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Andre, B.; Canhao, H.; Espnes, G.A.; Ferreira Rodrigues, A.M.; Gregorio, M.J.; Nguyen, C.; Sousa, R.; Gronning, K. |

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Is there an association between food patterns and life satisfaction among Norway's inhabitants ages 65 years and older? |
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Journal Article |
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2017 |
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Appetite |
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Appetite |
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110 |
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108-115 |
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Anxiety; Depression; Elderly adults; Food patterns; Life satisfaction |
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The lack of information regarding older adults' health and lifestyles makes it difficult to design suitable interventions for people at risk of developing unhealth lifestyles. Therefore, there is a need to increase knowledge about older adults' food patterns and quality of life. Our aim was to determine associations among food patterns, anxiety, depression, and life satisfaction in Norwegian inhabitants ages 65+. The Nord-Trondelag Health Study (The HUNT Study) is a large, population-based cohort study that includes data for 125 000 Norwegian participants. The cohort used for this study is wave three of the study, consisting of 11 619 participants age 65 and over. Cluster analysis was used to categorize the participants based on similarities in food consumption; two clusters were identified based on similarities regarding food consumption among participants. Significant differences between the clusters were found, as participants in the healthy food-patterns cluster had higher life satisfaction and lower anxiety and depression than those in the unhealthy food-patterns cluster. The associations among food patterns, anxiety, depression, and life satisfaction among older adults show the need for increased focus on interactions among food patterns, food consumption, and life satisfaction among the elderly in order to explore how society can influence these patterns. |
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Faculty of Medicine and Health Sciences, Department of Public Health and Nursing, Norwegian University of Science and Technology (NTNU), Norway; NTNU Center for Health Promotion Research, Norway |
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0195-6663 |
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PMID:27988367 |
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HUNT @ maria.stuifbergen @ |
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1878 |
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Sardahaee, F.S.; Holmen, T.L.; Micali, N.; Kvaloy, K. |

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Effects of single genetic variants and polygenic obesity risk scores on disordered eating in adolescents – The HUNT study |
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Journal Article |
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Year |
2017 |
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Appetite |
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118 |
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8-16 |
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Adolescents; Comt; Disordered eating; Eat-12; Hunt; Obesity polygenic risk score |
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PURPOSE: Improving the understanding of the role of genetic risk on disordered eating (DE). METHODS: A case-control study including 1757 (F: 979, M: 778) adolescents (aged 13-19 years) from the Nord-Trondelag Health Study (HUNT), an ethnically homogenous Norwegian population based study. Cases and controls were defined using a shortened version of the Eating Attitude Test. Logistic regression was employed to test for associations between DE phenotypes and 24 obesity and eating disorder susceptibility SNPs, and the joint effect of a subset of these in a genetic risk score (GRS). RESULTS: COMT was shown to be associated with poor appetite/undereating (OR: 0.6, CI 95%: 0.43-0.83, p = 0.002). Independent of obesity associations, the weighted GRS was associated to overeating in 13-15 year old females (OR: 2.07, CI 95%: 1.14-3.76, p = 0.017). Additionally, a significant association was observed between the GRS and loss of control over eating in the total sample (OR: 1.62, CI 95%: 1.01-2.61, p = 0.046). CONCLUSIONS: The COMT variant (rs4680) was associated with poor appetite/undereating. Our study further confirms prior findings that obesity risk also confers risk for loss of control over eating; and overeating amongst girls. |
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HUNT Research Center, Department of Public Health and Nursing, Faculty of Medicine and Health Science, Norwegian University of Science and Technology, Trondheim, Norway; Department of Research and Development, Levanger Hospital, Nord-Trondelag Health Trust, Levanger, Norway. Electronic address: kirsti.kvaloy@ntnu.no |
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PMID:28694222 |
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HUNT @ maria.stuifbergen @ |
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1975 |
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Cai, Y.; Hansell, A.L.; Blangiardo, M.; Burton, P.R.; de Hoogh, K.; Doiron, D.; Fortier, I.; Gulliver, J.; Hveem, K.; Mbatchou, S.; Morley, D.W.; Stolk, R.P.; Zijlema, W.L.; Elliott, P.; Hodgson, S. |

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Long-term exposure to road traffic noise, ambient air pollution, and cardiovascular risk factors in the HUNT and lifelines cohorts |
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Journal Article |
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2017 |
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European Heart Journal |
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Eur Heart J |
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38 |
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29 |
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2290-2296 |
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Air pollution; Blood glucose; Blood lipids; Systemic inflammation; Traffic noise |
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Aims: Blood biochemistry may provide information on associations between road traffic noise, air pollution, and cardiovascular disease risk. We evaluated this in two large European cohorts (HUNT3, Lifelines). Methods and results: Road traffic noise exposure was modelled for 2009 using a simplified version of the Common Noise Assessment Methods in Europe (CNOSSOS-EU). Annual ambient air pollution (PM10, NO2) at residence was estimated for 2007 using a Land Use Regression model. The statistical platform DataSHIELD was used to pool data from 144 082 participants aged >/=20 years to enable individual-level analysis. Generalized linear models were fitted to assess cross-sectional associations between pollutants and high-sensitivity C-reactive protein (hsCRP), blood lipids and for (Lifelines only) fasting blood glucose, for samples taken during recruitment in 2006-2013. Pooling both cohorts, an inter-quartile range (IQR) higher day-time noise (5.1 dB(A)) was associated with 1.1% [95% confidence interval (95% CI: 0.02-2.2%)] higher hsCRP, 0.7% (95% CI: 0.3-1.1%) higher triglycerides, and 0.5% (95% CI: 0.3-0.7%) higher high-density lipoprotein (HDL); only the association with HDL was robust to adjustment for air pollution. An IQR higher PM10 (2.0 microg/m3) or NO2 (7.4 microg/m3) was associated with higher triglycerides (1.9%, 95% CI: 1.5-2.4% and 2.2%, 95% CI: 1.6-2.7%), independent of adjustment for noise. Additionally for NO2, a significant association with hsCRP (1.9%, 95% CI: 0.5-3.3%) was seen. In Lifelines, an IQR higher noise (4.2 dB(A)) and PM10 (2.4 microg/m3) was associated with 0.2% (95% CI: 0.1-0.3%) and 0.6% (95% CI: 0.4-0.7%) higher fasting glucose respectively, with both remaining robust to adjustment for air/noise pollution. Conclusion: Long-term exposures to road traffic noise and ambient air pollution were associated with blood biochemistry, providing a possible link between road traffic noise/air pollution and cardio-metabolic disease risk. |
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Department of Epidemiology and Biostatistics, MRC-PHE Centre for Environment and Health, School of Public Health, Imperial College London, St Mary's Campus, Norfolk Place, W2 1PG, London, UK |
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0195-668X |
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PMID:28575405 |
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HUNT @ maria.stuifbergen @ |
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1895 |
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Thomsen, L.C.V.; McCarthy, N.S.; Melton, P.E.; Cadby, G.; Austgulen, R.; Nygard, O.K.; Johnson, M.P.; Brennecke, S.; Moses, E.K.; Bjorge, L.; Iversen, A.-C. |

