78 resultados para smokers


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Background: Not much is known about whether women who follow Pap testing recommendations report the same pattern of sexual behavior as women who do not.
Methods: Data come from part of a larger population-based computer-assisted telephone survey of 8656 Australians aged 16–64 years resident in Australian households with a fixed telephone line (Australian Longitudinal Study of Health and Relationships [ALSHR]). The main outcome measure in the current study was having had a Pap test in the past 2 years.
Results: Data on a weighted sample of 4052 women who reported sexual experience (ever had vaginal intercourse) were analyzed. Overall, 73% of women in the sample reported having a Pap test in the past 2 years. Variables individually associated with Pap testing behavior included age, education, occupation, cohabitation status, residential location, tobacco and alcohol use, body mass index (BMI), lifetime and recent number of opposite sex partners, sexually transmitted infection (STI) history, and condom reliance for contraception. In adjusted analyses, women in their 30s, those who lived with their partner, and nonsmokers were more likely to have had a recent Pap test. Those who drank alcohol at least weekly were more likely to have had a recent test than irregular drinkers or nondrinkers. Women with no sexual partners in the last year were less likely to have had a Pap test, and women who reported a previous STI diagnosis were more likely to have had a Pap test in the past 2 years.
Conclusions: There are differences in Pap testing behavior among Australian women related to factors that may affect their risk of developing cervical abnormalities. Younger women and regular smokers were less likely to report a recent test. Screening programs should consider the need to focus recruitment strategies for these women.

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Aims To examine the association of adolescent depression and anxiety symptoms with daily smoking and nicotine dependence in young adulthood.

Design A prospective cohort study of adolescent and young adult health (n = 1943). Teen assessments occurred at 6-monthly intervals, with two follow-up assessments in young adulthood (wave 7, 1998; wave 8, 2001–03).

Setting Victoria, Australia.

Participants Students who participated at least once during the first six (adolescent) waves of the cohort study.

Measurements Adolescent depression and anxiety symptomswere assessed using the Revised Clinical Interview Schedule (CIS-R).Young adult tobacco usewas defined as: daily use (6 or 7 days perweek) and dependent use (>4 on the Fagerstrom Test for Nicotine Dependence).

Findings Among adolescent ‘less than daily’ smokers, those with high levels of depression and anxiety symptoms had an increased risk of reporting nicotine dependence in young adulthood [odds ratio (OR) 3.3, 95% confidence interval (CI) 1.2–9.1] compared to young adults who had low levels of adolescent depression and anxiety symptoms, after adjusting for potential confounding factors. Similarly, in the adjusted model (OR 1.9, 95% CI 1.0–3.4), among adolescent ‘daily’ smokers, those with high levels of depression and anxiety symptoms had an almost two-fold increase in the odds of reporting nicotine dependence in young adulthood compared to young adults with low levels of adolescent depression and anxiety symptoms.

Conclusions Adolescent smokerswith depression and anxiety symptoms are at increased risk for nicotine dependence into young adulthood. They warrant vigilance from primary care providers in relation to tobacco use well into adulthood.

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Background: Whereas several epidemiological studies suggest that low dietary intake of vitamins C and E is linked to increased hip fracture in smokers and antioxidants (dietary and endogenous) are reduced in elderly osteoporotic women, none has demonstrated an effect of supplemental antioxidants on bone turnover.

Methods: In an observational study of 533 randomly selected women, we investigated the associations among the use of antioxidant supplements, vitamins C and E, serum levels of biochemical markers of bone turnover (C-telopeptide [CTx] and bone-specific alkaline phosphatase [BSAP]), and whole body bone mineral density (BMD).

Results: Twenty-two women were identified as current users of supplemental vitamin C or E. Duration of antioxidant supplement use was negatively associated with age-adjusted and weight-adjusted serum CTx, such that mean CTx levels (natural log transformed) were 0.022 units lower for each year of exposure. No significant differences were detected for adjusted serum BSAP or whole body BMD.

Conclusions: Our results suggest that antioxidant vitamin E or C supplements may suppress bone resorption in nonsmoking postmenopausal women. Coupling of bone formation and resorption may explain the absence of an effect on bone formation markers, given evidence of enhanced effects of antioxidants on osteoblast differentiation; this warrants further investigation. This work adds to the growing body of evidence that antioxidants may play a role in preventing osteoporosis.

