The core of the medical marijuana debate often centers not on its symptom relief capabilities, but on the possible risks it poses to both individual well-being and the wider community. This chapter will begin by analyzing the scientific data regarding the potential physical and psychological harm marijuana may cause to individuals. Following this, it will explore the potential societal repercussions of legalizing marijuana for medical purposes.
Smoke indicates danger
Given the established dangers of tobacco smoking, it’s reasonable to wonder if marijuana could have similar negative impacts on health. While marijuana lacks nicotine, its smoke still introduces pollutants into the lungs. Considering the links between tobacco smoking and various health problems like respiratory issues, cancer, emphysema, heart disease, pregnancy complications, and low birth weight, concerns about the potential harm of marijuana smoking are understandable.
Scientists have investigated the health risks of marijuana and tobacco smoke by comparing various factors, but definitive evidence showing one as more dangerous than the other remains elusive. Studies have indicated that, weight for weight, marijuana joints deposit significantly more tar in the lungs compared to tobacco cigarettes, owing to the absence of filters and the tendency of marijuana smokers to inhale larger volumes of smoke more deeply and hold it longer, increasing exposure to carcinogens.
However, commercially produced cigarettes are more densely packed and generate more smoke than hand-rolled joints. Furthermore, tobacco users generally smoke more frequently throughout the day compared to marijuana users. Consequently, daily tobacco consumption often results in significantly greater smoke intake compared to exclusive marijuana use. This makes direct comparisons of health damage between the two substances difficult. Compounding the problem is the fact that approximately 70% of marijuana users also smoke tobacco, making it challenging to isolate the specific effects of marijuana in epidemiological studies.
Unsurprisingly, clinical research suggests a higher incidence of respiratory illnesses among marijuana smokers compared to non-smokers. A study of outpatient visits at a large HMO revealed that marijuana users sought medical attention for respiratory issues more often than non-smokers of both marijuana and tobacco. However, the study also found that long-term marijuana smokers (over 10 years) did not seek treatment for respiratory illness more frequently than those who smoked for shorter periods. A possible explanation is that individuals who continued smoking for extended periods experienced fewer respiratory problems, while those who developed symptoms like shortness of breath likely quit sooner. Unfortunately, the survey did not inquire about cocaine use, which can exacerbate respiratory symptoms, and underreporting of tobacco, alcohol, and marijuana use by participants is also possible.
A study involving 446 volunteers compared the prevalence of chronic bronchitis symptoms (excessive coughing, sputum production, and wheezing) among regular marijuana smokers, tobacco smokers, and individuals who did not smoke. Approximately 33% of both marijuana and tobacco smokers experienced at least one of these symptoms, compared to only about 8% of nonsmokers. Smokers, regardless of tobacco use, experienced acute bronchitis episodes more than five times as frequently as nonsmokers. Furthermore, marijuana smokers exhibited poorer performance on lung function tests compared to nonsmokers.
Participants in this study who regularly smoked marijuana consumed an average of three to four joints daily, while tobacco users smoked an average of 20 cigarettes per day. Interestingly, habitual marijuana smokers who also smoked tobacco did not report a higher incidence of chronic bronchitis symptoms than those who smoked tobacco alone, suggesting that marijuana smoking does not exacerbate the harmful effects of tobacco smoking in this group.
However, another study revealed evidence of an interaction between marijuana and tobacco smoking, but this study involved individuals who smoked considerably less of both substances compared to the participants in the first study. Research suggests that the synergistic effects of toxic substances are often more easily detected at lower exposure levels. This may explain why the lighter smokers in the second study showed increased respiratory damage when using both marijuana and tobacco, while the heavier smokers in the first study did not. Regardless, both studies demonstrate that marijuana smoke negatively impacts respiratory function.
Regularly smoking either marijuana or tobacco causes damage to the lining of the bronchial airways. Prolonged exposure to smoke leads to inflammation and redness of the delicate tissues lining these passageways. Additionally, smoking alters the cells within the bronchial airways. Typically, these passages are lined with ciliated cells, which use their hairlike projections to move mucus towards the mouth. However, smoking leads to the replacement of these cells with cells that secrete excessive amounts of thick mucus, resulting in the characteristic “smoker’s cough.”
Bronchial injury, a more sensitive indicator of damage than chronic bronchitis symptoms, is even more pronounced in individuals who smoke both marijuana and tobacco. The damage extends to the interior of bronchial cells, leading to various abnormalities. Some of these changes, which are known precursors to cancer, have also been identified in the respiratory tracts of marijuana and hashish smokers who did not use tobacco.
Chronic obstructive pulmonary disease (COPD), characterized by a gradual and irreversible loss of elasticity in the airways, is another respiratory ailment linked to tobacco smoke. COPD sufferers experience shortness of breath and chronic bronchitis symptoms. While studies investigating whether marijuana smoke induces COPD have yielded inconsistent findings, with one study observing significant impairment of small airway function from smoking a single joint daily, and another failing to detect similar damage even in long-term, heavy marijuana smokers, the potential for marijuana smoke to cause COPD remains a concern.
