1000 resultados para tobacco smoking
Tobacco use is a major public health concern, and is associated with a number of mental illnesses as well as increased alcohol/other drug (AOD). Research into treatment for individuals experiencing such comorbidities is limited. Participants (n = 447) were those enrolled in the Depression and Alcohol Integrated and Single-focused Interventions project (Baker et al. 2010), and the Self Help for Alcohol/other drugs and DEpression project (Kay-Lambkin et al. Medical Journal of Australia 195:S44-S50, 2011a, Journal of Medical Internet Research 13(1):e11p11, b), who reported current depression and hazardous alcohol use at entry to the study. Smoking cessation was not targeted in, nor a goal of, treatment. After controlling for socioeconomic variables, tobacco use was not associated with higher levels of depressive symptoms at baseline; however heavy smokers (30+ cigarettes per day) consumed significantly more alcohol at baseline than did non-smokers (13 vs. 9 standard drinks per day). Baseline smoking severity did not impact on depression or alcohol use outcomes over a 12-month period. Reductions in tobacco use between baseline and 3-month follow-up were significantly associated with reductions in depression and alcohol consumption over the same time period. The study results suggest that tobacco use does not interfere with treatment for depression and alcohol use problems, and adds weight to the idea of considering specific treatment for tobacco use in the context of treatment for alcohol/other drug use.
Background & Aims: Esophageal adenocarcinoma arises from Barrett's esophagus (BE); patients with this cancer have a poor prognosis. Identification of modifiable lifestyle factors that affect the risk of progression from BE to esophageal adenocarcinoma might prevent its development. We investigated associations among body size, smoking, and alcohol use with progression of BE to neoplasia. Methods: We analyzed data from patients with BE identified from the population-based Northern Ireland BE register, diagnosed between 1993 and 2005 with specialized intestinal metaplasia (n = 3167). Data on clinical, demographic, and lifestyle factors related to diagnosis of BE were collected from hospital case notes. We used the Northern Ireland Cancer Registry to identify which of these patients later developed esophageal adenocarcinoma, adenocarcinomas of the gastric cardia, or esophageal high-grade dysplasia. Cox proportional hazards models were used to associate lifestyle factors with risk of progression.
Results: By December 31, 2008, 117 of the patients with BE developed esophageal high-grade dysplasia or adenocarcinomas of the esophagus or gastric cardia. Current tobacco smoking was significantly associated with an increased risk of progression (hazard ratio = 2.03; 95% confidence interval, 1.29-3.17) compared with never smoking, and across all strata of smoking intensity. Alcohol consumption was not related to risk of progression. Measures of body size were infrequently reported in endoscopy reports, and body size was not associated with risk of progression.
Conclusions: Smoking tobacco increases the risk of progression to cancer or high-grade dysplasia 2-fold among patients with BE, compared with patients with BE that have never smoked. Smoking cessation strategies should be considered for patients with BE.
BACKGROUND: Tobacco smoking is a major contributor to the public health burden and healthcare costs worldwide, but the determinants of smoking behaviours are poorly understood. We conducted a large individual-participant meta-analysis to examine the extent to which work-related stress, operationalised as job strain, is associated with tobacco smoking in working adults. METHODOLOGY AND PRINCIPAL FINDINGS: We analysed cross-sectional data from 15 European studies comprising 166 130 participants. Longitudinal data from six studies were used. Job strain and smoking were self-reported. Smoking was harmonised into three categories never, ex- and current. We modelled the cross-sectional associations using logistic regression and the results pooled in random effects meta-analyses. Mixed effects logistic regression was used to examine longitudinal associations. Of the 166 130 participants, 17% reported job strain, 42% were never smokers, 33% ex-smokers and 25% current smokers. In the analyses of the cross-sectional data, current smokers had higher odds of job strain than never-smokers (age, sex and socioeconomic position-adjusted odds ratio: 1.11, 95% confidence interval: 1.03, 1.18). Current smokers with job strain smoked, on average, three cigarettes per week more than current smokers without job strain. In the analyses of longitudinal data (1 to 9 years of follow-up), there was no clear evidence for longitudinal associations between job strain and taking up or quitting smoking. CONCLUSIONS: Our findings show that smokers are slightly more likely than non-smokers to report work-related stress. In addition, smokers who reported work stress smoked, on average, slightly more cigarettes than stress-free smokers.
