Publications
260 results found
Butt J, Jenab M, Willhauck-Fleckenstein M, et al., 2018, Prospective evaluation of antibody response to Streptococcus gallolyticus and risk of colorectal cancer, International Journal of Cancer, Vol: 143, Pages: 245-252, ISSN: 0020-7136
The gut microbiome is increasingly implicated in colorectal cancer (CRC) development. A subgroup of patients diagnosed with CRC show high antibody responses to Streptococcus gallolyticus subspecies gallolyticus (SGG). However, it is unclear whether the association is also present pre‐diagnostically. We assessed the association of antibody responses to SGG proteins in pre‐diagnostic serum samples with CRC risk in a case–control study nested within a prospective cohort. Pre‐diagnostic serum samples from 485 first incident CRC cases (mean time between blood draw and diagnosis 3.4 years) and 485 matched controls in the European Prospective Investigation into Nutrition and Cancer (EPIC) study were analyzed for antibody responses to 11 SGG proteins using multiplex serology. Odds ratios (OR) and 95% confidence intervals (CI) were estimated using multivariable conditional logistic regression models. Antibody positivity for any of the 11 SGG proteins was significantly associated with CRC risk with 56% positive controls compared to 63% positive cases (OR: 1.36, 95% CI: 1.04–1.77). Positivity for two or more proteins of a previously identified SGG 6‐marker panel with greater CRC‐specificity was also observed among 9% of controls compared to 17% of CRC cases, corresponding to a significantly increased CRC risk (OR: 2.17, 95% CI: 1.44–3.27). In this prospective nested case–control study, we observed a positive association between antibody responses to SGG and CRC development in serum samples taken before evident disease onset. Further work is required to establish the possibly etiological significance of these observations and whether SGG serology may be applicable for CRC risk stratification.
Lin C, Travis RC, Appleby PN, et al., 2018, Pre-diagnostic circulating insulin-like growth factor-I and bladder cancer risk in the European prospective investigation into cancer and nutrition, International Journal of Cancer, Vol: 143, Pages: 2351-2358, ISSN: 0020-7136
Previous in vitro and case-control studies have found an association between the insulin-like growth factor (IGF)-axis and bladder cancer risk. Circulating concentrations of IGF-I have also been found to be associated with an increased risk of several cancer types; however, the relationship between pre-diagnostic circulating IGF-I concentrations and bladder cancer has never been studied prospectively. We investigated the association of pre-diagnostic plasma concentrations of IGF-I with risk of overall bladder cancer and urothelial cell carcinoma (UCC) in a case-control study nested within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. A total of 843 men and women diagnosed with bladder cancer between 1992 and 2005 were matched with 843 controls by recruitment centre, sex, age at recruitment, date of blood collection, duration of follow-up, time of day and fasting status at blood collection using an incidence density sampling protocol. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using conditional logistic regression with adjustment for smoking status. No association was found between pre-diagnostic circulating IGF-I concentration and overall bladder cancer risk (adjusted OR for highest versus lowest fourth: 0.91, 95% CI: 0.66-1.24, Ptrend =0.40) or UCC (n of cases=776; 0.91, 0.65-1.26, Ptrend =0.40). There was no significant evidence of heterogeneity in the association of IGF-I with bladder cancer risk by tumour aggressiveness, sex, smoking status, or by time between blood collection and diagnosis (Pheterogeneity >0.05 for all). This first prospective study indicates no evidence of an association between plasma IGF-I concentrations and bladder cancer risk. This article is protected by copyright. All rights reserved.
Cramer DW, Fichorova RN, Terry KL, et al., 2018, Anti-CA15.3 and anti-CA125 antibodies and ovarian cancer risk: Results from the EPIC cohort, Cancer Epidemiology, Biomarkers and Prevention, Vol: 27, Pages: 790-804, ISSN: 1055-9965
BACKGROUND: Neoplastic and non-neoplastic events may raise levels of mucins, CA15.3 and CA125, and generate antibodies against them; but their impact on epithelial ovarian cancer (EOC) risk has not been fully defined. METHODS: CA15.3, CA125, and IgG1 antibodies against them were measured in 806 women who developed EOC and 1,927 matched controls from the European Prospective Investigation of Nutrition and Cancer. Associations between epidemiologic factors and anti-mucin antibodies were evaluated using generalized linear models; EOC risks associated with anti-mucin antibodies, by themselves or in combination with respective antigens, were evaluated using conditional logistic regression. RESULTS: In controls, lower antibodies against both mucins were associated with current smoking; and, in postmenopausal women, higher levels with longer oral contraceptive use and later-age-at and shorter-interval-since last birth. Lower anti-CA15.3 antibodies were associated with higher body mass and, in premenopausal women, more ovulatory cycles. Higher anti-CA15.3 and anti-CA125 antibodies were associated with higher risk for mucinous EOC occurring ≥ 3 years from enrollment. Long-term risk for serous EOC was reduced in women with low CA125 and high anti-CA125 antibodies relative to women with low concentrations of both. CONCLUSIONS: We found general support for the hypothesis that anti-mucin antibody levels correlate with risk factors for EOC. Antibodies alone or in combinations with their antigen may predict longer term risk of specific EOC types. IMPACT: Anti-CA125 and anti- CA15.3 antibodies alone or in perspective of antigens may be informative in the pathogenesis of EOC subtypes, but less useful for informing risk for all EOC.
Landais E, Moskal A, Mullee A, et al., 2018, Coffee and tea consumption and the contribution of their added ingredients to total energy and nutrient intakes in 10 European countries: benchmark data from the late 1990s, Nutrients, Vol: 10, ISSN: 2072-6643
BACKGROUND: Coffee and tea are among the most commonly consumed nonalcoholic beverages worldwide, but methodological differences in assessing intake often hamper comparisons across populations. We aimed to (i) describe coffee and tea intakes and (ii) assess their contribution to intakes of selected nutrients in adults across 10 European countries. METHOD: Between 1995 and 2000, a standardized 24-h dietary recall was conducted among 36,018 men and women from 27 European Prospective Investigation into Cancer and Nutrition (EPIC) study centres. Adjusted arithmetic means of intakes were estimated in grams (=volume) per day by sex and centre. Means of intake across centres were compared by sociodemographic characteristics and lifestyle factors. RESULTS: In women, the mean daily intake of coffee ranged from 94 g/day (~0.6 cups) in Greece to 781 g/day (~4.4 cups) in Aarhus (Denmark), and tea from 14 g/day (~0.1 cups) in Navarra (Spain) to 788 g/day (~4.3 cups) in the UK general population. Similar geographical patterns for mean daily intakes of both coffee and tea were observed in men. Current smokers as compared with those who reported never smoking tended to drink on average up to 500 g/day more coffee and tea combined, but with substantial variation across centres. Other individuals' characteristics such as educational attainment or age were less predictive. In all centres, coffee and tea contributed to less than 10% of the energy intake. The greatest contribution to total sugar intakes was observed in Southern European centres (up to ~20%). CONCLUSION: Coffee and tea intake and their contribution to energy and sugar intake differed greatly among European adults. Variation in consumption was mostly driven by geographical region.