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Dopamine is a key neurotransmitter of the mesolimbic reward pathway in the human brain, and tyrosine hydroxylase (TH) is the rate-limiting enzyme in dopamine biosynthesis. Consequently, the gene encoding TH is a strong candidate for involvement in the genetic component of addiction. The importance of this gene in nicotine dependence is supported by many studies showing a link between nicotine administration and TH expression. A functional tetranucleotide repeat polymorphism within intron 1 of the TH gene (HUMTH01-VNTR) has been shown to modify tobacco use in two independent Caucasian samples from the USA and Australia. Using information drawn from an eight-wave Australian population-based longitudinal study of adolescent health, we tested the effect of the HUMTH01-VNTR on nicotine dependence. Comparisons were made between dependent smokers and non-dependent smokers. These data provide further support for a protective association between the K4 allele and dependent smoking (odds ratio 0.54, 95% confidence interval 0.28-1.0). No associations were observed at any of three other common TH polymorphisms (rs6356, rs6357 and HUMTH01-PstI). Including these data, three independent studies, two of which use identical phenotypes, have now identified a protective relationship between the K4 allele of the functional HUMTH01-VNTR polymorphism and high-level smoking.

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This study reports pilot data on an association between tobacco dependence and a five-allele tetranucleotide repeat polymorphism in the first intron of the tyrosine hydroxylase (TH) gene. One hundred and twenty-six Australian adolescents who had participated in the Health in Transition Study (1993–1997), and who showed patterns of either dependent or nondependent smoking across four waves of data collection, consented to participation in the pilot study. The smoking status of those recruited was confirmed using a telephone-administered drug use questionnaire during 2000. Tobacco dependence was defined as smoking more than 6 days per week and more than 10 cigarettes per day during wave 5 (year 2000) and at lfeast one prior wave (n = 58). A second, more stringent phenotype included smoking within an hour of waking (n = 37). The control group comprised adolescents who had used tobacco but had remained low-level social smokers across each wave of data (n = 56). DNA was collected using a mouthwash procedure. Using the more strictly defined tobacco dependence phenotype, and after adjusting for sex, a significant protective association was found between the K4 allele and tobacco dependence (OR 0.27, 95% confidence interval [CI] 0.09, 0.82). No association was found using the liberal criteria of tobacco dependence (OR 0.51, 95% confidence interval [CI] 0.23, 1.2). These preliminary results replicate a previous association between tobacco use and the K4 allele of the TH gene (Lerman et al., 1997). The potential significance of including time to first cigarette in definitions of tobacco dependence and the possible role that these TH variants might play in tobacco dependence are discussed.

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Background: Although the relationship between cigarette smoking and cardiovascular disease (CVD) is well-established, the underlying mechanisms remain unclear. Smokers have a more atherogenic lipid profile but this may be mediated by lifestyle-related factors. Because detailed analysis of lipoprotein subclasses using nuclear magnetic resonance spectroscopy (NMR) may improve characterisation of lipid abnormalities, we applied the technique to investigate the relationships between smoking status, other lifestyle-related risk factors and lipoproteins in a contemporary cohort.

Methods: A total of 612 participants (360 women) aged 40-69 years at baseline (1990-1994) enrolled in the community-based Melbourne Collaborative Cohort Study had plasma lipoproteins measured using NMR. Data were analysed separately for men and women.

Results: After adjusting for other lifestyle-related risk factors, mean total low-density lipoprotein (LDL) particle concentration was higher for female smokers than non-smokers. Both medium and small LDL particle concentrations contributed to this difference. Both total high-density lipoprotein (HDL) and large HDL particle concentrations were lower for female smokers than non-smokers. The proportion at increased risk (according to NMR-determined particle size and number) was higher for female smokers than non-smokers. For men, there were few differences in lipoprotein measures related to smoking.

Conclusions: Female smokers have a more atherogenic lipoprotein profile than non-smokers, and this difference is independent of lifestyle-related risk factors. Lipoprotein profiles did not differ greatly between male smokers and non-smokers. These data reinforce the importance for women of not smoking.

