Cocaine Smoking

Abstract

Cocaine smoking is a type of non-tobacco products smoking: the inhaling of vaporized cocaine freebase, or crack, which carries the same molecule as snorted powder but reaches the brain within seconds. It is the decisive natural experiment in the psychology of addiction, holding the drug fixed and varying only the route of administration. Under the rate hypothesis, the reinforcing power of a dose scales with how fast it reaches the brain, so the near-vertical arrival of smoked cocaine pairs tightly with the dopamine reward signal and makes crack far more addictive than the identical dose snorted. Cocaine blocks the dopamine transporter, and imaging shows the subjective high tracks the speed of that blockade, not its eventual level. Three interactive demonstrations trace crack-versus-powder delivery, the rate-dependence of transporter occupancy, and the mapping from delivery speed to reinforcement.

Keywords: cocaine, crack, route of administration, rate hypothesis, dopamine transporter

Cocaine smoking is the sharpest case the psychology of addiction has to offer, because it isolates the one variable that most other comparisons confound. Powder cocaine and crack are the same molecule with the same pharmacological target; what differs is only the speed at which the drug reaches the brain (Hatsukami & Fischman, 1996). Holding the drug fixed and changing only the route turns a question about chemistry into a question about kinetics, and the answer is unambiguous: the faster route is far more addictive (Gossop et al., 1992).

That is why cocaine smoking sits at the center of the cognitive account of drug reward. The reward system does not read the mere presence of a drug; it reads the rate at which the drug's concentration climbs, and smoking produces the steepest climb available short of injection (Samaha & Robinson, 2005). Smoked cocaine therefore maximizes the phasic dopamine signal that drives learning and wanting, which is the mechanism this article traces from the chemistry of the freebase to the compulsive habit it so efficiently installs (Robinson & Berridge, 1993).

What Cocaine Smoking Is

Cocaine smoking is the practice of inhaling the vapor of cocaine freebase. In the Medical Subject Headings vocabulary, Cocaine Smoking (D000074101) is filed directly beneath Smoking, Non-Tobacco Products (D000073847), its parent category, which in turn sits beneath Smoking itself. MeSH is an indexing classification for retrieving the biomedical literature, not a theory of behavior, and it groups the practice by what the user does rather than by the pharmacology of the 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 drug is the same in either form. Cocaine is a stimulant that blocks the reuptake of dopamine, raising its concentration in the synapses of the reward pathway (Volkow et al., 1997). What changes between powder and crack is not the molecule but its physical form and the speed with which it can be delivered. Cocaine hydrochloride, the water-soluble salt, is a powder that is snorted or dissolved and injected; it decomposes at the temperatures needed to vaporize it, so it cannot usefully be smoked. Converting it to the un-ionized freebase yields a compound that vaporizes before it burns, and that vapor, inhaled, carries the cocaine across the lungs into the arterial blood and to the brain in a single circulation time (Cone, 1995).

That difference in route, not any difference in the drug, is the whole of the cognitive story. Snorted powder is absorbed across the nasal mucosa over several minutes; smoked freebase reaches the brain in seconds, producing the steep concentration spike that the reward system reads as a strong signal (Samaha & Robinson, 2005). The sections that follow treat cocaine smoking as the clean experiment that it is, and read off from it a general lesson about how the manner of use, not merely the choice of drug, governs the grip of a drug on cognition and behavior.

Cocaine Smoking and Cognition

Smoking cocaine 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 presence of cocaine but to the rate at which its action climbs; a fast climb produces a large, phasic dopamine signal and a tight association between the act and its reward (Volkow et al., 2004; Hyman et al., 2006). Because smoking produces the fastest climb available short of injection, it maximizes that signal for a drug whose molecular target is already one of the most directly rewarding known.

Table 1 sets crack and powder side by side on the variables that decide a drug's cognitive grip. The two columns hold the molecule constant and vary only the route; the pattern across the rows is the argument of this article in miniature.

