Non-Tobacco Products Smoking

Abstract

Non-tobacco products smoking is a type of smoking: the volatilizing and inhaling of a psychoactive substance other than tobacco, chiefly cocaine and cannabis, a category defined cognitively not by any one drug but by a shared route of administration. Smoking carries a lipophilic drug across the vast surface of the lungs into the arterial blood and to the brain within seconds, an arrival as steep as an intravenous injection and far faster than swallowing or snorting the same dose. Under the rate hypothesis, that speed—not the amount alone—is what makes a dose strongly reinforcing, because a sharp spike pairs tightly with the brain's dopamine reward signal. The clearest evidence is the crack-versus-powder natural experiment: one molecule, two routes, sharply different addictiveness. Three interactive demonstrations trace route-dependent delivery, the rate-to-reinforcement mapping, and the delay discounting behind a quit attempt.

Keywords: route of administration, rate hypothesis, addiction, crack cocaine, reinforcement

To the cognitive scientist, smoking a drug names a delivery method, not a substance. Tobacco is the usual cargo, but the same act carries cocaine, cannabis, and other volatile drugs, and it carries each of them by the same fast route. The Medical Subject Headings vocabulary gathers the non-tobacco cases under one heading precisely because the behavior—combust or heat, inhale, absorb across the lung—is the common element (Samaha & Robinson, 2005).

That common element is the whole of the cognitive story. Whatever the drug, inhaling its vapor or smoke delivers it to the brain in seconds, producing the steep concentration spike that the reward system reads as a strong signal (Robinson & Berridge, 1993). The route, more than the molecule, sets how addictive a given drug will be in practice. This article treats non-tobacco products smoking as the case that isolates that variable: by holding the drug fixed and changing only the route—powder cocaine snorted versus crack smoked—it shows reinforcement rising with the speed of arrival (Hatsukami & Fischman, 1996; Gossop et al., 1992).

What Non-Tobacco Products Smoking Is

Non-tobacco products smoking is the practice of inhaling the smoke or vapor of a psychoactive drug that is not tobacco. In the Medical Subject Headings vocabulary, Smoking, Non-Tobacco Products (D000073847) is filed directly beneath Smoking (D012907), its parent category, and gathers beneath itself the smoking of specific drugs, principally cocaine and cannabis. MeSH is an indexing classification for retrieving the biomedical literature, not a theory of behavior, and it groups these practices by what the smoker does rather than by the pharmacology of each drug. For once that indexing choice coincides with the cognitively decisive variable: the act of smoking is itself a route of administration, and the route is what the account below turns on.

The physical facts of that route are the same across drugs. Heating a volatile, lipophilic compound releases it as a vapor or in fine smoke particles; drawn into the lungs, it crosses the enormous alveolar surface into the pulmonary veins, reaches the left heart, and is pumped as an arterial bolus to the brain in a single circulation time—on the order of ten to twenty seconds (Samaha & Robinson, 2005). This is faster than an intravenous injection into a peripheral vein, which must return through the right heart and the lungs before reaching the brain, and far faster than swallowing a drug, whose absorption across the gut and first pass through the liver spread arrival over an hour or more (Grotenhermen, 2003).

What changes from drug to drug is only the cargo. Cocaine, a stimulant that blocks dopamine reuptake, and the cannabinoids of cannabis, which act at cannabinoid receptors, have different molecular targets and different subjective effects; but each, when smoked, is delivered on the same steep time-course, and each converges on the mesolimbic dopamine pathway that assigns motivational weight to the experience (Volkow et al., 2004; Koob & Volkow, 2016). The grouping by route is therefore not a cognitive accident: it collects the drugs whose addictiveness has been most sharply amplified by the manner of their use.

Types of Non-Tobacco Products Smoking

Within the Medical Subject Headings tree, Smoking, Non-Tobacco Products (D000073847) sits beneath its parent Smoking and has two narrower descriptors of its own, listed in Table 2. Each names the smoking of a specific drug, and each is a child by route rather than by pharmacology: the drugs differ in their molecular action but share the fast pulmonary delivery that the parent category picks out. The two are not exhaustive or mutually exclusive as a taxonomy of drug use—a person may smoke more than one substance, and many smoked drugs have no descriptor of their own—because MeSH is an indexing vocabulary for the literature, not a complete classification of behavior. They are listed here as the curated narrower terms that the vocabulary recognizes.

