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  • 1.
    Benetou, V.
    et al.
    Univ Athens, WHO Collaborating Ctr Nutr & Hlth, Unit Nutr Epidemiol & Nutr Publ Hlth, Dept Hyg Epidemiol & Med Stat,Sch Med, 75 Mikras Asias St, Athens 11527, Greece.
    Orfanos, P.
    Hellen Hlth Fdn, Athens, Greece;Univ Athens, WHO Collaborating Ctr Nutr & Hlth, Unit Nutr Epidemiol & Nutr Publ Hlth, Dept Hyg Epidemiol & Med Stat,Sch Med, 75 Mikras Asias St, Athens 11527, Greece.
    Feskanich, D.
    Harvard Med Sch, Boston, MA USA;Brigham & Womens Hosp, Dept Med, Channing Div Network Med, 75 Francis St, Boston, MA 02115 USA.
    Michaëlsson, Karl
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Pettersson-Kymmer, U.
    Umea Univ, Dept Pharmacol & Clin Neurosci, Umea, Sweden;Umea Univ, Dept Publ Hlth & Clin Med, Umea, Sweden.
    Byberg, Liisa
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Eriksson, S.
    Umea Univ, Dept Community Med, Umea, Sweden.
    Grodstein, F.
    Harvard Med Sch, Boston, MA USA;Brigham & Womens Hosp, Dept Med, Channing Div Network Med, 75 Francis St, Boston, MA 02115 USA.
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics. Karolinska Inst, Inst Environm Med, Div Nutr Epidemiol, Stockholm, Sweden.
    Jankovic, N.
    Wageningen Univ, Div Human Nutr, Wageningen, Netherlands;Univ Duisburg Essen, Inst Med Informat Biometry & Epidemiol, Ctr Clin Epidemiol, Fac Med, Essen, Germany.
    de Groot, L. C. P. G. M.
    Wageningen Univ, Div Human Nutr, Wageningen, Netherlands.
    Boffetta, P.
    Icahn Sch Med Mt Sinai, Inst Translat Epidemiol, New York, NY 10029 USA;Icahn Sch Med Mt Sinai, Tisch Canc Inst, New York, NY 10029 USA.
    Trichopoulou, A.
    Hellen Hlth Fdn, Athens, Greece.
    Mediterranean diet and hip fracture incidence among older adults: the CHANCES project2018In: Osteoporosis International, ISSN 0937-941X, E-ISSN 1433-2965, Vol. 29, no 7, p. 1591-1599Article in journal (Refereed)
    Abstract [en]

    The association between adherence to Mediterranean diet (MD) and hip fracture incidence is not yet established. In a diverse population of elderly, increased adherence to MD was associated with lower hip fracture incidence. Except preventing major chronic diseases, adhering to MD might have additional benefits in lowering hip fracture risk. Hip fractures constitute a major public health problem among older adults. Latest evidence links adherence to Mediterranean diet (MD) with reduced hip fracture risk, but still more research is needed to elucidate this relationship. The potential association of adherence to MD with hip fracture incidence was explored among older adults. A total of 140,775 adults (116,176 women, 24,599 men) 60 years and older, from five cohorts from Europe and the USA, were followed-up for 1,896,219 person-years experiencing 5454 hip fractures. Diet was assessed at baseline by validated, cohort-specific, food-frequency questionnaires, and hip fractures were ascertained through patient registers or telephone interviews/questionnaires. Adherence to MD was evaluated by a scoring system on a 10-point scale modified to be applied also to non-Mediterranean populations. In order to evaluate the association between MD and hip fracture incidence, cohort-specific hazard ratios (HR), adjusted for potential confounders, were estimated using Cox proportional-hazards regression and pooled estimates were subsequently derived implementing random-effects meta-analysis. A two-point increase in the score was associated with a significant 4% decrease in hip fracture risk (pooled adjusted HR 0.96; 95% confidence interval (95% CI) 0.92-0.99, p(heterogeneity) = 0.446). In categorical analyses, hip fracture risk was lower among men and women with moderate (HR 0.93; 95% CI 0.87-0.99) and high (HR 0.94; 95% CI 0.87-1.01) adherence to the score compared with those with low adherence. In this large sample of older adults from Europe and the USA, increased adherence to MD was associated with lower hip fracture incidence.

  • 2.
    Ferro, Ana
    et al.
    Univ Porto, Inst Saude Publ, EPIUnit, Rua Taipas 135, P-4050600 Porto, Portugal.
    Morais, Samantha
    Univ Porto, Inst Saude Publ, EPIUnit, Rua Taipas 135, P-4050600 Porto, Portugal.
    Rota, Matteo
    Univ Milan, Dept Biomed & Clin Sci, Milan, Italy;Univ Milan, Dept Clin Sci & Community Hlth DISCCO, Milan, Italy.
    Pelucchi, Claudio
    Univ Milan, Dept Clin Sci & Community Hlth DISCCO, Milan, Italy.
    Bertuccio, Paola
    Univ Milan, Dept Clin Sci & Community Hlth DISCCO, Milan, Italy.
    Bonzi, Rossella
    Univ Milan, Dept Clin Sci & Community Hlth DISCCO, Milan, Italy.
    Galeone, Carlotta
    Univ Milan, Dept Clin Sci & Community Hlth DISCCO, Milan, Italy.
    Zhang, Zuo-Feng
    UCLA, Dept Epidemiol, Fielding Sch Publ Hlth, Los Angeles, CA USA;Jonsson Comprehens Canc Ctr, Los Angeles, CA 90034 USA.
    Matsuo, Keitaro
    Aichi Canc Ctr, Div Mol Med, Res Inst, Nagoya, Aichi, Japan.
    Ito, Hidemi
    Aichi Canc Ctr, Div Mol Med, Res Inst, Nagoya, Aichi, Japan.
    Hu, Jinfu
    Harbin Med Univ, Dept Epidemiol, Harbin, Heilongjiang, Peoples R China.
    Johnson, Kenneth C.
    Univ Ottawa, Fac Med, Sch Epidemiol Publ Hlth & Prevent Med, Ottawa, ON, Canada.
    Yu, Guo-Pei
    Peking Univ, Med Informat Ctr, Beijing, Peoples R China.
    Palli, Domenico
    ISPO, Canc Res & Prevent Inst, Mol & Nutr Epidemiol Unit, Florence, Italy.
    Ferraroni, Monica
    Univ Milan, Dept Clin Sci & Community Hlth DISCCO, Milan, Italy.
    Muscat, Joshua
    Penn State Univ, Coll Med, Penn State Hershey Med Ctr, Dept Publ Hlth Sci, Hershey, PA USA.
    Malekzadeh, Reza
    Univ Tehran Med Sci, Digest Dis Res Inst, Digest Oncol Res Ctr, Tehran, Iran.
    Ye, Weimin
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
    Song, Huan
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden;Univ Iceland, Fac Med, Ctr Publ Hlth Sci, Reykjavik, Iceland.
    Zaridze, David
    Russian NN Blokhin Canc Res Ctr, Dept Epidemiol & Prevent, Moscow, Russia.
    Maximovitch, Dmitry
    Russian NN Blokhin Canc Res Ctr, Dept Epidemiol & Prevent, Moscow, Russia.
    Fernandez de Larrea, Nerea
    Inst Salud Carlos III, Natl Ctr Epidemiol, Environm & Canc Epidemiol Unit, Madrid, Spain;CIBERESP, Madrid, Spain.
    Kogevinas, Manolis
    CIBERESP, Madrid, Spain;Ctr Res Environm Epidemiol CREAL, ISGlobal, Barcelona, Spain;Hosp del Mar, Med Res Inst, IMIM, Barcelona, Spain;UPF, Barcelona, Spain.
    Vioque, Jesus
    Miguel Hernandez Univ, Campus San Juan, Alicante, Spain;ISABIAL FISABIO Fdn, Campus San Juan, Alicante, Spain.
    Navarrete-Munoz, Eva M.
    Miguel Hernandez Univ, Campus San Juan, Alicante, Spain;ISABIAL FISABIO Fdn, Campus San Juan, Alicante, Spain.
    Pakseresht, Mohammadreza
    Univ Tehran Med Sci, Digest Dis Res Inst, Digest Oncol Res Ctr, Tehran, Iran;Univ Alberta, Dept Agr Food & Nutr Sci, Edmonton, AB, Canada;Univ Leeds, Ctr Epidemiol & Biostat, Nutr Epidemiol Grp, Leeds, W Yorkshire, England.
    Pourfarzi, Farhad
    Univ Tehran Med Sci, Digest Dis Res Inst, Digest Oncol Res Ctr, Tehran, Iran;Ardabil Univ Med Sci, Digest Dis Res Ctr, Ardebil, Iran.
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics. Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, Stockholm, Sweden.
    Orsini, Nicola
    Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, Stockholm, Sweden.
    Bellavia, Andrea
    Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, Stockholm, Sweden.
    Håkansson, Niclas
    Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, Stockholm, Sweden.
    Mu, Lina
    Univ Buffalo, Sch Publ Hlth & Hlth Profess, Dept Epidemiol & Environm Hlth, Buffalo, NY USA.
    Pastorino, Roberta
    Univ Cattolica Sacro Cuore, IRCCS Fdn Policlin Agostino Gemelli, Inst Publ Hlth, Sect Hyg, Lgo F Vito 1, I-00168 Rome, Italy.
    Kurtz, Robert C.
    Mem Sloan Kettering Canc Ctr, Dept Med, 1275 York Ave, New York, NY 10021 USA.
    Derakhshan, Mohammad H.
    Univ Tehran Med Sci, Digest Dis Res Inst, Digest Oncol Res Ctr, Tehran, Iran;Univ Glasgow, Inst Cardiovasc & Med Sci, Glasgow, Lanark, Scotland.
    Lagiou, Areti
    Athens Technol Educ Inst, Sch Hlth Profess, Dept Publ Hlth & Community Hlth, Athens, Greece.
    Lagiou, Pagona
    Univ Athens, Sch Med, Dept Hyg Epidemiol & Med Stat, Athens, Greece;Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
    Boffetta, Paolo
    Icahn Sch Med Mt Sinai, Tisch Canc Inst, New York, NY 10029 USA.
    Boccia, Stefania
    Univ Cattolica Sacro Cuore, IRCCS Fdn Policlin Agostino Gemelli, Inst Publ Hlth, Sect Hyg, Lgo F Vito 1, I-00168 Rome, Italy.
    Negri, Eva
    Univ Milan, Dept Biomed & Clin Sci, Milan, Italy.
    La Vecchia, Carlo
    Univ Milan, Dept Clin Sci & Community Hlth DISCCO, Milan, Italy.
    Peleteiro, Barbara
    Univ Porto, Inst Saude Publ, EPIUnit, Rua Taipas 135, P-4050600 Porto, Portugal;Univ Porto, Fac Med, Dept Ciencias Saude Publ & Forenses & Educ Med, Al Prof Hernani Monteiro, P-4200319 Porto, Portugal.
    Lunet, Nuno
    Univ Porto, Inst Saude Publ, EPIUnit, Rua Taipas 135, P-4050600 Porto, Portugal;Univ Porto, Fac Med, Dept Ciencias Saude Publ & Forenses & Educ Med, Al Prof Hernani Monteiro, P-4200319 Porto, Portugal.
    Alcohol intake and gastric cancer: Meta-analyses of published data versus individual participant data pooled analyses (StoP Project)2018In: Cancer Epidemiology, ISSN 1877-7821, E-ISSN 1877-783X, Vol. 54, p. 125-132Article in journal (Refereed)
    Abstract [en]

    Background: Individual participant data pooled analyses allow access to non-published data and statistical reanalyses based on more homogeneous criteria than meta-analyses based on systematic reviews. We quantified the impact of publication-related biases and heterogeneity in data analysis and presentation in summary estimates of the association between alcohol drinking and gastric cancer.

