Course Of Alcohol Use Disorders Research Articles

Sleep-Related Predictors of Risk for Alcohol Use and Related Problems in Adolescents and Young Adults.

Growing evidence supports sleep and circadian rhythms as influencing alcohol use and the course of alcohol use disorder (AUD). Studying sleep/circadian-alcohol associations during adolescence and young adulthood may be valuable for identifying sleep/circadian-related approaches to preventing and/or treating AUD. This paper reviews current evidence for prospective associations between sleep/circadian factors and alcohol involvement during adolescence and young adulthood with an emphasis on the effects of sleep/circadian factors on alcohol use. The authors conducted a literature search in PsycInfo, PubMed, and Web of Science using the search terms "sleep" and "alcohol" paired with "adolescent" or "adolescence" or "young adult" or "emerging adult," focusing on the title/abstract fields, and restricting to English-language articles. Next, the search was narrowed to articles with a prospective/longitudinal or experimental design, a sleep-related measure as a predictor, an alcohol-related measure as an outcome, and confirming a primarily adolescent and/or young adult sample. This step was completed by a joint review of candidate article abstracts by two of the authors. The initial search resulted in 720 articles. After review of the abstracts, the list was narrowed to 27 articles reporting on observational longitudinal studies and three articles reporting on intervention trials. Noted for potential inclusion were 35 additional articles that reported on studies with alcohol-related predictors and sleep-related outcomes, and/or reported on candidate moderators or mediators of sleep-alcohol associations. Additional articles were identified via review of relevant article reference lists and prior exposure based on the authors' previous work in this area. Overall, the review supports a range of sleep/circadian characteristics during adolescence and young adulthood predicting the development of alcohol use and/or alcohol-related problems. Although sleep treatment studies in adolescents and young adults engaging in regular and/or heavy drinking show that sleep can be improved in those individuals, as well as potentially reducing alcohol craving and alcohol-related consequences, no studies in any age group have yet demonstrated that improving sleep reduces drinking behavior. Notable limitations include relatively few longitudinal studies and only two experimental studies, insufficient consideration of different assessment timescales (e.g., day-to-day vs. years), insufficient consideration of the multidimensional nature of sleep, a paucity of objective measures of sleep and circadian rhythms, and insufficient consideration of how demographic variables may influence sleep/circadian-alcohol associations. Examining such moderators, particularly those related to minoritized identities, as well as further investigation of putative mechanistic pathways linking sleep/circadian characteristics to alcohol outcomes, are important next steps.

Negative modulation of AMPA receptors bound to transmembrane AMPA receptor regulatory protein γ-8 blunts the positive reinforcing properties of alcohol and sucrose in a brain region-dependent manner in male mice.

The development and progression of alcohol use disorder (AUD) are widely viewed as maladaptive neuroplasticity. The transmembrane alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor (AMPAR) regulatory protein γ8 (TARP γ-8) is a molecular mechanism of neuroplasticity that has not been evaluated in AUD or other addictions. To address this gap in knowledge, we evaluated the mechanistic role of TARP γ-8 bound AMPAR activity in the basolateral amygdala (BLA) and ventral hippocampus (vHPC) in the positive reinforcing effects of alcohol, which drive repetitive alcohol use throughout the course of AUD, in male C57BL/6J mice. These brain regions were selected because they exhibit high levels of TARP γ-8 expression and send glutamate projections to the nucleus accumbens (NAc), which is a key nucleus in the brain reward pathway. Site-specific pharmacological inhibition of AMPARs bound to TARP γ-8 in the BLA via bilateral infusion of the selective negative modulator JNJ-55511118 (0-2µg/µl/side) significantly decreased operant alcohol self-administration with no effect on sucrose self-administration in behavior-matched controls. Temporal analysis showed that reductions in alcohol-reinforced response rate occurred > 25min after the onset of responding, consistent with a blunting of the positive reinforcing effects of alcohol in the absence of nonspecific behavioral effects. In contrast, inhibition of TARP γ-8 bound AMPARs in the vHPC selectively decreased sucrose self-administration with no effect on alcohol. This study reveals a novel brain region-specific role of TARP γ-8 bound AMPARs as a molecular mechanism of the positive reinforcing effects of alcohol and non-drug rewards.