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The antihypertensive MTHFR gene polymorphism rs17367504-G is a possible novel protective locus for preeclampsia |
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Journal Article |
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2017 |
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Journal of Hypertension |
Abbreviated Journal |
J Hypertens |
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35 |
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1 |
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132-139 |
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Adolescent; Adult; Alleles; Australia; Case-Control Studies; Female; Gene Frequency; Genetic Pleiotropy; Genome-Wide Association Study; Genotype; Humans; Hypertension/genetics; Inflammation/genetics; Methylenetetrahydrofolate Reductase (NADPH2)/*genetics; Norway; Polymorphism, Single Nucleotide; Pre-Eclampsia/*genetics; Pregnancy; Protective Factors; Young Adult |
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OBJECTIVE: Preeclampsia is a complex heterogeneous disease commonly defined by new-onset hypertension and proteinuria in pregnancy. Women experiencing preeclampsia have increased risk for cardiovascular diseases (CVD) later in life. Preeclampsia and CVD share risk factors and pathophysiologic mechanisms, including dysregulated inflammation and raised blood pressure. Despite commonalities, little is known about the contribution of shared genes (pleiotropy) to these diseases. This study aimed to investigate whether genetic risk factors for hypertension or inflammation are pleiotropic by also being associated with preeclampsia. METHODS: We genotyped 122 single nucleotide polymorphisms (SNPs) in women with preeclampsia (n = 1006) and nonpreeclamptic controls (n = 816) from the Norwegian HUNT Study. SNPs were chosen on the basis of previously reported associations with either nongestational hypertension or inflammation in genome-wide association studies. The SNPs were tested for association with preeclampsia in a multiple logistic regression model. RESULTS: The minor (G) allele of the intronic SNP rs17367504 in the gene methylenetetrahydrofolate reductase (MTHFR) was associated with a protective effect on preeclampsia (odds ratio 0.65, 95% confidence interval 0.53-0.80) in the Norwegian cohort. This association did not replicate in an Australian preeclampsia case-control cohort (P = 0.68, odds ratio 1.05, 95% confidence interval 0.83-1.32, minor allele frequency = 0.15). CONCLUSION: MTHFR is important for regulating transmethylation processes and is involved in regulation of folate metabolism. The G allele of rs17367504 has previously been shown to protect against nongestational hypertension. Our study suggests a novel association between this allele and reduced risk for preeclampsia. This is the first study associating the minor (G) allele of a SNP within the MTHFR gene with a protective effect on preeclampsia, and in doing so identifying a possible pleiotropic protective effect on preeclampsia and hypertension. |
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aDepartment of Gynecology and Obstetrics, Haukeland University Hospital bDepartment of Clinical Science, University of Bergen, Bergen, Norway cCentre for Genetic Origins of Health and Disease, University of Western Australia, Perth, Australia dDepartment of Cancer Research and Molecular Medicine, Centre of Molecular Inflammation Research, Norwegian University of Science and Technology, Trondheim eDepartment of Heart Disease, Haukeland University Hospital, Bergen, Norway fSouth Texas Diabetes and Obesity Institute, School of Medicine, University of Texas Rio Grande Valley, Brownsville, Texas, USA gDepartment of Obstetrics and Gynaecology, University of Melbourne, Parkville hPregnancy Research Centre, Department of Maternal-Fetal Medicine, Royal Women's Hospital, Parkville, Victoria iFaculty of Health Sciences, Curtin University, Perth, Western Australia, Australia |
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0263-6352 |
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PMID:27755385; PMCID:PMC5131692 |
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HUNT @ maria.stuifbergen @ |
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1996 |
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Bjorngaard, J.H.; Nordestgaard, A.T.; Taylor, A.E.; Treur, J.L.; Gabrielsen, M.E.; Munafo, M.R.; Nordestgaard, B.G.; Asvold, B.O.; Romundstad, P.; Davey Smith, G. |

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Heavier smoking increases coffee consumption: findings from a Mendelian randomization analysis |
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Journal Article |
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2017 |
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International Journal of Epidemiology |
Abbreviated Journal |
Int J Epidemiol |
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Coffee, tea, smoking, Mendelian randomization |
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Background: There is evidence for a positive relationship between cigarette and coffee consumption in smokers. Cigarette smoke increases metabolism of caffeine, so this may represent a causal effect of smoking on caffeine intake. Methods: We performed Mendelian randomization analyses in the UK Biobank ( N = 114 029), the Norwegian HUNT study ( N = 56 664) and the Copenhagen General Population Study (CGPS) ( N = 78 650). We used the rs16969968 genetic variant as a proxy for smoking heaviness in all studies and rs4410790 and rs2472297 as proxies for coffee consumption in UK Biobank and CGPS. Analyses were conducted using linear regression and meta-analysed across studies. Results: Each additional cigarette per day consumed by current smokers was associated with higher coffee consumption (0.10 cups per day, 95% CI: 0.03, 0.17). There was weak evidence for an increase in tea consumption per additional cigarette smoked per day (0.04 cups per day, 95% CI: -0.002, 0.07). There was strong evidence that each additional copy of the minor allele of rs16969968 (which increases daily cigarette consumption) in current smokers was associated with higher coffee consumption (0.16 cups per day, 95% CI: 0.11, 0.20), but only weak evidence for an association with tea consumption (0.04 cups per day, 95% CI: -0.01, 0.09). There was no clear evidence that rs16969968 was associated with coffee or tea consumption in never or former smokers or that the coffee-related variants were associated with cigarette consumption. Conclusions: Higher cigarette consumption causally increases coffee intake. This is consistent with faster metabolism of caffeine by smokers, but could also reflect a behavioural effect of smoking on coffee drinking. |
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School of Social and Community Medicine, University of Bristol, Bristol, UK |
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0300-5771 |
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PMID:29025033 |
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HUNT @ maria.stuifbergen @ |
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1881 |
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Carslake, D.; Davey Smith, G.; Gunnell, D.; Davies, N.; Nilsen, T.I.L.; Romundstad, P. |

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Confounding by ill health in the observed association between BMI and mortality: evidence from the HUNT Study using offspring BMI as an instrument |
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Journal Article |
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2017 |
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International Journal of Epidemiology |
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Int J Epidemiol |
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Body mass index; cohort study; confounding; instrumental variables; mortality; reverse causation |
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Background: The observational association between mortality and body mass index (BMI) is U-shaped, leading to highly publicized suggestions that moderate overweight is beneficial to health. However, it is unclear whether elevated mortality is caused by low BMI or if the association is confounded, for example by concurrent ill health. Methods: Using HUNT, a Norwegian prospective study, 32 452 mother-offspring and 27 747 father-offspring pairs were followed up to 2009. Conventional hazard ratios for parental mortality per standard deviation of BMI were estimated using Cox regression adjusted for behavioural and socioeconomic factors. To estimate hazard ratios with reduced susceptibility to confounding, particularly from concurrent ill health, the BMI of parents' offspring was used as an instrumental variable for parents' own BMI. The shape of mortality-BMI associations was assessed using cubic splines. Results: There were 18 365 parental deaths during follow-up. Conventional associations of mortality from all-causes, cardiovascular disease and cancer with parents' own BMI were substantially nonlinear, with elevated mortality at both extremes and minima at 21-25 kg m-2. Equivalent associations with offspring BMI were positive and there was no evidence of elevated parental mortality at low offspring BMI. The linear instrumental variable hazard ratio for all-cause mortality per standard deviation increase in BMI was 1.18 (95% confidence interval: 1.10, 1.26), compared with 1.05 (1.03, 1.06) in the conventional analysis. Conclusions: Elevated mortality rates at high BMI appear causal, whereas excess mortality at low BMI is likely exaggerated by confounding by factors including concurrent ill health. Conventional studies probably underestimate the adverse population health consequences of overweight. |
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Department of Public Health and General Practice, Norwegian University of Science and Technology, Trondheim, Norway |
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0300-5771 |
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PMID:29206928 |
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HUNT @ maria.stuifbergen @ |
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1896 |
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Paulsen, J.; Askim, A.; Mohus, R.M.; Mehl, A.; Dewan, A.; Solligard, E.; Damas, J.K.; Asvold, B.O. |

