Marijuana: History, Biology and Myths

Kirk Honda, M.A., LMFT

August 30, 2013

.

The use of cannabis has a long and complicated history and it has been debated among researchers, civil liberties proponents, policymakers, recreational users, medial patients, and doctors for centuries (Fortney & Kindschi, 2013).  Proponents claim cannabis shows promise as a valuable therapeutic agent for various medical conditions and that recreational use is relatively non-harmful and should therefore not be criminalized (Fortney & Kindschi, 2013).  Opponents claim cannabis is drug like any other, causing addiction and harm among its users.  In this paper, I will explore the history of cannabis, the prevalence of use, the psychophysiology of THC (the main psychoactive constituent), and the new definitions within DSM-5.

Definition of Terms

There are several terms for cannabis and its various forms and functions.  According to my observation of the literature, the word “cannabis” is often used as an umbrella term for all forms or a term for the plant species.  The word “hemp” usually refers to the forms used as rope, cloth, paper, etc.  The word “marijuana” is most often used for the recreational or medical drug.  However, it should be noted that some authors do not follow this convention of terms.  Other names for the recreational drug are hashish, bhang, weed, grass, reefer, pot, herb, ganja, old man, blanche, dagga, smoke, hash, dope, Mary Jane, hooch, joints, brew, cones, skunk, boom, gangster, kif, mull, buddha, hydro, yarndi, heads, and green.  Although some of these terms are rarely used or used only within particular groups.

History of Cannabis

Cannabis sativa, Cannabis indica, and Cannabis ruderalis are plants native to South Central Asia and have been cultivated by humans for thousands of years (Maccarrone & Alexander, 2012).  Cannabis is the cultivated plant with the longest history and has been used for centuries as food, fabrics, paper, and building material (Fortney & Kindschi, 2013; Kuhn, Swartzwelder, Wilson, Wilson, & Foster, 2008).  Cannabis was first brought to the Americas by European explorers in the early 1600s to produce rope, cloth, and other materials (Kuhn et al., 2008; Lynne-Landsman, Livingston, & Wagenaar, 2013).  For example, initial drafts of the American Declaration of Independence are purported to have been written on paper made from cannabis (Fortney & Kindschi, 2013).

Resourceful humans discovered that when cannabis is dried, the leaves and buds can be used as a psychoactive or medicinal substance (Kuhn et al., 2008; Lynne-Landsman et al., 2013).  The psychoactive properties have been used for over 2000 years in various cultures (e.g., ancient Romania, ancient China) and for religious, ritual, and psychoactive purposes (Fortney & Kindschi, 2013; Kuhn et al., 2008; Napchan, Buse, & Loder, 2011).  It has also been used medicinally as an appetite stimulant, a muscle relaxant, and a pain reliever (Kuhn et al., 2008).

Legal history in the U.S. The history of the legality of cannabis in the United States is a long and complicated story.  In general, cannabis was considered an extremely useful plant by the early European colonizers.  However, as cannabis became used recreationally, attitudes changed.  As a result, throughout the late 1800s, laws were passed regulating cannabis.  However, this did not stop hashish parlors – similar to opium dens at the time – from flourishing in U.S. cities.

Reefer Madness. By the early 1900s, due to a rise in recreational cannabis use and a societal attitude change regarding the recreational use of many substances (including alcohol), the government began regulating cannabis in the U.S. (Julien, 2004; Lynne-Landsman et al., 2013).  From substance to substance, this anti-substance movement had a wide variety of particular manifestations.  Anti-marijuana sentiment was fueled partially by racism against Mexicans.  Some historians argue that in the early 1900s, tensions in the southwestern states were growing between Mexican-Americans and European-Americans due to a shortage of jobs (particularly during the Great Depression) which resulted in an increase in anti-Mexican sentiment among White Americans which, in turn, resulted in an increase in anti-cannabis legislation since marijuana was associated with Mexicans (Fortney & Kindschi, 2013).  Additionally, the U.S. government initiated a propaganda campaign exaggerating the effects of cannabis use called “Reefer Madness.”  In the film Reefer Madness, young adults smoke marijuana and proceed to commit rape, murder, suicide, and other violence.  This, and several other campaigns, portrayed cannabis as evil, menacing, maddening, and crime-inducing (Julien, 2004). 

