α-5/α-3 nicotinic receptor subunit alleles increase risk for heavy smoking
Open accessAbstract
Twin studies indicate that additive genetic effects explain most of the variance in nicotine dependence (ND), a construct emphasizing habitual heavy smoking despite adverse consequences, tolerance and withdrawal. To detect ND alleles, we assessed cigarettes per day (CPD) regularly smoked, in two European populations via whole genome association techniques. In these approximately 7500 persons, a common haplotype in the CHRNA3-CHRNA5 nicotinic receptor subunit gene cluster was associated with CPD (nominal P=6.9 x 10(-5)). In a third set of European populations (n= approximately 7500) which had been genotyped for approximately 6000 SNPs in approximately 2000 genes, an allele in the same haplotype was associated with CPD (nominal P=2.6 x 10(-6)). These results (in three independent populations of European origin, totaling approximately 15 000 individuals) suggest that a common haplotype in the CHRNA5/CHRNA3 gene cluster on chromosome 15 contains alleles, which predispose to ND.
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The rs16969968 risk variant is associated with heavy smoking, early onset of smoking behavior, and a pleasurable buzz from tobacco.
“The rs16969968 risk variant is associated with heavy smoking (Berrettini et al. 2008;Bierut et al. 2008;Grucza et al. 2008;Stevens et al. 2008), early onset of smoking behavior (Weiss et al. 2008), and with a”
From Mechanisms of Nicotine Addiction (2021) · cites this paper as Berrettini et al. 2008
The Results (p. 3) associate a CHRNA3–CHRNA5 haplotype with cigarettes per day, supporting the heavy-smoking association at the haplotype level. The Discussion (p. 5) says rs16969968 itself was not genotyped in this paper's studies, so it does not establish that specific variant's association with heavy smoking. The printed citation attaches Berrettini et al. to heavy smoking, not to the separately cited early-onset claim or the buzz claim. (LLM, conf=0.87)
Experimental — accuracy not yet measuredIncreased risk of tobacco dependence is associated with rs6495308, rs578776, or rs1051730 in CHRNA3, and with rs1948 in CHRNB4.
“In addition to the rs16969968 SNP in CHRNA5, there is also increased risk of tobacco dependence in individuals carrying the rs6495308, rs578776, or rs1051730 SNPs in CHRNA3 (Berrettini et al. 2008;Saccone et al. 2009), and rs1948 in CHRNB4 (Schlaepfer et al. 2008).”
From Mechanisms of Nicotine Addiction (2021) · cites this paper as Berrettini et al. 2008
Table 2 (p. 2) identifies rs6495308 in CHRNA3 as associated with cigarettes smoked per day, which the paper uses as a measure relevant to nicotine dependence. Our copy does not identify rs578776 or rs1051730 as associated risk variants. The rs1948 claim is attached to Schlaepfer et al., not to Berrettini et al., so it is outside this citation assessment. (LLM, conf=0.87)
Experimental — accuracy not yet measuredAllelic variation in the α5/α3/β4 nAChR subunit gene cluster at chromosome 15q25 significantly increases risk of tobacco addiction.
“It has been shown that allelic variation in the α5/α3/β4 nAChR subunit gene cluster located in chromosome region 15q25 significantly increases risk of tobacco addiction (Saccone et al. 2007;Berrettini et al. 2008;Lips et al. 2010).”
From Mechanisms of Nicotine Addiction (2021) · cites this paper as Berrettini et al. 2008
The association with rs16969968 has been replicated either directly or using highly correlated SNPs by several groups.
“This association has been replicated either directly or using highly correlated SNPs by several groups (92–97).”
From Nicotine is a selective pharmacological chaperone of acetylcholine receptor number and stoichiometry. Implications for drug discovery (2009) · cites this paper as [92]
The second association with nicotine dependence tagged by rs578776 has been replicated in additional studies using the same SNP or a highly correlated SNP.
“This second association with nicotine dependence has been replicated in additional studies using the same SNP or a highly correlated SNP (92,95,96,98).”
From Nicotine is a selective pharmacological chaperone of acetylcholine receptor number and stoichiometry. Implications for drug discovery (2009) · cites this paper as [92]
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- Authors
- Berrettini, W., Yuan, X., Tozzi, F., Song, K., Francks, C., Chilcoat, H., Waterworth, D., Muglia, P., & Mooser, V
- Affiliations
- University of Pennsylvania (US)
- GlaxoSmithKline (United States) (US)
- University of Toronto (CA)
- Corresponding author
- Berrettini, W
- Venue
- Molecular Psychiatry
- Published
- 2008-01-29
- Volume
- 13
- Issue
- 4
- Pages
- 368-373
- ISSN
- 1359-4184 (ISSN-L)
- 1476-5578
- PMC
- PMC2507863
- OpenAlex
- W1511621596
- Cited by
- 465
- References
- 17
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 8 · 2023: 10 · 2022: 11 · 2021: 6 · 2020: 20 · 2019: 19 · 2018: 9 · 2017: 14 · 2016: 17 · 2015: 32 · 2014: 27 · 2013: 37 · 2012: 50
- FWCI
- 44.69
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Molecular Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion, other-oa)
- Funders
- National Institutes of Health (5p60da005186-25)
- U.S. Public Health Service (P60 05186)
- National Institute on Drug Abuse (P60-DA005186)
- NIH Clinical Center
- Topics
- Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Keywords
- nicotine dependence, heavy smoking, CHRNA3, CHRNA5, nicotinic acetylcholine receptors, genetic susceptibility, cigarettes per day, twin studies, additive genetic effects, whole-genome association studies
- MeSH terms
- Adult, Aged, Alleles, Chromosomes, Human, Pair 15, Female, Genotype, Humans, Male, Middle Aged, Nerve Tissue Proteins, Receptors, Nicotinic, Retrospective Studies, Sensitivity and Specificity, Tobacco Use Disorder, Linkage Disequilibrium, Case-Control Studies, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide, Microarray Analysis
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