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Author Grov, E.K.; Fossa, S.D.; Dahl, A.A. url  doi
  Title A controlled study of the influence of comorbidity on activities of daily living in elderly cancer survivors (the HUNT-3 survey) Type Journal Article
  Year 2017 Publication (up) Journal of Geriatric Oncology Abbreviated Journal J Geriatr Oncol  
  Volume 8 Issue 5 Pages 328-335  
  Keywords Adl; Activities of daily living; Cancer survivors; Comorbidity; Elderly; Home dwelling  
  Abstract OBJECTIVES: To examine the influence of somatic comorbidity on Activity of Daily Living (ADL) problems in cancer survivors >/=70years (ECSs) based on data from The Health Study of Nord-Trondelag County (HUNT-3) 2006-08. MATERIAL AND METHODS: Among participants of the HUNT-3 survey, 599 ECSs had a diagnosis of one invasive cancer according to both The Cancer Registry of Norway and self-report. Three controls without cancer aged >/=70years for each ECS were drawn from the HUNT-3 sample. We compared personal-ADL (P-ADL) and instrumental-ADL (I-ADL) problems for ECSs and differences between ADL problems for ECSs with and without comorbidity and controls with and without comorbidity. RESULTS: The prevalence of P-ADL problems was 3.5% among ECSs and 2.9% among controls (p=0.97) and for I-ADL 28.5% versus 21.4% (p=0.01), respectively. In bivariate analyses where ECSs versus controls was the dependent variable, presence of I-ADL problems, higher age, being female, paired relationship, poor self-rated health, hospitalization last year, and low level of neuroticism were associated being ECSs. In multivariate analyses, these variables, except I-ADL-problems and paired relationship, remained significantly associated being ECSs. No significant differences were shown for P-ADL problems when comparing ECSs and controls with comorbidity, and ECSs with and without comorbidity. ECSs with comorbidity reported significantly more I-ADL-problems than controls with comorbidity, and ECSs with comorbidity had significantly more I-ADL-problems than ECSs without comorbidity. CONCLUSION: Our results reflect common factors found in ADL studies in the elderly population. Health personnel have to be particularly observant on I-ADL problems among female ECSs, and those reporting poor self-rated health or comorbidity.  
  Address National Advisory Unit on Late Effects after Cancer Treatment, Oslo University Hospital, Norwegian Radium Hospital, 0424 Oslo, Norway; Faculty of Medicine, University of Oslo, 0316 Oslo, Norway  
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  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 1879-4068 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:28629695 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1917  
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Author Daneshvar, F.; Weinreich, M.; Daneshvar, D.; Sperling, M.; Salmane, C.; Yacoub, H.; Gabriels, J.; McGinn, T.; Smith, M.C. url  doi
  Title Cardiorespiratory Fitness in Internal Medicine Residents: Are Future Physicians Becoming Deconditioned? Type Journal Article
  Year 2017 Publication (up) Journal of Graduate Medical Education Abbreviated Journal J Grad Med Educ  
  Volume 9 Issue 1 Pages 97-101  
  Keywords *Cardiorespiratory Fitness; Cross-Sectional Studies; Education, Medical, Graduate; Exercise/*psychology; Female; Habits; Humans; Internal Medicine/*education; *Internship and Residency; Male; New York; Surveys and Questionnaires; Time Factors  
  Abstract BACKGROUND : Previous studies have shown a falloff in physicians' physical activity from medical school to residency. Poor fitness may result in stress, increase resident burnout, and contribute to mortality from cardiovascular disease and other causes. Physicians with poor exercise habits are also less likely to counsel patients about exercise. Prior studies have reported resident physical activity but not cardiorespiratory fitness age. OBJECTIVE : The study was conducted in 2 residency programs (3 hospitals) to assess internal medicine residents' exercise habits as well as their cardiorespiratory fitness age. METHODS : Data regarding physical fitness levels and exercise habits were collected in an anonymous cross-sectional survey. Cardiopulmonary fitness age was determined using fitness calculator based on the Nord-Trondelag Health Study (HUNT). RESULTS : Of 199 eligible physicians, 125 (63%) responded to the survey. Of respondents, 11 (9%) reported never having exercised prior to residency and 45 (36%) reported not exercising during residency (P < .001). In addition, 42 (34%) reported exercising every day prior to residency, while only 5 (4%) reported exercising daily during residency (P < .001), with 99 (79%) participants indicating residency obligations as their main barrier to exercise. We found residents' calculated mean fitness age to be 5.6 years higher than their mean chronological age (P < .001). CONCLUSIONS : Internal medicine residents reported significant decreases in physical activity and fitness. Residents attributed time constraints due to training as a key barrier to physical activity.  
