Cigarette smoking in male patients with chronic schizophrenia in a Chinese population: prevalence and relationship to clinical phenotypes.
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ABSTRACT:
SUBMITTER: Zhang XY
PROVIDER: S-EPMC3274516 | biostudies-other | 2012
REPOSITORIES: biostudies-other
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Project description:Schizophrenic patients have higher smoking rates than the general population. Studies show that smoking may be a form of self-medication in an attempt to alleviate cognitive deficits in schizophrenic patients of European background. This study examined the relationships between smoking and cognitive deficits in Chinese schizophrenic patients, which have previously received little systemic study. We recruited 580 male chronic patients meeting DSM-IV criteria for schizophrenia and 175 male control subjects who were matched on age and education. The subjects completed a detailed cigarette smoking questionnaire, the Fagerstrom Test for Nicotine Dependence (FTND), and the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS). Patients also were rated on the Positive and Negative Symptom Scale (PANSS), the Simpson and Angus Extrapyramidal Symptom Rating Scale (SAES), and the Abnormal Involuntary Movement Scale (AIMS). All five RBANS subscales except for the Visuospatial/Constructional index showed significantly lower cognitive performance for schizophrenics than normal controls. The schizophrenic smokers scored lower than the schizophrenic non-smokers on the RBANS total score and the Visuospatial/Constructional and Immediate Memory indices. Similarly, the control smokers scored lower than the control non-smokers on the RBANS total score and the Immediate Memory index . Also, the schizophrenic smokers consistently performed the poorest on the cognitive domains of the RBANS. Among the schizophrenic patients, smokers displayed significantly fewer negative symptoms than non-smokers. Using multivariate regression analysis the following variables were independently associated with the RBANS total score: years of education, PANSS negative symptom score, age at schizophrenia onset, and number of hospitalizations. Our results show that smoking is associated with significant cognitive impairment in both schizophrenic patients and normal controls, but the smokers with schizophrenia had a reduced level of negative symptoms, suggesting that the benefits of smoking for those with schizophrenia may be limited to certain aspects of a given clinical phenotype.
| S-EPMC3343009 | biostudies-other
Project description:Male schizophrenia patients are known to have a heavier smoking pattern compared with the general population. However, the mechanism for this association is not known, though hypothesis that smoking could alleviate symptomatology of schizophrenia and reduce side effects of antipsychotics has been suggested. The aims of this study were to validate the heavier smoking pattern among male schizophrenia patients and to investigate the possible mechanisms for the association. To enhance the reliability of the study, we recruited two large independent samples with 604 and 535 male Chinese schizophrenia patients, and compared their smoking pattern with that of 535 healthy male controls recruited from general population. Validated multiple indicators and multiple causes structure equation model and regression models were used to investigate the association of smoking with factors of schizophrenia symptomatology and with the usage of antipsychotics and their extra-pyramidal side effects (EPS). Schizophrenia patients had significantly heavier smoking pattern compared with healthy controls in our sample (42.4% vs. 16.8%, p<0.001 for current smoking prevalence; 23.5% vs. 43.3%, p<0.001 for smoking cessation rate; 24.5% vs. 3.0%, p<0.001 for heavy smoker proportion). Their smoking status was also found to be consistently and significantly associated with reduced negative factor scores for schizophrenia symptomatology (??=?-0.123, p?=?0.051 for sample-A; ??=?-0.103, p?=?0.035 for sample-B; ??=?-0.082, p?=?0.017 for the combined sample). However, no significant association was found between smoking and antipsychotics usage or risk of EPS. These results support that smoking is associated with improved negative symptoms, which could account for the heavier smoking pattern among schizophrenia patients.
