

One legacy of this history is that today advocates argue for the harmlessness of marijuana. Many Americans who have tried it once or twice would say cannabis did not really affect them. A marijuana joint in the 1970’s had about a 2% THC concentration. THC is the chemical responsible for the marijuana high. What many do not realize, however, is that today a joint has a THC concentration of 25% or more. Other cannabis products such as wax and shatter can be pure or near pure THC. Marijuana today is more than twelve times potent than it was fifty years ago.

This has a direct correlation with the rise in fatal overdoses. Many believe that one cannot die from cannabis overdose, and this was “pretty much” true. In 1999 there was only eight marijuana fatal overdoses, so while possible it was highly unlikely. Yet this is not the whole story, for the number of fatal overdoses is rising. In 2016 the figure climbed to 191.[12] As cannabis products become more potent the number of deaths by fatal overdose increased. This also means that today we should be able to see more readily the adverse side effects of this drug due to its increased potency.

2.2. Cannabis and Teenagers

The General Problem[13]

The teenager’s brain is still in the process of development. The brain does not finish developing until one reaches his or her mid-20’s (and thereafter the brain still remains plastic and malleable throughout most of adulthood). During development the brain establishes synapses based around skills through one’s daily activities. These stimulate the brain’s pleasure center and hence one’s life activities are in a sense programmed in this part of the brain.

Drugs introduce a shortcut to the brain’s pleasure center, i.e. the limbic system. These shortcuts create brain circuits centered on drug usage. For a teenager this means that his or her brain can literally become hardwired towards drug usage instead of ordinary, healthy life activities. This implies that the teenager will be more likely to become addicted to drugs, abuse other substances, and have a more difficult time leading a healthy lifestyle since these synapses are underdeveloped or eliminated. It should hence come as no surprise that a ten year study of cannabis usage amongst adolescents showed that teens who used marijuana were more likely to abuse drugs at higher rates in comparison to cannabis users who started as adults.[14] What is alarming is that most marijuana users start before they reach the age of 18 and one fourth of all cannabis users start by the time they reach 15 years of age.[15] We need to keep in mind on the other hand that the person remains a free, rational person. Drugs impair one’s ability to live as such but he or she still retains his or her personhood and ability to freely accept and continue abusing drugs or to reject them.

Marijuana and the Teenager’s Brain

A study by Duke University showed that cannabis smokers who started before the age of 17 had smaller brains and less grey matter.[16] Grey matter includes the thinking part of the brain controlling decision making and self-control. This means that cannabis users who started as teens should have both cognitive problems and issues controlling their behavior, and hence more likely to become violent.

The University of California at San Diego conducted a study showing that teens who were heavy marijuana users after being abstinent one month still performed worse on neurocognitive tests including attention, memory, and planning ability, in comparison to those who never used marijuana.[17] A Harvard study similarly found that heavy marijuana users before the age of 16 performed worse in executive functions such as solving problems, discerning patterns, and controlling impulses versus those who never smoked marijuana or did so at a later age (and both of these latter groups performed normally).[18]

Another study conducted by Duke University and the University of Otago studied IQ in 1000 people from birth to middle age. Researchers found that the IQ of cannabis users dropped as they aged but for nonusers their IQ remained the same. After one year of abstinence from cannabis, those who had started using marijuana as adults saw their brain function return while those who started using marijuana before the age of 18 did not and lost an average of 8 IQ points.[19]

2.3. Marijuana and Academic Performance

Given that marijuana has negative consequences for the health of the brain it should come as no surprise that marijuana users face several academic challenges versus nonusers. Cannabis users who started in their early teens are more likely to drop out of school and have worse academic performances.[20] One study showed that users who started consuming marijuana before they reached 16 years of age were more than twice as likely to drop out of school in comparison to nonusers.[21] Similarly, once substance abusing teens cut down their drug or alcohol usage it was shown that they attended school more regularly. For marijuana users this was only true once they had quit entirely.[22] The study also showed that marijuana users needed to be abstinent for three months in order for school attendance to start improving.

The pattern is also true for college students. One study showed that infrequent cannabis users who only smoked twice a month were two-thirds more likely to drop out of college versus nonusers.[23] The University of Maryland School of Public Health followed freshmen for ten years and found that those who abused substances and especially marijuana skipped more classes, spent less time studying, earned lower grades, dropped out at higher rates, and were more likely to be unemployed after college.[24]

A major study by Fergusson followed 1000 people from the age 15 to 25.[25] The group was divided into the six following groups based on the number of times he or she smoked marijuana by the time they reached age 21: 1-99 times, 100-199 times, 200-299 times, 300-399 times, >400 times, and nonusers. The researchers showed that the number of times marijuana was used is inversely proportional to obtaining a Bachelor's degree. The more one used marijuana, the less likely he or she graduated. The graduation rate in fact drops quite significantly; those who used cannabis 200-399 times had a 10% graduation rate whereas those who used it over 400 times had only a 2% graduation rate. In comparison, about one-third of nonusers and one-fourth of occasional users graduated college.

The study also showed that those who used cannabis more than 100 times also earned less money, felt less satisfied in their intimate relationships, and reported being unhappier. The researchers tested sixteen variables for explanation which included accounting for poverty, child abuse, and alcohol abuse, and found that the pattern remained consistent regardless of these variables. Hence, while there is a correlation between these poor academic outcomes and cannabis, it is possible that there are other variables involved which can explain why one is abusing marijuana and performing poorly in his or her studies. The Fergusson study, however, does show that there appears to be a causal connection between marijuana and poor academic performance since the researchers were able to eliminate sixteen other variables that could possibly affect the outcome.

