Neuroscience: The Brain in Addiction and Recovery

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    Takeaways

    • Alcohol is dually reinforcing because it can both activate the brain’s reward processing system that mediates pleasure and reduce the activity of the brain’s systems that mediate negative emotional states such as stress, anxiety, and emotional pain.
    • Repeated, excessive use of alcohol can lead to the development of addiction, which is associated with reduced reward function and increased activation of brain stress systems. The process of becoming addicted is thus accompanied by a shift in drinking motivation from positive reinforcement to negative reinforcement, during which drinking is motivated by attempts to reduce the emotional discomfort of acute and protracted withdrawal.
    • Addiction and its associated brain changes can be understood as a three-stage cycle involving binge/intoxication, withdrawal/negative affect, and preoccupation/anticipation.
    • The adaptability, or plasticity, of the brain is central to the development of addiction, to the effectiveness of evidence-based treatments, and to the neurological and psychological improvements in recovery.

    The plasticity of the human brain contributes to both the development of and recovery from alcohol use disorder (AUD). Within the brain, individual genetic and environmental factors interact at molecular, neuronal, and circuit levels to influence a person’s vulnerability to AUD.1,2 Thus, each person’s path to AUD is shaped by a unique set of variables, and as a result, different people will have different levels of severity and types of dysfunction that may require different treatment approaches.3

    Alcohol produces chemical imbalances in specific neurocircuits and can be neurotoxic. Chronic heavy drinking can, for example, damage brain regions involved in memory, decision-making, impulse control, attention, sleep regulation, and other cognitive functions.4,5 Once AUD develops and progresses, these and other brain changes can make it very difficult to stop drinking without assistance.1

    Here, we outline a framework for understanding alcohol-induced changes in the brain, which can help you appreciate the challenges faced by many patients with AUD when they try to cut back or quit drinking. We then describe evidence-based treatments you can recommend to patients to help the brain, and the patient as a whole, to recover.

    A note on drinking level terms in this Core article: Binge drinking brings a person’s blood alcohol concentration to 0.08 percent or more, which typically happens if a woman has 4 or more drinks, or a man has 5 or more drinks, within about 2 hours. Heavy drinking includes binge drinking and has been defined for women as 4 or more drinks on any day or 8 or more per week, and for men as 5 or more drinks on any day or 15 or more per week.

    How does the brain change as AUD develops?

    The brain mediates our motivation to repeat behaviors that lead to pleasurable, rewarding states or reduce uncomfortable, distressing physical or emotional states. In this context, drinking alcohol can be motivated by its ability to provide both relief from aversive states and reward. These dual, powerful reinforcing effects help explain why some people drink and why some people use alcohol to excess. With repeated heavy drinking, however, tolerance develops and the ability of alcohol to produce pleasure and relieve discomfort decreases.

    During acute and protracted withdrawal, a profound negative emotional state evolves, termed hyperkatifeia (hyper-kuh-TEE-fee-uh). Hyperkatifeia is defined as a hypersensitive negative emotional state comprised of symptoms such as dysphoria, malaise, irritability, pain, and sleep disturbances.6 Heavy drinking may also produce deficits in executive function that contribute to symptoms such as impulsivity, compulsivity, impaired cognitive function, and impaired decision making. These brain changes related to excessive alcohol use underlie many AUD symptoms.

    Below is a brief overview of the current knowledge of the brain structures and circuitry involved in the cycle of alcohol addiction,1 which aligns symptomatically with moderate to severe AUD.7 (The current AUD diagnostic criteria are listed in the Core articles on AUD and assessment.)

    • Alcohol produces pleasure. Alcohol produces pleasurable or rewarding effects by increasing activity in brain systems related to reward processing. In the basal ganglia, activation of opioid receptors in the nucleus accumbens may be responsible for some of the pleasure associated with alcohol intoxication (see Figure 1). In addition, alcohol causes the ventral tegmental area to send dopamine signals to the nucleus accumbens. Dopamine is critical for learning to associate alcohol and its related “cues”—people, places, or things—with the rewarding effects of alcohol. This learning process can lead to “incentive salience,” a motivation for reward that is driven by both a person’s current physiological state and previously learned associations between cues and the reward. Some people are initially drawn to alcohol more for its rewarding effects, while others seek it largely to alleviate physical or emotional discomfort, as detailed next.
    • Habit formation makes it harder to stop drinking. When drinking behavior patterns are repeated, the brain shifts control over the sequence of actions involved in drinking from conscious control via the prefrontal cortex to habit formation using the basal ganglia. This transition from incentive salience toward habitual responding, mediated by changes in brain circuitry, can make it more likely that someone will continue their drinking pattern and harder for them to stop.
    • Alcohol initially reduces, then promotes negative emotional states and pain. Alcohol may temporarily reduce negative emotional states in part by dampening activity in the extended amygdala. This brain structure mediates the fight or flight stress response and helps us learn to associate certain cues with danger or threat. Neurons interacting within the extended amygdala release stress-related neurotransmitters such as corticotropin releasing factor and dynorphin, which in turn influence other brain areas involved in stress responses, including the hypothalamus and brain stem structures.

