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Open-label pilot study of memantine in the treatment of compulsive buying

Jon E. Grant, JD, MD, MPH

Department of Psychiatry, University of Minnesota, Minneapolis, MN, USA

Brian L. Odlaug, BA

Department of Psychiatry, University of Minnesota, Minneapolis, MN, USA

Marc Mooney, PhD

Department of Psychiatry, University of Minnesota, Minneapolis, MN, USA

Robert O’Brien, BA

Department of Psychiatry, University of Minnesota, Minneapolis, MN, USA

Suck Won Kim, MD

Department of Psychiatry, University of Minnesota, Minneapolis, MN, USA

BACKGROUND: Although compulsive buying (CB) is relatively common, pharmacotherapy research for CB is limited. Memantine, an N-methyl-D-aspartate receptor antagonist, appears to reduce glutamate excitability and improve impulsive behaviors, suggesting it may help individuals with CB.

METHODS: Nine patients (8 females) with CB were enrolled in a 10-week open-label treatment study of memantine (dose ranging from 10 to 30 mg/d). Participants were enrolled from December 2008 until May 2010. The primary outcome measure was change from baseline to study endpoint on the Yale-Brown Obsessive Compulsive Scale–Shopping Version (Y-BOCS-SV).

RESULTS: Of the 9 participants, 8 (88.9%) completed the 10-week study. Y-BOCS-SV scores decreased from a mean of 22.0±1.3 at baseline to 11.0±5.3 at endpoint (P < .001). Hours spent shopping per week and money spent shopping both decreased significantly (P < .001). The mean effective dose of memantine was 23.4±8.1 mg/d. Memantine treatment was associated with diminished impulsive buying and improvements on cognitive tasks of impulsivity. In addition, the medication was well-tolerated.

CONCLUSIONS: These findings suggest that pharmacologic manipulation of the glutamate system may target the impulsive behavior underlying CB. Placebo-controlled, double-blind studies are warranted in order to confirm these preliminary findings in a controlled design.

KEYWORDS: buying, cognition, impulse control, shopping



Compulsive buying (CB) is characterized by a preoccupation with buying, frequently buying unneeded items or more than can be afforded, and shopping for longer periods of time than intended.1-3 Research has found that prevalence of CB ranges from 1.4% to 5.8% (n = 2,513)4 in the general population, 1.9% in college students (n = 791),5 and up to 9% in individuals seeking psychiatric treatment (n = 204).6 Females appear to be disproportionately affected by this disorder (80% to 93.2%).1-4,7

Currently, there is no FDA-approved pharmacologic treatment for CB, and effective treatment options are limited. Research suggests that individual or group cognitive-behavioral therapy may be effective in some individuals.7-9 However, few individuals seek these treatments and it can be difficult to find trained therapists. In terms of pharmacotherapy, controlled trials of fluvoxamine10 and escitalopram11 have failed to demonstrate significant benefit in reducing CB symptoms. However, an open-label study of 24 individuals treated with citalopram found that 71% responded to treatment.12 Additional treatment options are needed because not all individuals report improvement with these options.

Memantine has the potential to reduce CB behaviors via antagonism of the N-methyl-D-aspartate receptor antagonist (NMDA) receptors in the striatum.13-15 Additionally, and in contrast to the other potential treatments outlined above, memantine also may be capable of improving aspects of cognition by modulating glutamatergic neurotransmission in the cortex.16

Based on memantine’s potential mechanism of action, we conducted a pilot study to examine the tolerability and efficacy of memantine for CB treatment. The rationale for the use of memantine was 2-fold. First, glutamatergic dysfunction has been implicated in the pathophysiology of pathological gambling, a disorder with phenomenological and possible neurobiological links to CB.17 Clinical reports also support the possible efficacy of glutamatergic modulators to treat other impulse control disorders.13 Second, CB symptoms suggest dysfunction of cortically-dependent cognitive domains, and frontal lobe function has been found to be modulated by memantine in brain-imaging research.16 We hypothesized that memantine treatment would decrease shopping behaviors and be associated with improvements in cognitive flexibility and response inhibition in CB.



