Does the association between smoking and mortality differ due to frailty status? A secondary analysis from the Mexican Health and Aging Study.

BACKGROUND: despite the well-known adverse health effects of smoking, evidence of these effects on frail individuals is still scarce. AIMS: to assess whether frailty influences the association between smoking and mortality. METHODS: individuals ≥50 years from the Mexican Health and Aging Study were analysed. Mortality rates from a 17-year follow-up were compared between smoking status groups (never, previous and current) and other smoking behaviour-related characteristics (pack-years, age commenced and cessation). Baseline variables were included to adjust the Cox regression models. First, models were adjusted for the whole sample, including an interaction term between the frailty index (FI) and smoking variables. A second set of models were stratified by FI levels: 0.00-0.10, 0.11-0.20, 0.21-0.30 and ≥ 0.31. RESULTS: from a total 14,025 individuals, mean age was 62.4 (95% confidence interval [95% CI]: 62.1-62.8) and 53.9% were women (95% CI: 52.4-55.6). Main results from the survival analyses showed that when including FI interaction term with smoking status, comparing current to never smoking, the hazard ratio (HR) was 2.03 (95% CI: 1.07-3.85, P = 0.029), and comparing current to previous smoking, the HR was 2.13 (95% CI: 1.06-4.26, P = 0.032). Models stratified by FI levels showed a significant HR only for the two highest level groups. Similar results were found for the smoking behaviour-related characteristics. DISCUSSION: our results suggest that frailty could modify smoking mortality risk. Other smoking characteristics were impacted by frailty, in particular, cessation. It was noteworthy that having ≥10 years of tobacco cessation was beneficial for frail individuals. CONCLUSIONS: smoking has a higher toll on frail individuals, but ceasing is still beneficial for this group.

Clinical and microbiological characteristics and inflammatory profile during an exacerbation of COPD due to biomass exposure. A comparison with COPD due to tobacco exposure.

BACKGROUND: Patients with biomass exposure-related COPD (BE-COPD) is a prevalent disease in developing countries and requires a detailed study of its clinical and inflammatory characteristics, specifying interventions that may differ from tobacco exposure-related COPD (TE-COPD). The objective was to describe clinical characteristics, biomarkers of inflammation, T-helper cells, and microbiological agents during a COPD exacerbation in BE-COPD in comparison with TE-COPD. METHODS: A prospective observational study in patients with moderate or severe exacerbation was recruited either in the emergency room or the COPD clinic. At enrollment, nasopharyngeal swabs and sputum were collected to identify viral and bacterial pathogens. Blood samples were also collected to measure inflammatory biomarkers and T-helper cells levels. Days of hospitalization and mechanical ventilation requirement was evaluated. RESULTS: Clinical characteristics, vaccination history, hospitalization, history of exacerbations, and microbiological pattern between BE-COPD and TE-COPD were similar. The Th2 profile was higher in BE-COPD than in TE-COPD (2.10 [range 1.30-3.30] vs. 1.40 [range 1.20-1.80], p = 0.001). The Th2/Th1 ratio was higher in BE-COPD than TE-COPD (1.22 [range 0.58-2.57 ] vs. 0.71 [range 0.40-1.15], p = 0.004). The need of mechanical ventilation (MV) was higher in TE-COPD than BE-COPD (13% vs. 31.1%, p = 0.01). Nonvaccination history and high CRP levels were significantly associated with hospitalization [OR 1.48 (CI 95% 1.30-4.61, p = 0.005) and OR 1.17 (CI 95% 1.10-1.24, p = 0.001), respectively]. CONCLUSIONS: Clinical characteristics, inflammatory markers, and microbiological isolates were similar in both groups but BE-COPD show a tendency to present higher inflammatory Th2 cells and low requirement MV compared with TE-COPD.

Air quality in Mexico City during the COVID-19 lockdown possibly decreased COPD exacerbations.

The reduction of air pollution during the #COVID19 lockdown in Mexico City possibly reduced the exacerbation rate in #COPD patients due to biomass and tobacco despite that the self-isolation was not as strict as expected. https://bit.ly/3Iyv98t.

Women with COPD from biomass smoke have reduced serum levels of biomarkers of angiogenesis and cancer, with EGFR predominating, compared to women with COPD from smoking.