    Methods: We compared estimates obtained from conventional meta-analyses, using only data available in published reports from studies that take part in the Stomach Cancer Pooling (StoP) Project, with individual participant data pooled analyses including the same studies.

    Results: A total of 22 studies from the StoP Project assessed the relation between alcohol intake and gastric cancer, 19 had specific data for levels of consumption and 18 according to cancer location; published reports addressing these associations were available from 18, 5 and 5 studies, respectively. The summary odds ratios [OR, (95%CI)] estimate obtained with published data for drinkers vs. non-drinkers was 10% higher than the one obtained with individual StoP data [18 vs. 22 studies: 1.21 (1.07-1.36) vs. 1.10 (0.99-1.23)] and more heterogeneous (1(2): 63.6% vs 54.4%). In general, published data yielded less precise summary estimates (standard errors up to 2.6 times higher). Funnel plot analysis suggested publication bias.

    Conclusion: Meta-analyses of the association between alcohol drinking and gastric cancer tended to overestimate the magnitude of the effects, possibly due to publication bias. Additionally, individual participant data pooled analyses yielded more precise estimates for different levels of exposure or cancer subtypes.

  • 3. Kaluza, J
    et al.
    Håkansson, N
    Harris, H R
    Orsini, N
    Michaëlsson, Karl
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences.
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Influence of anti-inflammatory diet and smoking on mortality and survival in men and women: two prospective cohort studies.2018In: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The associations between an anti-inflammatory diet and both all-cause and cause-specific mortality have been studied previously; however, the influence of an anti-inflammatory diet on survival time has not been investigated. Moreover, the potential modification of these associations by smoking status remains unclear.

    OBJECTIVE: The aims of this study were to examine the associations between an anti-inflammatory diet index (AIDI) and all-cause and cause-specific mortality, to determine the association between the AIDI and differences in survival time and to assess effect modification by smoking status.

    METHODS: The study population included 68 273 Swedish men and women (aged 45-83 years) at baseline. The anti-inflammatory potential of the diet was estimated using the validated AIDI, which includes 11 potential anti-inflammatory and five potential pro-inflammatory foods. Cox proportional hazards and Laplace regression were used to estimate hazard ratios and differences in survival time.

    RESULTS: During 16 years of follow-up (1 057 959 person-years), 16 088 deaths [5980 due to cardiovascular disease (CVD) and 5252 due to cancer] were recorded. Participants in the highest versus lowest quartile of the AIDI had lower risks of all-cause (18% reduction, 95% CI: 14-22%), CVD (20%, 95% CI: 14-26%) and cancer (13%, 95% CI: 5-20%) mortality. The strongest inverse associations between the highest and lowest quartiles of AIDI and risk of mortality were observed in current smokers: 31%, 36% and 22% lower risks of all-cause, CVD and cancer mortality, respectively. The difference in survival time between current smokers in the lowest AIDI quartile and never smokers in the highest quartile was 4.6 years.

    CONCLUSION: Adherence to a diet with high anti-inflammatory potential may reduce all-cause, CVD and cancer mortality and prolong survival time especially amongst smokers.

  • 4.
    Kaluza, Joanna
    et al.
    Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, Stockholm, Sweden.; Warsaw Univ Life Sci SGGW, Dept Human Nutr, Nutr Res Lab, 159C Nowoursynowska St, PL-02776 Warsaw, Poland..
    Harris, Holly
    Fred Hutchinson Canc Res Ctr, Program Epidemiol, Div Publ Hlth Sci, Seattle, WA 98104 USA.
    Melhus, Håkan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical pharmacogenomics and osteoporosis.
    Michaëlsson, Karl
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics. Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, Stockholm, Sweden.
    Questionnaire-Based Anti-Inflammatory Diet Index as a Predictor of Low-Grade Systemic Inflammation.2018In: Antioxidants and Redox Signaling, ISSN 1523-0864, E-ISSN 1557-7716, Vol. 28, no 1, p. 78-84Article in journal (Refereed)
    Abstract [en]

    There is accumulating evidence that diet may be associated with markers of inflammation. We have evaluated if an empirically developed questionnaire-based Anti-Inflammatory Diet Index (AIDI) may predict low-grade systemic chronic inflammation in a Nordic population. The AIDI was developed using a 123-item food frequency questionnaire among 3503 women (56-74 years old) with high-sensitivity C-reactive protein (hsCRP) plasma concentration <20 mg/L. Using Spearman correlations, we identified 20 foods (AIDI-20) statistically significantly related to hsCRP. The median (range) of AIDI-20 was 8 (0-17) scores, and the median concentration of hsCRP in the lowest versus the highest quintile of AIDI-20 (≤6 vs. ≥11 scores) varied by 80% (1.8 vs. 1.0 mg/L, respectively). In a multivariable-adjusted linear regression model, women in the highest quintile of AIDI-20 compared with those in the lowest had a 26% (95% confidence interval [CI] 18-33%; p-trend <0.001) lower hsCRP concentration; each 1-score increment in the AIDI-20 was associated with a 0.06 (95% CI 0.04-0.08) mg/L lower hsCRP. The observed association between the AIDI-20 and hsCRP was robust by all hsCRP levels and in subgroups defined by inflammatory-related factors. Our results lead to the hypothesis that the empirically developed questionnaire-based dietary anti-inflammatory index may predict low-grade systemic inflammation. Antioxid. Redox Signal. 28, 78-84.

  • 5. Kaluza, Joanna
    et al.
    Harris, Holly
    Wallin, Alice
    Linden, Anders
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics. Karolinska Inst, Unit Nutr Epidemiol, Inst Environm Med, Stockholm, Sweden.
    Dietary Fiber Intake and Risk of Chronic Obstructive Pulmonary Disease: A Prospective Cohort Study of Men.2018In: Epidemiology, ISSN 1044-3983, E-ISSN 1531-5487, Vol. 29, no 2, p. 254-260Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The limited literature suggests that dietary fiber intake from whole grains, fruits, and vegetables is negatively associated with chronic obstructive pulmonary disease (COPD) via fiber's anti-inflammatory properties. Therefore, we investigated the association between total fiber and fiber sources and risk of COPD in the population-based prospective Cohort of Swedish Men (45,058 men, aged 45-79 years) with no history of COPD at baseline.

    METHODS: Dietary fiber intake was assessed with a self-administered questionnaire in 1997 and was energy-adjusted using the residual method. Cox proportional hazard regression models were used to estimate hazard ratios (HRs) with 95% confidence intervals (95% CIs) adjusted for potential confounders.

    RESULTS: During a mean follow-up of 13.1 years (1998-2012), 1,982 incident cases of COPD were ascertained via linkage to the Swedish health registers. A strong inverse association between total fiber intake (≥36.8 vs. <23.7 g/day) and COPD was observed in current smokers (hazard ratio [HR]=0.54; 95% confidence interval [CI]=0.43-0.67) and ex-smokers (HR=0.62, 95%CI=0.50-0.78) but not in never smokers (HR=0.93; 95%CI=0.60-1.45;P-interaction=0.04). For cereal fiber, HRs for highest vs. lowest quintile were 0.62 (95%CI=0.51-0.77,P-trend<0.001) in current smokers and 0.66 (95%CI=0.52-0.82,P-trend<0.001) in ex-smokers; for fruit fiber the HR was 0.65 (95%CI=0.52-0.81,P-trend<0.001) in current smokers and 0.77 (95%CI=0.61-0.98,P-trend=0.17) in ex-smokers; for vegetable fiber it was 0.71 (95%CI=0.57-0.88,P-trend=0.003) in current smokers and 0.92 (95%CI=0.71-1.19,P-trend=0.48) in ex-smokers.

    CONCLUSION: Our findings indicate that high fiber intake was inversely associated with COPD incidence in men who are current or ex-smokers.

  • 6.
    Khalili, Hamed
    et al.
    Harvard Med Sch, Gastroenterol Unit, Clin & Translat Epidemiol Unit, Massachusetts Gen Hosp, Boston, MA 02115 USA;Karolinska Inst, Clin Epidemiol Unit, Dept Med Solna, Inst Environm Med, Stockholm, Sweden.
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics. Karolinska Inst, Dept Med Epidemiol & Biostat, Inst Environm Med, Stockholm, Sweden.
    Reply to: The Association Between Consumption of Sweetened Beverages and the Risk of Inflammatory Bowel Disease2018In: Clinical Gastroenterology and Hepatology, ISSN 1542-3565, E-ISSN 1542-7714, Vol. 16, no 10, p. 1682-1682Article in journal (Other academic)
  • 7.
    Larsson, S. C.
    et al.
    Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, SE-17177 Stockholm, Sweden.
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics. Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, SE-17177 Stockholm, Sweden;Uppsala Univ, Dept Surg Sci, Uppsala, Sweden.
    Håkansson, N.
    Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, SE-17177 Stockholm, Sweden.
    Bäck, M.
    Karolinska Inst, Ctr Mol Med, Dept Med, Stockholm, Sweden;Karolinska Univ Hosp, Dept Cardiol, Stockholm, Sweden.
    Coffee consumption and risk of aortic valve stenosis: A prospective study2018In: NMCD. Nutrition Metabolism and Cardiovascular Diseases, ISSN 0939-4753, E-ISSN 1590-3729, Vol. 28, no 8, p. 803-807Article in journal (Refereed)
    Abstract [en]

    Background and aims: Coffee contains many biologically active compounds with potential adverse or beneficial effects on the cardiovascular system. Whether coffee consumption is associated with the risk of aortic valve stenosis (AVS) is unknown. The purpose of this study was therefore to examine the association between coffee consumption and AVS incidence.

