Will Nicotine Genetics and a Nicotine Vaccine Prevent Cigarette Smoking and Smoking-Related Diseases?

0860 B iotechnologies that aim to prevent smoking and tobacco-related disease may emerge as unintended by-products of research on the genetics of nicotine dependence and the effectiveness of nicotine vaccines for smoking cessation. For many advocates of tobacco control, any discussion of the genetics of smoking is anathema because of the tobacco industry's use of Fisher's [1] genetic hypothesis to argue that cigarette smoking did not cause lung cancer [2,3]. Advocates of tobacco control say that the goal of tobacco policy should be to eliminate cigarette smoking by imposing high taxes on tobacco products, preventing the tobacco industry from promoting its products, restricting access to tobacco and opportunities to smoke, and minimising nonsmokers' exposure to environmental tobacco smoke [4]. These policies have substantially reduced smoking prevalence in the developed countries that have adopted them [4]. Even if one agrees with these policies, as I do, it would be unwise to ignore evidence that genetic factors play a role in smoking initiation and persistence or neurobiological explanations of why some smokers fi nd it so diffi cult to quit. Indeed, the past misuse of genetic research on nicotine and the possible public misunderstanding of the role of nicotine vaccines make it all the more important for public health practitioners and genetic and neurobiological researchers to be well acquainted with some of the superfi cially attractive but mistaken ways in which this work may be used. In this short paper, I briefl y explain why it would be unwise to use genetic and neurobiological knowledge to prevent cigarette smoking and tobacco-related disease. However implausible these uses may seem to those who are well informed about the genetics of tobacco use or tobacco-control policy, it is the preventive uses of genetic information and nicotine vaccines that most excite the interest of the media and the public. The major challenges that these approaches face need to be widely understood if we are to prevent these superfi cially attractive but controversial uses from undermining effective control policies and the development of better methods of helping smokers to quit. Twin studies of cigarette smoking [5,6] estimate that the heritability of smoking initiation is 50% and that for smoking persistence is 70% [5,7,8]. There are a number of plausible " candidate genes " that predict an increased risk of nicotine dependence [5,8]. These include polymorphisms that affect nicotine metabolism, as well as dopamine receptors and transporters that …