We studied the influence of drinking and smoking habits on CYP2D6 metabolic
capacity measured by the use of debrisoquine as a substance test. We did n
ot find any significant differences in the frequency of subjects with CYP2D
6 deficiency (poor metabolizers) among four groups of healthy individuals:
nonsmokers/nondrinkers, smokers/drinkers, nondrinkers/smokers, and nonsmoke
rs/drinkers. We demonstrated that, among poor metabolizers, alcohol and tob
acco consumption was associated with higher metabolic ratios than it was wi
th the control group, but the differences were not statistically significan
t. Among extensive metabolizers, the lowest metabolic ratio (highest enzyme
activity) was detected for nondrinkers/smokers, intermediate values for sm
okers/drinkers, and the highest metabolic ratio (lowest enzyme activity) fo
r nonsmokers/drinkers. These variations were slight but statistically signi
ficant when logarithmic ratio values were applied. These results show that
smoking and drinking habits do not need to be taken into account when human
s are phenotyped for CYP2D6.