Background : Smoking is disproportionately prevalent among people with psychiatric illness.
Aims : To investigate smoking as a risk factor for major depressive disorder.
Method : A population-based sample of women was studied using case–control and retrospective cohort study designs. Exposure to smoking was self-reported, and major depressive disorder diagnosed using the Structured Clinical Interview for DSM–IV–TR (SCID–I/NP).
Results : Among 165 people with major depressive disorder and 806 controls, smoking was associated with increased odds for major depressive disorder (age-adjusted odds ratio (OR)=1.46, 95% CI 1.03–2.07). Compared with non-smokers, odds for major depressive disorder more than doubled for heavy smokers (>20 cigarettes/day). Among 671 women with no history of major depressive disorder at baseline, 13 of 87 smokers and 38 of 584 non-smokers developed de novo major depressive disorder during a decade of follow-up. Smoking increased major depressive disorder risk by 93% (hazard ratio (HR)=1.93, 95% CI 1.02–3.69); this was not explained by physical activity or alcohol consumption.
Conclusions : Evidence from cross-sectional and longitudinal data suggests that smoking increases the risk of major depressive disorder in women.
Programa de doctorado: Salud Pública (Epidemiología, Planificación y Nutrición)
Maternal smoking in pregnancy is associated with respiratory diseases in the offspring, possibly due to prenatal influences on the developing immune system. We investigated whether maternal smoking in pregnancy was associated with cord blood leukocyte numbers, including precursor dendritic cells, adjusting for concomitant factors. In a prospective healthy birth cohort study, total leukocyte counts were reduced in neonates of smoking mothers [10.7 (8.4-13.0), n=14] compared with nonexposed infants [14.7 (13.7-15.7), n=74, p=0.002] [geometric mean cells x 10(3)/microL (95% confidence interval)]. All leukocyte subsets were decreased, most prominently segmented neutrophils [4.3 (2.8-5.7) versus 6.2 (5.5-6.8), p=0.021], lymphocytes [3.8 (2.9-4.8) versus 5.0 (4.5-5.6), p=0.036], and myeloid precursor dendritic cells [12.7 cells/microL (9.1-17.8) versus 18.3 (15.8-21.2), p=0.055]. These differences persisted after adjustment for possible confounders. Predictors of myeloid precursor dendritic cell numbers in multivariable models were maternal smoking (-5.1 cells/microL, p=0.042), age (-0.5 cells/microL/y, p=0.035), and, marginally, asthma (+8.1 cells/microL, p=0.075). The decrease of all leukocytes in neonates of smoking mothers could be clinically significant and suggests a decreased cell production, increased peripheral recruitment, or retention in bone marrow. Given the importance of dendritic cells in early immune responses, their decrease might reflect an impact of maternal smoking on the developing fetal immune system.
Thesis (Master's)--University of Washington, 2016-06
BACKGROUND: We report on the prospective association between smoking and depression and health-related quality of life (HRQOL) in patients with coronary artery disease (CAD).
METHODS: Prospective study of 193 patients with assessment of depression occurring 3-, 6- and 9- months (T1, 2, and 3, respectively) following discharge from hospital for a cardiac event. HRQOL was assessed at T3. T1 depression was assessed by clinical interview; T2 and T3 depression was assessed by self-report. Smoking at time of cardiac event was assessed by self-report. Multivariate analyses controlled for known demographic, psychosocial and clinical correlates of depression.
RESULTS: Smoking at the time of index cardiac event increased the likelihood of being diagnosed with Major Depressive Disorder (MDD) at T1 by 4.30 [95% CI, 1.12-16.46; p < .05]. The likelihood of receiving a diagnosis of minor depression, dysthymia or MDD as a combined group was increased by 8.03 [95% CI, 2.35-27.46; p < .01]. Smoking did not reliably predict depression at T2 or T3 and did not reliably predict persistent depression. Smoking increased the likelihood of being classified as depressed according to study criteria at least once during the study period by 5.19 [95% CI, 1.51-17.82; p < .01]. Smoking independently predicted worse mental HRQOL.
CONCLUSIONS: The findings support a role for smoking as an independent predictor of depression in CAD patients, particularly in the first 3 months post-cardiac event. The well-established imperative to encourage smoking cessation in these patients is augmented and the findings may add to the evidence for smoking cessation campaigns in the primary prevention of depression.