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  • 11
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    Online Resource
    Genetic and environmental influences on the progression from alcohol use disorder to alcohol‐related medical conditions
    Wiley ; 2021
    In:  Alcoholism: Clinical and Experimental Research Vol. 45, No. 12 ( 2021-12), p. 2528-2535
    Details
    In: Alcoholism: Clinical and Experimental Research, Wiley, Vol. 45, No. 12 ( 2021-12), p. 2528-2535
    Abstract: Medical conditions related to alcohol use disorders (AUD) represent a substantial public health concern. However, only a subset of individuals with AUD develop these conditions and the extent to which genetic and environmental factors that are shared with AUD, versus those distinct from it, contribute to this progression has not yet been determined. Methods Using data from Swedish national registries for a cohort born from 1932 to 1970 ( N  = 1,319,214, 48.9% women), we conducted twin‐sibling biometric model fitting to examine the genetic and environmental sources of variance that contribute to the liability to alcohol‐related medical conditions (AMC). Progression to AMC, determined using medical registry data, was contingent on an AUD registration, which was determined using medical and criminal registry data. Results We identified AUD registrations in 3.2% of women and 9.2% of men. Among individuals with an AUD registration, 14.4% of women and 15.4% of men had an AMC registration. In the final models, we constrained the beta pathway from AUD to AMC and the genetic and unique environmental paths to be equal across sexes. The beta path was estimated at 0.59. AMC was modestly heritable in women ( A  = 0.32) and men ( A  = 0.30). The proportion of total heritability unique to AMC was 39.6% among women and 41.3% among men. A higher proportion of total environmental variance was unique to AMC: 76.7% for women and 77.2% for men. In a sensitivity analysis limited to liver‐related AMC, we observed similar results, with a slightly lower beta path from AUD to AMC (0.46) and higher proportions of AMC‐specific genetic (70.0% in women; 71.7% in men) and environmental (84.5% in both sexes) variance. Conclusions A moderate‐to‐substantial proportion of genetic and environmental variance that contributes to AMC risk is not shared with AUD, underscoring the need for additional gene identification efforts for AMC. Furthermore, the prominent influence of environmental factors specific to AMC provides a promising area for the identification of prevention targets. We did not observe significant sex differences in the etiology of AMC, although follow‐up is warranted in other well‐powered studies.
    Type of Medium: Online Resource
    ISSN: 0145-6008 , 1530-0277
    URL: Issue
    URL: Article
    DOI: 10.1111/acer.v45.12
    DOI: 10.1111/acer.14731
    Language: English
    Publisher: Wiley
    Publication Date: 2021
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  • 12
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    Assessment of a Modified DSM-5 Diagnosis of Alcohol Use Disorder in a Genetically Informative Population
    Wiley ; 2013
    In:  Alcoholism: Clinical and Experimental Research Vol. 37, No. 3 ( 2013-03), p. 443-451
    Details
    In: Alcoholism: Clinical and Experimental Research, Wiley, Vol. 37, No. 3 ( 2013-03), p. 443-451
    Type of Medium: Online Resource
    ISSN: 0145-6008
    URL: Issue
    URL: Article
    DOI: 10.1111/acer.2013.37.issue-3
    DOI: 10.1111/j.1530-0277.2012.01954.x
    Language: English
    Publisher: Wiley
    Publication Date: 2013
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  • 13
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    Associations Between Gestational Age at Birth and Alcohol Use in the Avon Longitudinal Study of Parents and Children
    Wiley ; 2016
    In:  Alcoholism: Clinical and Experimental Research Vol. 40, No. 6 ( 2016-06), p. 1328-1338
    Details
    In: Alcoholism: Clinical and Experimental Research, Wiley, Vol. 40, No. 6 ( 2016-06), p. 1328-1338
    Abstract: The relationship between gestational age at birth (GA) and alcohol use measures in early adulthood was examined in a large U.K. community‐based birth cohort (Avon Longitudinal Study of Parents and Children). Methods A series of linear and logistic regression models were used to test for main effects of a continuous measure of GA on a range of alcohol use measures, and moderation of these associations by sex. In addition, mediation analyses assessed the extent to which significant associations between GA and alcohol use operated indirectly, through influences of the parental environment and/or childhood measures of emotional and behavioral health (EBH). Results Earlier GA significantly predicted never drinking by age 18, but was not associated with other measures of alcohol use behavior among young adult drinkers (i.e., Self‐Rating of the Effects of Alcohol, Alcohol Use Disorders Identification Test, or DSM ‐ IV ‐ TR Criteria for Alcohol Dependence). The association between earlier GA and never drinking by age 18 was moderated by sex, such that females born early were less likely to have ever had a drink by age 18. In the full sample, childhood measures of EBH were found to mediate the association between earlier GA and never drinking by age 18. This association was not mediated by parenting factors. Conclusions Earlier GA is associated with never drinking alcohol in early adulthood, in females. Emotional and behavioral difficulties experienced in early childhood may mediate the relationship between earlier GA and never drinking by age 18.
