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Ruquaiijah Yearby uses Talib Kweli’s 2003 song “Get By” as a lens through which the reader can understand racialized health care disparities. In 1906, W. E. B. DuBois noted that social conditions, not genetics, impacted the health of blacks, causing racial disparities in mortality rates. Almost eighty years later, during the Reagan administration, the federal government identified racial health disparities as a problem in the Heckler Report on Black & Minority Health but focused on individual responsibility and solutions. In 2008, the Obama administration developed the Social Determinants of Health framework (“SDOH”), which recognizes that social factors outside an individual’s control impact individual health outcomes. The SDOH, often noted as the root cause of racial health disparities, are “conditions in the environments in which people are born, live, learn, work, play, worship, and age that affects a wide range of health, functioning, and quality-of-life outcomes and risks.” However, not only does the SDOH framework fail to acknowledge or discuss the ways that law is used to limit racial minorities’ equal opportunity to healthy conditions, but also some public health researchers and policymakers using the framework have tried to eliminate racial health disparities by focusing on individual responsibility.
Risk factors for salivary gland carcinoma are poorly understood. Although links between background radiation, smoking and obesity have been previously suggested, no studies have so far established any significant results. This study aimed to establish correlations between common environmental and lifestyle risk factors and different subtypes of salivary gland carcinoma.
A study of population data in Wales spanning 27 years was conducted; 2 national databases were used to identify 356 cases of primary salivary gland carcinoma over this period. Histological subtype of cancer and geographical location of each case was recorded. Public health data was used to establish radon levels, smoking, obesity and activity levels of populations in each geographical location. A population matched multivariate analysis of variance analysis was performed using histological subtype and risk factor data for each geographical location.
A significantly higher incidence of mucoepidermoid cancer in populations with higher background radon levels (p = 0.006), epithelial-myoepithelial cancer in populations with higher smoking levels (p = 0.029) and adenoid cystic cancer in populations with higher obesity levels (p = 0.028) was found.
To the authors’ knowledge, this is the first study to establish significant links between background radiation, smoking and obesity with different subtypes of salivary gland carcinoma.
Tobacco smoking rates are much higher in people who are in treatment or recovery for a substance use disorder (SUD) and/or mental health condition. Dependence on tobacco is a medical condition, though one that has historically been overlooked in both drug and alcohol and mental health settings. Smoking has a negative impact on substance use and mental health outcomes and contributes to the shorter life span these groups experience. In this chapter the importance of understanding the difference between tobacco and nicotine is discussed, and the prevalence of tobacco smoking and its impact on the health of people with a SUD and/or mental health condition is reviewed. A brief overview of population-level interventions is provided and a detailed section on individual-level interventions to help people quit smoking.
To determine the presence of cardiovascular (CV) risk (CVR) factors in university students and evaluate how these factors are affected from the knowledge, attitudes, and habits of the individuals regarding healthy lifestyle.
Starting from early ages, lifestyle habits such as lack of physical activity, unhealthy eating, and inappropriate drug use increase CV and metabolic risks of individuals.
In April–May 2018, sociodemographic characteristics of 770 undergraduate students, in addition to their knowledge, attitudes, and habits regarding their nutrition and physical activity status were obtained through face-to-face questionnaires. CVR factors were determined according to blood pressure, blood glucose, total cholesterol levels, and anthropometric measurements. Collected data were compared by CVR factor presence (CV[+] or CV[−]) in students.
The mean age of the participants was 22.3 ± 2.6 years. 59.6% were female and 71.5% were students of non-health sciences. In total, 274 individuals (35.9%) belonged to CV(+) group (mean risk number: 1.3 ± 0.5) with higher frequency in males (42.1% versus 31.6%, P < 0.05). The most common CVR factors were smoking (20.6%), high total cholesterol (7.5%), and hypertension/high blood pressure (6.0%). 15.5% of the participants regularly used at least one drug/non-pharmaceutical product. 11.3% complied the Mediterranean diet well. 21.9% of CV(+) stated consuming fast food at lunch compared to 14.3% of CV(−) (P < 0.05). 44.6% stated exercising below the CV-protective level.
This study showed one-third of university students was at CVR, independent of their sociodemographic characteristics. Furthermore, the students appear to perform below expectations in terms of nutrition and physical activity. Extensive additional measures are needed to encourage young individuals for healthy nutritional and physical activity habits.