Men and women age 18 to 65 were recruited from December 2008 through May 2010 via newspaper and poster advertising. Inclusion criteria consisted of a current diagnosis of CB using the following criteria: 1) preoccupation with buying (characterized by either an irresistible, intrusive, and/or senseless preoccupation with buying or buying more than one can afford; buying unneeded items or shopping for longer durations of time than originally intended), and 2) the preoccupation to buy results in marked distress, interferes with social or occupational functioning, and causes financial problems.2

Exclusion criteria included: 1) unstable medical illness or clinically significant abnormalities on laboratory tests or physical examination at initial screening; 2) current pregnancy or lactation; 3) a need for medication other than memantine, with possible psychotropic effects or unfavorable interactions; 4) clinically significant suicidality; 5) past 12-months axis I disorder determined by the Structured Clinic Interview for DSM-IV (SCID)18 and SCID-compatible modules for impulse-control disorders,6 except for nicotine dependence; 6) lifetime history of bipolar I disorder or bipolar II disorder, dementia, or any psychotic disorder determined by SCID; 7) positive urine drug screen at screening; 8) initiation of psychotherapy or behavior therapy within 3 months before study baseline; and 9) previous treatment with memantine.

The institutional review board for the University of Minnesota approved all study procedures. After a complete description of the study and opportunity for participants to ask questions, all participants provided written informed consent. This study was carried out in accordance with the Declaration of Helsinki and under the standards of good clinical practice. This study was registered on with identifier NCT00830375.

Study design

The study consisted of 8 weeks of open-label memantine. All eligible study participants were started on memantine, 10 mg/d for 2 weeks. The dose was increased to 20 mg/d after 2 weeks and to 30 mg/d after 4 weeks, unless remission of CB symptoms was attained at a lower dose (remission was defined as no shopping urges and no impulsive shopping behavior for the previous 2 weeks). Participants were seen every 2 weeks during the study. Safety and efficacy assessments were performed at each visit. Noncompliance with study medication (ie, failing to take medication for ≥3 consecutive days) resulted in discontinuation from the trial.

Efficacy and safety assessments

Participants were seen every 2 weeks for the 8-week study period. The primary outcome measure in this study was the Yale-Brown Obsessive Compulsive Scale–Shopping Version (Y-BOCS-SV).19 The Y-BOCS-SV is a reliable and valid, 10-item, clinician-administered scale that rates buying symptoms within the last 7 days on a severity scale from 0 to 4 for each item (total scores range from 0 to 40, with higher scores reflecting greater illness severity). The first 5 items of the Y-BOCS-SV comprise the buying urge/thought subscale (time occupied with urges/thoughts; interference and distress due to urges/thoughts; resistance against and control over urges/thoughts), and items 6 to 10 comprise the buying behavior subscale (time spent buying and amount of buying; interference and distress due to buying; ability to resist and control buying behavior). Scores ranging from 0 to 10 reflect minimal or mild symptoms; scores from 11 to 20 suggest moderate symptoms; severe symptoms are associated with scores from 21 to 30; and scores >30 reflect extreme buying symptoms.

Secondary measures administered at each visit in the study included:

Compulsive Buying Symptom Assessment Scale (CB-SAS).20 The CB-SAS is a modified version of the valid and reliable Gambling Symptom Assessment Scale assessing buying urges, thoughts, and behaviors during the previous 7 days. Each item is rated on a scale of 0 to 4, with a possible total score of 48. Higher scores reflect greater severity of CB symptoms.

Clinical Global Impression-Improvement and Severity scales (CGI-I, CGI-S).21 The CGI consists of 2 reliable and valid 7-item Likert scales used to assess severity and change in clinical symptoms. The CGI-I scale ranges from 1 = “very much improved” to 7 = “very much worse.” The CGI-S scale was used at each visit and ranges from 1 = “not ill at all” to 7 = “among the most extremely ill.”

Sheehan Disability Scale (SDS).22 The SDS is a 3-item, reliable, and valid scale that assesses functioning in 3 areas of life: work, social or leisure activities, and home and family life.

Hamilton Anxiety Rating Scale (HAM-A).23 The HAM-A is a reliable and valid, clinician-administered, 14-item scale that provides an overall measure of global anxiety.

Hamilton Depression Rating Scale (HAM-D).24 The HAM-D is a valid and reliable, 17-item, clinician-administered rating scale assessing severity of depressive symptoms.

Secondary measures used only at baseline and study endpoint included:

Perceived Stress Scale (PSS).25 The 14-item PSS is a reliable and valid self-report measure designed to assess the degree to which individuals find their lives to be unpredictable, uncontrollable, and stressful. Each question is answered on a 5-point scale (ranging from “never” to “very often”) based on experiences of the previous month. Scores range from 0 to 40, with higher scores indicating greater stress.

