Examining interactions between genetic risk for alcohol problems, peer deviance, and interpersonal traumatic events on trajectories of alcohol use disorder symptoms among African American college students

AbstractNumerous studies have demonstrated that genetic and environmental factors interact to influence alcohol problems. Yet prior research has primarily focused on samples of European descent and little is known about gene–environment interactions in relation to alcohol problems in non-European populations. In this study, we examined whether and how genetic risk for alcohol problems and peer deviance and interpersonal traumatic events independently and interactively influence trajectories of alcohol use disorder symptoms in a sample of African American students across the college years (N = 1,119; Mage= 18.44 years). Data were drawn from the Spit for Science study where participants completed multiple online surveys throughout college and provided a saliva sample for genotyping. Multilevel growth curve analyses indicated that alcohol dependence genome-wide polygenic risk scores did not predict trajectory of alcohol use disorder symptoms, while family history of alcohol problems was associated with alcohol use disorder symptoms at the start of college but not with the rate of change in symptoms over time. Peer deviance and interpersonal traumatic events were associated with more alcohol use disorder symptoms across college years. Neither alcohol dependence genome-wide polygenic risk scores nor family history of alcohol problems moderated the effects of these environmental risk factors on alcohol use disorder symptoms. Our findings indicated that peer deviance and experience of interpersonal traumatic events are salient risk factors that elevate risk for alcohol problems among African American college students. Family history of alcohol problems could be a useful indicator of genetic risk for alcohol problems. Gene identification efforts with much larger samples of African descent are needed to better characterize genetic risk for alcohol use disorders, in order to better understand gene–environment interaction processes in this understudied population.

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The role of pubertal timing in the link between family history of alcohol use disorder and late adolescent substance use

Drug and Alcohol Dependence ◽

10.1016/j.drugalcdep.2020.107955 ◽

2020 ◽

Vol 210 ◽

pp. 107955

Author(s):

Alexander S. Weigard ◽

Jillian E. Hardee ◽

Robert A. Zucker ◽

Mary M. Heitzeg ◽

Adriene M. Beltz

Keyword(s):

Substance Use ◽

Family History ◽

Alcohol Use ◽

Alcohol Use Disorder ◽

Pubertal Timing ◽

Adolescent Substance Use ◽

Late Adolescent ◽

Adolescent Substance ◽

History Of

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Parkinson’s disease determinants, prediction and gene–environment interactions in the UK Biobank

Journal of Neurology Neurosurgery & Psychiatry ◽

10.1136/jnnp-2020-323646 ◽

2020 ◽

Vol 91 (10) ◽

pp. 1046-1054 ◽

Cited By ~ 2

Author(s):

Benjamin Meir Jacobs ◽

Daniel Belete ◽

Jonathan Bestwick ◽

Cornelis Blauwendraat ◽

Sara Bandres-Ciga ◽

...

Keyword(s):

Risk Factors ◽

Parkinson’S Disease ◽

Parkinson's Disease ◽

Family History ◽

Genetic Risk ◽

Positive Family History ◽

Risk Scores ◽

Uk Biobank ◽

Gene Environment ◽

History Of

ObjectiveTo systematically investigate the association of environmental risk factors and prodromal features with incident Parkinson’s disease (PD) diagnosis and the interaction of genetic risk with these factors. To evaluate whether existing risk prediction algorithms are improved by the inclusion of genetic risk scores.MethodsWe identified individuals with an incident diagnosis of PD (n=1276) and controls (n=500 406) in UK Biobank. We determined the association of risk factors with incident PD using adjusted logistic regression models. We constructed polygenic risk scores (PRSs) using external weights and selected the best PRS from a subset of the cohort (30%). The PRS was used in a separate testing set (70%) to examine gene–environment interactions and compare predictive models for PD.ResultsStrong evidence of association (false discovery rate <0.05) was found between PD and a positive family history of PD, a positive family history of dementia, non-smoking, low alcohol consumption, depression, daytime somnolence, epilepsy and earlier menarche. Individuals with the highest 10% of PRSs had increased risk of PD (OR 3.37, 95% CI 2.41 to 4.70) compared with the lowest risk decile. A higher PRS was associated with earlier age at PD diagnosis and inclusion of the PRS in the PREDICT-PD algorithm led to a modest improvement in model performance. We found evidence of an interaction between the PRS and diabetes.InterpretationHere, we used UK Biobank data to reproduce several well-known associations with PD, to demonstrate the validity of a PRS and to demonstrate a novel gene–environment interaction, whereby the effect of diabetes on PD risk appears to depend on background genetic risk for PD.

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Family history of alcohol use disorder is associated with brain structural and functional changes in healthy first-degree relatives

European Psychiatry ◽

10.1016/j.eurpsy.2019.08.003 ◽

2019 ◽

Vol 62 ◽

pp. 107-115 ◽

Cited By ~ 3

Author(s):

Irina Filippi ◽

Nicolas Hoertel ◽

Eric Artiges ◽

Guillaume Airagnes ◽

Christophe Guérin-Langlois ◽

...