Criminalization. In the U.S., it was further criminalized in 1937 against the advice of the American Medical Association and the pharmaceutical industry (Fortney & Kindschi, 2013).  Since then, throughout the 20th century, cannabis has become progressively more regulated (Lynne-Landsman et al., 2013).  And then in the 1970s, cannabis possession became even more criminalized when it became classified by the federal government as a Schedule I substance (along with cocaine, heroin, and other such substances) since it met the following criteria: 1) high potential for abuse, 2) no current accepted medical use, and 3) lack of accepted safety for use under medical supervision (Kuhn et al., 2008; Lynne-Landsman et al., 2013; Napchan et al., 2011).  However, many debate the accuracy of this legal designation since marijuana has been shown to have safe medical uses (Kuhn et al., 2008).

Legalization. Beginning in the 1990s, American culture showed noticeable changes in the attitude toward cannabis in that voters began to decriminalize it.  Since 1996, eighteen U.S. states (including Washington State) have approved the use of medical marijuana for specific diseases (Fortney & Kindschi, 2013; Lynne-Landsman et al., 2013; Napchan et al., 2011).  It has been used medicinally to: 1) reduce nausea associated with chemotherapy, 2) reduce the pressure of the fluid in the eye due to glaucoma, 3) relieve pain, and 4) increase appetite in people with HIV/AIDS (Kuhn et al., 2008).  Various other medical uses are currently being researched.  And in 2012, Colorado and Washington furthered legalization of cannabis by passing ballot initiatives legalizing marijuana for recreational use (Fortney & Kindschi, 2013; Hartman, 2013).  Some claim that the recent legalization medical marijuana will lead to an increase in marijuana use, particularly among children.  However, initial research has shown no evidence of a significant increase in marijuana use after the enactment of medical marijuana laws (Lynne-Landsman et al., 2013).

Legal confusion. Even though 18 states have legalized its use for medical purposes and 2 states have legalized recreational use, the federal government still considers marijuana a Schedule I substance and prohibits pharmacies from distributing medical marijuana, so patients have to buy it from dispensaries (Fortney & Kindschi, 2013; Hartman, 2013; Lynne-Landsman et al., 2013).  Furthermore, some workers are being fired for testing positive for marijuana even though they are properly registered as medical marijuana patients (Hartman, 2013).  Courts in California, Michigan, Montana, Oregon, and Washington are rejecting claims made by fired employees seeking protection under medical marijuana statutes (Hartman, 2013).  Similarly, since marijuana is still a Schedule I substance according the federal government, state courts have rejected the argument that the Americans with Disabilities Act prohibits the discharge of employees who are medical marijuana patients (Hartman, 2013).  These contradictions between state law and federal law have yet to be worked out and are currently causing much legal confusion.

Prevalence

Among illicit drugs worldwide, cannabis is the most widely used (Batalla et al., 2013; Hirvonen et al., 2012; Julien, 2004; Jutras-Aswad et al., 2012; Smith, Longo, Fried, Hogan, & Cameron, 2010).  Around the globe, between 125 and 200 million people report having used cannabis in the past year – or an annual prevalence rate of 3% to 5% (Batalla et al., 2013; Smith et al., 2010).  It is also the most widely used illicit drug in the U.S. where more than 17 million individuals – or 6% of the population – used cannabis in 2010 (Substance Abuse and Mental Health Services Administration, as cited by Gizer, Gilder, Lau, Wang, Wilhelmsen, & Ehlers, 2013).  In the U.S., younger people use cannabis at much higher rates: 25% of American teenagers had used cannabis in the past month and 5% of high-school-age teens used cannabis daily (Partnership for a Drug-Free America, as cited in Julien, 2004).  In 2010, 33% of U.S. college students reported using cannabis in the past year, 18% reported using cannabis in the past month, and 4% reported daily use over the past 30 days (Neighbors, Foster, Walker, Kilmer, & Lee, 2013).  To put these rates in perspective, the past-month prevalence of alcohol use is 65% among U.S. college students as opposed to 18% having used cannabis (Neighbors et al., 2013).