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  Language English Summary Language Original Title  
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  ISSN 1949-8357 ISBN Medium  
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  Notes PMID:28261402; PMCID:PMC5330203 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1904  
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Author 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. url  doi
  Title The antihypertensive MTHFR gene polymorphism rs17367504-G is a possible novel protective locus for preeclampsia Type Journal Article
  Year 2017 Publication (up) Journal of Hypertension Abbreviated Journal J Hypertens  
  Volume 35 Issue 1 Pages 132-139  
  Keywords 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  
  Abstract 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.  
  Address 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  
  Corporate Author Thesis  
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  Language English Summary Language Original Title  
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  Series Volume Series Issue Edition  
  ISSN 0263-6352 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:27755385; PMCID:PMC5131692 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1996  
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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. url  doi
  Title Systematic Evaluation of Pleiotropy Identifies 6 Further Loci Associated With Coronary Artery Disease Type Journal Article
  Year 2017 Publication (up) Journal of the American College of Cardiology Abbreviated Journal J Am Coll Cardiol  
  Volume 69 Issue 7 Pages 823-836  
  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  
  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.  
  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  
  Corporate Author Myocardial Infarction Genetics and CARDIoGRAM Exome Consortia Investigators Thesis  
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  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0735-1097 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:28209224; PMCID:PMC5314135 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 2030  
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Author Gemes, K.; Malmo, V.; Laugsand, L.E.; Loennechen, J.P.; Ellekjaer, H.; Laszlo, K.D.; Ahnve, S.; Vatten, L.J.; Mukamal, K.J.; Janszky, I. url  doi
  Title Does Moderate Drinking Increase the Risk of Atrial Fibrillation? The Norwegian HUNT (Nord-Trondelag Health) Study Type Journal Article
  Year 2017 Publication (up) Journal of the American Heart Association Abbreviated Journal J Am Heart Assoc  
  Volume 6 Issue 10 Pages  
  Keywords Hunt; alcohol; atrial fibrillation; cohort study; epidemiology; moderate alcohol  
  Abstract BACKGROUND: Compelling evidence suggests that excessive alcohol consumption increases the risk of atrial fibrillation (AF), but the effect of light-moderate alcohol consumption is less certain. We investigated the association between alcohol consumption within recommended limits and AF risk in a light-drinking population. METHODS AND RESULTS: Among 47 002 participants with information on alcohol consumption in a population-based cohort study in Norway, conducted from October 2006 to June 2008, 1697 validated AF diagnoses were registered during the 8 years of follow-up. We used Cox proportional hazard models with fractional polynomials to analyze the association between alcohol intake and AF. Population attributable risk for drinking within the recommended limit (ie, at most 1 drink per day for women and 2 drinks per day for men without risky drinking) compared with nondrinking was also calculated. The average alcohol intake was 3.8+/-4.8 g/d. The adjusted hazard ratio for AF was 1.38 (95% confidence interval, 1.06-1.80) when we compared participants consuming >7 drinks per week with abstainers. When we modeled the quantity of alcohol intake as a continuous variable, the risk increased in a curvilinear manner. It was higher with heavier alcohol intake, but there was virtually no association at <1 drink per day for women and <2 drinks per day for men in the absence of risky drinking. The population attributable risk among nonrisky drinkers was 0.07% (95% confidence interval, -0.01% to 0.13%). CONCLUSIONS: Although alcohol consumption was associated with a curvilinearly increasing risk of AF in general, the attributable risk of alcohol consumption within recommended limits among participants without binge or problem drinking was negligible in this population.  
