Peter R. Finn’s research while affiliated with Indiana University Bloomington and other places

Borderline personality disorder (BPD) is highly comorbid with internalizing and externalizing psychopathology. The current study replicates findings indicating that BPD symptomatology is influenced by the distress subfactor of both the internalizing and the externalizing dimension of psychopathology. Confirmatory factor analysis of the covariance of continuous measures of externalizing pathology, internalizing pathology, and BPD symptoms was assessed in 837 young adults. The sample contained a range of externalizing severity from none to high severity, leading to an overrepresentation of externalizing problems. BPD symptoms were associated with both the externalizing dimension and the distress subfactor of the internalizing dimension. Interestingly, BPD had a stronger association with the externalizing dimension than observed in previous studies. Results replicated earlier findings using different and more dimensional measures. Findings indicated that BPD is more heavily influenced by the externalizing dimension of psychopathology within a high externalizing sample, such as those presenting for treatment of alcohol or substance use disorders.

Background Low working memory (WM) capacity is associated with alcohol use disorders (AUDs). The importance of WM to adaptive functioning has led to a recent influx of studies attempting to improve individual WM capacity using various cognitive training methods. The present study aimed to examine the efficacy of complex WM training for improving WM capacity among individuals with AUD. Methods Individuals were randomized to complete either adaptive WM training or active control training. We applied a methodologically rigorous and structured approach, including a battery of near and moderate transfer measures in those with AUDs and a control group. Additionally, we examined cognitive factors (at baseline) and other predictors of adherence, training task improvement, and transfer. Results Results suggest improved WM in individuals with AUDs and controls, as evidenced by improved scores on several transfer measures, after adaptive WM training. However, individuals with AUDs showed poorer adherence and less improvement on the training tasks themselves. Neither IQ, WM, sex, nor condition predicted adherence. Level of training task performance, baseline WM, and IQ predicted transfer task improvement. Conclusions This is the first study to rigorously examine both the efficacy of WM training in those with AUDs, and predictors of successful training program adherence and transfer in a large sample. Among study completers, results suggest that although AUD status does not predict training improvement and transfer. However, AUD status did predict lower program adherence. WM training was more effective in those with higher cognitive ability at baseline. This study provides direct translation to the development of cognitive interventions for treating AUD. This article is protected by copyright. All rights reserved.

Phishing is a fraudulent form of email that solicits personal or financial information from the recipient, such as a password, username, or social security or bank account number. The scammer may use the illicitly obtained information to steal the victim’s money or identity or sell the information to another party. The direct costs of phishing on consumers are exceptionally high and have risen substantially over the past 12 years. Phishing experiments that simulate real world conditions can provide cybersecurity experts with valuable knowledge they can use to develop effective countermeasures and prevent people from being duped by phishing emails. Although these experiments contravene widely accepted informed consent requirements and involve deception, we argue that they can be conducted ethically if risks are minimized, confidentiality and privacy are protected, potential participants have an opportunity to opt out of the research before it begins, and human subjects are debriefed after their participation ends.

Abnormalities in brain white matter (WM) structure have been reported in youths having a family history of substance use disorders (SUDs). It was hypothesized that these abnormalities constitute features of the liability for SUDs transmitted across generations. The association between severity of intergenerational risk for SUD, measured by the Transmissible Liability Index (TLI), and white matter microstructure was examined. Diffusion tensor imaging (DTI) measured WM microstructure in forty-four drug-naïve 10–14 year-olds (N = 19 with parental SUD). Metrics of WM microstructure (i.e., fractional anisotropy, radial diffusivity, mean diffusivity and axial diffusivity) were quantified across the whole brain and in four tracts of interest: anterior corona radiata, superior and inferior longitudinal fasciculi and superior fronto-occipital fasciculi. The TLI was completed by the youths, their parents and, when available, their teachers. The relationship between WM structure and TLI score across the entire group was evaluated using linear multiple regression and between group comparisons were also examined. Fractional anisotropy and radial diffusivity in multiple tracts across the brain were significantly associated with TLI scores. Confirming and extending prior research, the findings indicate that global atypicality in WM tracts was linearly related to liability for eventual SUD development in drug naïve youths.

Alcohol use disorder (AUD) has been consistently associated with elevated discounting rates for delayed rewards. However, there are few studies of delay discounting of losses in those with AUD even though their drinking behavior suggests that they discount future negative consequences of excessive drinking. The current study extends this literature by examining delay discounting of rewards and losses in a sample of those with AUD (n = 78) and healthy controls (n = 51) in 2 conditions: working memory (WM) load and no WM load. The AUD group discounted both rewards and losses at higher rates than the control group. The WM load increased discounting rates in the reward task but not in the loss task. There was also a significant Group × WM load interaction; the WM load increased discounting in control participants but not in AUD participants. These findings suggest that AUD is associated with a general propensity to discount future incentivized events regardless of nature of the incentive.