Aune D, Schlesinger S, Norat T, et al., 2018, Tobacco smoking and the risk of sudden cardiac death: a systematic review and meta-analysis of prospective studies, European Journal of Epidemiology, Vol: 33, Pages: 509-521, ISSN: 0393-2990
Smoking is an established risk factor for cardiovascular disease including coronary heart disease and stroke, however, data regarding smoking and sudden cardiac death have not been summarized in a meta-analysis previously. We therefore conducted a systematic review and meta-analysis to clarify this association. We searched the PubMed and Embase databases for studies of smoking and sudden cardiac death up to July 20th 2017. Prospective studies were included if they reported adjusted relative risk (RR) estimates and 95% confidence intervals (CIs) for smoking and sudden cardiac death. Summary RRs were estimated by use of a random effects model. Twelve prospective studies were included. The summary RR was 3.06 (95% CI 2.46-3.82, I2 = 41%, pheterogeneity = 0.12, n = 7) for current smokers and 1.38 (95% CI 1.20-1.60, I2 = 0%, pheterogeneity = 0.55, n = 7) for former smokers compared to never smokers. For four studies using non-current (never + former) smokers as the reference category the summary RR among current smokers was 2.08 (95% CI 1.70-2.53, I2 = 18%, pheterogeneity = 0.30). The results persisted in most of the subgroup analyses. There was no evidence of publication bias. These results confirm that smoking increases the risk of sudden cardiac death. Any further studies should investigate in more detail the effects of duration of smoking, number of cigarettes per day, pack-years, and time since quitting smoking and sudden cardiac death.
Aune D, Schlesinger S, Norat T, et al., 2018, Diabetes mellitus and the risk of sudden cardiac death: a systematic review and meta-analysis of prospective studies, Nutrition, Metabolism and Cardiovascular Diseases, Vol: 28, Pages: 543-556, ISSN: 0939-4753
BackgroundAlthough diabetes mellitus is an established risk factor for myocardial infarction and stroke, data on the association with sudden cardiac death are less extensive and the findings have not been entirely consistent. We therefore conducted a systematic review and meta-analysis of prospective studies on diabetes mellitus and risk of sudden cardiac death.Methods and resultsPubMed and Embase databases were searched up to July 18th 2017. Prospective studies that reported adjusted relative risk (RR) estimates and 95% confidence intervals (CIs) for the association between a diabetes diagnosis or pre-diabetes and risk of sudden cardiac death were included. Summary RRs were estimated by use of a random effects model. Nineteen population-based prospective studies (11 publications) (3610 cases, 249,225 participants) and 10 patient-based prospective studies (2713 cases, 55,098 participants) were included. The summary RR for diabetes patients vs. persons without diabetes was 2.02 (95% CI: 1.81–2.25, I2 = 0%, pheterogeneity = 0.91) in the population-based studies. The summary RR was 1.23 (95% CI: 1.05–1.44, I2 = 6%, pheterogeneity = 0.34) for the association between pre-diabetes and sudden cardiac death (n = 3 studies, 1000 sudden cardiac deaths, 18,360 participants). In the patient-based studies, the summary RR of sudden cardiac death for diabetes patients vs. patients without diabetes was 1.75 (95% CI: 1.51–2.03, I2 = 39%, pheterogeneity = 0.10) for all patients combined, 1.63 (95% CI: 1.36–1.97, I2 = 39%, n = 5) for coronary heart disease patients, and 1.85 (95% CI: 1.48–2.33, I2 = 0%, n = 3) for heart failure patients.ConclusionsThese results suggest that diabetes patients are at an increased risk of sudden cardiac death both in the general population and among different patient groups.
Li SX, Imamura F, Schulze MB, et al., 2018, Interplay between genetic predisposition, macronutrient intake and type 2 diabetes incidence: analysis within EPIC-InterAct across eight European countries, Diabetologia, Vol: 61, Pages: 1325-1332, ISSN: 0012-186X
AIMS/HYPOTHESIS: Gene-macronutrient interactions may contribute to the development of type 2 diabetes but research evidence to date is inconclusive. We aimed to increase our understanding of the aetiology of type 2 diabetes by investigating potential interactions between genes and macronutrient intake and their association with the incidence of type 2 diabetes. METHODS: We investigated the influence of interactions between genetic risk scores (GRSs) for type 2 diabetes, insulin resistance and BMI and macronutrient intake on the development of type 2 diabetes in the European Prospective Investigation into Cancer and Nutrition (EPIC)-InterAct, a prospective case-cohort study across eight European countries (N = 21,900 with 9742 incident type 2 diabetes cases). Macronutrient intake was estimated from diets reported in questionnaires, including proportion of energy derived from total carbohydrate, protein, fat, plant and animal protein, saturated, monounsaturated and polyunsaturated fat and dietary fibre. Using multivariable-adjusted Cox regression, we estimated country-specific interaction results on the multiplicative scale, using random-effects meta-analysis. Secondary analysis used isocaloric macronutrient substitution. RESULTS: No interactions were identified between any of the three GRSs and any macronutrient intake, with low-to-moderate heterogeneity between countries (I2range 0-51.6%). Results were similar using isocaloric macronutrient substitution analyses and when weighted and unweighted GRSs and individual SNPs were examined. CONCLUSIONS/INTERPRETATION: Genetic susceptibility to type 2 diabetes, insulin resistance and BMI did not modify the association between macronutrient intake and incident type 2 diabetes. This suggests that macronutrient intake recommendations to prevent type 2 diabetes do not need to account for differences in genetic predisposition to these three metabolic conditions.
Kröger J, Meidtner K, Stefan N, et al., 2018, Circulating Fetuin-A and risk of Type 2 Diabetes: a Mendelian randomization analysis, Diabetes, Vol: 67, Pages: 1200-1205, ISSN: 0012-1797
Fetuin-A, a hepatic-origin protein, is strongly positively associated with risk of type 2 diabetes in human observational studies, but it is unknown whether this association is causal. We aimed to study the potential causal relation of circulating fetuin-A to risk of type 2 diabetes in a Mendelian Randomization study with SNPs located in the fetuin-A-encodingAHSGgene. We used data from eight European countries of the prospective EPIC-InterAct case-cohort study including 10,020 incident cases. Plasma fetuin-A concentration was measured in a subset of 965 subcohort participants and 654 cases. A genetic score of theAHSGSNPs was strongly associated with fetuin-A (28% explained variation). Using the genetic score as instrumental variable of fetuin-A, we observed no significant association of a 50 µg/ml higher fetuin-A concentration with diabetes risk (HR 1.02 [95%-CI 0.97, 1.07]). Combining our results with those from the Diabetes Genetics Replication And Meta-analysis (DIAGRAM) consortium (12,171 cases) also did not suggest a clear significant relation of fetuin-A with diabetes risk. In conclusion, although there is mechanistical evidence for an effect of fetuin-A on insulin sensitivity and secretion, this study doesn't support a strong, relevant relationship between circulating fetuin-A and diabetes risk in the general population.
