Alexithymia disrupts emotion regulation processes and is associated with greater negative affect and alcohol problems.

OBJECTIVE: Alexithymia is common among people who abuse alcohol, yet the mechanisms by which alexithymia exerts its influence remain unclear. This analysis tested a model whereby the three subscales of the Toronto Alexithymia Scale exert an indirect effect on alcohol problems through difficulties with emotion regulation and psychological distress. METHOD: Men and women (n = 141) seeking alcohol use disorder (AUD) treatment completed the Toronto Alexithymia Scale, the Difficulties with Emotion Regulation Scale, the Brief Symptom Inventory, the Short Inventory of Problems, and the Alcohol Dependence Scale. RESULTS: The Difficulty Identifying Feelings subscale of the Toronto Alexithymia Scale was positively associated with alcohol problems through emotion dysregulation and psychological distress. The other two subscales, Difficulty Describing Feelings and Externally oriented Thinking, were not associated with any other variables. CONCLUSION: People with alexithymia may consume alcohol to help regulate undifferentiated states of emotional arousal. Given the prevalence of alexithymia among people who abuse alcohol, treatment supplements that enhance the identification of emotions are needed.

The Identification of Pretreatment Trajectories of Alcohol Use and Their Relationship to Treatment Outcome in Men and Women With Alcohol Use Disorder.

BACKGROUND: Few studies have focused on behavioral changes that occur prior to entering treatment for an alcohol use disorder (AUD). In 2 studies (Psychol Addict Behav, 27, 2013, 1159; J Stud Alcohol, 66, 2005, 369), pretreatment reductions in alcohol use were associated with better treatment outcomes. Identifying patterns of pretreatment change has the potential to inform clinical decision making. METHODS: This study sought to identify pretreatment change trajectories in individuals seeking outpatient treatment for AUD (N = 205) using finite mixture modeling based on changes in number of days abstinent per week (NDA). RESULTS: The analysis identified 3 pretreatment trajectory classes. Class 1 (High Abstinence-Minimal Increase; HA-MI) (n = 64; 31.2%) reported a high level of pretreatment NDA with minimal change during an 8-week pretreatment interval. Class 2 (Low Abstinence-Steady Increase; LA-SI) (n = 73; 35.6%) reported a low level of pretreatment NDA followed by a steady increase beginning 2 weeks prior to the phone screen. Class 3 (Nonabstinent-Accelerated Increase; NA-AI) (n = 68; 33.2%) reported no or very low levels of pretreatment NDA but demonstrated an increase following the phone screen. With regard to within-treatment change, Class 1 demonstrated the least and Class 3 demonstrated the most change in NDA. From baseline to 6-month follow-up, Class 3 added 2.31 abstinent days per week, Class 2 added 0.69 days, and Class 1 added 0.63 days. The increase in NDA for Class 3 was significantly different from the other 2 classes; however, Class 3 reported fewer overall days abstinent at 6-month follow-up. CONCLUSIONS: Study results have clinical and research implications including recommended changes to treatment protocols and research designs. Understanding the impact of pretreatment trajectories of alcohol use on within-treatment and posttreatment outcomes may provide important information about adapting treatment to increase efficiency and effectiveness.

The Shape of Change: Determining When Mechanisms of Behavior Change Are Active in Cognitive Behavioral Treatment for Alcohol Use Disorder Using Time-Varying Effect Modeling (TVEM).

OBJECTIVE: Research has identified several potential mechanisms of behavior change (MOBCs) in cognitive-behavioral therapy for alcohol use disorder, including alcohol abstinence self-efficacy (AASE), negative affect (NA), and positive affect (PA). However, little is known about when MOBCs affect clinical outcomes during alcohol use disorder treatment. Such information could advance MOBC research by identifying relationships between specific treatment content and variations in MOBCs. This study examined three MOBCs simultaneously to determine their timing and relative influence on percent days abstinent (PDA) and drinks per day (DPD). METHOD: Data were derived from a parent study assessing pretreatment change in drinking. Participants (n = 205) received 12 sessions of cognitive-behavioral therapy for alcohol use disorder. AASE, NA, and PA were measured at each treatment session, and time-varying effect models (TVEM) were used to examine their association with PDA and DPD. RESULTS: All three MOBCs were associated with PDA and DPD but varied with regard to time course, strength, and direction. For PDA, AASE was positively associated throughout treatment, NA was negatively associated from Sessions 1 to 10, and PA was positively associated from Sessions 1 to 3 and 11 to 12. For DPD, AASE was positively associated from Session 5 to the end of treatment, NA was positively associated throughout treatment although the strength of the association varied and was strongest at the beginning of treatment, and PA was positively associated from Sessions 5 to 12. CONCLUSIONS: Results show that MOBCs exert their effects at different times during treatment. In addition to replicating these results, future research should attempt to manipulate MOBCs directly and examine their influence on alcohol outcomes.