Microbiome Alterations in Alcohol Use Disorder and Alcoholic Liver Disease.

Microbiome alterations are emerging as one of the most important factors that influence the course of alcohol use disorder (AUD). Recent advances in bioinformatics enable more robust and accurate characterization of changes in the composition of the microbiome. In this study, our objective was to provide the most comprehensive and up-to-date evaluation of microbiome alterations associated with AUD and alcoholic liver disease (ALD). To achieve it, we have applied consistent, state of art bioinformatic workflow to raw reads from multiple 16S rRNA sequencing datasets. The study population consisted of 122 patients with AUD, 75 with ALD, 54 with non-alcoholic liver diseases, and 260 healthy controls. We have found several microbiome alterations that were consistent across multiple datasets. The most consistent changes included a significantly lower abundance of multiple butyrate-producing families, including Ruminococcaceae, Lachnospiraceae, and Oscillospiraceae in AUD compared to HC and further reduction of these families in ALD compared with AUD. Other important results include an increase in endotoxin-producing Proteobacteria in AUD, with the ALD group having the largest increase. All of these alterations can potentially contribute to increased intestinal permeability and inflammation associated with AUD and ALD.

Poor subjective sleep predicts compromised quality of life but not cognitive impairment in abstinent individuals with Alcohol Use Disorder.

How disrupted sleep contributes to cognitive dysfunction over the dynamic course of Alcohol Use Disorder (AUD) is an emerging topic of investigation. Here, the Pittsburgh Sleep Quality Index (PSQI) was used to evaluate subjective sleep in 90 individuals with AUD sober for an average of 3 months and in 50 healthy controls. Relative to controls, AUD individuals had higher global PSQI scores (worse sleep), higher scores on the Beck Depression Inventory (BDI-II), worse Quality of Life (QoL) indicators, and poorer performance on cognitive composite tests (executive functioning, attention and working memory, visual and verbal learning or memory). Among AUD individuals, a higher PSQI score correlated with a higher BDI-II score and worse QoL, but not with cognitive scales. Also noted in the AUD group were higher global PSQI scores in individuals also diagnosed with major depressive disorder (MDD) or generalized anxiety disorder (GAD). The four variables explained 29.8% of the variance in AUD PSQI scores. In women with AUD, the four factors explained 39.3% of the variance in PSQI scores (MDD was salient); in AUD men, the four measures explained 19.9% of the variance (QoL predominated). Together, these results suggest that poor PSQI-defined sleep does not predict cognitive performance in abstinent AUD individuals and further, that differential factors associate with poor sleep in men and women with AUD.

Family-Based Predictors of Alcohol Use Disorder (AUD) Recurrence and New Non-Alcohol Substance Use Disorder Onset Following Initial AUD Recovery

Knowledge of factors that predict alcohol use disorder (AUD) recurrence or the subsequent switching to a different substance use disorder (SUD) after initial AUD recovery is especially crucial for preventive efforts that seek to alter life courses dominated by problematic substance use. This study evaluated whether the proportions (or densities) of first-degree relatives with AUD and non-alcohol substance use disorder (NASUD) histories predicted AUD recurrence or a new NASUD onset in a family member (i.e., proband) following initial AUD episode recovery. This research is based on a prospective and multigenerational data set collected as part of the Oregon Adolescent Depression Project (OADP). The initial proband cohort was selected randomly from nine high schools in western Oregon. The sample for this research consisted of OADP probands with histories of AUD who recovered from their first AUD episode by age 30 (n = 244). Lifetime SUD histories were also assessed for first-degree adult relatives of probands (n = 790). In unadjusted and partially adjusted analyses, family densities of AUD predicted AUD recurrence among probands, and family densities of NASUDs predicted the onset of a new NASUD following first-episode AUD recovery. In fully adjusted analyses, the effect for AUD family histories on proband AUD recurrence remained, whereas the effect for family NASUD histories on new NASUD emergence was not maintained. Family SUD histories have predictive relevance for the course of AUD following initial recovery as well as some specificity for the type of SUD recurrence subsequently experienced.

