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Smokeless tobacco products have been linked to precancerous and cancers of oral cavity for long. Evidence was available on the association between smokeless tobacco (SLT) products and oral cancers at regional but not at global level. Present meta-analysis is aimed to evaluate the risk of oral cancer with the use of SLT products among \"ever\" versus \"never\" users. Studies published for the period (1960-2016) are retrieved using Pubmed, Indmed, EMBASE, and Google Scholar search engines for the subject \"ever\" versus \"never\" users of SLT products and estimated the risk association with oral cancer. Summary odds ratios (relative risk) are estimated and meta-analysis was performed using random-effects model. Thirty-seven studies from four of six WHO regions, Southeast Asia region (SEAR), the Eastern Mediterranean Region (EMR), Europe, and region of Americas (North and South) are included in the analysis. Significant risk with SLT products with oral cancer was found for SEAR (4.44, 95% CI = 3.51 to 5.61) and for EMR (1.28, 95% CI = 1.04 to 1.56). Significantly higher risk (p < .001) was found for females (5.83, 95% CI = 2.93 to 11.58). Product wise analysis for different SLT products revealed various levels of risk viz. gutkha (8.67, 95% CI = 3.59 to 20.93), pan tobacco / betel liquid (7.18, 95% CI = 5.48 to 9.41), oral snuff (4.18, 50% CI = 2.37 to 7.38), Mainpuri tobacco (3.32, 95% CI = 1.32 to 8.36), and snus (0.86, 95% CI = 0.58 to 1.29). A significant positive association was observed between SLT use and the risk of oral cancer, in SEAR, EMRs, and among women users. The present meta-analysis demonstrates SLT product use and the risk of oral cancer at global level. Moreover, the present analysis provided data on the risk associated with individual SLT product. The results fulfil the gap in the data on independent effect of individual SLT product use on the outcome of oral cancer at global level, conclusively. Chewing SLT products was associated with higher risk of oral cancer than other types of SLT. This can serve as a useful tool for policy makers in forming strict policies in controlling SLT menace. Hence, we propose that in addition to smoking, efforts should be directed towards SLT product cessation as well in reducing oral cancer incidence.

The rate of cigarette smoking is greater among persons with mental health and/or substance abuse problems. There are few population-based datasets with which to study tobacco mortality in these vulnerable groups. The Oregon Health Authority identified persons who received publicly-funded mental health or substance abuse services from January 1996 through December 2005. These cases were then matched to Oregon Vital Statistics records for all deaths (N= 148,761) in the period 1999-2005. The rate of tobacco-related death rates was higher among persons with substance abuse problems only (53.6%) and those with both substance abuse and mental health problems (46.8%), as compared to the general population (30.7%). The rate of tobacco-related deaths among persons with mental health problems (30%) was similar to that in the general population. Persons receiving substance abuse treatment alone, or receiving both substance abuse and mental health treatment, were more likely to die and more likely to die prematurely of tobacco-related causes as compared to the general population. Persons receiving mental health services alone were not more likely to die of tobacco-related causes, but tobacco-related deaths occurred earlier in this population.

Objectives Those with any psychiatric diagnosis have substantially greater rates of smoking and are less likely to quit smoking than those with no diagnosis. Using nationally representative data, we sought to provide estimates of smoking and longitudinal cessation rates by specific psychiatric diagnoses and mental health service use. Design and participants Data were analysed from a two-wave cohort survey of a US nationally representative sample (non-institutionalised adults): the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC; 2001–2002, n=43 093; 2004–2005, n=34 653). Main outcome measures We examined smoking rates (lifetime, past year and past year heavy) and cross-sectional quit rates among those with any lifetime or past year psychiatric diagnosis (DSM-IV). Importantly, we examined longitudinal quit rates and conducted analyses by gender and age categories. Results Those with any current psychiatric diagnosis had 3.23 (95% CI 3.11 to 3.35) times greater odds of currently smoking than those with no diagnosis, and were 25% less likely to have quit by follow-up (95% CI 20% to 30%). Prevalence varied by specific diagnoses (32.4% to 66.7%) as did cessation rates (10.3% to 17.9%). Comorbid disorders were associated with higher proportions of heavy smoking. Treatment use was associated with greater prevalence of smoking and lower likelihood of cessation. Conclusions Those with psychiatric diagnoses remained much more likely to smoke and less likely to quit, with rates varying by specific diagnosis. Our findings highlight the need to improve our ability to address smoking and psychiatric comorbidity both within and outside of healthcare settings. Such advancements will be vital to reducing mental illness-related disparities in smoking and continuing to decrease tobacco use globally.