  Address Regional Center for Health Care Improvement, St Olav's Hospital, Trondheim, Norway  
  Corporate Author Thesis  
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  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 2047-9980 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:29054845; PMCID:PMC5721892 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1901  
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Author Modalsli, E.H.; Asvold, B.O.; Snekvik, I.; Romundstad, P.R.; Naldi, L.; Saunes, M. url  doi
  Title The association between the clinical diversity of psoriasis and depressive symptoms: the HUNT Study, Norway Type Journal Article
  Year 2017 Publication (up) Journal of the European Academy of Dermatology and Venereology : JEADV Abbreviated Journal J Eur Acad Dermatol Venereol  
  Volume 31 Issue 12 Pages 2062-2068  
  Keywords  
  Abstract BACKGROUND: While a number of observational hospital-based studies have reported an association between psoriasis and depression, less is known about the clinical diversity of psoriasis and depressive symptoms. OBJECTIVE: To investigate the associations of inverse psoriasis, psoriasis severity and psoriasis duration with depressive symptoms in a general population. METHODS: We linked data from the population-based third Nord-Trondelag Health Study (HUNT3) to the Norwegian Prescription Database (NorPD) and Statistics Norway. Depressive symptoms were assessed using the Hospital Anxiety and Depression Scale (HADS). Associations between psoriasis and depressive symptoms (HADS >/= 8) were estimated using logistic regression. RESULTS: Among 37 833 participants in HUNT3, we found a weak association between any psoriasis and the prevalence of depressive symptoms [fully adjusted odds ratio (OR) 1.12, 95% confidence interval (CI) 0.97-1.28]. The association with depressive symptoms was stronger when psoriasis was characterized by inverse anatomical distribution (OR 1.32, 95% CI 1.02-1.70), requirement of systemic psoriasis medication (OR 1.47, 95% CI 1.00-2.17) or long disease duration (OR 1.33, 95% CI 1.09-1.64). Conversely, when there was no inverse psoriasis distribution, no requirement of systemic medication, or shorter disease duration, psoriasis was not meaningfully associated with depressive symptoms. CONCLUSION: Overall, depressive symptoms do not seem to be a major concern among subjects with psoriasis in a general Norwegian population. However, among subjects with inverse anatomical distribution, requirement of systemic psoriasis medication or long disease duration, depressive symptoms may be particularly important to address when evaluating the burden of psoriasis.  
  Address Department of Cancer Research and Molecular Medicine, Faculty of Medicine and Health Sciences, NTNU, Norwegian University of Science and Technology, Trondheim, Norway  
  Corporate Author Thesis  
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  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0926-9959 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:28662282 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1956  
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Author Simic, A.; Hansen, A.F.; Asvold, B.O.; Romundstad, P.R.; Midthjell, K.; Syversen, T.; Flaten, T.P. url  doi
  Title Trace element status in patients with type 2 diabetes in Norway: The HUNT3 Survey Type Journal Article
  Year 2017 Publication (up) Journal of Trace Elements in Medicine and Biology : Organ of the Society for Minerals and Trace Elements (GMS) Abbreviated Journal J Trace Elem Med Biol  
  Volume 41 Issue Pages 91-98  
  Keywords Aged; Diabetes Mellitus, Type 2/*blood/diagnosis/epidemiology; Female; *Health Surveys; Humans; Male; Middle Aged; Norway/epidemiology; Trace Elements/*blood; Case-control study; Hunt3; Trace elements; Type 2 diabetes; Whole blood  
  Abstract Several epidemiological studies have indicated that a number of trace elements may play a role in type 2 diabetes (T2D). We investigated the association between prevalent T2D and the concentrations of 25 trace elements in whole blood, and the relationships between T2D duration and blood levels of the trace elements that we found to be related to T2D prevalence. In this population based case-control study, 267 patients with self-reported T2D and 609 controls (frequency matched), were selected from the third Nord-Trondelag Health Survey. Trace element blood levels were determined by high resolution inductively coupled plasma-mass spectrometry. Multivariable conditional logistic regression and multivariable linear regression were used to estimate associations. The prevalence of T2D was positively associated with boron, calcium and silver, and inversely associated with indium, lead and magnesium (Ptrend<0.05). We found no statistical evidence for associations between blood levels of arsenic, bromine, cadmium, cesium, chromium, copper, gallium, gold, manganese, mercury, molybdenum, nickel, rubidium, selenium, strontium, tantalum, thallium, tin and zinc and T2D prevalence. After corrections for multiple testing, associations remained significant for calcium and lead (Qtrend<0.05), and borderline significant for magnesium, silver and boron. With increasing disease duration, higher calcium levels were observed (P<0.05). This study suggests an association between prevalent T2D and blood levels of boron, calcium, indium, lead, magnesium and silver.  