While many tobacco smokers accept the drawbacks of coughing and shortness of breath, the fear of cancer frequently motivates them to quit; others continue smoking not for pleasure, but to alleviate nicotine withdrawal symptoms. The question of whether marijuana users should share similar cancer concerns remains open, although cellular, genetic, and clinical research increasingly points to marijuana smoke as a significant risk factor for respiratory cancers.
Marijuana smoke shares many of the same carcinogenic compounds as tobacco smoke, and unfiltered marijuana smoke contains higher concentrations of polycyclic aromatic hydrocarbons (PAHs). Marijuana users often inhale more deeply than tobacco smokers, potentially exposing their lungs to even greater levels of these harmful substances. Moreover, preliminary research suggests elevated levels of an enzyme in marijuana smokers’ lung cells that converts PAHs into carcinogenic forms. These factors suggest a link between marijuana smoking and cancers of the lung, mouth, and throat.
While case reports have suggested an increased risk of cancers in tissues exposed to marijuana smoke, these reports have not been substantiated by controlled studies, making it difficult to isolate marijuana as the sole cause. Other factors, such as concurrent tobacco smoking, may contribute.
To date, only one large-scale study has investigated the link between marijuana smoking and cancer incidence, finding an increased risk of prostate cancer in male marijuana users who did not smoke tobacco. However, no link was found to other cancers, including those typically associated with tobacco smoking. This study was limited by the young age and short duration of marijuana use among the participants. The long latency period for cancers like lung cancer, coupled with the lower rates of long-term marijuana use and high rates of concurrent tobacco use, complicate research in this area.
Future research should benefit from the longer history of widespread marijuana use, providing a larger population for epidemiological studies. However, challenges remain, including the difficulty in finding exclusive marijuana smokers and the potential for underreporting of marijuana use.
In contrast to epidemiological studies, cellular-level research has provided compelling evidence of the carcinogenic potential of marijuana smoke, which has been shown to induce chromosomal changes and malignancies in isolated human and animal lung cells. These changes have also been observed in the lung cells of marijuana smokers, with even higher levels in those who also smoke tobacco.
A particularly compelling study found elevated levels of DNA aberrations linked to cancer development in the lymphocytes of pregnant women who exclusively smoked marijuana and their newborns, mirroring similar findings in the DNA of tobacco smokers.
Furthermore, marijuana smoking has been linked to increased mortality in men with AIDS, a significant concern given the prevalence of medical marijuana use within this population. While this association remains largely unexplained, it may be due to risky behaviors associated with marijuana use, or it could indicate that marijuana smoking further compromises the immune system in HIV-positive individuals. The increased risk of opportunistic infections and Kaposi’s sarcoma in marijuana-using AIDS patients raises questions about whether smoke, cannabinoids, or both are responsible for this effect.
Understanding the part played by cannabinoids
Most research on the physiological effects of marijuana centers on smoking, but some researchers have investigated the direct effects of cannabinoids on isolated cells, experimental animals, and humans. These studies often explore potential harm to the immune, cardiovascular, and reproductive/fetal health systems.
As previously discussed, biological studies indicate that cannabinoids can suppress the immune response to infection. In some experiments, white blood cells from animals exposed to THC and other cannabinoids showed a diminished ability to proliferate after infection. These animals sometimes produced fewer antibodies than normal or displayed impaired “killer cell” activity.
However, not all studies identify cannabinoids as immune suppressants, as some immune functions have been shown to increase in response to them. These seemingly contradictory results are understandable because immunity involves numerous physiological processes. Therefore, individual experiments cannot fully capture marijuana’s complex effects on the immune system. This is especially true for studies focusing on pure cannabinoids like THC, as marijuana contains a diverse range of chemicals that could influence immune activity.
Research on disease resistance in animals exposed to cannabinoids, while also requiring careful interpretation, offers a more comprehensive view of the overall impact on the immune system. For example, mice infected with pneumonia-causing bacteria succumbed to septic shock when injected with THC before and after infection, while those without THC exposure developed immunity and survived. This response varied based on the THC dosage and timing of the injection relative to the infection. Similarly, two doses of THC given before and after herpes simplex virus infection appeared to accelerate death in immunodeficient mice, whereas a single pre-infection dose did not. These experiments suggest that the timing of THC exposure relative to infection is a key determinant in whether THC suppresses the immune response.
While cannabinoids themselves might not significantly harm the immune system, smoking marijuana likely does. Marijuana smoke is associated with increased mortality in AIDS patients and can damage alveolar macrophages, crucial immune cells in the lungs. Studies show habitual marijuana smokers have twice as many alveolar macrophages as nonsmokers, suggesting the lungs are fighting infection. This number quadruples in those who also smoke tobacco.
