Common genetic variations affecting nicotine receptors in the nervous system dramatically raise the likelihood of children struggling with lifelong nicotine addiction by age 17, a new study by researchers from the University of Utah and University of Wisconsin-Madison has found.
Writing about their findings in the journal PLoS Genetics, the researchers said that their findings stressed the importance of public health efforts to reduce the number of youth who begin smoking.
The researchers revealed that the common gene variations, called single nucleotide polymorphisms (SNPs), were changes in a single unit of DNA.
They said that SNPs that are linked and inherited together are called a haplotype.
During a study, the research team observed that one haplotype for the nicotine receptor put European American smokers at greater risk of heavy nicotine dependence as adults, but only if they began daily smoking before the age of 17.
The researchers also found another haplotype that actually reduced the risk of adult heavy nicotine dependence for people who began smoking in their youth.
For their study, the researchers examined 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.
All smokers were assessed for their levels of nicotine dependence.
The researcher recorded the age when the subjects began daily smoking, 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.
It was found that the subjects 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.
The researchers also found that the presence of the high-risk haplotype did not significantly influence the risk of later addiction for people who began smoking at age 17 or older.
The high-risk haplotype was common in the three study populations, and European American populations in general, ranging in frequency from 38 percent to 41 percent.
The authors caution that different haplotype frequencies would likely be observed in different ethnic populations.
However, Dr. Robert Weiss, professor of human genetics at the University of Utah and lead author of the study, says: "We know that people who begin smoking at a young age are more likely to face severe nicotine dependence later in life. This finding suggests that genetic influences expressed during adolescence contribute to the risk of lifetime addiction severity produced from the early onset of tobacco use."
Dr. Nora Volkow, director of the National Institute on Drug Abuse (NIDA), says: "In recent years we've seen an explosion in the understanding of how small genetic variations can impact all aspects of health, including addiction. As we learn more about how both genes and environment play a role in smoking, we will be able to better tailor both prevention and cessation programs to individuals."