Cannabis Pharmacology

Currently, there are four forms of organic marijuana: 1) low-grade marijuana (average 2% THC), 2) high-grade marijuana (average 7% THC), 3) hashish (between 0% and 70% THC), and 4) hash oil (30% to 70% THC).  Synthetic forms of THC are also available for medical purposes.  Other synthetic cannabinoid compounds have been developed for recreational use (e.g., K2, Spice).  Cannabis is usually smoked in pipes, bongs, or joints.  It can be ingested orally by mixing it with food.  It can also be vaporized by a vaporizer which heats the plant releasing the psychoactive compounds for inhalation.

Psychophysiology. The pharmacodynamic effects of cannabis can vary widely depending on several factors including genetic differences among individual humans, plant strain differences, growing and harvesting factors, and drug potency (Fortney & Kindschi, 2013; Kuhn et al., 2008).  There are more than 400 different chemicals in a typical marijuana flower bud, including its most well-known and the principle psychoactive constituent tetrahydrocannabinol or THC (Fortney & Kindschi, 2013; Hirvonen et al., 2012; Julien, 2004; Kuhn et al., 2008; Napchan et al., 2011; Smith et al., 2010).  The psychoactive effects of cannabis involves THC activating cannabinoid receptors in humans

The two known cannabinoid receptors in humans, cannabinoid receptor type 1 and 2 (or CB1 and CB2, both G-protein coupled receptors), were discovered recently in the 1990s (Fortney & Kindschi, 2013; Julien, 2004; Napchan et al., 2011).  CB1 receptors are principally located and widely distributed in the peripheral and central nervous system, while CB2 receptors are located in the central nervous system, peripheral nervous system, gastrointestinal system, and immune system (Julien, 2004; Napchan et al., 2011).  Within the brain, there is a relatively large number of CB1 receptors, perhaps 10 to 20 times the number of opioid receptors and perhaps more than any other receptor in the body (Julien, 2004). 

CB1 receptors are located in various concentrations throughout the brain, with high densities found in: 1) the frontal cortex (associated with executive function, reasoning, decision-making, planning, problem solving, focused attention, response inhibition, and working memory), 2) the hippocampus (associated with several types of memory and formation of new memories), 3) the basal ganglia (associated with motivation and the planning of movement), 4) the cerebellum (associated with fine movement coordination), and 5) the spinal cord (associated with sensation and pain) (Hirvonen et al., 2012; Julien, 2004; Smith et al., 2010; Vaidya, Block, O’Leary, Ponto, Ghoneim, & Bechara, 2012).  CB1 receptors are also found in: 6) the medulla (associated with nausea and vomiting), the hypothalamus (associated with appetite), and 7) the amygdala (associated with fear and anxiety).  In other words, THC affects receptors throughout the body, affecting many systems.

Cannabinoid receptors are activated by three ligands: 1) endocannabinoids (produced by the body), 2) plant cannabinoids (such as THC), and 3) synthetic cannabinoids (such as dronabinol) (Napchan et al., 2011).  Primarily, CB1 receptors are located presynaptically, where they inhibit release of other neurotransmitters (Hirvonen et al., 2012).  Since the excitatory neurotransmitter glutamate and the inhibitory GABA are prominent throughout the nervous system, when THC is present at the synapses, both the excitation and the inhibition of neural circuits are slowed.  In other words, THC binds to the presynaptic CB1 receptor and inhibits both the activation and the inhibition of a neuronal pathway, and this produces various effects that are difficult to predict based on current knowledge of biology.

