TY - JOUR
T1 - Common genetic vulnerability for pathological gambling and alcohol dependence in men
AU - Slutske, Wendy S.
AU - Eisen, Seth
AU - True, William R.
AU - Lyons, Michael J.
AU - Goldberg, Jack
AU - Tsuang, Ming
PY - 2000/7
Y1 - 2000/7
N2 - Background: In comparison with alcohol dependence (AD), relatively little is known about the causes of pathological gambling (PG). Given the high rate of comorbidity between PG and AD, knowledge about the causes of AD may be applied to understanding those of PG. Methods: Subjects were adult male twin pairs from the Vietnam Era Twin Registry. Lifetime histories of PG and AD were assessed by structured psychiatric telephone interview. The validity of a continuum of PG liability was tested to determine whether the causes of subclinical PG, or problem gambling, are quantitatively or qualitatively distinct from those of DSM-III-R PG disorder. Genetic model- fitting methods were used to quantify the extent to which the genetic and environmental risk for PG could be explained by the risk for AD. Results: Tests of the continuity model of PG were all consistent with the hypothesis that subclinical PG and DSM-III-R PG disorder have many, perhaps all, of the same risk factors and thus differ quantitatively rather than qualitatively. Depending on the PG definition, between 12% and 20% of the genetic variation and between 3% and 8% of the nonshared environmental variation in the risk for PG were accounted for by the risk for AD. Conclusions: Subclinical PG, or problem gambling, may be a milder form of PG, rather than an etiologically distinct syndrome. Risk for AD accounts for a significant but modest proportion of the genetic and environmental risk for subclinical PG and DSM- III-R PG disorder.
AB - Background: In comparison with alcohol dependence (AD), relatively little is known about the causes of pathological gambling (PG). Given the high rate of comorbidity between PG and AD, knowledge about the causes of AD may be applied to understanding those of PG. Methods: Subjects were adult male twin pairs from the Vietnam Era Twin Registry. Lifetime histories of PG and AD were assessed by structured psychiatric telephone interview. The validity of a continuum of PG liability was tested to determine whether the causes of subclinical PG, or problem gambling, are quantitatively or qualitatively distinct from those of DSM-III-R PG disorder. Genetic model- fitting methods were used to quantify the extent to which the genetic and environmental risk for PG could be explained by the risk for AD. Results: Tests of the continuity model of PG were all consistent with the hypothesis that subclinical PG and DSM-III-R PG disorder have many, perhaps all, of the same risk factors and thus differ quantitatively rather than qualitatively. Depending on the PG definition, between 12% and 20% of the genetic variation and between 3% and 8% of the nonshared environmental variation in the risk for PG were accounted for by the risk for AD. Conclusions: Subclinical PG, or problem gambling, may be a milder form of PG, rather than an etiologically distinct syndrome. Risk for AD accounts for a significant but modest proportion of the genetic and environmental risk for subclinical PG and DSM- III-R PG disorder.
UR - http://www.scopus.com/inward/record.url?scp=0033936803&partnerID=8YFLogxK
U2 - 10.1001/archpsyc.57.7.666
DO - 10.1001/archpsyc.57.7.666
M3 - Article
C2 - 10891037
AN - SCOPUS:0033936803
VL - 57
SP - 666
EP - 673
JO - Archives of General Psychiatry
JF - Archives of General Psychiatry
SN - 0003-990X
IS - 7
ER -