Drinking motives in alcohol use disorder patients with and without social anxiety disorder

The high comorbidity of alcohol use disorders (AUD) and social anxiety disorder (SAD) is often explained by excessive drinking in social situations to self-medicate social anxiety. Indeed, the motive to drink alcohol to lower social fears was found to be elevated in socially anxious persons. However, this social anxiety specific motive has not been directly investigated in primarily alcohol dependent individuals. We explored social anxiety, the motivation to drink alcohol in order to cope with social fears, and social anxiety as a consequence of drinking in AUD with and without comorbid SAD. Male AUD inpatients with (AUD+SAD group, N=23) and without comorbid SAD (N=37) completed a clinical interview and a questionnaire assessment. AUD+SAD patients reported higher levels of depression and an elevated motive to drink due to social anxiety but did not experience more social fears as a consequence of drinking. Previous results concerning alcohol drinking motives in order to relieve social fears could be replicated in a clinical AUD sample. Additionally, our findings suggest comorbid AUD+SAD patients to be more burdened regarding broader psychopathological symptoms. Thus, accessibility to SAD-specific screening and treatment procedures may be beneficial for primary AUD patients.     

Understanding the Progression from Early Alcohol Use Experimentation to Alcohol Use Disorder: Testing Vulnerability by Experience Interactions Using a Two-Part Latent Growth Curve Model

Most adolescents experiment with alcohol, but a smaller percentage advance to heavy alcohol use (AU) and AU disorder (AUD). Understanding for whom and how early risk leads to AUD is of interest to prevention, treatment, and etiology of AUD. Informed by developmental and behavioral neuroscience theory, the current study tested whether temperament (effortful control, surgency, and negative affect), peer AU (multi-reporter), and AU with parents’ permission interacted to distinguish youth who experiment with alcohol from those who escalate to AUD. Community adolescents (N?=?765, 53% female) were assessed annually for seven years (M_age?=?11.8, range: 10–13 at Year 1; M_age?=?18.7; range?=?17–20 at year 7). Temperament by early experience interactions were expected to predict amount of AU. Amount of AU was expected to mediate the relationship between the interactions and AUD symptoms (assessed at Years 3 and 7, M_age?=?13.8 and 18.7) above and beyond a range of confounds (e.g., problem behavior and parental AU and AUD). Supporting hypotheses, effortful control and surgency interacted with AU with parents’ permission and peer AU, respectively, to predict higher amount of AU (R²?=?0.47) and AUD symptoms (R²?=?0.03). Results support developmental and behavioral neuroscience theory. High surgency and low effortful control in conjunction with peer AU and AU with parents’ permission were associated with large effects on AU and moderate mediated effects through AU to AUD. AU with parents’ permission was risky at low and high effortful control and protective when peers used alcohol.

     

An Examination of Alcohol Use Disorder Symptoms and Neighborhood Disorganization from Age 21 to 39

Living in disorganized neighborhoods characterized by high levels of poverty, crime, violence, and deteriorating buildings has been associated with increased alcohol consumption and mental health problems. Data drawn from the Seattle Social Development Project (N = 790), a theory‐driven longitudinal study originating in Seattle, WA, were used to estimate trajectories of Alcohol Use Disorder (AUD) symptoms from age 21 to 39. Time‐varying measures of neighborhood disorganization, psychological distress, and sociodemographic factors were associated with deviations from average AUD symptoms at each wave. Results indicated that, on average, AUD symptoms decreased as individuals got older. Living in more disorganized neighborhoods and experiencing psychological distress was associated with increased AUD symptoms after accounting for average reductions from AUD symptoms over time and time‐varying measures of relevant sociodemographic factors. Results of mediation analysis suggested that psychological distress is a mechanism by which disorganized neighborhoods increased risk of AUD from age 21 to 39.     