The National Academies of Sciences, Engineering, and Medicine in their 2017 report on the health effects of marijuana concluded that there is moderate evidence of an association between marijuana usage and impairment in learning, memory, and attention, and limited evidence of impairment of the three once the individual stopped using marijuana for an extended period of time.[26] (CDDA also argues this).[27] Since marijuana affects the person in such a manner this would explain the problems noted above concerning academic performance. This same report further concluded that there is limited evidence for an association between cannabis use and poor academic achievement and outcomes,[28] and between using marijuana and increased rates of low employment and lower income.[29]

2.4. Cannabis and Violence

Earlier we mentioned that studies showed marijuana impaired the part of the brain which determines one’s self-control. This means that we should expect to see problems with violence from cannabis users and research demonstrates this. One study showed that those addicted to cannabis were more prone to violence independently of other psychiatric problems and drug abuse.[30] Another study conducted on 12,000 students showed that cannabis users were three times as likely to become violent versus nonusers.

Those with psychiatric problems suffered worse. Those who have schizophrenia and are substance abusers are significantly more likely to become violent.[31] Another study on psychosis patients showed that about half of all patients who used marijuana became violent over a three year period and that the risk of violence was four times that of psychotic nonusers. Research also suggests that those with PTSD who consume marijuana have more severe symptoms and are more violent.[32]

One may reply to these studies asking where are some examples of such violence? Afterall one never hears of cases of cannabis-induced violence. Here are some examples: Raina Thaiday, mother of eight, marijuana user, murdered seven of her children and her niece with a knife then stabbed herself. Nikolas Cruz, marijuana user, killed 17, injured 17 more in Parkland, FL. Devin Kelley, marijuana user, killed 27, injured 20 more in Sutherland Springs, TX. Salaman Abedi, marijuana user, detonated a bomb in Manchester Arena, UK, killing 20 and injuring over 100 others. Richard Rojas, marijuana user, drove his car along the pavement of Times Square, killing one and injuring 22. Arcan Cetin, marijuana user, killed five at Cascade Mall in WA. Satoshi Uematsu, marijuana user, stabbed to death 19 and injured 26 more at a care facility in Sagamihara, Japan. Robert Dear, marijuana user, killed three, injured nine more at Planned Parenthood in Colorado Springs. Muhammad Youssef Abdulazeez, marijuana user, killed five and injured two more in Chattanooga, TN. Dylan Roof, marijuana user, murdered nine people at a church service in Charleston, SC. Michael Brown, whose death sparked race riots, was a marijuana user and was intoxicated with THC at the time of his death. The Boston marathon bombers were marijuana users and killed three, injured over 250 more. Jared Loughner, marijuana user, killed six, injured 14 more in Tucson, AZ. James Holmes, marijuana user, killed 12, injured 70 in Aurora, CO. Most of these examples are listed in a meta-analysis of cannabis and violence.[33] There are many examples that have made the news, only not the part about the perpetrator being high on drugs. I do acknowledge that in each case listed there are several other factors involved. What is pointed out here is a correlation that raises questions concerning the causes and whether marijuana is a statistically significant predictor for violence.

2.5. Cannabis, Psychosis, and Schizophrenia

Research has shown that cannabis worsens the symptoms of schizophrenia.[34] This is due to THC causing psychosis.[35] Part of the problem is the fact that schizophrenic patients who use cannabis are twice as likely to incorrectly take their medicine or not at all and six times more likely to drop out of therapy.[36] Not only do marijuana patients have poor adherence to their treatment plans but they have higher rates of relapse and more frequent hospitalizations versus nonusers.[37] Emergency room visits due to psychosis while on marijuana tripled in the United States between 2006 and 2014 from 30,000 to 90,000, and this demographic represented 11% of all emergency room visits.[38] Schizophrenic marijuana users demonstrated more disorganized thinking, paranoia, chronic symptoms, irritability, and hostility versus nonusers.[39] The more a schizophrenic patient used cannabis, the more aggravated his or her symptoms became.

One study shows that schizophrenic marijuana users relapse at three times the rate of nonusers.[40] Another study showed that nearly one-fourth of all schizophrenic patients abuse marijuana.[41] Over the course of thirty years, a third study showed that schizophrenic patients on marijuana had twice the number of hospitalizations and spent three times as many days in the hospital versus nonusers.[42]

Schizophrenic marijuana users in one study were shown to be diagnosed seven years younger than nonusers[43] and two to three years younger in another.[44] A third study showed a correlation between teens abusing marijuana and schizophrenia, that this demographic has higher rates of schizophrenia and are more likely to develop it later in life.[45]

The Swedish Conscript study evaluated 50,000 conscripts and showed a direct correlation between marijuana and schizophrenia.[46] The overall rate for schizophrenia in the sample population was 0.54%. Those who used weed no more than 10 times by age 18 had a risk of 1.16%, meaning that using marijuana no more than 10 times doubled one’s risk for schizophrenia. Those who used marijuana less than 50 times were three times more likely to develop schizophrenia, and those who used it more than 50 times were six times more likely. The risk for schizophrenia in marijuana users remained after the researchers accounted for eleven variables.

