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: 3.88). 04/2007; 190(4):449-56. DOI: 10.1007/s00213-006-0628-4
Source: PubMed


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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Available from: Hong-Qiang Sun, Dec 29, 2015
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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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    ABSTRACT: Performance improvements in cognitive tasks requiring executive functions are evident with nicotinic acetylcholine receptor (nAChR) agonists and activation of the underlying neural circuitry supporting these cognitive effects is thought to involve dopamine neurotransmission. As individual difference in response to nicotine may be related to a functional polymorphism in the gene encoding catechol-O-methyltransferase (COMT), an enzyme that strongly influences cortical dopamine metabolism, this study examined the modulatory effects of the COMT Val158Met polymorphism on the neural response to acute nicotine as measured with resting state electroencephalographic (EEG) oscillations. In a sample of 62 healthy nonsmoking adult males, a single dose (6 mg) of nicotine gum administered in a randomized, double-blind, placebo controlled design was shown to affect α oscillatory activity, increasing power of upper α oscillations in fronto-central regions of Met/Met homozygotes and in parietal/occipital regions of Val/Met heterozygotes. Peak α frequency was also found to be faster with nicotine (vs. placebo) treatment in Val/Met heterozygotes, who exhibited a slower α frequency compared to Val/Val homozygotes. The data tentatively suggest that interindividual differences in brain α oscillations and their response to nicotinic agonist treatment are influenced by genetic mechanisms involving COMT. This article is protected by copyright. All rights reserved.
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    • "Nonsmokers were defined as individuals who had smoked less than 100 cigarettes during their lifetime. Former smokers were defined as persons who had previously smoked more than one cigarette each day but had quit smoking for more than 1 year (de Leon and Diaz, 2005; Guo et al., 2007). If the subject was currently a nonsmoker , further questions were asked regarding previous smoking behavior including whether or not they had quit smoking. "
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    ABSTRACT: Some recent studies show an association between a functional polymorphism of BDNF gene (Val66Met) and the susceptibility to nicotine dependence and we hypothesized that this polymorphism was associated with smoking in both schizophrenia patients and healthy controls. The BDNF Val66Met gene polymorphism was genotyped in 690 chronic male schizophrenia patients (smoker/nonsmoker= 522/169) and 628 male controls (smoker/nonsmoker=322/306) using a case–control design. Nicotine dependence (ND) was assessed by the cigarettes smoked per day (CPD), the Heaviness of Smoking Index (HSI), and the Fagerstrom Test for ND (FTND). Patients also were rated on the Positive and Negative Symptom Scale (PANSS). The results showed no significant differences in BDNF Val66Met genotype and allele distributions between the patients and healthy controls or between smokers and nonsmokers in either patients or healthy controls alone. In patient groups, however, the smokers with the Met allele had significantly higher HSI scores (Met/Met: 2.8±1.7 vs. Met/Val: 2.2±1. 7 vs.Val/Val: 2.0±1.6, p<0.01) and a trend toward a significantly higher FTND score (p=0.09) than those with the Val/Val genotype. In addition, the smokers showed significantly lower PANSS negative symptom and total scores, longer duration of illness and more hospitalizations (all p<0.05). In the control group, the smokers with the Met allele started smoking significantly earlier than those with the Val/Val genotype (both p<0.05). These results suggest that the BDNF Val66Met polymorphism may affect a smoker’s response to nicotine in both schizophrenia and healthy controls from a Chinese Han population, but with differential effects in different aspects of smoking behaviors.
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    • "There was no gender difference in the genotype distribution. The allele frequencies in the present study are comparable to other studies with Chinese participants666768. Because of the limited number of subjects in the Met/Met group, we grouped the Val/Met and Met/Met subjects into the Met-carrier group in all subsequent analysis. "
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    ABSTRACT: Both genetic and environmental factors have been shown to influence decision making, but their relative contributions and interactions are not well understood. The present study aimed to reveal possible gene-environment interactions on decision making in a large healthy sample. Specifically, we examined how the frequently studied COMT Val(158)Met polymorphism interacted with an environmental risk factor (i.e., stressful life events) and a protective factor (i.e., parental warmth) to influence affective decision making as measured by the Iowa Gambling Task. We found that stressful life events acted as a risk factor for poor IGT performance (i.e., high reward sensitivity) among Met carriers, whereas parental warmth acted as a protective factor for good IGT performance (i.e., higher IGT score) among Val/Val homozygotes. These results shed some new light on gene-environment interactions in decision making, which could potentially help us understand the underlying etiology of several psychiatric disorders associated with decision making impairment.
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