    Methods and results: This prospective study included 71 178 men and women who provided information on their coffee consumption through a questionnaire at baseline. Incident cases of AVS were identified through linkage with the Swedish National Patient and Cause of Death Registers. During a mean follow-up of 15.2 years, 1295 participants (777 men and 518 women) were diagnosed with AVS. Coffee consumption was positively associated with risk of AVS in a dose - response manner after adjustment for age, sex, smoking, and other risk factors (P-trend = 0.005). The multivariable hazard ratios were was 1.11 (95% confidence interval 1.04 - 1.19) per 2 cups/day increase of coffee consumption and 1.65 (95% confidence interval 1.10 - 2.48) when comparing the highest (>= 6 cups/day) with the lowest (<0.5 cup/day) category of coffee consumption. The association was not modified by other risk factors.

    Conclusions: This study provides novel evidence that high coffee consumption is associated with an increased risk of AVS.

  • 8.
    Larsson, Susanna C.
    et al.
    Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, SE-17177 Stockholm, Sweden.
    Drca, Nikola
    Karolinska Inst, Karolinska Univ Hosp, Dept Cardiol, Stockholm, Sweden.
    Björck, Martin
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Vascular Surgery.
    Bäck, Magnus
    Karolinska Univ Hosp, Div Valvular & Coronary Dis, Stockholm, Sweden;Karolinska Inst, Dept Med, Ctr Mol Med, Stockholm, Sweden.
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences. Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, SE-17177 Stockholm, Sweden.
    Nut consumption and incidence of seven cardiovascular diseases2018In: Heart, ISSN 1355-6037, E-ISSN 1468-201X, Vol. 104, no 19, p. 1615-1620Article in journal (Refereed)
    Abstract [en]

    Background Nut consumption has been found to be inversely associated with cardiovascular disease mortality, but the association between nut consumption and incidence of specific cardiovascular diseases is unclear. We examined the association between nut consumption and incidence of seven cardiovascular diseases. Methods This prospective study included 61 364 Swedish adults who had completed a Food Frequency Questionnaire and were followed up for 17 years through linkage with the Swedish National Patient and Death Registers. Results Nut consumption was inversely associated with risk of myocardial infarction, heart failure, atrial fibrillation and abdominal aortic aneurysm in the age-adjusted and sex-adjusted analysis. However, adjustment for multiple risk factors attenuated these associations and only a linear, dose-response, association with atrial fibrillation (p(trend)=0.004) and a non-linear association (p(non-linearity)=0.003) with heart failure remained. Compared with no consumption of nuts, the multivariable HRs (95% CI) of atrial fibrillation across categories of nut consumption were 0.97 (0.93 to 1.02) for 1-3 times/month, 0.88 (0.79 to 0.99) for 1-2 times/week and 0.82 (0.68 to 0.99) for 3times/week. For heart failure, the corresponding HRs (95% CI) were 0.87 (0.80 to 0.94), 0.80 (0.67 to 0.97) and 0.98 (0.76 to 1.27). Nut consumption was not associated with risk of aortic valve stenosis, ischaemic stroke or intracerebral haemorrhage. Conclusions These findings suggest that nut consumption or factors associated with this nutritional behaviour may play a role in reducing the risk of atrial fibrillation and possibly heart failure. Trial registration number NCT01127711 and NCT01127698; Results.

  • 9.
    Larsson, Susanna C
    et al.
    Unit of Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Drca, Nikola
    Karolinska Inst, Karolinska Univ Hosp, Dept Cardiol, Stockholm, Sweden.
    Jensen-Urstad, Mats
    Karolinska Inst, Karolinska Univ Hosp, Dept Cardiol, Stockholm, Sweden.
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics. Unit of Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Chocolate consumption and risk of atrial fibrillation: Two cohort studies and a meta-analysis2018In: American Heart Journal, ISSN 0002-8703, E-ISSN 1097-6744, Vol. 195, p. 86-90Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Chocolate consumption has been inconsistently associated with risk of atrial fibrillation (AF). We investigated the association between chocolate consumption and risk of AF in Swedish adults from two cohort studies and conducted a meta-analysis to summarize available evidence from cohort studies on this topic.

    METHODS: Our study population comprised 40,009 men from the Cohort of Swedish Men and 32,486 women from the Swedish Mammography Cohort. Incident AF cases were ascertained through linkage with the Swedish National Patient Register. Published cohort studies of chocolate consumption in relation to risk of AF were identified by a PubMed search through September 14, 2017.

    RESULTS: During a mean follow-up of 14.6 years, AF was diagnosed in 9978 Swedish men and women. Compared with non-consumers, the multivariable hazard ratio of AF for those in the highest category of chocolate consumption (≥3-4 servings/week) was 0.96 (95% CI 0.88-1.04). In a random-effects meta-analysis of 5 cohort studies, including 180,454 participants and 16,356 AF cases, the hazard ratios of AF were 0.97 (95% CI 0.94-1.01) per 2 servings/week increase in chocolate consumption and 0.96 (95% CI 0.90-1.03) for the highest versus lowest category of chocolate consumption.

    CONCLUSION: Available data provide no evidence of an association of chocolate consumption with risk of AF.

  • 10.
    Larsson, Susanna C.
    et al.
    Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, S-17177 Stockholm, Sweden.
    Wallin, Alice
    Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, S-17177 Stockholm, Sweden.
    Håkansson, Niclas
    Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, S-17177 Stockholm, Sweden.
    Stackelberg, Otto
    Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, S-17177 Stockholm, Sweden;Stockholm South Gen Hosp, Dept Surg, Stockholm, Sweden.
    Bäck, Magnus
    Karolinska Univ Hosp, Div Valvular & Coronary Dis, Stockholm, Sweden;Karolinska Inst, Ctr Mol Med, Dept Med, Stockholm, Sweden.
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics. Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, S-17177 Stockholm, Sweden.
    Type 1 and type 2 diabetes mellitus and incidence of seven cardiovascular diseases2018In: International Journal of Cardiology, ISSN 0167-5273, E-ISSN 1874-1754, Vol. 262, p. 66-70Article in journal (Refereed)
    Abstract [en]

    Background: The association between type 1 diabetes mellitus (T1DM) and specific cardiovascular diseases (CVD) is uncertain. Furthermore, data on type 2 diabetes mellitus (T2DM) in relation to risk of aortic valve stenosis, atrial fibrillation, abdominal aortic aneurysm, and intracerebral hemorrhage are scarce and inconclusive. We examined the associations of T1DM and T2DM with incidence of seven CVD outcomes.

    Methods: This study comprised 71,483 Swedish adults from two population-based prospective cohorts. T1DM and T2DM diagnosis and incident CVD cases were ascertained through linkage with the population-based registers.

    Results: T1DM was associated with myocardial infarction (hazard ratio [HR] 3.26; 95% confidence interval [CI] 2.47-4.30), heart failure (HR 2.68; 95% CI 1.76-4.09), and ischemic stroke (HR 2.61; 95% CI 1.80-3.79). Increased risk of myocardial infarction, ischemic stroke, and heart failure was also observed in T2DM patients and the magnitude of the associations increased with longer T2DM duration. T2DM was also associated with an increased risk of aortic valve stenosis (HR 1.34; 95% CI 1.05-1.71) and with lower risk of abdominal aortic aneurysm (HR 0.57; 95% CI 0.40-0.82) and intracerebral hemorrhage (HR 0.51; 95% CI 0.30-0.88). Only long-term T2DM(>= 20 years) was associated with an increased risk of atrial fibrillation (HR 1.44; 95% CI 1.02-2.04).

    Conclusion: T1DM and T2DM are associated with increased risk of major CVD outcomes. Trial registration: The Cohort of Swedish Men and the Swedish Mammography Cohort are registered at clinicaltrials.gov as NCT01127711 and NCT01127698, respectively.

  • 11.
    Michaëlsson, Karl
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Lohmander, L S
    Turkiewicz, A
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Nilsson, P
    Englund, M
    Association between statin use and consultation or surgery for osteoarthritis of the hip or knee: a pooled analysis of four cohort studies.2017In: Osteoarthritis and Cartilage, ISSN 1063-4584, E-ISSN 1522-9653, Vol. 25, no 11, p. 1804-1813, article id S1063-4584(17)31102-0Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: Experimental findings and previous observational data have suggested lower risk of osteoarthritis (OA) with statin use but results are inconsistent. Large-scale studies with a clinically important outcome are needed. Thus, we aimed to determine whether statin use is associated with a reduced risk of developing clinically-defined hip or knee OA.

    DESIGN: Pooled analysis based on time-to-event analysis of four population-based large cohorts, encompassing in total 132,607 persons aged 57-91 years resident in southern and central Sweden. We studied the association between statin use and time to consultation or surgery for OA of the hip or knee by time-dependent exposure analysis and Cox regression.

    RESULTS: During 7.5 years of follow-up, we identified 7468 out- or inpatient treated cases of hip or knee OA. Compared with never use, current use of statins conferred no overall reduction in the risk of OA with an adjusted pooled hazard ratio (HR) of 1.04 (95% confidence intervals [95% CI] 0.99-1.10). We found no dose-response relation between duration of current statin use and the risk of OA, with similar HRs among patients with less than 1 year of use (HR 1.09; 95% CI 0.92-1.32) as in patients with use for 3 years or more (HR 1.05; 0.93-1.16). Results were comparable in those with low, medium and high dose of current statin use, without indications of heterogeneity of study results.

    CONCLUSION: Statin use is not associated with reduced risk of consultation or surgery for OA of the hip or knee.