    Type of Medium: Online Resource
    ISSN: 0145-6008 , 1530-0277
    URL: Issue
    URL: Article
    DOI: 10.1111/acer.2016.40.issue-6
    DOI: 10.1111/acer.13080
    Language: English
    Publisher: Wiley
    Publication Date: 2016
    detail.hit.zdb_id: 2046886-6
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  • 14
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    Genetic differences between suicide deaths and deaths of undetermined intent
    Wiley ; 2023
    In:  Suicide and Life-Threatening Behavior Vol. 53, No. 1 ( 2023-02), p. 100-109
    Details
    In: Suicide and Life-Threatening Behavior, Wiley, Vol. 53, No. 1 ( 2023-02), p. 100-109
    Abstract: Few, if any, prior studies have considered whether undetermined intent (UDI) deaths and suicide deaths differ with respect to genetic liability for suicidal behavior or psychopathology. Methods The authors used Swedish national registry data to identify suicide deaths ( N  = 31,835) and UDI deaths ( N  = 10,623); sociodemographic covariates; and registrations for psychopathology. Family genetic risk scores (FGRS) were derived for each form of psychopathology. The authors used LASSO models to assess genetic and phenotypic differences across outcomes. Results In the multivariate LASSO regressions, higher FGRS for major depression, bipolar disorder, and suicide death were associated with lower odds of UDI relative to unambiguous suicide (OR = 0.91–0.95), while those for alcohol and drug use disorders, ADHD, and criminal behavior were associated with higher odds of UDI relative to unambiguous suicide (OR = 1.04–1.12). When the corresponding phenotypic registration status for these outcomes was included in a subsequent model, the associations were attenuated and of small magnitude, but many remained different from OR = 1. Conclusions Aggregate genetic differences between unambiguous suicide decedents and UDI deaths are small, particularly when accounting for psychiatric comorbidity, but in some cases, statistically significant. These findings suggest that different analytic treatment of UDI deaths may be warranted depending on the research question. Replication in other samples, and using molecular genetic data, is necessary.
    Type of Medium: Online Resource
    ISSN: 0363-0234 , 1943-278X
    URL: Issue
    URL: Article
    DOI: 10.1111/sltb.v53.1
    DOI: 10.1111/sltb.12926
    Language: English
    Publisher: Wiley
    Publication Date: 2023
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  • 15
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    Meta‐Analysis of Genetic Influences on Initial Alcohol Sensitivity
    Wiley ; 2018
    In:  Alcoholism: Clinical and Experimental Research Vol. 42, No. 12 ( 2018-12), p. 2349-2359
    Details
    In: Alcoholism: Clinical and Experimental Research, Wiley, Vol. 42, No. 12 ( 2018-12), p. 2349-2359
    Abstract: Previous studies indicate that low initial sensitivity to alcohol may be a risk factor for later alcohol misuse. Evidence suggests that initial sensitivity is influenced by genetic factors, but few molecular genetic studies have been reported. Methods We conducted a meta‐analysis of 2 population‐based genome‐wide association studies of the Self‐Rating of the Effects of Alcohol scale. Our final sample consisted of 7,339 individuals (82.3% of European descent; 59.2% female) who reported having used alcohol at least 5 times. In addition, we estimated single nucleotide polymorphism ( SNP )‐based heritability and conducted a series of secondary aggregate genetic analyses. Results No individual locus reached genome‐wide significance. Gene and set based analyses, both overall and using tissue‐specific expression data, yielded largely null results, and genes previously implicated in alcohol problems and consumption were overall not associated with initial sensitivity. Only 1 gene set, related to hormone signaling and including core clock genes, survived correction for multiple testing. A meta‐analysis of SNP ‐based heritability resulted in a modest estimate of  = 0.19 ( SE  = 0.10), though this was driven by 1 sample ( N  = 3,683,  = 0.36, SE = 0.14, p  = 0.04). No significant genetic correlations with other relevant outcomes were observed. Conclusions Findings yielded only modest support for a genetic component underlying initial alcohol sensitivity. Results suggest that its biological underpinnings may diverge somewhat from that of other alcohol outcomes and may be related to core clock genes or other aspects of hormone signaling. Larger samples, ideally of prospectively assessed samples, are likely necessary to improve gene identification efforts and confirm the current findings.
