Common genetic variations affecting nicotine receptors in the nervous system can significantly increase the chance that European Americans who begin smoking by age 17 will struggle with life-long nicotine addiction. Published July 11 in the open-access journal PLoS Genetics, this research - led by scientists at the University of Utah together with colleagues from the University of Wisconsin - highlights the importance of preventing early exposure to tobacco through public health policies.
These common genetic variations, or single nucleotide polymorphisms (SNPs), are changes in a single unit of DNA. A haplotype is a set of SNPs that are statistically linked. The researchers found that one haplotype for the nicotine receptor put European American smokers at a greater risk of heavy nicotine dependence as adults, but only if they began daily smoking before the age of 17. A second haplotype actually reduced the risk of adult heavy nicotine dependence for people who began smoking in their youth.
The researchers studied 2,827 long-term European American smokers, recruited in Utah and Wisconsin, and to the National Heart, Lung, and Blood Institute's Lung Health Study. They assessed the level of nicotine dependence for all smokers, recording the age they began smoking daily, the number of years they smoked, and the average number of cigarettes smoked per day. DNA samples were taken from all smokers, and the researchers recorded the occurrence of common SNPs, grouped into four haplotypes, which had been identified earlier in a subset of participants.
They found that people who began smoking before the age of 17 and possessed two copies of the high-risk haplotype had from a 1.6-fold to almost 5-fold increase in risk of heavy smoking as an adult. For people who began smoking at age 17 or older, presence of the high-risk haplotype did not significantly influence their risk of later addiction.