Quality of Life Inventory (QoLI).26 The QoLI is a 16-item, self-administered rating scale that assesses life domains such as health, work, recreation, friendships, love relationships, home, self-esteem, and standard of living. Each item is rated according to importance in the respondent’s life and the level of satisfaction perceived by the respondent in that area of life.

Safety assessments at each visit included evaluations of sitting blood pressure, heart rate, and weight. Adverse effects were documented. Use of concomitant medications was recorded. Urine toxicology and urine pregnancy tests were performed only at screening. Compliance was monitored by pill count.

Neurocognitive assessments

Computerized neurocognitive assessments were administered at baseline and study endpoint. Participants undertook paradigms from the Cambridge Neuropsychological Test Automated Battery (CANTAB)27 quantifying aspects of impulsivity (relating to response inhibition) and cognitive flexibility.

Intra-dimensional/extra-dimensional set shift task (IDED). The IDED examines rule learning and behavioral flexibility.28 Participants attempt to learn a rule about which of 2 stimuli is correct. Once learning criterion is obtained (6 consecutive correct responses), the rule changes and the volunteer must adapt their behavior. There are 9 stages, requiring different components of set acquisition, reversal, and flexibility. Outcome measures include the number of errors made before obtaining learning criterion for the crucial ID and ED stages. Both stages involve the introduction of new stimuli; for ID shifting, participants must focus on the previously relevant dimension; for ED shifting, participants must inhibit and shift attention away from a previously relevant stimulus dimension to one that was previously irrelevant, ie, show cognitive flexibility.

Stop-signal test (SST). The SST quantifies the ability to suppress impulsive responses.29,30 Participants observe a series of arrows on a computer and make speeded motor responses depending on the direction of each arrow. On a subset of trials, an auditory beep (the “stop signal”) indicates the participant should inhibit their response for that particular trial. This task estimates the time taken by the participant’s brain to stop a prepotent response (ie, “stop-signal reaction time”). The median reaction time for “go” trials also is recorded.

Data analysis

All analyses were conducted with the Statistical Analysis System Version 9.1.3 (Cary, NC).

Values of P < .05 were considered statistically significant, based on 2-tailed tests.

In all efficacy analyses, only participants who returned for 1 visit after starting medication were included (n = 9). Comparisons within participants were evaluated with t tests for dependent samples. A mixed-model procedure for repeated measures, restricted maximum likelihood estimation analysis of covariance was used to test for the effect of treatment week on each outcome. Type I error rate in all post-hoc comparisons of between-treatment and baseline observations were controlled using Dunnett-Hsu adjustments. Changes in cognitive performance between baseline and end of treatment were assessed in CB patients using paired t tests. Performance of CB patients at baseline and at study endpoint were compared separately to baseline data from healthy volunteers using unpaired t tests.


A total of 10 participants meeting proposed diagnostic criteria for CB signed the informed consent and were enrolled in the study. A total of 9 patients (88.9% female; mean age 32±12.4 years [range 19 to 59]) returned for at least 1 visit following the baseline visit.

Demographic and clinical characteristics are detailed in TABLE 1. Of the 9 participants, 8 (88.9%) reported buying primarily from clothing stores. Over the previous 12 months, participants reported spending a mean of $26,750±$16,210 on unnecessary purchases that they reported were impulsive. With a mean gross yearly income of $58,875±$60,539, these impulsive purchases constituted an average of 61.04% of participants’ yearly income. The mean amount of credit card debt due to these unnecessary purchases was $21,933.30±$28,962.50. Impulsive shopping episodes were most commonly triggered by sales (n = 7; 77.7%), a “need” for an item (n = 6; 66.7%), to impress others (n = 5; 55.6%), and body image (n = 3; 33.3%). Illegal behaviors or legal problems were reported by 4 (44.4%) patients and included writing bad checks (n = 2; 22.2%), theft (n = 2; 22.2%), forgery (n = 1; 11.1%), and bankruptcy (n = 1; n = 11.1%).