| S-EPMC3744579 | biostudies-literature
Project description:The oral microbiota has been observed to be influenced by cigarette smoking and linked to several human diseases. However, research on the effect of cigarette smoking on the oral microbiota has not been systematically conducted in the Chinese population. We profiled the oral microbiota of 316 healthy subjects in the Chinese population by 16S rRNA gene sequencing. The alpha diversity of oral microbiota was different between never smokers and smokers (P = 0.002). Several bacterial taxa were first reported to be associated with cigarette smoking by LEfSe analysis, including Moryella (q = 1.56E-04), Bulleidia (q = 1.65E-06), and Moraxella (q = 3.52E-02) at the genus level and Rothia dentocariosa (q = 1.55E-02), Prevotella melaninogenica (q = 8.48E-08), Prevotella pallens (q = 4.13E-03), Bulleidia moorei (q = 1.79E-06), Rothia aeria (q = 3.83E-06), Actinobacillus parahaemolyticus (q = 2.28E-04), and Haemophilus parainfluenzae (q = 4.82E-02) at the species level. Two nitrite-producing bacteria that can increase the acidity of the oral cavity, Actinomyces and Veillonella, were also enriched in smokers with FDR-adjusted q-values of 3.62E-06 and 1.10E-06, respectively. Notably, we observed that two acid production-related pathways, amino acid-related enzymes (q = 6.19E-05) and amino sugar and nucleotide sugar metabolism (q = 2.63E-06), were increased in smokers by PICRUSt analysis. Finally, the co-occurrence analysis demonstrated that smoker-enriched bacteria were significantly positively associated with each other and were negatively correlated with the bacteria decreased in smokers. Our results suggested that cigarette smoking may affect oral health by creating a different environment by altering bacterial abundance, connections among oral microbiota, and the microbiota and their metabolic function.
| S-EPMC8195269 | biostudies-literature
Project description:Smoking is a risk factor for many human diseases. DNA methylation has been related to smoking, but genome-wide methylation data for smoking in Chinese populations is limited.We aimed to investigate epigenome-wide methylation in relation to smoking in a Chinese population.We measured the methylation levels at > 485,000 CpG sites (CpGs) in DNA from leukocytes using a methylation array and conducted a genome-wide meta-analysis of DNA methylation and smoking in a total of 596 Chinese participants. We further evaluated the associations of smoking-related CpGs with internal polycyclic aromatic hydrocarbon (PAH) biomarkers and their correlations with the expression of corresponding genes.We identified 318 CpGs whose methylation levels were associated with smoking at a genome-wide significance level (false discovery rate < 0.05), among which 161 CpGs annotated to 123 genes were not associated with smoking in recent studies of Europeans and African Americans. Of these smoking-related CpGs, methylation levels at 80 CpGs showed significant correlations with the expression of corresponding genes (including RUNX3, IL6R, PTAFR, ANKRD11, CEP135 and CDH23), and methylation at 15 CpGs was significantly associated with urinary 2-hydroxynaphthalene, the most representative internal monohydroxy-PAH biomarker for smoking.We identified DNA methylation markers associated with smoking in a Chinese population, including some markers that were also correlated with gene expression. Exposure to naphthalene, a byproduct of tobacco smoke, may contribute to smoking-related methylation.Zhu X, Li J, Deng S, Yu K, Liu X, Deng Q, Sun H, Zhang X, He M, Guo H, Chen W, Yuan J, Zhang B, Kuang D, He X, Bai Y, Han X, Liu B, Li X, Yang L, Jiang H, Zhang Y, Hu J, Cheng L, Luo X, Mei W, Zhou Z, Sun S, Zhang L, Liu C, Guo Y, Zhang Z, Hu FB, Liang L, Wu T. 2016. Genome-wide analysis of DNA methylation and cigarette smoking in Chinese. Environ Health Perspect 124:966-973;?http://dx.doi.org/10.1289/ehp.1509834.
| S-EPMC4937856 | biostudies-other
Project description:Recent studies demonstrate that brain-derived neurotrophic factor (BDNF) might be associated with nicotine addiction, and circulating BDNF is a biomarker of memory and general cognitive function. Moreover, studies suggest that a functional polymorphism of the BDNF Val66Met may mediate hippocampal-dependent cognitive functions. We aimed to explore the relationships between smoking, cognitive performance and BDNF in a normal Chinese Han population. We recruited 628 male healthy subjects, inducing 322 smokers and 306 nonsmokers, and genotyped them the BDNF Val66Met polymorphism. Of these, we assessed 114 smokers and 98 nonsmokers on the repeatable battery for the assessment of neuropsychological status (RBANS), and 103 smokers and 89 nonsmokers on serum BDNF levels. Smokers scored lower than the nonsmokers on RBANS total score (p?=?0.002), immediate memory (p?=?0.003) and delayed memory (p?=?0.021). BDNF levels among the smokers who were Val allele carriers were correlated with the degree of cognitive impairments, especially attention, as well as with the carbon monoxide concentrations. Our findings suggest that smoking is associated with cognitive impairment in a male Chinese Han population. The association between higher BDNF levels and cognitive impairment, mainly attention in smokers appears to be dependent on the BDNF Val66Met polymorphism.
