Evidence map›Paper›PMID 10090900›Full record

ArticleAmerican journal of human genetics1999

Linkage disequilibrium at the ADH2 and ADH3 loci and risk of alcoholism.

M Osier, A J Pakstis, J R Kidd, J F Lee, S J Yin, H C Ko, H J Edenberg, R B Lu, K K Kidd

Open access · bronzeAbstract read
In one paragraph

Article in American journal of human genetics, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 3 pooled it
10.0field-weighted citation impact, top 1% 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

68 citing papers in PubMed, 3 syntheses or guidelines pooled it, 262 citations in OpenAlex.

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8 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 6 institutions in 2 countries.

M OsierDepartment of Human Genetics, Yale University, New Haven, CT 06520-8005, USA.
A J Pakstis
J R Kidd
J F Lee
S J Yin
H C Ko
H J Edenberg
R B Lu
K K Kidd
Yale University · USBali Psychiatric Center · TWIndiana University School of MedicineNational Cheng Kung University · TWNational Defense Medical Center · TWTri-Service General Hospital · TW

Funding

CONTROLS FOR ASSOCIATION STUDIES OF ALCOHOLISMR01AA009379 · NIAAA · YALE UNIVERSITY · PI KIDD, KENNETH K. · 1992 to 2009
$2.7M
LABORATORY OF NEUROIMAGINGP30MH030929 · NIMH · YALE UNIVERSITY · PI HENINGER, GEORGE R · 1993 to 2000
$1.7M
NEUROPSYCHOPHARMACOLOGY--ANALYSIS OF PSYCHOTHERAPEUTIC DRUGS AND METABOLITESP50MH030929 · NIMH · YALE UNIVERSITY · PI BOWERS, MALCOLM B · 1985 to 1992
–
GENETIC STUDIES OF PSYCHIATRIC DISORDERSR01MH039239 · NIMH · YALE UNIVERSITY · PI KIDD, KENNETH K. · 1985 to 1998
–
GENETIC STUDIES OF PSYCHIATRIC DISORDERSR37MH039239 · NIMH · YALE UNIVERSITY · PI KIDD, KENNETH K. · 1987 to 1996
–
NIAAA NIH HHS AA09379-05NIMH NIH HHS MH30929NIMH NIH HHS MH39239
6 · The paper itself

Abstract

Two of the three class I alcohol dehydrogenase (ADH) genes (ADH2 and ADH3) encode known functional variants that act on alcohol with different efficiencies. Variants at both these genes have been implicated in alcoholism in some populations because allele frequencies differ between alcoholics and controls. Specifically, controls have higher frequencies of the variants with higher Vmax (ADH2*2 and ADH3*1). In samples both of alcoholics and of controls from three Taiwanese populations (Chinese, Ami, and Atayal) we found significant pairwise disequilibrium for all comparisons of the two functional polymorphisms and a third, presumably neutral, intronic polymorphism in ADH2. The class I ADH genes all lie within 80 kb on chromosome 4; thus, variants are not inherited independently, and haplotypes must be analyzed when evaluating the risk of alcoholism. In the Taiwanese Chinese we found that, only among those chromosomes containing the ADH3*1 variant (high Vmax), the proportions of chromosomes with ADH2*1 (low Vmax) and those with ADH2*2 (high Vmax) are significantly different between alcoholics and controls (P<10-5). The proportions of chromosomes with ADH3*1 and those with ADH3*2 are not significantly different between alcoholics and controls, on a constant ADH2 background (with ADH2*1, P=.83; with ADH2*2, P=.53). Thus, the observed differences in the frequency of the functional polymorphism at ADH3, between alcoholics and controls, can be accounted for by the disequilibrium with ADH2 in this population.

Indexed as

Genetic Predisposition to DiseaseAlcohol DehydrogenaseAlcoholismAllelesBase SequenceChinaChromosomes, Human, Pair 4Cloning, MolecularGene FrequencyGenetic VariationHaplotypesHumansIndians, Central AmericanLinkage DisequilibriumMexicoMolecular Sequence DataAlcohol Dehydrogenase

Identifiers

PMID10090900
PMCPMC1377839
OpenAlexW2126728005

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Texttitle and abstract
Read underepoch 390

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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.