Pharmacokinetics. The pharmacokineties of THC vary depending on the route of administration.  Inhaled THC (via pipe, bong, joint, vaporizer, etc.) causes psychotropic effects in seconds, a maximum blood concentration within minutes, a maximum level after 15-30 minutes, and a tapering down over 2-3 hours in most people (Fortney & Kindschi, 2013).  Ingested THC (via food infusion or synthetic pill) causes psychotropic effects within 30-90 minutes, a maximum blood concentration level after 2-3 hours, and an active duration of 4-12 hours (Fortney & Kindschi, 2013; Kuhn et al., 2008). 

THC can persist in the body for up to two weeks (longer for chronic and obese users) where it continues to affect mental and physical functions (Julien, 2004).  In other words, individuals may be adversely affected by cannabis use for several days even though the initial intoxication ended after a few hours. 

Since only minute quantities of THC are found in urine, testing for THC focuses on its inactive metabolite, carboxy-THC, which is much more slowly secreted (Julien, 2004).  For infrequent users (less than twice per week), urine will generally be carboxy-THC positive for 1 to 3 days (Julien, 2004).  For chronic daily users, urine will be positive for 30 days or longer (Julien, 2004).

Cannabis as a Medical Drug

Cannabis has been used for centuries for various medical purposes.  More recently, its uses have become recognized and utilized within mainstream U.S. medical practice.  Cannabis is currently being used: 1) as an appetite stimulant, 2) as a muscle relaxant, 3) as a pain reliever, and 4) to reduce nausea (Fortney & Kindschi, 2013; Kuhn et al., 2008; Lynne-Landsman et al., 2013).  There are many other purported medical uses such as an anti-anxiety agent, an anti-depression medication, and a treatment for ADHD.  However, much more research is necessary to test such claims, and since cannabis is becoming less stigmatized and less criminalized, much more research is likely on the horizon.

Cannabis as a Psychoactive Drug

For centuries, humans around the globe have been using cannabis as a psychoactive substance (Kuhn et al., 2008; Lynne-Landsman et al., 2013).  Our current knowledge of the effects of the substance comes from a variety of sources ranging from anecdotal to biochemical.

Positive subjective effects. Anecdotally, cannabis use leads to a feeling of being “high” and an elevated mood.  People report it simply makes them feel better.  This effect alone might explain why cannabis is the most widely used illicit drug.

More specifically, cannabis use produces several varied, difficult-to-explain subjective experiences including: 1) elevated mood; 2) relaxation; 3) hearing subtleties in speech or music; 4) perceiving visual images as being more intense or more meaningful; 5) feeling a sense of emotional well-being and euphoria; 6) feeling as though time is slowed; 7) feeling a sense of wonder about the world; 8) decreased aggression; and 9) decreased anxiety (Fortney & Kindschi, 2013; Julien, 2004; Kuhn et al., 2008).

Kuhn et al. (2008) hypothesize that the subjective sense of wonder could be due to the memory deficiencies that marijuana causes since the usual time-line that one experiences is distorted.  This might keep particular details in the present mind far longer than normal, giving the mind a chance to more fully experience a particular moment or detail.

Acute adverse effects. The most common acute adverse side effects are dizziness, impaired memory, disinhibition and risk taking, impaired attention, impaired learning, impaired motor activity, increased appetite, increased heart rate, anxiety, panic attacks, paranoia, sleepiness, and dry mouth (Fortney & Kindschi, 2013; Julien, 2004; Kuhn et al., 2008; Neighbors et al., 2013).  Research has shown that heart rates increase between 20 and 30 beats per minute (Kuhn et al., 2008).  Therefore, people with heart disease or high blood pressure may be at risk when using marijuana.  In pregnant women, THC crosses the placental barrier potentially causing complications to the pregnancy or the development of the fetus (Kuhn et al., 2008).  Also, due to the intoxicating effects of cannabis, people should avoid driving or operating machinery while under the influence (Fortney & Kindschi, 2013).  Furthermore, large doses can cause a number of temporary debilitating effects such as delusions, hallucinations, heavy confusion, depersonalization, and loss of insight (Julien, 2004).