    Type of Medium: Online Resource
    ISSN: 0145-6008 , 1530-0277
    URL: Issue
    URL: Article
    DOI: 10.1111/acer.2018.42.issue-12
    DOI: 10.1111/acer.13896
    Language: English
    Publisher: Wiley
    Publication Date: 2018
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  • 16
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    Multiple Mechanisms Influencing the Relationship Between Alcohol Consumption and Peer Alcohol Use
    Wiley ; 2015
    In:  Alcoholism: Clinical and Experimental Research Vol. 39, No. 2 ( 2015-02), p. 324-332
    Details
    In: Alcoholism: Clinical and Experimental Research, Wiley, Vol. 39, No. 2 ( 2015-02), p. 324-332
    Abstract: Alcohol consumption is typically correlated with the alcohol use behaviors of one's peers. Previous research has suggested that this positive relationship could be due to social selection, social influence, or a combination of both processes. However, few studies have considered the role of shared genetic and environmental influences in conjunction with causal processes. Methods This study uses data from a sample of male twins ( N  = 1,790) who provided retrospective reports of their own alcohol consumption and their peers' alcohol‐related behaviors, from adolescence into young adulthood (ages 12 to 25). Structural equation modeling was employed to compare 3 plausible models of genetic and environmental influences on the relationship between phenotypes over time. Results Model fitting indicated that one's own alcohol consumption and the alcohol use of one's peers are related through both genetic and shared environmental factors and through unique environmental causal influences. The relative magnitude of these factors, and their contribution to covariation, changed over time, with genetic factors becoming more meaningful later in development. Conclusions Peers' alcohol use behaviors and one's own alcohol consumption are related through a complex combination of genetic and environmental factors that act via correlated factors and the complementary causal mechanisms of social selection and influence. Understanding these processes can inform risk assessment as well as improve our ability to model the development of alcohol use.
    Type of Medium: Online Resource
    ISSN: 0145-6008 , 1530-0277
    URL: Issue
    URL: Article
    DOI: 10.1111/acer.2015.39.issue-2
    DOI: 10.1111/acer.12624
    Language: English
    Publisher: Wiley
    Publication Date: 2015
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  • 17
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    Sex Differences in the Pathways to Symptoms of Alcohol Use Disorder: A Study of Opposite‐Sex Twin Pairs
    Wiley ; 2015
    In:  Alcoholism: Clinical and Experimental Research Vol. 39, No. 6 ( 2015-06), p. 998-1007
    Details
    In: Alcoholism: Clinical and Experimental Research, Wiley, Vol. 39, No. 6 ( 2015-06), p. 998-1007
    Abstract: We sought to develop an empirical, broad‐based developmental model for sex differences in risk for symptoms of alcohol use disorders, here called alcohol problems ( AP s). Methods We assessed 18 risk factors in 5 developmental tiers in both members of 1,377 opposite‐sex dizygotic twin pairs from the Virginia population‐based twin registry. Analyses were conducted by structural modeling, examining within‐pair differences. Results The best‐fitting model explained 73% of the variance in men and 71% in women for last year AP . Forty‐nine percent of paths differed significantly across sexes. Ten variables had appreciably different predictive effects on AP in males versus females. Three were stronger in females: familial risk, early‐onset anxiety disorders, and nicotine dependence. Seven predictors had a stronger total effect in males: novelty seeking, conduct disorder, childhood sexual abuse, parental loss, neuroticism, low self‐esteem, and low marital satisfaction. Conclusions In a co‐twin control design, which matches sisters and brothers on genetic and familial–environmental background, we found numerous sex differences in predictors of last year AP . Factors that were more prominent in men and in women were diverse, reflecting both internalizing and externalizing psychopathology. The model was slightly more successful at predicting AP in men than in women.
