scholarly journals Relationship between self-reported task persistence and history of quitting smoking, plans for quitting smoking, and current smoking status in adolescents

2007 ◽  
Vol 32 (7) ◽  
pp. 1451-1460 ◽  
Author(s):  
Marc L. Steinberg ◽  
Jonathan A. Krejci ◽  
Kerstin Collett ◽  
Thomas H. Brandon ◽  
Douglas M. Ziedonis ◽  
...  
2020 ◽  
Vol 2020 ◽  
pp. 1-11 ◽  
Author(s):  
Askin Gülsen ◽  
Burcu Arpinar Yigitbas ◽  
Berat Uslu ◽  
Daniel Drömann ◽  
Oguz Kilinc

Background. Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SAR2-COV-2) and was first identified in Wuhan, China, in December of 2019, but quickly spread to the rest of the world, causing a pandemic. While some studies have found no link between smoking status and severe COVID-19, others demonstrated a significant one. The present study aimed to determine the relationship between smoking and clinical COVID-19 severity via a systematic meta-analysis approach. Methods. We searched the Google Scholar, PubMed, Scopus, Web of Science, and Embase databases to identify clinical studies suitable for inclusion in this meta-analysis. Studies reporting smoking status and comparing nonsevere and severe patients were included. Nonsevere cases were described as mild, common type, nonintensive care unit (ICU) treatment, survivors, and severe cases as critical, need for ICU, refractory, and nonsurvivors. Results. A total of 16 articles detailing 11322 COVID-19 patients were included. Our meta-analysis revealed a relationship between a history of smoking and severe COVID-19 cases (OR=2.17; 95% CI: 1.37–3.46; P<.001). Additionally, we found an association between the current smoking status and severe COVID-19 (OR=1.51; 95% CI: 1.12–2.05; P<.008). In 10.7% (978/9067) of nonsmokers, COVID-19 was severe, while in active smokers, severe COVID-19 occurred in 21.2% (65/305) of cases. Conclusion. Active smoking and a history of smoking are clearly associated with severe COVID-19. The SARS-COV-2 epidemic should serve as an impetus for patients and those at risk to maintain good health practices and discontinue smoking. The trial is registered with the International Prospective Register of Systematic Reviews (PROSPERO) CRD42020180173.


2020 ◽  
Vol 154 (Supplement_1) ◽  
pp. S150-S150
Author(s):  
H Li ◽  
M Arslan ◽  
Z Fu ◽  
H Lee ◽  
M Mikula

Abstract Introduction/Objective A subset of patients with an established diagnosis of UC develops signs of CD (de novo CD) following IPAA. While the etiology and risk factors of de novo CD remain largely unknown, preliminary studies have shown controversial results regarding family history of inflammatory bowel disease (IBD) and smoking history. Methods Patients that underwent IPAA for UC, with at least 1 year of follow-up, were identified (n=161; 1996 to 2018). We retrospectively reviewed the electronic medical records. Patients that were diagnosed with de novo CD during the follow-up period were further identified. Smoking history and family history of IBD were evaluated. Chi square test was performed to compare the frequencies. Odds ratio (OR) and 95% confidence intervals (CIs) were estimated by logistic regression model. P&lt;0.05 was considered statistically significant. Results 29 de novo CD were identified. At the time of proctocolectomy, the family history of IBD and smoking history was documented in 152 UC patients including 27 that subsequently developed de novo CD. 23 of 152 had a family history of IBD (12 UC, 9 CD and 2 IBD, NOS). 19/129 (14.7%) UC patients without a family history of any type of IBD, 4/9 (44.4%) with a family history of CD, and 4/12 (33.3%) with a family history of UC developed de novo CD. Patients with a family history of CD were more likely to develop de novo CD post IPAA than those without a family history of any type of IBD (OR 4.63, 95% CI 1.14-18.82, p=0.03). Family history of UC did not correlate with development of de novo CD (OR 2.90; 95% CI 0.79-10.57, p=0.108). At the time of proctocoletomy, 11 were current smokers, 25 were former smokers, and 116 never smoked. In de novo CD group, there were 4/27 (14.8 %) former smokers and 23/27 (85.2 %) never smokers. No de novo CD patient was current smoker. In the UC group that remained as UC following IPAA, 11/125 (8.8%) were current smokers, 21/125 (16.8 %) former smokers, and 93/125 (74.4 %) were never smokers. Current smoking status was not associated with development of de novo CD (p = 0.214). Conclusion Family history of CD may be a risk factor for developing de novo CD following IPAA for UC. Current smoking status was not associated with development of de novo CD following IPAA for UC.