Keyword(s):

Family History ◽

Alcohol Use ◽

Childhood Maltreatment ◽

Alcohol Use Disorder ◽

Grey Matter ◽

Brain Regions ◽

Whole Brain ◽

Childhood Trauma Questionnaire ◽

Functional Changes ◽

History Of

Abstract Background: Neuroimaging studies of vulnerability to Alcohol Use Disorder (AUD) have identified structural and functional variations which might reflect inheritable features in alcohol-naïve relatives of AUD individuals (FH+) compared to controls having no such family history (FH-). However, prior research did not simultaneously account for childhood maltreatment, any clinically significant disorder and maternal AUD. Therefore, we mainly aimed to investigate the brain structure and reward-related neural activations (fMRI), using whole-brain analysis in FH+ young adults with no prevalent confounders. Methods: 46 FH+ and 45 FH- male and female participants had no severe childhood maltreatment exposure, neither any psychiatric disorder or AUD, nor a prenatal exposure to maternal AUD. We used a 3 T MRI coupled with a whole brain voxel-based method to compare between groups the grey matter volumes and activations in response to big versus small wins during a Monetary Incentive Delay task. The Childhood Trauma Questionnaire score was used as confounding variable in the analyses to account for the remaining variance between groups. Results: Compared to FH- controls, FH+ participants had smaller grey matter volumes in the frontal and cingulate regions as well as in the bilateral nucleus accumbens and right insula. The FH+ participants’ fMRI datasets denoted a blunted activation in the middle cingulum with respect to FH- controls’ during the processing of reward magnitude, and a greater activation in the anterior cingulum in response to anticipation of a small win. Conclusions: Family history of alcohol use disorder is linked to structural and functional variations including brain regions involved in reward processes.

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Delineating genetic and familial risk for psychopathology in the ABCD study

10.1101/2020.09.08.20186908 ◽

2020 ◽

Author(s):

Clare E Palmer ◽

Robert John Loughnan ◽

Carolina Makowski ◽

Wesley Thompson ◽

Deanna Barch ◽

...

Keyword(s):

Family History ◽

Psychiatric Disorders ◽

Genetic Risk ◽

Familial Risk ◽

Risk Scores ◽

Typically Developing ◽

Polygenic Risk ◽

Hyperactivity Disorder ◽

History Of ◽

Risk Predictors

Psychiatric disorders place a huge burden on those affected and their families, as well as society. Nearly all psychiatric disorders have a heritable component and lifetime prevalence rates of several disorders are higher among first degree biological relatives of individuals with a diagnosis. Given that many psychiatric disorders have their onset in adolescence, estimating genetic risk during childhood may identify at-risk individuals for early intervention that can reduce this burden. Here we measured genetic risk for psychopathology using both polygenic risk scores (PRS) and family history in a large typically developing sample of 9-10 year old children from the Adolescent Brain and Cognitive Development (ABCD) StudySM and determined associations with a large battery of behavioural phenotypes. By including all genetic risk predictors in the same model, we were able to delineate unique behavioral associations across these measures. Polygenic risk for Attention Deficit Hyperactivity Disorder (ADHD) and depression (DEP) was associated with unique patterns of both externalizing and internalizing behaviors. Family history of conduct problems, depression and anxiety/stress additionally predicted unique behavioral variance across similar measures. These findings provide important insight into the potential predictive utility of PRS and family history in early adolescence and suggest that they may be signaling differential, additive information that could be useful for quantifying risk during development.

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Family History of Alcohol Abuse Associated with Higher Impulsivity in Patients with Alcohol Use Disorder: A Multisite Study

European Addiction Research ◽

10.1159/000505621 ◽

2020 ◽

Vol 26 (2) ◽

pp. 85-95 ◽

Cited By ~ 1

Author(s):

Lotfi Khemiri ◽

Anne Marije Kaag ◽

Leen Joos ◽

Geert Dom ◽

Johan Franck ◽

...

Keyword(s):

Family History ◽

Alcohol Use ◽

Alcohol Abuse ◽

Alcohol Use Disorder ◽

History Of

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The impact of sex, age at onset, recurrence, mode of ascertainment and medical complications on the family genetic risk score profiles for alcohol use disorder

Psychological Medicine ◽

10.1017/s0033291721003317 ◽

2021 ◽

pp. 1-9

Author(s):

Kenneth S. Kendler ◽

Henrik Ohlsson ◽

Jan Sundquist ◽

Kristina Sundquist

Keyword(s):