  • 12.
    Michaëlsson, Karl
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics. Karolinska Inst, Natl Inst Environm Med, Div Nutr Epidemiol, Stockholm, Sweden.
    Warensjö, Eva
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Melhus, Håkan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Clinical pharmacogenomics and osteoporosis.
    Byberg, Liisa
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Intake of milk or fermented milk combined with fruit and vegetable consumption in relation to hip fracture rates: A cohort study of Swedish women.2018In: Journal of Bone and Mineral Research, ISSN 0884-0431, E-ISSN 1523-4681, Vol. 33, no 3, p. 449-457Article in journal (Refereed)
    Abstract [en]

    Milk products may differ in pro-oxidant properties and their effects on fracture risk could potentially be modified by the intake of foods with antioxidant activity. In the population-based Swedish Mammography Cohort study, we aimed to determine how milk and fermented milk combined with fruit and vegetable consumption are associated with hip fracture. Women born 1914-1948 (n=61 240) answered food frequency and lifestyle questionnaires in 1987-1990 and 38 071 women contributed with updated information in 1997. During a mean follow-up of 22 years, 5827 women had a hip fracture (ascertained via official register data). Compared with a low intake of milk (<1 glass/day) and a high intake of fruits and vegetables (≥5 servings/day), a high intake of milk (≥3 glasses/day) with a concomitant low intake of fruits and vegetables (<2 servings/day) resulted in a HR of 2.49 (95% CI, 2.03-3.05). This higher hip fracture rate among high consumers of milk was only modestly attenuated with a concomitant high consumption of fruit and vegetables (HR 2.14; 95% CI 1.69-2.71). The combination of fruits and vegetables with fermented milk (yogurt or soured milk) yielded a different pattern with lowest rates of hip fracture in high consumers: HR 0.81 (95% CI, 0.68-0.97) for ≥2 servings/day of fermented milk and ≥5 servings/day of fruits and vegetables compared with low consumption of both fruit and vegetables and fermented milk. We conclude that the amount and type of dairy products as well as fruit and vegetable intake are differentially associated with hip fracture rates in women.

  • 13.
    Neumeyer, Sonja
    et al.
    German Canc Res Ctr, Div Canc Epidemiol, D-69120 Heidelberg, Germany.
    Banbury, Barbara L.
    Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98124 USA.
    Arndt, Volker
    German Canc Res Ctr, Div Clin Epidemiol & Aging Res, D-69120 Heidelberg, Germany.
    Berndt, Sonja I.
    NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
    Bezieau, Stephane
    CHU Nantes, Nantes Serv Genet Med, F-44093 Nantes, France.
    Bien, Stephanie A.
    Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98124 USA.
    Buchanan, Dan D.
    Univ Melbourne, Dept Pathol, Genet Epidemiol Lab, Colorectal Oncogen Grp, Melbourne, Vic 3010, Australia;Univ Melbourne, Ctr Epidemiol & Biostat, Melbourne Sch Populat & Global Hlth, Parkville, Vic 3010, Australia.
    Butterbach, Katja
    German Canc Res Ctr, Div Canc Epidemiol, D-69120 Heidelberg, Germany.
    Caan, Bette J.
    Kaiser Permanente Med Care Program Northern Calif, Div Res, Oakland, CA 94612 USA.
    Campbell, Peter T.
    Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA.
    Casey, Graham
    Univ Virginia, Ctr Publ Hlth Genom, Charlottesville, VA 22908 USA.
    Chan, Andrew T.
    Massachusetts Gen Hosp, Clin & Translat Epidemiol Unit, Boston, MA 02115 USA;Massachusetts Gen Hosp, Div Gastroenterol, Boston, MA 02115 USA;Brigham & Womens Hosp, Channing Div Network Med, 75 Francis St, Boston, MA 02115 USA;Harvard Med Sch, Boston, MA 02115 USA;Harvard Med Sch, Massachusetts Gen Hosp, Dept Med, Boston, MA 02115 USA.
    Chanock, Stephen J.
    NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
    Dai, James Y.
    Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98124 USA.
    Gallinger, Steven
    Mt Sinai Hosp, Lunenfeld Tanenbaum Res Inst, Toronto, ON M5G 1X5, Canada.
    Giovannucci, Edward L.
    Brigham & Womens Hosp, Channing Div Network Med, 75 Francis St, Boston, MA 02115 USA;Harvard Med Sch, Boston, MA 02115 USA;Harvard Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA;Harvard Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA;Harvard Med Sch, Dept Med, Boston, MA 02115 USA.
    Giles, Graham G.
    Univ Melbourne, Ctr Epidemiol & Biostat, Melbourne Sch Populat & Global Hlth, Parkville, Vic 3010, Australia;Canc Council Victoria, Canc Epidemiol & Intelligence Div, Melbourne, Vic 3010, Australia.
    Grady, William M.
    Univ Washington, Sch Med, Dept Med, Div Gastroenterol, Seattle, WA 98195 USA;Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98109 USA.
    Hampe, Jochen
    Tech Univ Dresden, Univ Hosp Dresden, Dept Med 1, D-01307 Dresden, Germany.
    Hoffmeister, Michael
    German Canc Res Ctr, Div Clin Epidemiol & Aging Res, D-69120 Heidelberg, Germany.
    Hopper, John L.
    Univ Melbourne, Ctr Epidemiol & Biostat, Melbourne Sch Populat & Global Hlth, Parkville, Vic 3010, Australia.
    Hsu, Li
    Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98124 USA.
    Jenkins, Mark A.
    Univ Melbourne, Ctr Epidemiol & Biostat, Melbourne Sch Populat & Global Hlth, Parkville, Vic 3010, Australia.
    Joshi, Amit
    Harvard Med Sch, Massachusetts Gen Hosp, Dept Med, Boston, MA 02115 USA;Harvard Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
    Larsson, Susanna C.
    Karolinska Inst Solna, Inst Environm Med, SE-17177 Stockholm, Sweden.
    Le Marchand, Loic
    Univ Hawaii, Ctr Canc, Epidemiol Program, Honolulu, HI 96822 USA.
    Lindblom, Annika
    Karolinska Univ Hosp Solna, Dept Clin Genet, SE-17177 Stockholm, Sweden;Karolinska Inst Solna, Dept Mol Med & Surg, SE-17177 Stockholm, Sweden.
    Moreno, Victor
    Bellvitge Biomed Res Inst IDIBELL, Catalan Inst Oncol, Barcelona 08028, Spain;CIBERESP, Madrid 28029, Spain;Univ Barcelona, E-08007 Barcelona, Spain.
    Lemire, Mathieu
    Ontario Inst Canc Res, Toronto, ON M5G 0A3, Canada.
    Li, Li
    Case Western Reserve Univ, Dept Family Med & Community Hlth, Cleveland, OH 44106 USA.
    Lin, Yi
    Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98124 USA.
    Offit, Kenneth
    Mem Sloan Kettering Canc Ctr, Clin Genet Serv, Dept Med, New York, NY 10065 USA.
    Newcomb, Polly A.
    Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98124 USA.
    Pharaoh, Paul D.
    Univ Cambridge, Ctr Canc Genet Epidemiol, Dept Publ Hlth & Primary Care, Cambridge CB2 8AR, England.
    Potter, John D.
    Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98124 USA.
    Qi, Lihong
    Univ Calif Davis, Dept Publ Hlth Sci, Sacramento, CA 95817 USA.
    Rennert, Gad
    Technion Israel Inst Technol, Bruce Rappaport Fac Med, Haifa, Israel;Natl Israeli Canc Control Ctr, Clalit Hlth Serv, IL-34361 Haifa, Israel;Carmel Hosp, Dept Community Med & Epidemiol, IL-34361 Haifa, Israel.
    Schafmayer, Clemens
    Univ Hosp Schleswig Holstein, Dept Gen & Thorac Surg, Campus Kiel, D-24118 Kiel, Germany.
    Schoen, Robert E.
    Univ Pittsburgh, Med Ctr, Dept Med & Epidemiol, Pittsburgh, PA 15213 USA.
    Slattery, Martha L.
    Univ Utah, Hlth Sci Ctr, Dept Internal Med, Salt Lake City, UT 84108 USA.
    Song, Mingyang
    Massachusetts Gen Hosp, Clin & Translat Epidemiol Unit, Boston, MA 02115 USA;Massachusetts Gen Hosp, Div Gastroenterol, Boston, MA 02115 USA;Harvard Med Sch, Massachusetts Gen Hosp, Dept Med, Boston, MA 02115 USA;Harvard Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
    Ulrich, Cornelia M.
    Univ Utah, Huntsman Canc Inst, Salt Lake City, UT 84112 USA;Univ Utah, Dept Populat Hlth Sci, Salt Lake City, UT 84112 USA.
    Win, Aung K.
    Univ Melbourne, Ctr Epidemiol & Biostat, Melbourne Sch Populat & Global Hlth, Parkville, Vic 3010, Australia;Royal Melbourne Hosp, Genet Med & Familial Canc Ctr, Parkville, Vic 3050, Australia.
    White, Emily
    Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98124 USA.
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics. Karolinska Inst Solna, Inst Environm Med, SE-17177 Stockholm, Sweden.
    Woods, Michael O.
    Mem Univ Newfoundland, Fac Med, St John, NF A1C 5S7, Canada.
    Wu, Anna H.
    Univ Southern Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
    Gruber, Stephen B.
    Univ Southern Calif, Keck Sch Med, Dept Med, Los Angeles, CA 90033 USA.
    Brenner, Hermann
    German Canc Res Ctr, Div Clin Epidemiol & Aging Res, D-69120 Heidelberg, Germany;German Canc Res Ctr, Div Prevent Oncol, D-69120 Heidelberg, Germany;Natl Ctr Tumor Dis NCT, D-69120 Heidelberg, Germany;German Canc Res Ctr, German Canc Consortium DKTK, D-69120 Heidelberg, Germany.
    Peters, Ulrike
    Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98124 USA.
    Chang-Claude, Jenny
    German Canc Res Ctr, Div Canc Epidemiol, D-69120 Heidelberg, Germany;Univ Canc Ctr Hamburg, Univ Med Ctr Hamburg Eppendorf, Genet Tumour Epidemiol Grp, D-20246 Hamburg, Germany.
    Mendelian randomisation study of age at menarche and age at menopause and the risk of colorectal cancer2018In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 118, no 12, p. 1639-1647Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Substantial evidence supports an association between use of menopausal hormone therapy and decreased colorectal cancer (CRC) risk, indicating a role of exogenous sex hormones in CRC development. However, findings on endogenous oestrogen exposure and CRC are inconsistent.

