Alcoholism Clinical and Experimental Research Journal Impact Factor & Information

Publisher: Research Society on Alcoholism (U.S.); National Council on Alcoholism and Drug Dependence (U.S.); International Society for Biomedical Research on Alcoholism, Wiley

Journal description

Founded by the National Council on Alcoholism and Drug Dependence, this journal gives readers direct access to the most significant and current findings on the nature and management of this serious health problem. Each month Alcoholism: Clinical and Experimental Research brings health care professionals and researchers the latest clinical studies and research findings on alcoholism, alcohol-induced syndromes and organ damage. Pertinent current papers in the major categories of basic science, clinical research, and treatment methods are included in each issue.

Current impact factor: 3.21

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 3.205
2013 Impact Factor 3.311
2012 Impact Factor 3.421
2011 Impact Factor 3.343
2010 Impact Factor 3.468
2009 Impact Factor 3.392
2008 Impact Factor 3.166
2007 Impact Factor 3.175
2006 Impact Factor 2.933
2005 Impact Factor 2.636
2004 Impact Factor 2.508
2003 Impact Factor 2.421
2002 Impact Factor 2.355
2001 Impact Factor 2.674
2000 Impact Factor 2.323
1999 Impact Factor 2.013
1998 Impact Factor 2.14
1997 Impact Factor 1.875
1996 Impact Factor 2.294
1995 Impact Factor 2.31
1994 Impact Factor 2.065
1993 Impact Factor 2.164
1992 Impact Factor 1.961

Impact factor over time

Impact factor

Additional details

5-year impact 3.72
Cited half-life 8.70
Immediacy index 0.64
Eigenfactor 0.02
Article influence 1.02
Website Alcoholism: Clinical and Experimental Research website
Other titles Alcoholism (Baltimore, Md.: Online), Alcoholism, ACER
ISSN 1530-0277
OCLC 44003050
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo
  • Conditions
    • Some journals have separate policies, please check with each journal directly
    • On author's personal website, institutional repositories, arXiv, AgEcon, PhilPapers, PubMed Central, RePEc or Social Science Research Network
    • Author's pre-print may not be updated with Publisher's Version/PDF
    • Author's pre-print must acknowledge acceptance for publication
    • Non-Commercial
    • Publisher's version/PDF cannot be used
    • Publisher source must be acknowledged with citation
    • Must link to publisher version with set statement (see policy)
    • If OnlineOpen is available, BBSRC, EPSRC, MRC, NERC and STFC authors, may self-archive after 12 months
    • If OnlineOpen is available, AHRC and ESRC authors, may self-archive after 24 months
    • Publisher last contacted on 07/08/2014
    • This policy is an exception to the default policies of 'Wiley'
  • Classification
    ​ yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: Ethanol (EtOH) inhibits Notch-mediated vascular smooth muscle cell (SMC) proliferation, an event that is key in vessel remodeling and atherogenesis. The object of this study was to determine whether EtOH inhibits Notch signaling in SMC at the level of γ-secretase, a protease that in concert with α-secretase catalyzes the release of the intracellular domain of the Notch receptor necessary for signaling. Methods: Human coronary artery SMCs (HCASMCs) were treated with a recombinant soluble Notch ligand, Delta-like ligand 4 (DLL4) (2 μg/ml), or transfected with a constitutively active Notch 1 intracellular domain (N1ICD), in the absence or presence of EtOH. EtOH (25 mM) treatment inhibited DLL4-stimulated CBF-1/RBP-Jk-dependent promoter activity (determined by luciferase assay) and downstream target gene HRT-3 mRNA levels. In contrast, EtOH had no effect on N1ICD-driven CBF-1/RBP-Jk-dependent promoter activity or HRT-3 expression. Results: These data suggest that EtOH inhibits Notch signaling at, or prior to, Notch intracellular domain (NICD) generation. γ-Secretase activity was determined in solubilized membrane preparations from HCASMC treated with/without EtOH (25 mM) or the γ-secretase inhibitor DAPT (20 μM) using (i) a fluorometric assay and (ii) Western blot detection of cleavage products using a Flag-tagged Notch-based substrate, N100Flag. EtOH inhibited basal and DLL4-stimulated γ-secretase activity, and SMC growth to a similar extent as DAPT, whereas it had no effect on α-secretase (TACE/ADAM17) activity also determined by fluorometric assay. Moreover, EtOH treatment inhibited the expression of caveolin-1, a lipid raft protein implicated in regulating γ-secretase activity, and altered its cellular distribution in HCASMC. Conclusions: EtOH inhibits Notch signaling in vascular SMCs at the level of γ-secretase activity, possibly by affecting lipid raft function. Such a response might be expected to result in attenuation of pathologic vessel remodeling and thus may contribute to moderate alcohols' cardioprotective effects.