Slowing the Tide of Alcohol Use Disorders

Alcohol use disorders (AUDs)—a spectrum including at-risk drinking, alcohol abuse, dependence, and addiction—is a highly prevalent problem worldwide with a substantial economic impact. The toll of alcohol on individual health and healthcare systems is devastating. Alcohol is estimated to be the fifth leading risk factor for global disability-adjusted life years. Tackling the problem of AUD requires a comprehensive strategy that includes solid action on price, availability, and marketing of alcohol. Restricting or banning alcohol advertising may reduce exposure to the risk posed by alcohol at the individual and general population level. Warning labels about the cancer risks associated with drinking have a high degree of public support and may be an inexpensive and acceptable way to educate the public. Religiosity may reduce risk behaviors and contribute to health decision making related to alcohol use.

     

Impulsivity in rodents with a genetic predisposition for excessive alcohol consumption is associated with a lack of a prospective strategy

Increasing evidence supports the hypothesis that impulsive decision-making is a heritable risk factor for an alcohol use disorder (AUD). Clearly identifying a link between impulsivity and AUD risk, however, is complicated by the fact that both AUDs and impulsivity are heterogeneous constructs. Understanding the link between the two requires identifying the underlying cognitive factors that lead to impulsive choices. Rodent models have established that a family history of excessive drinking can lead to the expression of a transgenerational impulsive phenotype, suggesting heritable alterations in the decision-making process. In the present study, we explored the cognitive processes underlying impulsive choice in a validated, selectively bred rodent model of excessive drinking—the alcohol-preferring (“P”) rat. Impulsivity was measured via delay discounting (DD), and P rats exhibited an impulsive phenotype as compared to their outbred foundation strain—Wistar rats. Steeper discounting in P rats was associated with a lack of a prospective behavioral strategy, which was observed in Wistar rats and was directly related to DD. To further explore the underlying cognitive factors mediating these observations, a drift diffusion model of DD was constructed. These simulations supported the hypothesis that prospective memory of the delayed reward guided choice decisions, slowed discounting, and optimized the fit of the model to the experimental data. Collectively, these data suggest that a deficit in forming or maintaining a prospective behavioral plan is a critical intermediary to delaying reward, and by extension, may underlie the inability to delay reward in those with increased AUD risk.     

Personality and the genetic risk for alcohol dependence

The extent to which the genetic risk for alcohol dependence (AD) and conduct disorder (CD) and their common genetic risk overlap with genetic factors contributing to variation in dimensions of personality was examined in a study of 6,453 individuals from 3,383 adult male and female same-sex and unlike-sex twin pairs from the Australian Twin Registry. The associations between the personality dimensions of positive emotionality, negative emotionality, and AD and CD risk were modest, whereas the associations between behavioral undercontrol and AD and CD risk were substantially higher. Genetic influences contributing to variation in behavioral undercontrol accounted for about 40% of the genetic variation in AD and CD risk and about 90% of the common genetic risk for AD and CD. These results suggest that genetic factors contributing to variation in dimensions of personality, particularly behavioral undercontrol, account for a substantial proportion of the genetic diathesis for AD and most of the common genetic diathesis for AD and CD among both men and women.     

Dietary restraint moderates genetic risk for binge eating

Dietary restraint is a prospective risk factor for the development of binge eating and bulimia nervosa. Although many women engage in dietary restraint, relatively few develop binge eating. Dietary restraint may increase susceptibility for binge eating only in individuals who are at genetic risk. Specifically, dietary restraint may be a behavioral exposure factor that activates genetic predispositions for binge eating. We investigated this possibility in 1,678 young adolescent and adult same-sex female twins from the Minnesota Twin Family Study and the Michigan State University Twin Registry. Twin moderation models were used to examine whether levels of dietary restraint moderate genetic and environmental influences on binge eating. Results indicated that genetic and nonshared environmental factors for binge eating increased at higher levels of dietary restraint. These effects were present after controlling for age, body mass index, and genetic and environmental overlap among dietary restraint and binge eating. Results suggest that dietary restraint may be most important for individuals at genetic risk for binge eating and that the combination of these factors could enhance individual differences in risk for binge eating.     

