A pilot study to examine the effects of smoking cessation on serum markers of inflammation in women at risk for cardiovascular disease.
Ontology highlight
ABSTRACT:
SUBMITTER: Reichert V
PROVIDER: S-EPMC2707500 | biostudies-other | 2009 Jul
REPOSITORIES: biostudies-other
Similar Datasets
Project description:ObjectiveTo evaluate longitudinal changes in 6 inflammatory markers that predict cardiovascular disease events among smokers making a quit attempt and to characterize their cross-sectional associations between smoking and smoking heaviness.Approach and resultsIn a longitudinal cohort study of contemporary smokers (n=1652), we evaluated (1) independent associations of smoking heaviness markers (exhaled carbon monoxide, cigarettes/d, pack-years) with inflammatory markers (C-reactive protein, D-dimer, fibrinogen, urinary F2 isoprostane:creatinine [F2:Cr] ratio, white blood cell [WBC] count, myeloperoxidase) and (2) the effects of smoking cessation and continued smoking on these inflammatory markers after 1 year, among the 888 smokers who made an aided quit attempt as part of a randomized comparative effectiveness trial or standard care. There were strong, independent associations between smoking heaviness markers and the F2:Cr ratio, WBC, and myeloperoxidase (all Padj<0.001), but not high-sensitivity C-reactive protein, D-dimer, or fibrinogen. Participants were mean (SD) 49.6 years old (11.6), 54% women, 34% non-white, and smoked 16.8 cigarettes/d (8.5) for 27.3 pack-years (18.6). After 1 year, the 344 successful abstainers gained more weight (4.0 [6.0] versus 0.4 [5.7] pounds; P<0.001) and had larger increases in insulin resistance scores (P=0.02) than continuing smokers. Despite these increases, abstainers had significant decreases in F2:Cr ratio (P<0.001) and WBC counts (P<0.001). Changes in other markers were not related to quitting.ConclusionsSmoking heaviness is associated with increased F2:Cr ratio, myeloperoxidase, and WBC counts. Cessation improves the F2:Cr ratio and WBC counts independent of weight change, suggesting reduced inflammation related to less oxidant stress.
| S-EPMC5269476 | biostudies-literature
Project description:Smoking increases mortality from all causes and has a crucial role in atherosclerotic cardiovascular disease (ASCVD). Active smoking and secondhand smoke exposure determine more than 30% of coronary heart disease (CHD) mortality. The exact mechanisms of cardiovascular damages are not well known, but the detrimental effect of smoking on endothelial function has long been recognized. Smoking elicits oxidative processes, negatively affects platelet function, fibrinolysis, inflammation and vasomotor function; all these proatherogenic effects double the 10-year risk of fatal events in smokers compared to non smokers. An intriguing issue about smoking is the vulnerability of female gender. The mortality from cardiovascular diseases (CVDs) is higher in female than male smokers and female smokers show a 25% higher risk of developing CHD than men with the same exposure to tobacco smoke. This female vulnerability seems to be related to genes involved in thrombin signaling. The effects of smoking cessation have also been extensively studied. Cessation at an early age (40 years) has an impressive 90% reduction in the excess risk of death. In this review we report recent data about the causal link between smoking and CVDs and about the benefits of smoking cessation.