  Address Department of Chemistry, NTNU, Norwegian University of Science and Technology, Trondheim, Norway  
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  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0946-672X ISBN Medium  
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  Notes PMID:28347468 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1979  
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Author url  doi
  Title Worldwide trends in blood pressure from 1975 to 2015: a pooled analysis of 1479 population-based measurement studies with 19.1 million participants Type Comment
  Year 2017 Publication (up) Lancet (London, England) Abbreviated Journal Lancet  
  Volume 389 Issue 10064 Pages 37-55  
  Keywords Bayes Theorem; *Blood Pressure; *Global Health; Humans; Prevalence; Risk Factors  
  Abstract BACKGROUND: Raised blood pressure is an important risk factor for cardiovascular diseases and chronic kidney disease. We estimated worldwide trends in mean systolic and mean diastolic blood pressure, and the prevalence of, and number of people with, raised blood pressure, defined as systolic blood pressure of 140 mm Hg or higher or diastolic blood pressure of 90 mm Hg or higher. METHODS: For this analysis, we pooled national, subnational, or community population-based studies that had measured blood pressure in adults aged 18 years and older. We used a Bayesian hierarchical model to estimate trends from 1975 to 2015 in mean systolic and mean diastolic blood pressure, and the prevalence of raised blood pressure for 200 countries. We calculated the contributions of changes in prevalence versus population growth and ageing to the increase in the number of adults with raised blood pressure. FINDINGS: We pooled 1479 studies that had measured the blood pressures of 19.1 million adults. Global age-standardised mean systolic blood pressure in 2015 was 127.0 mm Hg (95% credible interval 125.7-128.3) in men and 122.3 mm Hg (121.0-123.6) in women; age-standardised mean diastolic blood pressure was 78.7 mm Hg (77.9-79.5) for men and 76.7 mm Hg (75.9-77.6) for women. Global age-standardised prevalence of raised blood pressure was 24.1% (21.4-27.1) in men and 20.1% (17.8-22.5) in women in 2015. Mean systolic and mean diastolic blood pressure decreased substantially from 1975 to 2015 in high-income western and Asia Pacific countries, moving these countries from having some of the highest worldwide blood pressure in 1975 to the lowest in 2015. Mean blood pressure also decreased in women in central and eastern Europe, Latin America and the Caribbean, and, more recently, central Asia, Middle East, and north Africa, but the estimated trends in these super-regions had larger uncertainty than in high-income super-regions. By contrast, mean blood pressure might have increased in east and southeast Asia, south Asia, Oceania, and sub-Saharan Africa. In 2015, central and eastern Europe, sub-Saharan Africa, and south Asia had the highest blood pressure levels. Prevalence of raised blood pressure decreased in high-income and some middle-income countries; it remained unchanged elsewhere. The number of adults with raised blood pressure increased from 594 million in 1975 to 1.13 billion in 2015, with the increase largely in low-income and middle-income countries. The global increase in the number of adults with raised blood pressure is a net effect of increase due to population growth and ageing, and decrease due to declining age-specific prevalence. INTERPRETATION: During the past four decades, the highest worldwide blood pressure levels have shifted from high-income countries to low-income countries in south Asia and sub-Saharan Africa due to opposite trends, while blood pressure has been persistently high in central and eastern Europe. FUNDING: Wellcome Trust.  
