There is a lack of robust research investigating the association between neurocognitive impairments and chronic tobacco smoking in adolescents/young adults. Therefore, a systematic review and meta-analysis were conducted to examine this association by pooling cross-sectional studies published from 1980 to 2023. The systematic review assessed the neurocognitive performances between chronic tobacco smokers and non-smokers in each study. The meta-analysis included six studies that compared chronic tobacco smokers against non-smokers using neuropsychological tests covering three neurocognitive domains. The results showed a cross-sectional association between impairpments in motor impulsivity across two aspects: reaction delay and incongruent errors, with the effect size being (SDM = 0.615, p = 0.000) and (SDM = 0.593, p = 0.000) respectively. However, no significant associations were found for intelligence (SDM = 0.221, p = 0.425) or working memory (SDM = 0.150, p = 0.581). This study highlights the need for further research to explore a greater number of neurocognitive domains in the context of chronic smoking in adolescents/young adults, particularly motor impulsivity, intelligence and working memory, as well as the socioeconomic factors involved. There is also a need to further study the effects of emerging alternative nicotine administration methods in this age group.

Smoking is a potent cause of asthma exacerbations, chronic obstructive pulmonary disease (COPD) and many other health defects, and changes in DNA methylation (DNAm) have been identified as a potential link between smoking and these health outcomes. However, most studies of smoking and DNAm have been done using blood and other easily accessible tissues in humans, while evidence from more directly affected tissues such as the lungs is lacking. Here, we identified DNAm patterns in the lungs that are altered by smoking. We used an established mouse model to measure the effects of chronic smoke exposure first on lung phenotype immediately after smoking and then after a period of smoking cessation. Next, we determined whether our mouse model recapitulates previous DNAm patterns observed in smoking humans, specifically measuring DNAm at a candidate gene responsive to cigarette smoke, Cyp1a1. Finally, we carried out epigenome-wide DNAm analyses using the newly released Illumina mouse methylation microarrays. Our results recapitulate some of the phenotypes and DNAm patterns observed in human studies but reveal 32 differentially methylated genes specific to the lungs which have not been previously associated with smoking. The affected genes are associated with nicotine dependency, tumorigenesis and metastasis, immune cell dysfunction, lung function decline, and COPD. This research emphasizes the need to study CS-mediated DNAm signatures in directly affected tissues like the lungs, to fully understand mechanisms underlying CS-mediated health outcomes.

Introduction Chronic proton-pump inhibitor (PPI) prescription is on the rise in the last decade with an increased prevalence in the elderly population. For most patients, this class of drugs is the primary treatment for various diseases. Even though PPIs are generally safe, long-term use has been associated with multiple adverse effects like bone fractures. The extent of the association between PPI and fracture is still unclear in women aged between 50 and 65 years. Besides, many other variables and risk factors must be accounted for in the analysis of this relation. Methods This is a retrospective case-control study looking at women 50-65 years of age who presented to Genesys Health for a low-impact fall. Data were extracted from electronic medical records and fracture outcomes; PPI therapy exposure and duration were determined. Chi-square analysis was performed to determine the association between chronic PPI therapy and fracture outcome and independently analyzed for major risk factors of osteoporosis, including smoking, low body mass index, and cancer. Results Patients in the chronic PPI therapy group were found to have a decreased fracture outcome overall in each subcategory of risk factors. When adjusting for all risk factors, there was a significant but weak association between chronic PPI therapy and increased fracture outcome. Conclusion With different results from previous studies, this study sheds new light on this debate. More studies need to be carried out to determine the association between chronic PPI therapy and fracture outcomes in postmenopausal women.