Furthermore, marijuana smoke impairs the ability of alveolar macrophages to destroy harmful fungi, bacteria, and tumor cells, and it reduces their production of cytokines, essential for immune response coordination. These findings suggest marijuana smoking could be dangerous for individuals with weakened immune systems, such as AIDS and cancer patients (especially those undergoing chemotherapy), and organ transplant recipients.
Cannabinoids can also affect the cardiovascular system, with effects easier to measure than those on the immune system. Both smoked marijuana and THC can significantly increase heart rate. Oral THC, like smoked marijuana, can cause a dangerous drop in blood pressure upon standing, potentially leading to fainting. While this reaction typically subsides after a few days and poses little risk to young, healthy individuals, it could be problematic for older patients or those at risk of heart attack or stroke. As marijuana users from the 1960s reach the age where cardiovascular disease is common, the long-term effects of marijuana use on circulatory health will become clearer. Until then, individuals at risk of cardiovascular disease should avoid marijuana and THC.
Research also explores the impact of cannabinoids on reproduction. Animal studies involving THC injections suggest it inhibits various reproductive functions, from hormone secretion to sperm development and embryo implantation. However, these studies primarily used short-term treatments, making it difficult to assess the consequences of chronic marijuana or cannabinoid use.
Despite limited studies, research on human reproduction aligns with animal studies, suggesting THC affects fertility. While fertility research on marijuana users is inconsistent, it suggests a short-term decrease in reproductive hormones after use. Long-term users may develop a tolerance to THC’s inhibitory effects on luteinizing hormone, which regulates testosterone and estrogen. In women, this effect varies throughout the menstrual cycle, being most significant between ovulation and menstruation.
Without direct measures, both marijuana and THC likely decrease short-term fertility in both sexes. THC may also interfere with early pregnancy stages, particularly embryo implantation. Marijuana smoke poses an even greater risk to pregnant women and those trying to conceive, potentially harming fetal development as much as tobacco smoke.
Epidemiological studies investigating the effects of marijuana use on pregnancy and fetal development have yielded inconsistent results. Similar problems observed in infants of tobacco-smoking mothers, such as low birth weight, are also seen in marijuana users. However, a study of Jamaican women using marijuana tea for morning sickness showed no neurobiological or behavioral differences in their newborns compared to non-users.
Since 1978, the Ottawa Prenatal Prospective Study has tracked the impact of prenatal marijuana exposure on children’s cognitive function. The study has not found evidence that children whose mothers smoked marijuana during pregnancy perform below average on intelligence tests. While some early cognitive problems were observed in children of women who smoked at least one joint daily during pregnancy, these deficits disappeared by age 5. However, older children of marijuana users scored slightly lower on tasks measuring planning and self-control compared to nonsmokers and tobacco smokers. Children of tobacco smokers scored lower on language and cognitive skills tests, and these effects persisted until age 12. However, these differences in test scores were generally subtle, varying by less than 5 percent.
In conclusion, there are concerns that marijuana, especially when smoked, could worsen the health problems of those who use it for medicinal purposes. Definitive evidence on whether habitual marijuana smoking leads to respiratory cancer is still pending. It appears that marijuana smoking is likely more harmful than beneficial for individuals with chronic medical disorders or those with compromised respiratory or immune systems. Similarly, the potential risks of THC or smoked marijuana seem to outweigh the potential benefits for individuals at risk of cardiovascular disease, pregnant women, and couples trying to conceive.
Marijuana misuse
The potential for abuse and addiction is a prominent health concern linked to marijuana use; however, strong opinions differ on this matter, and limited research exists focusing specifically on marijuana’s medical applications. Despite this, insights from biological, clinical, and population studies offer a fairly comprehensive understanding of the effects of long-term marijuana consumption.
Due to its illegal status, marijuana use is sometimes automatically considered abuse. The IOM team, however, adopted the medical definition of substance abuse, defining it as repeated marijuana use that leads to personal harm. This aligns with the core definition of substance abuse found in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), a leading diagnostic tool in mental health. When marijuana use becomes compulsive and difficult to stop, even when it causes significant negative consequences, the condition is classified as substance dependence, a more severe diagnosis than abuse, according to the DSM-IV.
The physiological mechanisms underlying use and abuse
Even individuals who use marijuana without meeting the diagnostic criteria for abuse or dependence may still experience tolerance, physical dependence, and withdrawal. Tolerance, a common reaction to repeated drug use, occurs when increasing dosages are needed to achieve the desired effect. Physical dependence arises from the body’s adaptation to frequent drug exposure. While physical dependence can contribute to substance abuse, it doesn’t always lead to it. When someone physically dependent on a drug ceases using it, they are likely to experience withdrawal symptoms. Tolerance, physical dependence, and withdrawal are associated with many abused drugs, but also with substances like caffeine and nicotine, as well as certain non-addictive medications for pain, anxiety, and hypertension. For instance, abruptly stopping propranolol, a medication for high blood pressure, can cause withdrawal symptoms such as a temporary spike in blood pressure. To prevent this, patients must gradually reduce their propranolol dose before switching to another medication.