Difficulties in emotion regulation in treatment-seeking alcoholics with and without co-occurring mood and anxiety disorders.

Emotion regulation difficulties (ERD) are known to underlie mental health conditions including anxiety and depressive disorders and alcohol use disorder (AUD). Although AUD, mood, and anxiety disorders commonly co-occur, no study has examined the association between these disorders and ERD among AUD outpatients. In the current study, emotion regulation (ER) scores of AUD individuals with no co-occurring mental health condition were compared to the ER scores of individuals who met diagnostic criteria for co-occurring mood and/or anxiety disorders. Treatment-seeking AUD individuals (N=77) completed measures of emotion regulation, alcohol use and psychological functioning prior to beginning a 12-week outpatient cognitive-behaviorally oriented alcohol treatment program. Individuals were classified as having no co-occurring mood or anxiety disorder (AUD-0, n=24), one co-occurring disorder (AUD-1, n=34), or two or more co-occurring disorders (AUD-2, n=19). Between-group differences in emotion regulation, quantity/frequency of alcohol consumption, positive and negative affect, affective drinking situations, negative mood regulation expectancies, distress tolerance, alexithymia, trait mindfulness, and psychological symptom severity were examined. Compared with the AUD-0 group, the AUD-2 group reported significantly greater ERD, psychiatric distress and alcohol consumption, more frequent drinking in response to negative affect situations, greater interference from negative emotions, and less use of mindfulness skills. The AUD-1 group differed from AUD-0 group only on the DERS lack of emotional awareness (Aware) subscale. Emotion regulation scores in the AUD-0 group were comparable to those previously reported for general community samples, whereas levels of ERD in the AUD-1 and AUD-2 were similar to those found in other clinical samples. Implications for the inclusion of ER interventions among AUD patients who might most benefit from such an intervention are discussed.

Integrated physical map of the human essential tremor gene region (ETM2) on chromosome 2p24.3-p24.2.

A gene for autosomal dominant familial essential tremor maps to a 9.1 cM interval flanked by loci D2S224 and D2S405 (ETM2) on human chromosome 2p24.3-p24.2. The recombinatorial boundaries of the interval were refined on a radiation hybrid map to a 123 cR minimal critical region (MCR) between D2S224 and D2S2221. High-throughput non-isotopic screening of bacterial artificial chromosomes (BACs) was used to assemble a physical map of the region. A scaffold BAC map of 31 overlapping clones was ordered by their sequence tagged site (STS) content using PCR and Southern blotting. A complementary 3.9 Mb integrated physical map of the human ETM2 region was constructed by identifying GenBank contigs that contained seven BAC DNA sequences and common STSs. Thirty-three transcripts including five known genes (MATN3, LAPTM4A, SDC1, PUM2, and APOB) were identified in the MCR and ordered on an integrated contig by PCR and virtual mapping. This physical map will provide a template for genomic sequencing and the identification of a gene for essential tremor.

Haplotype analysis of the ETM2 locus in familial essential tremor.

The objective of this study was to analyze a sample of unrelated individuals with autosomal dominant essential tremor (ET) for a genetic association with loci in a candidate region (ETM2) on chromosome 2p24.1 that harbors a disease gene for ET. ET is a common movement disorder that is genetically linked to ETM2 in four large families. It is unknown whether this candidate locus is associated with dominantly inherited ET in other individuals. Based on information from previous genetic linkage studies, a linkage disequilibrium study was designed to compare individuals with a family history of ET (n=45) with normal controls (n=70). Three unreported dinucleotide polymorphic loci (etm1240, etm1231, and etm1234) were identified on a physical map of the ETM2 interval in a region of no recombination. The study sample was tested for allele frequency differences by the CLUMP program and haplotypes were analyzed by the FASTEHPLUS program. The allele frequencies were significantly different between ET cases and the control samples for the loci etm1231 (P< or =0.0419) and etm1234 (P<0.0001). A haplotype formed by the loci etm1231 and etm1234 occurred with a frequency of 29% in cases (n=45) and 9% in a white newborn sample (P<0.0001, n=35). The haplotype was not found in normal individuals older than 60 years without tremor (P=0.0063, n=35). This study provides evidence that an ancestral haplotype on chromosome 2p24.1 segregates with the ET disease phenotype in individuals with a family history of the disorder and will facilitate the search for a causative gene.