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Associations of obesity and lifestyle with the risk and mortality of bloodstream infection in a general population: a 15-year follow-up of 64 027 individuals in the HUNT Study |
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Journal Article |
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2017 |
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International Journal of Epidemiology |
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Int J Epidemiol |
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46 |
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5 |
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1573-1581 |
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Bacteraemia; alcohol drinking; exercise; obesity; sepsis; smoking |
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Background: Bloodstream infections (BSI) cause considerable morbidity and mortality, and primary prevention should be a priority. Lifestyle factors are of particular interest since they represent a modifiable target. Methods: We conducted a prospective cohort study among participants in the population-based Norwegian HUNT2 Survey, where 64 027 participants were followed from 1995-97 through 2011 by linkage to prospectively recorded information on BSI at local and regional hospitals. The exposures were: baseline body mass index (BMI) measurements; and self-reported smoking habits, leisure time physical activity and alcohol intake. The outcomes were hazard ratios (HR) of BSI and BSI mortality. Results: During 810 453 person-years and median follow-up of 14.8 years, 1844 (2.9%) participants experienced at least one BSI and 396 (0.62%) died from BSI. Compared with normal weight participants (BMI 18.5-24.9 kg/m2), the age- and sex-adjusted risk of a first-time BSI was 31% [95% confidence interval (CI) 14-51%] higher at BMI 30.0-34.9 kg/m2, 87% (95% CI 50-135%) higher at BMI 35.0-39.9 kg/m2 and 210% (95% CI 117-341%) higher at BMI >/= 40.0 kg/m2. The risk of BSI mortality was similarly increased. Compared with never-smokers, current smokers had 51% (95% CI 34-70%) and 75% (95% CI 34-129%) higher risks of BSI and BSI mortality, respectively. Physically inactive participants had 71% (95% CI 42-107%) and 108% (95% CI 37-216%) higher risks of BSI and BSI mortality, respectively, compared with the most physically active. Conclusions: Obesity, smoking and physical inactivity carry increased risk of BSI and BSI mortality. |
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Department of Endocrinology, St Olavs Hospital, Trondheim University Hospital, Trondheim, Norway |
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PMID:28637260 |
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HUNT @ maria.stuifbergen @ |
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1969 |
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Machiela, M.J.; Hofmann, J.N.; Carreras-Torres, R.; Brown, K.M.; Johansson, M.; Wang, Z.; Foll, M.; Li, P.; Rothman, N.; Savage, S.A.; Gaborieau, V.; McKay, J.D.; Ye, Y.; Henrion, M.; Bruinsma, F.; Jordan, S.; Severi, G.; Hveem, K.; Vatten, L.J.; Fletcher, T.; Koppova, K.; Larsson, S.C.; Wolk, A.; Banks, R.E.; Selby, P.J.; Easton, D.F.; Pharoah, P.; Andreotti, G.; Freeman, L.E.B.; Koutros, S.; Albanes, D.; Mannisto, S.; Weinstein, S.; Clark, P.E.; Edwards, T.E.; Lipworth, L.; Gapstur, S.M.; Stevens, V.L.; Carol, H.; Freedman, M.L.; Pomerantz, M.M.; Cho, E.; Kraft, P.; Preston, M.A.; Wilson, K.M.; Gaziano, J.M.; Sesso, H.S.; Black, A.; Freedman, N.D.; Huang, W.-Y.; Anema, J.G.; Kahnoski, R.J.; Lane, B.R.; Noyes, S.L.; Petillo, D.; Colli, L.M.; Sampson, J.N.; Besse, C.; Blanche, H.; Boland, A.; Burdette, L.; Prokhortchouk, E.; Skryabin, K.G.; Yeager, M.; Mijuskovic, M.; Ognjanovic, M.; Foretova, L.; Holcatova, I.; Janout, V.; Mates, D.; Mukeriya, A.; Rascu, S.; Zaridze, D.; Bencko, V.; Cybulski, C.; Fabianova, E.; Jinga, V.; Lissowska, J.; Lubinski, J.; Navratilova, M.; Rudnai, P.; Szeszenia-Dabrowska, N.; Benhamou, S.; Cancel-Tassin, G.; Cussenot, O.; Bueno-de-Mesquita, H.B.; Canzian, F.; Duell, E.J.; Ljungberg, B.; Sitaram, R.T.; Peters, U.; White, E.; Anderson, G.L.; Johnson, L.; Luo, J.; Buring, J.; Lee, I.-M.; Chow, W.-H.; Moore, L.E.; Wood, C.; Eisen, T.; Larkin, J.; Choueiri, T.K.; Lathrop, G.M.; Teh, B.T.; Deleuze, J.-F.; Wu, X.; Houlston, R.S.; Brennan, P.; Chanock, S.J.; Scelo, G.; Purdue, M.P. |

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Title |
Genetic Variants Related to Longer Telomere Length are Associated with Increased Risk of Renal Cell Carcinoma |
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Journal Article |
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2017 |
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European Urology |
Abbreviated Journal |
Eur Urol |
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72 |
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5 |
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747-754 |
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Genetic variants; Mendelian randomization; Renal cell carcinoma; Risk; Telomere length |
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Abstract |
BACKGROUND: Relative telomere length in peripheral blood leukocytes has been evaluated as a potential biomarker for renal cell carcinoma (RCC) risk in several studies, with conflicting findings. OBJECTIVE: We performed an analysis of genetic variants associated with leukocyte telomere length to assess the relationship between telomere length and RCC risk using Mendelian randomization, an approach unaffected by biases from temporal variability and reverse causation that might have affected earlier investigations. DESIGN, SETTING, AND PARTICIPANTS: Genotypes from nine telomere length-associated variants for 10 784 cases and 20 406 cancer-free controls from six genome-wide association studies (GWAS) of RCC were aggregated into a weighted genetic risk score (GRS) predictive of leukocyte telomere length. OUTCOME MEASUREMENTS AND STATISTICAL ANALYSIS: Odds ratios (ORs) relating the GRS and RCC risk were computed in individual GWAS datasets and combined by meta-analysis. RESULTS AND LIMITATIONS: Longer genetically inferred telomere length was associated with an increased risk of RCC (OR=2.07 per predicted kilobase increase, 95% confidence interval [CI]:=1.70-2.53, p<0.0001). As a sensitivity analysis, we excluded two telomere length variants in linkage disequilibrium (R(2)>0.5) with GWAS-identified RCC risk variants (rs10936599 and rs9420907) from the telomere length GRS; despite this exclusion, a statistically significant association between the GRS and RCC risk persisted (OR=1.73, 95% CI=1.36-2.21, p<0.0001). Exploratory analyses for individual histologic subtypes suggested comparable associations with the telomere length GRS for clear cell (N=5573, OR=1.93, 95% CI=1.50-2.49, p<0.0001), papillary (N=573, OR=1.96, 95% CI=1.01-3.81, p=0.046), and chromophobe RCC (N=203, OR=2.37, 95% CI=0.78-7.17, p=0.13). CONCLUSIONS: Our investigation adds to the growing body of evidence indicating some aspect of longer telomere length is important for RCC risk. PATIENT SUMMARY: Telomeres are segments of DNA at chromosome ends that maintain chromosomal stability. Our study investigated the relationship between genetic variants associated with telomere length and renal cell carcinoma risk. We found evidence suggesting individuals with inherited predisposition to longer telomere length are at increased risk of developing renal cell carcinoma. |
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Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department Health and Human Services, Bethesda, MS, USA. Electronic address: purduem@mail.nih.gov |
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0302-2838 |
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PMID:28797570; PMCID:PMC5641242 |
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HUNT @ maria.stuifbergen @ |
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1959 |
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Perreault, K.; Bauman, A.; Johnson, N.; Britton, A.; Rangul, V.; Stamatakis, E. |