Underage drinking as a predictor of alcohol use disorder among African Americans

This study aimed to examine the effect of underage drinking (UD) on alcohol use disorder (AUD) among African Americans. Data from the 2010 National Survey of Drug Use and Health (NSDUH) (N = 19 240; age range 25–75 years) were analysed for the study. Following regression analysis, African Americans with a history of underage drinking were found to be approximately four times more likely to experience AUD than their counterparts without a history of underage drinking. Within the underage drinking history group, those who are married and who had higher levels of education were less likely to have AUD compared to single persons who had lower levels of education. Age and gender did not predict AUD among those with a history of underage drinking. The findings of this study suggest that familial relationships may moderate the risks for AUD from UD. Primary socialisation theory might explain risk for AUD from UD among African Americans by way of intergenerational transmission of health values.     

Alcohol-Induced Amnesia and Personalized Drinking Feedback: Blackouts Predict Intervention Response

Alcohol-induced amnesia (“blackout”) is a reliable predictor of alcohol-related harm. Given its association with other negative consequences, experience of alcohol-induced amnesia may serve as a teachable moment, after which individuals are more likely to respond to intervention. To test this hypothesis, alcohol-induced amnesia was evaluated as a moderator of brief intervention effect on (a) alcohol-related consequences and (b) the proposed intervention mediators, protective behavioral strategies and peak blood alcohol concentration (BAC). Baseline alcohol risk measured using the Alcohol Use Disorders Identification Test (AUDIT) was also evaluated as a moderator to rule out the possibility that amnesia is simply an indicator of more general alcohol risk. College students (N = 198) reporting alcohol use in a typical week completed assessments at baseline and 1-month follow-up as part of a larger intervention trial. Participants were randomized to assessment only (AO; n = 58) or personalized feedback intervention (PFI; n = 140). Hierarchical regression was used to examine direct and indirect intervention effects. A significant group-by-amnesia interaction revealed that only PFI participants who had experienced alcohol-induced amnesia in the past month reported decreases in alcohol consequences at 1-month follow-up. The PFI reduced alcohol-related consequences indirectly through changes in peak BAC, but only among those who had experienced amnesia at baseline. In contrast, baseline alcohol risk (AUDIT) did not moderate intervention effects, and use of protective behavioral strategies did not statistically mediate intervention effects. Findings suggest that loss of memory for drinking events is a unique determinant of young adult response to brief alcohol intervention. Normative feedback interventions may be particularly effective for individuals who have experienced alcohol-induced amnesia in the past 30 days.     

Brain functions associated with verbal working memory tasks among young males with alcohol use disorders

This study aimed to investigate the differences in brain functions during verbal working memory between individuals with alcohol use disorders (AUD) and normal controls. fMRI was used to scan brain activations associated with verbal working memory while participants performed 2-back and 0-back tasks. A total of 21 young male college students participated in the study. Eleven of those who clinically met the criteria for AUD were assigned to the AUD group, whereas ten demographically similar subjects who were social drinkers but not AUD were assigned to the normal control group. The AUD group showed less activation in bilateral frontal and precentral, left superior temporal, left superior parietal, and left cerebellar cortex during the 2-back task relative to 0-back task compared to the normal control group. In contrast, the control group showed less activation only in the right uncus than the AUD group. These results suggest that subjects with AUD present abnormality in brain functioning during verbal working memory.     

Drinking motives as mediators in the relation between personality disorder symptoms and alcohol use disorder

Research shows high comorbidity between Cluster B Personality Disorders (PDs) and Alcohol Use Disorders (AUDs). Studies of personality traits and alcohol use have identified coping and enhancement drinking motives as mediators of the relation among impulsivity, negative affectivity or affectivity instability, and alcohol use. To the extent that certain PDs reflect extreme expression of these traits, drinking motives were hypothesized to mediate the relation between PD symptoms and presence/absence of an alcohol use disorder (AUD). This hypothesis was tested using a series of cross-sectional and prospective path models estimating the extent that coping and enhancement drinking motives mediated the relation between cluster A, B, and C PD symptom counts and AUD diagnosis among a sample of 168 young adults between ages 18 and 21. Enhancement motives mediated the cross-sectional relation between Cluster B symptoms and AUD. Prospectively, enhancement motives partially mediated the relation between Cluster B personality symptoms and AUD through the stability of Year 1 AUD to Year 3 AUD. Results suggest that enhancement motives may be especially important in understanding the relation between Cluster B personality disorders and AUDs.     