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Background: Risk prediction for CVD events has been shown to vary according to current smoking status, pack-years smoked over a lifetime, time since quitting and age at quitting. The latter two are closely and inversely related. It is not known whether the age at which one quits smoking is an additional important predictor of CVD events. The aim of this study was to determine whether the risk of CVD events varied according to age at quitting after taking into account current smoking status, lifetime pack-years smoked and time since quitting.
Findings.
We used the Cox proportional hazards model to evaluate the risk of developing a first CVD event for a cohort of participants in the Framingham Offspring Heart Study who attended the fourth examination between ages 30 and 74 years and were free of CVD. Those who quit before the median age of 37 years had a risk of CVD incidence similar to those who were never smokers. The incorporation of age at quitting in the smoking variable resulted in better prediction than the model which had a simple current smoker/non-smoker measure and the one that incorporated both time since quitting and pack-years. These models demonstrated good discrimination, calibration and global fit. The risk among those quitting more than 5 years prior to the baseline exam and those whose age at quitting was prior to 44 years was similar to the risk among never smokers. However, the risk among those quitting less than 5 years prior to the baseline exam and those who continued to smoke until 44 years of age (or beyond) was two and a half times higher than that of never smokers.
Conclusions:
Age at quitting improves the prediction of risk of CVD incidence even after other smoking measures are taken into account. The clinical benefit of adding age at quitting to the model with other smoking measures may be greater than the associated costs. Thus, age at quitting should be considered in addition to smoking status, time since quitting and pack-years when counselling individuals about their cardiovascular risk.

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Current prediction models for risk of cardiovascular disease (CVD) incidence incorporate smoking as a dichotomous yes/no measure. However, the risk of CVD associated with smoking also varies with the intensity and duration of smoking and there is a strong association between time since quitting and the risk of disease onset. This study aims to develop improved risk prediction equations for CVD incidence incorporating intensity and duration of smoking and time since quitting. The risk of developing a first CVD event was evaluated using a Cox’s model for participants in the Framingham offspring cohort who attended the fourth examination (1988–92) between the ages of 30 and 74 years and were free of CVD (n=3751). The full models based on the smoking variables and other risk factors, and reduced models based on the smoking variables and non-laboratory risk factors demonstrated good discrimination, calibration and global fit. The incorporation of both time since quitting among past smokers and pack-years among current smokers resulted in better predictive performance as compared to a dichotomous current/non-smoker measure and a current/quitter/never smoker measure. Compared to never smokers, the risk of CVD incidence increased with pack-years. Risk among those quitting more than five years prior to the baseline exam and within five years prior to the baseline exam were similar and twice as high as that of never smokers. A CVD risk equation incorporating the effects of pack-years and time since quitting provides an improved tool to quantify risk and guide preventive care.

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Objective To identify predictors of increasing waist circumference (WC) over a 5-year period in a contemporary population of Australian adults.

Design Longitudinal national cohort of adults participating in the Australian Diabetes, Obesity and Lifestyle Study (AusDiab).

Settings Australian adults in 2000 and 2005.

Subjects A total of 2521 men and 2726 women aged ≥25 years at baseline who participated in AusDiab and provided anthropometric measurements at baseline (1999–2000) and follow-up (2005).

Results A ≥5 % increase of baseline WC occurred in 27 % of men and 38 % of women over the 5-year period. In the multivariate analysis of the total population, there was a higher risk of ≥5 % gain in baseline WC in women, younger people, people with a lower baseline WC, people who never married compared with married/de facto, current smokers compared with never smokers, people with a poorer diet quality and people with a low energy intake. However, there was no significant association with many expected predictors of waist gain such as physical activity. There were some associations between other lifestyle factors and change of WC by sex, age, level of education and across WC categories, but the associations differed across these groups.

Conclusions A ≥5 % increase of baseline WC occurred in a significant proportion of men and women over the 5-year period. Of the behavioural factors, poor diet quality was the key predictor of the ≥5 % increase of baseline WC in this cohort. The findings highlight the need to understand better the causal role of lifestyle in regard to increasing WC over time.