2020 ◽  
Author(s):  
Askin Gulsen ◽  
Burcu Arpinar Yigitbas ◽  
Berat Uslu ◽  
Daniel Droemann ◽  
Oguz Kilinc

Background: Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SAR2-COV-2), and was first identified in Wuhan, China in December of 2019, but quickly spread to the rest of the world, causing a pandemic. While some studies have found no link between smoking status and severe COVID-19, others demonstrated a significant one. The present study aimed to determine the relationship between smoking and clinical COVID-19 severity via a systematic meta-analysis approach. Methods: We searched the Google Scholar, PubMed, Scopus, Web of Science, and Embase databases to identify clinical studies suitable for inclusion in this meta-analysis. Studies reporting smoking status and comparing non-severe and severe patients were included. Non-severe cases were described as mild, common type, non-intensive care unit (ICU) treatment, survivors, and severe cases as critical, need for ICU, refractory, and non-survivors. Results: A total of 16 articles detailing 11322 COVID-19 patients were included. Our meta-analysis revealed a relationship between a history of smoking and severe COVID-19 cases (OR=2.17; 95% CI: 1.37-3.46; P <.001). Additionally, we found an association between the current smoking status and severe COVID-19 (OR=1.51; 95% CI: 1.12-2.05; P <.008). In 10.7% (978/9067) of non-smokers, COVID-19 was severe, while in active smokers, severe COVID-19 occurred in 21.2% (65/305) of cases. Conclusion: Active smoking and a history of smoking are clearly associated with severe COVID-19. The SARS-COV-2 epidemic should serve as an impetus for patients and those at risk to maintain good health practices and discontinue smoking.


2021 ◽  
pp. 1-8
Author(s):  
Francesca Galluzzi ◽  
Veronica Rossi ◽  
Cristina Bosetti ◽  
Werner Garavello

<b><i>Introduction:</i></b> Smell and taste loss are characteristic symptoms of SARS-CoV-2 infection. The aim of this study is to investigate the prevalence and risk factors associated with olfactory and gustatory dysfunctions in coronavirus disease (COVID-19) patients. <b><i>Methods:</i></b> We conducted an observational, retrospective study on 376 patients with documented SARS-CoV-2 infection admitted to the San Gerardo Hospital in Monza, Italy, from March to July 2020. All patients answered a phone questionnaire providing information on age, sex, smoking status, and clinical characteristics. Adjusted odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were estimated through logistic regression models including relevant covariates. <b><i>Results:</i></b> The prevalence of olfactory and gustatory dysfunctions in COVID-19 patients was 33.5 and 35.6%, respectively. Olfactory dysfunctions were significantly directly associated with current smoking and history of allergy, the multivariable ORs being 6.53 (95% CI 1.16–36.86) for current smokers versus never smokers, and 1.89 (95% CI 1.05–3.39) for those with an allergy compared to those without any allergy. Respiratory allergy in particular was significantly associated with olfactory dysfunctions (multivariable OR 2.30, 95% CI 1.02–5.17). Significant inverse associations were observed for patients aged 60 years or more (multivariable OR 0.33, 95% CI 0.19–0.57) and hospitalization (multivariable OR 0.22, 95% CI 0.06–0.89). Considering gustatory dysfunctions, after allowance of other variables a significant direct association was found for respiratory allergies (OR 2.24, 95% CI 1.03–4.86), and an inverse association was found only for hospitalization (OR 0.21, 95% CI 0.06–0.76). <b><i>Conclusion:</i></b> Our study indicates that current smoking and history of allergy (particularly respiratory) significantly increase the risk for smell loss in COVID-19 patients; the latter is also significantly associated to taste loss. Hospitalization has an inverse association with the risk of olfactory and gustatory dysfunctions, suggesting that these may be symptoms characteristics of less severe SARS-CoV-2 infection.


