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  • 1
    Online Resource
    Online Resource
    Shared genetic risk between eating disorder‐ and substance‐use‐related phenotypes: Evidence from genome‐wide association studies
    Wiley ; 2021
    In:  Addiction Biology Vol. 26, No. 1 ( 2021-01)
    Details
    In: Addiction Biology, Wiley, Vol. 26, No. 1 ( 2021-01)
    Abstract: Eating disorders and substance use disorders frequently co‐occur. Twin studies reveal shared genetic variance between liabilities to eating disorders and substance use, with the strongest associations between symptoms of bulimia nervosa and problem alcohol use (genetic correlation [ r g ], twin‐based = 0.23‐0.53). We estimated the genetic correlation between eating disorder and substance use and disorder phenotypes using data from genome‐wide association studies (GWAS). Four eating disorder phenotypes (anorexia nervosa [AN] , AN with binge eating, AN without binge eating, and a bulimia nervosa factor score), and eight substance‐use‐related phenotypes (drinks per week, alcohol use disorder [AUD], smoking initiation, current smoking, cigarettes per day, nicotine dependence, cannabis initiation, and cannabis use disorder) from eight studies were included. Significant genetic correlations were adjusted for variants associated with major depressive disorder and schizophrenia. Total study sample sizes per phenotype ranged from ~2400 to ~537 000 individuals. We used linkage disequilibrium score regression to calculate single nucleotide polymorphism‐based genetic correlations between eating disorder‐ and substance‐use‐related phenotypes. Significant positive genetic associations emerged between AUD and AN ( r g = 0.18; false discovery rate q = 0.0006), cannabis initiation and AN ( r g = 0.23; q 〈 0.0001), and cannabis initiation and AN with binge eating ( r g = 0.27; q = 0.0016). Conversely, significant negative genetic correlations were observed between three nondiagnostic smoking phenotypes (smoking initiation, current smoking, and cigarettes per day) and AN without binge eating ( r gs = −0.19 to −0.23; qs 〈 0.04). The genetic correlation between AUD and AN was no longer significant after co‐varying for major depressive disorder loci. The patterns of association between eating disorder‐ and substance‐use‐related phenotypes highlights the potentially complex and substance‐specific relationships among these behaviors.
    Type of Medium: Online Resource
    ISSN: 1355-6215 , 1369-1600
    URL: Issue
    URL: Article
    DOI: 10.1111/adb.v26.1
    DOI: 10.1111/adb.12880
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 1495537-4
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  • 2
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    Online Resource
    Associations of delay discounting and drinking trajectories from ages 14 to 22
    Wiley ; 2022
    In:  Alcoholism: Clinical and Experimental Research Vol. 46, No. 4 ( 2022-04), p. 667-681
    Details
    In: Alcoholism: Clinical and Experimental Research, Wiley, Vol. 46, No. 4 ( 2022-04), p. 667-681
    Abstract: While drinking alcohol, one must choose between the immediate rewarding effects and the delayed reward of a healthier lifestyle. Individuals differ in their devaluation of a delayed reward based on the time required to receive it, i.e., delay discounting (DD). Previous studies have shown that adolescents discount more steeply than adults and that steeper DD is associated with heavier alcohol use in both groups. Methods In a large‐scale longitudinal study, we investigated whether higher rates of DD are an antecedent or a consequence of alcohol use during adolescent development. As part of the IMAGEN project, 2220 adolescents completed the Monetary Choice Questionnaire as a DD measure, the Alcohol Use Disorders Identification Test, and the Timeline Follow Back interview at ages 14, 16, 18, and 22. Bivariate latent growth curve models were applied to investigate the relationship between DD and drinking. To explore the consequences of drinking, we computed the cumulative alcohol consumption and correlated it with the development of discounting. A subsample of 221 participants completed an intertemporal choice task (iTeCh) during functional magnetic resonance imaging at ages 14, 16, and 18. Repeated‐measures ANOVA was used to differentiate between high‐risk and low‐risk drinkers on the development of neural processing during intertemporal choices. Results Overall, high rates of DD at age 14 predicted a greater increase in drinking over 8 years. In contrast, on average, moderate alcohol use did not affect DD from ages 14 to 22. Of note, we found indicators for less brain activity in top‐down control areas during intertemporal choices in the participants who drank more. Conclusions Steep DD was shown to be a predictor rather than a consequence of alcohol use in low‐level drinking adolescents. Important considerations for future longitudinal studies are the sampling strategies to be used and the reliability of the assessments.