Prospective analysis of comorbidity: tobacco and alcohol use disorders

Alcohol use disorders (AUD) and tobacco use disorders (TD) frequently co-occur. The authors examined AUD-TD comorbidity over time using a state-trait (ST) model. The ST model represents variance in AUD/TD as a traitlike factor that spans measurement occasion and identifies distinct sources of variance in AUD-TD comorbidity. The ST model was evaluated on 450 young adults (baseline age = 18.5 years; 51% with family history of alcoholism) assessed 5 times over 7 years. The ST model demonstrated superior fit over a first-order autoregressive model. The tendency to diagnose with AUD and TD was partially explained by family history of alcoholism; this relationship was mediated by childhood stressors, alcohol expectancies, and behavioral undercontrol. Results supported a common third-variable influence (vs. directional) model of comorbidity. The ST model is an important conceptual and methodological approach to the prospective study of comorbidity in general.     

A Role for Cognitive Rehabilitation in Increasing the Effectiveness of Treatment for Alcohol Use Disorders

Neurocognitive impairments are prevalent in persons seeking treatment for alcohol use disorders (AUDs). These impairments and their physical, social, psychological and occupational consequences vary in severity across persons, much like those resulting from traumatic brain injury; however, due to their slower course of onset, alcohol-related cognitive impairments are often overlooked both within and outside of the treatment setting. Evidence suggests that cognitive impairments can impede treatment goals through their effects on treatment processes. Although some recovery of alcohol-related cognitive impairments often occurs after cessation of drinking (time-dependent recovery), the rate and extent of recovery is variable across cognitive domains and individuals. Following a long hiatus in scientific interest, a new generation of research aims to facilitate treatment process and improve AUD treatment outcomes by directly promoting cognitive recovery (experience-dependent recovery). This review updates knowledge about the nature and course of cognitive and brain impairments associated with AUD, including cognitive effects of adolescent AUD. We summarize current evidence for indirect and moderating relationships of cognitive impairment to treatment outcome, and discuss how advances in conceptual frameworks of brain-behavior relationships are fueling the development of novel AUD interventions that include techniques for cognitive remediation. Emerging evidence suggests that such interventions can be effective in promoting cognitive recovery in persons with AUD and other substance use disorders, and potentially increasing the efficacy of AUD treatments. Finally, translational approaches based on cognitive science, neurophysiology, and neuroscience research are considered as promising future directions for effective treatment development that includes cognitive rehabilitation.     

Anosognosia for Memory Impairment in Addiction: Insights from Neuroimaging and Neuropsychological Assessment of Metamemory

In addiction, notably Alcohol Use Disorder (AUD), patients often have a tendency to fail to acknowledge the reality of the disease and to minimize the physical, psychological, and social difficulties attendant to chronic alcohol consumption. This lack of awareness can reduce the chances of initiating and maintaining sobriety. Presented here is a model focusing on compromised awareness in individuals with AUD of mild to moderate cognitive deficits, in particular, for episodic memory impairment—the ability to learn new information, such as recent personal experiences. Early in abstinence, alcoholics can be unaware of their memory deficits and overestimate their mnemonic capacities, which can be investigated with metamemory paradigms. Relevant neuropsychological and neuroimaging results considered suggest that the alcoholics’ impairment of awareness of their attenuated memory function can be a clinical manifestation explained mechanistically by neurobiological factors, including compromise of brain systems that result in a mild form of mnemonic anosognosia. Specifically, unawareness of memory impairment in AUD may result from a lack of personal knowledge updating attributable to damage in brain regions or connections supporting conscious recollection in episodic memory. Likely candidates are posterior parietal and medial frontal regions known to be integral part of the Default Mode Network (DMN) and the insula leading to an impaired switching mechanism between the DMN and the Central-Executive Control (i.e., Lateral Prefronto-Parietal) Network. The cognitive concepts and neural substrates noted for addictive disorders may also be relevant for problems in self-identification of functional impairment resulting from injury following war-related blast, sport-related concussion, and insidiously occurring dementia.     

