How addictive is cannabis? My detailed overview of addiction science
Cannabis has always had a strangely familiar presence in our culture—part taboo, part wellness trend, part rite of passage. Over the past decade, its visibility in Europe has grown substantially: legalization debates are on the political agenda, while CBD products are widespread in corner stores and lifestyle shops, marketed for everything from anxiety to sleep to chronic pain.
But for all this exposure, one question remains mysterious to most: Is cannabis actually addictive? And if it is, how addictive is it?
To find out, I went through the scientific studies looking at cannabis addiction in humans and animal models, as well as the long-term trends of addiction and remission, as compared with other drugs of abuse. Along the way, I learned that the potency of modern cannabis means only tiny quantities of the drug are entirely non-addictive, and that adolescent cannabis use is indeed very detrimental to the developing brain. Nonetheless, I also found that nearly all drugs of abuse are more harmful than marijuana.
The reward and addiction potential of cannabis
Dopamine is the single most important chemical responsible for motivation and reward in our brain. The pathway most responsible for reward and addiction links the dopamine-producing cells of the ventral tegmental area (VTA) and the nucleus accumbens (NAc). Dopamine released by VTA neurons onto the NAc is both sufficient and necessary for the development of addiction(1). By examining the amount of dopamine released in the NAc, researchers can gauge the addictive potential of any substance.
It is well-known that administering THC (the main psychoactive molecule in cannabis) to rodents will increase the dopamine released in their NAc(2). The extent to which this experience is rewarding to the animal, the more craving — so-called psychological dependence — develops.
N.B. There is also another kind of addiction: physical dependence. This manifests as physical withdrawal symptoms that make life intolerable without the drug: the nauseating dysphoria of heroin addicts or the brain fog before your morning coffee. Marijuana can only cause physical addiction rarely: if it’s used for falling asleep or managing chronic pain(3). The rest of the article discusses psychological addiction.
The dopaminergic effect of marijuana is substantially smaller than that of cocaine, amphetamine, or heroin. Due to regulations in human studies, researchers only administer THC doses found in a regular ‘joint,’ as defined by the US National Institute of Drug Abuse in the 70s. This amount does not cause a noticeable increase in NAc dopamine(2). In the four decades since that definition, however, THC content in cannabis has increased at least fourfold(4). In rodents, the body weight equivalent of a modern ‘joint’ is more than enough for a robust dopamine response.
When you chronically abuse THC, your finely tuned dopamine system cannot be in constant overdrive, so it decreases its sensitivity to dopamine. This means you have to increase the dose to feel the same pleasurable effect. The problem begins when you stop using cannabis: your dopamine system is less sensitive, so things that would normally be rewarding won’t feel as pleasurable (2). The withdrawal will be a psychological state of under-stimulation and jadedness. Fortunately, in adults the dopamine system eventually rebounds. But the story in adolescents is very different. Marijuana abuse during one’s teenage years can permanently damage the dopamine system of the maturing brain(5).
There is another important caveat. Due to the specific way THC acts on the dopamine system, it increases the reward potential of any kind of stimulation you obtain from your environment while high(6). That’s one of the reasons food or music take on a more sublime texture: the reward you receive from them is magnified. But crucially, this explains why drinking alcohol, smoking cigarettes, or using any other drug together with marijuana increases the chance of getting addicted to the co-administered substances(7). Their reward becomes higher too.
According to the human scientific literature, however, recreational marijuana use under 0.1–0.2 grams at a time seems to have no addictive potential to most people. The second class of addiction studies corroborates this notion.
Animal place preference and drug self-administration
The idea of conditioned place preference is very straightforward: a test chamber is split into two rooms with different visual cues (patterns) on the walls. The rat is placed in one of the rooms and is given a drug while it can see the distinct environment around it. On test day, the doorway is opened between the two rooms, allowing the rat to explore both freely. If the animal chooses to stay significantly longer in the drug-reward context (i.e., it remembers the context in which it got the drug), it has a conditioned place preference. The drug is concluded to be rewarding, hence addictive.
All drugs of abuse, including marijuana, induce conditioned place preference in rats. The human equivalent of 1 g of average modern cannabis on alternating days is sufficient to induce place preference similar to that of 5 mg/kg cocaine or 4 mg/kg morphine(8). A smaller dose of marijuana doesn’t provide a great enough reward, but interestingly, larger amounts begin evoking conditioned place aversion (the rat chooses to be in the unconditioned room instead).
This is a fascinating paradox: rats only get addicted to marijuana in medium doses. What is the explanation for this? A property of THC called the ‘rate-decreasing effect.’ After obtaining the highest reward at a medium dose, the more you increase the amount of THC, the more aversive its effects will be(9).
N.B. It is physically impossible to overdose on cannabis since it doesn’t directly interact with respiration. It is, however, contraindicated with heart conditions because of the rate-decreasing effect.