Aune D, Feng T, Schlesinger S, et al., 2018, Diabetes mellitus, blood glucose and the risk of atrial fibrillation: A systematic review and meta-analysis of cohort studies, Journal of Diabetes and its Complications, Vol: 32, Pages: 501-511, ISSN: 1056-8727
BACKGROUND: Diabetes and elevated blood glucose have been associated with increased risk of atrial fibrillation in a number of epidemiological studies, however, the findings have not been entirely consistent. We conducted a systematic review and meta-analysis to clarify the association. MATERIAL AND METHODS: We searched the PubMed and Embase databases for studies of diabetes and blood glucose and atrial fibrillation up to July 18th 2017. Cohort studies were included if they reported relative risk (RR) estimates and 95% confidence intervals (CIs) of atrial fibrillation associated with a diabetes diagnosis, prediabetes or blood glucose. Summary RRs were estimated using a random effects model. RESULTS: Thirty four studies were included in the meta-analysis of diabetes, pre-diabetes or blood glucose and atrial fibrillation. Thirty two cohort studies (464,229 cases, >10,244,043 participants) were included in the analysis of diabetes mellitus and atrial fibrillation. The summary RR for patients with diabetes mellitus versus patients without diabetes was 1.30 (95% CIs: 1.03-1.66), however, there was extreme heterogeneity, I2 = 99.9%) and evidence of publication bias with Begg's test, p < 0.0001. After excluding a very large and outlying study the summary RR was 1.28 (95% CI: 1.22-1.35, I2 = 90%, n = 31, 249,772 cases, 10,244,043 participants). The heterogeneity was mainly due to differences in the size of the association between studies and the results persisted in a number of subgroup and sensitivity analyses. The summary RR was 1.20 (95% CI: 1.03-1.39, I2 = 30%, n = 4, 2392 cases, 58,547 participants) for the association between prediabetes and atrial fibrillation. The summary RR was 1.11 (95% CI: 1.04-1.18, I2 = 61%, n = 4) per 20 mg/dl increase of blood glucose in relation to atrial fibrillation (3385 cases, 247,447 participants) and there was no evidence of nonlinearity, pnonlinearity = 0.34. CONCLUSIONS: This meta-analysis suggest that prediabetes and diabetes
Kaaks R, Fortner RT, Hüsing A, et al., 2018, Tumor-associated autoantibodies as early detection markers for ovarian cancer? A prospective evaluation., International Journal of Cancer, Vol: 143, Pages: 515-526, ISSN: 0020-7136
Immuno-proteomic screening has identified several tumor-associated autoantibodies (AAb) that may have diagnostic capacity for invasive epithelial ovarian cancer, with AAbs to P53 proteins and cancer-testis antigens (CTAGs) as prominent examples. However, the early detection potential of these AAbs has been insufficiently explored in prospective studies. We performed ELISA measurements of AAbs to CTAG1A, CTAG2, P53 and NUDT11 proteins, for 194 patients with ovarian cancer and 705 matched controls from the European EPIC cohort, using serum samples collected up to 36 months prior to diagnosis under usual care. CA125 was measured using electrochemo-luminiscence. Diagnostic discrimination statistics were calculated by strata of lead-time between blood collection and diagnosis. With lead times ≤6 months, ovarian cancer detection sensitivity at 0.98 specificity (SE98) varied from 0.19 [95% CI 0.08-0.40] for CTAG1A, CTAG2 and NUDT1 to 0.23 [0.10-0.44] for P53 (0.33 [0.11-0.68] for high-grade serous tumors). However, at longer lead-times, the ability of these AAb markers to distinguish future ovarian cancer cases from controls declined rapidly; at lead times >1 year, SE98 estimates were close to zero (all invasive cases, range: 0.01-0.11). Compared to CA125 alone, combined logistic regression scores of AAbs and CA125 did not improve detection sensitivity at equal level of specificity. The added value of these selected AAbs as markers for ovarian cancer beyond CA125 for early detection is therefore limited.
Dossus L, Franceschi S, Biessy C, et al., 2017, Adipokines and inflammation markers and risk of differentiated thyroid carcinoma:the EPIC study, International Journal of Cancer, Vol: 142, Pages: 1332-1342, ISSN: 0020-7136
Other than the influence of ionizing radiation and benign thyroid disease, little is known about the risk factors for differentiated thyroid cancer (TC) which is an increasing common cancer worldwide. Consistent evidence shows that body mass is positively associated with TC risk. As excess weight is a state of chronic inflammation, we investigated the relationship between concentrations of leptin, adiponectin, C-reactive protein, interleukin (IL)-6, IL-10 and tumor necrosis factor (TNF)-α and the risk of TC. A case-control study was nested within the European Prospective Investigation into Cancer and Nutrition (EPIC) study and included 475 first primary incident TC cases (399 women and 76 men) and 1,016 matched cancer-free cohort participants. Biomarkers were measured in serum samples using validated and highly sensitive commercially available immunoassays. Odds ratios (ORs) of TC by levels of each biomarker were estimated using conditional logistic regression models, adjusting for BMI and alcohol consumption. Adiponectin was inversely associated with TC risk among women (ORT3vs.T1 = 0.69, 95% CI: 0.49–0.98, Ptrend = 0.04) but not among men (ORT3vs.T1 = 1.36, 95% CI: 0.67–2.76, Ptrend = 0.37). Increasing levels of IL-10 were positively associated with TC risk in both genders and significantly so in women (ORT3vs.T1 = 1.59, 95% CI: 1.13–2.25, Ptrend = 0.01) but not in men (ORT3vs.T1 = 1.78, 95% CI: 0.80–3.98, Ptrend = 0.17). Leptin, CRP, IL-6 and TNF-α were not associated with TC risk in either gender. These results indicate a positive association of TC risk with IL-10 and a negative association with adiponectin that is probably restricted to women. Inflammation may play a role in TC in combination with or independently of excess weight.
van Duijnhoven FJB, Jenab M, Hveem K, et al., 2017, Circulating concentrations of vitamin D in relation to pancreatic cancer risk in European populations, International Journal of Cancer, Vol: 142, Pages: 1189-1201, ISSN: 0020-7136
Evidence from in vivo, in vitro and ecological studies are suggestive of a protective effect of vitamin D against pancreatic cancer (PC). However, this has not been confirmed by analytical epidemiological studies. We aimed to examine the association between pre-diagnostic circulating vitamin D concentrations and PC incidence in European populations. We conducted a pooled nested case-control study within the European Prospective Investigation into Cancer and Nutrition (EPIC) and the Nord-Trøndelag Health Study's second survey (HUNT2) cohorts. In total, 738 primary incident PC cases (EPIC n = 626; HUNT2 n = 112; median follow-up = 6.9 years) were matched to 738 controls. Vitamin D [25(OH)D2 and 25(OH)D3 combined] concentrations were determined using isotope-dilution liquid chromatography-tandem mass spectrometry. Conditional logistic regression models with adjustments for body mass index and smoking habits were used to estimate incidence rate ratios (IRRs) and 95% confidence intervals (95%CI). Compared with a reference category of >50 to 75 nmol/L vitamin D, the IRRs (95% CIs) were 0.71 (0.42–1.20); 0.94 (0.72–1.22); 1.12 (0.82–1.53) and 1.26 (0.79–2.01) for clinically pre-defined categories of ≤25; >25 to 50; >75 to 100; and >100 nmol/L vitamin D, respectively (p for trend = 0.09). Corresponding analyses by quintiles of season-standardized vitamin D concentrations also did not reveal associations with PC risk (p for trend = 0.23). Although these findings among participants from the largest combination of European cohort studies to date show increasing effect estimates of PC risk with increasing pre-diagnostic concentrations of vitamin D, they are not statistically significant.