OBJECTIVE: One of the most important mechanisms by which smoking contributes to cardiovascular disease is endothelial dysfunction, including arterial stiffness. However, the effects of smoking and smoking cessation on arterial stiffness remain unclear. This meta-analysis aimed to evaluate the effect of smoking and smoking cessation on arterial stiffness in the adult population.
RESULTS: Random effects models were used to compute pooled estimates of effect size (ES) and their respective 95% confidence intervals (95% CIs) and %change in pulse wave velocity (PWv) (m/s) for the acute and chronic effect of smoking and smoking cessation, and for the effect of smoking cessation vs. the pooled ES estimate for the effect of smoking cessation vs. maintaining this behaviour. Thirteen studies were included in the meta-analysis. Smoking cessation decreased the PWv (ES -0.52, 95% CI -1.02 to -0.03, 3.5% m/s) compared to those maintaining this behaviour. Pooled estimates of both smoking conventional cigarettes and vaping significantly increased the PWv (ES 0.68, 95% CI 0.39-0.98, 10.0% m/s; and ES 0.37, 95% CI 0.14-0.61, 4.7% m/s, respectively). In addition, smoking cessation was effective in reducing arterial stiffness but only in healthy subjects (ES -0.95, 95% CI -1.85 to -0.05, -6.7% m/s). The chronic effect of smoking showed non-significant results on arterial stiffness.
CONCLUSIONS: Our results show that arterial stiffness levels decrease after smoking cessation. These findings are of clinical importance, as smoking cessation partially reverses the effects of smoking on arterial stiffness.

The evidence on the effects of chronic tobacco smoking on neuropsychological functions is conflicting. The literature remains limited by inconsistent accounting for potentially confounding biomedical and psychiatric conditions. This study aimed to assess the neuropsychological functions of adult chronic tobacco smokers in comparison to group-matched non-smokers.
The study included 73 smokers and 84 group-matched non-smokers. The data was collected during the year 2019. After an initial interview to collect demographics and smoking profile, the subjects undertook neuropsychological assessments that targeted a wide range of cognitive domains.
The performance of smokers was poorer on almost all neuropsychological domains, namely selective attention (p ≤ .001, p = .044), alternating attention (p = .002) working memory (p ≤ .001), Short-term memory (p = .006 and .003), Long-term memory (p ≤ .001), processing accuracy (p ≤ .001), and executive function (p = .011 and .026). Smokers were intact on processing speed. Smoking accumulation and lower age onset of regular smoking were correlated with lower neuropsychological function.
Our findings add to the growing body of evidence suggesting that chronic tobacco smoking impacts cognition negatively.

BACKGROUND: Previous studies based on voxel-based morphometry (VBM) had revealed brain gray matter (GM) changes in chronic smokers relative to nonsmokers. However, not all studies reported entirely consistent findings, or even opposite. The aim of this study was to conduct a quantitative meta-analysis of VBM studies of chronic smokers.
METHODS: A systematic database search was conducted in PubMed and Web of Knowledge from January 1, 2000 to January 31, 2020 to identify eligible VBM studies. Meta-analysis was performed with the Seed-based d Mapping software package to compare alternations between chronic cigarette smokers and nonsmokers. In addition, meta-regression analysis were performed to examine the influences of cigarette per day, smoking history and FTND.
RESULTS: A total of 17 VBM studies including 905 smokers and 1344 nonsmokers met the inclusion criteria. The results of this meta-analysis showed that the chronic smokers showed a robust GM volume decrease in bilateral prefrontal cortex and left insular and a GM increase in the right lingual cortex and left occipital cortex. Moreover, meta-regression analysis showed that cigarette per day, smoking history and FTND were partly associated with GM changes in chronic smokers.
CONCLUSIONS: This meta-analysis indicated that chronic cigarette smokers had significant and robust brain GM alternations compared with nonsmokers. Longitudinal studies should be performed in the future to explore whether these brain regions could be used as potential therapeutic neuro-target for nicotine dependence.

Chronic smokers have a greater risk for altered chemosensation, unhealthy dietary patterns, and excessive adiposity. In an observational study of chronic smokers, we modeled relationships between chemosensation, fat/carbohydrate liking, smoking-associated dietary behaviors, and body mass index (BMI). Also tested in the model was liking for sweet electronic cigarette juice (e-juice). Smokers (n = 135, 37 ± 11 years) were measured for: Taste genetics (intensity of 6-n-propylthiouracil-PROP); taste (NaCl and quinine intensities) and olfactory (odor identification) function; liking for cherry e-juice; and weight/height to calculate BMI. Smokers survey-reported their food liking and use of smoking for appetite/weight control. Structural equation models tested direct and indirect relationships between chemosensation, fat/carbohydrate liking, dietary behaviors, and BMI. In good-fitting models, taste intensity was linked to BMI variation through fat/carbohydrate liking (greater PROP intensity→greater NaCl intensity→greater food liking→higher BMI). Olfactory function tended to predict sweet e-juice liking, which, in turn, partially mediated the food liking and BMI association. The path between smoking-associated dietary behaviors and BMI was direct and independent of chemosensation or liking. These findings indicate that taste associates with BMI in chronic smokers through liking of fats/carbohydrates. Future research should determine if vaping sweet e-juice could improve diet quality and adiposity for smokers.