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Does physical activity moderate the association between alcohol drinking and all-cause, cancer and cardiovascular diseases mortality? A pooled analysis of eight British population cohorts |
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Journal Article |
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Year |
2017 |
Publication |
British Journal of Sports Medicine |
Abbreviated Journal |
Br J Sports Med |
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Volume |
51 |
Issue |
8 |
Pages |
651-657 |
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Adult; Aged; Aged, 80 and over; Alcohol Drinking/*adverse effects; Cardiovascular Diseases/*mortality; England; *Exercise; Female; Health Surveys; Humans; Male; Middle Aged; Mortality; Neoplasms/*mortality; Proportional Hazards Models; Prospective Studies; Risk Factors; Cancer; Epidemiology; Physical activity; Public health |
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OBJECTIVE: To examine whether physical activity (PA) moderates the association between alcohol intake and all-cause mortality, cancer mortality and cardiovascular diseases (CVDs) mortality. DESIGN: Prospective study using 8 British population-based surveys, each linked to cause-specific mortality: Health Survey for England (1994, 1998, 1999, 2003, 2004 and 2006) and Scottish Health Survey (1998 and 2003). PARTICIPANTS: 36 370 men and women aged 40 years and over were included with a corresponding 5735 deaths and a mean of 353 049 person-years of follow-up. EXPOSURES: 6 sex-specific categories of alcohol intake (UK units/week) were defined: (1) never drunk; (2) ex-drinkers; (3) occasional drinkers; (4) within guidelines (<14 (women); <21 (men)); (5) hazardous (14-35 (women); 21-49 (men)) and (6) harmful (>35 (women) >49 (men)). PA was categorised as inactive (</=7 MET-hour/week), active at the lower (>7.5 MET-hour/week) and upper (>15 MET-hour/week) of recommended levels. MAIN OUTCOMES AND MEASURES: Cox proportional-hazard models were used to examine associations between alcohol consumption and all-cause, cancer and CVD mortality risk after adjusting for several confounders. Stratified analyses were performed to evaluate mortality risks within each PA stratum. RESULTS: We found a direct association between alcohol consumption and cancer mortality risk starting from drinking within guidelines (HR (95% CI) hazardous drinking: 1.40 (1.11 to 1.78)). Stratified analyses showed that the association between alcohol intake and mortality risk was attenuated (all-cause) or nearly nullified (cancer) among individuals who met the PA recommendations (HR (95% CI)). CONCLUSIONS: Meeting the current PA public health recommendations offsets some of the cancer and all-cause mortality risk associated with alcohol drinking. |
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Department of Epidemiology and Public Health, University College London, London, UK |
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0306-3674 |
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PMID:27581162 |
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HUNT @ maria.stuifbergen @ |
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1970 |
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Naicker, K.; Overland, S.; Johnson, J.A.; Manuel, D.; Skogen, J.C.; Sivertsen, B.; Colman, I. |

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Symptoms of anxiety and depression in type 2 diabetes: Associations with clinical diabetes measures and self-management outcomes in the Norwegian HUNT study |
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Journal Article |
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Year |
2017 |
Publication |
Psychoneuroendocrinology |
Abbreviated Journal |
Psychoneuroendocrinology |
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84 |
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116-123 |
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Anxiety; Depression; Diabetes self-management; Metabolic control; Type 2 diabetes |
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OBJECTIVE: To determine if symptoms of depression and anxiety are differentially associated with clinical diabetes measures and self-management behaviours in individuals with Type 2 diabetes, and whether these associations vary by patient sex. RESEARCH DESIGN AND METHODS: A cross-sectional analysis using data from 2035 adults with Type 2 diabetes in the Nord-Trondelag Health Study. Multivariate logistic regression was used to explore associations between symptoms of depression and anxiety and waist girth, HDL cholesterol, systolic blood pressure, triglycerides, c-reactive protein, glycemic control, diet adherence, exercise, glucose monitoring, foot checks for ulcers, and the subjective patient experience. Analyses were stratified by sex. RESULTS: Depression was associated with a lower likelihood of avoiding saturated fats (OR=0.20 [95% CI: 0.06, 0.68]) and increased odds of physical inactivity (OR=1.69 [95% CI: 1.37, 2.72]). Anxiety was associated with increased odds of eating vegetables (OR=1.66 [95% CI: 1.02, 2.73]), and an over two-fold increase of feeling that having diabetes is difficult. In women, anxiety was associated with elevated c-reactive protein levels (OR=1.57 [95% CI: 1.05, 2.34]). In men, depressive symptoms were associated with elevated HbA1c (OR=5.00 [95% CI: 1.15, 8.23). CONCLUSIONS: Symptoms of depression and anxiety were differentially associated with some key diabetes-related measures. Our results suggest sex-specific differences with respect to two important clinical outcomes (i.e., anxiety and CRP in women and depression and glycemic control in men). These findings should alert practitioners to the importance of detection and management of psychological symptoms in individuals with Type 2 diabetes. |
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School of Public Health and Preventive Medicine, University of Ottawa, Ontario Canada. Electronic address: icolman@uottawa.ca |
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0306-4530 |
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PMID:28704763 |
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HUNT @ maria.stuifbergen @ |
Serial |
1962 |
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Jaremko, J.L.; Azmat, O.; Lambert, R.G.; Bird, P.; Haugen, I.K.; Jans, L.; Weber, U.; Winn, N.; Zubler, V.; Maksymowych, W.P. |

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Title |
Validation of a Knowledge Transfer Tool for the Knee Inflammation MRI Scoring System for Bone Marrow Lesions According to the OMERACT Filter: Data from the Osteoarthritis Initiative |
Type |
Journal Article |
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Year |
2017 |
Publication |
The Journal of Rheumatology |
Abbreviated Journal |
J Rheumatol |
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Volume |
44 |
Issue |
11 |
Pages |
1718-1722 |
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Bone Marrow Lesion; Knee Joint; Mri; Omeract; Osteoarthritis; Scoring Methods |
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OBJECTIVE: To assess feasibility and reliability of scoring bone marrow lesions (BML) on knee magnetic resonance imaging (MRI) in osteoarthritis using the Outcome Measures in Rheumatology Knee Inflammation MRI Scoring System (KIMRISS), with a Web-based interface and online training with real-time iterative calibration. METHODS: Six readers new to the KIMRISS (3 radiologists, 3 rheumatologists) scored sagittal T2-weighted fat-saturated MRI in 20 subjects randomly selected from the Osteoarthritis Initiative data, at baseline and 1-year followup. In the KIMRISS, the reader moves a transparent overlay grid within a Web-based interface to fit bones, then clicks or touches each region containing BML per slice, to score 1 if BML is present. Regional and total scores are automatically calculated. Outcomes include the interreader intraclass correlation coefficients (ICC) and the smallest detectable change (SDC). RESULTS: Scoring took 3-12 min per scan and all readers rated the process as moderately to very user friendly. Despite a low BML burden (average score 2.8% of maximum possible) and small changes, interobserver reliability was moderate to high for BML status and change in the femur and tibia (ICC 0.78-0.88). Four readers also scored the patella reliably, whereas 2 readers were outliers, likely because of image artifacts. SDC of 1.5-5.6 represented 0.7% of the maximum possible score. CONCLUSION: We confirmed feasibility of knee BML scoring by new readers using interactive training and a Web-based touch-sensitive overlay system, finding high reliability and sensitivity to change. Further work will include adjustments to training materials regarding patellar scoring, and study in therapeutic trial datasets with higher burden of BML and larger changes. |
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J.L. Jaremko, MD, PhD, FRCPC, Department of Radiology and Diagnostic Imaging, Faculty of Medicine and Dentistry, University of Alberta; O. Azmat, MB, FRCP, Department of Radiology and Diagnostic Imaging, Faculty of Medicine and Dentistry, University of Alberta; R.G. Lambert, MB, FRCPC, Department of Radiology and Diagnostic Imaging, Faculty of Medicine and Dentistry, University of Alberta; P. Bird, MD, Division of Medicine, University of New South Wales; I.K. Haugen, MD, PhD, Department of Rheumatology, Diakonhjemmet Hospital; L. Jans, MD, PhD, Department of Radiology and Medical Imaging, Ghent University Hospital; U. Weber, MD, King Christian 10th Hospital for Rheumatic Diseases, and Institute of Regional Health Research, University of Southern Denmark; N. Winn, MBBS, FRCR, Department of Radiology, Robert Jones and Agnes Hunt Orthopaedic Hospital; V. Zubler, MD, Department of Radiology, Balgrist University Hospital; W.P. Maksymowych, MB ChB, FRCP(C), FACP, Division of Rheumatology, Faculty of Medicine and Dentistry, University of Alberta |
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0315-162X |
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PMID:28365581 |
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no |
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HUNT @ maria.stuifbergen @ |
Serial |
1932 |
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Author |
Videm, V.; Thomas, R.; Brown, M.A.; Hoff, M. |