Aune D, Schlesinger S, Henriksen T, et al., 2017, Physical activity and the risk of preterm birth: a systematic review and meta-analysis of epidemiological studies, BJOG-AN INTERNATIONAL JOURNAL OF OBSTETRICS AND GYNAECOLOGY, Vol: 124, Pages: 1816-1826, ISSN: 1470-0328
BackgroundPhysical activity has been inconsistently associated with risk of preterm birth, and the strength of the association and the shape of the dose–response relationship needs clarification.ObjectivesTo conduct a systematic review and dose–response meta‐analysis to clarify the association between physical activity and risk of preterm birth.Search strategyPubMed, Embase and Ovid databases were searched for relevant studies up to 9 February 2017.Selection criteriaStudies with a prospective cohort, case‐cohort, nested case‐control or randomized study design were included.Data collection and analysisData were extracted by one reviewer and checked for accuracy by a second reviewer. Summary relative risks (RRs) were estimated using a random effects model.Main resultsForty‐one studies (43 publications) including 20 randomized trials and 21 cohort studies were included. The summary RR for high versus low activity was 0.87 [95% confidence interval (CI): 0.70–1.06, I2 = 17%, n = 5] for physical activity before pregnancy, and it was 0.86 (95% CI: 0.78–0.95, I2 = 0%, n = 30) for early pregnancy physical activity. The summary RR for a 3 hours per week increment in leisure‐time activity was 0.90 (95% CI: 0.85–0.95, I2 = 0%, n = 5). There was evidence of a nonlinear association between physical activity and preterm birth, Pnonlinearity < 0.0001, with the lowest risk observed at 2–4 hours per week of activity.ConclusionThis meta‐analysis suggests that higher leisure‐time activity is associated with reduced risk of preterm birth. Further randomized controlled trials with sufficient frequency and duration of activity to reduce the risk and with larger sample sizes are needed to conclusively demonstrate an association.
Yang JJ, Yu D, Takata Y, et al., 2017, Dietary fat intake and lung cancer risk: a pooled analysis, Journal of Clinical Oncology, Vol: 35, Pages: 3055-+, ISSN: 0732-183X
PurposeDietary fat may play a role in lung carcinogenesis. Findings from epidemiologic studies, however, remain inconsistent. In this pooled analysis of 10 prospective cohort studies from the United States, Europe, and Asia, we evaluated the associations of total and specific types of dietary fat with lung cancer risk.MethodsCox regression was used to estimate hazard ratios (HRs) and 95% CIs in each cohort. Study-specific risk estimates were pooled by random- or fixed-effects meta-analysis. The first 2 years of follow-up were excluded to address potential influence of preclinical dietary changes.ResultsAmong 1,445,850 participants, 18,822 incident cases were identified (mean follow-up, 9.4 years). High intakes of total and saturated fat were associated with an increased risk of lung cancer (for highest v lowest quintile: HR, 1.07 and 1.14, respectively; 95% CI, 1.00 to 1.15 and 1.07 to 1.22, respectively; P for trend for both < .001). The positive association of saturated fat was more evident among current smokers (HR, 1.23; 95% CI, 1.13 to 1.35; P for trend < .001) than former/never smokers (P for interaction = .004), and for squamous cell and small cell carcinoma (HR, 1.61 and 1.40, respectively; 95% CI, 1.38 to 1.88 and 1.17 to 1.67, respectively; P for trend for both < .001) than other histologic types (P for heterogeneity < .001). In contrast, a high intake of polyunsaturated fat was associated with a decreased risk of lung cancer (HR, 0.92; 95% CI, 0.87 to 0.98 for highest v lowest quintile; P for trend = .02). A 5% energy substitution of saturated fat with polyunsaturated fat was associated with a 16% to 17% lower risk of small cell and squamous cell carcinoma. No associations were found for monounsaturated fat.ConclusionFindings from this large, international cohort consortium suggest that modifying dietary fat intake (ie, replacing saturated fat with polyunsaturated fat) may reduce lung cancer risk, particularly among smokers and for squamous ce
Aleksandrova K, Jenab M, Leitzmann M, et al., 2017, Physical activity, mediating factors and risk of colon cancer:insights into adiposity and circulating biomarkers from theEPIC Cohort, International Journal of Epidemiology, Vol: 46, Pages: 1823-1835, ISSN: 1464-3685
Background: There is convincing evidence that high physical activity lowers the risk of colon cancer; however, the underlying biological mechanisms remain largely unknown. We aimed to determine the extent to which body fatness and biomarkers of various biologically plausible pathways account for the association between physical activity and colon cancer.Methods: We conducted a nested case-control study in a cohort of 519 978 men and women aged 25 to 70 years followed from 1992 to 2003. A total of 713 incident colon cancer cases were matched, using risk-set sampling, to 713 controls on age, sex, study centre, fasting status and hormonal therapy use. The amount of total physical activity during the past year was expressed in metabolic equivalent of task [MET]-h/week. Anthropometric measurements and blood samples were collected at study baseline.Results: High physical activity was associated with a lower risk of colon cancer: relative risk ≥91 MET-h/week vs <91 MET-h/week = 0.75 [95% confidence interval (CI): 0.57 to 0.96]. In mediation analyses, this association was accounted for by waist circumference: proportion explained effect (PEE) = 17%; CI: 4% to 52%; and the biomarkers soluble leptin receptor (sOB-R): PEE = 15%; 95% CI: 1% to 50% and 5-hydroxyvitamin D (25[OH]D): PEE = 30%; 95% CI: 12% to 88%. In combination, these factors explained 45% (95% CI: 20% to 125%) of the association. Beyond waist circumference, sOB-R and 25[OH]D additionally explained 10% (95% CI: 1%; 56%) and 23% (95% CI: 6%; 111%) of the association, respectively.Conclusions: Promoting physical activity, particularly outdoors, and maintaining metabolic health and adequate vitamin D levels could represent a promising strategy for colon cancer prevention.