Demographic and clinical characteristics of individuals with compulsive buying

  Mean (± SD) [range], years
32 (12.4) [19 to 59]
Female, n (%) 8 (88.9%)
  White, n (%)
9 (100%)
Marital status, n (%)
7 (77.8%)
1 (11.1%)
1 (11.1%)
Education, n (%)
  High-school graduate
  Some college
  College graduate or post-college
2 (22.2%)
5 (55.6%)
2 (22.2%)
Unemployed, n (%) 4 (44.4%)
Age at CB onset
  Mean (± SD), [range], years
20.6 (9.6) [13 to 42]
Percentage of gross income spent compulsively in the previous 12 months
  Mean % (± SD)
61.0% (31.5)
Time spent shopping each week
  Mean (± SD) [range], hours
15.2 (8.75) [7 to 38.5]
Comorbid lifetime disorders, n (%)
  Any affective disorder
  Any anxiety disorder
  Alcohol abuse/dependence
  Nicotine dependence
  Attention-deficit/hyperactivity disorder
  Any other impulse-control disorder
6 (66.7%)
3 (33.3%)
1 (11.1%)
5 (55.6%)
2 (22.2%)
3 (33.3%)
CB: compulsive buying; SD: standard deviation.

Participants reported a mean (SD) overall Y-BOCS-SV score of 22±4 at baseline, corresponding to severe buying symptoms. Mean CGI-S scores at baseline were 4.4±0.6, indicating moderate to marked illness.

Five patients (55.6%) met diagnostic criteria for at least 1 lifetime co-occurring Axis I disorder: Any affective (n = 6; 66.7%), anxiety (n = 3; 33.3%), or impulse control (n = 3; 33.3%) disorder were the most common (TABLE 1). A high rate of lifetime nicotine dependence (n = 5; 55.6%) was also noted. A total of 6 participants (66.7%) were currently taking stable doses of psychotropics upon enrollment in the study. These medications included citalopram (n = 3), bupropion (n = 3), sertraline (n = 1), buspirone (n = 1), and duloxetine (n = 1). No significant differences between participants taking stable doses of psychotropics were found compared with those not taking medication.

Efficacy results

Of the 9 participants who returned for at least 1 visit, 8 (88.9%) completed the 10-week open-label study. The patient who discontinued treatment did so after reporting increasing anxiety to the study center.

Scores on the Y-BOCS-SV decreased from a mean of 22.0±4.0 at baseline to 11.0±5.3 (P < .001) at the end of 8 weeks (TABLE 2). Significant change was evident after 6 weeks of treatment (P = .0068) (FIGURE). Similar changes were seen on secondary measures as well (TABLE 2). Eight (88.9%) participants were “much” or “very much” improved by study endpoint (CGI-I score of 1 or 2). The mean effective dose of memantine was 23.4±8.1 mg/d.


Changes on primary and secondary measures across visits (n=9)

  Baseline Week 2 Week 4 Week 6 Week 8
Memantine dosage (mg)a 10
(10 to 10)
(10 to 20)
(10 to 30)
(10 to 30)
Y-BOCS-SV total score 22.0 (1.3) –0.7 (1.7) –6.9 (2.9) –8.4 (1.8)b –11.6 (1.4)c
Y-BOCS-SV-U/T 11.1 (1.1) –0.1 (0.8) –2.1 (1.1) –3.3 (1.5) –4.0 (0.9)d
Y-BOCS-SV-B 10.7 (0.7) –0.3 (1.4) –4.3 (2.1) –4.9 (1.4) –7.4 (1.3)d
CB-SAS total score 32.8 (1.7) –5.1 (1.9) –6.1 (4.0) –10.1 (2.7) –15.4 (3.9)c
HAM-A 5.9 (0.8) –1.3 (0.5) –0.5 (1.6) –1.6 (1.3) –1.9 (0.9)
HAM-D 5.8 (0.8) –0.6 (0.4) –0.5 (1.9) –1.9 (1.1) –2.4 (0.9)
SDS total score 15.9 (1.8) –4.6 (2.0) –3.6 (2.8) –7.3 (2.1)d –9.3 (2.1)c
CGI-S 4.4 (0.2) –0.3 (0.3) –0.8 (0.4) –1.0 (0.4) –1.8 (0.3)c
CGI-I (Investigator) 2.0 (0.2)
CGI-I (Patient) 2.0 (0.3)
Perceived Stress Scalee 27.1 (2.0) 17.6 (1.7)c
Quality of Life T-scoree 30.9 (4.3) 43.0 (4.6)c
Values for visits 2 to 5 reflect changes from baseline. All values shown as mean (standard error), unless otherwise indicated. All tests are repeated-measures regression models, using Dunnett-Hsu test comparing all treatment time points to baseline.
aMean (range)
bP < .05.
cP < .001.
dP < .01.
eOne-sample t test.
CB-SAS: Compulsive Buying Symptom Assessment Scale; CGI-I: Clinical Global Impression-Improvement Scale; CGI-S: Clinical Global Impression-Severity Scale;
HAM-A: Hamilton Anxiety Rating Scale; HAM-D: Hamilton Depression Rating Scale; SDS: Sheehan Disability Scale; Y-BOCS-SV: Yale-Brown Obsessive Compulsive Scale–Shopping Version; Y-BOCS-SV-B: Behavior subscale; Y-BOCS-SV-U/T: Urge-Thought subscale.