    Although alcohol initially suppresses activity in the extended amygdala and reduces stress responses, excessive alcohol use can lead to tolerance and the need to drink more to find relief. After drinking stops, during withdrawal, the amygdala circuits become hyperactive, leading to hyperkatifeia, or heightened negative emotional states, such as irritability, anxiety, dysphoria, and emotional pain. This discomfort, often described as misery, can motivate some people to drink alcohol again and repeat the cycle of drinking and withdrawal. Research suggests that among people with negative emotional states, self-medication with alcohol to help cope with mood symptoms increases the risk for developing AUD.8

    Like its effects on emotional pain, alcohol can temporarily reduce physical pain. Research suggests that reduction of pain only occurs at or above binge levels of drinking (reaching a blood alcohol concentration of 0.08% or above, typically after 4 or more drinks for women and 5 or more drinks for men within about 2 hours).9,10 As blood alcohol concentrations decrease, however, the sensation of pain returns even more intensely. This again leads to a cycle of misregulation,11 that is, using a “solution” that ultimately makes the problem worse. The discomfort or misery felt during withdrawal, including negative emotional states, is the leading precipitant of relapses in patients recovering from AUD.12,13

    • The brain becomes motivated to continue drinking. As noted earlier, negative emotional states or hyperkatifeia, can persist into protracted withdrawal and are a major driver for relapse in AUD.14 Also, the powerful effects of alcohol on neurocircuits relating to reward and relief cause the brain to attach strong motivational value or incentive salience to the cues associated with alcohol, whether in the immediate environment or recalled from memory. These environmental stimuli, or thoughts of them, can prompt a return to alcohol seeking via connections made between the prefrontal cortex and the basal ganglia using the neurotransmitter glutamate. Especially when combined with negative emotional or physical states, the sight or thought of alcohol or related cues can trigger cravings, or the urge to drink.
    • Executive function becomes dysregulated. Alcohol disrupts function in the prefrontal cortical areas involved in executive function, impulse control, decision-making, and emotional regulation.1 These functional deficits make it harder to withstand urges and avoid repeating the behaviors related to the addiction cycle, particularly in the face of stress and physical and emotional discomfort.1 In severe cases, impairments in prefrontal cortical function can persist despite months to years of abstinence, making it particularly difficult to recover from or compensate for deficits in executive function.15

    Figure 1. Conceptual framework for the neurobiological bases of addiction (and the brain areas involved)

    Addiction can be described as a repeating three-stage cycle, with each stage associated with different brain regions, neurocircuits, and neurotransmitters.1 Drawn from decades of research, this cycle models processes that people with addiction may experience repeatedly over the course of a day, weeks, or months.1,16,17

    Image
    Three Stages of the Addiction Cycle, Brain Regions Associated with Addiction, the basal ganglia is associated with the binge intoxication stage, the extended amygdala is associated with the withdrawal negative affect stage, the prefrontal cortex is associated with the preoccupation anticipation stage.

    The binge/intoxication stage (associated with circuits in the basal ganglia): The person drinks alcohol, which activates reward circuits and engages “incentive salience” circuits. Incentive salience circuits link the pleasurable, rewarding experience with “cues,” that is, the people, places, and things present when drinking, such that the cues themselves gain motivational significance. These and other neurocircuits help develop and strengthen habitual drinking and may lay the groundwork for compulsive use of alcohol. Neurotransmitters associated with this stage include dopamine, GABA, glutamate, and opioid peptides.

