AIM: To assess the promise and risks of technological applications of genetic research on liability to develop nicotine dependence. METHODS: We reviewed (i) the evidence on the genetics of nicotine dependence; (ii) the technical feasibility of using genetic information to reduce smoking uptake and increase cessation; and (iii) policy and ethical issues raised by the uses of genetic information on addiction liability. RESULTS: (i) Despite evidence from twin studies that genes contribute to addiction susceptibility, research to date has not identified commonly occurring alleles that are strongly predictive of developing nicotine addiction. Nicotine addiction is likely to involve multiple alleles of small effect that interact with each other and with the environment. (ii) Population screening for susceptibility alleles is unlikely to be effective or cost-effective. Tailoring of smoking cessation treatments with genetic information is more plausible but results to date have been disappointing. Population health strategies such as increased taxation and reduced opportunities to smoke are more efficient in reducing cigarette smoking. Tobacco harm reduction policies applied to populations may also play a role in reducing tobacco-related harm. (iii) Future uses of genomic information on addiction risk will need to assess the risks of medicalising addiction (e.g. pessimism about capacity to quit) and community concerns about genetic privacy. CONCLUSIONS: Nicotine genomics is a very new and underdeveloped field. On the evidence to date, its advocates would be wise to avoid extravagant claims about its preventive applications.
AIM: To assess the promise and risks of technological applications of genetic research on liability to develop nicotine dependence. METHODS: We reviewed (i) the evidence on the genetics of nicotine dependence; (ii) the technical feasibility of using genetic information to reduce smoking uptake and increase cessation; and (iii) policy and ethical issues raised by the uses of genetic information on addiction liability. RESULTS: (i) Despite evidence from twin studies that genes contribute to addiction susceptibility, research to date has not identified commonly occurring alleles that are strongly predictive of developing nicotine addiction. Nicotine addiction is likely to involve multiple alleles of small effect that interact with each other and with the environment. (ii) Population screening for susceptibility alleles is unlikely to be effective or cost-effective. Tailoring of smoking cessation treatments with genetic information is more plausible but results to date have been disappointing. Population health strategies such as increased taxation and reduced opportunities to smoke are more efficient in reducing cigarette smoking. Tobacco harm reduction policies applied to populations may also play a role in reducing tobacco-related harm. (iii) Future uses of genomic information on addiction risk will need to assess the risks of medicalising addiction (e.g. pessimism about capacity to quit) and community concerns about genetic privacy. CONCLUSIONS:Nicotine genomics is a very new and underdeveloped field. On the evidence to date, its advocates would be wise to avoid extravagant claims about its preventive applications.