Zamora-Ros R, Beraud V, Franceschi S, et al., 2017, Consumptiion of fruits,vegetables, and fruit juices and differentiated thyroid carcinoma risk in the European Investigation into Cancer and Nutrition (EPIC) study, International Journal of Cancer, Vol: 142, Pages: 449-459, ISSN: 1097-0215
Fruit and vegetable (F&V) intake is considered as probably protective against overall cancer risk, but results in previous studies are not consistent for thyroid cancer (TC). The purpose of this study is to examine the association between the consumption of fruits, vegetables, fruit juices and differentiated thyroid cancer risk within the European Prospective Investigation into Cancer and Nutrition (EPIC) study. The EPIC study is a cohort including over half a million participants, recruited between 1991 and 2000. During a mean follow-up of 14 years, 748 incident first primary differentiated TC cases were identified. F&V and fruit juice intakes were assessed through validated country-specific dietary questionnaires. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox regression models adjusted for potential confounding factors. Comparing the highest versus lowest quartile of intake, differentiated TC risk was not associated with intakes of total F&V (HR: 0.89; 95% CI: 0.68–1.15; p-trend = 0.44), vegetables (HR: 0.89; 95% CI: 0.69–1.14; p-trend = 0.56), or fruit (HR: 1.00; 95% CI: 0.79–1.26; p-trend = 0.64). No significant association was observed with any individual type of vegetable or fruit. However, there was a positive borderline trend with fruit juice intake (HR: 1.23; 95% CI: 0.98–1.53; p-trend = 0.06). This study did not find any significant association between F&V intakes and differentiated TC risk; however a positive trend with fruit juice intake was observed, possibly related to its high sugar content.
Perez-Cornago A, Appleby PN, Pischon T, et al., 2017, Tall height and obesity are associated with an increased risk of aggressive prostate cancer: results from the EPIC cohort study, BMC Medicine, Vol: 15, ISSN: 1741-7015
BackgroundThe relationship between body size and prostate cancer risk, and in particular risk by tumour characteristics, is not clear because most studies have not differentiated between high-grade or advanced stage tumours, but rather have assessed risk with a combined category of aggressive disease. We investigated the association of height and adiposity with incidence of and death from prostate cancer in 141,896 men in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort.MethodsMultivariable-adjusted Cox proportional hazards models were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs). After an average of 13.9 years of follow-up, there were 7024 incident prostate cancers and 934 prostate cancer deaths.ResultsHeight was not associated with total prostate cancer risk. Subgroup analyses showed heterogeneity in the association with height by tumour grade (P heterogeneity = 0.002), with a positive association with risk for high-grade but not low-intermediate-grade disease (HR for high-grade disease tallest versus shortest fifth of height, 1.54; 95% CI, 1.18–2.03). Greater height was also associated with a higher risk for prostate cancer death (HR = 1.43, 1.14–1.80). Body mass index (BMI) was significantly inversely associated with total prostate cancer, but there was evidence of heterogeneity by tumour grade (P heterogeneity = 0.01; HR = 0.89, 0.79–0.99 for low-intermediate grade and HR = 1.32, 1.01–1.72 for high-grade prostate cancer) and stage (P heterogeneity = 0.01; HR = 0.86, 0.75–0.99 for localised stage and HR = 1.11, 0.92–1.33 for advanced stage). BMI was positively associated with prostate cancer death (HR = 1.35, 1.09–1.68). The results for waist circumference were generally similar to those for BMI, but the associations were slightly stronger
Aune D, Sen A, Leitzmann MF, et al., 2017, Tobacco smoking and the risk of diverticular disease - a systematic review and meta-analysis of prospective studies, Colorectal Disease, Vol: 19, Pages: 621-633, ISSN: 1462-8910
AimThis systematic review and meta-analysis aimed to clarify whether tobacco smoking is associated with an increased risk of diverticular disease.MethodThe PubMed and Embase databases were searched for studies of smoking and diverticular disease up to 19 February 2016. Prospective studies that reported adjusted relative risk (RR) estimates and 95% confidence intervals (CIs) of diverticular disease associated with current or previous smoking were included. Summary RRs were estimated using a random effects model.ResultsWe identified five prospective studies which comprised 6076 cases of incident diverticular disease (diverticulosis and diverticulitis) among 385 291 participants and three studies with 1118 cases of complications related to diverticular disease (abscess or perforation) among 292 965. The summary RR for incident diverticular disease was 1.36 (95% CI 1.15–1.61, I2 = 84%, n = 4) for current smokers, 1.17 (95% CI 1.05–1.31, I2 = 49%, n = 4) for former smokers and 1.29 (95% CI 1.16–1.44, I2 = 62%, n = 5) for ever smokers. The summary RR was 1.11 (95% CI 0.99–1.25, I2 = 82%, n = 4) per 10 cigarettes per day. Although there was some indication of nonlinearity there was a dose-dependent positive association with increasing number of cigarettes smoked per day. There was some evidence that smoking also increases the risk of complications of diverticular disease, but the number of studies was small.ConclusionThe current meta-analysis provides evidence that tobacco smoking is associated with an increased incidence of diverticular disease and related complications.
Duell EJ, Lujan-Barroso L, Sala N, et al., 2017, Plasma microRNAs as biomarkers of pancreatic cancer risk in a prospective cohort study, International Journal of Cancer, Vol: 141, Pages: 905-915, ISSN: 0020-7136
Noninvasive biomarkers for early pancreatic ductal adenocarcinoma (PDAC) diagnosis and disease risk stratification are greatly needed. We conducted a nested case-control study within the Prospective Investigation into Cancer and Nutrition (EPIC) cohort to evaluate prediagnostic microRNAs (miRs) as biomarkers of subsequent PDAC risk. A panel of eight miRs (miR-10a, -10b, -21-3p, -21-5p, -30c, -106b, -155 and -212) based on previous evidence from our group was evaluated in 225 microscopically confirmed PDAC cases and 225 controls matched on center, sex, fasting status and age/date/time of blood collection. MiR levels in prediagnostic plasma samples were determined by quantitative RT-PCR. Logistic regression was used to model levels and PDAC risk, adjusting for covariates and to estimate area under the receiver operating characteristic curves (AUC). Plasma miR-10b, -21-5p, -30c and -106b levels were significantly higher in cases diagnosed within 2 years of blood collection compared to matched controls (all p-values <0.04). Based on adjusted logistic regression models, levels for six miRs (miR-10a, -10b, -21-5p, -30c, -155 and -212) overall, and for four miRs (-10a, -10b, -21-5p and -30c) at shorter follow-up time between blood collection and diagnosis (≤5 yr, ≤2 yr), were statistically significantly associated with risk. A score based on the panel showed a linear dose-response trend with risk (p-value = 0.0006). For shorter follow-up (≤5 yr), AUC for the score was 0.73, and for individual miRs ranged from 0.73 (miR-212) to 0.79 (miR-21-5p).