The rate hypothesis and the cocaine high

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 and weakens it (Robinson & Berridge, 1993). Cocaine is the cleanest test the hypothesis could ask for, because the identical molecule is used by two routes that differ sharply in speed, so delivery kinetics can be varied with the pharmacology held perfectly constant.

The outcome of that experiment is decisive. Across routes of the same drug, the faster the delivery, the more severe the dependence that follows, with smoked and injected cocaine producing markedly greater addiction than intranasal 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). Demo 1 makes the route selectable for a fixed cocaine dose and reads off the time to peak and the steepness of the leading edge.

Freebase chemistry: why crack can be smoked

The route is available only because of a chemical fact. Cocaine hydrochloride, the salt sold as powder, is water-soluble and melts at a high temperature at which the cocaine molecule itself decomposes; heating the powder destroys the drug before it can vaporize, so there is nothing useful to inhale. Treating the salt with a base frees the un-ionized cocaine, the freebase, which is volatile and vaporizes at a far lower temperature, well below the point of decomposition (Cone, 1995). The vapor can then be inhaled and absorbed across the lungs.

Crack is simply the freebase prepared with baking soda into a smokable solid, named for the sound it makes when heated. The chemistry matters cognitively only because it unlocks the fast route: the freebase conversion changes nothing about how cocaine acts in the brain, only whether the drug can be delivered by the steep pulmonary path that the rate hypothesis identifies as the most reinforcing (Hatsukami & Fischman, 1996). The same reasoning applies to every route-shifting innovation in which a change of preparation speeds a drug's arrival without altering the molecule.

Dopamine-transporter blockade and the speed of the high

Cocaine's molecular action is to block the dopamine transporter, the protein that clears dopamine from the synapse; with the transporter blocked, dopamine accumulates and the reward signal is amplified (Volkow et al., 1997). Positron-emission-tomography studies that labeled the transporter directly established two things. First, a cocaine high requires blocking a large fraction of the available transporters, on the order of half or more. Second, and decisively for the cognitive account, the intensity of the subjective high tracks not the eventual level of blockade but the rate at which the blockade is achieved: the faster the transporter is occupied, the bigger the high for the same final occupancy (Volkow et al., 1997).

This is the molecular face of the rate hypothesis. The smoked route occupies the transporter almost as fast as the drug can be delivered, producing a sharp rise in synaptic dopamine and a correspondingly intense rush; the snorted route reaches a similar occupancy slowly, and the slow rise yields a milder high despite comparable eventual blockade (Volkow et al., 2004). The reward is a property of the derivative, the speed of change, not of the steady state. Beyond this acute dopamine signal, repeated cocaine exposure drives broader adaptations across reward and cognitive-control circuitry that outlast any single dose (Volkow et al., 2011). Demo 2 lets the delivery speed be varied and shows transporter occupancy climbing against the subjective high it produces.

Incentive sensitization and the compulsive habit

The pharmacology sets up the learning, but conditioning sustains it. Under the incentive-sensitization theory, cues paired repeatedly with cocaine 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 smoked cocaine is an unusually effective teacher of these associations, because the tight pairing it produces is exactly the condition under which cue learning is strongest (Hyman et al., 2006).

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). The neurocircuitry analysis of addiction describes this as a cycle of binge and intoxication, withdrawal and negative affect, and preoccupation and anticipation, each stage recruiting its own circuitry and each deepened by the fast, repeated reward that the smoked route supplies (Koob & Volkow, 2016). Smoked cocaine is the route that most efficiently installs these learned changes, which is why it so reliably produces the most entrenched patterns of use.

Intertemporal choice and quitting

When a person who smokes cocaine considers stopping, the decision is an exercise in intertemporal choice: a near-certain immediate loss, the fast and intense reward, set against a delayed and probabilistic gain in health, money, and stability. People dependent on stimulants 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 immediacy that makes the smoked route reinforcing also makes its reward especially hard to trade against a delayed one.