Many adolescents start using tobacco, alcohol, and cannabis. Genetic vulnerability, parent characteristics in young adolescence, and interaction (GxE) and correlation (rGE) between these factors could contribute to the development of substance use. Using prospective data from the TRacking Adolescent Individuals’ Lives Survey (TRAILS; N = 1,645), we model latent parent characteristics in young adolescence to predict young adult substance use. Polygenic scores (PGS) are created based on genome-wide association studies (GWAS) for smoking, alcohol use, and cannabis use. Using structural equation modeling we model the direct, GxE, and rGE effects of parent factors and PGS on young adult smoking, alcohol use, and cannabis initiation. The PGS, parental involvement, parental substance use, and parent–child relationship quality predicted smoking. There was GxE such that the PGS amplified the effect of parental substance use on smoking. There was rGE between all parent factors and the smoking PGS. Alcohol use was not predicted by genetic or parent factors, nor by interplay. Cannabis initiation was predicted by the PGS and parental substance use, but there was no GxE or rGE. Genetic risk and parent factors are important predictors of substance use and show GxE and rGE in smoking. These findings can act as a starting point for identifying people at risk.
The high prevalence of smoking in individuals who are at ultra-high risk (UHR) for psychosis is well known and moderate cognitive deficits have also been found in UHR. However, the association between smoking and cognition in UHR is unknown and longitudinal studies are lacking.
A cohort study with 330 UHR individuals and 66 controls was conducted, as part of the European network of national schizophrenia networks studying gene–environment interactions (EU-GEI). At baseline and after 6, 12, and 24 months, smoking behavior was assessed with the Composite International Diagnostic Interview and cognitive functioning with a comprehensive test battery. Linear mixed-effects analyses were used to examine the multicross-sectional and prospective associations between (change in) smoking behavior and cognitive functioning, accounting for confounding variables.
At baseline, 53% of UHR and 27% of controls smoked tobacco. Smoking UHR and controls did not significantly differ from nonsmoking counterparts on the tested cognitive domains (speed of processing, attention/vigilance, working memory, verbal learning, or reasoning/problem solving) across different assessment times. Neither smoking cessation nor initiation was associated with a significant change in cognitive functioning in UHR.
No associations were found between smoking and cognitive impairment in UHR nor in controls. However, the fact that one in every two UHR individuals report daily use of tobacco is alarming. Our data suggest that UHR have fewer cognitive impairments and higher smoking cessation rates compared to patients with first-episode psychosis found in literature. Implications to promote smoking cessation in the UHR stage need further investigation.
Smoking is highly prevalent in the psychiatric population, and hospital admittance usually results in partial or complete smoking cessation. Tobacco use is known to affect the metabolism of certain psychoactive drugs, but whether smoking influences the plasma concentration of tricyclic antidepressants (TCAs) remains unclear. This article investigates the possible effect of smoking on the plasma concentration of TCAs. A systematic review of the literature available on PubMed and EMBASE as of October 2020 was carried out using PRISMA guidelines. Studies reporting plasma concentrations of any TCA in both a smoking and a non-smoking group were included and compared. Ten eligible studies were identified and included. In the eight studies investigating the effect of smoking on amitriptyline and/or nortriptyline, five studies found no significant effect. Two studies investigating the effect of smoking on imipramine found a significant effect, and one study investigating the effect of smoking on doxepin found no significant effect. The majority of studies included in this review were influenced by small study populations and other methodical issues. The effect of smoking on the plasma concentration of TCAs is still not entirely clear. There is a possibility that smoking affects the distribution of TCA metabolites, but this is probably not of clinical importance.
Moving away from the text-centered paradigm in film studies, the present research explores the relationship between the growing popularity of the film in Shanghai during the first two decades of the twentieth century and city governance in the International Settlement. It argues that the rise of movie halls contributed to creating a new kind of crowd that blended Chinese moviegoers with non-Chinese viewers. The emergence of the cinema as a space where people of different racial and ethnic origins encountered impelled the Shanghai Municipal Council – the governing body of the International Settlement in Shanghai – to respond by implementing new measures of public safety and altering its decades-long unspoken rules of segregation in the realm of everyday life. For Chinese enlightenment intellectuals and government officials, meanwhile, anxiety over their fellow Chinese's lack of basic decorum in public spaces arose with the intense intermingling of Chinese and non-Chinese filmgoers under the same roof. Thus, the cinema became a “contact zone” – a space of asymmetrical relations resulting not necessarily from colonists' exercise of colonial power but from the Chinese elite's wrapping of the discussion of movie theater etiquette reform within a political and ideological framework of modernization, patriotism, and anti-imperialism.
Smoking and nicotine dependence are particularly common in patients with a psychiatric disorder compared to the general population.
To study the prevalence of smoking in patients followed at the department of psychiatry and to assess their dependence on nicotine.
