Evidence map›Paper›PMID 35705636›Full record

SynthesisMolecular psychiatry2022

Alcohol use disorder is associated with DNA methylation-based shortening of telomere length and regulated by TESPA1: implications for aging.

Jeesun Jung, Daniel L McCartney, Josephin Wagner, Daniel B Rosoff, Melanie Schwandt, Hui Sun, Corinde E Wiers, Luana Martins de Carvalho, Nora D Volkow, Rosie M Walker and 7 more

Open access · hybridAbstract readMeta-Analysis
In one paragraph

Synthesis in Molecular psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

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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

17 authors at 4 institutions in 2 countries.

Jeesun JungSection on Clinical Genomics and Experimental Therapeutics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA.ORCID http://orcid.org/0000-0002-2668-5541
Daniel L McCartneyCentre for Genomic and Experimental Medicine, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK.ORCID http://orcid.org/0000-0003-3242-0360
Josephin WagnerSection on Clinical Genomics and Experimental Therapeutics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA.
Daniel B RosoffSection on Clinical Genomics and Experimental Therapeutics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA.
Melanie SchwandtOffice of the Clinical Director, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA.ORCID http://orcid.org/0000-0002-8355-4900
Hui SunOffice of the Clinical Director, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA.
Corinde E WiersLaboratory of Neuroimaging, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA.ORCID http://orcid.org/0000-0002-2934-8794
Luana Martins de CarvalhoLaboratory of Neuroimaging, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA.
Nora D VolkowLaboratory of Neuroimaging, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA.
Rosie M WalkerCentre for Genomic and Experimental Medicine, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK.ORCID http://orcid.org/0000-0002-1060-4479
Archie CampbellCentre for Genomic and Experimental Medicine, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK.ORCID http://orcid.org/0000-0003-0198-5078
David J PorteousCentre for Genomic and Experimental Medicine, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK.ORCID http://orcid.org/0000-0003-1249-6106
Andrew M McIntoshCentre for Genomic and Experimental Medicine, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK.ORCID http://orcid.org/0000-0002-0198-4588
Riccardo E MarioniCentre for Genomic and Experimental Medicine, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK.
Steve HorvathDepartment of Biostatistics, Fielding School of Public Health, University of California Los Angeles, Los Angeles, CA, USA.ORCID http://orcid.org/0000-0002-4110-3589
Kathryn L EvansCentre for Genomic and Experimental Medicine, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK.ORCID http://orcid.org/0000-0002-7884-5877
Falk W LohoffSection on Clinical Genomics and Experimental Therapeutics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA. falk.lohoff@nih.gov.ORCID http://orcid.org/0000-0002-0480-7755
Edinburgh Cancer Research · GBNational Institutes of Health · USNational Institute on Alcohol Abuse and Alcoholism · USUniversity of California, Los Angeles · US

Funding

Neurobiology of Substance Abuse and AddictionZIAAA000550 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI VOLKOW, NORA D. · 2009 to 2025
$115.1M
Clinical Genomics and Experimental TherapeuticsZIAAA000242 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI LOHOFF, FALK · 2015 to 2025
$26.7M
Intramural NIH HHS ZIA AA000242Wellcome Trust 104036/Z/14/ZWellcome Trust 220857/Z/20/Z
6 · The paper itself

Abstract

Chronic heavy alcohol consumption is associated with increased mortality and morbidity and often leads to premature aging; however, the mechanisms of alcohol-associated cellular aging are not well understood. In this study, we used DNA methylation derived telomere length (DNAmTL) as a novel approach to investigate the role of alcohol use on the aging process. DNAmTL was estimated by 140 cytosine phosphate guanines (CpG) sites in 372 individuals with alcohol use disorder (AUD) and 243 healthy controls (HC) and assessed using various endophenotypes and clinical biomarkers. Validation in an independent sample of DNAmTL on alcohol consumption was performed (N = 4219). Exploratory genome-wide association studies (GWAS) on DNAmTL were also performed to identify genetic variants contributing to DNAmTL shortening. Top GWAS findings were analyzed using in-silico expression quantitative trait loci analyses and related to structural MRI hippocampus volumes of individuals with AUD. DNAmTL was 0.11-kilobases shorter per year in AUD compared to HC after adjustment for age, sex, race, and blood cell composition (p = 4.0 × 10

Indexed as

Adaptor Proteins, Signal TransducingAgingAlcoholismTelomere ShorteningAlcohol DrinkingDNA MethylationGenome-Wide Association StudyHumansTelomereAdaptor Proteins, Signal TransducingTESPA1 protein, human

Identifiers

PMID35705636
PMCPMC9708583
OpenAlexW4282982593

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.