The two types bracket the argument. Cocaine smoking is the sharp case, where changing only the route transforms a moderately reinforcing stimulant into one of the most addictive forms of any drug (Hatsukami & Fischman, 1996). Marijuana smoking is the common case, where the fast route makes cannabis easy to titrate and more reinforcing than its slow oral form, and where the smoked delivery is also the source of much of the drug's respiratory harm (Hall & Degenhardt, 2009; Volkow et al., 2014). Both are instances of the same principle: the route decides the cognitive grip.

Non-Tobacco Products Smoking and Cognition

Smoking a drug recruits the ordinary machinery of reward learning, attention, and intertemporal choice, but it loads that machinery in a particular way. The shared mesolimbic dopamine pathway responds not to the mere presence of a drug but to the rate at which its concentration climbs; a fast climb produces a large, phasic dopamine signal and a tight association between the act and its reward (Volkow et al., 2004; Dani & Balfour, 2011). Because smoking produces the fastest climb available short of injection, it maximizes that signal whatever the drug it carries.

Table 1 sets the four common routes side by side on the variables that decide a drug's cognitive grip. The pattern is the argument of this article in miniature: the smoked route combines the steepest arrival with easy, repeatable self-dosing, which is why it so reliably produces the most compulsive patterns of use.

The rate hypothesis across drug classes

The central idea is the rate hypothesis: the reinforcing power of a dose depends on how fast it reaches the brain, not merely on how much arrives (Samaha & Robinson, 2005). A sharp concentration spike produces a tight, well-timed pairing between the act of use and the dopaminergic reward signal, strengthening the association that drives future wanting; a slow rise smears that signal across minutes or hours and weakens it (Robinson & Berridge, 1993). The hypothesis is route-general: it is a claim about delivery kinetics, so it holds whatever drug is in the pipe.

This is why smoking is such an effective way to maximize a drug's addictiveness. Of the practical routes, only intravenous injection rivals it for speed, and injection carries a needle, a stigma, and a barrier that smoking does not (Gossop et al., 1992). Smoking offers near-injection speed with none of that friction, plus puff-by-puff control that lets the user keep the brain concentration climbing in repeated steep steps—the pattern that most efficiently drives the shift from casual use to compulsive, habit-governed seeking (Everitt & Robbins, 2005). Demo 1 makes the route selectable for a fixed dose and reads off the time to peak and the steepness of the leading edge.

The crack demonstration

Cocaine supplies the cleanest test the rate hypothesis could ask for, because the same molecule is used by two routes that differ sharply in speed. Snorted as the hydrochloride powder, cocaine is absorbed across the nasal mucosa over minutes; converted to its volatile freebase and smoked as crack, the identical drug reaches the brain in seconds (Hatsukami & Fischman, 1996). Holding the molecule fixed and changing only the route isolates delivery speed from every pharmacological property of the drug itself.

The outcome is unambiguous: across routes of the same drug, the faster the delivery, the more severe the dependence that follows, with smoked and injected use producing markedly greater addiction than intranasal or oral use (Gossop et al., 1992). The crack epidemic was, in effect, a large natural experiment demonstrating the rate hypothesis at the level of populations: a change in the preparation and route of an already-available drug, with no change in the molecule, produced a far more addictive product (Hatsukami & Fischman, 1996). The same reasoning that explains why crack is more addictive than powder explains why smoking is the route of choice for maximizing the grip of many drugs. Demo 2 maps delivery rate onto a reinforcement index and marks the powder and crack cases on the same curve.

Intertemporal choice and quitting

When a person who smokes a drug considers stopping, the decision is an exercise in intertemporal choice: a near-certain immediate loss—the fast, steep reward—set against a delayed, probabilistic gain in health, money, and stability. People dependent on drugs tend to discount delayed rewards steeply, so the distant benefit is heavily devalued against the immediate cost of forgoing the next hit, and the steepness of that discounting tracks the severity of dependence (Volkow & Boyle, 2018). The very feature that makes the smoked route reinforcing—its immediacy—also makes its reward especially hard to trade against a delayed one.

Structured models of behavior change describe quitting as movement through stages—precontemplation, contemplation, preparation, action, maintenance—each with its own cognitive balance of perceived costs and benefits (Prochaska & DiClemente, 1983). Because craving and lapse are driven by momentary cues and states rather than stable traits, they are best captured as they happen, through ecological momentary assessment in the user's own environment (Shiffman et al., 2008). Demo 3 makes the discounting that underlies the quit decision adjustable, showing how a steeper discount rate flips the choice toward the immediate reward.

