Studies just published in Nature are reported here as:
The study, published today in the online edition of Nature Genetics, analyzes detailed genotypic and smoking data from more than 130,000 participants. Both of the new SNPs are common, and in smokers each copy carried associates with a small increase in smoking quantity – about half a cigarrette per day – but an approximately 10% increase in risk of lung cancer compared to non carriers. This is about one third of the increase in lung cancer risk conferred by the SNP on chromosome 15q25. But taken together these variants can identify a sizeable proportion of smokers whose health is at even greater risk than average from their habit, information which may serve as an additional spur to smoking cessation. The study, ‘Sequence variants at CHRNB3-CHRNA6 and CYP2A6 affect smoking behavior,’ can be found at http://www.nature.com/ng.
“Smoking is bad for anyone’s health. It is even worse for some, and today’s discoveries continue to strengthen our ability to identify who those people are and give them a compelling additional reason to quit. We plan to incorporate these SNPs into our testing products to do that. What we do not yet know is exactly how this additional risk is conferred. To some degree these variants suggest that those for whom nicotine is more addictive are driven to smoke more, increasing their exposure to environmental risk. But given the quite substantial corresponding increases in risk of lung cancer it may also be that they make people more susceptible to the noxious effects of tobacco smoke. What is clear is that these variants — which are all near genes that encode nicotine metabolizing enzymes and receptors — are giving us a solid starting point for finding answers to advance personal and public health,” said Kari Stefansson, executive chairman and president of research at deCODE and senior author on the paper.
These are newsworthy developments and this research can only be encouraged. However, this report on the findings limits the application of these these data to informing cessation efforts. No doubt, this will lead eventually to some sort of test where you can determine whether you are more susceptible to nicotine or lung cancer and therefore whether you should, even more than most, not start or quit smoking. (I can see groups arguing against this test on the basis that if the test comes up negative then that might be interpreted as a smoking pass of sorts).
Once again I have to argue the beautiful simplicity of tobacco harm reduction in that whether a person smokes on a regular basis out of little more than boredom with hardly a hint of actual need or whether they are genetically driven to consume nicotine the application and results of product substitution are the same -greatly reduced harm and total elimination of smoking related lung cancer risk.
– Paul L. Bergen