Regular marijuana users often develop tolerance to the drug’s effects relatively quickly. This may explain why frequent users appear less impaired than infrequent users after consuming similar amounts, despite having higher THC levels in their blood. However, tolerance seems to diminish after a week or two of abstinence. Interestingly, tolerance can develop at different rates for different effects of the same drug. For example, heroin users develop tolerance to the euphoric effects more rapidly than to the drug’s respiratory depressant effects. Consequently, they may increase their dosage to achieve the same high, inadvertently raising their risk of a fatal overdose due to asphyxiation.
While no marijuana user is known to have died from an overdose, tolerance to cannabinoids could outweigh the benefits of marijuana-based medicines for some patients. Conversely, developing tolerance to certain side effects of cannabinoids, like short-term memory loss or concentration difficulties, could be considered advantageous. Given that tolerance to different cannabinoids may develop at varying rates, it’s crucial to assess their individual effects on mood, movement, memory, and attention if they are to be used therapeutically.
Individuals who use marijuana or ingest oral THC (e.g., Marinol) may develop tolerance to some effects more quickly than others. In a study, daily marijuana smokers and THC pill users reported that the same dose made them feel less “high” over four days, but their drug-induced appetite increases did not decline. The marijuana group reported feeling “mellow” throughout the study, while the THC group did not. Similarly, some individuals who have used both smoked marijuana and oral THC for medical purposes have shared experiences that align with these study findings.
Animal studies have also investigated the development of cannabinoid tolerance. Similar to the clinical studies, animals receiving continuous THC developed tolerance to many of its initial effects, including memory impairment, reduced movement, and pain relief.
Research suggests that target cells for THC, specifically those with CB1 and CB2 receptors, adapt to chronic THC exposure in ways that contribute to tolerance. Many studies on brain cells have observed a decrease in the production of cannabinoid receptors under conditions mimicking prolonged cannabinoid exposure. However, tolerance to cannabinoids appears to develop at different rates in different brain regions, potentially explaining why some studies haven’t found a decline in cannabinoid receptors. This could also explain why tolerance to some effects of THC develops more quickly than to others. In addition to their effects on CB1 and CB2 receptors, cannabinoids may also desensitize other proteins in target cells.
While these basic studies on cannabinoids are interesting, their results should be interpreted cautiously. Most are short-term experiments that simulate long-term marijuana use by exposing animals to higher cannabinoid doses than typically experienced by marijuana users. Furthermore, cannabinoids behave differently in the body depending on whether they are inhaled, injected, or swallowed. While most people ingest cannabinoids through smoking, they are typically injected into laboratory animals. Nevertheless, some of the biochemical responses to chronic cannabinoid exposure observed in animals likely occur in humans as well, albeit perhaps in less pronounced ways.
Withdrawal from marijuana or THC can cause distinct symptoms, as reported in clinical studies and by adolescents in substance abuse treatment. These symptoms include restlessness, irritability, mild agitation, insomnia, sleep disturbance, nausea, and cramping. While uncomfortable, these symptoms are generally milder than those associated with alcohol withdrawal. Following very high doses of oral THC (equivalent to smoking five to ten joints per day for 10 to 20 days), withdrawal symptoms also included runny nose, sweating, and decreased appetite, but lasted only four days. In another study, participants taking about half as much THC for only four days reported longer-lasting withdrawal symptoms.
In animals, simply administering THC for several days or weeks and then discontinuing it does not provoke withdrawal symptoms because the drug lingers in the brain, allowing it to gradually adapt. A similar situation probably occurs in human marijuana users who go “cold turkey,” easing the process of withdrawal. However, by administering a chemical block that immediately interferes with THC’s effects, researchers can create a sort of instantaneous withdrawal in experimental animals that have been chronically exposed to THC. These animals exhibit dramatic symptoms, including hyperactivity and disorganized behavior, which also occur during withdrawal from opiate drugs.
Tolerance and withdrawal certainly contribute to a drug’s ca pacity for abuse. But ultimately the better a drug makes people feel, the more likely they are to abuse it. This effect, called reinforcement, generally depends on drug dosage. Caffeine, for example, is reinforcing for many people who drink a cup or two of coffee at a time but is aversive—that is, it makes most people feel worse, not better—if they consume the caffeine equivalent of six cups of coffee all at once. Reinforcement for a particular drug also varies from person to person. In the case of caffeine, research indicates that its effects are the most pleasurable for the least anxious people.