Cue conditioning and the compulsive habit

The pharmacology sets up the learning, but conditioning sustains it. Under the incentive-sensitization theory, cues paired repeatedly with a drug acquire incentive salience—they come to capture attention and elicit craving, a cue-driven wanting that is dissociable from, and can grow and persist independently of, the liking or pleasure the drug delivers (Berridge & Robinson, 2016). The steep, well-timed reward of a smoked drug is an unusually effective teacher of these associations, because the tight pairing it produces is exactly the condition under which cue learning is strongest.

As use continues, control of the behavior shifts from goal-directed action toward automatic, stimulus-driven habit, and in dependence toward frank compulsion—a transition mirrored in a shift of control from ventral to dorsal striatal circuits (Everitt & Robbins, 2005; Koob & Volkow, 2016). For cannabis specifically, imaging work documents the adaptations in reward and cognitive-control circuitry that accompany heavy use and help explain the craving and difficulty quitting that dependent users report (Zehra et al., 2018). Across drugs, the smoked route is the one that most efficiently installs these learned changes, which is why it so often produces the most entrenched habits.

Worked Example

Two numbers show why the route, not the molecule, governs the cognitive grip. The first is the per-dose steepness that the rate hypothesis says the reward system reads. Treat the brain as a one-compartment system filling toward a peak C_max with a delivery time constant τ, so a dose gives C(t) = C_max(1 − e^−t/τ), and the reinforcing quantity is the initial slope, C_max/τ. Hold the molecule and the eventual peak fixed at C_max = 300 ng/mL, and change only the route for cocaine: smoked as crack, τ ≈ 0.2 min; snorted as powder, τ ≈ 5 min.

- Smoked (crack): 300 / 0.2 = 1500 ng/mL per minute - Snorted (powder): 300 / 5 = 60 ng/mL per minute - Ratio: 1500 / 60 = 25 times the steepness, from the same molecule and the same peak

A twenty-five-fold steeper leading edge, with no change in the drug—the entire difference is the route (Samaha & Robinson, 2005; Hatsukami & Fischman, 1996).

The second number is how fast seconds really is. Peripheral venous blood must return to the right heart, pass through the lungs, and cross the left heart before it reaches the brain; drug absorbed in the lung itself skips the venous leg and the pulmonary transit, entering the arterial side directly. Take a lung-to-brain arterial time of about 11 seconds against an arm-vein-to-brain time of about 16 seconds:

- Smoked, lung to brain: ≈ 11 s - Intravenous, arm to brain: ≈ 16 s - Oral, across gut and liver first: ≈ 45 min = 2700 s

The smoked route is the fastest of all—slightly ahead of an injection and some two hundred times faster than swallowing the same drug (Samaha & Robinson, 2005; Grotenhermen, 2003). The reinforcing kick is a property of that arrival speed, not of the dose. Demo 1 varies the route and reads off both the time to peak and the steepness.

Discussion

Read cognitively, non-tobacco products smoking is the category that makes the route visible by varying it while holding the drug fixed. Its parent, smoking, is usually studied with tobacco, where route and molecule are confounded because nicotine is nearly always smoked. The non-tobacco cases break that confound. Crack and powder cocaine are the same molecule; smoked and oral cannabis are the same cannabinoids; in each pair the smoked form is more reinforcing, and the difference can be attributed to delivery speed rather than to anything about the drug (Hatsukami & Fischman, 1996; Grotenhermen, 2003).

That framing has a sharp implication for how drug harms should be reckoned. Schemes that rank drugs by harm treat the substance as the unit, but the smoking literature shows that the route can move a drug's addictiveness by an order of magnitude (Nutt et al., 2007). Acute toxicity, too, depends on how fast a dose arrives: the same amount delivered as a steep arterial bolus stresses the cardiovascular and central nervous systems far more than a slow oral rise (Gable, 2004). A cognitive account that puts delivery kinetics at the center therefore predicts what the harm data show—that the manner of use, not merely the choice of drug, is a primary determinant of outcome. The lesson generalizes to every route-shifting innovation, from freebasing to vaporizing: whenever a change in preparation speeds a drug's arrival at the brain, it raises that drug's cognitive grip, regardless of marketing category or molecular identity (Koob & Volkow, 2016).