    Type of Medium: Online Resource
    ISSN: 0145-6008 , 1530-0277
    URL: Issue
    URL: Article
    DOI: 10.1111/acer.2015.39.issue-6
    DOI: 10.1111/acer.12694
    Language: English
    Publisher: Wiley
    Publication Date: 2015
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  • 18
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    Alcohol use disorder and non‐fatal suicide attempt: findings from a Swedish National Cohort Study
    Wiley ; 2022
    In:  Addiction Vol. 117, No. 1 ( 2022-01), p. 96-105
    Details
    In: Addiction, Wiley, Vol. 117, No. 1 ( 2022-01), p. 96-105
    Abstract: Alcohol use disorder (AUD) is associated with increased risk of non‐fatal suicide attempt. We aimed to measure the strength and mechanistic nature of the association between AUD and increased suicide attempt and determine any causal pathways and/or shared risk factors. Design We used Cox proportional hazards models in population‐level and co‐relative analyses to evaluate the risk of first non‐fatal suicide attempt as a function of previous AUD. Setting and Participants We used continuously updated longitudinal nationwide Swedish registry data on native Swedes born from 1950 to 1970 ( n  = 2 229 619) and followed from age 15 until 2012. Measurements AUD and suicide attempt were identified using International Classification of Diseases (ICD)‐8, ICD‐9, and ICD‐10 codes. AUD was also identified using pharmacy and criminal records. Genetic and family environmental risks were derived based on relatedness via the Multi‐Generation Register and shared residency via the Population and Housing Census and the Total Population Register. Findings AUD was robustly associated with suicide attempt in crude models (hazard ratio [HR] = 15.24 [95% CI: 14.92, 15.56] ). In models adjusted for sociodemographic factors and psychiatric comorbidity, the association was attenuated: for women, HRs declined gradually across time, ranging from 5.55 (3.72, 8.29) during the observation period that ranged from age 15 to 19 years to 1.77 (1.65, 1.90) at age 40 or older. For men, the corresponding figures were 6.12 (4.07, 9.19) and 1.83 (1.72, 1.94); in contrast to women, risk of suicide attempt among men increased from age 15 to 29 before declining. In co‐relative models, a residual association remained, consistent with a causal path from AUD to suicide attempt. Conclusions In Sweden, alcohol use disorder appears to be an important predictor of suicide attempt even in the context of other psychiatric disorders. The observed association is likely the result of features that jointly impact risk of alcohol use disorder and suicide attempts (genetic liability, psychiatric illness, and childhood stressors) and a potentially causal pathway, acting independently or in conjunction with one another.
    Type of Medium: Online Resource
    ISSN: 0965-2140 , 1360-0443
    URL: Issue
    URL: Article
    DOI: 10.1111/add.v117.1
    DOI: 10.1111/add.15621
    Language: English
    Publisher: Wiley
    Publication Date: 2022
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  • 19
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    Risk of non‐fatal suicide attempt in individuals with substance use disorder: the roles of aggregate genetic liability and environmental exposures in a Swedish population‐based cohort
    Wiley ; 2022
    In:  Addiction Vol. 117, No. 11 ( 2022-11), p. 2943-2952
    Details
    In: Addiction, Wiley, Vol. 117, No. 11 ( 2022-11), p. 2943-2952
    Abstract: Substance use disorder (SUD) is related to widespread adverse consequences, including higher suicidality. Shared genetic liability has been demonstrated between SUD and suicidality. Here, we measured the factors that contribute to increased risk of non‐fatal suicide attempt among individuals with SUD by focusing upon aggregate genetic risks and both childhood and past‐year environmental factors. Design Longitudinal study. Family genetic risk scores and environmental factors (childhood, aged from 0 to 15 years, and the year preceding SUD registration) were used to predict the relative risk of non‐fatal suicide attempt using Cox proportional hazards models. Additional analyses employed a co‐relative design, accounting for genetic factors and shared familial environment, to test for potential causality. Setting and participants Based on longitudinal Swedish registry data, 228 617 individuals with SUD registrations from 1991 to 2015 were included. Measurements SUD and suicide attempts were identified using medical records (International Classification of Diseases codes). SUD was also identified using pharmacy and criminal registries. Findings In multivariable analyses that jointly accounted for all the selected potential predictors, individuals with SUD were at higher risk for non‐fatal suicide attempt if they had experienced a parental death [hazard ratio (HR) = 1.58; 95% confidence interval (CI) = 1.30, 1.93], were female (HR = 1.53, 95% CI = 1.49, 1.57), had low educational attainment (HR = 1.50, 95% CI = 1.46, 1.55), received social welfare (HR = 1.21, 95% CI = 1.17, 1.25) or had lived in a non‐intact family (HR = 1.11, 95% CI = 1.08, 1.14). In co‐relative analyses, low education was supported as a possible causal factor for suicide attempt. Aggregate genetic risks interacted with low education and being raised in a non‐intact family, with increased prevalence of suicide attempt in people with high genetic risks and unfavorable environmental exposures. Conclusions Aggregate genetic liability, childhood environmental experiences and specific socio‐economic indicators are important risk factors for non‐fatal suicide attempt among individuals with substance use disorder.