Quitting is correspondingly hard, and the difficulty is compounded by a treatment gap. Structured models describe behavior change as movement through stages, each with its own balance of perceived costs and benefits (Prochaska & DiClemente, 1983), and 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). Unlike opioid or nicotine dependence, cocaine use disorder has no medication approved to treat it; the evidence base rests on behavioral treatments such as contingency management, with pharmacotherapy still an open research problem (Kampman, 2019).

Worked Example

Two numbers show why the route, not the molecule, governs the cognitive grip of cocaine. 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: 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 much faster seconds is than minutes. Drug absorbed in the lung enters the arterial side of the circulation directly and reaches the brain in a single circulation time; drug snorted must cross the nasal mucosa slowly before any of it is carried centrally. Take a lung-to-brain time of about 11 seconds for the smoked route against about 240 seconds for the snorted route to begin delivering centrally:

- Smoked, lung to brain: ≈ 11 s - Snorted, across the nasal mucosa: ≈ 240 s (4 min) - Ratio: 240 / 11 ≈ 22 times faster to the brain

The intense rush of crack is a property of that arrival speed, not of the dose (Cone, 1995; Volkow et al., 1997). Demo 3 maps the delivery slope onto a reinforcement index and marks the crack and powder cases on the same curve.

Discussion

Read cognitively, cocaine smoking is the experiment that makes the route of administration visible by varying it while holding the drug perfectly fixed. Most comparisons between drugs confound molecule and route; cocaine does not, because crack and powder are the same cocaine and differ only in how fast they arrive (Hatsukami & Fischman, 1996). The result is that a moderately reinforcing stimulant becomes, by a change of preparation alone, one of the most addictive forms of any drug, and the cognitive account attributes that shift entirely to delivery kinetics and the phasic dopamine signal they produce (Volkow et al., 1997; Robinson & Berridge, 1993).

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 cocaine case shows that the route can move a drug's addictiveness by a large factor (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 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 is a primary determinant of outcome, and it generalizes beyond cocaine: whenever a change in preparation speeds a drug's arrival at the brain, it raises that drug's cognitive grip regardless of 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 to the changes that outlast acute intoxication (Volkow et al., 2011; Volkow et al., 2004). The second is the search for a pharmacotherapy: cocaine use disorder remains without an approved medication, and current work tests immunotherapies, dopamine-system modulators, and the consolidation of contingency management as the behavioral standard against which any drug must prove itself (Kampman, 2019; 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; Hyman et al., 2006).

Common Misconceptions

Crack is a different, more dangerous drug than powder cocaine.

Crack is the same cocaine molecule as powder, in its freebase form. What makes it more addictive is the route: smoked freebase reaches the brain in seconds, where snorted powder takes minutes, and the faster arrival produces a sharper, more reinforcing spike (Hatsukami & Fischman, 1996; Cone, 1995).

The cocaine high depends simply on how much dopamine is freed.

Imaging shows the subjective high tracks the rate at which the dopamine transporter is occupied, not merely the eventual level of occupancy. A fast rise to a given blockade produces a big high; a slow rise to the same blockade produces a mild one (Volkow et al., 1997).

If the dose is the same, snorting and smoking are equivalent.

The rate hypothesis holds that reinforcement scales with how fast the dose arrives, not just with how much. The same cocaine delivered as a steep smoked spike is far more reinforcing, and more acutely toxic, than the same amount snorted slowly (Samaha & Robinson, 2005; Gable, 2004).

There is a medication for cocaine addiction as there is for opioids.

There is not. No pharmacotherapy is approved for cocaine use disorder; the evidence base rests on behavioral treatments such as contingency management, and an effective medication remains an open research problem (Kampman, 2019).

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.

Contingency management.

A behavioral treatment that reinforces verified abstinence with tangible rewards; it is the best-supported intervention for cocaine use disorder in the absence of an approved medication.

Crack cocaine.

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

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.

Dopamine transporter.

The protein that clears dopamine from the synapse; cocaine blocks it, raising synaptic dopamine, and the speed of that blockade sets the intensity of the high.