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Fish and PUFA consumption are thought to play a role in mental health; however, many studies do not take into account multiple sources of PUFA. The present study analysed data from a sample of 935 randomly selected, population-based women aged 20–93 years. A validated and comprehensive dietary questionnaire ascertained the consumption of n-3 and n-6 PUFA. Another assessed fish and energy intake and provided data for a dietary quality score. The General Health Questionnaire-12 (GHQ-12) measured psychological symptoms and a clinical interview (Structured Clinical Interview for DSM-IV-TR Research Version, Non-patient edition) assessed depressive and anxiety disorders. Median dietary intakes of long-chain n-3 fatty acids (310 mg/d) were below suggested dietary target levels. The only PUFA related to categorical depressive and anxiety disorders was DHA. There was a non-linear relationship between DHA intake and depression; those in the second tertile of DHA intake were nearly 70 % less likely to report a current depressive disorder compared to those in the first tertile. The relationship of DHA to anxiety disorders was linear; for those in the highest tertile of DHA intake, the odds for anxiety disorders were reduced by nearly 50 % after adjustments, including adjustment for diet quality scores, compared to the lowest tertile. Those who ate fish less than once per week had higher GHQ-12 scores, and this relationship was particularly obvious in smokers. These are the first observational data to indicate a role for DHA in anxiety disorders, but suggest that the relationship between DHA and depressive disorders may be non-linear.

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To address increasing rates of overweight and obesity, a population-based telephone intervention was introduced in New South Wales, Australia. The Get Healthy Information and Coaching Service® (GHS) offered participants a 6-month coaching program or detailed self-help information. Determining the population reach of GHS is of public health importance to ensure that the program reaches disadvantaged groups. This paper describes the socio-demographic and risk profile of participants (n = 4828) in the first 18 months of operations, determines how representative they are of the population, assesses changes in participants’ socio-demographic profile and compares ‘information-only’ and ‘coaching’ participants. The results show that GHS users are representative of the adult population in relation to education, employment status, Aboriginal status, fruit and vegetable consumption and alcohol use. However, more female, middle-aged, English-speaking, rural and socially disadvantaged adults participated in GHS. Coaching Participants were more likely to be overweight and to be ex-smokers than the general population. There was substantial variability in GHS recruitment, when mass-reach television advertising was used, participants enrolled from a major city and from more disadvantaged communities. The GHS has broader population reach than many local interventions, but further efforts are needed to increase reach by Aboriginal communities, other minorities and men.

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Endothelial dysfunction is a hallmark of cardiovascular disease, and the l-arginine:NO pathway plays a critical role in determining endothelial function. Recent studies suggest that smoking, a well-recognized risk factor for vascular disease, may interfere with l-arginine and NO metabolism; however, this remains poorly characterized. Accordingly, we performed a series of complementary in vivo and in vitro studies to elucidate the mechanism by which cigarette smoke adversely affects endothelial function. In current smokers, plasma levels of asymmetrical dimethyl-arginine (ADMA) were 80% higher (P=0.01) than nonsmokers, whereas citrulline (17%; P<0.05) and N-hydroxy-l-arginine (34%; P<0.05) were significantly lower. Exposure to 10% cigarette smoke extract (CSE) significantly affected endothelial arginine metabolism with reductions in the intracellular content of citrulline (81%), N-hydroxy-l-arginine (57%), and arginine (23%), while increasing ADMA (129%). CSE significantly inhibited (38%) arginine uptake in conjunction with a 34% reduction in expression of the arginine transporter, CAT1. In conjunction with these studies, CSE significantly reduced the activity of eNOS and NO production by endothelial cells, while stimulating the production of reactive oxygen species. In conclusion, cigarette smoke adversely affects the endothelial l-arginine NO synthase pathway, resulting in reducing NO production and elevated oxidative stress. In conjunction, exposure to cigarette smoke increases ADMA concentration, the latter being a risk factor for cardiovascular disease.

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Objectives: Following the recent H1N1 influenza pandemic we were able to describe seropositivity in a repre-sentative sample of adults prior to the availability of a specific vaccine.

Methods: This cross-sectional serological study is set in the Barwon Statistical Division, Australia. Blood samples were collected from September 2009 through to May 2010, from 1184 individuals (569 men, 615 women; median age 61.7 years), randomly selected from electoral rolls. Serum was analysed for specific H1N1 immunity using a haemagglutina-tion inhibition test. A self-report provided information about symptoms, demographics and healthcare. Associations be-tween H1N1 infection, gender, households and occupation were determined using logistic regression, adjusting for age.

