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The aim of this study was to explore the association between traumatic brain injury and brain tumor development.

There is a widespread notion that obesity leads to gastro-oesophageal reflux but scientific evidence of an association is limited and inconsistent.To estimate the strength of the association between body mass and reflux symptoms, we performed a population based cross sectional interview study.Population based, randomly selected, middle aged or elderly persons in Sweden in 1995-1997.At face-to-face interviews we asked a stratified sample of Swedes about body measures and occurrence of reflux symptoms. Odds ratios (OR) with 95% confidence intervals (CI), calculated by logistic regression with multivariate adjustments for covariates, were the measures of association.Reflux symptoms occurring at least once a week more than five years before the interview were reported by 135 (16%) of the 820 interviewees. Among those who had ever been overweight during adulthood (body mass index (BMI)or =25 kg/m(2)), the OR of having recurrent reflux symptoms was 0.99 (95% CI 0.66-1.47) compared with those who were never overweight. There was no association between BMI at age 20, BMI 20 years before the interview, or maximum adult BMI and occurrence of reflux symptoms: ORs per unit increase in BMI were 1. 00 (95% CI 0.93-1.09), 1.03 (95% CI 0.96-1.10), and 1.01 (95% CI=0.95-1.07), respectively. There was no association between BMI and severity or duration of reflux symptoms.Gastro-oesophageal reflux symptoms occur independently of body mass index. Weight reduction may not be justifiable as an antireflux therapy.

We conducted a population-based cohort study to analyze the risk of developing cancers of the female genitals among 36,856 patients with a hospital discharge diagnosis of alcoholism (ICD-7: 307, 322; ICD-8: 291, 303; ICD-9: 291, 303, 305A) in Sweden between 1965 and 1995. The follow-up was done by linkages of national registries. Standardized incidence ratios (SIRs) and 95% confidence intervals (CIs) were computed based on nationwide specific cancer rates. The first year of follow-up was excluded from all analyses to minimize the impact of selection bias. We found that alcoholic women had excess risks for in situ cervical cancer (SIR, 1.7; 95% CI, 1.6-1.9), for invasive cervical cancer (SIR, 2.9; 95% CI, 2.4-3.5), and for cancer of the vagina (SIR, 4.6; 95% CI, 2.2-8.5) but not for cancer of the vulva (SIR, 1.0; 95% CI, 0.4-2.0). The fact that alcoholics had an excess risk also for the in situ cancer suggests that the observed excess in invasive cervical cancer may not only be attributable to less use of Pap smear screening among them. The alcoholic women may be at higher risk for the progression from human papillomavirus infection to a malignant lesion for lifestyle-related reasons (promiscuity, smoking, use of contraceptive hormones, and dietary deficiencies). We conclude that alcoholic women are at high risk for in situ and invasive cervical cancer and for cancer of the vagina.

Objective Both observational studies and randomized trials have shown that a diet rich in antioxidants can reduce systemic inflammation and oxidative stress, two conditions that, together with obesity and smoking, are established risk factors for stroke. However, the association between antioxidant intake and risk for stroke is poorly understood, particularly when studying possible interaction with sex. We investigated the relationship of nonenzymatic antioxidant capacity (NEAC) on risk for stroke in a large Swedish prospective cohort. Methods The cohort study included 34 555 men and women from the Swedish National March Cohort. NEAC was assessed using a detailed food frequency questionnaire, collected at baseline. We achieved complete follow-up from enrollment in 1997 through 2010 by record linkage to nationwide registers. We identified 1186 incident cases of a first stroke, of which 860 were ischemic, 201 hemorrhagic, and 125 unspecified. We used multivariable Cox proportional hazards models to estimate adjusted hazard ratios (HR) with 95% confidence intervals (CIs). Results Compared with women in the lowest quartile of NEAC, women in the highest quartile had a 27% lower incidence of total stroke (HR, 0.73; 95% CI, 0.53–0.99; P trend = 0.03) and 35% lower incidence of ischemic stroke (HR, 0.65; 95% CI, 0.43–0.99; P trend = 0.01). Among men, the relationship between NEAC and risk for stroke was not statistically significant and all HRs were close to unity. Conclusion Findings from the present study suggest that dietary antioxidant capacity from different foods and beverages is inversely associated with risk for stroke, more specifically ischemic stroke, in women.

Background: Results from randomized trials of antioxidant supplementation have cast doubt on observational data linking diets high in antioxidants to a reduced risk of cardiovascular diseases. We hypothesized that supplementation of one or a few antioxidants might not simulate the complex actions of all antioxidants in the human diet. We therefore investigated the association between dietary Non Enzymatic Antioxidant Capacity (NEAC), reflecting the antioxidant potential of the whole diet, and the risk of myocardial infarction (MI). Methods: In the Swedish National March Cohort, 34 543 men and women free from cardiovascular diseases and cancer were followed through record linkages from 1997 until 2010. NEAC was assessed with a validated food-frequency questionnaire at baseline. The distribution of NEAC was categorized into sex-specific quartiles. We fitted multivariable Cox proportional hazards regression models to estimate hazard ratios (HRs) with 95% confidence intervals (CIs). Results: During a mean follow-up time of 12.7 years, we identified 1142 incident cases of MI. Successively higher quartiles (Qs) of dietary NEAC were accompanied by a monotonic trend of decreasing MI incidence, both for overall MI (HR Q4 vs Q1: 0.77; 95% CI: 0.61–0.96; p for trend ¼ 0.008) and non-fatal MI (HR Q4 vs Q1: 0.72; 95% CI: 0.56–0.92; p for trend ¼ 0.004). No such association was found for fatal MI. Conclusions: A diet rich in antioxidants might protect from MI.