This was a cross-sectional, descriptive and analytical study. The study focused on patients followed at the department of psychiatry of the regional hospital of Gabes. Sociodemographic and clinical data were assessed. Fagerstrom questionnaire in its validated French version was used to assess the nicotine dependence. Data were analyzed using the software SPSS (20th edition).
100 patients were included. They were male (60%) and single (50%) and with a mean age of 45.3 years [18-71]. The three most common pathologies were anxiety disorders (31%), schizophrenia (30%) and depression (29%). Among the patients surveyed 48% were smokers. Of which, 93.7% smoked cigarettes, 20.8% snorted chewing tobacco and 12.5% smoked hookah. The average number of pack-years was 11.6, with an average of 22.8 cigarettes per day. The mean duration of regular smoking was 19.1 years. Regarding nicotine dependence, 42% of patients were dependent. Regarding the degree of dependency, 43.7% were heavily dependent, 25% were weakly dependent and 18.8% were moderately dependent. Smoking was significantly associated with the male gender (p≤10-3), alcoholism (p=0.002) and schizophrenia (p=0.006).
Results of our study show that smoking is frequent in patients followed at the psychiatry department. This aspect should be taken into account during the psychiatric evaluation, especially when therapeutic resistance occurs.
Alcohol consumption, smoking and mood disorders are leading contributors to the global burden of disease and are highly comorbid. Yet, their interrelationships have remained elusive. The aim of this study was to examine the multi-cross-sectional and longitudinal associations between (change in) smoking and alcohol use and (change in) number of depressive symptoms.
In this prospective, longitudinal study, 6646 adults from the general population were included with follow-up measurements after 3 and 6 years. Linear mixed-effects models were used to test multi-cross-sectional and longitudinal associations, with smoking behaviour, alcohol use and genetic risk scores for smoking and alcohol use as independent variables and depressive symptoms as dependent variables.
In the multi-cross-sectional analysis, smoking status and number of cigarettes per day were positively associated with depressive symptoms (p < 0.001). Moderate drinking was associated with less symptoms of depression compared to non-use (p = 0.011). Longitudinally, decreases in the numbers of cigarettes per day and alcoholic drinks per week as well as alcohol cessation were associated with a reduction of depressive symptoms (p = 0.001–0.028). Results of genetic risk score analyses aligned with these findings.
While cross-sectionally smoking and moderate alcohol use show opposing associations with depressive symptoms, decreases in smoking behaviour as well as alcohol consumption are associated with improvements in depressive symptoms over time. Although we cannot infer causality, these results open avenues to further investigate interventions targeting smoking and alcohol behaviours in people suffering from depressive symptoms.
Smoking pipes discovered in archaeological contexts demonstrate that Indigenous peoples of the Pacific Northwest of North America have practiced smoking for over 4,500 years. Archaeometry and ancient residue metabolomics provide evidence for the association of particular plants with these artifacts. In this article, we synthesize recent research on ancient smoking and present current knowledge on the spatiotemporal distribution of smoking in the past. The presence of stone smoking pipes in the archaeological record is paired with our understanding of past plant use based on chemical residue analyses to create a picture of precontact smoking practices. Archaeological pipe data demonstrate that smoking was a widely distributed practice in the inland Northwest over the past several thousand years, but not on the coast. Distributional data—including positive and negative evidence from chemical residue studies—show that tobacco was an important smoke plant in the region as early as around 1,410 years ago and as far north as the mid-Columbia region. Ancient residue metabolomics contributes to a richer understanding of past use of specific plants through the identification of tobacco species and other indigenous plants, including Rhus glabra, Cornus sericia, and Salvia sp., as contributing to the chemical residues in ancient pipes.
While acknowledging the disproportionate role of Islamic jurisprudence in studies of Islam generally, as a body of texts it provides a valuable site to trace the ways in which the natural sciences were on the one hand instrumentalized and appropriated by jurists to address ritual and social issues, and on the other demonstrates how these sciences provided the basis for legal thinking. The case of the Great Smoking Debate of the seventeenth–eighteenth centuries is discussed at length to show in detail how medicine shaped legal categories.
Depression is a common and serious mental illness that begins early in life. An association between cardiovascular disease (CVD) and subsequent depression is clear in adults. We examined associations between individual CVD risk factors and depression in young people.
We searched MEDLINE, EMBASE, and PsycINFO databases from inception to 1 January 2020. We extracted data from cohort studies assessing the longitudinal association between CVD risk factors [body mass index (BMI), smoking, systolic blood pressure (SBP), total cholesterol, high-density lipoprotein] and depression, measured using a validated tool in individuals with mean age of 24 years or younger. Random effect meta-analysis was used to combine effect estimates from individual studies, including odds ratio (OR) for depression and standardised mean difference for depressive symptoms.