| S-EPMC6338731 | biostudies-literature
Project description:Background: The oral microbiome, which consists of various habitats, has been shown to be influenced by smoking. However, differences in the tongue microbiomes of current and former smokers, as well as their resultant functional consequences, have rarely been investigated in East Asian populations. Methods: We used 16S rRNA amplicon sequencing of tongue-coating samples obtained from East Asian subjects who were current, former, or never smokers to identify differences in their tongue microbiomes and related metagenomic functions. Two sets of participants from 2016 to 2017 (n = 657 and n = 187, respectively) were analyzed separately. Results: We found significant differences between the overall microbiome compositions of current versus never smokers (p = 0.0015), but not between former versus never smokers (p = 0.43) based on the weighted UniFrac distance. Twenty-nine of 43 investigated genera showed significantly different expression levels in current versus never smokers. Neisseria and Capnocytophaga were less abundant, and Streptococcus and Megasphaera were more abundant in current smokers. Moreover, the abundances of metagenomic pathways, including those related to nitrate reduction and the tricarboxylic acid cycle, were significantly different between current and never smokers. Conclusions: The tongue microbiomes and related metagenomic pathways of current smokers differ from those of never smokers among East Asians.
| S-EPMC7170382 | biostudies-literature
Project description:BackgroundObesity is a multifactorial abnormality which has an underlying genetic control but requires environmental influences to trigger. Numerous epidemiological studies have examined the roles of physical inactivity and dietary factors in obesity development. Interactions between obesity-related genes and these lifestyles have also been confirmed. However, less attention has been paid to these complex relationship between cigarette smoking, alcohol drinking and obesity. The purpose of this study was to assess whether cigarette smoking and alcohol drinking were associated with body mass index (BMI), and whether these lifestyle factors modified the genetic variance of BMI.MethodsSubjects were twins recruited through the Chinese National Twin Registry, aged 18 to 79 years, and the sample comprised 6121 complete male twin pairs. Information on height, weight, cigarette smoking and alcohol drinking status were assessed with self-report questionnaires. The associations of cigarette smoking and alcohol drinking with BMI were evaluated by linear regression models. Further, structure equation models were conducted to estimate whether cigarette smoking and alcohol drinking status modified the degree of genetic variance of BMI.ResultsAfter adjustment for a variety of socio-demographic and lifestyle factors, former smokers had higher BMI (β = 0.475; 95 % CI, 0.196 to 0.754) whereas moderate to heavy smokers had lower BMI (β = -0.115; 95 % CI, -0.223 to -0.007) when compared with nonsmokers. BMI decreased with increased cigarette pack-years (β = -0.008; 95 % CI, -0.013 to -0.003). These effects still existed substantially in within-MZ twin pair analyses. By contrast, current alcohol drinking had no significant influence on BMI when additionally controlled for shared factors in within-pair analyses. Genetic modification by alcohol drinking was statistically significant for BMI (β = -0.137; 95 % CI, -0.215 to -0.058), with the intake of alcohol decreasing the additive genetic component of BMI.ConclusionsCigarette smoking was negatively associated with BMI independent of genetic influences. The influence of genes on BMI was moderated by alcohol drinking, such that for individuals who were regular drinkers, genetic factors became less influential. Our findings highlight gene-alcohol interaction in finding candidate genes of BMI and elucidating the etiological factors of obesity.