Results: Of 1184 individuals, 129 (58 men, 71 women) were seropositive. Gender-adjusted age-specific prevalence was: 8.3% 20-29 years, 13.5% 30-39, 10.4% 40-49, 6.5% 50-59, 9.7% 60-69, 10.3% 70-79, 18.8% 80+. Standardised preva-lence was 10.3% (95%CI 9.6-11.0). No associations were detected between seropositivity and gender (OR=0.82, 95%CI 0.57-1.19) or being a healthcare worker (OR=1.43, 95%CI 0.62-3.29). Smokers (OR=1.86, 95%CI 1.09-3.15) and those socioeconomically disadvantaged (OR=2.52, 95%CI 1.24-5.13) were at increased risk. Among 129 seropositive individu-als, 31 reported symptoms that were either mild (n = 13) or moderate (time off work, doctor visit, n = 18). For age <60, 39.6% of seropositive individuals reported symptoms, whereas the proportion was 13.2% for age 60+.

Conclusions: Following the pandemic, the proportion of seropositive adults was low, but significant subclinical infection was found. Social disadvantage increased the likelihood of infection. The low symptom rate for older ages may relate to pre-existing immunity.

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Background: The effectiveness of lifestyle interventions in reducing diabetes incidence has been well established. Little is known, however, about factors influencing the reach of diabetes prevention programs. This study examines the predictors of enrolment in the Sydney Diabetes Prevention Program (SDPP), a community-based diabetes prevention program conducted in general practice, New South Wales, Australia from 2008–2011.

Methods:
SDPP was an effectiveness trial. Participating general practitioners (GPs) from three Divisions of General Practice invited individuals aged 50–65 years without known diabetes to complete the Australian Type 2 Diabetes Risk Assessment tool. Individuals at high risk of diabetes were invited to participate in a lifestyle modification program. A multivariate model using generalized estimating equations to control for clustering of enrolment outcomes by GPs was used to examine independent predictors of enrolment in the program. Predictors included age, gender, indigenous status, region of birth, socio-economic status, family history of diabetes, history of high glucose, use of anti-hypertensive medication, smoking status, fruit and vegetable intake, physical activity level and waist measurement.

Results:
Of the 1821 eligible people identified as high risk, one third chose not to enrol in the lifestyle program. In multivariant analysis, physically inactive individuals (OR: 1.48, P = 0.004) and those with a family history of diabetes (OR: 1.67, P = 0.000) and history of high blood glucose levels (OR: 1.48, P = 0.001) were significantly more likely to enrol in the program. However, high risk individuals who smoked (OR: 0.52, P = 0.000), were born in a country with high diabetes risk (OR: 0.52, P = 0.000), were taking blood pressure lowering medications (OR: 0.80, P = 0.040) and consumed little fruit and vegetables (OR: 0.76, P = 0.047) were significantly less likely to take up the program.

Conclusions: Targeted strategies are likely to be needed to engage groups such as smokers and high risk ethnic groups. Further research is required to better understand factors influencing enrolment in diabetes prevention programs in the primary health care setting, both at the GP and individual level.

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Background and objective: Natural killer (NK) and natural killer T (NKT)-like cells represent a small but important proportion of effector lymphocytes that we have previously shown to be major sources of pro-inflammatory cytokines and granzymes. We hypothesized that these cells would be increased in the airway in chronic obstructive pulmonary disease (COPD), accompanied by reduced expression of the inhibitory receptor CD94 (Kp43) and increased expression of cytotoxic mediators granzyme B and perforin.
Methods: We measured NK and NKT-like cells and their expression of CD94 in the blood of COPD patients (n = 71; 30 current and 41 ex-smokers), smokers (16) and healthy controls (25), and bronchoalveolar lavage fluid (BALF) from a cohort of subjects (19 controls, 12 smokers, 33 COPD). Activation was assessed by measuring CD69 in blood and the cytotoxic potential of NK cells by measuring granzymes A and B, and using a cytotoxicity assay in blood and BALF.
Results: In blood in COPD, there were no significant changes in the proportion of NK or NKT-like cells or expression of granzyme A or NK cytotoxic potential versus controls. There was, however, increased expression of granzyme B and decreased expression of CD94 by both cell types versus controls. The proportion of NK and NKT-like cells were increased in BALF in COPD, associated with increased NK cytotoxicity, increased expression of granzyme B and decreased expression of the inhibitory receptor CD94 by both cell types.
Conclusions: Treatment strategies that target NK and NKT-like cells, their cytotoxicity and production of inflammatory mediators in the airway may improve COPD morbidity.