Walking to work in Canada: health benefits, socio-economic characteristics and urban-regional variations

<p>Abstract</p> <p>Background</p> <p>There is mounting concern over increasing rates of physical inactivity and overweight/obesity among children and adult in Canada. There is a clear link between the amount of walking a person does and his or her health. The purpose of this paper is to assess the health factors, socio-economic characteristics and urban-regional variations of walking to work among adults in Canada.</p> <p>Methods</p> <p>Data is drawn from two cycles of the Canadian Community Health Survey: 2001 and 2005. The study population is divided into three groups: non-walkers, lower-duration walkers and high-duration walkers. Logistic regression modeling tests the association between levels of walking and health related outcomes (diabetes, high blood pressure, stress, BMI, physical activity), socio-economic characteristics (sex, age, income, education) and place of residence (selected Census Metropolitan Areas).</p> <p>Results</p> <p>In 2005, the presence of diabetes and high blood pressure was not associated with any form of walking. Adults within the normal weight range were more likely to be high-duration walkers. Females and younger people were more likely to be lower-duration walkers but less likely to be high-duration walkers. There was a strong association between SES (particularly relative disadvantage) and walking to work. In both 2001 and 2005, the conditions influencing walking to work were especially prevalent in Canada's largest city, Toronto, as well as in several small to medium sized urban areas including Halifax, Kingston, Hamilton, Regina, Calgary and Victoria.</p> <p>Conclusion</p> <p>A number of strategies can be followed to increase levels of walking in Canada. It is clear that for many people walking to work is not possible. However, strategies can be developed to encourage adults to incorporate walking into their daily work and commuting routines. These include mass transit walking and workplace walking programs.</p

Television Viewing and Incident Cardiovascular Disease: Prospective Associations and Mediation Analysis in the EPIC Norfolk Study

Background: Although television viewing time is detrimentally associated with intermediate cardiovascular risk factors, the relationship with incident total (i.e. combined fatal and non-fatal) cardiovascular disease (CVD), non-fatal CVD and coronary heart disease is largely unknown. This study examined whether television viewing time is associated with these three outcomes, independently of physical activity energy expenditure and other confounding variables. Methodology/Principal Findings: A population-based cohort of 12,608 men and women (aged 61.4 +/- 9.0), free from stroke, myocardial infarction and cancer at baseline in 1998-2000 were followed up until 2007 (6.9 +/- 1.9 years). Participants self-reported education, smoking, alcohol use, antihypertensive, lipid lowering and antidepressant medication, disease history, total energy intake, sleep duration, physical activity and television viewing. BMI, waist circumference, blood pressure, triglycerides, HDL cholesterol and glycated haemoglobin (HbA(1c)) were measured by standardized procedures; a clustered metabolic risk score was constructed. Every one hour/day increase in television viewing was associated with an increased hazard for total (HR = 1.06, 95% CI = 1.03-1.08; 2,620 cases), non-fatal CVD (HR = 1.06, 95% CI = 1.03-1.09; 2,134 cases), and coronary heart disease (HR = 1.08, 95% CI = 1.03-1.13; 940 cases), independent of gender, age, education, smoking, alcohol, medication, diabetes status, CVD family history, sleep duration and physical activity energy expenditure. Energy intake, BMI, waist circumference, blood pressure, triglycerides, HDL cholesterol, HbA(1c) and the clustered metabolic risk score only partially mediated these associations. Conclusions: These results indicate that the most prevalent leisure time (sedentary) behaviour, television viewing, independently contributes to increased CVD risk. Recommendations on reducing television viewing time should be considered

The relationship between body size and mortality in the linked Scottish Health Surveys: cross-sectional surveys with follow-up

Objective: To investigate the relationship between body mass index (BMI), waist circumference (WC) or waist–hip ratio (WHR) and all-cause mortality or cause-specific mortality. Design: Cross-sectional surveys linked to hospital admissions and death records. Subjects: In total, 20 117 adults (aged 18–86 years) from a nationally representative sample of the Scottish population. Measurements: Cox proportional hazards models were used to estimate hazard ratios (HRs) for all-cause, or cause-specific, mortality. The three anthropometric measurements BMI, WC and WHR were the main variables of interest. The following were adjustment variables: age, gender, smoking status, alcohol consumption, survey year, social class and area of deprivation. Results: BMI-defined obesity (greater than or equal to30 kg m−2) was not associated with increased risk of mortality (HR=0.93; 95% confidence interval=0.80–1.08), whereas the overweight category (25–&#60;30 kg m−2) was associated with a decreased risk (0.80; 0.70–0.91). In contrast, the HR for a high WC (mengreater than or equal to102 cm, womengreater than or equal to88 cm) was 1.17 (1.02–1.34) and a high WHR (mengreater than or equal to1, women&#8805;0.85) was 1.34 (1.16–1.55). There was an increased risk of cardiovascular disease (CVD) mortality associated with BMI-defined obesity, a high WC and a high WHR categories; the HR estimates for these were 1.36 (1.05–1.77), 1.41 (1.11–1.79) and 1.44 (1.12–1.85), respectively. A low BMI (&#60;18.5 kg m−2) was associated with elevated HR for all-cause mortality (2.66; 1.97–3.60), for chronic respiratory disease mortality (3.17; 1.39–7.21) and for acute respiratory disease mortality (11.68; 5.01–27.21). This pattern was repeated for WC but not for WHR. Conclusions: It might be prudent not to use BMI as the sole measure to summarize body size. The alternatives WC and WHR may more clearly define the health risks associated with excess body fat accumulation. The lack of association between elevated BMI and mortality may reflect the secular decline in CVD mortality.</p

Asthma and COPD in cystic fibrosis intron-8 5T carriers. A population-based study

BACKGROUND: Carriers of cystic fibrosis intron-8 5T alleles with high exon-9 skipping could have increased annual lung function decline and increased risk for asthma or chronic obstructive pulmonary disease (COPD). METHODS: We genotyped 9131 individuals from the adult Danish population for cystic fibrosis 5T, 7T, 9T, and F508del alleles, and examined associations between 11 different genotype combinations, and annual FEV(1 )decline and risk of asthma or COPD. RESULTS: 5T heterozygotes vs. 7T homozygous controls had no increase in annual FEV(1 )decline, self-reported asthma, spirometry-defined COPD, or incidence of hospitalization from asthma or COPD. In 5T/7T heterozygotes vs. 7T homozygous controls we had 90% power to detect an increase in FEV(1 )decline of 8 ml, an odds ratio for self-reported asthma and spirometry-defined COPD of 1.9 and 1.7, and a hazard ratio for asthma and COPD hospitalization of 1.8 and 1.6, respectively. Both 5T homozygotes identified in the study showed evidence of asthma, while none of four 5T/F508del compound heterozygotes had severe pulmonary disease. 7T/9T individuals had annual decline in FEV(1 )of 19 ml compared with 21 ml in 7T homozygous controls (t-test:P = 0.03). 6.7% of 7T homozygotes without an F508del allele in the cystic fibrosis transmembrane conductance regulator gene reported asthma vs. 11% of 7T/9T individuals with an F508del allele (χ(2):P = 0.01) and 40% of 7T homozygotes with an F508del allele (P = 0.04). 7T homozygotes with vs. without an F508del allele also had higher incidence of asthma hospitalization (log-rank:P = 0.003); unadjusted and adjusted equivalent hazard ratios for asthma hospitalization were 11 (95%CI:1.5–78) and 6.3 (0.84–47) in 7T homozygotes with vs. without an F508del allele. CONCLUSION: Polythymidine 5T heterozygosity is not associated with pulmonary dysfunction or disease in the adult Caucasian population. Furthermore, our results support that F508del heterozygosity is associated with increased asthma risk independently of the 5T allele

Vitamin D improves endothelial dysfunction and restores myeloid angiogenic cell function via reduced CXCL-10 expression in systemic lupus erythematosus.

Patients with systemic lupus erythematosus (SLE) have accelerated cardiovascular disease and dysfunctional endothelial repair mechanisms. Myeloid angiogenic cells (MACs), derived from circulating monocytes, augment vascular repair by paracrine secretion of pro-angiogenic factors. We observed that SLE MACs are dysfunctional and secrete pro-inflammatory cytokines. We also found that the vitamin D receptor was transiently expressed during MAC differentiation and that in vitro, calcitriol increased differentiation of monocytes into MACs in both SLE and in a model using the prototypic SLE cytokine, interferon-alpha. The active form of vitamin D (calcitriol) restored the SLE MAC phenotype towards that of healthy subjects with reduced IL-6 secretion, and normalised surface marker expression. Calcitriol also augmented the angiogenic capacity of MACs via the down-regulation of CXCL-10. In SLE patients treated with cholecalciferol for 12 weeks, the improvement in endothelial function correlated with increase in serum 25(OH)D concentrations independently of disease activity. We also show that MACs were able to positively modulate eNOS expression in human endothelial cells in vitro, an effect further enhanced by calcitriol treatment of SLE MACs. The results demonstrate that vitamin D can positively modify endothelial repair mechanisms and thus endothelial function in a population with significant cardiovascular risk

Iron Behaving Badly: Inappropriate Iron Chelation as a Major Contributor to the Aetiology of Vascular and Other Progressive Inflammatory and Degenerative Diseases

The production of peroxide and superoxide is an inevitable consequence of aerobic metabolism, and while these particular "reactive oxygen species" (ROSs) can exhibit a number of biological effects, they are not of themselves excessively reactive and thus they are not especially damaging at physiological concentrations. However, their reactions with poorly liganded iron species can lead to the catalytic production of the very reactive and dangerous hydroxyl radical, which is exceptionally damaging, and a major cause of chronic inflammation. We review the considerable and wide-ranging evidence for the involvement of this combination of (su)peroxide and poorly liganded iron in a large number of physiological and indeed pathological processes and inflammatory disorders, especially those involving the progressive degradation of cellular and organismal performance. These diseases share a great many similarities and thus might be considered to have a common cause (i.e. iron-catalysed free radical and especially hydroxyl radical generation). The studies reviewed include those focused on a series of cardiovascular, metabolic and neurological diseases, where iron can be found at the sites of plaques and lesions, as well as studies showing the significance of iron to aging and longevity. The effective chelation of iron by natural or synthetic ligands is thus of major physiological (and potentially therapeutic) importance. As systems properties, we need to recognise that physiological observables have multiple molecular causes, and studying them in isolation leads to inconsistent patterns of apparent causality when it is the simultaneous combination of multiple factors that is responsible. This explains, for instance, the decidedly mixed effects of antioxidants that have been observed, etc...Comment: 159 pages, including 9 Figs and 2184 reference