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.

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 smoked cocaine is so much more addictive than snorted.

Reinforcement.

The strengthening of a behavior by its consequences; cocaine use is reinforced by the reward its delivery produces, most strongly when that delivery is fast.

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.

Transporter occupancy.

The fraction of dopamine transporters blocked by cocaine, measured by positron emission tomography; a cocaine high requires high occupancy, but its intensity tracks the speed of occupancy.

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 cocaine cues come to drive craving independently of pleasure. Faculty · 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

Eric J. Nestler

(Nash Family Department of Neuroscience, Icahn School of Medicine at Mount Sinai). A molecular neuroscientist of addiction whose synthesis of reward-related learning and memory links cocaine's acute dopamine action to the lasting changes that sustain compulsive use. Faculty · 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 the rapid delivery of cocaine to the brain 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 transporter-occupancy studies showed that the cocaine high tracks the speed of dopamine-transporter blockade. Faculty · Wikipedia

Frequently Asked Questions

What is cocaine smoking?

It is the inhaling of vaporized cocaine freebase, known as crack. The Medical Subject Headings vocabulary files it beneath non-tobacco products smoking, because the category is defined by the method, inhaling a volatilized drug, rather than by any property unique to the drug.

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 across the nasal mucosa 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.

Why can crack be smoked when powder cannot?

Powder cocaine is the hydrochloride salt, which decomposes at the temperature needed to vaporize it, so heating it destroys the drug. Converting it to the freebase yields a compound that vaporizes at a much lower temperature, below the point of decomposition, so the vapor can be inhaled and absorbed in the lungs.

How does cocaine act in the brain?

Cocaine blocks the dopamine transporter, the protein that normally clears dopamine from the synapse. With the transporter blocked, dopamine accumulates in the reward pathway and its signal is amplified, which is read as reward and drives the learning that underlies addiction.

Why does a faster route produce a bigger high?

Imaging shows the subjective high tracks the rate at which the dopamine transporter is occupied, not just the final level of occupancy. Smoking occupies the transporter almost as fast as the drug arrives, producing a sharp dopamine rise and an intense rush, where the slow rise of snorting yields a milder high at comparable occupancy.

What is the rate hypothesis?

It is the proposal that the reinforcing power of a 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. Cocaine is its cleanest test, because the same molecule can be delivered fast or slow.

Is there a medication to treat cocaine addiction?

No medication is approved for cocaine use disorder, unlike opioid or nicotine dependence. Treatment rests on behavioral approaches, especially contingency management, which rewards verified abstinence, while an effective pharmacotherapy remains an active research problem.

Why is smoked cocaine so hard to quit?

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

Cone, E. J. (1995). Pharmacokinetics and pharmacodynamics of cocaine. Journal of Analytical Toxicology, 19(6), 459–478. https://doi.org/10.1093/jat/19.6.459

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

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

Hyman, S. E., Malenka, R. C., & Nestler, E. J. (2006). Neural mechanisms of addiction: The role of reward-related learning and memory. Annual Review of Neuroscience, 29, 565–598. https://doi.org/10.1146/annurev.neuro.29.051605.113009

Kampman, K. M. (2019). The treatment of cocaine use disorder. Science Advances, 5(10), eaax1532. https://doi.org/10.1126/sciadv.aax1532

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., Wang, G.-J., Fischman, M. W., Foltin, R. W., Fowler, J. S., Abumrad, N. N., Vitkun, S., Logan, J., Gatley, S. J., Pappas, N., Hitzemann, R., & Shea, C. E. (1997). Relationship between subjective effects of cocaine and dopamine transporter occupancy. Nature, 386(6627), 827–830. https://doi.org/10.1038/386827a0

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., Wang, G.-J., Fowler, J. S., Tomasi, D., & Telang, F. (2011). Addiction: Beyond dopamine reward circuitry. Proceedings of the National Academy of Sciences, 108(37), 15037–15042. https://doi.org/10.1073/pnas.1010654108

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