    METHODS: We used a Mendelian randomisation approach to test for a causal effect of age at menarche and age at menopause as surrogates for endogenous oestrogen exposure on CRC risk. Weighted genetic risk scores based on 358 single-nucleotide polymorphisms associated with age at menarche and 51 single-nucleotide polymorphisms associated with age at menopause were used to estimate the association with CRC risk using logistic regression in 12,944 women diagnosed with CRC and 10,741 women without CRC from three consortia. Sensitivity analyses were conducted to address pleiotropy and possible confounding by body mass index.

    RESULTS: Genetic risk scores for age at menarche (odds ratio per year 0.98, 95% confidence interval: 0.95-1.02) and age at menopause (odds ratio 0.98, 95% confidence interval: 0.94-1.01) were not significantly associated with CRC risk. The sensitivity analyses yielded similar results.

    CONCLUSIONS: Our study does not support a causal relationship between genetic risk scores for age at menarche and age at menopause and CRC risk.

  • 14. Rasouli, B
    et al.
    Ahlqvist, E
    Alfredsson, L
    Andersson, T
    Carlsson, Per-Ola
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Groop, L
    Löfvenborg, J E
    Martinell, Mats
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Family Medicine and Preventive Medicine.
    Rosengren, A
    Tuomi, T
    Wolk, Alicja
    Carlsson, S
    Coffee consumption, genetic susceptibility and risk of latent autoimmune diabetes in adults: A population-based case-control study.2018In: Diabetes & Metabolism, ISSN 1262-3636, E-ISSN 1878-1780, Vol. 44, no 4, p. 354-360, article id S1262-3636(18)30087-9Article in journal (Refereed)
    Abstract [en]

    AIM: Coffee consumption is inversely related to risk of type 2 diabetes (T2D). In contrast, an increased risk of latent autoimmune diabetes in adults (LADA) has been reported in heavy coffee consumers, primarily in a subgroup with stronger autoimmune characteristics. Our study aimed to investigate whether coffee consumption interacts with HLA genotypes in relation to risk of LADA.

    METHODS: This population-based study comprised incident cases of LADA (n=484) and T2D (n=1609), and also 885 healthy controls. Information on coffee consumption was collected by food frequency questionnaire. Odds ratios (ORs) with 95% CIs of diabetes were calculated and adjusted for age, gender, BMI, education level, smoking and alcohol intake. Potential interactions between coffee consumption and high-risk HLA genotypes were calculated by attributable proportion (AP) due to interaction.

    RESULTS: Coffee intake was positively associated with LADA in carriers of high-risk HLA genotypes (OR: 1.14 per cup/day, 95% CI: 1.02-1.28), whereas no association was observed in non-carriers (OR: 1.04, 95% CI: 0.93-1.17). Subjects with both heavy coffee consumption (≥4 cups/day) and high-risk HLA genotypes had an OR of 5.74 (95% CI: 3.34-9.88) with an estimated AP of 0.36 (95% CI: 0.01-0.71; P=0.04370).

    CONCLUSION: Our findings suggest that coffee consumption interacts with HLA to promote LADA.

  • 15.
    Sarajlic, Philip
    et al.
    Center for Molecular Medicine, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics. Unit of Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Bäck, Magnus
    Center for Molecular Medicine, Department of Medicine, Karolinska Institutet, Stockholm, Sweden; Heart and Vascular Theme - Division of Valvular and Coronary Disease, Karolinska University Hospital, Stockholm, Sweden.
    Larsson, Susanna C.
    Unit of Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Physical Activity Does Not Reduce Aortic Valve Stenosis Incidence2018In: Circulation Journal, ISSN 1346-9843, E-ISSN 1347-4820, Vol. 82, no 9, p. 2372-2374Article in journal (Refereed)
    Abstract [en]

    Background: Physical activity is associated with lower risk of coronary and cerebrovascular disease but its potential role in prevention of aortic valve stenosis (AVS) is unclear.

    Methods and Results: We investigated whether physical activity influences AVS risk in a cohort of 69,288 adults. During a mean follow-up of 15.3 years, 1,238 AVS cases were diagnosed. No associations were observed between AVS and walking/bicycling (>= 1h/day vs. almost never: hazard ratio 0.92, 95% CI 0.74-1.15) or exercise (>= 4hs/week vs. <1 h/week: hazard ratio 1.18, 95% CI 0.97-1.43).

    Conclusions: Physical activity did not reduce the incidence of AVS.