  Address  
  Corporate Author NCD Risk Factor Collaboration (NCD-RisC) Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0140-6736 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:27863813; PMCID:PMC5220163 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1897  
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Author Karlsen, T.; Nauman, J.; Dalen, H.; Langhammer, A.; Wisloff, U. url  doi
  Title The Combined Association of Skeletal Muscle Strength and Physical Activity on Mortality in Older Women: The HUNT2 Study Type Journal Article
  Year 2017 Publication (up) Mayo Clinic Proceedings Abbreviated Journal Mayo Clin Proc  
  Volume 92 Issue 5 Pages 710-718  
  Keywords Aged; Aged, 80 and over; Cardiovascular Diseases/*mortality; *Cause of Death; *Exercise; Female; Hand Strength; Humans; Leg/physiology; *Muscle Strength; Norway/epidemiology; Predictive Value of Tests; Prognosis; Proportional Hazards Models; Prospective Studies  
  Abstract OBJECTIVE: To assess the isolated and combined associations of leg and arm strength with adherence to current physical activity guidelines with all-cause and cause-specific mortality in healthy elderly women. PATIENTS AND METHODS: This was a prospective cohort study of 2529 elderly women (72.6+/-4.8 years) from the Norwegian Healthy survey of Northern Trondelag (second wave) (HUNT2) between August 15, 1995, and June 18, 1997, with a median of 15.6 years (interquartile range, 10.4-16.3 years) of follow-up. Chair-rise test and handgrip strength performances were assessed, and divided into tertiles. The hazard ratio (HR) of all-cause and cause-specific mortality by tertiles of handgrip strength and chair-rise test performance, and combined associations with physical activity were estimated by using Cox proportional hazard regression models. RESULTS: We observed independent associations of physical activity and the chair-rise test performance with all-cause and cardiovascular mortality, and between handgrip strength and all-cause mortality. Despite following physical activity guidelines, women with low muscle strength had increased risk of all-cause mortality (HR chair test, 1.37; 95% CI, 1.07-1.76; HR handgrip strength, 1.39; 95% CI, 1.05-1.85) and cardiovascular disease mortality (HR chair test, 1.57; 95% CI, 1.01-2.42). Slow chair-test performance was associated with all-cause (HR, 1.32; 95% CI, 1.16-1.51) and cardiovascular disease (HR, 1.41; 95% CI, 1.14-1.76) mortality. The association between handgrip strength and all-cause mortality was dose dependent (P value for trend <.01). CONCLUSION: Handgrip strength and chair-rise test performance predicted the risk of all-cause and CVD mortality independent of physical activity. Clinically feasible tests of skeletal muscle strength could increase the precision of prognosis, even in elderly women following current physical activity guidelines.  
  Address Faculty of Medicine, K.G. Jebsen Center of Exercise in Medicine, Department of Circulation and Medical Imaging, NTNU, Norwegian University of Science and Technology, Trondheim, Norway; School of Human Movement & Nutrition Sciences, University of Queensland, Australia  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0025-6196 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:28473035 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1938  
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Author Nauman, J.; Nes, B.M.; Lavie, C.J.; Jackson, A.S.; Sui, X.; Coombes, J.S.; Blair, S.N.; Wisloff, U. url  doi
  Title Prediction of Cardiovascular Mortality by Estimated Cardiorespiratory Fitness Independent of Traditional Risk Factors: The HUNT Study Type Journal Article
  Year 2017 Publication (up) Mayo Clinic Proceedings Abbreviated Journal Mayo Clin Proc  
  Volume 92 Issue 2 Pages 218-227  
  Keywords Adult; Aged; *Cardiorespiratory Fitness; Cardiovascular Diseases/*mortality; Cause of Death; Female; Humans; Male; Middle Aged; Myocardial Ischemia/mortality; Norway/epidemiology; Predictive Value of Tests; Proportional Hazards Models; Prospective Studies; Registries; Risk Factors; Stroke/mortality  
  Abstract OBJECTIVE: To assess the predictive value of estimated cardiorespiratory fitness (eCRF) and evaluate the additional contribution of traditional risk factors in cardiovascular disease (CVD) mortality prediction. PARTICIPANTS AND METHODS: The study included healthy men (n=18,721) and women (n=19,759) aged 30 to 74 years. A nonexercise algorithm estimated cardiorespiratory fitness. Cox proportional hazards models evaluated the primary (CVD mortality) and secondary (all-cause, ischemic heart disease, and stroke mortality) end points. The added predictive value of traditional CVD risk factors was evaluated using the Harrell C statistic and net reclassification improvement. RESULTS: After a median follow-up of 16.3 years (range, 0.04-17.4 years), there were 3863 deaths, including 1133 deaths from CVD (734 men and 399 women). Low eCRF was a strong predictor of CVD and all-cause mortality after adjusting for established risk factors. The C statistics for eCRF and CVD mortality were 0.848 (95% CI, 0.836-0.861) and 0.878 (95% CI, 0.862-0.894) for men and women, respectively, increasing to 0.851 (95% CI, 0.839-0.863) and 0.881 (95% CI, 0.865-0.897), respectively, when adding clinical variables. By adding clinical variables to eCRF, the net reclassification improvement of CVD mortality was 0.014 (95% CI, -0.023 to 0.051) and 0.052 (95% CI, -0.023 to 0.127) in men and women, respectively. CONCLUSION: Low eCRF is independently associated with CVD and all-cause mortality. The inclusion of traditional clinical CVD risk factors added little to risk discrimination and did not improve the classification of risk beyond this simple eCRF measurement, which may be proposed as a practical and cost-effective first-line approach in primary prevention settings.  