Marijuana is indisputably reinforcing to many people. Some have argued that marijuana has a relatively low potential for abuse, based on experiments in which animals—who willingly dose themselves with cocaine—did not self-administer THC. Other studies indicate that THC is rewarding to animals in relatively mild doses but that, like many reinforcing drugs, it is aversive in large amounts. Cannabinoids have also been shown to unleash a surge of dopamine, a chemical generally associated with reinforcement, in rats; however, the mechanism by which cannabinoids exert this effect appears to be different from that of other abused drugs such as cocaine and heroin. It is also important to note that the dopamine “reward” system in the brain responds to a wide variety of stimuli, not all of which are dangerous substances. For example, from animal studies we know that dopamine levels also rise in response to feelings of sexual attraction and when eating sweet foods. Based on similarities in brain structure and function, this is probably true of humans as well.
As people progress from tolerance to physical dependence to drug abuse, their craving intensifies despite mounting problems caused by their behavior. This intense desire for a drug is the toughest part of addiction to overcome. As a result, most recovering addicts suffer a relapse within one year of becoming drug-free. Animal studies suggest that this tendency to relapse results from long-term changes in brain function brought on by addiction. These alterations appear to persist for months or years after the last use of an addictive drug.
Anticraving medications have been developed for nicotine and alcohol, while methadone reduces cravings for heroin as it blocks the drug’s euphoric effects.
Research on cravings has focused on nicotine, alcohol, cocaine, and opiate drugs. It has not specifically addressed marijuana, so it remains unknown whether marijuana induces similar changes in brain function.
Using Marijuana and Developing Dependence
To understand the risk of marijuana addiction, it’s helpful to analyze usage patterns and dependence. Researchers have investigated who uses marijuana, how often and why users become abusers, and how these patterns compare to those of other abused substances.
Surveys reveal that while a large number of Americans (33% of those over 12, or about 70 million people in 1997) have experimented with marijuana or hashish, only a small percentage (5%) are current users. Marijuana use is highest among young adults (18-25) and decreases significantly after age 34. This suggests that many individuals try marijuana during adolescence, often due to peer influence and a desire to fit in, but discontinue use as they mature. However, factors beyond simple experimentation likely play a role in continued marijuana use.
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A study of 456 high school students who had tried marijuana revealed that those who became regular, but not heavy, users did so primarily to improve their mood, suggesting a motivation rooted in psychological needs rather than social pressures. This aligns with broader research indicating that young adults often use drugs regularly to fulfill internal needs rather than seeking external validation.
Only about 28% of the high school experimenters continued using marijuana. Many who quit cited concerns about its negative impact on their health or relationships. Others stopped when they acquired more responsibilities or reduced contact with other marijuana users, and parental disapproval played a greater role in their decision than peer influence.
However, individuals using marijuana for medical purposes, typically those over 35, face different circumstances than recreational users. While there is a lack of scientific research specifically examining medical marijuana use and abuse, various individual and environmental factors likely contribute to the risk of abuse or addiction. These factors warrant consideration when assessing the potential risks associated with medical marijuana.
Certain demographic groups exhibit a higher susceptibility to drug dependence. National surveys show that men are 1.6 times more likely than women to develop dependence on illicit drugs. White Americans have approximately double the risk of drug dependence compared to African Americans. Individuals between 25 and 44 are estimated to be over three times more likely to abuse drugs than those over 45.
Adolescents are particularly susceptible to drug dependence, experiencing behavioral consequences at lower levels of use than adults. Young individuals already dependent on other substances, particularly alcohol or tobacco, are at a heightened risk of marijuana dependence. Research on over 200 delinquent youth in residential treatment found that they were dependent on an average of more than three substances. Among those who had used marijuana more than six times, over 80% developed dependence, a significantly higher rate than observed in the general population.
Parents who attribute rebellious behavior in their children to marijuana use may be mistaken, as research suggests that such adolescents often exhibited behavioral issues prior to using the drug. This aligns with other findings indicating that children with greater difficulties are more likely to initiate drug use, abuse, and dependence at an earlier age.
Individuals with psychiatric disorders are also at a significantly elevated risk for drug abuse; approximately 76% of drug-dependent men and 65% of drug-dependent women have at least one co-occurring psychiatric disorder, with alcohol abuse being the most common. In women with drug dependence, phobias and major depression are almost as prevalent as alcohol abuse. Furthermore, antisocial personality disorder and its childhood precursor, conduct disorder, are frequently observed in the psychiatric profiles of substance abusers.
Genetic factors may play a role in a person’s susceptibility to drug abuse, including marijuana. A study of over 8,000 male twins revealed a heritable component in the enjoyment of marijuana’s effects. It’s plausible that individuals who find marijuana pleasurable are more likely to continue its use, potentially leading to abuse, compared to those who do not enjoy it. This research, along with a similar study on female twins, suggests a genetic predisposition towards regular marijuana use in some who experiment with the drug. However, the decision to try marijuana initially seems to be most heavily influenced by an individual’s family and social surroundings.