Current Directions

Three fronts are active. The first is brain-imaging work that resolves how route and rate shape the dopamine response and the downstream adaptations of reward and cognitive-control circuitry, extending the crack-era behavioral findings to the level of receptor occupancy and circuit function, and increasingly across drug classes including cannabis (Volkow et al., 2004; Zehra et al., 2018). The second is the application of the rate account to the fast-widening landscape of inhaled and vaporized products: as more drugs are formulated for rapid pulmonary delivery, the same kinetics that made crack more addictive than powder become a recurring regulatory question, sharpening the case for treating route as a first-class variable in abuse-liability assessment (Nutt et al., 2007; Volkow & Boyle, 2018). The third is methodological: ecological momentary assessment is maturing into the standard way to capture craving, cue exposure, and lapse as they unfold in real settings, which is where the cue-conditioning side of the account can be tested rather than inferred (Shiffman et al., 2008). Underlying all three is a deepening neurocircuitry model of how the fast, repeated reward of a smoked drug drives the transition from voluntary use to compulsion (Koob & Volkow, 2016).

Common Misconceptions

How addictive a drug is, is a fixed property of the drug.

Addictiveness depends heavily on the route of administration. The same cocaine molecule is far more addictive smoked as crack than snorted as powder, because the smoked route delivers it to the brain in seconds rather than minutes (Hatsukami & Fischman, 1996; Gossop et al., 1992).

Smoking a drug is just a less serious way of using it than injecting.

Smoking rivals intravenous injection for speed of delivery to the brain, and can even exceed it, because drug absorbed in the lung reaches the arterial side directly. Its reinforcing power is correspondingly high; the absence of a needle lowers the barrier to use, not the addictiveness (Samaha & Robinson, 2005).

If the total dose is the same, the method of taking it does not matter.

The rate hypothesis holds that reinforcement scales with how fast the dose arrives, not just with how much. The same dose delivered as a steep smoked spike is far more reinforcing—and more acutely toxic—than the same amount taken slowly by mouth (Robinson & Berridge, 1993; Gable, 2004).

Smoked cannabis and an edible are interchangeable because the drug is the same.

The cannabinoids are the same, but the kinetics are not. Smoking delivers THC within minutes and allows puff-by-puff titration; an edible is delayed by an hour or more and is hard to adjust, so the two produce different patterns of effect and of reinforcement (Grotenhermen, 2003; Volkow et al., 2014).

Glossary

Addiction.

A disorder of compulsive drug seeking and use maintained by learned changes in reward, attention, and motivation; its severity depends heavily on the route and rate of drug delivery.

Arterial bolus.

A concentrated slug of drug delivered to the arterial blood and carried to the brain in a single circulation; smoking produces one because the drug is absorbed directly in the lungs.

Crack cocaine.

The smokable freebase form of cocaine; chemically the same drug as powder cocaine, but delivered by a far faster route and so markedly more reinforcing.

Craving.

An intense, often cue-triggered desire to use a drug; in incentive-sensitization theory it is the subjective face of sensitized wanting.

Delay discounting.

The decline in the subjective value of a reward as its delivery is postponed; steep discounting devalues the delayed benefits of quitting against the immediate reward of use.

Freebase.

The un-ionized, volatile form of a drug that can be vaporized and smoked; converting cocaine hydrochloride to freebase is what makes it smokable as crack.

Incentive salience.

The motivational property—wanting—that a reward and its cues acquire through conditioning, making them attractive and able to command attention independently of pleasure.

Lipophilic.

Fat-soluble; a property that lets a drug cross the lung membrane and the blood–brain barrier quickly, which is what makes fast smoked delivery possible.

Mesolimbic dopamine pathway.

The midbrain-to-striatum projection that signals reward and assigns motivational weight to experiences; its phasic response is largest when a drug arrives fast.

Pulmonary absorption.

Uptake of a drug across the large surface of the lungs; fast and efficient, delivering an arterial bolus to the brain within seconds, as in smoking any volatile drug.

Rate hypothesis.

The proposal that the reinforcing power of a drug dose scales with how quickly it reaches the brain, not just with the peak concentration; it explains why the smoked route is so addictive across drug classes.

Reinforcement.

The strengthening of a behavior by its consequences; drug use is reinforced by the reward its delivery produces and, as dependence forms, by relief of withdrawal.

