scholarly journals Tobacco Smoke and CYP1A2 Activity in a US Population with Normal Liver Enzyme Levels

2021 ◽  
Vol 18 (5) ◽  
pp. 2225
Author(s):  
Alexis Garduno ◽  
Tianying Wu
Keyword(s):  
Liver Enzyme ◽  
Liver Enzymes ◽  
Smoking Status ◽  
Caffeine Intake ◽  
Tobacco Exposure ◽  
Normal Range ◽  
Alcoholic Fatty Liver ◽  
Smoking Intensity ◽  
Cyp1a2 Activity ◽  
Never Smokers

Non-alcoholic fatty liver disease (NAFLD) is common among 30% of American adults. Former and current smokers are at higher risk for NAFLD compared to never smokers. The ratio of urine caffeine metabolites to caffeine intake—namely, urine caffeine metabolite indices—has previously been used as a proxy for CYP1A2 activity, which is one of the main liver metabolizing enzymes. CYP1A2 activity is associated with NAFLD progression. No studies to our knowledge have examined the associations of liver enzymes, smoking intensity, and secondhand smoke (SES) with CYP1A2 activity (using caffeine metabolite indices) across smoking status. We analyzed national representative samples from the 2009–2010 National Health and Nutrition Examination Survey (NHANES). Interestingly, even within a normal range, several liver enzymes were associated with caffeine metabolite indices, and patterns of many of these associations varied by smoking status. For instance, within a normal range, aspartate aminotransferase (AST) in never smokers and bilirubin in current smokers were inversely associated with 1-methyluric acid and 5-acetylamino-6-amino-3-methyluracil (URXAMU). Furthermore, we observed a common pattern: across all smoking statuses, higher AST/alanine aminotransferase (AST/ALT) was associated with 1-methyluric acid and URXAMU. Moreover, in current smokers, increased lifelong smoking intensity was associated with reduced caffeine metabolite indices, but acute cigarette exposure as measured by SES levels was associated with increased caffeine metabolite indices among never smokers. In summary, commonly used liver enzyme tests can reflect the CYP1A2 activity even within a normal range, but the selection of these enzymes depends on the smoking status; the associations between smoking and the CYP1A2 activity not only depend on the intensity but also the duration of tobacco exposure.

scholarly journals Current Smoking Dose-Dependently Associated with Decreasedβ-Cell Function in Chinese Men without Diabetes

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Chun Wang ◽  
Yijun Wang ◽  
Junxia Wu ◽  
Suyi Liu ◽  
Ying Zhu ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Cell Function ◽  
Smoking Status ◽  
Oral Glucose ◽  
Model Assessment ◽  
Current Smoking ◽  
Chinese Men ◽  
Smoking Intensity ◽  
Chronic Smoking ◽  
Never Smokers

The aim of this study was to evaluate the associations between chronic smoking and insulin resistance andβ-cell function in Chinese men without diabetes. A total of 1,568 participants were recruited by multistage sampling. Using homeostatic model assessment (HOMA), geometric means of insulin resistance (HOMA-IR) andβ-cell function (HOMA-β) with 95% confidence interval (CI) were calculated by general linear model. Odds ratios (ORs) with 95% CI were estimated to evaluate the associations between smoking status and insulin resistance andβ-cell deficiency under a logistic regression model. Current smokers had higher levels of 2 h glucose (6.66 versus 6.48 mmol/L) for oral glucose tolerance test and lower levels of fasting insulin (5.68 versus 6.03 mU/L) than never smokers. The adjusted means for HOMA-β(%) were 54.86 in current smokers and 58.81 in never smokers (P=0.0257). Current smoking was associated withβ-cell deficiency (OR 1.29, 95% CI 1.01–1.64) compared to never smoking. Theβ-cell function gradually decreased with increasing smoking intensity (Ptrend=0.0026), and the differences were statistically significant when the pack-year of smoking was 20 or above. No association was observed between smoking status and HOMA-IR. Our study suggested that chronic smoking may dose-dependently suppress insulin secretion in Chinese men.

scholarly journals Effect of cranberry supplementation on liver enzymes and cardiometabolic risk factors in patients with NAFLD: a randomized clinical trial