  • 16.
    Schumacher, Fredrick R.
    et al.
    Case Western Reserve Univ, Dept Populat & Quantitat Hlth Sci, Cleveland, OH 44106 USA;Univ Hosp, Seidman Canc Ctr, Cleveland, OH USA;Royal Marsden NHS Fdn Trust, London, England.
    Al Olama, Ali Amin
    Univ Cambridge, Dept Clin Neurosci, Cambridge, England;Royal Marsden NHS Fdn Trust, London, England;Univ Cambridge, Strangeways Res Lab, Ctr Canc Genet Epidemiol, Dept Publ Hlth & Primary Care, Cambridge, England.
    Berndt, Sonja I.
    NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA;Royal Marsden NHS Fdn Trust, London, England.
    Benlloch, Sara
    Inst Canc Res, London, England;Univ Cambridge, Strangeways Res Lab, Ctr Canc Genet Epidemiol, Dept Publ Hlth & Primary Care, Cambridge, England.
    Ahmed, Mahbubl
    Inst Canc Res, London, England.
    Saunders, Edward J.
    Inst Canc Res, London, England.
    Dadaev, Tokhir
    Inst Canc Res, London, England.
    Leongamornlert, Daniel
    Inst Canc Res, London, England.
    Anokian, Ezequiel
    Inst Canc Res, London, England.
    Cieza-Borrella, Clara
    Inst Canc Res, London, England.
    Goh, Chee
    Inst Canc Res, London, England.
    Brook, Mark N.
    Inst Canc Res, London, England.
    Sheng, Xin
    Univ Southern Calif, Keck Sch Med, Dept Prevent Med, Norris Comprehens Canc Ctr, Los Angeles, CA USA.
    Fachal, Laura
    Fdn Publ Galega Med Xenom SERGAS, CIBERER, Grp Med Xenom, IDIS, Santiago De Compostela, Spain;Univ Cambridge, Dept Oncol, Ctr Canc Genet Epidemiol, Strangeways Lab, Cambridge, England.
    Dennis, Joe
    Univ Cambridge, Strangeways Res Lab, Ctr Canc Genet Epidemiol, Dept Publ Hlth & Primary Care, Cambridge, England.
    Tyrer, Jonathan
    Univ Cambridge, Strangeways Res Lab, Ctr Canc Genet Epidemiol, Dept Publ Hlth & Primary Care, Cambridge, England.
    Muir, Kenneth
    Univ Manchester, Div Populat Hlth, Hlth Serv Res & Primary Care, Manchester, Lancs, England;Univ Warwick, Warwick Med Sch, Coventry, W Midlands, England.
    Lophatananon, Artitaya
    Univ Manchester, Div Populat Hlth, Hlth Serv Res & Primary Care, Manchester, Lancs, England;Univ Warwick, Warwick Med Sch, Coventry, W Midlands, England.
    Stevens, Victoria L.
    Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA.
    Gapstur, Susan M.
    Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA.
    Carter, Brian D.
    Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA.
    Tangen, Catherine M.
    Fred Hutchinson Canc Res Ctr, SWOG Stat Ctr, 1124 Columbia St, Seattle, WA 98104 USA.
    Goodman, Phyllis J.
    Fred Hutchinson Canc Res Ctr, SWOG Stat Ctr, 1124 Columbia St, Seattle, WA 98104 USA.
    Thompson, Ian M., Jr.
    CHRISTUS Santa Rosa Hosp Med Ctr, San Antonio, TX USA.
    Batra, Jyotsna
    Queensland Univ Technol, Inst Hlth & Biomed Innovat, Brisbane, Qld, Australia;Australian Prostate Canc Res Ctr Qld, Translat Res Inst, Brisbane, Qld, Australia;Queensland Univ Technol, Sch Biomed Sci, Brisbane, Qld, Australia.
    Chambers, Suzanne
    Griffith Univ, Menzies Hlth Inst Queensland, Nathan, Qld, Australia;Canc Council Queensland, Fortitude Valley, Qld, Australia.
    Moya, Leire
    Queensland Univ Technol, Inst Hlth & Biomed Innovat, Brisbane, Qld, Australia;Australian Prostate Canc Res Ctr Qld, Translat Res Inst, Brisbane, Qld, Australia;Queensland Univ Technol, Sch Biomed Sci, Brisbane, Qld, Australia.
    Clements, Judith
    Queensland Univ Technol, Inst Hlth & Biomed Innovat, Brisbane, Qld, Australia;Australian Prostate Canc Res Ctr Qld, Translat Res Inst, Brisbane, Qld, Australia;Queensland Univ Technol, Sch Biomed Sci, Brisbane, Qld, Australia.
    Horvath, Lisa
    Chris OBrien Lifehouse COBLH, Camperdown, NSW, Australia;Garvan Inst Med Res, Sydney, NSW, Australia.
    Tilley, Wayne
    Univ Adelaide, Dame Roma Mitchell Canc Res Ctr, Adelaide, SA, Australia.
    Risbridger, Gail P.
    Monash Univ, Dept Anat & Dev Biol, Prostate Canc Res Program, Monash Biomed Discovery Inst Canc Program, Clayton, Vic, Australia;Peter MacCallum Canc Ctr, Canc Res Div, Melbourne, Vic, Australia.
    Gronberg, Henrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
    Aly, Markus
    Karolinska Inst, Dept Mol Med & Surg, Stockholm, Sweden;Karolinska Univ Hosp, Dept Urol, Stockholm, Sweden.
    Nordstrom, Tobias
    Karolinska Inst, Danderyds Hosp, Dept Clin Sci, Stockholm, Sweden;Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
    Pharoah, Paul
    Univ Cambridge, Dept Oncol, Ctr Canc Genet Epidemiol, Strangeways Lab, Cambridge, England;Univ Cambridge, Strangeways Res Lab, Ctr Canc Genet Epidemiol, Dept Publ Hlth & Primary Care, Cambridge, England.
    Pashayan, Nora
    UCL, Dept Appl Hlth Res, London, England;Univ Cambridge, Dept Oncol, Ctr Canc Genet Epidemiol, Strangeways Lab, Cambridge, England.
    Schleutker, Johanna
    Univ Turku, Inst Biomed, Turku, Finland;Turku Univ Hosp, Dept Med Genet, Tyks Microbiol & Genet, Turku, Finland.
    Tammela, Teuvo L. J.
    Univ Tampere, Fac Med & Life Sci, Tampere, Finland;Tampere Univ Hosp, Dept Urol, Tampere, Finland.
    Sipeky, Csilla
    Univ Turku, Inst Biomed, Turku, Finland.
    Auvinen, Anssi
    Univ Tampere, Sch Hlth Sci, Dept Epidemiol, Tampere, Finland.
    Albanes, Demetrius
    NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
    Weinstein, Stephanie
    NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics. Karolinska Inst, Inst Environm Med, Div Nutr Epidemiol, Stockholm, Sweden.
    Hakansson, Niclas
    Karolinska Inst, Inst Environm Med, Div Nutr Epidemiol, Stockholm, Sweden.
    West, Catharine M. L.
    Univ Manchester, Christie NHS Fdn Trust, Manchester, Lancs, England;Univ Manchester, Manchester Acad Hlth Sci Ctr, Manchester Canc Res Ctr, Div Canc Sci, Manchester, Lancs, England.
    Dunning, Alison M.
    Univ Cambridge, Dept Oncol, Ctr Canc Genet Epidemiol, Strangeways Lab, Cambridge, England.
    Burnet, Neil
    Univ Cambridge, Cambridge Univ Hosp NHS Fdn Trust, Ctr Oncol, Dept Oncol, Cambridge, England.
    Mucci, Lorelei A.
    Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
    Giovannucci, Edward
    Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
    Andriole, Gerald L.
    Washington Univ, Sch Med, St Louis, MO USA.
    Cussenot, Olivier
    Tenon Hosp, CeRePP, Paris, France;UPMC, Sorbonne Univ, Tenon Hosp, GRC ONCOTYPE URO 5, Paris, France.
    Cancel-Tassin, Geraldine
    Tenon Hosp, CeRePP, Paris, France;UPMC, Sorbonne Univ, Tenon Hosp, GRC ONCOTYPE URO 5, Paris, France.
    Koutros, Stella
    NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
    Freeman, Laura E. Beane
    NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
    Sorensen, Karina Dalsgaard
    Aarhus Univ, Dept Clin Med, Aarhus, Denmark;Aarhus Univ Hosp, Dept Mol Med, Aarhus, Denmark.
    Orntoft, Torben Falck
    Aarhus Univ, Dept Clin Med, Aarhus, Denmark;Aarhus Univ Hosp, Dept Mol Med, Aarhus, Denmark.
    Borre, Michael
    Aarhus Univ, Dept Clin Med, Aarhus, Denmark;Aarhus Univ Hosp, Dept Urol, Aarhus, Denmark.
    Maehle, Lovise
    Oslo Univ Hosp, Dept Med Genet, Oslo, Norway.
    Grindedal, Eli Marie
    Oslo Univ Hosp, Dept Med Genet, Oslo, Norway.
    Neal, David E.
    Univ Oxford, Nuffield Dept Surg Sci, Oxford, England;Univ Cambridge, Addenbrookes Hosp, Dept Oncol, Cambridge, England;Canc Res UK, Cambridge Res Inst, Cambridge, England;Univ Oxford, John Radcliffe Hosp, Fac Med Sci, Oxford, England.
    Donovan, Jenny L.
    Univ Bristol, Sch Social & Community Med, Bristol, Avon, England.
    Hamdy, Freddie C.
    Univ Oxford, Nuffield Dept Surg Sci, Oxford, England;Univ Oxford, John Radcliffe Hosp, Fac Med Sci, Oxford, England.
    Martin, Richard M.
    Univ Bristol, Sch Social & Community Med, Bristol, Avon, England.
    Travis, Ruth C.
    Univ Oxford, Nuffield Dept Populat Hlth, Canc Epidemiol Unit, Oxford, England.
    Key, Tim J.
    Univ Oxford, Nuffield Dept Populat Hlth, Canc Epidemiol Unit, Oxford, England.
    Hamilton, Robert J.
    Princess Margaret Canc Ctr, Dept Surg Oncol, Toronto, ON, Canada.
    Fleshner, Neil E.
    Princess Margaret Canc Ctr, Dept Surg Oncol, Toronto, ON, Canada.
    Finelli, Antonio
    NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA;Princess Margaret Canc Ctr, Div Urol, Toronto, ON, Canada.
    Ingles, Sue Ann
    Univ Southern Calif, Keck Sch Med, Dept Prevent Med, Norris Comprehens Canc Ctr, Los Angeles, CA USA.
    Stern, Mariana C.
    Univ Southern Calif, Keck Sch Med, Dept Prevent Med, Norris Comprehens Canc Ctr, Los Angeles, CA USA.
    Rosenstein, Barry S.
    NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA;Icahn Sch Med Mt Sinai, Dept Radiat Oncol, New York, NY 10029 USA;Icahn Sch Med Mt Sinai, Dept Genet & Genom Sci, New York, NY 10029 USA.
    Kerns, Sarah L.
    Univ Rochester, Med Ctr, Dept Radiat Oncol, Rochester, NY 14642 USA.
    Ostrer, Harry
    NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA;Albert Einstein Coll Med, Dept Pathol, Bronx, NY 10467 USA.
    Lu, Yong-Jie
    Queen Mary Univ London, Barts Canc Inst, Ctr Mol Oncol, London, England.
    Zhang, Hong-Wei
    NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA;Second Mil Med Univ, Shanghai, Peoples R China.
    Feng, Ninghan
    Nanjing Med Univ, Wuxi Hosp 2, Wuxi, Peoples R China.
    Mao, Xueying
    Queen Mary Univ London, Barts Canc Inst, Ctr Mol Oncol, London, England.
    Guo, Xin
    Chongqing Med Univ, Affiliated Hosp 1, Dept Urol, Chongqing, Peoples R China.
    Wang, Guomin
    Fudan Univ, Zhongshan Hosp, Dept Urol, Med Coll, Shanghai, Peoples R China.
    Sun, Zan
    China Med Univ, Peoples Hosp, Peoples Hosp Liaoning Prov, Shenyang, Peoples R China.
    Giles, Graham G.
    Canc Council Victoria, Canc Epidemiol & Intelligence Div, Melbourne, Vic, Australia;Univ Melbourne, Melbourne Sch Populat & Global Hlth, Ctr Epidemiol & Biostati, Melbourne, Vic, Australia.
    Southey, Melissa C.
    Monash Univ, Sch Clin Sci Monash Hlth, Precis Med, Clayton, Vic, Australia.
    MacInnis, Robert J.
    Canc Council Victoria, Canc Epidemiol & Intelligence Div, Melbourne, Vic, Australia;Univ Melbourne, Melbourne Sch Populat & Global Hlth, Ctr Epidemiol & Biostati, Melbourne, Vic, Australia.
    FitzGerald, Liesel M.
    Univ Tasmania, Menzies Inst Med Res, Hobart, Tas, Australia;Canc Council Victoria, Canc Epidemiol & Intelligence Div, Melbourne, Vic, Australia.
    Kibel, Adam S.
    Brigham & Womens Hosp, Div Urol Surg, 75 Francis St, Boston, MA 02115 USA.
    Drake, Bettina F.
    Washington Univ, Sch Med, St Louis, MO USA.
    Vega, Ana
    Fdn Publ Galega Med Xenomica SERGAS, Grp Med Xenom, CIBERER, IDIS, Santiago De Compostela, Spain.
    Gomez-Caamano, Antonio
    SERGAS, Dept Radiat Oncol, Complexo Hosp Univ Santiago, Santiago De Compostela, Spain.
    Szulkin, Robert
    Scandinavian Dev Serv, Danderyd, Sweden;Karolinska Inst, Dept Neurobiol Care Sci & Soc, Div Family Med, Huddinge, Sweden.
    Eklund, Martin
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
    Kogevinas, Manolis
    Univ Pompeu Fabra, Barcelona, Spain;Hosp del Mar, Res Inst, IMIM, Barcelona, Spain;CIBER Epidemiol & Salud Publ CIBERESP, Madrid, Spain;ISGlobal, Ctr Res Environm Epidemiol CREAL, Barcelona, Spain.
    Llorca, Javier
    Univ Cantabria, IDIVAL, Santander, Spain;CIBER Epidemiol & Salud Publ CIBERESP, Madrid, Spain.