Effects of Comt Genotype on Behavioral Symptomatology in the 22q11.2 Deletion Syndrome

The 22q11.2 Deletion Syndrome (DiGeorge/velocardiofacial syndrome) is associated with elevated rates of psychosis, and is also characterized by severe attentional difficulties and executive dysfunction. Behavioral manifestations of this syndrome could result from haploinsufficiency of the catechol-O-methyltransferase (COMT) gene, located within the 22q11 region. The goal of the present study was to examine COMT genotype in relation to behavioral symptomatology in this syndrome. Val^158/108Met was genotyped in 38 patients (16 Met/-, 22 Val/-) with confirmed 22q11.2 deletions who had received the Child Behavior Checklist (CBCL) as part of a comprehensive evaluation. Results indicated that the Val genotype was associated with significantly greater internalizing and externalizing behavioral symptomatology in children with 22q11.2 deletions. Val allele status was associated with a greater-than-four-fold increase in risk for clinically significant behavior problems in children with this syndrome. These data are consistent with previous findings of increased psychopathology associated with the Val genotype in normal individuals and suggest that a functional genetic polymorphism in the 22q11 region may influence behavior in individuals with COMT haploinsufficiency.     

The Links Between Social Anxiety Disorder,Insomnia Symptoms,and Alcohol Use Disorders: Findings From a Large Sample of Adolescents in the United States

Social anxiety disorder (SAD) is associated with increased risk of developing an alcohol use disorder (AUD). Most of the current literature has focused on the role of acute stress responding in this relation; however, both SAD and AUDs also are linked to insomnia symptoms (i.e., difficulty falling or staying asleep). As adolescence is a sensitive period for the onset of these disorders, the present study examined if insomnia symptoms might partially account for the SAD-AUD link in a large sample of adolescents. Data from the National Comorbidity Survey–Adolescent Supplement were examined. Participants (N = 10,140) completed interviews to assess past 12-month SAD and AUD diagnostic status as well as insomnia symptoms. Analyses tested whether insomnia symptoms accounted for a significant proportion of the SAD-AUD relation. Results indicated that insomnia symptoms were positively related to both SAD and AUD status, and the relation between SAD and AUD status was significantly reduced when insomnia symptoms were included in the model. Findings remained significant after controlling for the effects of age, gender, posttraumatic stress disorder, major depressive disorder, and other drug dependence status. Experimental examination and intensive longitudinal assessment of these relationships are needed before strong conclusions can be inferred about causality and temporal relationships. The current findings do indicate insomnia may be an important indirect and stigma-free treatment target to address in prevention and treatment efforts for SAD, AUDs, and their co-occurrence.     

Better the Devil You Know? High-Risk Individuals’ Anticipated Psychological Responses to Genetic Testing for Melanoma Susceptibility

Purpose: The psychological consequences of genetic testing for mutations among individuals at increased risk of developing melanoma remain unexamined. The present study aimed to explore anticipated emotional, behavioral, cognitive, and familial responses to hypothetical genetic testing for melanoma susceptibility. Methods: Forty semi-structured interviews were undertaken with affected (n=20) and unaffected (n=20) individuals at either high or average risk of developing melanoma due to family history. Results: In-depth thematic analysis revealed that, in response to being identified as a mutation carrier, most participants with a family history anticipated calmly accepting their increased risk; either increasing precaution adoption or maintaining already vigilant behavioral practices; perceiving such information as important and valuable; and communicating genetic test results to family members, despite the acknowledgement of potential difficulties. In response to being identified as a non-carrier, the majority of participants expected to feel relieved; to maintain current precautionary health practices; to still perceive themselves at some risk of developing melanoma; and to be wary of the potential negative behavioral consequences of disclosing such information to family members. Women appeared more likely than men to acknowledge the potential for depression and worry following genetic testing. In contrast, more males than females expected to carry a gene mutation, and viewed their current preventive practices as optimum. Conclusion: Genetic testing for melanoma risk is likely to elicit a complex array of emotional, behavioral, cognitive, and familial responses for both testees and their family members, and these responses are likely to bear subtle differences for males and females.     