Schlesinger S, Chan DSM, Vingeliene S, et al., 2017, Carbohydrates, glycemic index, glycemic load, and breast cancer risk: a systematic review and dose-response meta-analysis of prospective studies, NUTRITION REVIEWS, Vol: 75, Pages: 420-441, ISSN: 0029-6643
Context: The investigation of dose–response associations between carbohydrate intake, glycemic index, glycemic load, and risk of breast cancer stratified by menopausal status, hormone receptor status, and body mass index (BMI) remains inconclusive. Objective: A systematic review and dose–response meta-analyses was conducted to investigate these associations. Data Sources: As part of the World Cancer Research Fund/American Institute for Cancer Research Continuous Update Project, PubMed was searched up to May 2015 for relevant studies on these associations. Study Selection: Prospective studies reporting associations between carbohydrate intake, glycemic index, or glycemic load and breast cancer risk were included. Data Extraction: Two investigators independently extracted data from included studies. Results: Random-effects models were used to summarize relative risks (RRs) and 95%CIs. Heterogeneity between subgroups, including menopausal status, hormone receptor status, and BMI was explored using meta-regression. Nineteen publications were included. The summary RRs (95%CIs) for breast cancer were 1.04 (1.00–1.07) per 10 units/d for glycemic index, 1.01 (0.98–1.04) per 50 units/d for glycemic load, and 1.00 (0.96–1.05) per 50 g/d for carbohydrate intake. For glycemic index, the association appeared slightly stronger among postmenopausal women (summary RR per 10 units/d, 1.06; 95%CI, 1.02–1.10) than among premenopausal women, though the difference was not statistically significant (Pheterogeneity = 0.15). Glycemic load and carbohydrate intake were positively associated with breast cancer among postmenopausal women with estrogen-negative tumors (summary RR for glycemic load, 1.28; 95%CI, 1.08–1.52; and summary RR for carbohydrates, 1.13; 95%CI, 1.02–1.25). No differences in BMI were detected. Conclusions: Menopausal and hormone receptor status, but not BMI, might be potential influencing factors for the associations
Perez-Cornago A, Travis RC, Appleby PN, et al., 2017, Fruit and vegetable intake and prostate cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC), International Journal of Cancer, Vol: 141, Pages: 287-297, ISSN: 1097-0215
Several dietary factors have been studied in relation to prostate cancer; however, most studies have not reported on subtypes of fruit and vegetables or tumor characteristics, and results obtained so far are inconclusive. This study aimed to examine the prospective association of total and subtypes of fruit and vegetable intake with the incidence of prostate cancer overall, by grade and stage of disease, and prostate cancer death. Lifestyle information for 142,239 men participating in the European Prospective Investigation into Cancer and Nutrition from 8 European countries was collected at baseline. Multivariable Cox regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). After an average follow-up time of 13.9 years, 7,036 prostate cancer cases were identified. Compared with the lowest fifth, those in the highest fifth of total fruit intake had a significantly reduced prostate cancer risk (HR = 0.91; 95% CI = 0.83–0.99; p-trend = 0.01). No associations between fruit subtypes and prostate cancer risk were observed, except for citrus fruits, where a significant trend was found (HR = 0.94; 95% CI = 0.86–1.02; p-trend = 0.01). No associations between total and subtypes of vegetables and prostate cancer risk were observed. We found no evidence of heterogeneity in these associations by tumor grade and stage, with the exception of significant heterogeneity by tumor grade (pheterogeneity<0.001) for leafy vegetables. No significant associations with prostate cancer death were observed. The main finding of this prospective study was that a higher fruit intake was associated with a small reduction in prostate cancer risk. Whether this association is causal remains unclear.
Aune D, Sen A, o'Hartaigh B, et al., 2017, Resting heart rate and the risk of cardiovascular disease, total cancer, and all-cause mortality - A systematic review and dose-response meta-analysis of prospective studies, Nutrition, Metabolism and Cardiovascular Diseases, Vol: 27, Pages: 504-517, ISSN: 0939-4753
Background and aimEpidemiological studies have reported increased risk of cardiovascular disease, cancer and all-cause mortality with greater resting heart rate, however, the evidence is not consistent. Differences by gender, adjustment for confounding factors, as well as the potential impact of subclinical disease are not clear. A previous meta-analysis missed a large number of studies, and data for atrial fibrillation have not been summarized before. We therefore aimed to clarify these associations in a systematic review and meta-analysis of prospective studies.Methods and resultsPubMed and Embase were searched up to 29 March 2017. Summary RRs and 95% confidence intervals (CIs) were calculated using random effects models. Eighty seven studies were included. The summary RR per 10 beats per minute increase in resting heart rate was 1.07 (95% CI: 1.05–1.10, I2 = 61.9%, n = 31) for coronary heart disease, 1.09 (95% CI: 1.00–1.18, I2 = 62.3%, n = 5) for sudden cardiac death, 1.18 (95% CI: 1.10–1.27, I2 = 74.5%, n = 8) for heart failure, 0.97 (95% CI: 0.92–1.02, I2 = 91.4%, n = 9) for atrial fibrillation, 1.06 (95% CI: 1.02–1.10, I2 = 59.5%, n = 16) for total stroke, 1.15 (95% CI: 1.11–1.18, I2 = 84.3%, n = 35) for cardiovascular disease, 1.14 (95% CI: 1.06–1.23, I2 = 90.2%, n = 12) for total cancer, and 1.17 (95% CI: 1.14–1.19, I2 = 94.0%, n = 48) for all-cause mortality. There was a positive dose–response relationship for all outcomes except for atrial fibrillation for which there was a J-shaped association.ConclusionThis meta-analysis found an increased risk of coronary heart disease, sudden cardiac death, heart failure, atrial fibrillation, stroke, cardiovascular disease, total cancer and all-cause mortality with greater resting heart rate.