    The withdrawal/negative affect stage (associated with circuits in the extended amygdala): When the person stops drinking, reward circuit activity decreases while stress circuits activate. Together, these changes fuel negative emotional states such as anxiety, dysphoria, and irritability. The person feels alcohol is needed for temporary relief from discomfort and emotional pain. This stage involves (1) the loss of reward neurotransmitters—as in a hypodopaminergic state, (2) the activation of stress neurotransmitters—such as corticotropin releasing factor, dynorphin, norepinephrine, hypocretin, and vasopressin—and possibly proinflammatory immune agents, and (3) the inhibition of anti-stress neurotransmitters—such as neuropeptide Y, nociceptin, endocannabinoids, and oxytocin.

    The preoccupation/anticipation stage (associated with circuits in the prefrontal cortex): The person with an addiction has impairments in executive function processes that normally limit impulsive and compulsive responses. The person has strong urges or cravings to drink, especially in response to stress, related negative emotions, and cues that are part of the incentive salience circuits activated in the first stage of the cycle. Neurotransmitters associated with this stage include glutamate and ghrelin.

    While people who drink heavily often enter the addiction cycle via the binge/intoxication stage, they can also enter via the withdrawal/negative affect stage (by attempting, for example, to self-medicate physical or emotional pain), or the preoccupation/anticipation stage (by attempting, for example, to self-medicate a high impulsivity condition).

    For more information, see this seven-minute video on the Neurocircuitry of AUD.

    What do healthcare professionals who work with adolescents need to know about alcohol?

    The developing adolescent brain is particularly vulnerable to alcohol-related harm. Alcohol is a powerful reinforcer in adolescents because the brain’s reward system is fully developed while the executive function system is not, and because there is a powerful social aspect to adolescent drinking. Specifically, prefrontal regions involved in executive functions and their connections to other brain regions are not fully developed in adolescents, which may make it harder for them to regulate the motivation to drink. Because the brain is adaptable and learns quickly during adolescence, and because alcohol is such a strong reinforcer for adolescents, alcohol use is more likely to be repeated, become a habit, and eventually evolve into a problematic drinking pattern that may lead to AUD.

    When adolescents drink heavily, alcohol can disrupt critical brain development patterns18,19 by accelerating the volume decline in frontal cortical gray matter that typically occurs in early adolescence and by slowing the volume increase in white matter that typically occurs in late adolescence.20 In addition, heavy drinking in adolescence increases the risk for developing AUD later in life, with the earlier the onset of any drinking, the greater the AUD risk.21,22

    In short, alcohol use during adolescence can interfere with structural and functional brain development and increase the risk for AUD not only during adolescence but also into adulthood. To help clinicians prevent alcohol-related harm in adolescents, NIAAA developed a quick and effective screening tool and a clinician’s guide (see Resources below).

    How does the brain recover?

    Just as brain plasticity contributes to the development of AUD, it can be harnessed to help the brain heal and to establish healthy behavior patterns that facilitate recovery. The extent of the brain’s capacity to return to “normal” following long-term sobriety is not fully understood.23 However, a growing number of studies indicate that at least some AUD-induced brain changes—and the changes in thinking, feeling, and behaving that accompany them—can improve and possibly reverse with months of abstinence.15,24 Even in individuals with lingering alterations in brain circuitry and function due to AUD, there is evidence that other circuits can compensate to help restore compromised function.20,25,26

    Healthcare professionals offer two types of evidence-based treatments for AUD that help the brain and the patient as a whole to recover: FDA-approved AUD medications and behavioral healthcare.

    • Medications. Medications to treat AUD can facilitate healthy brain changes by helping people to cut down or quit drinking. Three non-addicting medications are FDA-approved to treat AUD and can be easily prescribed in primary care—acamprosate, naltrexone, and disulfiram. Acamprosate helps prevent relapse by acting to blunt the activity of glutamatergic neurocircuits, which drive the emotional discomforts of anxiety, irritability, dysphoria, and insomnia. This emotional discomfort often occurs during protracted abstinence, and often triggers a relapse.27 Naltrexone, an opioid receptor antagonist, reduces the pleasurable effects of alcohol by interfering with its effects on opioid peptide activity in the basal ganglia circuitry.28,29 In contrast, disulfiram does not work on brain circuitry, but instead interferes with alcohol metabolism by preventing the breakdown of the toxic alcohol metabolite acetaldehyde. Consuming alcohol while taking disulfiram causes acetaldehyde to build up in the blood stream, producing facial flushing, throbbing headache, nausea, and other highly aversive effects.30 Each of these medications can help the patient maintain sobriety, or reduce drinking significantly, which may allow behavioral health treatments to be applied to best advantage.
    • Behavioral healthcare. When people become preoccupied with drinking alcohol, their cognitive control neurocircuits can struggle to regulate urges to drink, particularly when under stress.31 Alcohol also can directly damage these brain circuits, making it even harder to regulate urges. Neuroimaging studies indicate that behavioral health interventions for AUD can normalize activity in the reward and stress circuitry of the brain, while strengthening cognitive networks that help inhibit the drive to drink.32 For example, therapeutic approaches that teach mindfulness and coping skills can alter neural circuits associated with craving and help people tolerate and resist urges to drink.33,34 Other behavioral health interventions include cognitive behavioral therapy, motivational enhancement therapy, contingency management, couples and family counseling, and twelve-step facilitation to encourage active involvement in mutual support groups such as AA, SMART Recovery, and Secular AA (See Resources, below).