Anxiety and paranoia. Occasionally, marijuana use can result in an acute panic reaction and perhaps even prompting a trip to the hospital (Julien, 2004; Kuhn et al., 2008).  According to Julien (2004), studies have shown that 50 to 60 percent of cannabis users have reported at least one anxiety experience.  It has also been observed to cause mild paranoia (Julien, 2004).  For example, an intoxicated man at the shopping mall might feel as though everyone knows he is high and is judging him.

Impaired concentration. Research has shown the frontal cortex to be responsible for executive functioning processes such as decision making, planning, problem solving, focused attention, response inhibition, cognitive flexibility, and working memory (Smith et al., 2010).  Reports of impaired concentration and cognition due to cannabis use are consistent with biological findings since many of the brain’s CB1 receptors are located in the frontal cortex.

For example, studies have shown that heavy marijuana users showed impairment in their ability to problem solve – they often repeatedly made the same mistake on a test (Kuhn et al., 2008).

Impaired memory. The hippocampus is involved in several types of memory, particularly the formation of new memories (Kuhn et al., 2008; Smith et al., 2010).  Therefore, the reports of memory loss due to marijuana use likely involve the effects of THC on CB1 receptors in the hippocampus (Kuhn et al., 2008).  For example, according to research described in Kuhn et al. (2008), after participants smoked one joint, they were significantly impaired in their ability to recall the details of a story they listened to while high.  However, if they heard the story the day before they used marijuana, the participants could recall the story normally.  This is evidence that marijuana impairs the ability to form new memories but not the ability to recall older memories.

Overdose risk. According to Kuhn et al. (2008), there have been no reported lethal overdoses from marijuana.  However, its effects can indeed lead to injury or death.  For example, heavy use can result in decreased attention and concentration which can impair one’s ability to drive a car effectively.  Kuhn et al. (2008) also identify reports of small children unknowingly eating large amounts of cannabis in cookies and going into coma, although no citation was given.

Long-term adverse effects. Chronic cannabis use is associated with a pattern of apathy, loss of goal-directed behavior, impaired cognition, depression, addiction, impaired functioning of the lungs, and possibly even psychosis (Gizer, et al., 2013; Kuhn et al., 2008).  Many researchers (e.g., Fortney & Kindschi, 2013) recommend people under the age of 21 should avoid cannabinoids due to the risk of permanent impaired cognitive and emotional development.  In other words, when young people use marijuana, they risk permanently altering the development of their brain which may lead to permanent impairment and/or personality change.

Gateway hypothesis. Early cannabis use is associated with progression to other illicit drug use – otherwise known as the gateway drug hypothesis (Gizer et al., 2013).  This hypothesis is considered fact by many in our culture which causes much anxiety when parents learn their teenaged child is using marijuana occasionally.  Studies have shown that early cannabis exposure permanently alters dopamine receptor D2 and proenkephalin (an endogenous opioid polypeptide hormone) expression in the mesocorticolimbic system which may produce drug-seeking behavior later in life (Jutras-Aswad et al., 2012).  However, research has also shown little to no association between early cannabis use and later “harder” illicit drug use.  In other words, the jury is still out.

Psychosis risk. Research efforts have focused on cannabis use and its association with mental disorders such as psychosis (Jutras-Aswad et al., 2012).  For example, emerging research suggests that early marijuana use (by age 12) may increase a person’s chance of developing a psychotic disorder, particularly for predisposed individuals (Julien, 2004; Kuhn et al., 2008).  However, this may be a correlation rather than a causation in that early substance use may be an indication of early self-medication of an already emerging psychopathology (Julien, 2004).  Therefore, more research is needed.