The Clinical Course of Alcohol Use Disorder Depicted by Digital Biomarkers.

Aims: This study introduces new digital biomarkers to be used as precise, objective tools to measure and describe the clinical course of patients with alcohol use disorder (AUD).Methods: An algorithm is outlined for the calculation of a new digital biomarker, the recovery and exacerbation index (REI), which describes the current trend in a patient's clinical course of AUD. A threshold applied to the REI identifies the starting point and the length of an exacerbation event (EE). The disease patterns and periodicity are described by the number, length, and distance between EEs. The algorithms were tested on data from patients from previous clinical trials (n = 51) and clinical practice (n = 1,717).Results: Our study indicates that the digital biomarker-based description of the clinical course of AUD might be superior to the traditional self-reported relapse/remission concept and conventional biomarkers due to higher data quality (alcohol measured) and time resolution. We found that EEs and the REI introduce distinct tools to identify qualitative and quantitative differences in drinking patterns (drinks per drinking day, phosphatidyl ethanol levels, weekday and holiday patterns) and effect of treatment time.Conclusions: This study indicates that the disease state—level, trend and periodicity—can be mathematically described and visualized with digital biomarkers, thereby improving knowledge about the clinical course of AUD and enabling clinical decision-making and adaptive care. The algorithms provide a basis for machine-learning-driven research that might also be applied for other disorders where daily data are available from digital health systems.

Clinical characteristics and efficiency of antidepressant therapy of mood disorders with comorbid alcohol use disorder

Aim. To determine the nosological and clinical features of mood disorders (MD) with comorbid alcohol use disorder (AUD) and efficiency of antidepressant therapy. Materials and methods . We examined 88 patients with MD and comorbid AUD – 33 females (37.5%) and 55 males (62.5%). The first group included 31 patients with AUD without comorbid affective symptoms, the second group contained 29 patients with MD without AUD, the third group included 28 patients with AUD and MD. In the study, we applied clinical-psychopathologic, clinical-dynamic, and statistical methods with Pearson’s χ 2 test, Mann – Whitney U -test (for comparison of independent samples), Kruskal – Wallis test (for more than two independent samples), and Wilcoxon test (for comparison of dependent samples). At the level of statistical significance, no differences between the groups according to the gender – age composition were revealed ( p = 0.115 – according to gender composition, р = 0.248 – according to age composition, Pearson’s χ 2 test). Results . The patients with the diagnosis of AUD with comorbid MD showed worse dynamics of the reduction of depressive [from 24.0 (18.3; 33.0) to 9.0 (4.3; 12.0) points according to the Structured Interview Guide for the Hamilton Depression Rating Scale – Seasonal Affective Disorder (SIGH-SAD) ( р = 0.001, Wilcoxon test)] and anxiety [from 20.5 (12.5; 25.0) to 5.5 (3.3; 8.0) points according to the Hamilton Anxiety Rating Scale (HARS) ( р = 0.001, Wilcoxon test)] symptoms against the background of the therapy with initially lower indices compared to the group with MD alone [from 27.0 (21.0; 36.0) to 6.0 (5.0; 11.0) points according to SIGH-SAD ( р = 0.001, Wilcoxon test) (intergroup differences upon admission р = 0.046; upon discharge р = 0.683, Mann – Whitney U -test) and from 21.0 (14.0; 29.0) to 5.0 (3; 10.5) points according to HARS ( р = 0.001, Wilcoxon test) (intergroup differences upon admission р = 0.082; upon discharge р = 0.825, Mann – Whitney U -test)]. The course of AUD is characterized by a larger extent of malignancy in the group with a comorbidity: decrease in pathological alcohol craving from 31.5 (16.3; 43.5) points to 8 (2.3; 14.8) ( р = 0.001, Wilcoxon test) in the group with a comorbidity and from 29.5 (21.8; 37.0) to 7 (3.0; 11.3) points with AUD alone ( р = 0.001, Wilcoxon test) (intergroup differences upon admission р = 0.058; upon discharge р = 0.04, Mann – Whitney U -test on the Obsessive Compulsive Drinking Scale (OCDS). Conclusion. Clinical-dynamic characteristics of MD with comorbid AUD result in therapeutic difficulties associated with comparatively worse dynamics of reduction of the symptoms of both diseases.