    Together, medication and behavioral health treatments can facilitate functional brain recovery. For more details, see the Core article on treatment.

    In closing, brain alterations underlying addiction not only drive the addiction process itself but also make it difficult for many people with AUD to change their drinking behavior, particularly if they are struggling to cope with the considerable discomfort of acute or protracted withdrawal. You can promote healthy changes in the brains and behaviors of patients with AUD by encouraging them to take a long-term, science-based approach to getting better. For practical, evidence-based tips on supporting your patients with AUD, see the Core articles on treatment, referral, and recovery.

    Resources

    Neurobiology of Alcohol Use Disorder

    Alcohol Use Disorder Medication Guides

    Adolescent Primary Care

    Mutual Support Groups

    More resources for a variety of healthcare professionals can be found in the Additional Links for Patient Care.

    References

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    3. Litten RZ, Ryan ML, Falk DE, Reilly M, Fertig JB, Koob GF. Heterogeneity of alcohol use disorder: understanding mechanisms to advance personalized treatment. Alcohol Clin Exp Res. 2015;39(4):579-584. doi:10.1111/acer.12669
    4. Sullivan EV, Harris RA, Pfefferbaum A. Alcohol’s Effects on Brain and Behavior. Alcohol Res Health. 2010;33(1-2):127-143.
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    6. Koob GF, Powell P, White A. Addiction as a Coping Response: Hyperkatifeia, Deaths of Despair, and COVID-19. Am J Psychiatry. 2020;177(11):1031-1037. doi:10.1176/appi.ajp.2020.20091375
    7. Goldstein RB, Chou SP, Smith SM, et al. Nosologic Comparisons of DSM-IV and DSM-5 Alcohol and Drug Use Disorders: Results From the National Epidemiologic Survey on Alcohol and Related Conditions-III. J Stud Alcohol Drugs. 2015;76(3):378-388. doi:10.15288/jsad.2015.76.378
    8. Crum RM, Mojtabai R, Lazareck S, et al. A prospective assessment of reports of drinking to self-medicate mood symptoms with the incidence and persistence of alcohol dependence. JAMA Psychiatry. 2013;70(7):718-726. doi:10.1001/jamapsychiatry.2013.1098
    9. Egli M, Koob GF, Edwards S. Alcohol dependence as a chronic pain disorder. Neurosci Biobehav Rev. 2012;36(10):2179-2192. doi:10.1016/j.neubiorev.2012.07.010
    10. Thompson T, Oram C, Correll CU, Tsermentseli S, Stubbs B. Analgesic Effects of Alcohol: A Systematic Review and Meta-Analysis of Controlled Experimental Studies in Healthy Participants. J Pain. 2017;18(5):499-510. doi:10.1016/j.jpain.2016.11.009
    11. Baumeister RF, Heatherton TF, Tice DM. Losing Control: How and Why People Fail at Self-Regulation. Academic Press; 1994.
    12. Lowman C, Allen J, Stout RL. Replication and extension of Marlatt’s taxonomy of relapse precipitants: overview of procedures and results. The Relapse Research Group. Addict Abingdon Engl. 1996;91 Suppl:S51-71.
    13. Marlatt GA. Determinants of Relapse: Implications for the Maintenance of Behavior Change. In: Davidson PO, Davidson SM, eds. Behavioral Medicine: Changing Health Lifestyles. Brunner/Mazel; 1980:410-452.
    14. Witkiewitz K, Villarroel NA. Dynamic Association Between Negative Affect and Alcohol Lapses Following Alcohol Treatment. J Consult Clin Psychol. 2009;77(4):633-644. doi:10.1037/a0015647
    15. Le Berre AP, Fama R, Sullivan EV. Executive Functions, Memory, and Social Cognitive Deficits and Recovery in Chronic Alcoholism: A Critical Review to Inform Future Research. Alcohol Clin Exp Res. 2017;41(8):1432-1443. doi:10.1111/acer.13431