The link between neuropsychological impairments and chronic tobacco smoking is not clear and in the current literature there is a lack of robust analyses investigating this association. A systematic review of the literature was conducted in order to identify relevant longitudinal and cross-sectional studies conducted from 1946 to 2017. A meta-analysis was performed from 24 studies testing the performance of chronic tobacco smokers compared with non-smokers on neuropsychological tests related to eight different neuropsychological domains. The results revealed a cross-sectional association between neuropsychological impairments and chronic tobacco smoking in cognitive impulsivity, non-planning impulsivity, attention, intelligence, short term memory, long term memory, and cognitive flexibility, with the largest effect size being related to cognitive impulsivity (SDM = 0.881, p <0.005), and the smallest effect size being related to intelligence (SDM = 0.164, p < 0.05) according to Cohen\'s benchmark criteria. No association was found between chronic smoking and motor impulsivity (SDM = 0.105, p = 0.248). Future research is needed to investigate further this association by focusing on better methodologies and alternative methods for nicotine administration.

Both chronic smoking and trait anxiety have been associated with dysregulations in psychobiological stress response systems. However, these factors have not been studied in conjunction. We expected trait anxiety and smoking status to attenuate stress reactivity. Furthermore, we expected an allostatic load effect resulting in particularly attenuated stress reactivity in high-anxious smokers. In addition, high-anxious smokers were expected to exhibit increased urges to smoke in response to stress.
115 smokers and 37 nonsmokers, aged 18-64 years, completed a laboratory session including mental stressors such as evaluated public speaking and mental arithmetic. Trait anxiety was assessed using Spielberger\'s State-Trait Anxiety Inventory. Cardiovascular autonomic indices, salivary cortisol, and the desire to smoke were measured at baseline, during stressors, and at recovery.
Regression analyses showed that smokers exhibited attenuated cardiovascular stress responses in comparison to nonsmokers. Higher trait anxiety predicted attenuated systolic blood pressure responses to stress. No interaction effect of smoking status and trait anxiety was found in stress response measures. Higher trait anxiety predicted an increased desire to smoke in response to stress among smokers.
Results indicate that both smoking status and trait anxiety are associated with blunted sympatho-adrenal cardiovascular stress reactivity. Elevated urges to smoke in response to stress found among smokers with high trait anxiety suggest an important role of anxiety in smoking propensity and relapse.

BACKGROUND: Smoking has been known to cause endothelial dysfunction and bronchial carcinoma and duration of smoking has been implicated in the effects of smoking on regular smokers. This study evaluated the effects of long-term smoking on some coagulation markers in chronic smokers.
METHODS: A total of 78 chronic smokers (age, 41 ± 20 years) where grouped according to duration of time they have smoked (2-6 years, 7-11 years, 12-16 years and 17-21 years), and included in the study. Bleeding time (BT), whole-blood clotting time (WBCT), total platelet count (TPC), prothrombin time (PT) and activated partial thromboplastin time with kaolin (APTTK) were estimated in the subjects using standard operative procedures.
METHODS: Graph pad prism software (Statmate) version 2.0 and SPSS version 20.0 were used for the statistical analysis and the test of significance was calculated using paired Student\'s t-test.
RESULTS: There was an inverse correlation between the durations of smoking and BT, WBCT, PT and APTTK coagulation markers and a linear correlation between the different durations and TPC, in the chronic smokers. The strongest effects was in the 12-16 years and 17-21 years duration (P < 0.05).
CONCLUSIONS: The study revealed that long-term chronic cigarette-smoking can lead to haemostatic dysfunction in chronic smokers. Smoking should be generally discouraged as it could have far-reaching medical implications on this group of subjects, especially in bleeding emergency cases.