Evidence map›Paper›PMID 32860857›Full record

ArticleAlcohol (Fayetteville, N.Y.)2020

Adolescent low-dose ethanol drinking in the dark increases ethanol intake later in life in C57BL/6J, but not DBA/2J mice.

Jennifer T Wolstenholme, Rabha M Younis, Wisam Toma, M Imad Damaj

Abstract read
In one paragraph

Article in Alcohol (Fayetteville, N.Y.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. 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

4 authors.

Jennifer T WolstenholmeDepartment of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, VA, United States; Virginia Commonwealth University, Alcohol Research Center, Richmond, VA, United States. Electronic address: jennifer.wolstenholme@vcuhealth.org.
Rabha M YounisDepartment of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, VA, United States; Department of Pharmacotherapy & Outcomes Science, School of Pharmacy, Virginia Commonwealth University, Richmond, VA, United States.
Wisam TomaDepartment of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, VA, United States.
M Imad DamajDepartment of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, VA, United States; Translational Research Initiative for Pain and Neuropathy, Virginia Commonwealth University, Richmond, VA, United States.

Funding

Project 5 - Genetic architecture of alcohol use disorder using cross-trait genetic correlations and public next-generation sequencing studiesP50AA022537 · NIAAA · VIRGINIA COMMONWEALTH UNIVERSITY · PI JILL C BETTINGER · 2014 to 2026
$19.6M
VCU Center for Drug Addiction ResearchP30DA033934 · NIDA · VIRGINIA COMMONWEALTH UNIVERSITY · PI Matthew Sean Halquist · 2014 to 2026
$13.8M
Histone methylation as a potential mechanism for myelin deficits and behavioral alterations following adolescent binge ethanolR01AA026347 · NIAAA · VIRGINIA COMMONWEALTH UNIVERSITY · PI WOLSTENHOLME, JENNIFER T · 2018 to 2022
$1.7M
NIAAA NIH HHS P50 AA022537NIAAA NIH HHS R01 AA026347NIDA NIH HHS P30 DA033934
6 · The paper itself

Abstract

Alcohol is the most widely used and abused drug among youth in the United States. Youths aged 12-20 years old drink almost 11% of all alcohol consumed in the United States, and typically these young people are consuming alcohol in the form of binge drinking. Particularly concerning is that the risk of developing an alcohol use disorder over their lifetime increases the younger one begins to drink. Here we investigated the impact of ethanol drinking in early adolescence on adult ethanol intake using C57BL/6J and DBA/2J mice. We modeled low-dose drinking in adolescent mice using a modified Drinking in the Dark (DID) model where the total ethanol intake during adolescence was similar between the strains to specifically ask whether low-dose ethanol exposure in the high-alcohol preferring C57BL/6J strain will also lead to increased ethanol intake in adulthood. Our results show that low-dose ethanol drinking in early adolescence dramatically increases adult intake, but only in the alcohol-preferring C57BL/6J strain. Early adolescent ethanol exposure had no effect on ethanol intake in the alcohol-nonpreferring DBA/2J mice. These data add to the growing evidence that low-dose ethanol exposures, below the pharmacologically relevant dose, can also contribute to increased drinking in adulthood, but the effect may be influenced by genetic background.

Indexed as

Alcohol DrinkingDarknessEthanolAdolescentAge FactorsAnimalsDisease Models, AnimalHumansMaleMiceMice, Inbred C57BLMice, Inbred DBASpecies SpecificityEthanoladolescenceadulthoodDIDethanolintakemice

Identifiers

PMID32860857
PMCPMC7721983

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.