The main causes of COPD are smoking (COPD-TS) and exposure to biomass smoke (COPD-BS), considered as different phenotypes. The association of COPD-TS with lung cancer (LC) is well established, but not in COPD-BS. Thus, we studied the serum concentration of cytokines that participate in inflammation, angiogenesis, and tumor progression, used frequently as LC biomarkers, in women with COPD-BS compared with COPD-TS (n = 70). Clinical and physiological characteristics and the serum concentration (multiplex immunoassay) of 16 cytokines were evaluated. The analysis revealed that women with COPD-BS were shorter and older, and had lower concentrations of 12 serum cytokines: 6 proinflammatory and angiogenic IL-6Rα, PECAM-1, leptin, osteopontin, prolactin, and follistatin; and 6 that participate in angiogenesis and in tumor progression FGF-2, HGF, sVEGFR-2, sHER2/neu, sTIE-2, G-CSF, and SCF. Notably, there was a significant increase in sEGFR in women with COPD-BS compared to women with COPD-TS. PDGF-AA/BB and sTIE-2 did not change. These findings suggest that women with COPD-BS have markedly decreased proinflammatory, angiogenic, and tumor progression potential, compared to women with COPD-TS, with sEGFR as the predominant mediator, which might reflect a differential pattern of inflammation in women exposed to BS, favoring the development of chronic bronchitis.

Participation of the miR-22-HDAC4-DLCO Axis in Patients with COPD by Tobacco and Biomass.

Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitation and systemic inflammation. The main causes of COPD include interaction between genetic and environmental factors associated with tobacco smoking (COPD-TS) and/or exposure to biomass smoke (COPD-BS). Several microRNAs (miRNAs) control posttranscriptional regulation of COPD-TS associated gene expression. The miR-22-HDAC4-IL-17 axis was recently characterized. It is still unknown, however, whether this axis, participates in COPD-BS. To investigate, 50 patients diagnosed with severe-to-very severe COPD GOLD (Global Initiative for Chronic Obstructive Lung Disease) stages III/IV, were recruited, 25 women had COPD-BS (never smokers, exposed heavily to BS) and 25 had COPD-TS. Serum levels of miRNA-22-3p were measured by RT (Reverse Transcription)-qPCR, while the concentration of HDAC4 (Histone deacetylase 4) was detected by ELISA. Additionally, we looked for association between serum HDAC4 and DLCOsb (Single-breath diffusing capacity of the lung for carbon monoxide), as % of predicted by age, height, and gender, one of the main differences described between COPD-BS and COPD-TS. Women with COPD-BS were older and shorter and had a higher DLCOsb %P (percent predicted) compared to COPD-TS. Serum miR-22-3p was downregulated in COPD-BS relative to COPD-TS. In contrast, the concentration of HDAC4 was higher in COPD-BS compared to COPD-TS. Furthermore, a positive correlation between serum HDAC4 levels and DLCOsb %P was observed. We concluded that the miR-22-HDAC4-DLCO axis behaves differently in patients with COPD-BS and COPD-TS.

miR-34a in serum is involved in mild-to-moderate COPD in women exposed to biomass smoke.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities. The main causes of COPD are Gene-environment interactions associated with tobacco smoking (COPD-TS) and biomass smoke (COPD-BS). It is well know that microRNAs (miRNAs) participate in the control of post-transcriptional regulation and are involved in COPD-TS; nevertheless, those miRNAS are participating in the COPD-BS are unidentified. Thus, we studied which miRNAs are involved in COPD-BS (GOLD stages I-II). METHODS: In the screening phase, the profile of the miRNAs was analyzed in serum samples (n = 3) by means of a PCR array. Subsequently, the miRNAs were validated with RT-qPCR (n = 25) in the corresponding study groups. Additionally, the serum concentration of Notch1 was measured comparing COPD-BS vs COPD-TS. RESULTS: miR-34a was down-regulated in COPD- BS vs COPD-TS. In the other study groups, three miRNAs were differentially expressed: miR-374a was down-regulated in COPD-BS vs C, miR-191-5p was up-regulated in COPD-BS vs H-BS, and miR-21-5p was down-regulated in COPD-TS compared to the C group. Moreover, the serum concentration of Notch1, one of the targets of miR-34a, was increased in COPD-BS compared to women with COPD-TS. CONCLUSIONS: This is the first study in patients with COPD due to biomass that demonstrates miRNA expression differences between patients. The observations support the concept that COPD by biomass has a different phenotype than COPD due to tobacco smoking, which could have important implications for the treatment of these diseases.