Abstract Objective We conducted a prospective cohort study of the Clinical Practice Research Database to estimate rates of varenicline and nicotine replacement therapy (NRT) prescribing and the relative effects on smoking cessation, and mental health. Methods We used multivariable logistic regression, propensity score matched regression, and instrumental variable analysis. Exposure was varenicline or NRT prescription. Mental disorders were bipolar, depression, neurotic disorder, schizophrenia, or prescriptions of antidepressants, antipsychotics, hypnotics/anxiolytics, mood stabilizers. Outcomes were smoking cessation, and incidence of neurotic disorder, depression, prescription of antidepressants, or hypnotics/anxiolytics. Follow-ups were 3, 6, and 9 months, and at 1, 2, and 4 years. Results In all patients, NRT and varenicline prescribing declined during the study period. Seventy-eight thousand four hundred fifty-seven smokers with mental disorders aged ≥18 years were prescribed NRT (N = 59 340) or varenicline (N = 19 117) from September 1, 2006 to December 31, 2015. Compared with smokers without mental disorders, smokers with mental disorders had 31% (95% CI: 29% to 33%) lower odds of being prescribed varenicline relative to NRT, but had 19% (95% CI: 15% to 24%) greater odds of quitting at 2 years when prescribed varenicline relative to NRT. Overall, varenicline was associated with decreased or similar odds of worse mental health outcomes than NRT in patients both with and without mental disorders, although there was some variation when analyses were stratified by mental disorder subgroup. Conclusions Smoking cessation medication prescribing may be declining in primary care. Varenicline was more effective than NRT for smoking cessation in patients with mental disorders and there is not clear consistent evidence that varenicline is adversely associated with poorer mental health outcomes. Implications Patients with mental disorders were less likely to be prescribed varenicline than NRT. We triangulated results from three analytical techniques. We found that varenicline was more effective than NRT for smoking cessation in patients with mental disorders. Varenicline was generally associated with similar or decreased odds of poorer mental health outcomes (ie, improvements in mental health) when compared with NRT. We report these findings cautiously as our data are observational and are at risk of confounding.

Diabetes is far more prevalent in smokers than non-smokers, but the underlying mechanisms of vulnerability are unknown. Here we show that the diabetes-associated gene Tcf7l2 is densely expressed in the medial habenula (mHb) region of the rodent brain, where it regulates the function of nicotinic acetylcholine receptors. Inhibition of TCF7L2 signalling in the mHb increases nicotine intake in mice and rats. Nicotine increases levels of blood glucose by TCF7L2-dependent stimulation of the mHb. Virus-tracing experiments identify a polysynaptic connection from the mHb to the pancreas, and wild-type rats with a history of nicotine consumption show increased circulating levels of glucagon and insulin, and diabetes-like dysregulation of blood glucose homeostasis. By contrast, mutant Tcf7l2 rats are resistant to these actions of nicotine. Our findings suggest that TCF7L2 regulates the stimulatory actions of nicotine on a habenula–pancreas axis that links the addictive properties of nicotine to its diabetes-promoting actions. The transcription factor TCF7L2 mediates two important responses to nicotine in the medial habenula region of the rodent brain: aversion to nicotine, and regulation of blood sugar levels through a polysynaptic habenula–pancreas circuit.

Abstract Introduction High rates of tobacco use among people with serious mental illness (SMI), along with their unique needs, suggest the importance of developing tailored smoking cessation interventions for this group. Previous early-phase work empirically validated the design and content of Learn to Quit, a theory-based app designed for this population. Methods In a pilot randomized controlled trial, we compared the feasibility, acceptability, and preliminary efficacy of Learn to Quit versus QuitGuide, an app designed for the general population. All participants received nicotine replacement therapy and technical assistance. Daily smokers with SMI (N = 62) participated in the trial with outcomes assessed at weeks 4, 8, 12, and 16. Results Compared to QuitGuide, Learn to Quit participants had similar number of days of app use (34 vs. 32, p = .754), but larger number of app interactions (335 vs. 205; p = .001), longer durations of app use (4.24 hrs. vs. 2.14 hrs; p = .044), and higher usability scores (85 vs. 79, p = .046). At week 16, Learn to Quit led to greater reductions in cigarettes per day (12.3 vs. 5.9 for QuitGuide; p = 0.10). Thirty-day point prevalence abstinence was verified in 12% of Learn to Quit participants versus 3% of QuitGuide participants (odds ratio = 3.86, confidence interval = 0.41 to 36, p = .239). Changes in psychiatric symptoms and adverse events were not clinically significant between conditions. Conclusions This pilot trial provides strong evidence of Learn to Quit’s usability, feasibility, and safety. Preliminary evidence suggests the app may be efficacious. A randomized controlled efficacy trial is needed to test the app in a larger sample of smokers with SMI. Implications This study suggests that the Learn to Quit app is a feasible approach to deliver smoking cessation treatment in patients with co-occurring tobacco use disorder and SMI. This means that, if found efficacious, this technology could be used to deploy smoking cessation treatment to larger segments of this population, hence improving public health. Therefore, a randomized controlled trial should be conducted to examine the efficacy of this digital intervention.