    Castano-Vinyals, Gemma
    Univ Pompeu Fabra, Barcelona, Spain;Hosp del Mar, Res Inst, IMIM, Barcelona, Spain;CIBER Epidemiol & Salud Publ CIBERESP, Madrid, Spain;ISGlobal, Ctr Res Environm Epidemiol CREAL, Barcelona, Spain.
    Penney, Kathryn L.
    Harvard Med Sch, Boston, MA USA;Brigham & Womens Hosp, Dept Med, Div Network Med, 75 Francis St, Boston, MA 02115 USA.
    Stampfer, Meir
    Harvard Med Sch, Boston, MA USA;Brigham & Womens Hosp, Dept Med, Div Network Med, 75 Francis St, Boston, MA 02115 USA.
    Park, Jong Y.
    H Lee Moffitt Canc Ctr & Res Inst, Dept Canc Epidemiol, Tampa, FL USA.
    Sellers, Thomas A.
    H Lee Moffitt Canc Ctr & Res Inst, Dept Canc Epidemiol, Tampa, FL USA.
    Lin, Hui-Yi
    Louisiana State Univ, Hlth Sci Ctr, Sch Publ Hlth, Biostat Program, New Orleans, LA USA.
    Stanford, Janet L.
    Univ Washington, Sch Publ Hlth, Dept Epidemiol, Seattle, WA 98195 USA;Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, 1124 Columbia St, Seattle, WA 98104 USA.
    Cybulski, Cezary
    Pomeranian Med Univ, Dept Genet & Pathol, Int Hereditary Canc Ctr, Szczecin, Poland.
    Wokolorczyk, Dominika
    Pomeranian Med Univ, Dept Genet & Pathol, Int Hereditary Canc Ctr, Szczecin, Poland.
    Lubinski, Jan
    Pomeranian Med Univ, Dept Genet & Pathol, Int Hereditary Canc Ctr, Szczecin, Poland.
    Ostrander, Elaine A.
    NHGRI, NIH, Bethesda, MD 20892 USA.
    Geybels, Milan S.
    Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, 1124 Columbia St, Seattle, WA 98104 USA.
    Nordestgaard, Borge G.
    Copenhagen Univ Hosp, Herlev & Gentofte Hosp, Dept Clin Biochem, Herlev, Denmark;Univ Copenhagen, Fac Hlth & Med Sci, Copenhagen, Denmark.
    Nielsen, Sune F.
    Copenhagen Univ Hosp, Herlev & Gentofte Hosp, Dept Clin Biochem, Herlev, Denmark;Univ Copenhagen, Fac Hlth & Med Sci, Copenhagen, Denmark.
    Weischer, Maren
    Copenhagen Univ Hosp, Herlev & Gentofte Hosp, Dept Clin Biochem, Herlev, Denmark.
    Bisbjerg, Rasmus
    Copenhagen Univ Hosp, Herlev & Gentofte Hosp, Dept Urol, Herlev, Denmark.
    Roder, Martin Andreas
    Copenhagen Univ Hosp, Rigshosp, Dept Urol, Copenhagen Prostate Canc Ctr, Copenhagen, Denmark.
    Iversen, Peter
    Copenhagen Univ Hosp, Rigshosp, Dept Urol, Copenhagen Prostate Canc Ctr, Copenhagen, Denmark.
    Brenner, Hermann
    German Canc Res Ctr, German Canc Consortium DKTK, Heidelberg, Germany;Natl Ctr Tumor Dis NCT, Heidelberg, Germany;German Canc Res Ctr, Div Clin Epidemiol & Aging Res, Heidelberg, Germany;German Canc Res Ctr, Div Prevent Oncol, Heidelberg, Germany.
    Cuk, Katarina
    German Canc Res Ctr, Div Clin Epidemiol & Aging Res, Heidelberg, Germany.
    Holleczek, Bernd
    Saarland Canc Registry, Saarbrucken, Germany.
    Maier, Christiane
    Univ Hosp Ulm, Inst Human Genet, Ulm, Germany.
    Luedeke, Manuel
    Univ Hosp Ulm, Inst Human Genet, Ulm, Germany.
    Schnoeller, Thomas
    Univ Hosp Ulm, Dept Urol, Ulm, Germany.
    Kim, Jeri
    Univ Texas MD Anderson Canc Ctr, Dept Genitourinary Med Oncol, Houston, TX 77030 USA.
    Logothetis, Christopher J.
    Univ Texas MD Anderson Canc Ctr, Dept Genitourinary Med Oncol, Houston, TX 77030 USA.
    John, Esther M.
    Canc Prevent Inst Calif, Fremont, CA USA;Stanford Univ, Sch Med, Stanford Canc Inst, Stanford, CA USA;Stanford Univ, Sch Med, Dept Hlth Res & Policy Epidemiol, Stanford, CA USA.
    Teixeira, Manuel R.
    Univ Porto, Biomed Sci Inst ICBAS, Porto, Portugal;Portuguese Oncol Inst Porto, Dept Genet, Porto, Portugal.
    Paulo, Paula
    Portuguese Oncol Inst Porto, Dept Genet, Porto, Portugal.
    Cardoso, Marta
    Portuguese Oncol Inst Porto, Dept Genet, Porto, Portugal.
    Neuhausen, Susan L.
    City Hope Natl Med Ctr, Beckman Res Inst, Dept Populat Sci, Duarte, CA USA.
    Steele, Linda
    City Hope Natl Med Ctr, Beckman Res Inst, Dept Populat Sci, Duarte, CA USA.
    Ding, Yuan Chun
    City Hope Natl Med Ctr, Beckman Res Inst, Dept Populat Sci, Duarte, CA USA.
    De Ruyck, Kim
    Univ Ghent, Fac Med & Hlth Sci, Basic Med Sci, Ghent, Belgium.
    De Meerleer, Gert
    Univ Ghent, Fac Med & Hlth Sci, Basic Med Sci, Ghent, Belgium.
    Ost, Piet
    Ghent Univ Hosp, Dept Radiotherapy, Ghent, Belgium.
    Razack, Azad
    Univ Malaya, Dept Surg, Fac Med, Kuala Lumpur, Malaysia.
    Lim, Jasmine
    Univ Malaya, Dept Surg, Fac Med, Kuala Lumpur, Malaysia.
    Teo, Soo-Hwang
    Subang Jaya Med Ctr, Outpatient Ctr, CRM, Selangor, Malaysia.
    Lin, Daniel W.
    Univ Washington, Dept Urol, Seattle, WA 98195 USA;Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, 1124 Columbia St, Seattle, WA 98104 USA.
    Newcomb, Lisa F.
    Univ Washington, Dept Urol, Seattle, WA 98195 USA;Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, 1124 Columbia St, Seattle, WA 98104 USA.
    Lessel, Davor
    Univ Med Ctr Hamburg Eppendorf, Inst Human Genet, Hamburg, Germany.
    Gamulin, Marija
    NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA;Univ Hosp Ctr Zagreb, Div Med Oncol, Urogenital Unit, Dept Oncol, Zagreb, Croatia.
    Kulis, Tomislav
    Univ Zagreb, Sch Med, Univ Hosp Ctr Zagreb, Dept Urol, Zagreb, Croatia.
    Kaneva, Radka
    Med Univ Sofia, Dept Med Chem & Biochem, Mol Med Ctr, Sofia, Bulgaria.
    Usmani, Nawaid
    Univ Alberta, Cross Canc Inst, Dept Oncol, Edmonton, AB, Canada;Cross Canc Inst, Div Radiat Oncol, Edmonton, AB, Canada.
    Singhal, Sandeep
    Univ Alberta, Cross Canc Inst, Dept Oncol, Edmonton, AB, Canada;Cross Canc Inst, Div Radiat Oncol, Edmonton, AB, Canada.
    Slavov, Chavdar
    Med Univ Sofia, Dept Urol, Sofia, Bulgaria;Med Univ Sofia, Alexandrovska Univ Hosp, Sofia, Bulgaria.
    Mitev, Vanio
    Med Univ Sofia, Dept Med Chem & Biochem, Mol Med Ctr, Sofia, Bulgaria.
    Parliament, Matthew
    Univ Alberta, Cross Canc Inst, Dept Oncol, Edmonton, AB, Canada;Cross Canc Inst, Div Radiat Oncol, Edmonton, AB, Canada.
    Claessens, Frank
    Katholieke Univ Leuven, Dept Cellular & Mol Med, Mol Endocrinol Lab, Leuven, Belgium.
    Joniau, Steven
    Univ Hosp Leuven, Dept Urol, Leuven, Belgium.
    Van den Broeck, Thomas
    Katholieke Univ Leuven, Dept Cellular & Mol Med, Mol Endocrinol Lab, Leuven, Belgium;Univ Hosp Leuven, Dept Urol, Leuven, Belgium.
    Larkin, Samantha
    Univ Southampton, Southampton Gen Hosp, Southampton, Hants, England.
    Townsend, Paul A.
    Univ Manchester, Div Canc Sci,Hlth Innovat Manchester, Manchester Canc Res Ctr,NIHR Manchester Biomed Re, Fac Biol Med & Hlth,Manchester Acad Hlth Sci Ctr, Manchester, Lancs, England.
    Aukim-Hastie, Claire
    Univ Surrey, Guildford, Surrey, England.
    Dominguez, Manuela Gago
    Univ Calif San Diego, Moores Canc Ctr, La Jolla, CA 92093 USA;Galician Fdn Genom Med, Genom Med Grp,SERGAS, Inst Invest Sanitaria Santiago de Compostela IDIS, Complejo Hosp Univ Santiago,Serv Galego Saude, Santiago De Compostela, Spain.
    Castelao, Jose Esteban
    Complexo Hosp Univ Vigo, Inst Invest Biomed Galicia IISGS, CHUVI Hosp, Genet Oncol Unit, Vigo, Spain.
    Martinez, Maria Elena
    Univ Calif San Diego, Moores Canc Ctr, Dept Family Med & Publ Hlth, La Jolla, CA 92093 USA.
    Roobol, Monique J.
    Erasmus Univ, Med Ctr, Dept Urol, Rotterdam, Netherlands.
    Jenster, Guido
    Erasmus Univ, Med Ctr, Dept Urol, Rotterdam, Netherlands.
    van Schaik, Ron H. N.
    Erasmus Univ, Med Ctr, Dept Clin Chem, Rotterdam, Netherlands.
    Menegaux, Florence
    Univ Paris Saclay, Univ Paris Sud, INSERM, Canc & Environm Grp,Ctr Res Epidemiol & Populat H, Villejuif, France.
    Truong, Therese
    Univ Paris Saclay, Univ Paris Sud, INSERM, Canc & Environm Grp,Ctr Res Epidemiol & Populat H, Villejuif, France.
    Koudou, Yves Akoli
    Univ Paris Saclay, Univ Paris Sud, INSERM, Canc & Environm Grp,Ctr Res Epidemiol & Populat H, Villejuif, France.
    Xu, Jianfeng
    NorthShore Univ HealthSyst, Program Personalized Canc Care, Evanston, IL USA.
    Khaw, Kay-Tee
    Univ Cambridge, Clin Gerontol Unit, Cambridge, England.
    Cannon-Albright, Lisa
    George E Wahlen Dept Vet Affairs Med Ctr, Salt Lake City, UT USA;Univ Utah, Sch Med, Dept Med, Div Genet Epidemiol, Salt Lake City, UT USA.
    Pandha, Hardev
    Univ Surrey, Guildford, Surrey, England.
    Michael, Agnieszka
    Univ Surrey, Guildford, Surrey, England.
    Thibodeau, Stephen N.
    Mayo Clin, Dept Lab Med & Pathol, Rochester, MN USA.
    McDonnell, Shannon K.
    Mayo Clin, Div Biomed Stat & Informat, Rochester, MN USA.
    Schaid, Daniel J.
    Mayo Clin, Dept Lab Med & Pathol, Rochester, MN USA.
    Lindstrom, Sara
    Univ Washington, Sch Publ Hlth, Dept Epidemiol, Seattle, WA 98195 USA.
    Turman, Constance
    Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Program Genet Epidemiol & Stat Genet, Boston, MA USA.
    Ma, Jing
    Harvard Med Sch, Boston, MA USA;Brigham & Womens Hosp, Dept Med, Div Network Med, 75 Francis St, Boston, MA 02115 USA.
    Hunter, David J.
    Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Program Genet Epidemiol & Stat Genet, Boston, MA USA.
    Riboli, Elio
    Imperial Coll London, Sch Publ Hlth, Dept Epidemiol & Biostat, London, England.
    Siddiq, Afshan
    Queen Mary Univ London, Genom England, London, England.
    Canzian, Federico
    German Canc Res Ctr, Genom Epidemiol Grp, Heidelberg, Germany.
    Kolonel, Laurence N.
    Univ Hawaii, Ctr Canc, Epidemiol Program, Honolulu, HI 96822 USA. Geisel Sch Med Dartmouth, Dept Biomed Data Sci, Lebanon, NH USA. Geisel Sch Med Dartmouth, Dept Mol & Syst Biol, Hanover, NH USA.
    Le Marchand, Loic
    Univ Hawaii, Ctr Canc, Epidemiol Program, Honolulu, HI 96822 USA. Geisel Sch Med Dartmouth, Dept Biomed Data Sci, Lebanon, NH USA. Geisel Sch Med Dartmouth, Dept Mol & Syst Biol, Hanover, NH USA.
    Hoover, Robert N.
    NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
    Machiela, Mitchell J.
    NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
    Cui, Zuxi
    Case Western Reserve Univ, Dept Populat & Quantitat Hlth Sci, Cleveland, OH 44106 USA.
    Kraft, Peter
    Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Program Genet Epidemiol & Stat Genet, Boston, MA USA.
    Conti, David V.
    Univ Southern Calif, Keck Sch Med, Dept Prevent Med, Norris Comprehens Canc Ctr, Los Angeles, CA USA.
    Easton, Douglas F.
    Univ Cambridge, Dept Oncol, Ctr Canc Genet Epidemiol, Strangeways Lab, Cambridge, England;Univ Cambridge, Strangeways Res Lab, Ctr Canc Genet Epidemiol, Dept Publ Hlth & Primary Care, Cambridge, England.
    Wiklund, Fredrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
    Chanock, Stephen J.
    NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
    Henderson, Brian E.
    Univ Southern Calif, Keck Sch Med, Dept Prevent Med, Norris Comprehens Canc Ctr, Los Angeles, CA USA.
    Kote-Jarai, Zsofia
    Inst Canc Res, London, England.
    Haiman, Christopher A.
    Univ Southern Calif, Keck Sch Med, Dept Prevent Med, Norris Comprehens Canc Ctr, Los Angeles, CA USA.
    Eeles, Rosalind A.
    Inst Canc Res, London, England;Royal Marsden NHS Fdn Trust, London, England.
    Association analyses of more than 140,000 men identify 63 new prostate cancer susceptibility loci2018In: Nature Genetics, ISSN 1061-4036, E-ISSN 1546-1718, Vol. 50, no 7, p. 928-936Article in journal (Refereed)
    Abstract [en]