Women with COPD by biomass show different serum profile of adipokines, incretins, and peptide hormones than smokers.

BACKGROUND: The main causes of COPD are tobacco smoking (COPD-TS) and biomass smoke exposure (COPD-BS). COPD-TS is known to induce changes in adipokines, incretins, and peptide hormones, frequent biomarkers of inflammation; however, it is unknown if similar changes occur in COPD-BS. METHODS: Clinical and physiological characteristics, and serum concentration of C-peptide, ghrelin, GIP, GLP-1, glucagon, insulin, leptin, PAI-1, resistin, and visfatin were measured in women with COPD-BS, COPD-TS, and healthy controls. Data were compared with one-way ANOVA and Tukey's post hoc test; nonparametric were expressed as median (interquartile ranges), with Kruskal-Wallis and Dunn's post-hoc test. Multivariate analysis, age, BMI, MS, and FEV1% pred with levels of inflammatory mediators in COPD women. RESULTS: FEV1% pred, FVC% pred, and FEV1/FVC ratio were decremented in COPD. In COPD-TS increased C-peptide, ghrelin, GIP, GLP-1, and leptin, and reduced glucagon, PAI-1, resistin, and visfatin. In COPD-BS enlarged ghrelin, insulin, leptin, and PAI-1 comparatively with COPD-TS and control, while C-peptide and GLP-1 relatively with controls; conversely, glucagon, and resistin were reduced. Multivariate analysis showed association of ghrelin, insulin, PAI-1, and visfatin with BS exposure. CONCLUSIONS: women with COPD-BS have a distinct profile of adipokines, incretins, and peptide hormones, and specifically with ghrelin, insulin, PAI-1, and visfatin related to BS exposure.

Use of varenicline for more than 12 months for smoking cessation in heavy chronic obstructive pulmonary disease smokers unmotivated to quit: a pilot study.

INTRODUCTION: Use of varenicline for as long as necessary to achieve abstinence has not been studied. The aim of this study was to test whether smokers with mild-to-moderate chronic obstructive pulmonary disease (COPD) are able to quit if they use varenicline for a sufficient length of time. METHODS: A total of 30 heavy smokers with COPD took varenicline for sufficiently long enough for smoking cessation. Smokers were allowed to smoke without a fixed quit date. The main endpoints were the time of voluntary abstinence (VA) and the continuous abstinence rate (CAR) at 12 and 18 months. RESULTS: Of 28 subjects, eight subjects continued to smoke and 20 subjects stopped smoking, demonstrating a CAR up to 18 months (71%). Median time of treatment was 6 (range 3-24) and 2 (range 1-8) months for abstainers and non-abstainers, respectively, and the median time of VA for abstainers was 4 (range 1-21) months. CONCLUSIONS: Use of varenicline for more than the traditional 12 recommended weeks may be a good strategy to increase the cessation rate in heavy smokers with mild COPD.

Prevalence of chronic obstructive pulmonary disease in asymptomatic smokers.

BACKGROUND: Physicians do not routinely recommend smokers to undergo spirometry unless they are symptomatic. OBJECTIVE: To test the hypothesis that there are a significant number of asymptomatic smokers with chronic obstructive pulmonary disease (COPD), we estimated the prevalence of COPD in a group of asymptomatic smokers. METHODS: Two thousand nine hundred and sixty-one smokers with a cumulative consumption history of at least 10 pack-years, either smokers with symptoms or smokers without symptoms (WOS) were invited to perform a spirometry and complete a symptom questionnaire. RESULTS: Six hundred and thirty-seven (21.5%) smokers had no symptoms, whereas 2,324 (78.5%) had at least one symptom. The prevalence of COPD in subjects WOS was 1.5% when considering the whole group of smokers (45/2,961) and 7% when considering only the group WOS (45/637). From 329 smokers with COPD, 13.7% were WOS. Subjects WOS were younger, had better lung function and lower cumulative consumption of cigarettes, estimated as both cigarettes per day and pack-years. According to severity of airflow limitation, 69% vs 87% of subjects were classified as Global Initiative for Chronic Obstructive Lung Disease stages I-II in the WOS and smokers with symptoms groups, respectively (P<0.001). A multivariate analysis showed that forced expiratory volume in 1 second (mL) was the only predictive factor for COPD in asymptomatic smokers. CONCLUSION: Prevalence of COPD in asymptomatic smokers is 1.5%. This number of asymptomatic smokers may be excluded from the benefit of an "early" intervention, not just pharmacological but also from smoking cessation counseling. The higher forced expiratory volume in 1 second may contribute to prevent early diagnosis.