Growing evidence suggests that glutamate neurotransmission plays a critical role in alcohol addiction. Cue-induced change of glutamate has been observed in animal studies but never been investigated in humans. This work investigates cue-induced change in forebrain glutamate in individuals with alcohol use disorder (AUD). A total of 35 subjects (17 individuals with AUD and 18 healthy controls) participated in this study. The glutamate concentration was measured with single-voxel 1H-MR spectroscopy at the dorsal anterior cingulate. Two MRS sessions were performed in succession, the first to establish basal glutamate levels and the second to measure the change in response to alcohol cues. The changes in glutamate were quantified for both AUD subjects and controls. A mixed model ANOVA and t-tests were performed for statistical analysis. ANOVA revealed a main effect of cue-induced decrease of glutamate level in the anterior cingulate cortex (ACC). A significant interaction revealed that only AUD subjects showed significant decrease of glutamate in the ACC. There were no significant group differences in the level of basal glutamate. However, a negative correlation was found between the basal glutamate level and the number of drinking days in the past 2 weeks for the AUD subjects. Collectively, our results indicate that glutamate in key areas of the forebrain reward circuit is modulated by alcohol cues in early alcohol dependence.

Marc Potenza and colleagues1 advocated classifying “excessive sexual behaviour” as an addictive disorder in ICD-11. Sex has components of liking and wanting that share neural systems with many other motivated behaviours.2 However, experimental studies do not support key elements of addiction such as escalation of use, difficulty regulating urges, negative effects, reward deficiency syndrome, withdrawal syndrome with cessation, tolerance, or enhanced late positive potentials. A key neurobiological feature of addiction is the increased responsiveness of glutamate neurons that synapse on the nucleus accumbens. These changes might affect long-term sensitisation of the mesocorticolimbic dopamine pathway, as manifested by a range of symptoms including cue-induced craving and compulsive drug use.3 To date, research on the effects of sex on glutamate function and its modulation of dopamine pathways is scarce. Sex is a primary reward, with unique peripheral representation. Engagement in sex is positively associated with health and life satisfaction. Sex does not allow for supraphysiological stimulation. Research in this area has yet to investigate actual partnered sexual behaviours. Experimental work has been limited to sexual cues, or secondary rewards, using images. More research is needed, but data concerning frequent or excessive sex do not support its inclusion as an addiction. Also, data are not sufficient to differentiate between compulsive and impulsive models. Many other approaches exist, including well-supported non-pathological models.4 Potenza and colleagues5 also stated that addiction criteria were not met for sexual behaviours: we agree with this earlier conclusion.

Executive working memory capacity (eWMC) is central to adaptive decision-making. Research has revealed reduced eWMC and higher rates of impulsive decision making in individuals with alcohol use disorders (AUDs: DSM-IV Alcohol Dependence of Alcohol Abuse) and antisocial psychopathology (AP). Recent work has shown that placing a load on working memory (WM) further increases impulsive decision making on the delay discounting (DD) task in those with AUDs and AP. The current study examined the effects of an attention refocusing manipulation to offset the effects of this WM-load on DD rates in control subjects, those with AUDs without AP, and AUDs with AP (AUD-AP). Results revealed that 1) the AUD-AP group had higher DD rates (i.e., more impulsive decision-making) than the AUD group, followed by controls, and 2) attention refocusing after a load is placed on WM was associated with lower DD rates compared to the load without refocusing in both AUD groups, but not controls. Results suggest that refocusing attention after a cognitive load may be an effective cognitive strategy for reducing the impulsivity-enhancing effects of cognitive load on decision making in individuals with AUDs and AP.

Background: Alcohol use disorders (AUDs) are associated with increased discounting of delayed rewards and reduced executive working memory (eWM) capacity. This association is amplified when comorbid with antisocial psychopathology (AP). Furthermore, recent studies suggest that reduced WM capacity is associated with disinhibited decisions reflected by increased impulsive decision-making on the delay discounting of rewards task. While discounting of delayed rewards is well studied, the discounting of delayed losses (DDL) has received significantly less experimental attention. Methods: The current study investigated: 1) the rate of DDL in individuals with AUD only (n=61), AUD with comorbid AP (n=79) and healthy controls (n=64); 2) the relationship between eWM capacity and discounting of delayed losses; and 3) the effect of a WM load on discounting of delayed losses. Discounting performance was assessed using a computerized discounting of delayed losses task. Results: Results showed that the AUD-only and AUD-AP groups had higher rates of DDL and lower eWM capacity compared to the control groups. Lower individual eWM capacity was associated with increased discounting of delayed losses. However, WM load did not increase discounting rates overall. Conclusions: These results support the hypothesis that greater discounting of delayed losses is associated with AUD and comorbid AP problems and lower individual eWM capacity. This article is protected by copyright. All rights reserved.