led the Fagerstrom Tolerance Questionnaire (FTQ). For the TPH study, the participants were divided into three categories: those who had never smoked, regular smokers who had a low degree of dependence (scores of 0 to 3 on the 11-point FTQ), and regular smokers with a high degree of dependence (FTQ scores of 7 or higher). Dr. Sullivan and his colleagues analyzed the participants' TPH genes and found that the 779A allele was strongly associated with whether participants initiated smoking, but, unlike the University of Pennsylvania study, not strongly associated with an early age of smoking initiation.
"The fact that there is not complete agreement is not surprising," Dr. Sullivan says. "The two studies used different populations of subjects and were not designed to test the same hypothesis. Nonetheless, the two studies appear to have captured a similar influence that plays a role in the web of factors that underlies smoking initiation."
"It is rare to find confirmation of a candidate gene related to addiction, and these studies make a good case for an association between the TPH gene variant and smoking initiation," says Dr. Rebekah Rasooly of NIDA's Division of Neuroscience and Behavioral Research. "This kind of association helps us to better understand the factors that influence young potential smokers. They are the most vulnerable to becoming regular smokers and need to clearly understand all the risks associated with smoking that first cigarette."
- Lerman, C., et al. Tryptophan hydroxylase gene variant and smoking behavior. American Journal of Medical Genetics 105(6):518-520, 2001. [Abstract]
- Sullivan, P.F., et al. Association of the tryptophan hydroxylase gene with smoking initiation but not progression to nicotine dependence. American Journal of Medical Genetics 105(5):479-484, 2001. [Abstract]
Volume 17, Number 2 (May 2002)