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Title |
Self-reported Diagnosis of Rheumatoid Arthritis or Ankylosing Spondylitis Has Low Accuracy: Data from the Nord-Trondelag Health Study |
Type |
Journal Article |
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Year |
2017 |
Publication |
The Journal of Rheumatology |
Abbreviated Journal |
J Rheumatol |
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Volume |
44 |
Issue |
8 |
Pages |
1134-1141 |
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Ankylosing Spondylitis; Epidemiology; Rheumatoid Arthritis |
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OBJECTIVE: Self-reported diagnoses of inflammatory arthritis are not accurate. The primary study aim was to ascertain self-reported diagnoses of rheumatoid arthritis (RA) and ankylosing spondylitis (AS) in the Norwegian population-based Nord-Trondelag Health Study (HUNT) using hospital case files. The secondary aim was to provide updated estimates of the prevalence and incidence of RA and AS. METHODS: All inhabitants >/= 20 years old from the county of Nord-Trondelag were invited. Data from 70,805 unique participants from HUNT2 (1995-1997) and HUNT3 (2006-2008) were included. For participants who self-reported RA or AS, case files from all 3 hospitals in the catchment area were evaluated using standardized diagnostic criteria. RESULTS: Of 2703 self-reported cases of RA, 19.1% were verified in hospital files. Of 1064 self-reported cases of AS, 15.8% were verified. Of 259 cases self-reporting both RA and AS, 8.1% had RA and 5.4% had AS. Overall, a self-report of 1 or both diagnoses could not be verified in 82.1%, including 22.8% with insufficient information or no case file. The prevalence of RA was 768 (95% CI 705-835) per 100,000. The incidence of RA from HUNT2 to HUNT3 was 0.48 (0.41-0.56) per 1000 per year. The prevalence of AS was 264 (228-305) per 100,000. The incidence of AS from HUNT2 to HUNT3 was 0.19 (0.15-0.24) per 1000 per year. CONCLUSION: Self-reported diagnoses of RA and AS are often false-positive. The prevalence and incidence of RA were comparable to reports from similar populations. The incidence of AS was higher than previously reported in a mixed population from Norway. |
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V. Videm, MD, PhD, Professor, Department of Laboratory Medicine, Children's and Women's Health, NTNU, and Senior Consultant, Department of Immunology and Transfusion Medicine, St. Olavs Hospital; R. Thomas, MBBS, FRACP, MD, Professor, Translational Research Institute, University of Queensland; M.A. Brown, MBBS, MD, Director of Genomics, Queensland University of Technology, Institute of Health and Biomedical Research, Princess Alexandra Hospital; M. Hoff, MD, PhD, Associate Professor, Department of Public Health and General Practice and Department of Neuroscience, NTNU, and Senior Consultant, Department of Rheumatology, St. Olavs Hospital |
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0315-162X |
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PMID:28412703 |
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HUNT @ maria.stuifbergen @ |
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2001 |
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Hansen, A.G.; Stovner, L.J.; Hagen, K.; Helvik, A.-S.; Thorstensen, W.M.; Nordgard, S.; Bugten, V.; Eggesbo, H.B. |

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Paranasal sinus opacification in headache sufferers: A population-based imaging study (the HUNT study-MRI) |
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Journal Article |
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2017 |
Publication |
Cephalalgia : an International Journal of Headache |
Abbreviated Journal |
Cephalalgia |
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37 |
Issue |
6 |
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509-516 |
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Paranasal sinuses; headache; magnetic resonance imaging; migraine; opacification; sinus headache; tension headache |
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Background The association between headache and paranasal sinus disease is still unclear. Because of symptom overlap, the two conditions are not easily studied on the basis of symptoms alone. The aim of the present study was to investigate whether paranasal sinus opacification on magnetic resonance imaging (MRI) was associated with migraine, tension-type headache (TTH) or unclassified headache. Methods This was a cross-sectional study of 844 randomly selected participants (442 women, age range 50-65 years, mean age 57.7 years). Based on 14 headache questions, participants were allocated to four mutually exclusive groups: migraine, TTH, unclassified headache or headache free. On MRI, opacifications as mucosal thickening, polyps/retention cysts and fluid in the five paired sinuses were measured and recorded if >/=1 mm. For each participant, opacification thickness was summed for each sinus and, in addition, a total sum of all sinuses was calculated. Opacification in each sinus was compared between headache-free participants and the headache groups using non-parametric tests, and the total sum was compared by logistical regression. Results No significant association was found between paranasal sinus opacification and headache in general, nor when headache was differentiated into migraine, TTH and unclassified headache. This was also true in separate analyses of mucosal thickening and fluid and of opacification from each paranasal sinus. Conclusion Migraine, TTH and unclassified headache were found not to be associated with an increased degree of paranasal sinus opacification at MRI. |
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5 Department of Radiology and Nuclear Medicine, Oslo University Hospital, Oslo, Norway |
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0333-1024 |
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PMID:27215544 |
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HUNT @ maria.stuifbergen @ |
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1921 |
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Sun, Y.-Q.; Langhammer, A.; Wu, C.; Skorpen, F.; Chen, Y.; Nilsen, T.I.L.; Romundstad, P.R.; Mai, X.-M. |