Aune D, Sen A, Leitzmann MF, et al., 2017, Body mass index and physical activity and the risk of diverticular disease: a systematic review and meta-analysis of prospective studies., European Journal of Nutrition, Vol: 56, Pages: 2423-2438, ISSN: 1436-6215
PURPOSE: We conducted a systematic review and meta-analysis of prospective studies of the association between body mass index (BMI) and physical activity and diverticular disease risk. METHODS: PubMed and Embase databases were searched up to February 7, 2017. Summary relative risks and 95% confidence intervals (95% CIs) were calculated using a random effects model and nonlinear associations were modeled using fractional polynomial models. RESULTS: Six cohort studies of BMI and diverticular disease risk (28,915 cases, 1,636,777 participants) and five cohort studies of physical activity and diverticular disease risk (2080 cases, 147,869 participants) were included. The summary relative risk (RR) of incident diverticular disease for a 5 unit BMI increment was 1.28 (95% CI: 1.18-1.40, I (2) = 77%, n = 6) for diverticular disease, 1.31 (95% CI: 1.09-1.56, I (2) = 74%, n = 2) for diverticulitis, and 1.20 (95% CI: 1.04-1.40, I (2) = 56%, n = 3) for diverticular disease complications. There was no evidence of a nonlinear association between BMI and diverticular disease risk (p nonlinearity = 0.22), and risk increased even within the normal weight range. Compared to a BMI of 20, the summary RR for a BMI of 22.5, 25.0, 27.5, 30.0, 32.5, 35.0, 37.5, and 40.0 was 1.15 (1.07-1.23), 1.31 (1.17-1.47), 1.50 (1.31-1.71), 1.71 (1.52-1.94), 1.96 (1.77-2.18), 2.26 (2.00-2.54), 2.60 (2.11-3.21), and 3.01 (2.06-4.39), respectively. The summary RR was 0.76 (95% CI: 0.63-0.93, I (2) = 54%, n = 5) for high vs. low physical activity and 0.74 (95% CI: 0.57-0.97, I (2) = 39.5%, p heterogeneity = 0.20, n = 2) for high vs. low vigorous physical activity. CONCLUSIONS: These results suggest that even moderate increases in BMI may increase the risk of diverticular disease as well as diverticular disease complications and that a higher le
Aune D, Sen A, Vatten LJ, 2017, Hypertension and the risk of endometrial cancer: a systematic review and meta-analysis of case-control and cohort studies, Scientific Reports, Vol: 7, ISSN: 2045-2322
A history of hypertension has been associated with increased risk of endometrial cancer in several studies, but the results have not been consistent. We conducted a systematic review and meta-analysis of case-control and cohort studies to clarify the association between hypertension and endometrial cancer risk. PubMed and Embase databases were searched up to 27th of February 2016. Prospective and case-control studies which reported adjusted relative risk estimates and 95% confidence intervals of endometrial cancer associated with a hypertension diagnosis were included. Summary relative risks were estimated using a random effects model. Twenty case-control studies and 6 cohort studies were included. The summary RR was 1.61 (95% CI: 1.41-1.85, I2=86%) for all studies, 1.73 (95% CI: 1.45-2.06, I2=89%) for case-control studies and 1.32 (95% CI: 1.12-1.56, I2=47%) for cohort studies. The association between hypertension and endometrial cancer was weaker, but still significant, among studies with adjustment for smoking, BMI, oral contraceptive use, and parity, compared to studies without such adjustment. This meta-analysis suggest an increased risk of endometrial cancer among patients with hypertension, however, further studies with more comprehensive adjustments for confounders are warranted to clarify the association.
Fedirko V, Hao QT, Gewirtz AT, et al., 2017, Exposure to bacterial products lipopolysaccharide and flagellin and hepatocellular carcinoma: a nested case-control study, BMC MEDICINE, Vol: 15, ISSN: 1741-7015
Background:Leakage of bacterial products across the gut barrier may play a role in liver diseases which often precede the development of liver cancer. However, human studies, particularly from prospective settings, are lacking.Methods:We used a case-control study design nested within a large prospective cohort to assess the association between circulating levels of anti-lipopolysaccharide (LPS) and anti-flagellin immunoglobulin A (IgA) and G (IgG) (reflecting long-term exposures to LPS and flagellin, respectively) and risk of hepatocellular carcinoma. A total of 139 men and women diagnosed with hepatocellular carcinoma between 1992 and 2010 were matched to 139 control subjects. Multivariable rate ratios (RRs), including adjustment for potential confounders, hepatitis B/C positivity, and degree of liver dysfunction, were calculated with conditional logistic regression.Results:Antibody response to LPS and flagellin was associated with a statistically significant increase in the risk of hepatocellular carcinoma (highest vs. lowest quartile: RR = 11.76, 95% confidence interval = 1.70–81.40; P trend = 0.021). This finding did not vary substantially by time from enrollment to diagnosis, and did not change after adjustment for chronic infection with hepatitis B and C viruses.Conclusions:These novel findings, based on exposures up to several years prior to diagnosis, support a role for gut-derived bacterial products in hepatocellular carcinoma development. Further study into the role of gut barrier failure and exposure to bacterial products in liver diseases is warranted.
Schlesinger S, Aleksandrova K, Abar L, et al., 2017, Adult weight gain and colorectal adenomas - a systematic review and meta-analysis., Annals of Oncology, Vol: 28, ISSN: 1569-8041
Background: Colorectal adenomas are known as precursors for the majority of colorectal carcinomas. While weight gain during adulthood has been identified as a risk factor for colorectal cancer, the association is less clear for colorectal adenomas. We conducted a systematic review and meta-analysis to quantify the evidence on this association. Methods: : We searched MEDLINE up to September 2016 to identify observational (prospective, cross-sectional and retrospective) studies on weight gain during adulthood and colorectal adenoma occurrence and recurrence. We conducted meta-analysis on high weight gain versus stable weight, linear and non-linear dose-response meta-analyses to analyze the association. Summary odds ratios (OR) and 95% confidence intervals (95% CI) were estimated using a random effects model. Results: For colorectal adenoma occurrence, the summary OR was 1.39 (95% CI: 1.17-1.65; I 2 :43%, N =9 studies, cases=5,507) comparing high (midpoint: 17.4 kg) versus stable weight gain during adulthood and with each 5 kg weight gain the odds increased by 7% (2%-11%; I 2 :65%, N =7 studies). Although there was indication of non-linearity ( Pnon-linearity <0.001) there was an increased odds of colorectal adenoma throughout the whole range of weight gain. Three studies were identified investigating the association between weight gain and colorectal adenoma recurrence and data were limited to draw firm conclusions. Conclusions: Even a small amount of adult weight gain was related to a higher odds of colorectal adenoma occurrence. Our findings add to the benefits of weight control in adulthood regarding colorectal adenomas occurrence, which might be relevant for early prevention of colorectal cancer.
Aune D, Giovannucci E, Boffetta P, et al., 2017, Fruit and vegetable intake and the risk of cardiovasculardisease, total cancer and all-cause mortality – a systematicreview and dose-response meta-analysis of prospectivestudies, International Journal of Epidemiology, Vol: 46, Pages: 1029-1056, ISSN: 1464-3685
Background: Questions remain about the strength and shape of the dose response relationship between fruit and vegetable intake and risk of cardiovascular disease, cancer and mortality, and the effects of specific types of fruit and vegetables. We conducted a systematic review and meta analysis to clarify these questions. Methods and Results: PubMed and Embase were searched up to 29th of September 2016. Prospective studies of fruit and vegetable intake and cardiovascular disease, total cancer and all cause mortality were included. Summary RRs were calculated using a random effects model and the mortality burden globally was estimated. Ninety five studies (142 publications) were included. For fruits and vegetables combined, the summary RR per 200 g/day was 0.92 (95% CI: 0.90 0.94, I2=0%, n=15) for coronary heart disease, 0.84 (95% CI: 0.76 0.92, I2=73%, n=10) for stroke, 0.92 (95% CI: 0.90 0.95, I2=31%, n=13) for cardiovascular disease, 0.97 (95% CI: 0.95 0.99, I2=49%, n=12) for total cancer, and 0.90 (95% CI: 0.87 0.93, I2=83%, n=15) for all cause mortality. Similar associations were observed for fruits and vegetables separately. Reductions in risk were observed up to 700 800 g/day for all outcomes except cancer (600 g/day). Inverse associations were observed between apples or pears, citrus fruits, green leafy vegetables, cruciferous vegetables, and salads and cardiovascular disease and mortality, and between green yellow vegetables and cruciferous vegetables and total cancer risk. An estimated 5.6 and 7.8 million premature deaths worldwide in 2013 may be attributable to a fruit and vegetable intake below 500 and 800 grams per day, respectively. Conclusion: Fruits and vegetable intakes were associated with reduced risk of cardiovascular disease, cancer and mortality. These results supports public health recommendations to increase fruit and vegetable intake for chronic disease prevention.