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Kourosh Masnadi Shirazi ◽  
Elham Shirinpour ◽  
Arman Masnadi Shirazi ◽  
Zeinab Nikniaz
Keyword(s):  
Risk Factors ◽  
Clinical Trial ◽  
Placebo Group ◽  
Hepatic Steatosis ◽  
Liver Enzyme ◽  
Cardiometabolic Risk ◽  
Liver Enzymes ◽  
Cardiometabolic Risk Factors ◽  
Alcoholic Fatty Liver ◽  
The Mean

Abstract Background We aimed to evaluate the effect of cranberry supplementation on serum liver enzymes, hepatic steatosis, and cardiometabolic risk factors in patients with non-alcoholic fatty liver (NAFLD). Methods In the present parallel-designed randomized controlled clinical trial, 110 patients with NAFLD were enrolled. The patients were randomized to receive 144 mg cranberry capsule or placebo for 6 months. The primary efficacy of the treatment was lipid profile, glycemic measurements, and liver enzyme levels. Results The data were reported for 46 in the supplementation group and 48 in the placebo group. The patient’s mean (SD) age was 43.16 (11.08) years. No significant differences between groups were observed regarding the post-intervention level of liver enzyme. The mean after-intervention levels of total cholesterol (p < 0.001) and triglyceride (p = 0.01) were significantly lower in the intervention group compared with the placebo group. At the end of the study, the mean insulin and HOMA-IR levels were significantly lower in the cranberry group compared with the placebo group. Significantly more patients in the cranberry group experienced a decrease in steatosis level compared with the control group. Conclusion The results of the present study showed that cranberry supplementation had a positive effect on some lipid profiles, insulin resistance, and hepatic steatosis in patients with NAFLD. Trial registration IRCT20200725048200N1; first registration date: 11.8.2020.

scholarly journals Cigarette Smoking and Incident Stroke in Blacks of the Jackson Heart Study

2020 ◽  
Vol 9 (12) ◽  
Author(s):  
Adebamike A. Oshunbade ◽  
Wondwosen K. Yimer ◽  
Karen A. Valle ◽  
Donald Clark ◽  
Daisuke Kamimura ◽  
...  
Keyword(s):  
Cigarette Smoking ◽  
Smoking Status ◽  
Jackson Heart Study ◽  
Smoking Intensity ◽  
Heart Study ◽  
Increased Risk ◽  
Significant Difference ◽  
Never Smokers ◽  
The Relationship ◽  
Dose Dependent

Background Blacks are disproportionately affected by stroke compared with whites; however, less is known about the relationship between stroke and cigarette smoking in blacks. Therefore, we evaluated the relationship between cigarette smoking and all incident stroke in the JHS (Jackson Heart Study). Methods and Results JHS participants without a history of stroke (n=4410) were classified by self‐reported baseline smoking status into current, past (smoked at least 400 cigarettes/life), or never smokers at baseline (2000–2004). Current smokers were further classified by smoking intensity (number of cigarettes smoked per day [1–19 and ≥20]) and followed up for incident stroke (through 2015). Hazard ratios (HRs) for incident stroke for current and past smoking compared with never smoking were estimated with adjusted Cox proportional hazard regression models. After adjusting for cardiovascular risk factors, the risk for stroke in current smokers was significantly higher compared with never smokers (HR, 2.48; 95% CI, 1.60–3.83) but there was no significant difference between past smokers and never smokers (HR, 1.10; 95% CI, 0.74–1.64). There was a dose‐dependent increased risk of stroke with smoking intensity (HR, 2.28 [95% CI, 1.38–3.86] and HR, 2.78 [95% CI, 1.47–5.28] for current smokers smoking 1–19 and ≥20 cigarettes/day, respectively). Conclusions In a large cohort of blacks, current cigarette smoking was associated with a dose‐dependent higher risk of all stroke. In addition, past smokers did not have a significantly increased risk of all stroke compared with never smokers, which suggests that smoking cessation may have potential benefits in reducing the incidence of stroke in blacks.

scholarly journals Non-alcoholic fatty liver disease in polycystic ovary syndrome women

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Young Bin Won ◽  
Seok Kyo Seo ◽  
Bo Hyon Yun ◽  
SiHyun Cho ◽  
Young Sik Choi ◽  
...  
Keyword(s):  
Risk Factors ◽  
Liver Disease ◽  
Fatty Liver ◽  
Liver Enzyme ◽  
Fatty Liver Disease ◽  
Polycystic Ovary ◽  
Insulin Level ◽  
University Hospital ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