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Associations of serum 25-hydroxyvitamin D level with incidence of lung cancer and histologic types in Norwegian adults: a case-cohort analysis of the HUNT study |
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Journal Article |
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2017 |
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European Journal of Epidemiology |
Abbreviated Journal |
Eur J Epidemiol |
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Case-cohort study; Histologic types; Lung cancer; Pulmonary adenocarcinoma; Serum 25-hydroxyvitamin D [25(OH)D]; Vitamin D |
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Previous prospective studies have shown inconsistent associations between serum 25-hydroxyvitamin D [25(OH)D] level and lung cancer incidence. The aim of the present study was to explore the associations of serum 25(OH)D levels with incidence of lung cancer overall and different histologic types. We performed a population-based prospective case-cohort study including 696 incident lung cancer cases and 5804 individuals in a subcohort who participated in the second survey of the Nord-Trondelag Health Study in Norway. Cox proportional hazards regression models counting for the case-cohort design were used to estimate hazard ratios (HRs) with 95% confidence interval (CIs) for lung cancer overall or histologic types in relation to serum 25(OH)D levels. Compared with the fourth season-specific quartile of 25(OH)D (median 68.0 nmol/L), lower 25(OH)D levels were not associated with the incidence of overall, small or squamous cell lung cancer. However, the risk of adenocarcinoma was lower in the second and third quartiles (median 39.9 and 51.5 nmol/L) compared with the fourth quartile, with HRs of 0.63 (95% CI 0.41-0.98) and 0.58 (0.38-0.88), respectively. The associations of lower levels of 25(OH)D with a reduced risk of adenocarcinoma were only observed in the overweight/obese subjects [HRs for second and third quartiles: 0.40 (0.22-0.72) and 0.50 (0.27-0.92)] but not in the normal weight subjects [HRs: 0.95 (0.52-1.75) and 0.60 (0.32-1.10)]. Serum 25(OH)D levels were not associated with the risk of lung cancer in general. The observation that lower 25(OH)D levels were associated with a lower risk of adenocarcinoma should be interpreted with caution. |
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Department of Public Health and Nursing, NTNU, Norwegian University of Science and Technology, Trondheim, Norway |
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0393-2990 |
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PMID:29080012 |
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HUNT @ maria.stuifbergen @ |
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2007 |
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Felde, G.; Ebbesen, M.H.; Hunskaar, S. |

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Anxiety and depression associated with urinary incontinence. A 10-year follow-up study from the Norwegian HUNT study (EPINCONT) |
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Journal Article |
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2017 |
Publication |
Neurourology and Urodynamics |
Abbreviated Journal |
Neurourol Urodyn |
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36 |
Issue |
2 |
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322-328 |
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Adult; Aged; Aged, 80 and over; Anxiety/*epidemiology/etiology/psychology; Depression/*epidemiology/etiology/psychology; Female; Humans; Incidence; Longitudinal Studies; Middle Aged; Norway; Prevalence; Risk Factors; Urinary Incontinence/*complications/psychology; Young Adult; Epincont; Hads; Hunt; anxiety; depression; epidemiology; urinary incontinence |
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AIMS: Firstly, to investigate the association between depression, anxiety and urinary incontinence (UI) in a 10-year longitudinal study of women. Secondly, to investigate the association between possible differences in the stress- and urgency components of UI and different severities of depression and anxiety by age groups. METHODS: In a longitudinal, population-based survey study, the EPINCONT part of the HUNT study in Norway, we analyzed questionnaire data on UI, depression and anxiety from 16,263 women from 20 years of age. A multivariate logistic regression model was used to predict the odds of developing anxiety and depression among the women with and without UI at baseline and the odds of developing UI among the women with and without anxiety or depression at baseline. RESULTS: For women with any UI at baseline we found an association with the incidence of depression and anxiety symptoms, OR 1.45 (1.23-1.72) and 1.26 (1.8-1.47) for mild depression and anxiety respectively. For women with depression or anxiety symptoms at baseline we found an association with the incidence of any UI with OR 2.09 (1.55-2.83) and 1.65 (1.34-2.03) for moderate/severe symptom-score for depression and anxiety, respectively, for the whole sample. CONCLUSIONS: In this study, both depression and anxiety are shown to be risk factors for developing UI with a dose-dependent trend. UI is associated with increased incidence of depression and anxiety. Neurourol. Urodynam. 36:322-328, 2017. (c) 2015 The Authors. Neurourology and Urodynamics Published by Wiley Periodicals, Inc. |
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National Centre for Emergency Primary Health Care, Uni Research Health, Bergen, Norway |
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PMID:26584597 |
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HUNT @ maria.stuifbergen @ |
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1902 |
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Author |
Webb, T.R.; Erdmann, J.; Stirrups, K.E.; Stitziel, N.O.; Masca, N.G.D.; Jansen, H.; Kanoni, S.; Nelson, C.P.; Ferrario, P.G.; Konig, I.R.; Eicher, J.D.; Johnson, A.D.; Hamby, S.E.; Betsholtz, C.; Ruusalepp, A.; Franzen, O.; Schadt, E.E.; Bjorkegren, J.L.M.; Weeke, P.E.; Auer, P.L.; Schick, U.M.; Lu, Y.; Zhang, H.; Dube, M.-P.; Goel, A.; Farrall, M.; Peloso, G.M.; Won, H.-H.; Do, R.; van Iperen, E.; Kruppa, J.; Mahajan, A.; Scott, R.A.; Willenborg, C.; Braund, P.S.; van Capelleveen, J.C.; Doney, A.S.F.; Donnelly, L.A.; Asselta, R.; Merlini, P.A.; Duga, S.; Marziliano, N.; Denny, J.C.; Shaffer, C.; El-Mokhtari, N.E.; Franke, A.; Heilmann, S.; Hengstenberg, C.; Hoffmann, P.; Holmen, O.L.; Hveem, K.; Jansson, J.-H.; Jockel, K.-H.; Kessler, T.; Kriebel, J.; Laugwitz, K.L.; Marouli, E.; Martinelli, N.; McCarthy, M.I.; Van Zuydam, N.R.; Meisinger, C.; Esko, T.; Mihailov, E.; Escher, S.A.; Alver, M.; Moebus, S.; Morris, A.D.; Virtamo, J.; Nikpay, M.; Olivieri, O.; Provost, S.; AlQarawi, A.; Robertson, N.R.; Akinsansya, K.O.; Reilly, D.F.; Vogt, T.F.; Yin, W.; Asselbergs, F.W.; Kooperberg, C.; Jackson, R.D.; Stahl, E.; Muller-Nurasyid, M.; Strauch, K.; Varga, T.V.; Waldenberger, M.; Zeng, L.; Chowdhury, R.; Salomaa, V.; Ford, I.; Jukema, J.W.; Amouyel, P.; Kontto, J.; Nordestgaard, B.G.; Ferrieres, J.; Saleheen, D.; Sattar, N.; Surendran, P.; Wagner, A.; Young, R.; Howson, J.M.M.; Butterworth, A.S.; Danesh, J.; Ardissino, D.; Bottinger, E.P.; Erbel, R.; Franks, P.W.; Girelli, D.; Hall, A.S.; Hovingh, G.K.; Kastrati, A.; Lieb, W.; Meitinger, T.; Kraus, W.E.; Shah, S.H.; McPherson, R.; Orho-Melander, M.; Melander, O.; Metspalu, A.; Palmer, C.N.A.; Peters, A.; Rader, D.J.; Reilly, M.P.; Loos, R.J.F.; Reiner, A.P.; Roden, D.M.; Tardif, J.-C.; Thompson, J.R.; Wareham, N.J.; Watkins, H.; Willer, C.J.; Samani, N.J.; Schunkert, H.; Deloukas, P.; Kathiresan, S. |