| S-EPMC7399440 | biostudies-literature
Project description:ImportanceThe time course of cardiovascular disease (CVD) risk after smoking cessation is unclear. Risk calculators consider former smokers to be at risk for only 5 years.ObjectiveTo evaluate the association between years since quitting smoking and incident CVD.Design, setting, and participantsRetrospective analysis of prospectively collected data from Framingham Heart Study participants without baseline CVD (original cohort: attending their fourth examination in 1954-1958; offspring cohort: attending their first examination in 1971-1975) who were followed up through December 2015.ExposuresTime-updated self-reported smoking status, years since quitting, and cumulative pack-years.Main outcomes and measuresIncident CVD (myocardial infarction, stroke, heart failure, or cardiovascular death). Primary analyses included both cohorts (pooled) and were restricted to heavy ever smokers (≥20 pack-years).ResultsThe study population included 8770 individuals (original cohort: n = 3805; offspring cohort: n = 4965) with a mean age of 42.2 (SD, 11.8) years and 45% male. There were 5308 ever smokers with a median 17.2 (interquartile range, 7-30) baseline pack-years, including 2371 heavy ever smokers (406 [17%] former and 1965 [83%] current). Over 26.4 median follow-up years, 2435 first CVD events occurred (original cohort: n = 1612 [n = 665 among heavy smokers]; offspring cohort: n = 823 [n = 430 among heavy smokers]). In the pooled cohort, compared with current smoking, quitting within 5 years was associated with significantly lower rates of incident CVD (incidence rates per 1000 person-years: current smoking, 11.56 [95% CI, 10.30-12.98]; quitting within 5 years, 6.94 [95% CI, 5.61-8.59]; difference, -4.51 [95% CI, -5.90 to -2.77]) and lower risk of incident CVD (hazard ratio, 0.61; 95% CI, 0.49-0.76). Compared with never smoking, quitting smoking ceased to be significantly associated with greater CVD risk between 10 and 15 years after cessation in the pooled cohort (incidence rates per 1000 person-years: never smoking, 5.09 [95% CI, 4.52-5.74]; quitting within 10 to <15 years, 6.31 [95% CI, 4.93-8.09]; difference, 1.27 [95% CI, -0.10 to 3.05]; hazard ratio, 1.25 [95% CI, 0.98-1.60]).Conclusions and relevanceAmong heavy smokers, smoking cessation was associated with significantly lower risk of CVD within 5 years relative to current smokers. However, relative to never smokers, former smokers' CVD risk remained significantly elevated beyond 5 years after smoking cessation.
| S-EPMC6704757 | biostudies-literature
Project description:IntroductionWhereas the overall association between smoking and rheumatoid arthritis (RA) must be regarded as established, considerably less is known about how much smoking is needed to increase the risk of RA, that is, the effect of smoking intensity, duration and cessation.MethodsThe Swedish Mammography Cohort, including 34,101 women aged 54 to 89 years, was followed up from January 1, 2003 through December 31, 2010 (219 RA cases identified). Relative risks (RR) and their 95% confidence intervals (CI) were estimated as rate ratios using Cox proportional hazards model.ResultsThere was a statistically significant association between smoking intensity (RR comparing 1 to 7 cigarettes/day vs never smoking 2.31 (95% CI: 1.59, 3.36)) as well as duration of smoking (comparing 1 to 25 years vs never smoking RR = 1.60 (95% CI: 1.07, 2.38)) and risk of RA. Compared to never smokers, the risk was still significantly elevated 15 years after smoking cessation (RR = 1.99 (95% CI: 1.23, 3.20)). However, among former smokers, the risk of RA seemed to be decreasing over time since stopping smoking: women who stopped smoking 15 years before the start of the follow-up had 30% lower risk of RA compared to those who stopped only a year before start of the follow-up (RR = 0.70 (95% CI: 0.24,2.02)).ConclusionsThis prospective study highlights that even light cigarette smoking is associated with increased risk of RA in women and that smoking cessation may reduce, though not remove, this risk.
| S-EPMC3672738 | biostudies-literature
Project description:BACKGROUND:Weight gain frequently occurs after smoking cessation (SC); the risk of new-onset diabetes mellitus increases for several years after SC. However, no large-scale, randomized controlled trials have examined the effects of nutritional guidance on post-SC cardiovascular risk. The current trial will enroll individuals who successfully quit smoking with the help of a SC clinic and who gain weight, to determine the effects of nutritional guidance on cardiovascular, glucose, and lipid metabolism biomarkers. METHODS/DESIGN:This is a multicenter, prospective, parallel-group, randomized controlled trial. Some 250 individuals who successfully quit smoking with the help of a SC clinic and who gain weight (an increase of ??1.25% Body Mass Index (BMI) between the first and the fifth visit to the SC clinic) will be enrolled within 1 month of the final (fifth) visit to the SC clinic. These participants will be randomly assigned to an intervention group (125 individuals receiving nutritional guidance) or a control group (125 individuals not receiving nutritional guidance). A registered dietitian will provide nutritional guidance once every 3 months for a total of three sessions. The primary endpoint for this trial will be the level of adiponectin, a predictor of cardiovascular risk that reflects weight and smoking status. Secondary endpoints will be levels of cardiovascular, glucose, and lipid metabolism biomarkers, BMI, abdominal circumference, and the percentage of individuals who quit smoking for a prolonged period. DISCUSSION:This trial will determine the benefits of nutritional guidance with respect to post-SC weight gain. The findings should provide useful information for devising a quality protocol for SC education to prevent cardiovascular disease. TRIAL REGISTRATION:The study is registered at the University Hospital Medical Information Network Clinical Trials Registry ( UMIN000030282 ). Registered on 6 December 2017.