    Type of Medium: Online Resource
    ISSN: 0965-2140 , 1360-0443
    URL: Issue
    URL: Article
    DOI: 10.1111/add.v117.11
    DOI: 10.1111/add.15965
    Language: English
    Publisher: Wiley
    Publication Date: 2022
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  • 20
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    Polygenic Risk Score Prediction of Alcohol Dependence Symptoms Across Population‐Based and Clinically Ascertained Samples
    Wiley ; 2018
    In:  Alcoholism: Clinical and Experimental Research Vol. 42, No. 3 ( 2018-03), p. 520-530
    Details
    In: Alcoholism: Clinical and Experimental Research, Wiley, Vol. 42, No. 3 ( 2018-03), p. 520-530
    Abstract: Despite consistent evidence of the heritability of alcohol use disorders ( AUD s), few specific genes with an etiological role have been identified. It is likely that AUD s are highly polygenic; however, the etiological pathways and genetic variants involved may differ between populations. The aim of this study was thus to evaluate whether aggregate genetic risk for AUD s differed between clinically ascertained and population‐based epidemiological samples. Methods Four independent samples were obtained: 2 from unselected birth cohorts (Avon Longitudinal Study of Parents and Children [ ALSPAC ], N  =   4,304; FinnTwin12 [FT12], N  =   1,135) and 2 from families densely affected with AUD s, identified from treatment‐seeking patients (Collaborative Study on the Genetics of Alcoholism, N  =   2,097; Irish Affected Sib Pair Study of Alcohol Dependence, N  =   706). AUD symptoms were assessed with clinical interviews, and participants of European ancestry were genotyped. Genomewide association was conducted separately in each sample, and the resulting association weights were used to create polygenic risk scores in each of the other samples (12 total discovery–validation pairs), and from meta‐analyses within sample type. We then tested how well these aggregate genetic scores predicted AUD outcomes within and across sample types. Results Polygenic scores derived from 1 population‐based sample ( ALSPAC ) significantly predicted AUD symptoms in another population‐based sample (FT12), but not in either clinically ascertained sample. Trend‐level associations (uncorrected p  〈   0.05) were found for polygenic score predictions within sample types but no or negative predictions across sample types. Polygenic scores accounted for 0 to 1% of the variance in AUD symptoms. Conclusions Though preliminary, these results provide suggestive evidence of differences in the genetic etiology of AUD s based on sample characteristics such as treatment‐seeking status, which may index other important clinical or demographic factors that moderate genetic influences. Although the variance accounted for by genomewide polygenic scores remains low, future studies could improve gene identification efforts by amassing very large samples, or reducing genetic heterogeneity by informing analyses with other phenotypic information such as sample characteristics. Multiple complementary approaches may be needed to make progress in gene identification for this complex disorder.
    Type of Medium: Online Resource
    ISSN: 0145-6008 , 1530-0277
    URL: Issue
    URL: Article
    DOI: 10.1111/acer.2018.42.issue-3
    DOI: 10.1111/acer.13589
    Language: English
    Publisher: Wiley
    Publication Date: 2018
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