    Type of Medium: Online Resource
    ISSN: 0145-6008 , 1530-0277
    URL: Issue
    URL: Article
    DOI: 10.1111/acer.v46.4
    DOI: 10.1111/acer.14799
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2046886-6
    detail.hit.zdb_id: 3167872-5
    SSG: 15,3
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  • 3
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    Online Resource
    Genetic comorbidity between major depression and cardio‐metabolic traits, stratified by age at onset of major depression
    Wiley ; 2020
    In:  American Journal of Medical Genetics Part B: Neuropsychiatric Genetics Vol. 183, No. 6 ( 2020-09), p. 309-330
    Details
    In: American Journal of Medical Genetics Part B: Neuropsychiatric Genetics, Wiley, Vol. 183, No. 6 ( 2020-09), p. 309-330
    Abstract: It is imperative to understand the specific and shared etiologies of major depression and cardio‐metabolic disease, as both traits are frequently comorbid and each represents a major burden to society. This study examined whether there is a genetic association between major depression and cardio‐metabolic traits and if this association is stratified by age at onset for major depression. Polygenic risk scores analysis and linkage disequilibrium score regression was performed to examine whether differences in shared genetic etiology exist between depression case control status ( N cases = 40,940, N controls = 67,532), earlier ( N = 15,844), and later onset depression ( N = 15,800) with body mass index, coronary artery disease, stroke, and type 2 diabetes in 11 data sets from the Psychiatric Genomics Consortium, Generation Scotland, and UK Biobank. All cardio‐metabolic polygenic risk scores were associated with depression status. Significant genetic correlations were found between depression and body mass index, coronary artery disease, and type 2 diabetes. Higher polygenic risk for body mass index, coronary artery disease, and type 2 diabetes was associated with both early and later onset depression, while higher polygenic risk for stroke was associated with later onset depression only. Significant genetic correlations were found between body mass index and later onset depression, and between coronary artery disease and both early and late onset depression. The phenotypic associations between major depression and cardio‐metabolic traits may partly reflect their overlapping genetic etiology irrespective of the age depression first presents.
    Type of Medium: Online Resource
    ISSN: 1552-4841 , 1552-485X
    URL: Issue
    URL: Article
    DOI: 10.1002/ajmg.b.v183.6
    DOI: 10.1002/ajmg.b.32807
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 2143866-3
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    How alcohol makes the epigenetic clock tick faster and the clock reversing effect of abstinence
    Wiley ; 2022
    In:  Addiction Biology Vol. 27, No. 5 ( 2022-09)
    Details
    In: Addiction Biology, Wiley, Vol. 27, No. 5 ( 2022-09)
    Abstract: This study investigated the recently reported association between alcohol dependence and accelerated ageing and the potential effects of abstinence and relapse on DNA methylation status using Levine's epigenetic clock to estimate DNA methylation age in two independent cohorts. The first sample comprised 88 (15 female) detoxified patients with alcohol use disorder (AUD) and 32 (5 female) healthy control (CON) subjects (NCT02615977), and the second included 69 (10 female) AUD patients that were followed up for 12 months with respect to relapse ( n  = 38, 4 female) and abstinence ( n  = 31, 6 female) (NCT01679145). To account for the different aspects of ageing captured by various clocks, we performed additional analyses of the first‐generation Horvath clock and next‐generation Zhang clock. To account for the genetic liability of AUD and its potential influence on DNA methylation, we calculated a polygenic risk score for alcohol dependence. We found that ageing was accelerated by 3.64 years in AUD patients compared with the CON group according to Levine's DNAm PhenoAge. Furthermore, in a second longitudinal sample, we found that abstaining AUD patients displayed a decrease in DNAm PhenoAge by 3.1 years, but we found an over proportional increase by 2.7 years in those who relapsed. Polygenic risk did not affect epigenetic ageing within our sample. These results confirm the age acceleration associated with AUD and provide the first evidence for a recovery of this effect upon abstinence from alcohol.
    Type of Medium: Online Resource
    ISSN: 1355-6215 , 1369-1600
    URL: Issue
    URL: Article
    DOI: 10.1111/adb.v27.5
    DOI: 10.1111/adb.13198
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 1495537-4
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