Dependence. Despite myths proclaiming that cannabis is non-addictive, regular use of cannabis can lead to a harmful habit, tolerance, and withdrawal symptoms, which are the hallmarks of dependence and addiction (Fortney & Kindschi, 2013; Hirvonen et al., 2012; Kuhn et al., 2008).  Research has found that as many as one in every ten persons who start using cannabis will develop dependence (Julien, 2004).  In the U.S., lifetime rates of cannabis dependence are estimated to range from 1% to 4% (Gizer et al., 2013).  Of those who use cannabis, between 9% and 25% will eventually develop dependence (Batalla et al., 2013; Jutras-Aswad et al., 2012).  To put these figures in perspective, of those who use alcohol, about 15% will eventually develop dependence, and of those who use tobacco, 32% will become dependent (Batalla et al., 2013).

According the Kuhn et al. (2008), the dependence on other substances, aside from marijuana, often involves intense cravings that dominate one’s behavior, whereas dependence on marijuana does not produce these cravings.  However, other studies have shown that chronic users will crave cannabis after ceasing use (Julien, 2004). 

Compared to other substances, cannabis has a delayed progression to dependence (Jutras-Aswad et al., 2012).  Therefore, individuals are generally not at-risk of developing an addiction after initial use, but over time, a dependence may develop.

Family, twin, and adoption studies have shown that cannabis dependence is influenced by heritability (Jutras-Aswad et al., 2012).  Therefore, people with addiction in their family history should be wary when initiating use of cannabis and other substances.

In my clinical experience, chronic marijuana users report a “psychological habit” rather than a “body addiction,” meaning they use every day against their better judgment, but if they stopped, they would not feel the “body crash” associated with other substance withdrawal such as caffeine or nicotine.  However, some research has shown that some individuals do in fact experience physical withdrawal symptoms.

Tolerance and withdrawal. Evidence has been found that tolerance is the result of downregulation in brain CB1 receptors (Julien, 2004).  Therefore, when a chronic cannabis user ceases use, it may take some time for the CB1 receptors to upregulate – resulting in withdrawal symptoms.  Withdrawal symptoms include irritability, anxiety, cravings, aggression, depression, restlessness, insomnia, sweating, and nausea (Julien, 2004; Kuhn et al., 2008).  These symptoms begin within 48 hours of last use and usually last 7 to 10 days (Julien, 2004).  The debilitating effects of cessation are the major reason why there is almost universal relapse when attempting to quit (Julien, 2004).

Myths

It is a myth that marijuana causes sterility (Kuhn et al., 2008).  However, marijuana can in fact alter the production of hormones leading, in men, to decreased sperm count, erectile dysfunction, and/or increased breast tissue; and in women it can lead to decreased ovulation and irregular menstrual cycles (Julien, 2004; Kuhn et al., 2008).  

Although marijuana smoke is indeed harmful to the lungs, it is a myth that marijuana smoke is 10 to 100 times more toxic than cigarette smoke.  Instead, it has been shown that marijuana smoke and tobacco smoke damage the lungs similarly (Kuhn et al., 2008).  And although marijuana smoke is inhaled more deeply and for longer periods of time, cigarette addicts typically inhale much more smoke throughout the day.  Therefore, it appears that chronic marijuana smokers have a similar risk (for diseases such as lung cancer) as chronic cigarette smokers.

According to Kuhn et al. (2008), the myth that marijuana use kills brain cells was based on rat studies that involved administering abnormally large doses of THC (hundreds of times larger) over long periods of time.  Therefore, unless an individual lives in a constant cloud of cannabis smoke, marijuana use is not likely to cause brain cell death.

Many people have the impression that cannabis is as dangerous as cocaine and heroin.  However, according to Fortney & Kindschi (2013), claims of this high degree of harm to individuals and society are overstated.  Cannabis may actually be helpful while imposing little risk to individuals (Fortney & Kindschi, 2013).

Another myth worth mentioning is the cultural belief that cannabis use causes someone to become a “loser.”  In my psychotherapy practice, parents of teen marijuana users are mainly concerned their child will grow up to be a depressed, apathetic lump on the couch with no ambitions and no friends.  Even though attitudes are changing, our culture continues to view marijuana as an evil menace.  After reviewing the research and upon witnessing many of these pot-smoking teens develop into normal adults, it is my opinion that these worries are exaggerated.  This is not to say there are not adverse effects.  However, the extreme anxiety and urgency that parents feel is probably unwarranted in most cases.