Prevalence and diagnosis of chronic obstructive pulmonary disease among smokers at risk. A comparative study of case-finding vs. screening strategies.

BACKGROUND: Early diagnosis of chronic obstructive pulmonary disease (COPD) remains the main intervention to prevent disease progression. However, conflicting results exist on the utility of two different diagnostic strategies that preclude freely recommending one strategy in favor of the other. Spirometry was used to determine the effectiveness of a symptom-based (case-finding) strategy vs. a screening strategy to detect COPD in smokers. METHODS: The case-finding strategy was undertaken during the COPD Day campaign in smokers with respiratory symptoms who were willing to submit to lung function testing. Screening was carried out with smokers attending a smoking cessation program. A short standardized questionnaire on respiratory symptoms along with spirometry were carried out and analyzed for both strategies. RESULTS: We evaluated 2781 smokers (mean pack/years 23.38): 1999 from the case-finding strategy and 782 from the smoking cessation program strategy (SCS). Prevalence of COPD according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria was 10.1 and 13.3%, respectively (p < 0.01). With the exception of dyspnea (70.6% vs. 72.5%, p = 0.72), prevalence of symptoms such as cough (61.5 vs. 37, p < 0.001), phlegm (60.4 vs. 38.2, p < 0.001) and wheezing (56.7 vs.15.06, p < 0.001) was higher among smokers from the case-finding strategy. Multivariate logistic regression analysis showed that dyspnea [OR = 2.09 (95% CI 1.41-3.1)] was the only common predictor of COPD after jointly and separately analyzing case-finding and screening strategies. CONCLUSIONS: For early diagnosis of COPD in a primary care setting, a screening strategy aimed at all smokers may be more useful than a case-finding strategy.

[Proposal of Latin-American guidelines for smoking cessation]. / Guías de atención médica para dejar de fumar. Una propuesta para Latinoamérica.

OBJECTIVE: Although prevalence of tobacco smoking is different in the Latin American regions, the consequences on health are similar. MATERIAL AND METHODS: Therefore, guidelines on treatment are needed and ideally speaking must be useful in the different countries. In order to make quick recommendations useful in the region we made a search in PubMed from the last 5 years with the titles "Smoking cessation guidelines" and "Smoking cessation treatment meta-analysis" to know the content of different guidelines and with the titles of "Nicotine replacement therapy", "Nicotine chewing gum", "Nicotine patches", "Nicotine inhaler", "Bupropion therapy", "Varenicline therapy" and "Individual and group behavioural counselling for smoking cessation" to determine the efficacy of each intervention. RESULTS AND CONCLUSION: Our recommendation based on the availability of pharmacotherapy and human resources is that medical advice and behavioural group counseling must be primary interventions either adding, or not, first line drugs for smoking cessation.

Guías de atención médica para dejar de fumar. Una propuesta para Latinoamérica / Proposal of Latin-American guidelines for smoking cessation

Objetivo. Aunque la prevalencia del tabaquismo es diferente en cada país de América, los daños a la salud se presentan en la misma proporción. Por ello, es indispensable contar con guías de tratamiento que idealmente sean de utilidad para todos los países. Material y métodos. Para hacer recomendaciones puntuales de utilidad a la región se realizó una búsqueda en PubMed de los últimos cinco años, con los títulos "Smoking cessation guidelines" y "Smoking cessation treatment meta-analysis" para conocer el contenido de las diferentes guías y de los títulos "Nicotine replacement therapy", "Nicotine chewing gum", "Nicotine patches" "Nicotine inhaler", "Bupropion therapy", "Varenicline therapy" e "Individual and grupal behavioural counselling for smoking cessation" para determinar la eficacia de cada intervención. Resultados y conclusión. Nuestra recomendación basada en la disponibilidad de medicamentos y de recursos humanos es que el consejo médico y la terapia conductual grupal deben ser acciones primarias acompañadas, o no, de medicamentos de primera línea.

