They looked at their own long-term study of 1,000 citizens of New Zealand from birth to age 38 to identify whether people at high genetic risk got hooked on cigarettes more quickly as teenagers and whether, as adults, they had a harder time quitting.
Study participants with a high-risk genetic profile were found to be more likely to convert to daily smoking as teenagers and then progress more rapidly to heavy smoking. When assessed at age 38, the higher-risk individuals had smoked heavily for more years, and had more often developed nicotine dependence and were likely to have failed in their attempt to quit.
"Genetic risk accelerated the development of smoking behavior. Teens at a high genetic risk transitioned quickly from trying cigarettes to becoming regular, heavy smokers," Daniel Belsky, a post-doctoral research fellow at Duke University's Center for the Study of Aging and Human Development and the Duke Institute for Genome Sciences and Policy, said.
The Duke researchers developed a new "genetic risk score" for the study by examining prior genome-wide associations (GWAS) of adult smokers.
The studies scanned the entire genomes of tens of thousands of smokers to identify variants that were more common in the heaviest smokers.
The variants they identified were located in and around genes that affect how the brain responds to nicotine and how nicotine is metabolized.
In their first step, the researchers found that the genetic risk score they developed was able to predict heavy smoking among individuals in two large databases created by other researchers.
Then they turned to their New Zealand sample of 880 individuals of European descent to see whether the genetic risk score predicted who initiated smoking, who progressed to heavy smoking, and who developed nicotine dependence and experienced relapse after quitting.
The findings have been published in JAMA Psychiatry.