| S-EPMC6172844 | biostudies-other
Project description:Smoking is associated with an increased risk of total and cause-specific death, but the rate of mortality risk reduction after quitting compared with continuing to smoke is uncertain. There is inadequate or insufficient evidence to infer the presence or absence of a causal relationship between smoking and ovarian cancer and colorectal cancer.To assess the relationship between cigarette smoking and smoking cessation on total and cause-specific mortality in women.Prospective observational study of 104,519 female participants in the Nurses' Health Study with follow-up from 1980 to 2004.Hazard ratios (HRs) for total mortality, further categorized into vascular and respiratory diseases, lung cancer, other cancers, and other causes.A total of 12,483 deaths occurred in this cohort, 4485 (35.9%) among never smokers, 3602 (28.9%) among current smokers, and 4396 (35.2%) among past smokers. Compared with never smokers, current smokers had an increased risk of total mortality (HR, 2.81; 95% confidence interval [CI], 2.68-2.95) and all major cause-specific mortality. The HR for cancers classified by the 2004 surgeon general's report to be smoking-related was 7.25 (95% CI, 6.43-8.18) and 1.58 (95% CI, 1.45-1.73) for other cancers. Compared with never smokers, the HR for colorectal cancer was 1.63 (95% CI, 1.29-2.05) for current smokers and 1.23 (95% CI, 1.02-1.49) for former smokers. A significant association was not observed for ovarian cancer. Significant trends were observed for earlier age at initiation of smoking for total mortality (P = .003), respiratory disease mortality (P = .001), and all smoking-related cancer mortality (P = .001). The excess risk for all-cause mortality decreases to the level of a never smoker 20 years after quitting, with different time frames for risk reduction observed across outcomes. Approximately 64% of deaths among current smokers and 28% of deaths among former smokers were attributable to cigarette smoking.Most of the excess risk of vascular mortality due to smoking in women may be eliminated rapidly upon cessation and within 20 years for lung diseases. Postponing the age of smoking initiation reduces the risk of respiratory disease, lung cancer, and other smoking-related cancer deaths but has little effect on other cause-specific mortality. These data suggest that smoking is associated with an increased risk of colorectal cancer mortality but not ovarian cancer mortality.
| S-EPMC2879642 | biostudies-other
Project description:ObjectiveThere is some evidence for biomarker feedback when combined with cessation counseling for reducing smoking in pregnancy. This randomized controlled pilot study evaluated feasibility and potential efficacy of a social-cognitive theory (SCT)-based biomarker feedback intervention among pregnant Alaska Native (AN) smokers.MethodsParticipants were randomly assigned to receive three study calls (10-20 min each): (1) biomarker feedback intervention (n = 30) including personalized cotinine results and feedback on their baby's likely exposure to carcinogen metabolite NNAL, or (2) contact control usual care condition based on the 5As (n = 30). Assessments were conducted at baseline, post-treatment, and delivery.ResultsHigh rates of treatment compliance, study retention, and treatment acceptability were observed in both groups. 7-day point prevalence smoking abstinence rates at delivery verified with urinary cotinine were the same in both study groups (20% intent-to-treat analysis, 26% per-protocol). SCT-based measures did not change differentially from baseline by study group.ConclusionThis trial supports the feasibility and acceptability of providing biomarker feedback within the clinical care delivery system, but the intervention did not promote increased smoking cessation during pregnancy compared to usual care.Practice implicationsEfforts are needed to promote the usual care and to develop alternative biomarker feedback messaging for pregnant AN women.