Alcohol Use ◽

Genetic Risk ◽

Criminal Behavior ◽

Alcohol Use Disorder ◽

Genetic Risk Score ◽

Age At Onset ◽

Risk Scores ◽

Medical Complications ◽

The Family ◽

The Impact

Abstract Background Alcohol use disorder (AUD) is clinically heterogeneous. We examine its potential genetic heterogeneity as a function of sex, age, clinical features and mode of ascertainment. Methods In the Swedish population born 1932–1995 (n = 5 829 952), we examined the genetic risk profiles for AUD, major depression (MD), anxiety disorders, bipolar disorder, drug use disorder (DUD), attention deficit-hyperactivity disorder (ADHD) and criminal behavior (CB) in 361 124 cases of AUD subdivided by sex, age at onset (AAO), recurrence, mode of ascertainment and medical complications. Family genetic risk scores (FGRS), calculated from 1st to 5th-degree relatives controlling of cohabitation, assesses genetic risk from phenotypes in the family, not from DNA variants. Results FGRS profiles differed modestly across sex with all scores higher in females. Differences were more pronounced for AAO and recurrence with the FGRS for AUD, DUD, ADHD and CB substantially higher in cases with early AAO or high recurrence rates. Genetic profiles differed considerably by mode of ascertainment, with higher FGRS for AUD and most other disorders in patients seen in hospital v. primary care settings. Cases of AUD with medical complications had higher FGRS for AUD. AUD cases comorbid with MD and DUD had higher FGRS risk for AUD, but this genetic may be less specific given increases in FGRS for multiple other disorders. Conclusions From a genetic perspective, AUD differs substantially as a function of AAO, recurrence, mode of ascertainment and patterns of comorbidity, suggesting caution in cross-sample comparisons of AUD cohorts that differ in these features.

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Cortical Thickness in Adolescents with a Family History of Alcohol Use Disorder

Alcoholism Clinical and Experimental Research ◽

10.1111/acer.13543 ◽

2017 ◽

Vol 42 (1) ◽

pp. 89-99 ◽

Cited By ~ 18

Author(s):

Kate E. Henderson ◽

Jatin G. Vaidya ◽

John R. Kramer ◽

Samuel Kuperman ◽

Douglas R. Langbehn ◽

...

Keyword(s):

Family History ◽

Alcohol Use ◽

Cortical Thickness ◽

Alcohol Use Disorder ◽

History Of

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Parental Family History of Alcohol Use Disorder and Neural Correlates of Response Inhibition in Children From the Adolescent Brain Cognitive Development (ABCD) Study

Alcoholism Clinical and Experimental Research ◽

10.1111/acer.14343 ◽

2020 ◽

Vol 44 (6) ◽

pp. 1234-1244 ◽

Cited By ~ 3

Author(s):

Briana Lees ◽

Laika Aguinaldo ◽

Lindsay M. Squeglia ◽

Maria Alejandra Infante ◽

Natasha E. Wade ◽

...

Keyword(s):

Cognitive Development ◽

Family History ◽

Alcohol Use ◽

Response Inhibition ◽

Alcohol Use Disorder ◽

Neural Correlates ◽

History Of ◽

Parental Family

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Environmental influences predominate in remission from alcohol use disorder in young adult twins

Psychological Medicine ◽

10.1017/s003329171200044x ◽

2012 ◽

Vol 42 (11) ◽

pp. 2421-2431 ◽

Cited By ~ 10

Author(s):

V. V. McCutcheon ◽

J. D. Grant ◽

A. C. Heath ◽

K. K. Bucholz ◽

C. E. Sartor ◽

...

Keyword(s):

Young Adult ◽

Family History ◽

Alcohol Use ◽

Alcohol Use Disorder ◽

Telephone Interview ◽

Environmental Influences ◽

Familial Influences ◽

History Of ◽

Adult Twins ◽

Alcohol Abuse And Dependence

BackgroundFamilial influences on remission from alcohol use disorder (AUD) have been studied using family history of AUD rather than family history of remission. The current study used a remission phenotype in a twin sample to examine the relative contributions of genetic and environmental influences to remission.MethodThe sample comprised 6183 twins with an average age of 30 years from the Australian Twin Registry. Lifetime history of alcohol abuse and dependence symptoms and symptom recency were assessed with a structured telephone interview. AUD was defined broadly and narrowly as history of two or more or three or more abuse or dependence symptoms. Remission was defined as absence of symptoms at time of interview among individuals with lifetime AUD. Standard bivariate genetic analyses were conducted to derive estimates of genetic and environmental influences on AUD and remission.ResultsEnvironmental influences alone accounted for remission in males and for 89% of influences on remission in females, with 11% due to genetic influences shared with AUD, which decreased the likelihood of remission. For women, more than 80% of influences on remission were distinct from influences on AUD, and environmental influences were from individual experiences only. For men, just over 50% of influences on remission were distinct from those on AUD, and the influence of environments shared with the co-twin were substantial. The results for the broad and narrow phenotypes were similar.ConclusionsThe current study establishes young adult remission as a phenotype distinct from AUD and highlights the importance of environmental influences on remission.

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