Military Combat, Posttraumatic Stress Disorder, and the Course of Alcohol Use Disorders in a Cohort of Australian Vietnam War Veterans.

The present study examined the course of diagnosed alcohol use disorders (AUDs) in a cohort of Australian veterans of the Vietnam War (N = 388) who were assessed 22 and 36 years after returning home. Standardized interviews provided data on AUDs, posttraumatic stress disorder (PTSD), other psychiatric diagnoses, and combat exposure. Overall, 148 veterans (38.1%) had no history of alcohol-related diagnoses, 151 veterans (38.9%) had a past AUD diagnosis that was not current at the second assessment point, and 89 veterans (22.9%) had a current AUD diagnosis at the second assessment. Less education, lower intelligence test scores, and misconduct were individual risk factors for AUDs, as were first-interview diagnoses of PTSD, antisocial personality disorder, generalized anxiety, and dysthymia, but not depression; these variables were all nonsignificant after controlling for combat exposure and PTSD. Multinomial regression was used to assess the relative contributions of combat exposure and PTSD to the course of AUDs. Combat exposure and PTSD had different patterns of association with AUDs whereby combat exposure, but not PTSD, was associated with a history of AUDs, odds ratio (OR) = 1.02, but not with current AUDs, whereas PTSD, but not combat exposure, was associated with current AUDs, OR = 3.37. Current numbing and avoidance symptoms were associated with current AUDs, OR = 4.48. The results do not support a mutual maintenance model of PTSD and AUDs but are consistent with a self-medication model, which suggests treatment for PTSD may have beneficial effects on AUDs.

Medication Utilization for Alcohol Use Disorder in a Commercially Insured Population.

Examine patterns of alcohol use disorder (AUD) medication use and identify factors associated with prescription fill among commercially insured individuals with an index AUD visit. Using 2008-2018 claims data from a large national insurer, estimate days to first AUD medication using cause-specific hazards approach to account for competing risk of benefits loss. Aged 17-64 with ≥ 1 AUD visit. Days to AUD medication fill. A total of 13.3% of the 151,128 with an index visit filled an AUD prescription after that visit, while 69.8% lost benefits before filling and 17.0% remained enrolled but did not fill (median days observed = 305). Almost half (46.3%) of those who filled a prescription received substance use disorder (SUD) inpatient care within 7days before the fill, and 63.4% received SUD outpatient care. Likelihood of medication use was higher for those aged 26-35, 36-45, and 46-55years relative to 56-64years (e.g., 26-35: hazard ratio = 1.29 [95% confidence interval 1.23-1.36]); those diagnosed with moderate/severe AUD (2.05 [1.98-2.12]), co-occurring opioid use disorder (OUD) (1.33 [1.26-1.39]), or severe mental illness (1.31 [1.27-1.35]); those with a chronic alcohol-related diagnosis (1.08 [1.04-1.12]); and those whose index visit was in an inpatient/emergency department (1.27 [1.23-1.31]) or intermediate care setting (1.13 [1.07-1.20]) relative to outpatient. Likelihood of use was higher in later years relative to 2008 (e.g., 2018:2.02 [1.89-2.15]) and higher for those who received the majority of AUD care in a practice with a psychiatrist/addiction medicine specialist (1.13 [1.10-1.16]). Likelihood of use was lower for those diagnosed with a SUD other than AUD or OUD (0.88 [0.85-0.92]), those with an acute alcohol-related condition (0.79 [0.75-0.84]), and males (0.71 [0.69-0.73]). While AUD medication use increased and was more common among individuals with greater severity, few patients who could benefit from medications are using them. More efforts are needed to identify and treat individuals in non-acute care settings earlier in their course of AUD.