    Genome-wide association studies (GWAS) and fine-mapping efforts to date have identified more than 100 prostate cancer (PrCa)-susceptibility loci. We meta-analyzed genotype data from a custom high-density array of 46,939 PrCa cases and 27,910 controls of European ancestry with previously genotyped data of 32,255 PrCa cases and 33,202 controls of European ancestry. Our analysis identified 62 novel loci associated (P < 5.0 x 10(-8)) with PrCa and one locus significantly associated with early-onset PrCa (<= 55 years). Our findings include missense variants rs1800057 (odds ratio (OR) = 1.16; P = 8.2 x 10(-9); G>C, p.Pro1054Arg) in ATM and rs2066827 (OR = 1.06; P = 2.3 x 10(-9); T>G, p.Val109Gly) in CDKN1B. The combination of all loci captured 28.4% of the PrCa familial relative risk, and a polygenic risk score conferred an elevated PrCa risk for men in the ninetieth to ninety-ninth percentiles (relative risk = 2.69; 95% confidence interval (CI): 2.55-2.82) and first percentile (relative risk = 5.71; 95% CI: 5.04-6.48) risk stratum compared with the population average. These findings improve risk prediction, enhance fine-mapping, and provide insight into the underlying biology of PrCa1.

  • 17.
    Stattin, Karl
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Michaëlsson, Karl
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Larsson, Susanna C
    Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, Stockholm, Sweden.
    Wolk, Alicja
    Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, Stockholm, Sweden.
    Byberg, Liisa
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Leisure-Time Physical Activity and Risk of Fracture: A Cohort Study of 66,940 Men and Women2017In: Journal of Bone and Mineral Research, ISSN 0884-0431, E-ISSN 1523-4681, Vol. 32, no 8, p. 1599-1606Article in journal (Refereed)
    Abstract [en]

    Physical activity has been associated with reduced risk of fracture, but it is not known how the intensity or frequency of physical activity influences this risk reduction. We aim to compare the risk of hip fracture and fracture of any locale between men and women with different levels of leisure-time walking/bicycling and exercise. A total of 37,238 women (born 1914-1948) from the Swedish Mammography Cohort and 45,906 men (born 1918-1952) from the Cohort of Swedish Men were followed for a maximum of 17 years. Exposure and covariate information was collected through a self-administered questionnaire in 1997. Incident fractures (5153 individuals with hip fracture and 15,043 with any type of fracture) and comorbidities were gathered from national and local patient registries. Hazard ratios (HRs) were calculated using Cox proportional hazards regression. Individuals who walked/bicycled less than 20 minutes per day had a lower rate of hip fracture (multivariable adjusted HR = 0.77; 95% confidence interval [CI] 0.70 to 0.85) and any fracture (HR = 0.87; 95% CI 0.82 to 0.92) compared with those who hardly ever walked/bicycled. These reduced rates were also evident in both sexes, in different age categories, for vertebral fractures and for non-hip, non-vertebral fractures. Those who reported exercise 1 hour per week had a lower rate of hip fracture (HR = 0.87; 95% CI 0.80 to 0.96) and any fracture (HR = 0.94; 95% CI 0.89 to 0.99) compared with those who exercised less than 1 hour per week. Only minor differences in HRs were observed in individuals with moderate compared with higher levels of walking/bicycling or exercise. Walking/bicycling and exercise showed almost equal reductions in rate of fracture when compared with those in a joint category with lowest activity. In conclusion, both moderate and high self-reported frequency of physical activity is associated with reduced future risk of fracture.

  • 18.
    Stilling, Frej
    et al.
    Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, Stockholm, Sweden.
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics. Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, Stockholm, Sweden.
    Religa, Dorota
    Karolinska Inst, Dept Neurobiol Care Sci & Soc, Stockholm, Sweden;Karolinska Univ Hosp, Theme Aging, Stockholm, Sweden.
    Leppert, Jerzy
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Centre for Clinical Research, County of Västmanland.
    Bergkvist, Leif
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Centre for Clinical Research, County of Västmanland.
    Michaëlsson, Karl
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Larsson, Susanna C.
    Karolinska Inst, Inst Environm Med, Unit Nutr Epidemiol, Stockholm, Sweden.
    Adipose tissue fatty acid composition and cognitive impairment2018In: Nutrition (Burbank, Los Angeles County, Calif.), ISSN 0899-9007, E-ISSN 1873-1244, Vol. 54, p. 153-157Article in journal (Refereed)
    Abstract [en]

    Objective: The aim of this study was to examine the association among adipose tissue eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), arachidonic acid (AA), and the ratios of EPA to AA and DHA to AA with impaired cognitive function.

    Methods: This cross-sectional analysis comprised 481 men participating in the Cohort of Swedish Men Clinical and for whom adipose tissue fatty acid composition and results from a telephone-based cognitive test were available. Impaired cognitive function was defined using a predefined cutoff on the cognitive test. Binomial log-linear regression models were used to estimate prevalence ratios. In secondary analyses, Cox proportional hazards models were used to estimate relative risk for incident dementia ascertained by linkage with population-based registers.

    Results: We observed a graded reduction in the prevalence of impaired cognitive function across tertiles of adipose tissue EPA/AA- ratio (P-trend = 0.01); compared with the lowest tertile, the multivariable-adjusted prevalence ratios were, respectively, 0.89 (95% confidence interval [CI], 0.67-1.17) and 0.64 (95% CI, 0.45-0.91) for the second and third tertiles. EPA, DHA, and the DHA/AA ratio showed similar patterns of association; however, the CIs included the null. AA alone was not associated with impaired cognitive function. Although with lower precision, estimates obtained from the prospective analysis were broadly consistent with the main analysis.

    Conclusions: Findings from this study suggest that a high ratio of EPA to AA in adipose tissue may be associated with better cognitive function. A similar association was observed with EPA, DHA, and the ratio of DHA to AA, but the results did not exclude a null association.

  • 19.
    Warensjö Lemming, Eva
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Liisa, Byberg
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics. Institute of Environmental Medicine (IMM), C6, Nutritional Epidemiology, Stockholm, Sweden.
    Michaëlsson, Karl
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    A comparison between two healthy diet scores, the modified Mediterranean diet score and the Healthy Nordic Food Index, in relation to all-cause and cause-specific mortality2018In: British Journal of Nutrition, ISSN 0007-1145, E-ISSN 1475-2662, Vol. 119, no 7, p. 836-846Article in journal (Refereed)
    Abstract [en]

    High adherence to healthy diets has the potential to prevent disease and prolong life span, and healthy dietary pattern scores have each been associated with disease and mortality. We studied two commonly promoted healthy diet scores (modified Mediterranean diet score (mMED) and the Healthy Nordic Food Index (HNFI)) and the combined effect of the two scores in association with all-cause and cause-specific mortality (cancer, CVD and ischaemic heart disease). The study included 38 428 women (median age of 61 years) from the Swedish Mammography Cohort. Diet and covariate data were collected in a questionnaire. mMED and HNFI were generated and categorised into low-, medium- and high-adherence groups, and in nine combinations of these. Multivariable-adjusted hazard ratios (HR) of register-ascertained mortality and 95 % CI were calculated in Cox proportional hazards regression analysis. During follow-up (median: 17 years), 10 478 women died. In the high-adherence categories compared with low-adherence categories, the HR for all-cause mortality was 0·76 (95 % CI 0·70, 0·81) for mMED and 0·89 (95 % CI 0·83, 0·96) for HNFI. Higher adherence to mMED was associated with lower mortality in each stratum of HNFI in the combined analysis. In general, mMED, compared with HNFI, was more strongly associated with a lower cause-specific mortality. In Swedish women, both mMED and HNFI were inversely associated with all-cause and cardiovascular mortality. The combined analysis, however, indicated an advantage to be adherent to the mMED. The present version of HNFI did not associate with mortality independent of mMED score.

    The full text will be freely available from 2019-04-15 13:27
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