Based on meta-analysis of seven studies, comprising 15 753 participants, high BMI was associated with subsequent depression [pooled OR 1.61; 95% confidence interval (CI) 1.21–2.14; I2 = 31%]. Based on meta-analysis of eight studies, comprising 30 539 participants, smoking was associated with subsequent depression (pooled OR 1.73; 95% CI 1.36–2.20; I2 = 74%). Low, but not high, SBP was associated with an increased risk of depression (pooled OR 3.32; 95% CI 1.68–6.55; I2 = 0%), although this was based on a small pooled high-risk sample of 893 participants. Generalisability may be limited as most studies were based in North America or Europe.
Targeting childhood/adolescent smoking and obesity may be important for the prevention of both CVD and depression across the lifespan. Further research on other CVD risk factors including blood pressure and cholesterol in young people is required.
Structural variation in subcortical brain regions has been linked to substance use, including the most commonly used substances nicotine and alcohol. Pre-existing differences in subcortical brain volume may affect smoking and alcohol use, but there is also evidence that smoking and alcohol use can lead to structural changes.
We assess the causal nature of the complex relationship of subcortical brain volume with smoking and alcohol use, using bi-directional Mendelian randomisation.
Mendelian randomisation uses genetic variants predictive of a certain ‘exposure’ as instrumental variables to test causal effects on an ‘outcome’. Because of random assortment at meiosis, genetic variants should not be associated with confounders, allowing less biased causal inference. We used summary-level data of genome-wide association studies of subcortical brain volumes (nucleus accumbens, amygdala, caudate, hippocampus, pallidum, putamen and thalamus; n = 50 290) and smoking and alcohol use (smoking initiation, n = 848 460; cigarettes per day, n = 216 590; smoking cessation, n = 378 249; alcoholic drinks per week, n = 630 154; alcohol dependence, n = 46 568). The main analysis, inverse-variance weighted regression, was verified by a wide range of sensitivity methods.
There was strong evidence that liability to alcohol dependence decreased amygdala and hippocampal volume, and smoking more cigarettes per day decreased hippocampal volume. From subcortical brain volumes to substance use, there was no or weak evidence for causal effects.
Our findings suggest that heavy alcohol use and smoking can causally reduce subcortical brain volume. This adds to accumulating evidence that alcohol and smoking affect the brain, and likely mental health, warranting more recognition in public health efforts.
To assess changes in daily habits, food choices and lifestyle of adult Brazilians before and during the COVID-19 pandemic.
This observational study was carried out with Brazilian adults through an online questionnaire 5 months after the social distance measures implementation. The McNemar, McNemar–Bowker and Wilcoxon tests were used to investigate differences before and during the COVID pandemic period, adopting the statistical significance of P < 0·05.
Totally, 1368 volunteers aged 18+ years.
The volunteers reported a lower frequency of breakfast, morning and lunch snacks (P < 0·05) and a higher frequency of evening snacks and other meal categories during the pandemic period (P < 0·05). The results showed an increase in the consumption of bakery products, instant meals and fast food, while the consumption of vegetables and fruits decreased (P < 0·005). There was a significant increase in the frequency of consumption of alcoholic beverages (P < 0·001), but a reduction in the dose (P < 0·001), increased frequency of smoking (P = 0·007), an increase in sleep and screen time in hours and decrease in physical activity (P < 0·001).
It was possible to observe an increase in screen time, hours of sleep, smoking and drinking frequency. On the other hand, there was a reduction in the dose of alcoholic beverages but also in the practice of physical activity. Eating habits also changed, reducing the performance of daytime meals and increasing the performance of nighttime meals. The frequency of consumption of instant meals and fast food has increased, while consumption of fruits and vegetables has decreased.
Electronic cigarettes have been a popular alternative to tobacco smoking. The effect of tobacco smoking on nasal airway resistance has been investigated before; however, the effect of the aerosol generated by electronic cigarettes is still unknown. This study aimed to evaluate the short-term effects of e-cigarettes on nasal airway resistance.
Sixty-one participants were recruited into a vapers group and a control group. The vapers group was instructed to smoke for 5 minutes, and their nasal resistance was measured pre-procedure and at 1 and 5 minutes post-procedure. The results were compared between both groups.
Repeated measures analysis of variance demonstrated that vaping has no statistically significant effect on total nasal airway resistance.
Although the differences between both groups were not statistically significant overall, the vapers group showed a reduction in nasal airway resistance in the short term.