2.6. Cannabis and Addiction

Marijuana itself is Addictive

It is a common myth perpetuated by the cannabis legalization organism that one does not get addicted to the drug, but this is certainly not the case. There is a lot of research demonstrating that marijuana users are addicted and the rate of addiction is increasing given the increase in its popularity due to the legalization efforts in America.[47]

The DEA in its 2014 report on marijuana notes that from 1998 to 2008 the treatment admission rate for marijuana substance abuse rose 30% nationally and in California 117%.[48] In 2012 marijuana was the drug with the highest proportion of abuse or dependence of all illicit drug use, accounting for nearly 60%.[49] More sobering is the fact that in 2011 40% of primary marijuana treatment admissions were under the age of 20 and that 32% of treatment admissions had first used marijuana by the age of 14.[50]

While marijuana is not physically toxic like other substances, it does cause a mainly psychological dependency. Research shows that cannabis withdrawal leads to symptoms such as anger, aggression, decreased appetite, irritability, nervousness, anxiety, restlessness, sleep difficulties, chills, depression, stomach pain, sweating, and shakiness.[51]

Cannabis and Alcohol Addiction

Research also shows that those who abuse marijuana are also more likely to abuse alcohol.[52] In particular, teens who abuse cannabis are more at risk for abusing alcohol as adults.[53]

Cannabis and Other Drug Abuse

Research has also suggested that early marijuana usage is a precursor to substance abuse. One study analyzed 300 pairs of twins and found that those who used cannabis by the age of 17 were 2.1 to 5.2 times more likely to abuse other drugs and become dependent upon them versus the twin who did not use marijuana.[54] The correlation remained after accounting for several risk factors such as child abuse, psychological illnesses, and early alcohol and tobacco initiation.

Another study showed a strong relationship between cocaine and marijuana abuse.[55] 62% of those who used cocaine started using marijuana before they reached 15 years of age. In comparison, less than 1% of adults who never tried marijuana used cocaine. This means that over 99% of cocaine users had either tried marijuana  at some point in their lives while on cocaine or first started out using marijuana and moved on to cocaine.

The National Center of Addiction and Substance Abuse at Columbia University reported that teens who used marijuana at least once a month were 26 times likelier versus teens who never used marijuana to abuse other drugs such as meth, cocaine, and heroin.[56] The National Academies of Sciences, Engineering, and Medicine’s 2017 report concluded that there is moderate evidence of a statistical association between marijuana usage and becoming addicted to and abusing other drugs including alcohol, tobacco, and illicit drugs.[57]

2.7. Cannabis and Driving

Several studies have also shown a correlation between marijuana usage and impaired driving. One study in Nova Scotia found that marijuana alone was associated with a fourfold increased rate of collisions.[58] Another study showed that drivers with low levels of cannabis metabolites were twice as likely to cause a fatal motor accident, and heavy usage quadrupled the risk.[59] A third study showed that heavy marijuana users were nine times more likely to be injured in a car accident.[60] It should come as no surprise that since Colorado’s legalization of marijuana the number of traffic fatalities due to cannabis impair drivers doubled.[61]

One study showed that in 2012 12% of all fatal car accidents involved a driver using marijuana.[62] Interestingly enough, 15% of all bike crash victims used cannabis.[63] Researchers have also found that those who drive within a few hours after smoking marijuana were twice as likely to be in a serious or fatal motor accident.[64] An Australian study on airline pilots found that pilots who smoked marijuana were still severely impaired the next day unfit to fly.[65] An interesting feature about this study is that the pilots did not perceive themselves to be impaired. The DEA lists four full pages of statistics on marijuana and driving.[66] The National Academies of Sciences, Engineering, and Medicine report after surveying the research on this question concluded that there is substantial evidence of a statistical link between cannabis users and increased risk of vehicle accidents.[67]

2.8. Heart Attack and Strokes

The National Academies of Sciences, Engineering, and Medicine (NAM) in its 400 page report on marijuana and its health effects found that there is limited evidence of a statistical association between smoking marijuana and triggering a heart attack.[68] It also concluded that there is no evidence to judge either way whether there is a statistical association between chronic marijuana usage and heart attack risk. A third conclusion was that there is limited evidence of a link between cannabis usage and strokes and internal brain hemorrhages.[69]

2.9. Respiratory Problems

The same NAM report also concluded that there may be a link between smoking marijuana occasionally and an increased risk of chronic obstructive pulmonary disease, which causes irreversible lung damage.[70] It also found that there is substantial evidence of a link between smoking marijuana long term and worse respiratory symptoms such as injured airways, coughing, phlegm wheeze, and chronic bronchitis.[71] There is also moderate research between those who stopped smoking marijuana and seeing improvement in these symptoms.

3. Medical Marijuana

Legalization advocates argue that marijuana is a medicine and so it should be legalized. In fact, if this premise is true, then a kind of moral imperative seems to appear demanding access to this “medicine”. The legalization proponents in the media make emotional pleas in precisely this manner. We have all seen those pathos driven pleas of mothers and fathers seeking medical help for his or her child who claim that only marijuana can help or save them. This is the strongest argument for marijuana’s legalization, but also its greatest charade.

It must be noted first and foremost that if marijuana is to be treated as a medicine, then any medical usage of marijuana needs to be subjected to the same rigorous medical testing as any drug. Failure to do this is irresponsible and endangers people. Marijuana needs to be proven to be as effective and safe of a treatment like any other drug.