    Alcoholism Clinical and Experimental Research 10/2015; DOI:10.1111/acer.12875
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    ABSTRACT: Background Fetal alcohol spectrum disorders (FASD) are often characterized by disruptive behavior problems and there are few effective interventions available. GoFAR is a novel, 3-part intervention designed to improve self-regulation and adaptive living skills of children with FASD by improving metacognitive control of emotions and arousal.Methods The intervention has 3 components: (i) GoFAR: a “serious game” designed to teach a metacognitive control strategy in a computer game environment; (ii) parent training on child behavioral regulation; and (iii) Behavior Analog Therapy (BAT) sessions, a practical application of the metacognitive learning methodology by parent and child in the context of learning adaptive skills. The learning strategy (FAR) teaches the child to Focus and make a plan, Act out the plan, and Reflect back on the plan. Thirty families were randomized to 3 groups: (i) GoFAR (n = 10); (ii) FACELAND (n = 10); or (iii) CONTROL (n = 10). The 2 intervention groups, GoFAR and FACELAND, used computer games to instruct children. Both groups also received 5 sessions of parent training followed by 5 sessions of joint parent/child therapy (BAT). Assessment of disruptive behavior, including frequency of temper tantrums, frustration tolerance, impulsivity, destructiveness, aggression, and maintaining attention were carried out before enrollment at Mid-Treatment, when game play and parent training were completed, and finally, after completing the BAT sessions.ResultsParental report of disruptive behavior overall was significantly reduced in the GoFAR group after the first components, game play and parent training, and after the BAT sessions in the FACELAND group with no changes in the CONTROL group over time.Conclusions The GoFAR® game was well received by children and effective in teaching the required skills. Mastering the FAR metacognitive strategy was associated with a reduction in disruptive behaviors in children with FASD suggesting that effective interventions can improve outcomes for this high-risk group.
    Alcoholism Clinical and Experimental Research 10/2015; DOI:10.1111/acer.12885
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    ABSTRACT: Background Existing pharmacological treatments for alcohol use disorder (AUD) and other substance use disorders (SUDs) have demonstrated only modest efficacy. Although the field has recently emphasized testing and developing new compounds to treat SUDs, there are numerous challenges inherent to the development of novel medications, and this is particularly true for SUDs. Thus, research to date has tended toward the “repurposing” approach, in which medications developed to treat other mental or physical conditions are tested as SUD treatments. Often, potential treatments are examined across numerous drugs of abuse. Several repurposed medications have shown promise in treating a specific SUD, but few have shown efficacy across multiple SUDs. Examining similarities and differences between AUD and other SUDs may shed light on these findings and offer directions for future research.Methods This qualitative review discusses similarities and differences in neural circuitry and molecular mechanism(s) across alcohol and other substances of abuse, and examines studies of pharmacotherapies for AUD and other SUDs.ResultsSubstances of abuse share numerous molecular targets and involve much of the same neural circuitry, yet compounds tested because they putatively target common mechanisms have rarely indicated therapeutic promise for multiple SUDs.Conclusions The lack of treatment efficacy across SUDs may be partially explained by limitations inherent in studying substance users, who comprise a highly heterogeneous population. Alternatively, medications may fail to show efficacy across multiple SUDs due to the fact that the differences between drug mechanisms are more important than their commonalities in terms of influencing treatment response. We suggest that exploring these differences could support novel treatment development, aid in identifying existing medications that may hold promise as treatments for specific SUDs, and ultimately advance translational research efforts.