The rate-decreasing effect is also evident in self-administration studies. Here, you train an animal to press a lever for a reward. You then attach an intravenous catheter into its neck and place it in a test chamber, where it can self-administer the drug through the catheter by pulling on the lever.
Since THC was first isolated from hashish in the 60s, it has been notoriously tricky to get rodents to self-administer it(10). One reason is the rate-decreasing effect. Even if some animals get hooked on THC, they can’t go on consistently administering higher doses because pretty soon, they will be completely overwhelmed by the aversive effects (as anyone who’s had a profoundly disturbing paranoia on edibles knows).
The other explanation is found in brain circuitry: cannabinoids make it harder to remember the dopaminergic reward they produced. It is well-established that THC prevents the consistent flow of encoding short-term memories in the hippocampus(11). This area is closely linked to both the VTA and NAc, in a network that encodes the environmental memory of the reward(12). So when THC disrupts hippocampal function, it prevents the reward from being entrenched in the broader context of the drug-taking experience(13). This ‘forgetfulness’ is considerably different from a traditional drug experience (like that of cocaine), where the dopamine reward firmly encodes drug cues through the hippocampus.
N.B. Even a more potent synthetic cannabinoid, WIN 55,212–2, fails to establish a reliable model of cannabinoid addiction. Even if a rat gets hooked on WIN 55,212–2, but then the researcher substitutes it with THC, the animal stops taking the drug(14). Frustrated, the researchers found a more convenient model, the squirrel monkey. Turned out, this species reliably self-administered THC, synthetic cannabinoids, and endocannabinoids(15). Moreover, they had robust drug abuse, strong environmental conditioning, and high relapse rates. But when scientists focused on our closer evolutionary relatives, the old-world primates, they again failed to establish reliable self-administration(9). Which gives squirrel monkeys the venerable distinction as the animal kingdom’s biggest stoners.
Human addiction data and comparison with other drugs
Several studies on addiction epidemiology provide excellent resources to examine marijuana dependence rates in a shifting legalization climate — in the US between the years 2008 and 2016(16). During this period, 41 states enacted legislation to legalize or decriminalize some form of marijuana. In teens, cannabis use was declining, except in the few states that legalized recreational use, where cannabis use disorder (CUD — as defined by the Diagnostic and Statistics Manual of Mental Disorders) increased alarmingly by 25% soon after. Despite significantly higher use in adults, CUD did not increase among them.
To put these numbers into context, here’s the lifetime probability of developing dependence on four commonly abused substances following the first use(17):
Cocaine dependence develops four times quicker than the others, but by a decade after first trying it, more people will be addicted to cigarettes than to cocaine.
The lifetime cumulative probability of dependence remains highest for nicotine users at 67%.
In comparison, 23% of alcohol users, 21% of cocaine users, and 9% of cannabis users develop addiction at some point in their lives.
Another study tracked the lifetime probability of transitioning from milder substance abuse to full-blown dependence. It was 27% for alcohol, 16% for cocaine, and 9% for cannabis(18).
The implications of these results are striking. Whereas nicotine is the most addictive commonly abused substance, the probability of developing cannabis addiction is only 9%. And it remains at 9% for both first-time users and individuals with CUD. Thus, diluting marijuana with tobacco in cigarettes is much more likely to get someone addicted to nicotine than marijuana.
A study by addiction specialists from the UK ranking the harm of commonly abused drugs reinforces this idea(19). A meta-analysis of remission from cannabis dependence closely correlates with this data: 50% at four years and 81% at ten years, numbers much higher than for amphetamine, cocaine, or opioids(20). The data suggest that the key for marijuana and all other addictions is that the sooner someone faces their problem, the easier it is to renounce the substance before it morphs too much into their everyday identity and mental state.
Lastly, I list the most common psychosocial factors that lead not only to cannabis, but to most forms of addiction(21):
Commonly diagnosed mental health issues, such as ADHD, major depression, bipolar disorder, or social anxiety disorder.
A low socioeconomic status and educational achievement.
Previous history of substance abuse or family history of substance abuse (in particular, alcohol).
Resorting to cannabis to cope with a negative life circumstance like physical abuse, parental separation, loss of a parent, or divorce.
The earlier the age of onset of frequent marijuana use; and the more it is used in solitude.
As a neuroscience student, the limitations of my questioning lie in biology. But addiction is just as much a social issue as it is a biological one. Mental illnesses of all kinds burgeon in non-supportive environments, where anyone can become captive to the seemingly most innocent of pleasures. For more on the critical psychosocial aspects of addiction, I highly recommend Johann Hari’s Chasing the Scream, a forceful inquiry into the history of the war on drugs. Whatever the legalization debate in countries around the world, I hope that scientific rationality, and not a policy of fear or ignorance, will guide political and societal decision-making.
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