Secondly, medical marijuana is to be treated like a drug. One does not smoke their allergy medicine for example, make Tylenol laced brownies, or lace hard candies with morphine. These sorts of activities are rightly condemned as irresponsible and dangerous. The chemical properties that are deemed medicinally beneficial ought to be put in a proper form for adequate dosage, not smoked, vaped, or other methods used by marijuana addicts. Many medical societies are in fact against smoking marijuana for supposed medical benefits because of how dangerous such an activity actually is to one’s health.[72] Marijuana smoke contains toxic chemicals such as ammonia, benzene, toluene, and naphtha­lene in levels greater than tobacco smoke, making marijuana smoke a significant risk factor for several respiratory illnesses.[73]

It must be also noted that there are already THC and CBD based drugs that are FDA approved, meaning that it is a moot point to use marijuana for medical reasons when there are already marijuana-based drugs, like nabilone and dronabinol that have proved to be effective in treating nausea induced by chemotherapy for example.[74] Research has also shown that users of these drugs do not get high as easily from them, making these treatment options harder to abuse.

Marijuana is hailed as a miracle drug by many advocates that can cure several diseases and manage chronic pain. However, research has not given support for the majority of these claims of medical benefit. A recent four year Australian study across 1500 patients in fact suggests that marijuana may not only be of no benefit to pain management, but even make symptoms worse and have no impact on opiod usage.[75] If this is true then two arguments for marijuana’s legalization have been effectively undermined; for advocates argue that one, marijuana can manage pain, and two, help relieve the opioid crisis.

The 2017 National Academies of Sciences, Engineering, and Medicine (NAM) report on marijuana, The Health Effects of Cannabis and Cannabinoids, is a monumental work in the marijuana literature for it dissects the medical research on marijuana across many topics and spans thousands of research papers. It is an unparalleled source of information for our topic. In the following pages here we will report its findings for multiple topics.

3.1. Marijuana and Cancer

The NAM report found that there is insufficient evidence to make any statement on the efficacy of marijuana in cancer and glioma treatment.[76] It further concluded that there is moderate evidence of no statistical association between using cannabis and lung, neck, and head cancers. There is some limited evidence suggesting however that there is an association between cannabis usage and testicular cancer. Many other cancers the report concluded that for many other cancers there was no or insufficient evidence to give an opinion one way or another.[77]

3.2. Marijuana and Anorexia

On the topic of anorexia, the NAM report investigated AIDS wasting syndrome, cancer-associated anorexia-cachexia syndrome, and anorexia nervosa. For the first syndrome the report did not find any good primary literature and stated that this question is not being currently investigated due to the fact that there are effective therapies already developed.[78] Despite this, there is some limited evidence that marijuana can be of benefit here; however, the NAM report also observed that medical cannabinoids have little to no impact on appetite and weight for these patients.[79] For cancer-associated anorexia-cachexia syndrome the authors wrote “no benefit has been demonstrated” and the limited research on anorexia nervosa suggests that marijuana has no real effects on patients suffering from this syndrome.[80]

3.3. Marijuana as an Ineffective Treatment for Several Maladies

The NAM report found no sufficient evidence for marijuana’s medical usage for irritable bowel syndrome, but observed that research on this topic is also limited.[81] Concerning epilepsy the NAM report found no sufficient evidence either way due to the fact that the only good research did not have any control groups.[82]

Concerning spasticity the report investigated multiple sclerosis and spinal cord injury and concluded for the latter that there was no evidence either way and for the former oral cannabinoids are effective, but their effects have not produced any benefits on the Ashworth scale.[83] Similar conclusions of limited or no evidence are made concerning Tourette syndrome,[84] amyotrophic lateral sclerosis,[85] Huntington’s disease,[86] Parkinson’s disease,[87] and dystonia.[88] Evidence suggests that marijuana is ineffective for treating dementia[89] and glaucoma.[90] There is, however, limited evidence that cannabis can be useful in achieving better outcomes after traumatic brain injury or intracranial hemorrhage[91] and moderate evidence that cannabinoids is an effective treatment for improving sleep short term.[92]

3.4. Marijuana and Drug Usage

On the psychological effects of marijuana, the NAM report also analyzes several psychological illnesses and what probable effects marijuana may have on it. The NAM report notes that by its estimates in surveying the literature on addiction that evidence is inconclusive as to whether marijuana can be a treatment for other drug addictions.[93] There is, on the other hand, moderate evidence of an association between cannabis usage and increased risk of overdose injuries, especially among children in states with legalized marijuana.[94]

3.5. Problematic Usage of Marijuana

The NAM report concluded that there is substantial evidence of a correlation between the frequency of cannabis use and the progression of developing problematic cannabis use, meaning that the more one consumes marijuana, the more he or she is likely to become addicted and abuse it.[95] The question then is what variables are risk factors which may explain this result. The report concluded that there is moderate to substantial evidence that the following are not risk factors for abusing marijuana: anxiety, personality disorders, bipolar, ADHD, stimulant treatment for ADHD during adolescence, and nicotine or alcohol alone. The following were found to be risk factors: limited evidence for childhood anxiety and depression; moderate evidence for major depressive disorder, exposure to multiple drug abuse, and in adolescence: frequency of marijuana use, oppositional behavior, earlier first alcohol consumption, nicotine use, parents abusing substances, poor academic performance, antisocial behavior, and sex abuse; and substantial evidence for just being male, being male and a cigarette user, and early cannabis usage. [96] There is also moderate evidence of an association between marijuana abuse and a history of psychiatric treatment and substantial evidence for being male and the severity of marijuana abuse, with a caveat that the rate of recurrence of marijuana abuse does not differ whether one is male or female.[97]