AbstractTo evaluate risk factors leading to non-alcoholic fatty liver disease (NAFLD) occurrence in polycystic ovarian syndrome (PCOS) women. A retrospective cohort study of a total of 586 women diagnosed with PCOS aged 13–35 years at the gynecology department at a university hospital was done to evaluate PCOS phenotype, metabolic syndrome (MetS) diagnosis, body composition, insulin sensitivity, sex hormones, lipid profile, liver function, and transient elastography (TE). In PCOS women with NAFLD compared to those without, MetS diagnosis (Hazard ratio [HR] 5.6, 95% Confidence interval [CI] 2.2–14.4, p < 0.01) and hyperandrogenism (HA) (HR 4.4, 95% CI 1.4–13.4, p = 0.01) were risk factors significantly associated with subsequent NAFLD occurrence, whereas 2-h insulin level in 75 g glucose tolerance test (GTT) (HR 1.2, 95% CI 0.5–2.5, p = 0.70) and body mass index (BMI) > 25 kg/m2 (HR 2.2, 95% CI 0.6–8.0, p = 0.24) was not. Among NAFLD patients who underwent TE, a higher number of MetS components indicated a worse degree of fibrosis and steatosis. MetS diagnosis and HA at PCOS diagnosis were risk factors associated with NAFLD, while 2-h insulin level in 75 g GTT and obesity were not. Although elevated aspartate aminotransferase levels were significant for NAFLD risk, liver enzyme elevations may not be present until late liver damage. Further prospective studies of PCOS women with MetS or HA are warranted to determine whether patients without liver enzyme elevations should undergo preemptive liver examinations.

scholarly journals Associations between smoking and blood-group, and the risk of dyslipidaemia amongst French women

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
C. J. MacDonald ◽  
A. L. Madika ◽  
G. Severi ◽  
A. Fournier ◽  
M. C. Boutron-Ruault
Keyword(s):  
Blood Group ◽  
Smoking Status ◽  
Effect Modification ◽  
Blood Groups ◽  
Cross Sectional ◽  
Increased Risk ◽  
Cardio Vascular Disease ◽  
Never Smokers ◽  
Cardio Vascular ◽  
Incident Cases

AbstractDyslipidaemia is a major risk factor for cardio-vascular disease, as it promotes atherosclerosis. While cross-sectional studies have identified higher serum cholesterol amongst individuals with the A blood group, there is less evidence from prospective studies whether this translates into a higher risk of dyslipidaemia that requires treatment, nor if this genetic factor interacts with smoking status. This study aimed to prospectively determine potential associations between smoking, ABO blood groups, and risk of incident dyslipidaemia requiring treatment, and to assess associations over strata of blood ABO group. We assessed associations between blood ABO group, smoking and dyslipidaemia in 74,206 women participating in the E3N cohort. We included women who did not have cardiovascular disease at baseline. Logistic regression was used to determine associations between ABO group, smoking and prevalent dyslipidaemia at baseline. Cox proportional hazard models were then used to determine if blood ABO group and smoking were associated with the risk of incident dyslipidaemia, amongst women free of dyslipidaemia at baseline. At baseline 28,281 women with prevalent dyslipidaemia were identified. Compared to the O-blood group, the non-O blood group was associated higher odds of with prevalent dyslipidaemia (ORnon-O = 1.09 [1.06: 1.13]). Amongst the women free of dyslipidaemia at baseline, 6041 incident cases of treated dyslipidaemia were identified during 454,951 person-years of follow-up. The non-O blood groups were associated with an increased risk of dyslipidaemia when compared to the O-group (HRnon-O = 1.16 [1.11: 1.22]), specifically the A blood-group (HRA = 1.18 [1.12: 1.25]). Current smokers were associated with an increased risk of incident dyslipidaemia (HR smokers = 1.27 [1.16: 1.37]), compared to never-smokers. No evidence for effect modification between smoking and ABO blood group was observed (p-effect modification = 0.45), although the highest risk was observed among AB blood group women who smoked (HR = 1.76 [1.22: 2.55]). In conclusion, the non-O blood groups, specifically the A group were associated with an increased risk of dyslipidaemia. Current smokers were associated with a 30% increased risk of dyslipidaemia. These results could aid in personalised approaches to the prevention of cardiovascular risk-factors.