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Title |
Systematic Evaluation of Pleiotropy Identifies 6 Further Loci Associated With Coronary Artery Disease |
Type |
Journal Article |
|
Year |
2017 |
Publication |
Journal of the American College of Cardiology |
Abbreviated Journal |
J Am Coll Cardiol |
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Volume |
69 |
Issue |
7 |
Pages |
823-836 |
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Keywords |
Case-Control Studies; Coronary Artery Disease/epidemiology/*genetics; Female; Gene Frequency; *Genetic Loci; *Genetic Pleiotropy; Genome-Wide Association Study; Humans; Male; Odds Ratio; Polymorphism, Single Nucleotide; cholesteryl ester transfer protein; expression quantitative trait loci; genetics; genome-wide association; single nucleotide polymorphism |
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Abstract |
BACKGROUND: Genome-wide association studies have so far identified 56 loci associated with risk of coronary artery disease (CAD). Many CAD loci show pleiotropy; that is, they are also associated with other diseases or traits. OBJECTIVES: This study sought to systematically test if genetic variants identified for non-CAD diseases/traits also associate with CAD and to undertake a comprehensive analysis of the extent of pleiotropy of all CAD loci. METHODS: In discovery analyses involving 42,335 CAD cases and 78,240 control subjects we tested the association of 29,383 common (minor allele frequency >5%) single nucleotide polymorphisms available on the exome array, which included a substantial proportion of known or suspected single nucleotide polymorphisms associated with common diseases or traits as of 2011. Suggestive association signals were replicated in an additional 30,533 cases and 42,530 control subjects. To evaluate pleiotropy, we tested CAD loci for association with cardiovascular risk factors (lipid traits, blood pressure phenotypes, body mass index, diabetes, and smoking behavior), as well as with other diseases/traits through interrogation of currently available genome-wide association study catalogs. RESULTS: We identified 6 new loci associated with CAD at genome-wide significance: on 2q37 (KCNJ13-GIGYF2), 6p21 (C2), 11p15 (MRVI1-CTR9), 12q13 (LRP1), 12q24 (SCARB1), and 16q13 (CETP). Risk allele frequencies ranged from 0.15 to 0.86, and odds ratio per copy of the risk allele ranged from 1.04 to 1.09. Of 62 new and known CAD loci, 24 (38.7%) showed statistical association with a traditional cardiovascular risk factor, with some showing multiple associations, and 29 (47%) showed associations at p < 1 x 10(-4) with a range of other diseases/traits. CONCLUSIONS: We identified 6 loci associated with CAD at genome-wide significance. Several CAD loci show substantial pleiotropy, which may help us understand the mechanisms by which these loci affect CAD risk. |
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Address |
Center for Human Genetic Research, Massachusetts General Hospital, Boston, Massachusetts; Cardiovascular Research Center, Massachusetts General Hospital, Boston, Massachusetts; Department of Medicine, Harvard Medical School, Boston, Massachusetts; Program in Medical and Population Genetics, Broad Institute, Cambridge, Massachusetts; Cardiology Division, Massachusetts General Hospital, Boston, Massachusetts |
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Corporate Author |
Myocardial Infarction Genetics and CARDIoGRAM Exome Consortia Investigators |
Thesis |
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English |
Summary Language |
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Original Title |
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Abbreviated Series Title |
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Series Volume |
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Series Issue |
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Edition |
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ISSN  |
0735-1097 |
ISBN |
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Medium |
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Area |
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Expedition |
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Conference |
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Notes |
PMID:28209224; PMCID:PMC5314135 |
Approved |
no |
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Call Number |
HUNT @ maria.stuifbergen @ |
Serial |
2030 |
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Permanent link to this record |
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Author |
Zhou, W.; Fritsche, L.G.; Das, S.; Zhang, H.; Nielsen, J.B.; Holmen, O.L.; Chen, J.; Lin, M.; Elvestad, M.B.; Hveem, K.; Abecasis, G.R.; Kang, H.M.; Willer, C.J. |

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Title |
Improving power of association tests using multiple sets of imputed genotypes from distributed reference panels |
Type |
Journal Article |
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Year |
2017 |
Publication |
Genetic Epidemiology |
Abbreviated Journal |
Genet Epidemiol |
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Volume |
41 |
Issue |
8 |
Pages |
744-755 |
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Keywords |
Gwas; genotype imputation; multiple reference panels; population-specific; study power |
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Abstract |
The accuracy of genotype imputation depends upon two factors: the sample size of the reference panel and the genetic similarity between the reference panel and the target samples. When multiple reference panels are not consented to combine together, it is unclear how to combine the imputation results to optimize the power of genetic association studies. We compared the accuracy of 9,265 Norwegian genomes imputed from three reference panels-1000 Genomes phase 3 (1000G), Haplotype Reference Consortium (HRC), and a reference panel containing 2,201 Norwegian participants from the population-based Nord Trondelag Health Study (HUNT) from low-pass genome sequencing. We observed that the population-matched reference panel allowed for imputation of more population-specific variants with lower frequency (minor allele frequency (MAF) between 0.05% and 0.5%). The overall imputation accuracy from the population-specific panel was substantially higher than 1000G and was comparable with HRC, despite HRC being 15-fold larger. These results recapitulate the value of population-specific reference panels for genotype imputation. We also evaluated different strategies to utilize multiple sets of imputed genotypes to increase the power of association studies. We observed that testing association for all variants imputed from any panel results in higher power to detect association than the alternative strategy of including only one version of each genetic variant, selected for having the highest imputation quality metric. This was particularly true for lower frequency variants (MAF < 1%), even after adjusting for the additional multiple testing burden. |
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Address |
Department of Human Genetics, University of Michigan Medical School, Ann Arbor, Michigan, United States of America |
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Corporate Author |
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English |
Summary Language |
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Original Title |
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Series Editor |
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Series Title |
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Abbreviated Series Title |
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Series Volume |
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Series Issue |
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Edition |
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ISSN  |
0741-0395 |
ISBN |
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Medium |
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Area |
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Expedition |
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Conference |
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Notes |
PMID:28861891 |
Approved |
no |
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Call Number |
HUNT @ maria.stuifbergen @ |
Serial |
2026 |
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Permanent link to this record |
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Author |
Rasouli, B.; Andersson, T.; Carlsson, P.-O.; Grill, V.; Groop, L.; Martinell, M.; Midthjell, K.; Storm, P.; Tuomi, T.; Carlsson, S. |

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Title |
Use of Swedish smokeless tobacco (snus) and the risk of Type 2 diabetes and latent autoimmune diabetes of adulthood (LADA) |
Type |
Journal Article |
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Year |
2017 |
Publication |
Diabetic Medicine : a Journal of the British Diabetic Association |
Abbreviated Journal |
Diabet Med |
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Volume |
34 |
Issue |
4 |
Pages |
514-521 |
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Keywords |
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Abstract |
AIMS: It has been suggested that moist snuff (snus), a smokeless tobacco product that is high in nicotine and widespread in Scandinavia, increases the risk of Type 2 diabetes. Previous studies are however few, contradictory and, with regard to autoimmune diabetes, lacking. Our aim was to study the association between snus use and the risk of Type 2 diabetes and latent autoimmune diabetes of adulthood (LADA). METHOD: Analyses were based on incident cases (Type 2 diabetes, n = 724; LADA, n = 200) and population-based controls (n = 699) from a Swedish case-control study. Additional analyses were performed on cross-sectional data from the Norwegian HUNT study (n = 21 473) with 829 prevalent cases of Type 2 diabetes. Odds ratios (OR) were estimated adjusted for age, BMI family history of diabetes and smoking. Only men were included. RESULTS: No association between snus use and Type 2 diabetes or LADA was seen in the Swedish data. For Type 2 diabetes, the OR for > 10 box-years was 1.00 [95% confidence interval (CI), 0.47 to 2.11] and for LADA 1.01 (95% CI, 0.45 to 2.29). Similarly, in HUNT, the OR for Type 2 diabetes in ever-users was estimated at 0.91 (95% CI, 0.75 to 1.10) and in heavy users at 0.92 (95% CI, 0.46 to 1.83). CONCLUSION: The risk of Type 2 diabetes and LADA is unrelated to the use of snus, despite its high nicotine content. This opens the possibility of the increased risk of Type 2 diabetes seen in smokers may not be attributed to nicotine, but to other substances in tobacco smoke. |
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Address |
Epidemiology Unit, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden |
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Corporate Author |
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Thesis |
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English |
Summary Language |
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Abbreviated Series Title |
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ISSN  |
0742-3071 |
ISBN |
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Notes |
PMID:27353226 |
Approved |
no |
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Call Number |
HUNT @ maria.stuifbergen @ |
Serial |
1972 |
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Permanent link to this record |
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Author |
Haug, E.B.; Horn, J.; Fraser, A.; Markovitz, A.R.; Rich-Edwards, J.W.; Davey Smith, G.; Romundstad, P.R.; Asvold, B.O. |