FIGURE: Y-BOCS-SV total score change with memantine
aY-BOCS-SV score at visit was significantly lower than baseline score.
Y-BOCS-SV: Yale-Brown Obsessive Compulsive Scale–Shopping Version.

On cognitive tasks, CB patients were compared with healthy controls at baseline (TABLE 3). At baseline, CB patient performance trended toward significance when compared with healthy controls on the number of directional errors on the stop signal task (P = .056) and stop-signal reaction time (SSRT) (P = .058). Within-group analyses of CB patients at baseline and study endpoint, however, showed a significant improvement in SSRT (P = .0097).


Performance on cognitive tasks in compulsive buying and age/sex-matched healthy controls

  Performance (mean±SD) Comparisons
  Compulsive buyers
baseline vs
baseline vs
CB endpoint vs
  Baseline Endpoint   T P T P T P
IDED stages completed 8.33±0.33 8.78±0.67 8.88±0.43 –1.11 0.284 –1.58 0.133 –0.45 0.661
IDED total errors 18.89±9.23 16±10.84 15.22±12.56 0.61 0.551 0.710 0.490 0.14 0.889
IDED total errors (adjusted) 23.89±20.16 18.78±17.84 15.22±12.56 0.58 0.577 1.09 0.289 0.49 0.632
SST directional errors 5.11±5.78 2.33±2.18 1±1.58 1.35 0.196 2.06 0.056 1.49 0.157
SST median go reaction time 475±144.94 502.83±211.89 486±76.79 –0.33 0.749 –0.20 0.843 0.22 0.826
SST SSRT 211.64±72.0 140.19±11.85 154.37±43.2 2.94 0.0097 2.05 0.058 –0.95 0.357
Trend of significant impairment for CB patients at baseline compared to age/gender matched healthy controls on SST performance (both directional errors and stop-signal
reaction time); SSRT improved significantly from baseline to endpoint in CB patients
CB: compulsive buying; IDED: intra-dimensional/extra-dimensional; P: 2-tailed t test; SD: standard deviation; SSRT: Stop Signal Reaction Time; SST: Stop Signal Task; T: t test;
2 samples assuming equal variances.
Safety results

The incidence and severity of adverse events were consistent with prior studies,17 and no unexpected experiences were reported. Most adverse experiences were of mild-to-moderate intensity, and all adverse events resolved without sequelae. Of the 9 patients returning for at least 1 visit, 8 (88.9%) completed the study, and 1 dropped out after the second visit because of increasing anxiety. Following discontinuation of the study medication, the participant reported full remission of anxiety symptoms. The most common side effects reported were dizziness (n = 3; 33%), decreased appetite (n = 1; 11%), anxiety (n = 1; 11%), and tinnitus (n = 1; 11%). In addition, mean values in HAM-D and HAM-A scores remained at low levels throughout the study.

Clinical vignette

Kathy is a 38-year-old, married female with 2 children. She works full-time and lives in an upper-middle class suburban home. In late adolescence, Kathy began to spend irresponsibly; however, over the past 5 years, Kathy’s spending behavior worsened significantly. She reports having severe urges to shop and enjoys the attention she receives from coworkers and family members over having the “latest fashions.” Although Kathy makes nearly $60,000 annually, her shopping has resulted in credit card debt, no savings or retirement accounts, and owing money to multiple family members and friends. She has several closets filled with unused makeup and clothing and is several months behind in credit card payments. She has been reprimanded at work for decreased productivity as a result of hours of browsing online retailers for the best “deals.” She reports significant anxiety and stress over her inability to pay bills and cannot fall asleep at night. As a result, she reports that her intake of alcohol has increased significantly over the past 2 years to cope with these feelings.