3.6. Marijuana and Anxiety

In its analysis of experiments on anxiety, the NAM report concluded that there is limited evidence that cannabidiol may improve anxiety symptoms short term, but the research methods behind the different studies that the NAM report authors considered all had problematic flaws. Long term, on the other hand, is a different story. There is good evidence that daily cannabis usage has a correlation with anxiety symptoms, and that heavy usage is associated with social phobia disorder.[98] In fact regular cannabis usage has moderate evidence supporting an increased risk of social anxiety disorder.[99] The report also concluded that there is limited evidence between using cannabis and developing any anxiety disorder[100] and that near daily usage increases anxiety symptoms.[101]

3.7. Marijuana and Depression

In its investigations on depression, the NAM report concluded that there is some limited evidence suggesting that nabiximols, dronabinol and nabilone are ineffective treatments for reducing depression in patients with chronic pain or multiple sclerosis.[102] Later on the report concluded that there is moderate evidence that cannabis usage may in fact increase the risk of developing depression by a small amount.[103]

3.8. Marijuana and PTSD

The NAM report in its discussion of PTSD notes that nabilone may be effective for improving PTSD symptoms but the study was limited.[104] On the other hand, the report also concluded that there is some limited evidence that cannabis usage may actually increase the severity of PTSD symptoms.[105] It has been shown however that there is moderate evidence of a statistical association between those who abuse marijuana and suffering an increased severity of PTSD symptoms.[106]

3.9. Marijuana and Schizophrenia

On the topic of schizophrenia the NAM report concluded that there is substantial evidence between cannabis usage and the development of schizophrenia and psychosis, noting that heavy users are at higher risk.[107] Research also indicates that there is moderate evidence suggesting that there is a statistical association between historical cannabis usage and improved cognitive performance in patients with psychotic disorders.[108] We must, however, remain skeptical about this result given the fact that there are clear links between marijuana intoxication and impaired memory, learning and attention.[109] Furthermore, there is limited evidence that cannabis usage can increase positive symptoms of schizophrenia (which includes hallucinations, delusions, confused thoughts, and troubled concentration) but none concerning the negative symptoms of schizophrenia (such as lack of pleasure, troubled speech, withdrawal from society, not taking care of oneself).[110]

3.10. Marijuana and Bipolar Disorders

There is limited evidence that regular or daily marijuana users are at a greater risk for developing bipolar disorder,[111] and moderate evidence that marijuana use increases symptoms of mania and hypomania in bipolar patients.[112]

3.11. Marijuana and Suicide

On the question of suicide, the NAM report concluded that there is moderate evidence of a statistical association between marijuana usage and increased incidences of suicide ideation, suicide attempts, and increased suicide completions.[113] Heavy users faced higher rates in each category.

3.12. Marijuana and Pregnancy

The authors of the report concluded there is limited evidence of an association between pregnant mothers smoking marijuana and having pregnancy complications[114] and the admittance of newborns into NICU.[115] There is substantial evidence of children suffering low birth weight whose mother smoked marijuana.[116] The report found insufficient evidence to judge whether maternal marijuana usage could be linked to later problems in children such as sudden death syndrome, later substance abuse, and cognitive and academic performance.[117]

I want to note here that the FDA’s website cautions that there is potential adverse effects due to cannabis use in pregnant women “including fetal growth restriction, low birth weight, preterm birth, small-for-gestational age, neonatal intensive care unit (NICU) admission, and stillbirth.”[118] Maternal marijuana usage also may impact fetal brain development due to the results of some studies on animals.[119] Hence, while there is not a lot of evidence concerning the impact of marijuana on pregnant women and the fetus, there is some possible evidence that cannabis can have serious side effects and for this reason pregnant women should avoid consuming it.

4. Correlation and Causation

A frequent mantra of discussions involving empirical studies is “correlation does not equal causation”. Those who disagree with the evidence I have presented here may answer in such a manner, but does such a reply really say anything or is it moreso a feel-good platitude? The fact that correlation does not equal causation is something we must remind ourselves constantly so as to avoid false beliefs. If one observed for example that whenever it rains there was always worms on the ground, this does not mean that worms fell down from the sky in the rain droplets.

On the other hand, the statement that “correlation does not equal causation” can also be used as a tool of the skeptic. One can easily use this true statement and twist it to his or her own needs. Any study disproving of his or her accepted worldview can be conveniently dismissed. Consider this scenario. A person might become convinced that arsenic has a healing property for some illness and started self-medicating with daily doses. If a second person found out and pointed out the empirical facts concerning arsenic as being a poisonous chemical to man, could not the first person just as easily reply “correlation does not equal causation”?

In the first situation with the worms our true platitude is used correctly to eliminate an irrational belief but used in the second to reinforce a false belief concerning arsenic. The intellectual use of “correlation does not equal causation” requires an intellectual virtue of prudence in order to seek out which scenario is the truth. If one uses the proposition “correlation does not equal causation” as a “I-win” button in discussions, then he or she is not really interested in a discussion of the evidence but in naysaying whatever is counter to his or her particular world belief. It is good to remind a partner in dialogue of this true concerning correlation and causation in order to provoke deeper reflection on the sources themselves, but not for the purpose of shutting down the conversation.

In our case now concerning marijuana it must be first noted that there are of course several factors which can mitigate the effect of marijuana and reduce or eliminate marijuana completely from being a variable of significant predictive value for one’s entrance into a particular demographic. A teenager using cannabis might have other factors such as a dysfunctional family and a parent’s alcohol abuse that can further help explain why the teen is performing poorly at school.