    Alcoholism Clinical and Experimental Research 09/2015; DOI:10.1111/acer.12884
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    ABSTRACT: Background: Alcohol dependence is a devastating illness affecting a large population, and new pharmacological treatments with good efficacy are greatly needed. One potential candidate is varenicline, a smoking cessation agent with partial agonist action at α4 β2 nicotinic acetylcholine receptors. Methods: A total of 160 subjects, 30 to 70 years of age, fulfilling DSM-IV criteria for alcohol dependence without any serious physical or mental disorders, were recruited through advertisement at 3 university clinics in Sweden during March 2009 to January 2011. After a 2-week placebo run-in period, subjects received 2 mg varenicline daily (titrated from 0.5 mg during first week) or placebo for 12 weeks in a double-blind manner. Results: The primary outcome was the proportion of heavy drinking days, measured by self-reported alcohol consumption. Primary and secondary outcomes were calculated as a mean over the 10-week steady-state active treatment period. In the primary outcome analysis, no effect of varenicline over placebo was found (p = 0.73 for the intention to treat [ITT] and 0.92 for per protocol [PP]). Secondary outcome analysis found a significant reduction of specific alcohol marker phosphatidylethanol (PEth) in the blood in the varenicline group compared to placebo (p = 0.02 ITT). Craving (p = 0.048 PP) and Alcohol Use Disorders Identification Test (AUDIT) scores (p = 0.015 ITT) were also reduced in the active treatment group. PEth more strongly correlated with self-reported alcohol consumption than carbohydrate-deficient ttransferrin and γ-glutamyl transferase, and correlation coefficients were higher in the varenicline group than in the placebo group for all markers. Conclusions: Although the results of the main outcome of this study did not support an effect of varenicline in alcohol-dependent individuals, the secondary analyses of PEth, craving and AUDIT score support an effect of varenicline on alcohol consumption. The disclosure of a treatment effect and the lack of a clear placebo effect when using PEth as outcome variable, together with a nonsymmetric bias associated with self-reported data, strongly argue for using the specific biomarker PEth in studies of treatments of alcohol dependence.
    Alcoholism Clinical and Experimental Research 09/2015; DOI:10.1111/acer.12854
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    ABSTRACT: Background: Gestational alcohol exposure causes lifelong physical and neurocognitive deficits collectively referred to as fetal alcohol spectrum disorders (FASDs). Micronutrient deficiencies are common in pregnancies of alcohol-abusing women. Here we show the most common micronutrient deficiency of pregnancy-iron deficiency without anemia-significantly worsens neurocognitive outcomes following perinatal alcohol exposure. Methods: Pregnant rats were fed iron-deficient (ID) or iron-sufficient diets from gestational day 13 to postnatal day (P) 7. Pups received alcohol (0, 3.5, 5.0 g/kg) from P 4 to P 9, targeting the brain growth spurt. At P 32, learning was assessed using delay or trace eyeblink classical conditioning (ECC). Cerebellar interpositus nucleus (IPN) and hippocampal CA1 cellularity was quantified using unbiased stereology. Results: Global analysis of variance revealed that ID and alcohol separately and significantly reduced ECC learning with respect to amplitude (ps ≤ 0.001) and conditioned response [CR] percentage (ps ≤ 0.001). Iron and alcohol interacted to reduce CR percentage in the trace ECC task (p = 0.013). Both ID and alcohol significantly reduced IPN (ps < 0.001) and CA1 cellularity (ps < 0.005). CR amplitude correlated with IPN cellularity (delay: r = 0.871, trace: r = 0.703, ps < 0.001) and CA1 cellularity (delay: r = 0.792, trace: r = 0.846, ps < 0.001) across both tasks. The learning impairments persisted even though the offsprings' iron status had normalized. Conclusions: Supporting our previous work, gestational ID exacerbates the associative learning deficits in this rat model of FASD. This is strongly associated with cellular reductions within the ECC neurocircuitry. Significant learning impairments in FASD could be the consequence, in part, of pregnancies in which the mother was also iron inadequate.
