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

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

Research output: Contribution to journalArticle


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 (US)
Pages (from-to)143-152
Number of pages10
JournalPsychiatric Genetics
Issue number4
StatePublished - Aug 2013
Externally publishedYes


  • genetics
  • KORA
  • PsyCoLaus
  • SHIP
  • smoking

ASJC Scopus subject areas

  • Genetics(clinical)
  • Psychiatry and Mental health
  • Genetics
  • Biological Psychiatry

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    Tozzi, F., Teumer, A., Munafò, M., Rawal, R., Kazeem, G., Gerbaulet, M., McArdle, W., Chilcoat, H., Döring, A., Dahmen, N., Mooser, V., Nauck, M., Ring, S. M., Rubio, J. P., Vollenweider, P., Waeber, G., John, U., Völzke, H., Homuth, G., ... Grabe, H. J. (2013). A genomewide association study of smoking relapse in four European population-based samples. Psychiatric Genetics, 23(4), 143-152. https://doi.org/10.1097/YPG.0b013e32835fc94b