  Address K.G. Jebsen Center for Exercise in Medicine, Department of Circulation and Medical Imaging, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0025-6196 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:27866655 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1963  
Permanent link to this record
 

 
Author Marouli, E.; Graff, M.; Medina-Gomez, C.; Lo, K.S.; Wood, A.R.; Kjaer, T.R.; Fine, R.S.; Lu, Y.; Schurmann, C.; Highland, H.M.; Rueger, S.; Thorleifsson, G.; Justice, A.E.; Lamparter, D.; Stirrups, K.E.; Turcot, V.; Young, K.L.; Winkler, T.W.; Esko, T.; Karaderi, T.; Locke, A.E.; Masca, N.G.D.; Ng, M.C.Y.; Mudgal, P.; Rivas, M.A.; Vedantam, S.; Mahajan, A.; Guo, X.; Abecasis, G.; Aben, K.K.; Adair, L.S.; Alam, D.S.; Albrecht, E.; Allin, K.H.; Allison, M.; Amouyel, P.; Appel, E.V.; Arveiler, D.; Asselbergs, F.W.; Auer, P.L.; Balkau, B.; Banas, B.; Bang, L.E.; Benn, M.; Bergmann, S.; Bielak, L.F.; Bluher, M.; Boeing, H.; Boerwinkle, E.; Boger, C.A.; Bonnycastle, L.L.; Bork-Jensen, J.; Bots, M.L.; Bottinger, E.P.; Bowden, D.W.; Brandslund, I.; Breen, G.; Brilliant, M.H.; Broer, L.; Burt, A.A.; Butterworth, A.S.; Carey, D.J.; Caulfield, M.J.; Chambers, J.C.; Chasman, D.I.; Chen, Y.-D.I.; Chowdhury, R.; Christensen, C.; Chu, A.Y.; Cocca, M.; Collins, F.S.; Cook, J.P.; Corley, J.; Galbany, J.C.; Cox, A.J.; Cuellar-Partida, G.; Danesh, J.; Davies, G.; de Bakker, P.I.W.; de Borst, G.J.; de Denus, S.; de Groot, M.C.H.; de Mutsert, R.; Deary, I.J.; Dedoussis, G.; Demerath, E.W.; den Hollander, A.I.; Dennis, J.G.; Di Angelantonio, E.; Drenos, F.; Du, M.; Dunning, A.M.; Easton, D.F.; Ebeling, T.; Edwards, T.L.; Ellinor, P.T.; Elliott, P.; Evangelou, E.; Farmaki, A.-E.; Faul, J.D.; Feitosa, M.F.; Feng, S.; Ferrannini, E.; Ferrario, M.M.; Ferrieres, J.; Florez, J.C.; Ford, I.; Fornage, M.; Franks, P.W.; Frikke-Schmidt, R.; Galesloot, T.E.; Gan, W.; Gandin, I.; Gasparini, P.; Giedraitis, V.; Giri, A.; Girotto, G.; Gordon, S.D.; Gordon-Larsen, P.; Gorski, M.; Grarup, N.; Grove, M.L.; Gudnason, V.; Gustafsson, S.; Hansen, T.; Harris, K.M.; Harris, T.B.; Hattersley, A.T.; Hayward, C.; He, L.; Heid, I.M.; Heikkila, K.; Helgeland, O.; Hernesniemi, J.; Hewitt, A.W.; Hocking, L.J.; Hollensted, M.; Holmen, O.L.; Hovingh, G.K.; Howson, J.M.M.; Hoyng, C.B.; Huang, P.L.; Hveem, K.; Ikram, M.A.; Ingelsson, E.; Jackson, A.U.; Jansson, J.-H.; Jarvik, G.P.; Jensen, G.B.; Jhun, M.A.; Jia, Y.; Jiang, X.; Johansson, S.; Jorgensen, M.E.; Jorgensen, T.; Jousilahti, P.; Jukema, J.W.; Kahali, B.; Kahn, R.S.; Kahonen, M.; Kamstrup, P.R.; Kanoni, S.; Kaprio, J.; Karaleftheri, M.; Kardia, S.L.R.; Karpe, F.; Kee, F.; Keeman, R.; Kiemeney, L.A.; Kitajima, H.; Kluivers, K.B.; Kocher, T.; Komulainen, P.; Kontto, J.; Kooner, J.S.; Kooperberg, C.; Kovacs, P.; Kriebel, J.; Kuivaniemi, H.; Kury, S.; Kuusisto, J.; La Bianca, M.; Laakso, M.; Lakka, T.A.; Lange, E.M.; Lange, L.A.; Langefeld, C.D.; Langenberg, C.; Larson, E.B.; Lee, I.