On the contrary now, we know several effects THC has on the brain and how it disrupts sense and time perception, physical activity, coordination, memory, and attention amongst other distortions of man’s cognitive life. Given these pharmacological effects, if a study reinforces conclusions such as the correlation between marijuana and being impaired operating motor vehicles, then it would follow that given these pharmacological effects in addition it is a reasonable belief to assent to the proposition “marijuana causes impaired driving”.

There comes a point in empirical studies that there is overwhelming evidence to support a particular conclusion. Referring back to the arsenic example, it may be the case that there is a study which showed arsenic cured cancer, despite 99 other studies showing that arsenic is highly poisonous. The arsenic defender can reply that correlation does not equal causation and can footnote that one study as a source. Studies of the empirical can never guarantee absolute necessity or certainty of a particular result. That one study is evidence of this. This does not mean however it is reasonable to believe that arsenic is a medically significant substance for promoting health. It remains an irrational act to self-medicate on the authority of that one study given the evidence for the contrary.

It must also be acknowledged that not all studies are created equally. Some have built in biases and cannot be reproduced given the lack of integrity. Others could have been contaminated in some manner. Still others may have methodological factors which limits what conclusions can be drawn from the observations made, such as whether one tested their data to determine whether other variables influenced the correlation between the variable being tested and the observed outcomes. Much of the evidence presented in these pages here comes from a single report by the National Academies of Sciences, Engineering, and Medicine. This report is significant because it is a meta-analysis of thousands of research articles and only cited evidence from studies that were deemed sound methodologically and so cannot be reproached for lack of integrity.


Marijuana has been given an excellent propaganda machine by advocates who claim that marijuana is a medicinally significant drug. The NAM report amongst other cited medical sources present a different story. Some of the claims made about marijuana are bold face lies such as the supposed safety of driving after marijuana consumption and some of the proposed medical benefits for patients with PTSD, depression, and bipolar for example. Most of the medical claims about marijuana at this point are either erroneous or lacking sufficient data.

As Catholics, we need to arm ourselves with the medical facts concerning marijuana so that we can effectively engage the culture and reverse the trend that seeks to legalize marijuana. With recourse to such medical facts we can rationally demonstrate why it is against public interest to legalize this dangerous substance.


[1] A special thanks to Mandy Reimer for her advice and comments on this text.

[2] I want to acknowledge two books as significant contributions to the public discourse on marijuana: Marijuana Debunked by Ed Gogek and Tell Your Children by Alex Berenson. Both are book length investigations of the themes presented here and where many of the references came from. Three more notable sources are the DEA’s The Dangers and Consequences of Marijuana Abuse, May 2014 and Lessons Learned from Marijuana Legalization in Four U.S. States and D.C. published by Smart Approaches to Marijuana, March 2018, and The Health Effects of Cannabis and Cannabinoids, 2017, published by the National Academies of Sciences, Engineering, and Medicine.

[3] CDDA, 159.

[4] Tell Your Children, xviii-xix.


[6] Ibid.

[7] Ibid.

[8]All information concerning THC’s role on the brain come from the following:

[9] Ibid.

[10] Ibid.

[11] Ibid.

[12] Cf. Tell Your Children, xx.

[13] Cf. Marijuana Debunked, 31-32.

[14]  Louisa Degenhardt, PhD et al. “Outcomes of occasional cannabis use in adolescence: 10-year follow-up study in Victoria, Australia” (Apr. 2010) British Journal of Psychiatry.

[15] Substance Abuse and Mental Health Services Administration, Results from the 2011 National Survey on Drug Use and Health: Summary of National Findings, NSDUH Series H-44, HHS Publication NO (SMA) 12-4713. Rockville, MD: Substance Abuse and Mental Health Services Administration, 2012.

[16] W. Wilson et al. “Brain morphological changes and early marijuana use: a magnetic resonance and positron emission tomography study” (Feb. 2000) Journal of Addictive Diseases.

[17] Krista Lisdahl Medina et al. “Neuropsychological functioning in adolescent marijuana users: Subtle deficits detectable after a month of abstinence” (Sept. 2007) Journal of the International Neuropsychological Society.

[18] Staci A. Gruber et al. “Age of Onset of Marijuana Use and Executive Function” (Sept. 2012) Psychology of Addictive Behaviors. See also Blest-Hopley, Grace et al. “Is the Adolescent Brain at Greater Vulnerability to the Effects of Cannabis? A Narrative Review of the Evidence.” Frontiers in psychiatry vol. 11 859. 26 Aug. 2020, doi:10.3389/fpsyt.2020.00859.

[19] Madeline H. Meier et al. “Persistent cannabis users show neuropsychological decline from childhood to midlife” (Aug. 27, 2012) Proceedings of the National Academy of Sciences. Note: Fn 11 gives date July 30, 2012.

[20] Ibid.

[21] J.W. Bray et al. “The relationship between marijuana initiation and dropping out of high school” (Jan. 2000) Health Economics.

[22] J. Engberg and A.R. Morral “Reducing substance use improves adolescents’ school attendance” (Dec. 2006) Addiction.

[23] David Schick “Study: Marijuana use increases risk of academic problems” (June 7, 2013) USA Today.

[24] Center on Young Adult Health and Development (May 2013) “The Academic Opportunity Costs of Substance Use During College”.