Objective. Although prevalence of tobacco smoking is different in the Latin American regions, the consequences on health are similar. Material and Methods. Therefore, guidelines on treatment are needed and ideally speaking must be useful in the different countries. In order to make quick recommendations useful in the region we made a search in PubMed from the last 5 years with the titles "Smoking cessation guidelines" and "Smoking cessation treatment meta-analysis" to know the content of different guidelines and with the titles of "Nicotine replacement therapy", "Nicotine chewing gum", "Nicotine patches", "Nicotine inhaler", "Bupropion therapy", "Varenicline therapy" and "Individual and grupal behavioural counselling for smoking cessation" to determine the efficacy of each intervention. Results and conclusion. Our recommendation based on the availability of pharmacotherapy and human resources is that medical advice and behavioural grupal counseling must be primary interventions either adding, or not, first line drugs for smoking cessation.

[Differences in inflammatory markers in a non-smoking and smoking Mexican population]. / Diferencias de marcadores de inflamación entre fumadores y no fumadores en una población mexicana.

INTRODUCTION: Cigarette smoking is one of the main risk factors for the development of cancer, chronic obstructive pulmonary disease and cardiovascular disease, most of which exhibit an inflammatory component at some stage of their time-course. However, little is known about the early presence of proinflammatory markers in healthy smokers. MATERIAL AND METHODS: We conducted a 16-month, cross-sectional study to determine the presence of inflammatory markers in a group of smokers pronounced in good health after an exhaustive medical exam. Of an initial population of 1,806 smokers and non-smokers who underwent anthropometric, biochemical, radiographic and ultrasound studies plus exercise testing, 317 smokers and 297 non-smokers (the control group) found to have no alterations were ultimately selected and paired by age and gender. Their test data were then compared. RESULTS: In comparison with non-smokers, smokers showed higher levels of C-reactive protein, hemoglobin, hematocrit, platelets, lipid profile and cardiovascular risk. They also showed lower values of total proteins, albumin and lactic dehydrogenase. CONCLUSIONS: Even though laboratory value results were considered to be within normal range, smokers showed increased levels of prothrombotic and proinflammatory molecules. Therefore, tobacco smoking can be considered an inflammatory syndrome whose final outcome could be one of the many organic disorders that characterize and accompany this entity.

Association among C-reactive protein, Fatty liver disease, and cardiovascular risk.

Nonalcoholic fatty liver disease (NAFLD) is associated with several metabolic disturbances involving inflammation. Ultrasensitive C-reactive protein (uCRP), a marker of coronary heart disease and other chronic diseases, has not been investigated in NAFLD. We tested the relationship between uCRP and NAFLD in middle-aged asymptomatic subjects, independently of other metabolic disturbances associated with metabolic syndrome and cardiovascular risk. We compared 310 subjects with steatosis visible on ultrasound (cases) with 630 and without (controls). Body mass index (BMI), blood pressure and serum levels of uCRP, glucose, lipids, and lipoproteins were measured in all subjects. Differences between groups and the impact of serum uCRP levels were tested by univariate and multivariate logistic regression analysis. Cases were statistically different from controls in the frequency of metabolic syndrome (66.4% vs. 26.7%; P < 0.001). Cases were significantly older (P < 0.001), and had significantly higher values for BMI, glucose, total cholesterol and triglycerides (P < 0.001), and mean uCRP concentrations (4.5 vs. 2.79 mg/L; P < 0.001). By univariate analysis, variables significantly associated with cases were glucose (OR, 4.09; 95% CI, 2.98-5.61), BMI (OR 5.54; 95% CI, 4.09-7.49), and uCRP (OR 7.06; 95% CI, 4.51-11.02). By multivariate analysis, uCRP levels were associated with hepatic steatosis (OR 5.83; 95% CI, 3.07-11.06). Cardiovascular risk was also higher in subjects with NAFLD (4.7 vs. 2.8). Subjects with hepatic steatosis showed an increased concentration of uCRP independently of other metabolic disturbances; this suggests an increased risk of cardiovascular diseases and could be used as a marker of chronic inflammation.