Poor mental health has consistently been associated with substance use (smoking, alcohol drinking, cannabis use, and consumption of caffeinated drinks). To properly inform public health policy it is crucial to understand the mechanisms underlying these associations, and most importantly, whether or not they are causal.
In this pre-registered systematic review, we assessed the evidence for causal relationships between mental health and substance use from Mendelian randomization (MR) studies, following PRISMA. We rated the quality of included studies using a scoring system that incorporates important indices of quality, such as the quality of phenotype measurement, instrument strength, and use of sensitivity methods.
Sixty-three studies were included for qualitative synthesis. The final quality rating was ‘−’ for 16 studies, ‘– +’ for 37 studies, and ‘+’for 10 studies. There was robust evidence that higher educational attainment decreases smoking and that there is a bi-directional, increasing relationship between smoking and (symptoms of) mental disorders. Another robust finding was that higher educational attainment increases alcohol use frequency, but decreases binge-drinking and alcohol use problems, and that mental disorders causally lead to more alcohol drinking without evidence for the reverse.
The current MR literature increases our understanding of the relationship between mental health and substance use. Bi-directional causal relationships are indicated, especially for smoking, providing further incentive to strengthen public health efforts to decrease substance use. Future MR studies should make use of large(r) samples in combination with detailed phenotypes, a wide range of sensitivity methods, and triangulate with other research methods.
This narrative review provides mechanistic insight into the biological link between smoking and/or chronic excess alcohol consumption, and increased risk of developing sarcopenia. Although the combination of excessive alcohol consumption and smoking is often associated with ectopic adipose deposition, this review is focused on the context of a reduced caloric intake (leading to energy deficit) that also may ensue due to either lifestyle habit. Smoking is a primary cause of periodontitis and chronic obstructive pulmonary disease that both induce swallowing difficulties, inhibit taste and mastication, and are associated with increased risk of muscle atrophy and mitochondrial dysfunction. Smoking may contribute to physical inactivity, energy deficit via reduced caloric intake, and increased systemic inflammation, all of which are factors known to suppress muscle protein synthesis rates. Moreover, chronic excess alcohol consumption may result in gut microbiota dysbiosis and autophagy-induced hyperammonemia, initiating the up-regulation of muscle protein breakdown and down-regulation of muscle protein synthesis via activation of myostatin, AMPK and REDD1, and deactivation of IGF-1. Future research is warranted to explore the link between oral healthcare management and personalised nutrition counselling in light of potential detrimental consequences of chronic smoking on musculoskeletal health outcomes in older adults. Experimental studies should investigate the impact of smoking and chronic excess alcohol consumption on the gut–brain axis, and explore biomarkers of smoking-induced oral disease progression. The implementation of behavioural change interventions and health policies regarding smoking and alcohol intake habits may mitigate the clinical and financial burden of sarcopenia on the healthcare system.
The aim of this study was to systematically assess the association between smoking and cardiovascular disease (CVD) and disease progression among novel coronavirus pneumonia (coronavirus disease 2019 (COVID-19)) cases. PubMed database and Cochrane Library database were searched by computer to seek the epidemiological data of COVID-19 cases and literatures regarding CVDs from 1 Jan to 6 October 2020. Two researchers independently conducted literature screening, data collection and the assessment of the risk of bias of the studies included. RevMan 5.2 software was employed for meta-analysis. Funnel plot was adopted to assess the publication bias. On the whole, 21 studies comprising 7041 COVID-19 cases were included. As revealed from the meta-analysis, 14.0% (984/7027) of cases had a history of smoking, and 9.7% (675/6931) were subject to underlying CVDs. Cases with a history of smoking achieved a higher rate of COVID-19 disease progression as opposed to those having not smoked (OR 1.53, 95% CI 1.29–1.81, P < 0.00001), while no significant association could be found between smoking status and COVID-19 disease progression (OR 1.23, 95% CI 0.93–1.63, P = 0.15). Besides, smoking history elevated the mortality rate by 1.91-fold (OR 1.91, 95% CI 1.35–2.69, P = 0.0002). Moreover, underlying CVD elevated the incidence of severe disease by 2.87-fold (OR 2.87, 95% CI 2.29–3.61, P < 0.00001) and mortality by 3.05-fold (OR 3.05, 95% CI 1.82–5.11, P < 0.0001) in COVID-19 cases. As demonstrated from the current evidence, smoking displays a strong association with COVID-19 disease progression and mortality, and intensive tobacco control is imperative. Moreover, cases with CVD show a significantly elevated risk of disease progression and death when subject to COVID-19. However, the association between COVID-19 and CVD, and the potential effect exerted by smoking in the development of the two still require further verifications by larger and higher quality studies.