DSM-5

In most cultures, around the globe, people use various recreational and medicinal substances such as alcohol, marijuana, opium, etc.  Since many individuals seek help regarding their use of substances, the DSM-5 (APA, 2013) attempts to establish a boundary between normal use and disordered use.

The new definition for Cannabis Use Disorder in the recently published DSM-5 has additions and subtractions in comparison to the DSM-IV definition (APA, 1994).  First, the term “Cannabis Use Disorder” has replaced “Cannabis Dependence.”  Second, there is no longer a distinction between physiological and psychological dependence – both are subsumed under Cannabis Use Disorder.  Third, some of the other specifiers have changed including the addition of Mild (2-3 symptoms), Moderate (4-5 symptoms), and Severe (6 or more).  Fourth, to qualify for the diagnosis, a patient only need meet two of the criteria instead of three.  Fifth, four new criteria were added including: 1) craving, 2) recurrent use resulting in a failure to fulfill major role obligations at work, school, or home, 3) continued use despite having interpersonal problems caused by use, and 4) use in situations in which it is physically hazardous.  The most notable additional criterion is craving.  

The original umbrella definition remained: a problematic pattern of use leading to clinically significant impairment or distress, as manifested by the following criteria, occurring within a 12-month period.  Also, the original seven criteria remained in the definition including: 1) the substance is taken in larger amounts or over a longer period than intended; 2) unsuccessful in cutting back; 3) a great deal of time spent obtaining it, using it and recovering from it; 4) important activities are given up because of use; 5) continued use despite knowledge of problem; 6) tolerance (more is needed or diminished effect); and 7) withdrawal symptoms or avoidance of withdrawal symptoms.

The DSM-5 defines “Cannabis Intoxication” as clinically significant problematic behavioral or psychological changes (e.g., impaired coordination, euphoria, anxiety, sensation of slowed time, impaired judgment, social withdrawal) due to use and two or more of the following: 1) conjuctival injection (or reddening of the eyes), 2) increased appetite, 3) dry mouth, or 4) tachycardia (or increased heart rate).

According to the DSM-5, the definition of “Cannabis Withdrawal” is three or more of the following symptoms that develop within one week after cessation of chronic cannabis use causing clinically significant distress or impairment: 1) irritability, 2) anxiety, 3) sleep difficulty, 4) decreased appetite, 5) restlessness, 6) depressed mood, or 7) at least one of the following: pain, tremors, sweating, fever, chills or headache.

Conclusion

Since cannabis is becoming increasingly less criminalized (particularly in my home state of Washington), we could all benefit by bringing cannabis out from the darkness and into the light of day.  I think we can all agree that marijuana can become a problem for some individuals.  However, as with substances such as caffeine and alcohol, perhaps our relationship with marijuana can be more balanced.  I hope, as our culture relaxes its attitudes, cannabis research will increase greatly, shedding light on new medical uses.

 

For example, a mother recently told me her son performs better in school now that he is smoking marijuana.  At first she was, of course, highly disapproving of his marijuana use.  However, as his grades improved, she wondered if his use was reducing his lifelong, debilitating ADHD symptoms (which have not responded well to traditional ADHD medications).  According to recent exploratory research (e.g., Strohbeck-Kuehner, Skopp & Mattern, 2008), THC may ameliorate ADHD symptoms in some individuals.  If THC can be shown to have an overall benefit, should we not consider it as a treatment for ADHD?  Given today’s attitudes, I cannot imagine our society reacting accurately to an MD prescribing THC to a teen.  Until we change our laws and attitudes, we will not be able to approach the topic with maturity.

