Common Genetic Vulnerability for Nicotine and Alcohol Dependence in Men

True, William R.; Xian, Hong; Scherrer, Jeffrey F.; Madden, Pamela A. F.; Bucholz, Kathleen K.; Heath, Andrew C.; Eisen, Seth A.; Lyons, Michael J.; Goldberg, Jack; Tsuang, Ming T.

doi:10.1001/archpsyc.56.7.655

Cited by 453 publications

(363 citation statements)

References 48 publications

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“…Koopmans et al, 1997;Swan et al, 1997) and dependence (e.g. Prescott and Kendler, 1995;True et al, 1999). If, as this evidence suggests, alcohol and tobacco use disorders operate as stable traits, then the association between the two may exist at the level of the trait, and hence the association over a long-term interval should have a similar magnitude to that of a short-term interval than would be expected by a timebound, stochastic process.…”

Section: Alcohol-tobacco Comorbiditymentioning

confidence: 99%

“…Those studies that are based on substance use disorders have primarily been cross-sectional in nature and have used lifetime disorders (e.g. Batel et al, 1995;Breslau, 1995;Glassman et al, 1990;True et al, 1999; but see Sher et al, 1996;Jackson et al, 2000). It is questionable whether comorbidity truly exists if the criteria are based on a lifetime timeframe, as opposed to the same point in time.…”

Section: Alcohol-tobacco Comorbiditymentioning

confidence: 99%

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Alcohol and tobacco use disorders in a general population: short-term and long-term associations from the St. Louis Epidemiological Catchment Area Study

Jackson

Sher

Wood

et al. 2003

Drug and Alcohol Dependence

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Background-Although research using clinical and convenience samples has shown alcohol use disorders (AUD) to be highly comorbid with tobacco dependence (TD), little work has examined this association prospectively using population-based data. The AUD-TD association was prospectively examined using data from the St. Louis Epidemiological Catchment Area (ECA) Study and its 1-year follow-up as well as from a 16-year follow-up on a subsample of ECA data.Method-Respondents were 3004 (2564, 85%, at Wave 2) participants in the St. Louis household ECA sample, including 444 participants at Year 16 follow-up. At baseline, the sample was predominately White (58%; 38% Black), female (60%), and 44.3 years. Past-year AUD and TD were diagnosed at all waves according to DSM-III criteria.Results-AUDs and TDs were cross-sectionally associated at Years 1, 2, and 16. Controlling for demographics, Year 1 TD prospectively predicted Year 2 AUD, and Year 1 AUD prospectively predicted Year 16 TD. We found evidence for prediction of onset and persistence of both AUD and TD at short-term but not long-term follow-up. Prospective findings were reduced and no longer reached significance when concurrent diagnoses at follow-up were included in the regression models.Conclusions-We observed short-term and long-term associations between AUD and TD. These associations were mediated through concurrent diagnoses with the other substance use disorder.

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Section: Alcohol-tobacco Comorbiditymentioning

confidence: 99%

Section: Alcohol-tobacco Comorbiditymentioning

confidence: 99%

Alcohol and tobacco use disorders in a general population: short-term and long-term associations from the St. Louis Epidemiological Catchment Area Study

Jackson

Sher

Wood

et al. 2003

Drug and Alcohol Dependence

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“…Understanding the contribution of allelic variation to AD will aid in defining neurochemical pathways that are altered in the brain to produce addiction and to better understand mechanisms that may be shared with other habit-forming behaviors in humans, such as cigarette smoking. 3 Candidate gene studies and linkage-based genome scans have identified multiple chromosomal regions as sources of potential susceptibility to AD as well as other addictions, showing some convergent findings. 4 Examples of this convergence are the genes encoding alcohol dehydrogenase IB (ADH1B) and aldehyde dehydrogenase 2 (ALDH2), which were originally based on the mechanism of the association of ADH1B and ALDH2 polymorphisms with AD in that the isoenzymes encoded by these alleles lead to an accumulation of acetaldehyde during alcohol metabolism.…”

Section: Introductionmentioning

confidence: 99%

Nucleotide sequence variation within the human tyrosine kinase B neurotrophin receptor gene: association with antisocial alcohol dependence

Anderson

Neyer

et al. 2007

Pharmacogenomics J

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To identify sequence variants in genes that may have roles in neuronal responses to alcohol, we resequenced the 5 0 region of tyrosine kinase B neurotrophin receptor gene (NTRK2) and determined linkage disequilibrium (LD) values, haplotype structure, and performed association analyses using 43 single nucleotide polymorphisms (SNPs) covering the entire NTRK2 region in a Finnish Caucasian sample of 229 alcohol-dependent subjects with antisocial personality disorder (ASPD) and 287 healthy controls. Individually, three SNPs were associated with alcohol dependence and alcohol abuse (AD) (P-value from 0.0019 to 0.0059, significance level was set at Pp0.01 corrected for multiple testing), whereas a common 18 locus haplotype within the largest LD block of NTRK2, a 119-kb region containing the 5 0 flanking region and exons 1-15, was marginally overrepresented in control subjects compared to AD individuals (global P ¼ 0.057). Taken together, these results support a role for the NTRK2 gene in addiction in a Caucasian population with AD and a subtype of ASPD.

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“…Once smoking is initiated, the heritability for persistence to regular smoking has been estimated at 28-84%, 12,[15][16][17][19][20][21] for number of cigarettes smoked at 45-86% [21][22][23][24][25][26] and for diagnosed ND at 31-75%. 19,21,27 A genetic influence on nicotine withdrawal symptoms and smoking cessation has also been identified with heritability estimated at 26-48 and 50-58%, respectively. [28][29][30] Taken together, these studies suggest a substantial genetic contribution to most aspects of smoking.…”

Section: Introductionmentioning

confidence: 99%

Overview of the pharmacogenomics of cigarette smoking

Tyndale

2007

Pharmacogenomics J

102

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Cigarette smoking increases the risk of numerous health problems, including cancer, cardiovascular and pulmonary disorders, making smoking the leading cause of preventable death in the world. Nicotine is primarily responsible for the highly addictive properties of cigarettes. Although the majority of smokers express a desire to quit, few are successful in doing so. Twin and family studies have indicated substantial genetic contributions to smoking behaviors. One major research focus has been to elucidate the specific genes involved; this has been accomplished primarily through genome-wide linkage analyses and candidate gene association studies. Much attention has focused on genes involved in the neurotransmitter pathways for the brain reward system and genes altering nicotine metabolism. This paper reviews the current state of knowledge for genetic factors implicated in smoking behaviors, and examines how genetic variations may affect therapeutic outcomes for drugs used to assist smoking cessation.

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Common Genetic Vulnerability for Nicotine and Alcohol Dependence in Men

Cited by 453 publications

References 48 publications

Alcohol and tobacco use disorders in a general population: short-term and long-term associations from the St. Louis Epidemiological Catchment Area Study

Alcohol and tobacco use disorders in a general population: short-term and long-term associations from the St. Louis Epidemiological Catchment Area Study

Nucleotide sequence variation within the human tyrosine kinase B neurotrophin receptor gene: association with antisocial alcohol dependence

Overview of the pharmacogenomics of cigarette smoking

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