| S-EPMC4827244 | biostudies-literature
Project description:ObjectiveThe aim of this study was to examine if cholinergic receptor nicotinic beta 3 subunit (CHRNB3) was a common genetic basis for both nicotine dependence and schizophrenia.MethodsTwo CHRNB3 promoter single nucleotide polymorphisms (SNPs) were genotyped in 773 patients with schizophrenia and 302 healthy volunteers. Associations between smoking, schizophrenia, smoking+schizophrenia and CHRNB3 were analyzed. The mRNA expression of CHRNB3 in human brains was examined, and the expression correlations between CHRNB3 and dopaminergic and GABAergic receptor genes were evaluated.ResultsThe association between CHRNB3 and smoking was significant in the total sample, less significant in the smoking with schizophrenia, and suggestive in the smoking without schizophrenia. CHRNB3 had significant mRNA expression that was correlated with dopaminergic or GABAergic receptor expression in human brains. The two CHRNB3 SNPs had significant cis-acting regulatory effects on CHRNB3 mRNA expression.ConclusionsRisk for smoking behavior was associated with CHRNB3. CHRNB3 mRNA is abundant in human brain and could play important role in the pathogenesis of smoking behavior.
| S-EPMC8341072 | biostudies-literature
Project description:BackgroundCigarette smoking is a leading risk factor for morbidity and premature mortality in the United States, yet information about smoking prevalence and trends is not routinely available below the state level, impeding local-level action.MethodsWe used data on 4.7 million adults age 18 and older from the Behavioral Risk Factor Surveillance System (BRFSS) from 1996 to 2012. We derived cigarette smoking status from self-reported data in the BRFSS and applied validated small area estimation methods to generate estimates of current total cigarette smoking prevalence and current daily cigarette smoking prevalence for 3,127 counties and county equivalents annually from 1996 to 2012. We applied a novel method to correct for bias resulting from the exclusion of the wireless-only population in the BRFSS prior to 2011.ResultsTotal cigarette smoking prevalence varies dramatically between counties, even within states, ranging from 9.9% to 41.5% for males and from 5.8% to 40.8% for females in 2012. Counties in the South, particularly in Kentucky, Tennessee, and West Virginia, as well as those with large Native American populations, have the highest rates of total cigarette smoking, while counties in Utah and other Western states have the lowest. Overall, total cigarette smoking prevalence declined between 1996 and 2012 with a median decline across counties of 0.9% per year for males and 0.6% per year for females, and rates of decline for males and females in some counties exceeded 3% per year. Statistically significant declines were concentrated in a relatively small number of counties, however, and more counties saw statistically significant declines in male cigarette smoking prevalence (39.8% of counties) than in female cigarette smoking prevalence (16.2%). Rates of decline varied by income level: counties in the top quintile in terms of income experienced noticeably faster declines than those in the bottom quintile.ConclusionsCounty-level estimates of cigarette smoking prevalence provide a unique opportunity to assess where prevalence remains high and where progress has been slow. These estimates provide the data needed to better develop and implement strategies at a local and at a state level to further reduce the burden imposed by cigarette smoking.
| S-EPMC3987818 | biostudies-literature
Project description:Schizophrenia is associated with a high prevalence of smoking. Functional connectivity between the dorsal anterior cingulate (dACC) and limbic regions including the ventral striatum, extended amygdala and parahippocampal areas has been previously implicated in the genetics and clinical severity of smoking. In this study, we test the hypothesis that dACC functional circuits are key paths for the high risk of smoking comorbidity in schizophrenia. Resting state functional magnetic resonance imaging (fMRI) was performed using the dACC as a seed region in smoking and nonsmoking patients with schizophrenia (n = 54), matched controls (n = 65), and nonpsychotic first-degree relatives (n = 24). Multiple regions had decreased connectivity with the dACC in schizophrenia patients when compared with matched controls (n = 65). Several of these functional circuits were also associated with nicotine addiction severity; the largest cluster included limbic areas such as the parahippocampal, extended amygdala, ventral striatal, and posterior insula regions, indicating an overlap of schizophrenia and nicotine addiction on to this circuit. These same functional connectivity-defined circuits were also significantly impaired in schizophrenia nonsmokers compared with control nonsmokers and in nonpsychotic first-degree relatives. Functional connectivity between the dACC and limbic regions is inherently abnormal in schizophrenia, related to its genetic liability regardless of smoking, and overlaps with a nicotine addiction-related circuit. Our findings establish a biologically defined brain circuit mechanism that contributes to the high prevalence of smoking.
| S-EPMC3796082 | biostudies-other