Efecto del daño de vías dopaminérgicas mesencefálicas en la conducta adictiva al tabaco: Revisión generadora de una hipótesis / Mesencephalic dopaminergic tract lesions in tobacco addiction behavior: A review of mechanisms of disease and an hypothesis

El tabaquismo es la enfermedad prevenible que se relaciona con más problemas de salud y causas de muerte en el mundo. Se ha estimado una prevalencia de 1,100 millones de personas en el mundo con adicción al tabaco. La adicción a la nicotina depende de múltiples factores; está documentado que el sistema nervioso central desempeña un importante papel en su desarrollo a través de la estimulación de receptores neuronales dopaminérgicos por la nicotina. La dopamina tiene su principal síntesis en las neuronas de la sustancia nigra y área tegmental ventral del mesencéfalo, las cuales se proyectan hacia los núcleos básales y núcleo accumbens. Los estudios en animales sugieren que el sistema dopaminérgico está involucrado de manera importante en la adicción a la nicotina. Las lesiones neurotóxicas del sistema mesolfmbico o la administración sistémica de un bloqueador del receptor de nicotina reduce la administración de nicotina en roedores; sin embargo, estos hallazgos se han realizado en modelos animales, siendo difícil corroborarlos en humanos porque no se puede experimentar en ellos y causarles daño tóxico o vascular de las vías dopaminérgicas mesencefálicas. Una estrategia circunstancial apropiada podría llevarse a cabo analizando la conducta en términos de adicción de sujetos con lesiones del mesencéfalo, secundarias a un evento vascular cerebral.

Tobacco use, a well known cause of death, represents a preventable disease related to many health problems. Epidemiológical studies estimate a prevalence of 1,100 million tobacco dependent people. Nicotine addiction depends on multiple factors; studies have reported that the central nervous system plays an important role through the stimulation of neuronal dopaminergic nicotine receptors. The main dopamine synthesis sites are located in the neurons of the substantia nigra and the ventral tegmental area of the mesencephalus, which are projected towards the basal ganglia and accumbens nuclei. In vivo studies suggest that the dopaminergic cistern is highly implicated in nicotine dependence, showing that the neurotoxic lesions of the mesolimbic system or the systemic administration of nicotine receptor blockers reduce the quantity of nicotine administered. Nevertheless, these studies have been carried out in animal models; thus, such findings can not be confirmed in humans due to methodological limitations (i.e. it is unethical to produce toxic or vascular damage of the mesencephalic dopaminergic tracts). It could be possible to carry out such a study in patients with mesencephalic injuries secondary to stroke.

Smoking is not associated with nonalcoholic fatty liver disease.

AIM: To analyze the relationship between smoking and nonalcoholic fatty liver disease (NAFLD). METHODS: This is a cross-sectional study of a healthy population, carried out in a check-up unit of a university hospital in Mexico City. We enrolled 933 subjects, 368 current smokers (cases) and 565 persons who had never smoked (controls). Demographic, metabolic and biochemical variables were measured in the two groups. NAFLD was determined by ultrasound and metabolic syndrome according to ATPIII. RESULTS: A total of 548 men (205 cases and 343 controls) and 337 women (114 cases and 223 controls) were included in the analysis. Statistical differences between cases and controls were observed only in high blood pressure prevalence (6.6% vs 11.3%, P < 0.05; cases and controls respectively), high-density lipoproteins (1.00 +/- 0.26 vs 1.06 +/- 0.28 mmol/L, P < 0.005), triglycerides (2.18 +/- 1.49 vs 1.84 +/- 1.1 mmol/L, P < 0.001), and erythrocyte sedimentation rate (11.3 +/- 9.3 vs 13.5 +/- 11.9 mm/h, P < 0.001). No differences were observed in the prevalence of NAFLD (22.27% vs 29.68%, P = NS) and metabolic syndrome (41.69% vs 36.74%, P = NS). Univariate analysis showed that smoking was not a risk factor for NAFLD (OR = 0.89, 95% CI 0.65-1.21). CONCLUSION: No differences in NAFLD prevalence were observed between current smokers and nonsmokers, and furthermore, no differences were observed in heavy smokers (more than 20 packs/year), indicating that there is no relationship between smoking and NAFLD.