Kathy presented with significant urges to engage in buying behavior with a baseline Y-BOCS-SV score of 25 and CGI-S score of 5, corresponding with being “severely ill.” On the self-report CB-SAS scale, Kathy scored a 33. She was prescribed memantine, 10 mg/d. Reporting minimal symptom improvement after 2 weeks, the dose was increased to 20 mg/d. After 4 weeks, Kathy reported less preoccupation with shopping and noted a reduction in her shopping behavior (Y-BOCS-SV = 15; CGI = 3). Because she was tolerating the medication well, the dose of memantine was increased to 30 mg/d. After 2 weeks, Kathy’s Y-BOCS-SV score was reduced to 7 with a CGI-S score of 2 (“borderline ill”) and CB-SAS score of 8. Her productivity at work improved as she no longer felt preoccupied with online browsing for “deals.” She had started paying back her credit card debt, giving the unused items in her closet to charity, and reported that her overall mood and sleep had improved.


This pilot study—the first to examine the efficacy of an NMDA receptor antagonist in the treatment of CB—found that CB symptoms improved significantly in a majority of participants. The current study also explored effects of memantine treatment on specific cognitive functions, assessed with CANTAB, and found that stop-signal reaction time significantly improved with memantine treatment in CB. These findings suggest that pharmacologic modulation of the glutamate system may reduce behaviors associated with CB, and may do so by improving neurocognitive function related to dysfunction of right frontal and bilateral cingulate cortices. Because impaired performance on the SST task has been linked with damage to the right inferior frontal gyrus,31 and because memantine appears to modulate activity in the prefrontal cortex,16 memantine may target inhibitory control mechanisms resulting in shopping behavior despite adverse consequences.

Although memantine may be a promising treatment for CB, prior pharmacologic studies in CB have shown that particular treatments have not been effective for all individuals with CB.10-12,32 These earlier results may reflect the heterogeneity of individuals with CB and how this heterogeneity may necessitate individually tailored treatment approaches.33 It is possible that individuals with CB and impaired inhibitory control may respond preferentially to memantine. Although this notion remains speculative and requires additional studies to examine its appropriateness, one future direction for the treatment of CB may be to better define cognitive subtypes of CB to guide pharmacologic treatment selection. Future placebo-controlled studies may target examination of memantine based on groups specifically characterized by inhibitory control.

This study represents, to our knowledge, the first trial of a glutamatergic agent in CB, and the results are promising. Nonetheless, there exist several important limitations. First, the study was open label, and it is possible that patient and clinician bias may have influenced the results. In addition, placebo response rates in CB studies have been high (33.3% to 54.5%),10-12 and therefore these results could be due to the placebo effect. Interestingly, however, the assessment of cognitive tasks was blinded and confirmed the positive open-label results. Third, the sample size was very small and the results may not generalize to a larger population of compulsive buyers. Finally, this study did not assess treatment effects beyond an 8-week treatment period, and it is possible that memantine’s therapeutic effects might not endure beyond 8 weeks.


This investigation suggests that memantine may be effective in the acute treatment of CB. As effective treatments for CB emerge, it becomes increasingly important that physicians and mental health care providers screen for CB in order to provide timely treatment. However, given the open-label design of the study and the small number of patients participating, the interpretation of the efficacy results of this study is limited.

ACKNOWLEDGMENTS: This study was funded by internal funds. Dr. Grant, Mr. Odlaug, and Dr. Kim contributed to the design, implementation, and collection of data for this study. Dr. Grant and Mr. Odlaug drafted the initial manuscript. Dr. Mooney and Mr. O’Brien performed the statistical analysis and assisted with the editing of the manuscript. Each author has studied the manuscript in this submitted form, agrees to be cited as a coauthor, and has accepted the order of authorship.

DISCLOSURES: Dr. Grant has received research grants from Psyadon Pharmaceuticals and the National Institute on Drug Abuse. Dr. Mooney has received grant/research support from the National Institute on Drug Abuse. Mr. Odlaug, Mr. O’Brien, and Dr. Kim report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.


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CORRESPONDENCE: Jon E. Grant, JD, MD, MPH, Department of Psychiatry, University of Minnesota School of Medicine, 2450 Riverside Avenue, Minneapolis, MN 55454 USA E-MAIL: