Huerta J.M.,Murcia Regional Health Council |
Huerta J.M.,CIBER ISCIII |
Chirlaque M.-D.,Murcia Regional Health Council |
Chirlaque M.-D.,CIBER ISCIII |
And 23 more authors.
Stroke | Year: 2013
Background and Purpose-: Large-scale prospective epidemiological data testing the association between physical activity (PA) and cerebrovascular diseases (CVDs) are scarce, particularly in Europe. The objective was to assess the risk of CVD according to PA levels in adults. Methods-: We included a total of 13 576 men and 19 416 women aged 29 to 69 years and participating in the European Prospective Investigation into Cancer and Nutrition cohort in Spain, recruited between 1992 and 1996 and followed-up until 2006 to ascertain incident CVD events. The validated European Prospective Investigation into Cancer and Nutrition PA questionnaire was used to assess metabolic equivalent × hours per week dedicated to different types of PA. Hazard ratios of CVD by PA levels were estimated using multivariate Cox regression. Extensive baseline data collected on diet, lifestyle habits, medical history, and anthropometry were available to adjust for. Results-: A total of 210 transient ischemic attacks and 442 stroke cases (80% ischemic, 10% hemorrhagic, 7% subarachnoid hemorrhage, and 3% mixed or unspecified) were registered after 12.3 years of mean follow-up. Recreational activity was inversely associated with risk of CVD in women but not in men. Women walking for ≥3.5 hours per week were at lower risk of stroke than those who did not engage in regular walking. No significant associations were found for other leisure time activities or vigorous PA with CVD in either sex. Conclusions-: Recreational PA of moderate intensity was inversely associated with stroke incidence in women, whereas PA showed no effect on CVD risk in men. Increasing time dedicated to activities such as walking would be expected to help to reduce the stroke burden in women. © 2012 American Heart Association, Inc. Source
Agudo A.,Catalan Institute of Nanoscience and Nanotechnology |
Bonet C.,Catalan Institute of Nanoscience and Nanotechnology |
Travier N.,Catalan Institute of Nanoscience and Nanotechnology |
Gonzalez C.A.,Catalan Institute of Nanoscience and Nanotechnology |
And 50 more authors.
Journal of Clinical Oncology | Year: 2012
Purpose: Our aim was to assess the impact of cigarette smoking on the risk of the tumors classified by the International Agency for Research on Cancer as causally associated with smoking, referred to as tobacco-related cancers (TRC). Methods: The study population included 441,211 participants (133,018 men and 308,193 women) from the European Prospective Investigation Into Cancer and Nutrition. We investigated 14,563 participants who developed a TRC during an average follow-up of 11 years. The impact of smoking cigarettes on cancer risk was assessed by the population attributable fraction (AFp), calculated using the adjusted hazard ratios and 95% CI for current and former smokers, plus either the prevalence of smoking among cancer cases or estimates from surveys in representative samples of the population in each country. Results: The proportion of all TRC attributable to cigarette smoking was 34.9% (95% CI, 32.5 to 37.4) using the smoking prevalence among cases and 36.2% (95% CI, 33.7 to 38.6) using the smoking prevalence from the population. The AF p were above 80% for cancers of the lung and larynx, between 20% and 50% for most respiratory and digestive cancers and tumors from the lower urinary tract, and below 20% for the remaining TRC. Conclusion: Using data on cancer incidence for 2008 and our AFp estimates, about 270,000 new cancer diagnoses per year can be considered attributable to cigarette smoking in the eight European countries with available data for both men and women (Italy, Spain, United Kingdom, the Netherlands, Greece, Germany, Sweden, Denmark). © 2012 by American Society of Clinical Oncology. Source
Demetriou C.A.,Cyprus Institute of Neurology and Genetics |
Demetriou C.A.,Imperial College London |
Chen J.,Mount Sinai School of Medicine |
Polidoro S.,Molecular and Genetic Epidemiology Unit |
And 45 more authors.
PLoS ONE | Year: 2013
Reproductive factors have been linked to both breast cancer and DNA methylation, suggesting methylation as an important mechanism by which reproductive factors impact on disease risk. However, few studies have investigated the link between reproductive factors and DNA methylation in humans. Genome-wide methylation in peripheral blood lymphocytes of 376 healthy women from the prospective EPIC study was investigated using LUminometric Methylation Assay (LUMA). Also, methylation of 458877 CpG sites was additionally investigated in an independent group of 332 participants of the EPIC-Italy sub-cohort, using the Infinium HumanMethylation 450 BeadChip. Multivariate logistic regression and linear models were used to investigate the association between reproductive risk factors and genome wide and CpG-specific DNA methylation, respectively. Menarcheal age was inversely associated with global DNA methylation as measured with LUMA. For each yearly increase in age at menarche, the risk of having genome wide methylation below median level was increased by 32% (OR:1.32, 95%CI:1.14-1.53). When age at menarche was treated as a categorical variable, there was an inverse dose-response relationship with LUMA methylation levels (OR12-14vs.≤11 yrs:1.78, 95%CI:1.01-3.17 and OR≥15vs.≤11 yrs:4.59, 95%CI:2.04-10.33; P for trend<0.0001). However, average levels of global methylation as measured by the Illumina technology were not significantly associated with menarcheal age. In locus by locus comparative analyses, only one CpG site had significantly different methylation depending on the menarcheal age category examined, but this finding was not replicated by pyrosequencing in an independent data set. This study suggests a link between age at menarche and genome wide DNA methylation, and the difference in results between the two arrays suggests that repetitive element methylation has a role in the association. Epigenetic changes may be modulated by menarcheal age, or the association may be a mirror of other important changes in early life that have a detectable effect on both methylation levels and menarcheal age. © 2013 Demetriou et al. Source
Abete I.,Health Research Institute BIODONOSTIA |
Arriola L.,Basque Government |
Etxezarreta N.,Basque Government |
Mozo I.,Basque Government |
And 34 more authors.
European Journal of Nutrition | Year: 2015
Introduction: There is still a scientific debate on the exact role played by obesity on stroke risk.Objective: The aim of the study was to analyze the association between obesity, measured by different indices such as body mass index (BMI), waist circumference (WC), waist-to-hip ratio (WHR) and a new one called A Body Shape Index (ABSI) and the risk of total and ischemic stroke.Subjects/methods: A total of 41,020 subjects (15,490 men and 25,530 women) aged 29–69 years participated in the study. All participants were recruited between 1992 and 1996 and followed up until 2008 to ascertain incident cerebrovascular disease events. Cox proportional hazards models were designed to estimate the relative risk and 95 % CI between obesity and cerebrovascular disease incidence.Results: After 13.8 years of follow-up, a total of 674 stroke cases (55.3 % in men) were registered (531 ischemic, 79 hemorrhagic, 42 subarachnoid hemorrhage and 22 unspecified). WC fourth quartile (HR 1.95; 95 % CI 1.20–3.19) and WHR fourth quartile (HR 1.58; 95 % CI 1.12–2.25) were positively associated with total stroke only in men. BMI was not associated with stroke incidence. The new index, ABSI, was significantly associated with total stroke incidence only in men (HR 1.54; 95 % CI 1.06–2.23).Conclusions: Data from the Spanish EPIC cohort study show a strong association of WC and WHR with the relative risk of suffering a stroke only in men, while no associations were found for BMI. It supports the suggestion of other authors of using more than one obesity index in the study of stroke risk prediction. © 2014, Springer-Verlag Berlin Heidelberg. Source