    16. Administration (US) SA and MHS, General (US) O of the S. The Neurobiology of Substance Use, Misuse, and Addiction. US Department of Health and Human Services; 2016. Accessed October 25, 2021. https://www.ncbi.nlm.nih.gov/books/NBK424849/
    17. Kwako LE, Koob GF. Neuroclinical Framework for the Role of Stress in Addiction. Chronic Stress Thousand Oaks Calif. 2017;1. doi:10.1177/2470547017698140
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    19. Ruan H, Zhou Y, Luo Q, et al. Adolescent binge drinking disrupts normal trajectories of brain functional organization and personality maturation. NeuroImage Clin. 2019;22:101804. doi:10.1016/j.nicl.2019.101804
    20. Pfefferbaum A, Desmond JE, Galloway C, Menon V, Glover GH, Sullivan EV. Reorganization of Frontal Systems Used by Alcoholics for Spatial Working Memory: An fMRI Study. NeuroImage. 2001;14(1):7-20. doi:10.1006/nimg.2001.0785
    21. Hingson RW, Heeren T, Winter MR. Age at drinking onset and alcohol dependence: age at onset, duration, and severity. Arch Pediatr Adolesc Med. 2006;160(7):739-746. doi:10.1001/archpedi.160.7.739
    22. Hingson R, Heeren T, Zakocs R, Winter M, Wechsler H. Age of first intoxication, heavy drinking, driving after drinking and risk of unintentional injury among U.S. college students. J Stud Alcohol. 2003;64(1):23-31. doi:10.15288/jsa.2003.64.23
    23. Zahr NM, Pfefferbaum A. Alcohol’s Effects on the Brain: Neuroimaging Results in Humans and Animal Models. Alcohol Res Curr Rev. 2017;38(2):183-206.
    24. Fritz M, Klawonn AM, Zahr NM. Neuroimaging in alcohol use disorder: From mouse to man. J Neurosci Res. Published online April 22, 2019. doi:10.1002/jnr.24423
    25. Koob GF, BS MAA, McCracken M, Moal ML. Alcohol: Neurobiology of Addiction. Vol 3. 1st edition. Academic Press; 2021.
    26. Rosenbloom MJ, Pfefferbaum A. Magnetic Resonance Imaging of the Living Brain. Alcohol Res Health. 2008;31(4):362-376.
    27. Mason BJ, Heyser CJ. Acamprosate: a prototypic neuromodulator in the treatment of alcohol dependence. CNS Neurol Disord Drug Targets. 2010;9(1):23-32. doi:10.2174/187152710790966641
    28. Garbutt JC, Greenblatt AM, West SL, et al. Clinical and biological moderators of response to naltrexone in alcohol dependence: a systematic review of the evidence. Addict Abingdon Engl. 2014;109(8):1274-1284. doi:10.1111/add.12557
    29. Hendershot CS, Wardell JD, Samokhvalov AV, Rehm J. Effects of naltrexone on alcohol self‐administration and craving: meta‐analysis of human laboratory studies. Addict Biol. 2017;22(6):1515-1527. doi:10.1111/adb.12425
    30. DailyMed - ANTABUSE- disulfiram tablet. Accessed February 2, 2022. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=12850de3-c97c-42c1-b8d3-55dc6fd05750
    31. Koob GF. A Role for Brain Stress Systems in Addiction. Neuron. 2008;59(1):11-34. doi:10.1016/j.neuron.2008.06.012
    32. Zilverstand A, Parvaz MA, Moeller SJ, Goldstein RZ. Cognitive interventions for addiction medicine: Understanding the underlying neurobiological mechanisms. Prog Brain Res. 2016;224:285-304. doi:10.1016/bs.pbr.2015.07.019
    33. Garland EL, Howard MO. Mindfulness-based treatment of addiction: current state of the field and envisioning the next wave of research. Addict Sci Clin Pract. 2018;13(1):14. doi:10.1186/s13722-018-0115-3
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    Earn CME/CE Credit

    We invite healthcare professionals including primary care physicians, physician assistants, nurses, pharmacists, and psychologists to complete a post-test after reviewing this article to earn FREE continuing education (CME/CE) credit. This CME/CE credit opportunity is jointly provided by the Postgraduate Institute for Medicine and NIAAA.