    Alcoholism Clinical and Experimental Research 09/2015; DOI:10.1111/acer.12876
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    ABSTRACT: Background: Identifying and engaging excessive alcohol users in primary care may be an effective way to improve patient health outcomes, reduce alcohol-related acute care events, and lower costs. Little is known about what structures of primary care team communication are associated with alcohol-related patient outcomes. Methods: Using a sociometric survey of primary care clinic communication, this study evaluated the relation between team communication networks and alcohol-related utilization of care and costs. Between May 2013 and December 2013, a total of 155 healthcare employees at 6 primary care clinics participated in a survey on team communication. Three-level hierarchical modeling evaluated the link between connectedness within the care team and the number of alcohol-related emergency department visits, hospital days, and associated medical care costs in the past 12 months for each team's primary care patient panel. Results: Teams (n = 31) whose registered nurses displayed more strong (at least daily) face-to-face ties and strong (at least daily) electronic communication ties had 10% fewer alcohol-related hospital days (rate ratio [RR] = 0.90; 95% confidence interval [CI]: 0.84, 0.97). Furthermore, in an average team size of 19, each additional team member with strong interaction ties across the whole team was associated with $1,030 (95% CI: -$1,819, -$241) lower alcohol-related patient healthcare costs per 1,000 team patients in the past 12 months. Conversely, teams whose primary care practitioner (PCP) had more strong face-to-face communication ties and more weak (weekly or several times a week) electronic communication ties had 12% more alcohol-related hospital days (RR = 1.12; 95% CI: 1.03, 1.23) and $1,428 (95% CI: $378, $2,478) higher alcohol-related healthcare costs per 1,000 patients in the past 12 months. The analyses controlled for patient age, gender, insurance, and comorbidity diagnoses. Conclusions: Excessive alcohol-using patients may fair better if cared for by teams whose face-to-face and electronic communication networks include more team members and whose communication to the PCP has been streamlined to fewer team members.
    Alcoholism Clinical and Experimental Research 09/2015; 39(10). DOI:10.1111/acer.12831
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    ABSTRACT: Background: Chronic alcohol consumption is a critical contributing factor to ischemic stroke, as it enhances ischemia-induced glutamate release, leading to more severe excitotoxicity and brain damage. But the neural mechanisms underlying this phenomenon are poorly understood. Methods: We evaluated the effects of chronic alcohol exposure on the modulation of ischemia-induced glutamate release via CB1 and CB2 cannabinoid receptors during middle cerebral artery occlusion, using in vivo microdialysis coupled with high-performance liquid chromatography, in alcohol-naïve rats or rats after 1 or 30 days of withdrawal from chronic ethanol intake (6% v/v for 14 days). Results: Intra-dorsal hippocampus (DH) infusions of ACEA or JWH133, selective CB1 or CB2 receptor agonists, respectively, decreased glutamate release in the DH in alcohol-naïve rats in a dose-dependent manner. Such an effect was reversed by co-infusions of SR141716A or AM630, selective CB1 or CB2 receptor antagonists, respectively. After 30 days, but not 1 day of withdrawal, ischemia induced an enhancement in glutamate release in the DH, as compared with non-alcohol-treated control group. Intra-DH infusions of JWH133, but not ACEA, inhibited ischemia-induced glutamate release in the DH after 30 days of withdrawal. Finally, 1 day of withdrawal did not alter the protein level of CB1 or CB2 receptors in the DH, as compared to non-alcohol-treated control rats. Whereas 30 days of withdrawal robustly decreased the protein level of CB1 receptors, but failed to alter the protein level of CB2 receptors, in the DH, as compared to non-alcohol-treated control rats. Conclusions: Together, these findings suggest that loss of expression/function of CB1 receptors, but not CB2 receptors in the DH, is correlated with the enhancement of ischemia-induced glutamate release after prolonged alcohol withdrawal.