History of suicidality and alcohol craving trajectories during inpatient treatment for alcohol use disorder

BackgroundAlcohol use is associated with an increased risk of completed suicide, but it is unclear whether past suicidality affects the course of alcohol use disorder (AUD). We examined whether a history of suicidal ideation or attempts is associated with treatment response in individuals with AUD. Methods146 participants underwent inpatient detoxification and residential treatment for AUD. Reductions in craving during treatment were used as an index of treatment response. Participants were assessed for history of suicidality using the Columbia-Suicide Severity Rating Scale and divided into three groups: no history of suicidal ideation or attempts (N = 76), history of suicidal ideation without attempts (N = 50), and history of suicide attempts (N = 20). Alcohol craving was measured weekly during treatment using the Penn Alcohol Craving Scale and compared across groups. ResultsIndividuals with a history of suicide attempts showed higher levels of craving throughout treatment compared to those without a history of suicidality. Associations between past suicide attempts and craving remained significant after adjusting for age, sex, alcohol use disorder severity, comorbid psychopathology, and benzodiazepine treatment. Participants in all groups had significant reductions in alcohol craving by the end of treatment. ConclusionsOur findings suggest that a history of suicide attempts is associated with higher levels of craving throughout inpatient treatment for AUD. These results support current guidelines on assessing suicidal ideation in patients with substance use disorders.

Prevalence, incidence, recovery, and recurrence of alcohol use disorders from childhood to age 30

BackgroundLittle is known about the course of alcohol use disorders (AUDs) in representative samples during high-risk periods of adolescence and early adulthood. The primary objective of this research is to describe the prevalence and course of initial AUD episodes experienced between childhood and age 30 in a regionally representative cohort sample. MethodsStudy data are from an epidemiological study of 816 youth. Participants were initially selected at random from nine high schools in western Oregon, USA. Four waves of data collection were conducted between ages 16 and 30. AUD course milestones are referenced to participants’ age. ResultsResults indicated that male participants (43%) were significantly more likely to be diagnosed with a lifetime AUD than female participants (28%), OR [CI95] = 1.97 [1.47–2.65], and rate of first incidence was especially high between ages 18 and 24.9, a developmental period that also corresponded to the peak interval in prevalence rates. The rate of first AUD incidence substantially diminished beginning around age 25. Among those with an initial AUD episode, 87% recovered by age 30 and, of these, the average episode length was 23 months. Among recovered cases, 33% went on to experience a second AUD episode (i.e., a recurrence) after a minimum 12-month asymptomatic recovery period. Risk for recurrence remained relatively high within the 5 years following initial AUD offset. ConclusionsAUDs are common lifetime conditions in representative samples, whereby most affected individuals by age 30 experience a time-limited course rather than a recurring or persistent course.

Indexing the 'dark side of addiction': substance-induced affective symptoms and alcohol use disorders.