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Title |
Pre-pregnancy Blood Pressure and Offspring Sex in the HUNT Study, Norway |
Type |
Journal Article |
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Year |
2017 |
Publication |
American Journal of Hypertension |
Abbreviated Journal |
Am J Hypertens |
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Volume |
30 |
Issue |
9 |
Pages |
e7-e8 |
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Keywords |
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Abstract |
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Address |
Department of Endocrinology, St. Olavs Hospital, Trondheim University Hospital, Trondheim, Norway |
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English |
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Abbreviated Series Title |
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ISSN  |
0895-7061 |
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Notes |
PMID:28633300 |
Approved |
no |
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Call Number |
HUNT @ maria.stuifbergen @ |
Serial |
1923 |
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Permanent link to this record |
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Author |
Retnakaran, R.; Wen, S.W.; Tan, H.; Zhou, S.; Ye, C.; Shen, M.; Smith, G.N.; Walker, M.C. |

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Title |
Response to Pre-Pregnancy Blood Pressure and Offspring Sex in the HUNT Study, Norway |
Type |
Journal Article |
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Year |
2017 |
Publication |
American Journal of Hypertension |
Abbreviated Journal |
Am J Hypertens |
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Volume |
30 |
Issue |
9 |
Pages |
e9 |
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Abstract |
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Address |
Department of Epidemiology and Community Medicine, University of Ottawa, Ottawa, Ontario, Canada |
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English |
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0895-7061 |
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Notes |
PMID:28633294 |
Approved |
no |
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Call Number |
HUNT @ maria.stuifbergen @ |
Serial |
1973 |
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Permanent link to this record |
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Author |
Brumpton, B.; Mai, X.-M.; Langhammer, A.; Laugsand, L.E.; Janszky, I.; Strand, L.B. |

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Title |
Prospective study of insomnia and incident asthma in adults: the HUNT study |
Type |
Journal Article |
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Year |
2017 |
Publication |
The European Respiratory Journal |
Abbreviated Journal |
Eur Respir J |
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Volume |
49 |
Issue |
2 |
Pages |
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Keywords |
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Abstract |
Insomnia is highly prevalent among asthmatics; however, few studies have investigated insomnia symptoms and asthma development. We aimed to investigate the association between insomnia and the risk of incident asthma in a population-based cohort.Among 17 927 participants free from asthma at baseline we calculated odds ratios and 95% confidence intervals for the risk of incident asthma among those with insomnia compared to those without. Participants reported sleep initiation problems, sleep maintenance problems and nonrestorative sleep. Chronic insomnia was defined as those reporting one or more insomnia symptom at baseline and 10 years earlier. Incident asthma was defined by questions on asthma at baseline and follow-up (average 11 years).The prevalence of sleep initiation problems, sleep maintenance problems and nonrestorative sleep were 1%, 1% and 5%, respectively. The multi-adjusted odds ratios were 1.18 (95% CI 0.97-1.44), 1.30 (95% CI 1.03-1.64) and 1.70 (95% CI 1.37-2.11) for people with one, two and three insomnia symptoms, respectively, compared with people without symptoms (p<0.01 for trend). The risk of developing asthma in those with chronic insomnia was three times higher (adjusted OR 3.16, 95% CI 1.37-6.40) than those without.Insomnia symptoms were associated with increased risk of incident asthma in this study. |
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Address |
Dept of Public Health and General Practice, Faculty of Medicine, Norwegian University of Science and Technology, NTNU, Trondheim, Norway |
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English |
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ISSN  |
0903-1936 |
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Notes |
PMID:28153868 |
Approved |
no |
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Call Number |
HUNT @ maria.stuifbergen @ |
Serial |
1887 |
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Permanent link to this record |
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Author |
Burgel, P.-R.; Paillasseur, J.-L.; Janssens, W.; Piquet, J.; Ter Riet, G.; Garcia-Aymerich, J.; Cosio, B.; Bakke, P.; Puhan, M.A.; Langhammer, A.; Alfageme, I.; Almagro, P.; Ancochea, J.; Celli, B.R.; Casanova, C.; de-Torres, J.P.; Decramer, M.; Echazarreta, A.; Esteban, C.; Gomez Punter, R.M.; Han, M.L.K.; Johannessen, A.; Kaiser, B.; Lamprecht, B.; Lange, P.; Leivseth, L.; Marin, J.M.; Martin, F.; Martinez-Camblor, P.; Miravitlles, M.; Oga, T.; Sofia Ramirez, A.; Sin, D.D.; Sobradillo, P.; Soler-Cataluna, J.J.; Turner, A.M.; Verdu Rivera, F.J.; Soriano, J.B.; Roche, N. |

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Title |
A simple algorithm for the identification of clinical COPD phenotypes |
Type |
Journal Article |
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Year |
2017 |
Publication |
The European Respiratory Journal |
Abbreviated Journal |
Eur Respir J |
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Volume |
50 |
Issue |
5 |
Pages |
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Keywords |
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Abstract |
This study aimed to identify simple rules for allocating chronic obstructive pulmonary disease (COPD) patients to clinical phenotypes identified by cluster analyses.Data from 2409 COPD patients of French/Belgian COPD cohorts were analysed using cluster analysis resulting in the identification of subgroups, for which clinical relevance was determined by comparing 3-year all-cause mortality. Classification and regression trees (CARTs) were used to develop an algorithm for allocating patients to these subgroups. This algorithm was tested in 3651 patients from the COPD Cohorts Collaborative International Assessment (3CIA) initiative.Cluster analysis identified five subgroups of COPD patients with different clinical characteristics (especially regarding severity of respiratory disease and the presence of cardiovascular comorbidities and diabetes). The CART-based algorithm indicated that the variables relevant for patient grouping differed markedly between patients with isolated respiratory disease (FEV1, dyspnoea grade) and those with multi-morbidity (dyspnoea grade, age, FEV1 and body mass index). Application of this algorithm to the 3CIA cohorts confirmed that it identified subgroups of patients with different clinical characteristics, mortality rates (median, from 4% to 27%) and age at death (median, from 68 to 76 years).A simple algorithm, integrating respiratory characteristics and comorbidities, allowed the identification of clinically relevant COPD phenotypes. |
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Address |
Dept of Respiratory Medicine, Cochin Hospital, AP-HP, Paris, France |
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Initiatives BPCO, EABPCO, Leuven and 3CIA study groups |
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English |
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0903-1936 |
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Notes |
PMID:29097431 |
Approved |
no |
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Call Number |
HUNT @ maria.stuifbergen @ |
Serial |
1894 |
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Permanent link to this record |
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Author |
Sun, Y.-Q.; Chen, Y.; Langhammer, A.; Skorpen, F.; Wu, C.; Mai, X.-M. |

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Title |
Passive smoking in relation to lung cancer incidence and histologic types in Norwegian adults: the HUNT study |
Type |
Journal Article |
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Year |
2017 |
Publication |
The European Respiratory Journal |
Abbreviated Journal |
Eur Respir J |
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Volume |
50 |
Issue |
4 |
Pages |
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Address |
Dept of Public Health and Nursing, NTNU, Norwegian University of Science and Technology, Trondheim, Norway |
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0903-1936 |
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Notes |
PMID:29025890 |
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no |
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