[25] D.M. Fergusson and J.M. Boden “Cannabis use and later life outcomes” (June 2008) Addiction.

[26] The Health Effects of Cannabis and Cannabinoids, 275.

[27] CDDA, 164.

[28] The Health Effects of Cannabis and Cannabinoids, 279.

[29] Ibid, 281.

[30] Todd M. Moore and Gregory L. Stuart “A review of the literature on marijuana and interpersonal violence” (Jan.-Feb. 2005) Aggression and Violent Behavior.

[31] Elizabeth Walsh, MCRPsych et al. “Violence and schizophrenia: Examining the evidence” (June 2002) British Journal of Psychiatry.

[32] Deborah Brauser “Medical Marijuana May Worsen PTSD Symptoms, Increase Violence” (Dec. 15, 2014) S.T., Stefanovics E., Rosenheck R.A. Marijuana Use is Associated with Worse Outcomes in Symptom Severity and Violent Behavior in Patients with PTSD. J. Clin. Psychiatry. 2015;76:1174–1180. doi: 10.4088/JCP.14m09475.

[33] Miller, Norman S et al. “A Review of Cases of Marijuana and Violence.” International journal of environmental research and public health vol. 17,5 1578. 29 Feb. 2020, doi:10.3390/ijerph17051578.

[34] L. San et al. “Factors associated with relapse in patients with schizophrenia” (Feb. 2013) International Journal of Psychiatry in Clinical Practice.

[35] Robin Murray et al, “Cannabis use and outcome of recent onset psychosis” (June 2005), European Psychiatry. “The environment and schizophrenia: the role of cannabis use” (July 2005) Schizophrenia Bulletin. “What is the mechanism whereby cannabis use increases risk of psychosis?” (June 2008), Neurotoxicity Research. “The acute effects of synthetic intravenous 9-tetrahydrocannabinol on psychosis, mood, and cognitive functioning” (Oct. 2009), Psychological Medicine.

[36] R. Miller et al. “A prospective study of cannabis use as a risk factor for non-adherence and treatment dropout in first-episode schizophrenia” (Sept. 2009) Schizophrenia Research.

[37] Stanley Zammit, Theresa H.M. Moore, Anne Lingford-Hughes, Thomas R.E. Barnes, Peter B. Jones, Margaret Burke, & Glyn Lewis. “Effects of cannabis use on outcomes of psychotic disorders: systematic review” (2008) British Journal of Psychiatry.

D.H. Linszen et al. “Cannabis use and the course of recent-onset schizophrenic disorders.” (Apr. 1994) Archives of General Psychiatry.

[38] Tell Your Children, xxvi.

[39] D. Caspari “Cannabis and schizophrenia: results of a follow-up study” (Feb. 1999) European Archives of Psychiatry and Clinical Neuroscience.

[40] M.J. Martinez-Arevalo et al. “Cannabis consumption as a prognostic factor in schizophrenia” (May 1994) British Journal of Psychiatry.

[41] Bob Green, MSW et al. “Cannabis use and misuse prevalence among people with psychosis” (Oct. 2005) British Journal of Psychiatry.

[42] E. Manrique-Garcia et al. “Prognosis of schizophrenia in persons with and without a history of cannabis use” (Sept. 2014) Psychological Medicine.

[43] N.D. Veen et al. “Cannabis use and age at onset of schizophrenia” (Mar. 2004) American Journal of Psychiatry.

[44] G. Sugranyes et al. “Cannabis use and age of diagnosis of schizophrenia” (Mar. 2004) European Psychiatry.

[45] Louisa Degenhard & Wayne Hall. “Is Cannabis Use a Contributory Cause of Psychosis?” (Aug. 2006). Canadian Journal of Psychiatry, 51(9):556.

[46] Lancet Dec 26, 1987, Cannabis and schizophrenia. A longitudinal study of Swedish conscripts.

[47] See for example A.J. Budney et al. “Adults seeking treatment for marijuana dependence: a comparison with cocaine-dependent treatment seekers” (Nov. 1998) Experimental and Clinical Psychopharmacology.

[48] The Dangers and Consequences of Marijuana Abuse, Drug Enforcement Administration, May 2014, 23.

[49] Ibid, 24.

[50] Ibid, 24.

[51] A.J. Budney et al “Review of the validity and significance of cannabis withdrawal syndrome” (Nov. 2004) American Journal of Psychiatry.

[52] Louisa Degenhard, Wayne Hall, & Michael Lynskey. “The relationship between cannabis use and other substance use in the general population” (2001) Drug and Alcohol Dependence, 64:319-327.L. Degenhardt, PhD et al. “Alcohol, tobacco and cannabis use among Australians a comparison of their associations with other drug use and use disorders, affective and anxiety disorders and psychosis” (Nov. 2001) Addiction.

[53] Louisa Degenhardt, PhD et al. “Outcomes of occasional cannabis use in adolescence: 10-year follow-up study in Victoria, Australia” (Apr. 2010) British Journal of Psychiatry.

[54] Lynskey, M.T., et al. Escalation of drug use in early-onset cannabis users vs. co-twin controls. Journal of the American Medical Association 289(4):427-433, 2003.

[55] Gfroerer, Joseph C., et al. “Initiation of Marijuana Use: Trends, Patterns and Implications.” Department of Health and Human Services, Substance Abuse and Mental Health Services Administration, Office of Applied

Studies. July 2002.