The emergence of negative affective symptoms during the course of alcohol use disorders (AUDs) (e.g. 'dark side' symptoms) has been suggested theoretically; however, the description of their occurrence is limited. This study operationalized two negative affect symptoms and tested the strength of association between these phenotypes and (1) indicators of the clinical course of the severity of AUD, (2) comorbid Axis I psychiatric disorders, suicidal behaviors and trait neuroticism and (3) whether participants reported drinking to relieve the negative affective symptoms. A retrospective cross-sectional study was used to evaluate associations, using logistic regression, between the two negative affective symptoms and clinical measures of AUD severity and progression as well as comorbidity with other psychiatric disorders and conditions, adjusted for demographic characteristics. US community-based studies. A total of 2568 individuals with AUDs obtained from larger population studies that targeted individuals of European American (n=1663), Mexican American and American Indian (n=905) ancestry. Semi-Structured Assessment for the Genetics of Alcoholism was used to ascertain the two 'dark side' phenotypes, clinical diagnoses, the clinical course of AUD and associated symptoms. The two phenotypes were: (1) being anxious or depressed when trying to cut down or stop drinking and (2) experiencing disabling depression for more than 24hours while drinking. Both phenotypes were found to be rare in mild and moderate use disorder and highly prevalent in severe AUDs. Having an independent anxiety or affective disorder and elevated scores on trait neuroticism were also associated significantly with the occurrence of both symptoms, as was alcohol 'craving', elevated treatment-seeking, suicidal behaviors and drinking to relieve the symptoms. Affective symptoms are common in severe alcohol use disorders are associated with a history of independent affective/anxiety disorders, neuroticism and suicidal behaviors; and may promote further heavy drinking.

A study on the factors that influence the clinical course of alcohol use disorder in Korea

A study on the factors that influence the clinical course of alcohol use disorder in Korea

RADAR study: protocol for an observational cohort study to identify early warning signals on the pathways to alcohol use disorder

IntroductionHarmful alcohol consumption, particularly alcohol use disorder (AUD), is a worldwide health priority, contributing substantially to global morbidity and mortality. The peak age of onset of AUD is 18–24, thus...

Natural Course of Co-Occurring PTSD and Alcohol Use Disorder Among Recent Combat Veterans.

Posttraumatic stress disorder (PTSD) and alcohol use disorder (AUD) commonly co-occur in veterans, yet little is known about the longitudinal course of PTSD and drinking in comorbid populations. This study assessed the natural course of daily alcohol consumption and weekly changes in PTSD symptoms in 112 recent combat veterans over the course of 11 months. Latent class growth mixture modeling was used to classify individuals into distinct classes with similar PTSD symptom and alcohol use growth trajectories. We then investigated theorized predictors of class membership including sociodemographics; pre-, peri-, and postdeployment factors; coping; symptom severity; and number of mental health/substance use appointments attended. Results revealed that most participants had severe and nonremitting PTSD. Trajectories for alcohol use included gradual and drastic declines, and chronic low-level drinking. The use of behavioral health services (odds ratio = 2.47) and fewer current stressors (odds ratio = 0.42) predicted AUD remission. Because little variation was observed in the PTSD course, our study did not observe coordinated fluctuations of PTSD symptoms and heavy drinking. Our findings suggest that treatment impacts the course of AUD and that recent combat veterans who do not seek PTSD treatment may have chronic and severe PTSD symptoms.

Socio-contextual factors are linked to differences in the course of problem drinking in midlife: A discordant-twin study.

Course of alcohol use disorders (AUD) during midlife is understudied, and most research designs are unable to attribute an unambiguous environmental explanation to observed findings. Test whether socio-contextual factors are linked to differences in the course of problem drinking during midlife. Participants were 163 monozygotic and dizygotic twin pairs concordant for a history of AUD but discordant on problem drinking in the past 10 years. Frequency of drinking with spouse, and peer and emotional problems were associated with discordance. Socio-contextual factors are linked to differences in course of problem drinking in midlife and are not confounded by genetic effects. (Am J Addict 2015;24:193-196).

Alcohol use disorder clinical course research: informing clinicians' treatment planning now and in the future.

