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Guo S, Chen DF, Zhou DF, Sun HQ, Wu GY, Haile CN et al. Association of functional catechol O-methyl transferase (COMT) Val108Met polymorphism with smoking severity and age of smoking initiation in Chinese male smokers. Psychopharmacology 190: 449-456

Institute of Mental Health, Peking University, Beijing, 100083, China.
Psychopharmacology (Impact Factor: 3.99). 04/2007; 190(4):449-56. DOI: 10.1007/s00213-006-0628-4
Source: PubMed

ABSTRACT Catechol-O-methyltransferase (COMT) is an enzyme involved in the degradation and inactivation of the neurotransmitter dopamine, which is important in mediating drug reward such as nicotine in tobacco smoke. Different COMT alleles encode enzyme whose activity varies from three- to fourfold that may affect dopamine levels and alter subjective effects of nicotine. Recent evidence also suggests that a COMT polymorphism may be especially important in determining an individual's predisposition to developing nicotine dependence.
We studied the COMT Val108Met polymorphism in a male population of 203 current smokers, 66 former smokers, and 102 non-smokers. The age-adjusted odds ratios were estimated by multiple logistic regression models.
The results showed no significant association of the COMT Val108Met with initiation, persistent smoking, or smoking cessation. However, current smokers with the Met allele had significantly higher Fagerstrom Test for Nicotine Dependence scores (7.5 +/- 2.1 vs 6.8 +/- 1.8, p = 0.018) and started smoking significantly earlier (18.4 +/- 4.9 vs 20.1 +/- 5.9 years, p = 0.036).
These results suggest that the COMT Val108Met polymorphism may not influence smoking status in a Chinese male population but may influence the age at which smoking started and smoking severity among smokers. However, the findings must be regarded as preliminary because of the relatively small sample size and marginal associations and should be replicated in a larger cohort.

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    • "In non-smokers, oscillatory changes due to acute nicotine administration are limited primarily to í µí»¼ rhythms, with increases observed in both PAF (Foulds et al. 1994; Harkrider et al. 2001) and frontal upper frequency í µí»¼ 2 power (Fisher et al. 2012a) during resting states, and increases in anterior í µí»¼ 2 during working memory tasks (Fisher et al. 2012b, 2013). Nicotine-induced oscillatory response differences between smokers and non-smokers may reflect genetic factors, including COMT (Beuten et al. 2006; Colilla et al. 2005; Guo et al. 2007), involved in smoking initiation and progression to dependence (Kendler et al. 1999; Maes et al. 2004) or individual differences in EEG. Little is known about the genetics underlying EEG traits or pharmacologically modulated EEG, but twin studies show that heritability of resting EEG oscillations is substantial (Stassen et al. 1987), particularly for PAF (Posthuma et al. 2001; Smit et al. 2005, 2006) and í µí»¼-band oscillations with 80–90% heritability estimates (Van Beijsterveldt & van Baal 2002; Van Beijsterveldt et al. 1996). "
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    • "Third, given the risk of chance findings in genetic association studies and in an attempt to resolve the discrepancy between studies of the COMT rs4680 polymorphism and both heaviness of smoking (light vs. heavy smokers, as defined above) and persistent smoking (current smokers vs. ex-smokers), we combined our data with those from previous studies in community samples (Breitling et al., 2009; David et al., 2002; Guo et al., 2007; Omidvar et al., 2009; Shiels et al., 2008). We used our prepregnancy heaviness of smoking and first trimester persistent smoking data as described above. "
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    • "Numerous heritable factors (e.g. DRD4 (McClernon et al., 2007), DRD2 (Radwan et al., 2007), COMT (Beuten et al., 2006; Guo et al., 2007), etc) also clearly influence nicotine dependence. "
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