Despite the increased risk of abuse in certain individuals, marijuana is generally considered to have a low addiction potential. Compared to other addictive substances, a relatively small proportion of marijuana users become dependent on it. While a larger number of people experiment with and use marijuana than other illicit drugs like cocaine or heroin, instances of marijuana abuse are comparatively infrequent. Large-scale surveys, such as the National Comorbidity Survey and the Epidemiological Catchment Area Program, have estimated that around 5% of the U.S. population has experienced marijuana dependence at some point in their lives. In contrast, nearly 14% of adults have met the criteria for alcohol dependence, and 36% for tobacco dependence.
While marijuana use presents a risk of dependence and abuse that warrants careful consideration when evaluating its potential medical applications, especially for vulnerable individuals like adolescents, those with psychological or social challenges, and those predisposed to substance abuse, its abuse potential seems relatively low compared to alcohol, tobacco, and some prescription drugs and can likely be managed in a clinical setting under a doctor’s supervision.
Psychological damage
While the physical risks of marijuana use are relatively well-documented, its psychological consequences are less clear. Interestingly, certain psychoactive properties of marijuana, such as the ability to reduce anxiety, induce sedation, and create euphoria, may actually offer therapeutic benefits for specific patients. This duality, coupled with the fact that most psychological research focuses on the effects of intoxication and recreational marijuana use, makes it challenging to predict the psychological effects of medical marijuana use.
It stands to reason that individuals using marijuana solely for medicinal purposes would have different psychological experiences compared to recreational users, as the context of psychoactive drug use heavily influences psychological responses. Existing research predominantly involves individuals with prior marijuana experience, leaving a gap in our understanding of potential adverse psychological reactions in first-time or infrequent users. Furthermore, most psychological studies examine the effects of single, often high, doses, which doesn’t accurately reflect the chronic exposure typical of medical marijuana use. A deeper understanding of the subtle effects of low doses of marijuana and cannabinoids is crucial for their application in medical treatments. Even at levels insufficient to induce a “high,” marijuana and THC can alter mood, cognition, and performance in tasks requiring attention and coordination.
Marijuana’s recreational appeal largely stems from its ability to generate temporary feelings of well-being or euphoria in most users. Many report heightened physical and emotional sensitivity, increased talkativeness, and greater social engagement when under its influence. However, due to its suppression of short-term memory and learning, individuals using marijuana may struggle to maintain coherent conversations and experience a distorted sense of time.
Negative mood changes can also occur, particularly in inexperienced users following high doses administered through smoking or ingestion. Anxiety and paranoia are the most commonly reported acute reactions, followed by panic, depression, depersonalization, delusions, illusions, and hallucinations. These symptoms typically resolve within hours with reassurance and a supportive environment. Approximately 17% of regular marijuana smokers report having experienced at least one of these symptoms, usually early in their drug use.
High doses of marijuana can negatively impact cognitive function. Studies using positron emission tomography to visualize brain activity have revealed that smoking marijuana can cause circulatory irregularities, specifically a restriction of blood flow to the temporal lobe, an area crucial for auditory attention. This reduced blood flow correlated with impaired performance on listening tasks. Conversely, marijuana use seems to increase blood flow to the frontal lobes and lateral cerebellum, brain regions involved in higher-level cognitive functions like abstract thought, motor control, emotional regulation, movement coordination, and certain types of learning. While the definitive interpretation of these changes in cerebral blood flow remains unclear due to the relative novelty of brain activity measurement techniques, they generally support the idea that marijuana can impair cognitive abilities.
Early reports in the 1970s suggesting marijuana use led to structural brain changes have not been substantiated by more advanced research methods. More recent studies indicate that heavy marijuana users may exhibit subtle cognitive deficits after a period of abstinence; however, the validity of these findings has been questioned due to potential disparities in cognitive abilities between users and non-users in the control groups.
Furthermore, marijuana has been shown to affect psychomotor skills, which require a combination of attention and coordination, and are necessary for activities like driving. Psychomotor processes encompass the ability to control movement, maintain focus, and react appropriately to environmental stimuli. Research involving experienced pilots demonstrated impaired performance on flight simulator tests up to 24 hours after smoking marijuana, despite the pilots’ initial belief that their performance would not be affected.
This evidence strongly suggests that marijuana impairs cognitive and psychomotor performance, necessitating caution among medical marijuana users, similar to the precautions taken when using strong painkillers or alcohol. Operating vehicles or dangerous machinery while under the influence of marijuana or THC is clearly inadvisable.
A controversial purported effect of marijuana is the “amotivational syndrome,” a term used to describe a loss of interest in activities such as school, work, and social engagement, primarily among young people. While heavy marijuana use is often cited as the cause, conclusive evidence linking the drug directly to these symptoms is lacking.
Attributing a lack of motivation solely to marijuana use requires rigorous investigation. Ideally, a person’s behavior and personality would need to be assessed before and after becoming a regular marijuana user. However, ethical considerations prevent inducing heavy marijuana use for research purposes, limiting studies to observational data from self-initiated users. Epidemiological surveys could identify young people who have become marijuana users and explore the relationship between motivation and marijuana use. However, even if a correlation is found, it would not definitively prove that marijuana use causes a lack of motivation.