    Alcoholism Clinical and Experimental Research 09/2015; 39(10). DOI:10.1111/acer.12845
  • Alcoholism Clinical and Experimental Research 09/2015; DOI:10.1111/acer.12877
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    ABSTRACT: Deficits in neuronal plasticity underlie many neurobehavioral and cognitive problems presented in fetal alcohol spectrum disorder (FASD). Our laboratory has developed a ferret model showing that early alcohol exposure leads to a persistent disruption in ocular dominance plasticity (ODP). For instance, a few days of monocular deprivation results in a robust reduction of visual cortex neurons' responsiveness to stimulation of the deprived eye in normal animals, but not in ferrets with early alcohol exposure. Previously our laboratory demonstrated that overexpression of serum response factor (SRF) exclusively in astrocytes can improve neuronal plasticity in FASD. Here, we test whether neuronal overexpression of SRF can achieve similar effects. Ferrets received 3.5 g/kg alcohol intraperitoneally (25% in saline) or saline as control every other day between postnatal day 10 to 30, which is roughly equivalent to the third trimester of human gestation. Animals were given intracortical injections of a Herpes Simplex Virus-based vector to express either green fluorescent protein or a constitutively active form of SRF in infected neurons. They were then monocularly deprived by eyelid suture for 4 to 5 days after which single-unit recordings were conducted to determine whether changes in ocular dominance had occurred. Overexpression of a constitutively active form of SRF by neurons restored ODP in alcohol-treated animals. This effect was observed only in areas near the site of viral infection. Overexpression of SRF in neurons can restore plasticity in the ferret model of FASD, but only in areas near the site of infection. This contrasts with SRF overexpression in astrocytes which restored plasticity throughout the visual cortex. Copyright © 2015 by the Research Society on Alcoholism.
    Alcoholism Clinical and Experimental Research 09/2015; DOI:10.1111/acer.12844
  • Alcoholism Clinical and Experimental Research 09/2015; 39(10). DOI:10.1111/acer.12849
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    ABSTRACT: Chronic alcohol exposure exerts numerous adverse effects, although the specific mechanisms underlying these negative effects on different tissues are not completely understood. Alcohol also affects core properties of the circadian clock system, and it has been shown that disruption of circadian rhythms confers vulnerability to alcohol-induced pathology of the gastrointestinal barrier and liver. Despite these findings, little is known of the molecular interactions between alcohol and the circadian clock system, especially regarding implications for tissue-specific susceptibility to alcohol pathologies. The aim of this study was to identify changes in expression of genes relevant to alcohol pathologies and circadian clock function in different tissues in response to chronic alcohol intake. Wild-type and circadian Clock(Δ19) mutant mice were subjected to a 10-week chronic alcohol protocol, after which hippocampal, liver, and proximal colon tissues were harvested for gene expression analysis using a custom-designed multiplex magnetic bead hybridization assay that provided quantitative assessment of 80 mRNA targets of interest, including 5 housekeeping genes and a predetermined set of 75 genes relevant for alcohol pathology and circadian clock function. Significant alterations in expression levels attributable to genotype, alcohol, and/or a genotype by alcohol interaction were observed in all 3 tissues, with distinct patterns of expression changes observed in each. Of particular interest was the finding that a high proportion of genes involved in inflammation and metabolism on the array was significantly affected by alcohol and the Clock(Δ19) mutation in the hippocampus, suggesting a suite of molecular changes that may contribute to pathological change. These results reveal the tissue-specific nature of gene expression responses to chronic alcohol exposure and the Clock(Δ19) mutation and identify specific expression profiles that may contribute to tissue-specific vulnerability to alcohol-induced injury in the brain, colon, and liver. Copyright © 2015 by the Research Society on Alcoholism.