Background Multiple studies have demonstrated that rates of smoking and nicotine dependence are increased in individuals with anxiety disorders. However, significant variability exists in the epidemiological literature exploring this relationship, including study design (cross-sectional versus prospective), the population assessed (random sample versus clinical population) and diagnostic instrument utilized. Methods We undertook a systematic review of population-based observational studies that utilized recognized structured clinical diagnostic criteria ( Diagnostic and Statistical Manual of Mental Disorders (DSM) or International Classification of Diseases (ICD)) for anxiety disorder diagnosis to investigate the relationship between cigarette smoking, nicotine dependence and anxiety disorders. Results In total, 47 studies met the predefined inclusion criteria, with 12 studies providing prospective information and 5 studies providing quasiprospective information. The available evidence suggests that some baseline anxiety disorders are a risk factor for initiation of smoking and nicotine dependence, although the evidence is heterogeneous and many studies did not control for the effect of comorbid substance use disorders. The identified evidence however appeared to more consistently support cigarette smoking and nicotine dependence as being a risk factor for development of some anxiety disorders (for example, panic disorder, generalized anxiety disorder), although these findings were not replicated in all studies. A number of inconsistencies in the literature were identified. Conclusions Although many studies have demonstrated increased rates of smoking and nicotine dependence in individuals with anxiety disorders, there is a limited and heterogeneous literature that has prospectively examined this relationship in population studies using validated diagnostic criteria. The most consistent evidence supports smoking and nicotine dependence as increasing the risk of panic disorder and generalized anxiety disorder. The literature assessing anxiety disorders increasing smoking and nicotine dependence is inconsistent. Potential issues with the current literature are discussed and directions for future research are suggested.

The burden of chronic, non-communicable diseases in low-income and middle-income countries is increasing. We outline a framework for monitoring of such diseases and review the mortality burden and the capacity of countries to respond to them. We show data from WHO data sources and published work for prevalence of tobacco use, overweight, and cause-specific mortality in 23 low-income and middle-income countries with a high burden of non-communicable disease. Data for national capacity for chronic disease prevention and control were generated from a global assessment that was done in WHO member states in 2009–10. Although reliable data for cause-specific mortality are scarce, non-communicable diseases were estimated to be responsible for 23·4 million (or 64% of the total) deaths in the 23 countries that we analysed, with 47% occurring in people who were younger than 70 years. Tobacco use and overweight are common in most of the countries and populations we examined, but coverage of cost-effective interventions to reduce these risk factors is low. Capacity for prevention and control of non-communicable diseases, including monitoring and surveillance operations nationally, is inadequate. A surveillance framework, including a minimum set of indicators covering exposures and outcomes, is essential for policy development and assessment and for monitoring of trends in disease. Technical, human, and fiscal resource constraints are major impediments to the establishment of effective prevention and control programmes. Despite increasing awareness and commitment to address chronic disease, concrete actions by global partners to plan and implement cost-effective interventions are inadequate.

Although pulmonary fibrosis can occur in the absence of a clear-cut inciting agent, and without a clinically clear initial acute inflammatory phase, it is more commonly associated with severe lung injury. This may be due to respiratory infections, chronic granulomatous diseases, medications, and connective tissue disorders. Pulmonary fibrosis is associated with permanent pulmonary architectural distortion and irreversible lung dysfunction. Available clinical, radiographic, and autopsy data has indicated that pulmonary fibrosis is central to severe acute respiratory distress syndrome (SARS) and MERS pathology, and current evidence suggests that pulmonary fibrosis could also complicate infection by SARS-CoV-2. The aim of this review is to explore the current literature on the pathogenesis of lung injury in COVID-19 infection. We evaluate the evidence in support of the putative risk factors for the development of lung fibrosis in the disease and propose risk mitigation strategies. We conclude that, from the available literature, the predictors of pulmonary fibrosis in COVID-19 infection are advanced age, illness severity, length of ICU stay and mechanical ventilation, smoking and chronic alcoholism. With no proven effective targeted therapy against pulmonary fibrosis, risk reduction measures should be directed at limiting the severity of the disease and protecting the lungs from other incidental injuries.