The potential for marijuana to induce severe and persistent psychotic disorders remains a key question. Clinical reports describe marijuana-induced states resembling psychoses like schizophrenia, depression, and mania, with symptoms lasting a week or longer. Some argue that the variety of symptoms observed argues against a specific “marijuana psychosis.” Others argue that heavy marijuana use, or even acute use in susceptible individuals, can trigger psychosis characterized by confusion, amnesia, delusions, hallucinations, anxiety, and agitation. Regardless of these differing views, there is general agreement that marijuana use alone, without other contributing factors, is unlikely to cause a psychosis that lasts longer than the period of intoxication.
Drug abuse frequently co-occurs with mental illness, and consequently, research suggests a higher prevalence of marijuana use among individuals with schizophrenia, although not universally. The nature of the link between marijuana and schizophrenia remains complex. While a consensus exists that heavy marijuana use can trigger schizophrenic episodes in vulnerable individuals, it is generally accepted that the drug does not cause the underlying disorder itself. Studies suggest that individuals with schizophrenia may favor marijuana over alcohol and cocaine, potentially seeking symptom relief, though the reasons for this preference are unclear. However, individuals with schizophrenia or a family history of the condition should be aware of the increased risk of adverse psychiatric reactions associated with marijuana use.
Certain psychological effects of marijuana hold potential medical value. Specifically, the anti-anxiety properties of cannabinoids could alleviate conditions exacerbated by anxiety, such as movement disorders or nausea. Moreover, the euphoric effects of marijuana might enhance the efficacy of marijuana-based medications for pain relief or appetite stimulation. Conversely, euphoria or sedation induced by cannabinoids could mask symptoms, potentially leading users to mistakenly believe that marijuana improves their condition. This poses a risk if it leads patients to prioritize marijuana over more effective conventional treatments with fewer adverse effects. Therefore, the IOM researchers recommended that future clinical trials of cannabinoid drugs include an evaluation of their psychological impact.
Does medical marijuana pose a threat to society?
Many involved in the IOM study on medical marijuana’s potential harms were concerned that acknowledging its possible therapeutic benefits would diminish its perceived danger, especially among young people. However, if marijuana-derived medicines were developed, they would share a characteristic with many effective medications: the potential for harm if misused. While exploring how medical marijuana use might encourage drug abuse is important, it’s also essential to recognize that this risk isn’t unique to marijuana.
The central question isn’t whether marijuana has both benefits and risks, but whether perceived benefits will lead to increased abuse. Another concern is that marijuana use could lead to the use of more dangerous drugs, resulting in a broader increase in illicit substance abuse.
The “gateway drug” concept suggests that marijuana leads to the use of more dangerous drugs like cocaine or heroin, which pose greater threats to individual health and society. This concept also reflects consistent patterns of drug use from adolescence into adulthood. Marijuana, being the most commonly used illegal drug, is often the first illicit substance encountered, even by those who later use other drugs. However, most future drug users typically experiment with alcohol and nicotine before marijuana, often before they are legally old enough to do so.
Discussions about marijuana as a gateway drug often conflate two distinct ideas. The first, the “stepping stone” hypothesis, suggests marijuana has pharmacological properties that drive users to try harder drugs. The second, more prevalent theory proposes that marijuana introduces individuals to the world of illegal substances, increasing peer pressure and access to other drugs.
The stepping-stone hypothesis applies to marijuana only in that individuals who enjoy its effects might be more drawn to mood-altering substances in general. The factors that lead people to use marijuana, such as physiological responses, psychological state, and social context, may also predispose them to using harder drugs. The gateway theory adds that marijuana’s illegal status serves as a pathway to harder drugs.
Individuals prone to using illicit drugs beyond marijuana often share characteristics like early alcohol or nicotine use, heavy marijuana use, and psychiatric disorders. While early alcohol and nicotine use appears to increase the likelihood of experimenting with illegal drugs, it doesn’t necessarily lead to heavy drug use. Similarly, experimental or infrequent marijuana users are less likely to progress to harder drugs than daily users. One study found that young adults who had used marijuana 10-99 times were unlikely to have tried other illicit drugs, while over half of those who had used it more than 100 times had.
Data on the gateway phenomenon is often misinterpreted. For example, one study concluded that marijuana’s role as a gateway drug had increased based on interviews with daily crack cocaine or heroin users. However, this represents a tiny fraction of the adult population. While most interviewees had used marijuana before harder drugs, this doesn’t necessarily apply to all marijuana users.
Another limitation of many gateway theory studies is their focus on drug use rather than drug dependence. They can only show that marijuana users are more likely to try other drugs compared to non-users, but not that they become dependent on or frequent users of harder drugs. The real value of this research lies in identifying factors that predict progression from one illegal drug to a harder one.