Route of administration.

The path by which a drug enters the body—smoked, injected, snorted, or swallowed; it sets the speed of arrival at the brain and so, under the rate hypothesis, the strength of reinforcement.

Self-titration.

Adjusting the dose moment to moment to reach a desired effect; the puff-by-puff control of smoking makes fine self-titration possible, which the slow oral route does not.

Key Researchers

Kent C. Berridge

(Department of Psychology, University of Michigan). A co-originator of the incentive-sensitization theory of addiction, whose dissociation of wanting from liking explains how drug cues come to drive craving independently of pleasure. Faculty · Google Scholar · Wikipedia

Wayne Hall

(National Centre for Youth Substance Use Research, University of Queensland). An addiction epidemiologist whose syntheses of the adverse health effects of cannabis frame the harms of the most widely smoked non-tobacco drug. Faculty · ORCID · Google Scholar · Wikipedia

Dorothy K. Hatsukami

(Department of Psychiatry and Behavioral Sciences, University of Minnesota). An addiction researcher whose canonical review of crack versus cocaine hydrochloride established that route, not molecule, drives the difference in their addictiveness. Faculty

George F. Koob

(National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health). An addiction neuroscientist whose neurocircuitry analysis maps the transition from impulsive use to compulsive seeking across drug classes. Faculty · Google Scholar · Wikipedia

Terry E. Robinson

(Department of Psychology, University of Michigan). A co-originator of the incentive-sensitization theory and author, with Samaha, of the rate account of why rapid drug delivery promotes addiction. Faculty · ORCID · Google Scholar · Wikipedia

Nora D. Volkow

(National Institute on Drug Abuse, National Institutes of Health). The director of NIDA and a pioneer of addiction brain imaging, whose work shows how fast drug delivery shapes the dopamine response and the circuitry of compulsion. Faculty · Wikipedia

Frequently Asked Questions

What counts as non-tobacco products smoking?

It is the smoking or inhaling of a psychoactive drug other than tobacco. The Medical Subject Headings vocabulary files two specific types beneath it, cocaine smoking (crack) and marijuana smoking, but the category is really about the method, inhaling a volatilized drug, rather than about any single substance.

Why does the route of administration matter so much?

Because reinforcement depends on how fast a drug reaches the brain, not just on how much. Smoking carries a drug across the lungs into the arterial blood and to the brain in seconds, producing a steep concentration spike that the reward system reads as a strong signal. The same dose taken slowly by mouth is far less reinforcing.

Why is crack more addictive than powder cocaine if it is the same drug?

It is the same molecule delivered by a faster route. Snorted powder is absorbed over minutes; crack, the volatile freebase, is smoked and reaches the brain in seconds. The faster arrival produces a sharper, more strongly reinforcing spike, which is why the smoked form is markedly more addictive.

Is smoking a drug really as fast as injecting it?

Yes, and sometimes faster. A drug absorbed in the lungs enters the arterial side of the circulation directly, whereas a peripheral injection must first return through the right heart and the lungs. Both reach the brain in well under half a minute, far ahead of oral use.

What is the rate hypothesis?

It is the proposal that the reinforcing power of a drug dose scales with how quickly it reaches the brain, not merely with the peak amount. A sharp spike pairs tightly with the brain's reward signal; a slow rise smears that signal and weakens the learned association. It is a claim about delivery kinetics, so it applies to any smoked drug.

Does the drug being smoked change the cognitive account?

The molecular target differs (cocaine blocks dopamine reuptake, cannabinoids act at cannabinoid receptors), but the delivery kinetics and the shared reward circuitry do not. Whatever the drug, the smoked route gives it a fast, steep arrival and recruits the same mesolimbic dopamine pathway, so the same rate-based account holds.

Is smoked cannabis different from an edible?

In kinetics, yes. Smoking delivers THC within minutes and lets the user adjust the dose puff by puff; an edible is delayed by an hour or more and is hard to titrate. The cannabinoids are the same, but the faster, controllable smoked route is more reinforcing and produces a different pattern of use.

Why is quitting a smoked drug so hard?

The immediacy that makes the smoked reward strong also makes it hard to trade against a delayed benefit. Dependent users discount delayed rewards steeply, so the distant gains of quitting are heavily devalued against the immediate hit, and cue-driven craving, learned through the tight pairing the fast route produces, pulls toward relapse.