Dialysis has been used in the treatment of patients with end-stage renal disease since the 1960s. Recently, several large observational studies have been conducted to assess whether early initiation of dialysis prolongs survival, as compared with late initiation. However, these studies have used analytic approaches which are likely to suffer from either lead-time bias or immortal-time bias. In this paper, the authors demonstrate that recently developed methods in the causal inference literature can be used to avoid both types of bias and accurately estimate the ideal time for dialysis initiation from observational data. This is illustrated using data from a nationwide population-based cohort of patients with chronic kidney disease in Sweden (1996-2003). © 2011 The Author.

Gout patients might be at an increased risk of cancer because of obesity and heavy alcohol drinking, but uric acid has antioxidant properties, which may protect against carcinogenesis. We compared the incidence of cancer among 16 857 gout patients admitted to hospitals in Sweden during 1965-1995 with that of the national population. A total of 1425 malignant neoplasms were diagnosed in gout patients (standardized incidence ratio 1.25, 95% confidence limits 1.18, 1.31). The incidence of cancers of the oral cavity and pharynx, colon, liver and biliary tract, pancreas, lung, skin (melanoma and nonmelanoma), endometrium and kidney, as well as of malignant melanoma was increased among gout patients. With the exception of lung cancer, the risk remained elevated during the entire follow-up. This study provides no evidence of a protective effect of uric acid. Hyperuricemia may be an early manifestation of the carcinogenic process. © 2009 Wotters Kluwer Health|Lippincott Williams & Wilkins.

Cancer epidemiologyCancer type: stomach and esophageal adenocarcinomaStudy design: cohortStudy size:521457Description of cohort(s) studied: 368010 women and 153447 men from 10 european countriesExposure(s) evaluated:88-266 food itemsConfounders controlled for: h.pylori infectionImpact on risk: risk for gastric cancer and Total meat intake PR=5.32, 95%CI=2.1-13.4Processed meat OR=2.67, 95%CI=1.2-5.93Dietary modulation of cancer & cancer biomarkers Dietary item or component studied:meat, processed meatOutcome studied (cancer or cancer biomarker): stomach and esophageal adenocarcinomaStudy type (in vitro, animals, humans): humansTissue/biological material/sample size:30ml bloodMode of exposure (if in vivo):through normal dietImpact on outcome (including dose-response):red meat and noncardia cancer (HR 1.73, CI 95%=1.03-2.88,P=0.19)Poultry meat and esophageal cancer HR 1.14, CI95%=1-1.3Processed meat and gastric cancer HR 2.45, 955CI=1.43-4.21, P=0.02Processed meat and esophageal cancer HR=3.54, CI95%=1.57-7.99, P=0.002. KEYWORDS CLASSIFICATION: Adenocarcinoma;Adult;Aged;complications;cancer epidemiology;Cardia;Case-Control Studies;Confidence Intervals;dietary modulation of cancer & cancer biomarkers;epidemiology;etiology;Esophageal Neoplasms;Europe;Female;Follow-Up Studies;Food Habits;Helicobacter Infections;Helicobacter pylori;Humans;Incidence;Life Style;microbiology;Male;Meat;Middle Aged;Odds Ratio;Proportional Hazards Models;Prospective Studies;Questionnaires;Research;Risk Assessment;Risk Factors;Spain;Stomach Neoplasms. BACKGROUND: Dietary factors are thought to have an important role in gastric and esophageal carcinogenesis, but evidence from cohort studies for such a role is lacking. We examined the risks of gastric cancer and esophageal adenocarcinoma associated with meat consumption within the European Prospective Investigation Into Cancer and Nutrition (EPIC) cohort. METHODS: A total of 521,457 men and women aged 35-70 years in 10 European countries participated in the EPIC cohort. Dietary and lifestyle information was collected at recruitment. Cox proportional hazard models were used to examine associations between meat intake and risks of cardia and gastric non-cardia cancers and esophageal adenocarcinoma. Data from a calibration substudy were used to correct hazard ratios (HRs) and 95% confidence intervals (CIs) for diet measurement errors. In a nested case-control study, we examined interactions between Helicobacter pylori infection status (i.e., plasma H. pylori antibodies) and meat intakes. All statistical tests were two-sided. RESULTS: During a mean follow-up of 6.5 years, 330 gastric adenocarcinoma and 65 esophageal adenocarcinomas were diagnosed. Gastric non-cardia cancer risk was statistically significantly associated with intakes of total meat (calibrated HR per 100-g/day increase = 3.52; 95% CI = 1.96 to 6.34), red meat (calibrated HR per 50-g/day increase = 1.73; 95% CI = 1.03 to 2.88), and processed meat (calibrated HR per 50-g/day increase = 2.45; 95% CI = 1.43 to 4.21). The association between the risk of gastric non-cardia cancer and total meat intake was especially large in H. pylori-infected subjects (odds ratio per 100-g/day increase = 5.32; 95% CI = 2.10 to 13.4). Intakes of total, red, or processed meat were not associated with the risk of gastric cardia cancer. A positive but non-statistically significant association was observed between esophageal adenocarcinoma cancer risk and total and processed meat intake in the calibrated model. In this study population, the absolute risk of development of gastric adenocarcinoma within 10 years for a study subject aged 60 years was 0.26% for the lowest quartile of total meat intake and 0.33% for the highest quartile of total meat intake. CONCLUSION: Total, red, and processed meat intakes were associated with an increased risk of gastric non-cardia cancer, especially in H. pylori antibody-positive subjects, but not with cardia gastric cancer.