[56] “Non-Medical Marijuana II: Rite of Passage or Russian Roulette?” CASA Reports. April 2004. Chapter V, 15.

[57] The Health Effects of Cannabis and Cannabinoids, 371.

[58] M. Asbridge et al. “Cannabis and traffic collision risk: findings from a case-crossover study of injured drivers presenting to emergency departments” (Apr. 2014) International Journal of Public Health.

[59] B. Laumon et al. “Cannabis intoxication and fatal road crashes in France: population based case-control study” (Dec. 2005) British Medical Journal.

[60] S. Blows et al. “Marijuana use and car crash injury” (May 2005) Addiction.

[61] Salomonsen-Sautel et al. “Trends in fatal motor vehicle crashes before and after marijuana commercialization in Colorado” (July 2014) Drug and Alcohol Dependence.

[62] Joanne E. Brady and Guohua Li “Trends In Alcohol And Other Drugs Detected In Fatally Injured Drivers In The United States, 1999-2010” (Jan. 2014) American Journal of Epidemiology.

[63] M. Asbridge et al. “Cycling-related crash risk and the role of cannabis and alcohol: a case-crossover study” (Sept. 2014) Preventive Medicine.

[64] Mark Asbridge, Jill A. Hayden, & Jennifer L. Cartwright. (Feb 2012). Acute cannabis consumption and motor vehicle collision risk: systematic review of observational studies and meta-analysis. British Medical Journal.

[65] Australian Transport Safety Bureau (Mar. 2004) “Cannabis and its Effects on Pilot Performance and Flight Safety: A Review” ISBN 1 977071 57 9.

[66] The Dangers and Consequences of Marijuana Abuse, 25-29.

[67] The Health Effects of Cannabis and Cannabinoids, 230.

[68] Ibid, 166.

[69] Ibid, 170.

[70] Ibid, 186.

[71] Ibid, 192.

[72] Such as the American Academy of Pediatrics, Glaucoma Research Foundation, and American Society of Addiction Medicine.

[73] “Making Sense of Bioethics: Column 156: The Smoke over Medical Marijuana” National Catholic Bioethics Center, June 30, 2018. URL:

[74] The Health Effects of Cannabis and Cannabinoids, 94.

[75] Campbell G, Hall WD, Peacock A, Lintzeris N, Bruno R, Larance B, Nielsen S, Cohen M, Chan G, Mattick RP, Blyth F, Shanahan M, Dobbins T, Farrell M, Degenhardt L. Effect of cannabis use in people with chronic non-cancer pain prescribed opioids: findings from a 4-year prospective cohort study. Lancet Public Health. 2018 Jul;3(7):e341-e350. doi: 10.1016/S2468-2667(18)30110-5. PMID: 29976328; PMCID: PMC6684473.

[76] The Health Effects of Cannabis and Cannabinoids, 91.

[77] Ibid, 157.

[78] Ibid, 95.

[79] Ibid, 95-97,

[80] Ibid, 96-97.

[81] Ibid, 98-99.

[82] Ibid, 99-101.

[83] Ibid, 101-103.

[84] Ibid, 104.

[85] Ibid, 105-106.

[86] Ibid, 107.

[87] Ibid, 110.

[88] Ibid, 111

[89] Ibid, 113

[90] Ibid, 114. Note that both the American Glaucoma Society and Canadian Glaucoma Society advise against using marijuana for treating glaucoma.

[91] Ibid, 115-116.

[92] Ibid, 123.

[93] Ibid, 116-118.

[94] Ibid, 236.

[95] Ibid, 337.

[96] Ibid, 347-348.

[97] Ibid, 350.

[98] Ibid, 119-120.

[99] Ibid, 318.

[100] Ibid, 318.

[101] Ibid, 320.

[102] Ibid, 121.

[103] Ibid, 310.

[104] Ibid, 124.

[105] Ibid, 323.

[106] Ibid, 351.

[107] Ibid, 295.

[108] Ibid, 303.

[109] Ibid, 302. Cf. chapter 11.

[110] Ibid, 303.

[111] Ibid, 305.

[112] Ibid, 307.

[113] Ibid, 314.

[114] Ibid, 249.

[115] Ibid, 254.

[116] Ibid, 253.

[117] Ibid, 260.

[118] The FDA cites these three studies: Gray, et al. Identifying Prenatal Cannabis Exposure and Effects of Concurrent Tobacco Exposure on Neonatal Growth. Clinical Chemistry. 2010; 56(9): 1442-1450. Gunn, et al. Prenatal Exposure to cannabis and maternal and child health outcomes: a systematic review and meta-analysis. BMJ Open. 2016; 6:e009986. Hayatbakhsh, et al.  Birth Outcomes associated with cannabis use before and during pregnancy.  Pediatric Research. 2012; 71 (2): 215-219. FDA URL:

[119] Silva, et al. Prenatal tetrahydrocannabinol (THC) alters cognitive function and amphetamine response from weaning to adulthood in the rat. Neurotoxicol and Teratol 2012; 34(1): 63-71. Trezza, et al. Effects of perinatal exposure to delta-9-tetrahydrocannabinol on the emotional reactivity of the offspring: a longitudinal behavioral study in Wistar rats. Psychopharmacology (Berl) 2008; 198(4): 529-537. Campolongo, et al. Perinatal exposure to delta-9-tetrahydrocannabinol causes enduring cognitive deficits associated with alteration of cortical gene expression and neurotransmission in rats. Addict Biol 2007; 12(3-4): 485–495.

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