    CME/CE Activity — Neuroscience: The Brain in Addiction and Recovery

    Released on 5/6/2022
    Expires on 5/10/2023

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    Learning Objectives

    After completing this activity, the participant should be better able to:

    • Discuss brain changes involved in the development and maintenance of AUD.
    • Identify reasons the adolescent brain is particularly susceptible to alcohol-related harm.
    • Describe the importance of neuroplasticity in addiction and recovery.

    Contributors

    Contributors to this article for the NIAAA Core Resource on Alcohol include the writers for the full article, content contributors to subsections, reviewers, and editorial staff. These contributors included both experts external to NIAAA as well as NIAAA staff.

    NIAAA Writers

    George F. Koob, PhD
    Director, NIAAA

    Aaron White, PhD
    Senior Scientific Advisor to
    the NIAAA Director, NIAAA

    External Reviewers

    Louis E. Baxter Sr., MD, DFASAM
    Assistant Professor Medicine, ADM
    Fellowship Director, Howard University
    Hospital, Washington, DC;
    Assistant Clinical Professor Medicine
    Rutgers Medical School, Newark, NJ

    Hector Colon-Rivera MD, MRO
    Medical Director of Asociacion
    Puertorriquenos En Marcha, Inc;
    Attending at University of Pittsburgh Medical
    Center, Philadelphia, PA

    Olivier George, PhD
    Associate Professor, Adjunct Codirector Arc
    Animal Core, Department of Neuroscience,
    Scripps Research, CA

    John H. Krystal, MD
    Chair, Department of Psychiatry
    Yale School of Medicine, New Haven, CT

    Patricia E. Molina, MD, PhD
    Professor and Department Head of Physiology,
    Louisiana State University,
    New Orleans, LA

    Alan F. Schatzberg, MD
    Kenneth T. Norris, Jr. Professor, Department
    of Psychiatry and Behavioral Sciences,
    Stanford University, Stanford, CA

    Kimberly Tallian, PharmD, APh, BCPP, FASHP, FCCP, FCSHP
    Advance Practice Pharmacist, Psychiatry,
    Scripps Mercy Hospital;
    Adjunct Clinical Professor, School of Pharmacy
    and Pharmaceutical Sciences,
    University of California San Diego,
    La Jolla, California

    NIAAA Reviewers

    George F. Koob, PhD
    Director, NIAAA

    Patricia Powell, PhD
    Deputy Director, NIAAA

    Nancy Diazgranados, MD, MS, DFAPA
    Deputy Clinical Director, NIAAA

    Lorenzo Leggio, MD, PhD
    NIDA/NIAAA Senior Clinical Investigator and Section Chief;
    NIDA Branch Chief;
    NIDA Deputy Scientific Director;
    Senior Medical Advisor to the NIAAA Director

    Falk W. Lohoff, MD
    Lasker Clinical Research Scholar;
    Chief, Section on Clinical Genomics and Experimental Therapeutics, NIAAA

    Aaron White, PhD
    Senior Scientific Advisor to
    the NIAAA Director, NIAAA

    Editorial Team

    NIAAA

    Raye Z. Litten, PhD
    Editor and Content Advisor for the Core Resource on Alcohol,
    Director, Division of Treatment and Recovery, NIAAA

    Laura E. Kwako, PhD
    Editor and Content Advisor for the Core Resource on Alcohol,
    Health Scientist Administrator,
    Division of Treatment and Recovery, NIAAA

    Maureen B. Gardner
    Project Manager, Co-Lead Technical Editor, and
    Writer for the Core Resource on Alcohol,
    Division of Treatment and Recovery, NIAAA

    Contract Support

    Elyssa Warner, PhD
    Co-Lead Technical Editor,
    Ripple Effect

    Daria Turner, MPH
    Reference and Resource Analyst,
    Ripple Effect

    Lia Bennett, MPH
    Educational Consultant,
    Ripple Effect

    To learn more about CME/CE credit offered as well as disclosures, visit our CME/CE General Information page. You may also click here to learn more about contributors.

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