A genomewide association study of smoking relapse in four European population-based samples

Federica Tozzi, Alexander Teumer, Marcus Munafo, Rajesh Rawal, Gbenga Kazeem, Marcel Gerbaulet, Wendy McArdle, Howard Chilcoat, Angela Doering, Norbert Dahmen, Vincent Mooser, Matthias Nauck, Susan M. Ring, Justin P. Rubio, Peter Vollenweider, Gerard Waeber, Ulrich John, Henry Voelzke, Georg Homuth, Harald J. FreybergerUwe Voelker, George Davey Smith, Christian Gieger, Martin Preisig, Hans J. Grabe*

*Corresponding author for this work

Research output: Contribution to journalArticle (Academic Journal)peer-review

4 Citations (Scopus)

Abstract

OBJECTIVES: Genomewide association studies (GWAS) have identified clear evidence of genetic markers for nicotine dependence. Other smoking phenotypes have been tested, but the results are less consistent. The tendency to relapse versus the ability to maintain long-term abstinence has received little attention in genetic studies; thus, our aim was to provide a better biological understanding of this phenotype through the identification of genetic loci associated with smoking relapse. METHODS: We carried out a GWAS on data from two European population-based collections, including a total of 835 cases (relapsers) and 990 controls (abstainers). Top-ranked findings from the discovery phase were tested for replication in two additional independent European population-based cohorts. RESULTS: Of the seven top markers from the discovery phase, none were consistently associated with smoking relapse across all samples and none reached genomewide significance. A single-nucleotide polymorphism rs1008509, within the Xylosyltransferase II (XYLT2) gene, was suggestively associated with smoking relapse in the discovery phase (β=-0.504; P=5.6E-06) and in the first replication sample (ALSPAC) (β=-0.27; P=0.004; n=1932), but not in the second sample (KORA) (β=0.19; P=0.138; n=912). We failed to identify an association between loci implicated previously in other smoking phenotypes and smoking relapse. CONCLUSION: Although no genomewide significant findings emerged from this study, we found that loci implicated in other smoking phenotypes were not associated with smoking relapse, which suggests that the neurobiology of smoking relapse and long-term abstinence may be distinct from biological mechanisms implicated in the development of nicotine dependence.
Original languageEnglish
Pages (from-to)143-152
Number of pages10
JournalPsychiatric Genetics
Volume23
Issue number4
DOIs
Publication statusPublished - Aug 2013

Structured keywords

  • Brain and Behaviour
  • Tobacco and Alcohol

Keywords

  • ALSPAC
  • genetics
  • KORA
  • PsyCoLaus
  • SHIP
  • smoking
  • CARDIOVASCULAR RISK-FACTORS
  • NICOTINE DEPENDENCE
  • WIDE ASSOCIATION
  • ADULT TWINS
  • TOBACCO USE
  • CESSATION
  • METAANALYSIS
  • BEHAVIOR
  • ABSTINENCE
  • DISEASE

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