-T.; Lehtimaki, T.; Lewis, C.E.; Li, H.; Li, J.; Li-Gao, R.; Lin, H.; Lin, L.-A.; Lin, X.; Lind, L.; Lindstrom, J.; Linneberg, A.; Liu, Y.; Liu, Y.; Lophatananon, A.; Luan, J.'an; Lubitz, S.A.; Lyytikainen, L.-P.; Mackey, D.A.; Madden, P.A.F.; Manning, A.K.; Mannisto, S.; Marenne, G.; Marten, J.; Martin, N.G.; Mazul, A.L.; Meidtner, K.; Metspalu, A.; Mitchell, P.; Mohlke, K.L.; Mook-Kanamori, D.O.; Morgan, A.; Morris, A.D.; Morris, A.P.; Muller-Nurasyid, M.; Munroe, P.B.; Nalls, M.A.; Nauck, M.; Nelson, C.P.; Neville, M.; Nielsen, S.F.; Nikus, K.; Njolstad, P.R.; Nordestgaard, B.G.; Ntalla, I.; O'Connel, J.R.; Oksa, H.; Loohuis, L.M.O.; Ophoff, R.A.; Owen, K.R.; Packard, C.J.; Padmanabhan, S.; Palmer, C.N.A.; Pasterkamp, G.; Patel, A.P.; Pattie, A.; Pedersen, O.; Peissig, P.L.; Peloso, G.M.; Pennell, C.E.; Perola, M.; Perry, J.A.; Perry, J.R.B.; Person, T.N.; Pirie, A.; Polasek, O.; Posthuma, D.; Raitakari, O.T.; Rasheed, A.; Rauramaa, R.; Reilly, D.F.; Reiner, A.P.; Renstrom, F.; Ridker, P.M.; Rioux, J.D.; Robertson, N.; Robino, A.; Rolandsson, O.; Rudan, I.; Ruth, K.S.; Saleheen, D.; Salomaa, V.; Samani, N.J.; Sandow, K.; Sapkota, Y.; Sattar, N.; Schmidt, M.K.; Schreiner, P.J.; Schulze, M.B.; Scott, R.A.; Segura-Lepe, M.P.; Shah, S.; Sim, X.; Sivapalaratnam, S.; Small, K.S.; Smith, A.V.; Smith, J.A.; Southam, L.; Spector, T.D.; Speliotes, E.K.; Starr, J.M.; Steinthorsdottir, V.; Stringham, H.M.; Stumvoll, M.; Surendran, P.; 't Hart, L.M.; Tansey, K.E.; Tardif, J.-C.; Taylor, K.D.; Teumer, A.; Thompson, D.J.; Thorsteinsdottir, U.; Thuesen, B.H.; Tonjes, A.; Tromp, G.; Trompet, S.; Tsafantakis, E.; Tuomilehto, J.; Tybjaerg-Hansen, A.; Tyrer, J.P.; Uher, R.; Uitterlinden, A.G.; Ulivi, S.; van der Laan, S.W.; Van Der Leij, A.R.; van Duijn, C.M.; van Schoor, N.M.; van Setten, J.; Varbo, A.; Varga, T.V.; Varma, R.; Edwards, D.R.V.; Vermeulen, S.H.; Vestergaard, H.; Vitart, V.; Vogt, T.F.; Vozzi, D.; Walker, M.; Wang, F.; Wang, C.A.; Wang, S.; Wang, Y.; Wareham, N.J.; Warren, H.R.; Wessel, J.; Willems, S.M.; Wilson, J.G.; Witte, D.R.; Woods, M.O.; Wu, Y.; Yaghootkar, H.; Yao, J.; Yao, P.; Yerges-Armstrong, L.M.; Young, R.; Zeggini, E.; Zhan, X.; Zhang, W.; Zhao, J.H.; Zhao, W.; Zhao, W.; Zheng, H.; Zhou, W.; Rotter, J.I.; Boehnke, M.; Kathiresan, S.; McCarthy, M.I.; Willer, C.J.; Stefansson, K.; Borecki, I.B.; Liu, D.J.; North, K.E.; Heard-Costa, N.L.; Pers, T.H.; Lindgren, C.M.; Oxvig, C.; Kutalik, Z.; Rivadeneira, F.; Loos, R.J.F.; Frayling, T.M.; Hirschhorn, J.N.; Deloukas, P.; Lettre, G. url  doi
  Title Rare and low-frequency coding variants alter human adult height Type Journal Article
  Year 2017 Publication (up) Nature Abbreviated Journal Nature  
  Volume 542 Issue 7640 Pages 186-190  