Marijuana is a gateway drug in the sense that its use typically precedes the use of other illicit substances. However, marijuana use itself doesn’t appear to be a cause or significant predictor of hard drug abuse. Instead, intense marijuana use, psychiatric disorders, and a family history of psychological problems or alcoholism are more consistent predictors.
It’s also important to note that research on drug progression has focused on recreational use. The pattern of drug progression among medical users may differ. A study of non-medical use of psychoactive prescription drugs (tranquilizers, antidepressants, and opiate painkillers) didn’t find a clear or consistent sequence of drug use following abuse of these medications. Currently, data neither supports nor refutes the idea that legalizing medical marijuana would increase drug abuse among medical users.
A related concern is whether medical marijuana use would encourage drug use in society in general. Without medical marijuana approval, we can only speculate. However, we can draw reasonable inferences from the abuse patterns of opiate drugs (like morphine and codeine), drug abuse patterns in the Netherlands and parts of the US where marijuana was decriminalized in the 1970s, and the short-term consequences of California’s 1996 medical marijuana legalization.
Opiates can be considered analogous to marijuana-based medicines, as both have the potential for abuse and medical benefit. Earlier in the century, some doctors worried that liberal opiate use would lead to addiction. These fears proved unfounded, and it’s now recognized that doctors often unnecessarily limit opiate doses to pain patients due to addiction concerns. Today, opiates are carefully regulated by medical caregivers and rarely diverted from legitimate use to the black market.
There’s no evidence that medical opiate or cocaine use has increased the perception that illicit use of these drugs is safe or acceptable. While some patients may abuse these substances for their psychoactive effects or divert them to recreational users, similar issues have occurred with other medications, especially Schedule II drugs under the Controlled Substances Act. Dispensing and manufacturing of Schedule II drugs are strictly controlled, and doctors are advised to monitor their use by patients at risk for drug abuse.
Two studies examining the effects of marijuana decriminalization have produced somewhat conflicting conclusions. The “Monitoring the Future” survey of high school seniors found that students in states that had decriminalized marijuana didn’t report using the drug more than students in states where it remained illegal between 1975 and 1980. However, a study based on drug-related emergency room (ER) cases concluded that decriminalization had increased marijuana use, showing a greater increase between 1975 and 1978 in the number of ER patients who had used marijuana in states that had decriminalized it in 1975-1976, compared to states that didn’t.
However, the ER study also found that by 1978, the proportion of marijuana users among ER patients was roughly equal in states that did and did not decriminalize marijuana. Before decriminalization, states where marijuana remained illegal had higher rates of marijuana use than those that eventually legalized it. In contrast to marijuana use, rates of other illicit drug use among ER patients were substantially higher in states that did not decriminalize marijuana. This suggests multiple explanations for the relatively greater increase in marijuana use in decriminalized states: it may have led to increased use, or where marijuana remained illegal, people may have been less likely to differentiate it from other illicit substances, increasing the use of hard drugs.
WEIGHING MARIJUANA’S HARMS
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The primary negative effect of using marijuana in a single, high dose is impaired motor skills. Some users may also experience negative emotions, ranging from mild unease to significant distress. Individuals with pre-existing mental health conditions, particularly those prone to addiction, face a higher risk when using marijuana or marijuana-derived drugs. However, the scope of these potential acute side effects remains within acceptable limits for prescription drugs.
A more significant concern regarding medical marijuana is the potential for long-term side effects resulting from extended use. These effects are twofold: the long-term consequences of smoking and the dangers of prolonged THC exposure. Similar to tobacco smoke, marijuana smoke is linked to a greater risk of cancer, lung damage, and adverse pregnancy outcomes. Therefore, smoked marijuana is unlikely to be a safe long-term treatment option for chronic conditions.
Dependence is a less common side effect of long-term marijuana use, typically affecting only vulnerable individuals, especially conduct-disordered adolescents. People with mental health issues and those susceptible to substance abuse may also be at increased risk of becoming dependent on medical marijuana.
Besides the risks associated with smoking, the inconsistent composition of marijuana cigarettes poses another problem. The cannabinoid content can vary depending on growing conditions, and dried leaves can be contaminated with harmful bacteria and fungi.
Concerns that medical marijuana legalization might increase recreational use or general drug abuse are not supported by solid evidence. Research suggests that if marijuana were as strictly regulated as other potentially addictive medications, it wouldn’t pose a greater risk of abuse. However, this hasn’t been directly studied. Even if medical marijuana were to decrease the perceived harms of marijuana, this perception shouldn’t influence the legal regulation of marijuana-based treatments. Federal drug approval is determined by a drug’s individual safety and effectiveness, not by broader societal perceptions.
Marijuana is a potent drug with various effects on the body and mind. However, aside from smoking-related damage, its side effects are similar to those of many approved medications. While the efficacy of medical marijuana still needs further research, current data indicate that marijuana and its components could be beneficial in treating various conditions.
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