Pharmacogenetic Optimization of Smoking Cessation Treatment

Trends Pharmacol Sci. 2017 Jan;38(1):55-66. doi: 10.1016/j.tips.2016.09.006. Epub 2016 Oct 3.

Abstract

Worldwide, approximately one billion people smoke cigarettes. Cigarette smoking persists in part because long-term smoking cessation rates are modest on existing treatments. Smoking cessation outcomes are influenced by genetic factors, including genetic variation in enzymes that metabolize nicotine and smoking cessation medications, as well as in receptor targets for nicotine and treatment medications. For example, smokers with genetically slow nicotine metabolism have higher cessation success on behavioural counseling and nicotine patches compared with smokers with genetically fast nicotine metabolism. In this review, we highlight new progress in our understanding of how genetic variation in the pharmacological targets of nicotine and smoking cessation medications could be used to tailor smoking cessation therapy, increase quit rates, and reduce tobacco-related harm.

Keywords: metabolism; nicotine; pharmacogenetics; smoking cessation; tobacco; treatment.

Publication types

  • Review
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cytochrome P-450 CYP2A6 / genetics
  • Cytochrome P-450 CYP2B6 / genetics
  • Genetic Variation
  • Humans
  • Nicotine / metabolism
  • Organic Cation Transport Proteins / genetics
  • Organic Cation Transporter 2
  • Pharmacogenetics*
  • Polymorphism, Single Nucleotide
  • Receptors, Dopamine D4 / genetics
  • Receptors, Nicotinic / genetics
  • Smoking Cessation* / methods

Substances

  • Organic Cation Transport Proteins
  • Organic Cation Transporter 2
  • Receptors, Nicotinic
  • SLC22A2 protein, human
  • Receptors, Dopamine D4
  • Nicotine
  • CYP2A6 protein, human
  • CYP2B6 protein, human
  • Cytochrome P-450 CYP2A6
  • Cytochrome P-450 CYP2B6