SNPwatch gives you the latest news about research linking various traits and conditions to individual genetic variations. These studies are exciting because they offer a glimpse into how genetics may affect our bodies and health; but in most cases, more work is needed before this research can provide information of value to individuals. For that reason it is important to remember that like all information we provide, the studies we describe in SNPwatch are for research and educational purposes only. SNPwatch is not intended to be a substitute for professional medical advice; you should always seek the advice of your physician or other appropriate healthcare professional with any questions you may have regarding diagnosis, cure, treatment or prevention of any disease or other medical condition.
Despite the success of genome-wide association studies, many experts rightly point out the need to remember that most common diseases have a significant environmental component. For example, cigarette smoking increases one’s risk of lung cancer 10- to 20-fold, according to the National Cancer Institute. But other studies have found that even after controlling for smoking, having first-degree relatives with lung cancer increases one’s own risk by a modest amount, suggesting at least a small genetic component.
A trio of papers published today in Nature and Nature Genetics has found a SNP on chromosome 15 that is linked to lung cancer risk. Two of the studies, by Hung et al. and Amos et al., matched lung cancer cases and healthy controls for smoking behavior and compared their genotypes across 300,000 SNPs. Both studies found that one copy of the A version of rs1051730 increased subjects’ odds of lung cancer by about 1.3 times compared to those with none; having two copies increased subjects’ odds by 1.8 times. (23andMe users can see their genotype at rs1051730 in the Genome Explorer (now called Browse Raw Data).)
A 1.8-fold increase may not seem like much compared to the 10- to 20-fold increase seen for smokers. But if this genetic effect is independent of the effect of smoking, smokers with the AA genotype might find themselves at 18- to 36-fold increased risk compared to nonsmokers with the GG genotype.
A third study questions whether the SNP’s effect on lung cancer risk is truly independent of smoking. Thorgeirsson et al. found evidence that the same SNP, rs1051730, is actually linked to nicotine dependence. On average, each copy of the A version increased the number of cigarettes subjects smoked by about one cigarette per day. The authors also reported that most of the increased risk of lung cancer conferred by the A version was due to its effect on smoking. Thus, an environmental component itself appears to have a genetic component.
However, the effect of rs1051730 on smoking quantity was seen only if a subject smoked at all. Genotype at rs1051730 wasn’t connected with whether subjects smoke, only with how much they smoke once they start.
So in the nature vs. nurture debate, perhaps there is room for free will after all.