References

Berridge, K. C., & Robinson, T. E. (2016). Liking, wanting, and the incentive-sensitization theory of addiction. American Psychologist, 71(8), 670–679. https://doi.org/10.1037/amp0000059

Dani, J. A., & Balfour, D. J. K. (2011). Historical and current perspective on tobacco use and nicotine addiction. Trends in Neurosciences, 34(7), 383–392. https://doi.org/10.1016/j.tins.2011.05.001

Everitt, B. J., & Robbins, T. W. (2005). Neural systems of reinforcement for drug addiction: From actions to habits to compulsion. Nature Neuroscience, 8(11), 1481–1489. https://doi.org/10.1038/nn1579

Gable, R. S. (2004). Comparison of acute lethal toxicity of commonly abused psychoactive substances. Addiction, 99(6), 686–696. https://doi.org/10.1111/j.1360-0443.2004.00744.x

Gossop, M., Griffiths, P., Powis, B., & Strang, J. (1992). Severity of dependence and route of administration of heroin, cocaine and amphetamines. British Journal of Addiction, 87(11), 1527–1536. https://doi.org/10.1111/j.1360-0443.1992.tb02660.x

Grotenhermen, F. (2003). Pharmacokinetics and pharmacodynamics of cannabinoids. Clinical Pharmacokinetics, 42(4), 327–360. https://doi.org/10.2165/00003088-200342040-00003

Hall, W., & Degenhardt, L. (2009). Adverse health effects of non-medical cannabis use. The Lancet, 374(9698), 1383–1391. https://doi.org/10.1016/S0140-6736(09)61037-0

Hatsukami, D. K., & Fischman, M. W. (1996). Crack cocaine and cocaine hydrochloride: Are the differences myth or reality? JAMA, 276(19), 1580–1588. https://doi.org/10.1001/jama.1996.03540190052029

Koob, G. F., & Volkow, N. D. (2016). Neurobiology of addiction: A neurocircuitry analysis. The Lancet Psychiatry, 3(8), 760–773. https://doi.org/10.1016/S2215-0366(16)00104-8

Nutt, D., King, L. A., Saulsbury, W., & Blakemore, C. (2007). Development of a rational scale to assess the harm of drugs of potential misuse. The Lancet, 369(9566), 1047–1053. https://doi.org/10.1016/S0140-6736(07)60464-4

Prochaska, J. O., & DiClemente, C. C. (1983). Stages and processes of self-change of smoking: Toward an integrative model of change. Journal of Consulting and Clinical Psychology, 51(3), 390–395. https://doi.org/10.1037/0022-006X.51.3.390

Robinson, T. E., & Berridge, K. C. (1993). The neural basis of drug craving: An incentive-sensitization theory of addiction. Brain Research Reviews, 18(3), 247–291. https://doi.org/10.1016/0165-0173(93)90013-P

Samaha, A.-N., & Robinson, T. E. (2005). Why does the rapid delivery of drugs to the brain promote addiction? Trends in Pharmacological Sciences, 26(2), 82–87. https://doi.org/10.1016/j.tips.2004.12.007

Shiffman, S., Stone, A. A., & Hufford, M. R. (2008). Ecological momentary assessment. Annual Review of Clinical Psychology, 4, 1–32. https://doi.org/10.1146/annurev.clinpsy.3.022806.091415

Volkow, N. D., Fowler, J. S., & Wang, G.-J. (2004). The addicted human brain viewed in the light of imaging studies: Brain circuits and treatment strategies. Neuropharmacology, 47(Suppl 1), 3–13. https://doi.org/10.1016/j.neuropharm.2004.07.019

Volkow, N. D., Baler, R. D., Compton, W. M., & Weiss, S. R. B. (2014). Adverse health effects of marijuana use. New England Journal of Medicine, 370(23), 2219–2227. https://doi.org/10.1056/NEJMra1402309

Volkow, N. D., & Boyle, M. (2018). Neuroscience of addiction: Relevance to prevention and treatment. American Journal of Psychiatry, 175(8), 729–740. https://doi.org/10.1176/appi.ajp.2018.17101174

Zehra, A., Burns, J., Liu, C. K., Manza, P., Wiers, C. E., Volkow, N. D., & Wang, G.-J. (2018). Cannabis addiction and the brain: A review. Journal of Neuroimmune Pharmacology, 13(4), 438–452. https://doi.org/10.1007/s11481-018-9782-9