2011 ◽  
Vol 26 (4) ◽  
pp. 360-367 ◽  
Author(s):  
Katherine Webber ◽  
Andrew N Davies

Context: observational studies in North America suggest alcohol dependence is a common problem in advanced cancer patients and is associated with a high burden of physical and psychological symptoms. The prevalence of all types of alcohol use disorders, and the relationship between alcohol use disorders and symptoms, has not been studied. Objectives: this observational, cross-sectional study was designed to determine the prevalence of alcohol use disorders in patients with advanced cancer and establish if such patients have a higher symptom burden. Methods: sequential patients referred to the palliative medicine team at a United Kingdom cancer centre completed the Alcohol Use Disorders Identification Test, Hospital Anxiety and Depression Scale (HADS) and Memorial Symptom Assessment Scale-Short Form (MSAS-SF). Results: 120 patients participated in the study. Twenty-two (18%) patients screened positively for the presence of an alcohol use disorder. This study found no significant association between alcohol use disorders and the presence of anxiety ( P = 0.38) or depression ( P = 0.81) on the HADS or the global distress index subscale ( P = 0.142), physical symptom distress index subscale ( P = 0.734), or the psychological distress index subscale ( P = 0.154) on the MSAS-SF. Current smoking status was the only independent predictor for the presence of an alcohol use disorder ( P < 0.001). Seven (6%) patients screened positively for high-risk alcohol use disorders. Current smoking status ( P < 0.001) and male gender ( p < 0.001) were independent predictors of this problem. Conclusions: alcohol use disorders in this cohort of patients were not associated with a higher symptom burden, and the prevalence was lower than the general United Kingdom population.


2005 ◽  
Vol 41 (1) ◽  
pp. 134-140 ◽  
Author(s):  
Karl-Heinz Ladwig ◽  
Jens Baumert ◽  
Hannelore Löwel ◽  
Angela Döring ◽  
Heinz-Erich Wichmann

2013 ◽  
Vol 22 (6) ◽  
pp. 581-589 ◽  
Author(s):  
Carla J. Berg ◽  
Hefei Wen ◽  
Janet R. Cummings ◽  
Jasjit S. Ahluwalia ◽  
Benjamin G. Druss

Pain ◽  
2011 ◽  
Vol 152 (1) ◽  
pp. 60-65 ◽  
Author(s):  
Joseph W. Ditre ◽  
Brian D. Gonzalez ◽  
Vani N. Simmons ◽  
Leigh Anne Faul ◽  
Thomas H. Brandon ◽  
...  

2019 ◽  
Vol 11 (1) ◽  
Author(s):  
Luhang Han ◽  
Hongmei Zhang ◽  
Akhilesh Kaushal ◽  
Faisal I. Rezwan ◽  
Latha Kadalayil ◽  
...  

Abstract Background Adolescence is a period characterized by major biological development, which may be associated with changes in DNA methylation (DNA-M). However, it is unknown to what extent DNA-M varies from pre- to post-adolescence, whether the pattern of changes is different between females and males, and how adolescence-related factors are associated with changes in DNA-M. Methods Genome-scale DNA-M at ages 10 and 18 years in whole blood of 325 subjects (n = 140 females) in the Isle of Wight (IOW) birth cohort was analyzed using Illumina Infinium arrays (450K and EPIC). Linear mixed models were used to examine DNA-M changes between pre- and post-adolescence and whether the changes were gender-specific. Adolescence-related factors and environmental exposure factors were assessed on their association with DNA-M changes. Replication of findings was attempted in the comparable Avon Longitudinal Study of Parents and Children (ALSPAC) cohort. Results In the IOW cohort, after controlling for technical variation and cell compositions at both pre- and post-adolescence, 15,532 cytosine–phosphate–guanine (CpG) sites (of 400,825 CpGs, 3.88%) showed statistically significant DNA-M changes from pre-adolescence to post-adolescence invariant to gender (false discovery rate (FDR) = 0.05). Of these 15,532 CpGs, 10,212 CpGs (66%) were replicated in the ALSPAC cohort. Pathway analysis using Ingenuity Pathway Analysis (IPA) identified significant biological pathways related to growth and development of the reproductive system, emphasizing the importance of this period of transition on epigenetic state of genes. In addition, in IOW, we identified 1179 CpGs with gender-specific DNA-M changes. In the IOW cohort, body mass index (BMI) at age 10 years, age of growth spurt, nonsteroidal drugs use, and current smoking status showed statistically significant associations with DNA-M changes at 15 CpGs on 14 genes such as the AHRR gene. For BMI at age 10 years, the association was gender-specific. Findings on current smoking status were replicated in the ALSPAC cohort. Conclusion Adolescent transition is associated with changes in DNA-M at more than 15K CpGs. Identified pathways emphasize the importance of this period of transition on epigenetic state of genes relevant to cell growth and immune system development.


Sign in / Sign up

Export Citation Format

Share Document