    Alcoholism Clinical and Experimental Research 09/2015; 39(10). DOI:10.1111/acer.12834
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    ABSTRACT: Background The P2X4 receptor (P2X4R) is thought to be involved in regulating alcohol-consuming behaviors, and ethanol (EtOH) has been reported to inhibit P2X4Rs. Ivermectin is an antiparasitic agent that acts as a positive allosteric modulator of the P2X4R. This study examined the effects of systemically and centrally administered ivermectin on alcohol drinking of replicate lines of high-alcohol-drinking (HAD-1/HAD-2) rats, and the effects of lentiviral-delivered short-hairpin RNAs (shRNAs) targeting P2rx4 on EtOH intake of female HAD-2 rats.Methods For the first experiment, adult male HAD-1 and HAD-2 rats were given 24-hour free-choice access to 15% EtOH versus water. Dose–response effects of ivermectin (1.5 to 7.5 mg/kg, intraperitoneally [i.p.]) on EtOH intake were determined; the effects of ivermectin were then examined for 2% w/v sucrose intake over 5 consecutive days. In the second experiment, female HAD-2 rats were trained to consume 15% EtOH under 2-hour limited access conditions, and dose–response effects of intracerebroventricular (ICV) administration of ivermectin (0.5 to 2.0 μg) were determined over 5 consecutive days. The third experiment determined the effects of microinfusion of a lentivirus expressing P2rx4 shRNAs into the posterior ventral tegmental area (VTA) on 24-hour EtOH free-choice drinking of female HAD-2 rats.ResultsThe highest i.p. dose of ivermectin reduced alcohol drinking (30 to 45%) in both rat lines, but did not alter sucrose intake. HAD-2 rats appeared to be more sensitive than HAD-1 rats to the effects of ivermectin. ICV administration of ivermectin reduced 2-hour limited access intake (~35%) of female HAD-2 rats; knockdown of P2rx4 expression in the posterior VTA reduced 24-hour free-choice EtOH intake (~20%).Conclusions Overall, the results of this study support a role for P2X4Rs within the mesolimbic system in mediating alcohol-drinking behavior.
    Alcoholism Clinical and Experimental Research 09/2015; DOI:10.1111/acer.12836
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    ABSTRACT: Alcoholics have been reported to have reduced levels of magnesium in both their extracellular and intracellular compartments. Calcium-dependent potassium channels (BK) are known to be one of ethanol (EtOH)'s better known molecular targets. Using outside-out patches from hippocampal neuronal cultures, we examined the consequences of altered intracellular Mg(2+) on the effects that EtOH has on BK channels. We find that the effect of EtOH is bimodally influenced by the Mg(2+) concentration on the cytoplasmic side. More specifically, when internal Mg(2+) concentrations are ≤200 μM, EtOH decreases BK activity, whereas it increases activity when Mg(2+) is at 1 mM. Similar results are obtained when using patches from HEK cells expressing only the α-subunit of BK. When patches are made with the actin destabilizer cytochalasin D present on the cytoplasmic side, the potentiation caused by EtOH becomes independent of the Mg(2+) concentration. Furthermore, in the presence of the actin stabilizer phalloidin, EtOH causes inhibition even at Mg(2+) concentrations of 1 mM. Internal Mg(2+) can modulate the EtOH effects on BK channels only when there is an intact, internal actin interaction with the channel, as is found at synapses. We propose that the EtOH-induced decrease in cytoplasmic Mg(2+) observed in frequent/chronic drinkers would decrease EtOH's actions on synaptic (e.g., actin-bound) BK channels, producing a form of molecular tolerance. Copyright © 2015 by the Research Society on Alcoholism.
    Alcoholism Clinical and Experimental Research 09/2015; 39(9):1671-9. DOI:10.1111/acer.12821
  • Alcoholism Clinical and Experimental Research 09/2015; DOI:10.1111/acer.12858
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    ABSTRACT: Alcohol-dependent patients are known to be generally more unfairness sensitive. The ultimatum game (UG) is an experimental task designed to provoke feelings of perceived unfairness. A previous study using the UG has reported more unfairness sensitivity in patients with alcohol dependence than in a nondependent control group; it has been speculated that this increased sensitivity might be due to a difficulty in impulse control. However, the mechanism of this relationship has not been clarified. Therefore, the relationship between unfairness sensitivity in interpersonal relationships and impulsivity was investigated using UG and delay discounting (DD) paradigms. Subjects were 32 individuals with alcohol dependency and 36 healthy control individuals; both groups performed UG and DD tasks. Participants with alcohol dependence rejected monetary offers deemed unfair at a significantly higher rate than did control participants. Moreover, the proportion of accepting unfairness was negatively correlated with impulsivity in patients with alcohol dependence. Perceived unfairness is related to impulsivity in patients with alcohol dependence. These results provide insights concerning the psychopathology of alcohol dependence. Copyright © 2015 by the Research Society on Alcoholism.
    Alcoholism Clinical and Experimental Research 09/2015; 39(10). DOI:10.1111/acer.12832