I am not promoting its use – I certainly know many people, both clinically and personally, who have been negatively affected by the substance, both in the short-term and the long-term.  I am merely promoting a more accurate and unbiased view of the substance, free from the exaggerated propaganda that pervaded the 20th century.  Therefore, clinicians, family members and those who use cannabis can all potentially benefit by increasing our understanding of the substance and reflecting upon our attitudes.

References

American Psychiatric Association (1994). Diagnostic and statistical manual of mental disorders: DSM-IV. Washington, DC: American Psychiatric Association.

American Psychiatric Association (2013). Diagnostic and statistical manual of mental disorders: DSM-5. Washington, D.C: American Psychiatric Association.

Batalla, A., Bhattacharyya, S., Yu, M., Fusar-Poli, P., Crippa, J. A., Nogue, S., Torrens, M., Pujol, J. Farre´, M., & Martin-Santos, R. (2013). Structural and functional imaging studies in chronic cannabis users: A systematic review of adolescent and adult findings. Plos one, 8(2), 1-18.

Fortney, L. & Kindschi, J. (2013). Medical marijuana: Navigating the controversy. Integrative Medicine Alert, June 2013, 64-69.

Gizer, I. R., Gilder, D. A., Lau, P., Wang, T., Wilhelmsen, K. C., & Ehlers, C. L. (2013). Contributions of ethnicity to differential item functioning of cannabis abuse and dependence symptoms. Journal of Studies on Alcohol and Drugs, March 201

3, 320-328.

Hartman, H. L. (2013). Legalized marijuana and the workplace: Preparing for the trend. Employee Relations Law Journal, 38(4), 72-75.

Hirvonen, J., Goodwin, R. S., Li, C., Terry, G. E., Zoghbi, S. S., Morse, C., Pike, V. W., Volkow, N. D., Huestis, M. A., & Innis, R. B. (2012). Molecular Psychiatry, 17, 642–649

Julien, R. M. (2004). A primer of drug action: A concise, nontechnical guide to the actions, uses, and side effects. New York, NY: Worth Publishers.

Jutras-Aswad, D., Jacobs, M. M., Yiannoulos, G., Roussos, P., Bitsios, P., Nomura, Y., Liu, X., Hurd, Y. L. (2012). Cannabis-dependence risk relates to synergism between neuroticism and proenkephalin SNPs associated with amygdala gene expression: Case-control study. Plos One, 7(6), 1-9.

Kuhn, C., Swartzwelder, S., Wilson, W., Wilson, L. H., & Foster, J. (2008). Buzzed: The straight facts about the most used and abused drugs from alcohol to ecstasy. New York, NY: W.W. Norton.

Lynne-Landsman, S. D., Livingston, M. D., & Wagenaar, A. C. (2013). Effects of state medical marijuana laws on adolescent marijuana use. American Journal of Public Health, 103(8), 1500-1506.

Maccarrone, M. & Alexander, S. (2012). Cannabinoid research in the 2010s. British Journal of Pharmacology, 165, 2409–2410.

Napchan, U., Buse, D. C., & Loder, E. W. (2011). The use of marijuana or synthetic cannabinoids for the treatment of headache. Headache, March 2011, 502-505.

Neighbors, C., Foster, D. W., Walker, D. D., Kilmer, J. R., & Lee, C. M. (2013). Social identity as a moderator of the association between perceived norms and marijuana use. Journal of Studies on Alcohol and Drugs, May 2013, 479-483.

Smith, A. M., Longo, C. A., Fried, P. A., Hogan, M. J., & Cameron, I. (2010). Effects of marijuana on visuospatial working memory: an fMRI study in young adults. Psychopharmacology, 210, 429–438.

Strohbeck-Kuehner, P., Skopp, G., & Mattern, R. (2008). Cannabis improves symptoms of ADHD. Cannabinoids, 3(1), 1-3.

Vaidya, J. G., Block, R. I., O’Leary, D. S., Ponto, L. B., Ghoneim, M. M., & Bechara, A. (2012). Effects of chronic marijuana use on brain activity during monetary decision-making. Neuropsychopharmacology, 37, 618–629.