Effects of COMT genotype on behavioral symptomatology in the 22q11.2 Deletion Syndrome.

The 22q11.2 Deletion Syndrome (DiGeorge/velocardiofacial syndrome) is associated with elevated rates of psychosis, and is also characterized by severe attentional difficulties and executive dysfunction. Behavioral manifestations of this syndrome could result from haploinsufficiency of the catechol-O-methyltransferase (COMT) gene, located within the 22q11 region. The goal of the present study was to examine COMT genotype in relation to behavioral symptomatology in this syndrome. Val158/108Met was genotyped in 38 patients (16 Met/-, 22 Val/-) with confirmed 22q11.2 deletions who had received the Child Behavior Checklist (CBCL) as part of a comprehensive evaluation. Results indicated that the Val genotype was associated with significantly greater internalizing and externalizing behavioral symptomatology in children with 22q11.2 deletions. Val allele status was associated with a greater-than-four-fold increase in risk for clinically significant behavior problems in children with this syndrome. These data are consistent with previous findings of increased psychopathology associated with the Val genotype in normal individuals and suggest that a functional genetic polymorphism in the 22q11 region may influence behavior in individuals with COMT haploinsufficiency.     

Alcohol use disorders and psychological distress: a prospective state-trait analysis

The present study examined the association between alcohol use disorders (AUDs) and psychological distress over an 11-year period using a sample of 378 young adults (46% men, 54% women: baseline age = 18.5; 51% with paternal history of alcoholism). The authors examined this relation using a state-trait model, which decomposes variance in a given construct into a general traitlike factor that spans measurement occasion and more situational, occasion-specific variability. Trait AUD and trait distress were correlated (r =.43), suggesting that the tendency to meet criteria for an AUD is associated with the tendency to experience psychological distress. Much of this association was due to 3rd variables (primarily neuroticism but also childhood stressors and behavioral undercontrol), supporting a common 3rd-variable influence model of comorbidity.     

Changes in Hypothesized Mechanisms of Change Before and After Initiating Abstinence in Cognitive-Behavioral Therapy for Women With Alcohol Use Disorder

Abstinence self-efficacy, coping skills, and therapeutic alliance are hypothesized mechanisms of behavioral change (MOBCs) in cognitive-behavioral therapy (CBT) for alcohol use disorder (AUD). However, little is known about when these hypothesized MOBCs change during treatment or in relation to the initiation of abstinence from alcohol, which the current study investigated. Patient-reported abstinence self-efficacy, drinking-related coping skills, and therapeutic alliance were measured at every session throughout a 12-session clinical trial that previously showed equivalent drinking reductions in female-specific individual- and group-based CBT for AUD. Participants (N = 121 women) were classified into subgroups based on whether and when they first initiated 14 days of continuous abstinence from alcohol during treatment. Interrupted time-series analyses evaluated the magnitude and timing of change in MOBC variables in relation to the initiation of abstinence. All three MOBC measures showed gradual improvements throughout treatment (within-subjects d = 0.03 to 0.09 change per week). Participants who initiated abstinence during treatment experienced additional sudden improvements in abstinence self-efficacy (d = 0.47) and coping skills (d = 0.27), but not therapeutic alliance (d = -0.02), the same week they initiated abstinence. Participants who were already abstinent when treatment started maintained higher abstinence self-efficacy and coping skills, but not therapeutic alliance, throughout treatment compared to participants who never initiated abstinence. Initiating abstinence may help facilitate improvements in abstinence self-efficacy and drinking-related coping skills. Clinicians may help patients anticipate when and how much these variables are expected to improve during treatment and encourage initiation of abstinence to potentially help facilitate improvements in abstinence self-efficacy and coping skills.