The clinical course of alcohol use disorder (AUD) has been widely researched over the past half-century and has been used to advance our understanding of the treatment of AUD. Nevertheless, new directions in AUD clinical course research could enhance its value in informing clinical decision-making in patient-centered treatment of AUD. An overview, a critical analysis, and a discussion of AUD clinical course research are presented. This article discusses three research directions that promote the advancement of the knowledge regarding the clinical course of AUD to better inform clinical decision-making in patient-centered treatment of AUD. Specifically, we hypothesized that (a) real-time data collection of the clinical course of AUD via ecological momentary assessment would help elucidate near real-time associations between risk factors and alcohol use, (b) future research designs should use person-centered and dynamic analyses of alcohol use over time, and (c) adaptive treatment designs would provide personalized and optimized AUD treatment. Consequently, the field will advance the development of clinical decision-making support systems to better inform clinicians and clients in making informed AUD treatment decisions. In addition, such research would advance clinical practice with more attention to theory and expansion of the study of the clinical course of AUD to include areas of life functioning besides alcohol use. These research directions have the potential to build a scientific knowledge base that could improve our understanding of AUD among individuals with alcohol problems, would allow providers to predict patient outcomes during and after treatment, and would offer practical strategies regarding steps that could ultimately improve the clinical course of AUD.

Alcohol use disorder in women: Risks and consequences of an adolescent onset and persistent course.

Women are more vulnerable to the deleterious effects of both acute and protracted alcohol use than men, but women's lower levels of alcohol consumption and alcohol use disorder (AUD) have resulted in a paucity of investigations on the development of alcohol problems in women. In particular, it is not clear to what extent the cascading effects of key etiological factors that contribute to an especially severe course of AUD in men also underlie the development of AUD in women. To fill this gap, we examined the adolescent risk factors and adult consequences associated with an adolescent onset and persistent course of AUD in a community sample of women (n = 636) from ages 17 to 29. Women with AUD exhibited greater psychopathology and psychosocial impairment than those without, with an adolescent onset and persistent course indicative of the greatest severity. Notably, high levels of impairment across all women with AUD reduced the utility of onset and course to differentiate profiles of risk and impairment. In contrast to previous work in men, even women whose AUD symptoms desisted continued to exhibit impairment, suggesting that an adolescent onset of AUD is associated with enduring consequences for women's health and functioning, even after ostensible "recovery."

Anxiety disorders and risk for alcohol use disorders: The moderating effect of parental support

BackgroundThere have been mixed findings on the temporal relation between anxiety disorders and alcohol use disorders (AUDs), suggesting that the pathway to AUDs may differ among individuals. The aim of the current study was to test whether parental support moderated the association between anxiety disorders and the development of AUDs. We also tested whether our effects differed as a function of age of AUD onset. Methods817 individuals were assessed for lifetime diagnoses of psychopathology during 4-waves between adolescence (mean age=16) and adulthood (mean age=30). ResultsProportional hazards model analyses indicated that baseline anxiety disorders interacted with baseline perceived maternal support to prospectively predict onset of AUDs. At high levels of maternal support, anxiety disorders were associated with a reduced risk for AUD onset (HR=0.74, 95% CI=0.55–1.00). However, this effect was more robust for AUDs that developed prior to age 20. At low levels of maternal support, anxiety disorders were associated with an increased risk for AUD onset (HR=1.65, 95% CI=1.21–2.26). This effect was present for AUDs that developed across adolescence and adulthood. Paternal support was not associated with AUDs and did not interact with anxiety disorders. ConclusionsPrevention and intervention efforts targeted at maternal support in adolescents with anxiety disorders may be valuable, as this may represent a factor that has a significant impact on the developmental course of AUDs.

