Evidence map›Paper›PMID 28847377›Full record

ArticleAlcohol (Fayetteville, N.Y.)2017

A GABRA2 polymorphism improves a model for prediction of drinking initiation.

Samuel Kuperman, Grace Chan, John Kramer, Leah Wetherill, Laura Acion, Howard J Edenberg, Tatiana M Foroud, John Nurnberger, Arpana Agrawal, Andrey Anokhin and 6 more

Open access · greenAbstract readMulticenter Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Alcohol (Fayetteville, N.Y.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.9field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. GABAPsychopharmacology · 2018
    Review
  4. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors at 6 institutions in 1 country.

Samuel KupermanDepartment of Psychiatry, University of Iowa Carver College of Medicine, Iowa City, IA, USA. Electronic address: samuel-kuperman@uiowa.edu.
Grace ChanDepartment of Psychiatry, University of Connecticut Health Center, Farmington, CT, USA.
John KramerDepartment of Psychiatry, University of Iowa Carver College of Medicine, Iowa City, IA, USA.
Leah WetherillDepartment of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, USA.
Laura AcionDepartment of Psychiatry, University of Iowa Carver College of Medicine, Iowa City, IA, USA.
Howard J EdenbergDepartment of Biochemistry & Molecular Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
Tatiana M ForoudDepartment of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, USA.
John NurnbergerDepartment of Psychiatry, Indiana University School of Medicine, Indianapolis, IN, USA.
Arpana AgrawalDepartment of Psychiatry, Washington University School of Medicine, St. Louis, MO, USA.
Andrey AnokhinDepartment of Psychiatry, Washington University School of Medicine, St. Louis, MO, USA.
Andrew BrooksDepartment of Genetics, Rutgers University, Piscataway, NJ, USA.
Victor HesselbrockDepartment of Psychiatry, University of Connecticut Health Center, Farmington, CT, USA.
Michie HesselbrockDepartment of Psychiatry, University of Connecticut Health Center, Farmington, CT, USA.
Marc SchuckitDepartment of Psychiatry, University of California San Diego School of Medicine, La Jolla, CA, USA.
Jay TischfieldDepartment of Genetics, Rutgers University, Piscataway, NJ, USA.
Xiangtao LiuDepartment of Psychiatry, University of Iowa Carver College of Medicine, Iowa City, IA, USA.
Indiana University School of MedicineUniversity of Iowa · USUConn Health · USRutgers, The State University of New Jersey · USWashington University in St. Louis · USUniversity of California San Diego · US

Funding

Subject CollectionU10AA008401 · NIAAA · SUNY DOWNSTATE MEDICAL CENTER · PI JAY Arnold TISCHFIELD · 1989 to 2026
$162.7M
NEUROPHYSIOLOGY IN CHILDREN AT HIGH RISK FOR ALCOHOLISMR37AA005524 · NIAAA · SUNY DOWNSTATE MEDICAL CENTER · PI PORJESZ, BERNICE · 2001 to 2010
$4.6M
NEUROPHYSIOLOGY IN CHILDREN AT HIGH RISK FOR ALCOHOLISMR01AA005524 · NIAAA · SUNY DOWNSTATE MEDICAL CENTER · PI PORJESZ, BERNICE · 1986 to 2015
$3.0M
ETHANOL TOLERANCE IN NEUROHYPOPHYSISF31AA005524 · NIAAA · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI KNOTT, THOMAS KRIS · 1998 to 2000
$9k
NIAAA NIH HHS F31 AA005524NIAAA NIH HHS R01 AA005524NIAAA NIH HHS R37 AA005524NIAAA NIH HHS U10 AA008401
6 · The paper itself

Abstract

backgroundSurvival analysis was used to explore the addition of a single nucleotide polymorphism (SNP) and covariates (sex, interview age, and ancestry) on a previously published model's ability to predict onset of drinking. A SNP variant of rs279871, in the chromosome 4 gene encoding gamma-aminobutyric acid receptor (GABRA2), was selected due to its associations with alcoholism in young adults and with behaviors that increased risk for early drinking.

methodsA subsample of 674 adolescents (ages 14-17) participating in the Collaborative Study on the Genetics of Alcoholism (COGA) was examined using a previously derived Cox proportional hazards model containing: 1) number of non-drinking related conduct disorder (CD) symptoms, 2) membership in a high-risk alcohol-dependent (AD) family, 3) most best friends drank (MBFD), 4) Achenbach Youth Self Report (YSR) externalizing score, and 5) YSR social problems score. The above covariates along with the SNP variant of GABRA2, rs279871, were added to this model. Five new prototype models were examined. The most parsimonious model was chosen based on likelihood ratio tests and model fit statistics.

resultsThe final model contained four of the five original predictors (YSR social problems score was no longer significant and hence dropped from subsequent models), the three covariates, and a recessive GABRA2 rs279871 TT genotype (two copies of the high-risk allele containing thymine). The model indicated that adolescents with the high-risk TT genotype were more likely to begin drinking than those without this genotype.

conclusionsThe joint effect of the gene (rs279871 TT genotype) and environment (MBFD) on adolescent alcohol initiation is additive, but not interactive, after controlling for behavior problems (CD and YSR externalizing score). This suggests that the impact of the high-risk TT genotype on the onset of drinking is affected by controlling for peer drinking and does not include genotype-by-environment interactions.

Indexed as

AdolescentAdolescent BehaviorFemaleGenetic Predisposition to DiseaseHumansMalePolymorphism, Single NucleotidePredictive Value of TestsReceptors, GABA-AUnderage DrinkingGABRA2 protein, humanReceptors, GABA-AAdolescentAlcoholDrinking initiationGABRA2rs279871Survival analysis modeling

Identifiers

PMID28847377
PMCPMC5657392
OpenAlexW2728978071

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.