| S-EPMC6421103 | biostudies-literature
Project description:Smoking has a well-documented detrimental effect on risk for myocardial infarction and stroke, but less information is available regarding peripheral artery disease (PAD), particularly among women.To prospectively assess the association of current smoking status, cumulative smoking exposure, and smoking cessation with incident symptomatic PAD in women.Prospective cohort study.U.S. female health care professionals in the Women's Health Study.39,825 women with no cardiovascular disease who were prospectively followed for a median of 12.7 years.Incidence of symptomatic PAD. Cox proportional hazards models were used to compare PAD risk across smoking categories.178 confirmed PAD events occurred. Across the 4 smoking categories (never, former, <15 cigarettes/d, and ?15 cigarettes/d), age-adjusted incidence rates were 0.12, 0.34, 0.95, and 1.63 per 1000 person-years of follow-up, respectively. Multivariate adjustment had little effect on this relationship (adjusted hazard ratios [HRs], 3.14 [95% CI, 2.01 to 4.90], 8.93 [CI, 5.02 to 15.89], and 16.95 [CI, 10.77 to 26.67], respectively, vs. women who never smoked). Additional adjustment for high-sensitivity C-reactive protein and soluble intercellular adhesion molecule-1 levels among women with available blood samples (28,314 participants, 117 events) attenuated risk estimates (HR, 5.58 [CI, 2.61 to 11.93] for smoking <15 cigarettes/d and 9.52 [CI, 5.17 to 17.53] for smoking ?15 cigarettes/d). Lifetime exposure showed a strong dose-response relationship; fully adjusted HRs for smoking abstinence of fewer than 10, 10 to 29, and 30 or more pack-years were 2.52 (CI, 1.49 to 4.25), 6.75 (CI, 4.33 to 10.52), and 11.09 (CI, 6.94 to 17.72), respectively. Compared with current smokers, the adjusted HRs for fewer than 10 years, 10 to 20 years, more than 20 years, or lifelong abstinence were 0.39 (CI, 0.24 to 0.66), 0.28 (CI, 0.17 to 0.46), 0.16 (CI, 0.10 to 0.26), and 0.08 (CI, 0.05 to 0.12), respectively.The use of symptomatic PAD as the a priori primary end point excludes asymptomatic disease.Among initially healthy women, smoking is a potent risk factor for symptomatic PAD and was associated with subclinical inflammation. Smoking cessation substantially reduces risk for PAD, but an increased occurrence of PAD persists even among former smokers who maintain abstinence.The National Heart, Lung, and Blood Institute and National Cancer Institute.
| S-EPMC3111942 | biostudies-literature
Project description:Background: Smoking exerts detrimental effects during the progression of atherosclerotic vascular disease. Serum cystatin C is useful in the evaluation of early renal dysfunction and serves as a cardiovascular prognostic marker. This study measured changes in serum cystatin C after smoking cessation (SC). Methods and Results: In this study, patients who visited the SC clinic for the first time and succeeded in SC for 1 year were enrolled. In the entire cohort of 86 patients, body mass index (BMI, P<0.001) and waist circumference (WC, P<0.001) increased significantly at 3 months after SC compared with baseline. These values were further increased significantly (BMI, P<0.001; WC, P<0.001) from 3 months to 1 year after SC. Serum cystatin C decreased significantly at 3 months (P=0.045) after SC, and remained unchanged (P=0.482) from 3 months to 1 year after SC. Percent change from baseline to 3 months after SC in serum cystatin C was correlated with the percent change in serum monocyte chemoattractant protein 1 (P=0.047). Conclusions: Serum cystatin C, a marker of chronic kidney disease, was significantly reduced at 3 months after SC.
| S-EPMC7897701 | biostudies-literature
Project description:Pharmacogenetic clinical trials seek to identify genetic modifiers of treatment effects. When a trial has collected data on many potential genetic markers, a first step in analysis is to screen for evidence of pharmacogenetic effects by testing for treatment-by-marker interactions in a statistical model for the outcome of interest. This approach is potentially problematic because (i) individual significance tests can be overly sensitive, particularly when sample sizes are large; and (ii) standard significance tests fail to distinguish between markers that are likely, on biological grounds, to have an effect, and those that are not. One way to address these concerns is to perform Bayesian hypothesis tests [Berger (1985) Statistical decision theory and Bayesian analysis. New York: Springer; Kass and Raftery (1995) J Am Stat Assoc 90:773-795], which are typically more conservative than standard uncorrected frequentist tests, less conservative than multiplicity-corrected tests, and make explicit use of relevant biological information through specification of the prior distribution. In this article we use a Bayesian testing approach to screen a panel of genetic markers recorded in a randomized clinical trial of bupropion versus placebo for smoking cessation. From a panel of 59 single-nucleotide polymorphisms (SNPs) located on 11 candidate genes, we identify four SNPs (one each on CHRNA5 and CHRNA2 and two on CHAT) that appear to have pharmacogenetic relevance. Of these, the SNP on CHRNA5 is most robust to specification of the prior. An unadjusted frequentist test identifies seven SNPs, including these four, none of which remains significant upon correction for multiplicity. In a panel of 43 randomly selected control SNPs, none is significant by either the Bayesian or the corrected frequentist test.
| S-EPMC2655206 | biostudies-literature