Risk Factors for Olfactory and Gustatory Dysfunctions in Patients with SARS-CoV-2 Infection

2021 ◽  
pp. 1-8
Author(s):  
Francesca Galluzzi ◽  
Veronica Rossi ◽  
Cristina Bosetti ◽  
Werner Garavello
Keyword(s):  
Risk Factors ◽  
Smoking Status ◽  
Inverse Association ◽  
Current Smoking ◽  
Logistic Regression Models ◽  
Respiratory Allergies ◽  
History Of ◽  
Never Smokers ◽  
Smell Loss ◽  
Relevant Covariates

<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.

scholarly journals Smoking status and second-hand smoke biomarkers in COPD, asthma and healthy controls

2020 ◽  
Vol 6 (2) ◽  
pp. 00192-2019 ◽  
Author(s):  
Matteo Bradicich ◽  
Macé M. Schuurmans
Keyword(s):  
Sensitivity And Specificity ◽  
Smoking Status ◽  
Final Analysis ◽  
Integrated Approach ◽  
Second Hand Smoke ◽  
Healthy Controls ◽  
Tobacco Exposure ◽  
Urinary Cotinine ◽  
Pubmed Database ◽  
Shs Exposure

IntroductionTobacco smoke worsens COPD and asthma. For healthy individuals, quantifying active and second-hand smoke (SHS) exposure clarifies the epidemiology of tobacco consumption and the efficacy of nonsmoking measures. Identifying tobacco exposure biomarkers and cut-offs might allow the creation of sensitive and specific tests.AimWe describe the state-of-the-art serum, urinary cotinine and exhaled carbon monoxide (CO) cut-offs for assessing smoking status and SHS exposure in adult patients with COPD or asthma, and healthy controls.MethodologyAfter a keyword research in the PubMed database, we included papers reporting on the cut-offs of the investigated biomarkers in one of the populations of interest. Papers published before 2000, not in English, or reporting only data on nonadult subjects or on pregnant women were excluded from the analysis. 14 papers were included in the final analysis. We summarised diagnostic cut-offs for smoking status or SHS exposure in COPD, asthmatic and healthy control cohorts, reporting sensitivity and specificity when available.ConclusionSerum and urinary cotinine and exhaled CO are easy-to-standardise, affordable and objective tests for assessing smoking status and SHS exposure. Evidence on cut-offs with good sensitivity and specificity values is available mainly for healthy controls. For COPD and asthmatic patients, most of the currently available evidence focuses on exhaled CO, while studies on the use of cotinine with definite sensitivity and specificity values are still missing. Solid evidence on SHS exposure is available only for healthy controls. An integrated approach with a combination of these markers still needs evaluation.

scholarly journals Self-reported and cotinine-verified smoking and increased risk of incident hearing loss

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Woncheol Lee ◽  
Yoosoo Chang ◽  
Hocheol Shin ◽  
Seungho Ryu
Keyword(s):  
Smoking Status ◽  
Objective Measure ◽  
Self Report ◽  
Urinary Cotinine ◽  
Increased Risk ◽  
Former Smokers ◽  
Never Smokers ◽  
Time Varying Covariates ◽  
New Onset

AbstractWe examined the associations of smoking status and urinary cotinine levels, an objective measure of smoking, with the development of new-onset HL. This cohort study was performed in 293,991 Korean adults free of HL who underwent a comprehensive screening examination and were followed for up to 8.8 years. HL was defined as a pure-tone average of thresholds at 0.5, 1.0, and 2.0 kHz ≥ 25 dB in both ears. During a median follow-up of 4.9 years, 2286 participants developed new-onset bilateral HL. Self-reported smoking status was associated with an increased risk of new-onset bilateral HL. Multivariable-adjusted HRs (95% CIs) for incident HL comparing former smokers and current smokers to never-smokers were 1.14 (1.004–1.30) and 1.40 (1.21–1.61), respectively. Number of cigarettes, pack-years, and urinary cotinine levels were consistently associated with incident HL. These associations were similarly observed when introducing changes in smoking status, urinary cotinine, and other confounders during follow-up as time-varying covariates. In this large cohort of young and middle-aged men and women, smoking status based on both self-report and urinary cotinine level were independently associated with an increased incidence of bilateral HL. Our findings indicate smoking is an independent risk factor for HL.

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