Aune D, Sen A, Schlesinger S, et al., 2017, Body mass index, abdominal fatness, fat mass and the risk of atrial fibrillation: a systematic review and dose–response meta-analysis of prospective studies, European Journal of Epidemiology, Vol: 32, Pages: 181-192, ISSN: 1573-7284
Different adiposity measures have been associ-ated with increased risk of atrial fibrillation, however,results have previously only been summarized for BMI.We therefore conducted a systematic review and meta-analysis of prospective studies to clarify the associationbetween different adiposity measures and risk of atrialfibrillation. PubMed and Embase databases were searchedup to October 24th 2016. Summary relative risks (RRs)were calculated using random effects models. Twenty-nineunique prospective studies (32 publications) were included.Twenty-five studies (83,006 cases, 2,405,381 participants)were included in the analysis of BMI and atrial fibrillation.The summary RR was 1.28 (95% confidence interval:1.20–1.38, I2=97%) per 5 unit increment in BMI, 1.18(95% CI: 1.12–1.25, I2=73%, n=5) and 1.32 (95% CI:1.16–1.51, I2=91%, n=3) per 10 cm increase in waistand hip circumference, respectively, 1.09 (95% CI:1.02–1.16, I2=44%, n=4) per 0.1 unit increase in waist-to-hip ratio, 1.09 (95% CI: 1.02–1.16, I2=94%, n=4)per 5 kg increase in fat mass, 1.10 (95% CI: 0.92–1.33,I2=90%, n=3) per 10% increase in fat percentage,1.10 (95% CI: 1.08–1.13, I2=74%, n=10) per 5 kgincrease in weight, and 1.08 (95% CI: 0.97–1.19,I2=86%, n=2) per 5% increase in weight gain. Theassociation between BMI and atrial fibrillation was non-linear,pnonlinearity\0.0001, with a stronger association athigher BMI levels, however, increased risk was observedeven at a BMI of 22–24 compared to 20. In conclusion,general and abdominal adiposity and higher body fat massincrease the risk of atrial fibrillation.
Huang J, Zagai U, Hallmans G, et al., 2016, Helicobacter pylori infection, chronic corpus atrophic gastritis and pancreatic cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort: a nested case-control study, International Journal of Cancer, Vol: 140, Pages: 1727-1735, ISSN: 1097-0215
The association between H. pylori infection and pancreatic cancer risk remains controversial. We conducted a nested case-control study with 448 pancreatic cancer cases and their individually matched control subjects, based on the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, to determine whether there was an altered pancreatic cancer risk associated with H. pylori infection and chronic corpus atrophic gastritis. Conditional logistic regression models were applied to calculate odds ratios (ORs) and corresponding 95% confidence intervals (CIs), adjusted for matching factors and other potential confounders. Our results showed that pancreatic cancer risk was neither associated with H. pylori seropositivity (OR=0.96; 95% CI: 0.70, 1.31) nor CagA seropositivity (OR=1.07; 95% CI: 0.77, 1.48). We also did not find any excess risk among individuals seropositive for H. pylori but seronegative for CagA, compared with the group seronegative for both antibodies (OR=0.94; 95% CI: 0.63, 1.38). However, we found that chronic corpus atrophic gastritis was non-significantly associated with an increased pancreatic cancer risk (OR=1.35; 95% CI: 0.77, 2.37), and although based on small numbers, the excess risk was particularly marked among individuals seronegative for both H. pylori and CagA (OR=5.66; 95% CI: 1.59, 20.19, p value for interaction < 0.01). Our findings provided evidence supporting the null association between H. pylori infection and pancreatic cancer risk in western European populations. However, the suggested association between chronic corpus atrophic gastritis and pancreatic cancer risk warrants independent verification in future studies, and, if confirmed, further studies on the underlying mechanisms.
Aune D, Keum N, Giovannucci E, et al., 2016, Nut consumption and risk of cardiovascular disease, total cancer, all-cause and cause-specific mortality: a systematic review and dose-response meta-analysis of prospective studies, BMC Medicine, Vol: 14, ISSN: 1741-7015
Background: Although nut consumption has been associated with a reduced risk of cardiovascular disease and all-cause mortality, data on less common causes of death has not been systematically assessed. Previous reviews missed several studies and additional studies have since been published. We therefore conducted a systematic review and meta-analysis of nut consumption and risk of cardiovascular disease, total cancer, and all-cause and cause-specific mortality. Methods: PubMed and Embase were searched for prospective studies of nut consumption and risk of cardiovascular disease, total cancer, and all-cause and cause-specific mortality in adult populations published up to July 19, 2016. Summary relative risks (RRs) and 95% confidence intervals (CIs) were calculated using random-effects models. The burden of mortality attributable to low nut consumption was calculated for selected regions. Results: Twenty studies (29 publications) were included in the meta-analysis. The summary RRs per 28 grams/day increase in nut intake was for coronary heart disease, 0.71 (95% CI: 0.63-0.80, I2=47%, n=11), stroke, 0.93 (95% CI: 0.83-1.05, I2=14%, n=11), cardiovascular disease, 0.79 (95% CI: 0.70-0.88, I2=60%, n=12), total cancer, 0.85 (95% CI: 0.76-0.94, I2=42%, n=8), all-cause mortality, 0.78 (95% CI: 0.72-0.84, I2=66%, n=15), and for mortality from respiratory disease, 0.48 (95% CI: 0.26-0.89, I2=61%, n=3), diabetes, 0.61 (95% CI: 0.43-0.88, I2=0%, n=4), neurodegenerative disease, 0.65 (95% CI: 0.40-1.08, I2=5.9%, n=3), infectious disease, 0.25 (95% CI: 0.07-0.85, I2=54%, n=2), and kidney disease, 0.27 (95% CI: 0.04-1.91, I2=61%, n=2). The results were similar for tree nuts and peanuts. If the associations are causal, an estimated 4.4 million premature deaths in the America, Europe, South-East Asia and Western Pacific would be attributable to a nut intake below 20 grams per day in 2013.Conclusion: Higher nut intake is associated with reduced risk of cardiovascular disease, total c
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