Commentary on Tuithofet al. (2013): Implications of the DSM-5 revision for the analysis of persistence/remission of alcohol use disorder

The findings of Tuithof et al. [1] are consistent with studies of the course of DSM-IV [2] alcohol use disorder (AUD) in the general population, demonstrating that many episodes of AUD are of limited duration and many individuals who have experienced remission of AUD symptoms drink at levels that may increase the risk of relapse [3–7]. A prospective study based on just two data points is of limited utility for yielding valid inferences about a dynamic process such as persistence/remission of AUD, in that at least three data points are necessary to chart the chronic relapsing pattern that characterizes a substantial proportion of individuals with lifetime AUD in long-term prospective studies [8–11]. In fact, retrospective data, despite limitations related to recall error and selective survival, may actually tell us more about the recovery process than prospective data with single follow-up [3]. Despite the inherent limitations of its study design, this study nonetheless raises some interesting questions about how the persistence of AUD is related to remission, how has this changed under the DSM-5 and what new research opportunities may arise out of these changes. Under the DSM-IV, individuals who meet the criteria for alcohol dependence at t1 but do not satisfy the requirements for persistent dependence or full remission (cessation of all AUD symptoms) at t2 fall into the category of partial remission, comprising alcohol abuse and/or subclinical dependence symptoms. Individuals who do not satisfy the requirements for persistent abuse include both those who have progressed to dependence and those in full remission. Thus, the absence of persistence does not necessarily signify full remission. Retrospective studies of US population samples have shown that partial remission of dependence is common, peaking in prevalence at ≈40% 5–9 years after onset of dependence [4]. Individuals in partial remission drink more and have a lower quality of life than those in full remission, but drink less and have a higher quality of life than those with persistent dependence [12,13]. Because individuals in partial remission are distinct from those with persistent or fully remitted AUD, a clearer picture of the significance of factors associated with the course of DSM-IV AUD could be obtained by excluding partial remission cases from analyses or including them as a separate outcome category in multinomial models. The proposed DSM-5 revision [14] does not recognize partial remission as a course specifier for AUD [15]. Among individuals with AUD (2+ positive criteria) at t1, those with subclinical levels of AUD symptoms at t2 count as fully remitted, along with those who are asymptomatic. In addition, the newly added criterion of craving, which may persist even after discontinuation of drinking, does not preclude achievement of remission. Thus, full remission and persistent AUD are more complementary under the DSM-5 than they were under the DSM-IV; i.e., there are no longer any cases that fall between these categories. However, regardless of whether partial remission is formally recognized or subsumed under full remission, the residual presence of cases with a subclinical level of symptoms reduces the contrast between persistent and asymptomatic cases. Thus, challenges remain with dichotomous outcome measures when modeling correlates of remission or persistence. However, the DSM-5 definition of AUD as a unitary latent construct whose symptoms vary along a continuum of severity suggests new approaches to the study of persistence/remission that may overcome some of the limitations of a dichotomous outcome measure. One such approach is to examine correlates of increase/decrease in AUD severity, and to see whether a change of a given magnitude has different correlates depending on the base level of severity. That is, does a drop from 8 to 5 positive criteria between t1 and t2 have the same correlates as a drop from 4 to 1? Similarly, does the impact of a given decrease in severity on changes in consumption and quality of live vary based on initial severity level? Results of such an approach would at least be suggestive of factors that differentially affect the early versus later stages of recovery, and they would clearly distinguish factors associated with remission of AUD of varying severity levels. The addition of craving as a criterion for DSM-5 AUD also suggests new opportunities for analyses. Unlike most AUD criteria, which reflect or result from but do not cause heavy drinking, craving can reinforce excessive consumption, which may in turn lead to the persistence of other AUD symptoms. By studying the unique contribution of craving to the course of AUD, i.e., its impact net of the number of other AUD criteria, we may be able to draw valuable inferences related to the benefits of medical treatment for the alleviation of craving. In summary, the proposed DSM-5 criteria for AUD should facilitate multiple new analytic approaches that will enhance our understanding of factors associated with the course of AUD and implications for treatment.