  Keywords ADAMTS Proteins/genetics; Adult; Alleles; Body Height/*genetics; Cell Adhesion Molecules/genetics; Female; Gene Frequency/*genetics; Genetic Variation/*genetics; Genome, Human/genetics; Glycoproteins/genetics/metabolism; Glycosaminoglycans/biosynthesis; Hedgehog Proteins/genetics; Humans; Intercellular Signaling Peptides and Proteins/genetics/metabolism; Interferon Regulatory Factors/genetics; Interleukin-11 Receptor alpha Subunit/genetics; Male; Multifactorial Inheritance/genetics; NADPH Oxidase 4; NADPH Oxidases/genetics; Phenotype; Pregnancy-Associated Plasma Protein-A/metabolism; Procollagen N-Endopeptidase/genetics; Proteoglycans/biosynthesis; Proteolysis; Receptors, Androgen/genetics; Somatomedins/metabolism  
  Abstract Height is a highly heritable, classic polygenic trait with approximately 700 common associated variants identified through genome-wide association studies so far. Here, we report 83 height-associated coding variants with lower minor-allele frequencies (in the range of 0.1-4.8%) and effects of up to 2 centimetres per allele (such as those in IHH, STC2, AR and CRISPLD2), greater than ten times the average effect of common variants. In functional follow-up studies, rare height-increasing alleles of STC2 (giving an increase of 1-2 centimetres per allele) compromised proteolytic inhibition of PAPP-A and increased cleavage of IGFBP-4 in vitro, resulting in higher bioavailability of insulin-like growth factors. These 83 height-associated variants overlap genes that are mutated in monogenic growth disorders and highlight new biological candidates (such as ADAMTS3, IL11RA and NOX4) and pathways (such as proteoglycan and glycosaminoglycan synthesis) involved in growth. Our results demonstrate that sufficiently large sample sizes can uncover rare and low-frequency variants of moderate-to-large effect associated with polygenic human phenotypes, and that these variants implicate relevant genes and pathways.  
  Address Department of Medicine, Faculty of Medicine, Universite de Montreal, Montreal, Quebec, H3T 1J4, Canada  
  Corporate Author MAGIC Investigators Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0028-0836 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:28146470; PMCID:PMC5302847 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1953  
Permanent link to this record
 

 
Author Justice, A.E.; Winkler, T.W.; Feitosa, M.F.; Graff, M.; Fisher, V.A.; Young, K.; Barata, L.; Deng, X.; Czajkowski, J.; Hadley, D.; Ngwa, J.S.; Ahluwalia, T.S.; Chu, A.Y.; Heard-Costa, N.L.; Lim, E.; Perez, J.; Eicher, J.D.; Kutalik, Z.; Xue, L.; Mahajan, A.; Renstrom, F.; Wu, J.; Qi, Q.; Ahmad, S.; Alfred, T.; Amin, N.; Bielak, L.F.; Bonnefond, A.; Bragg, J.; Cadby, G.; Chittani, M.; Coggeshall, S.; Corre, T.; Direk, N.; Eriksson, J.; Fischer, K.; Gorski, M.; Neergaard Harder, M.; Horikoshi, M.; Huang, T.; Huffman, J.E.; Jackson, A.U.; Justesen, J.M.; Kanoni, S.; Kinnunen, L.; Kleber, M.E.; Komulainen, P.; Kumari, M.; Lim, U.; Luan, J.'an; Lyytikainen, L.-P.; Mangino, M.; Manichaikul, A.; Marten, J.; Middelberg, R.P.S.; Muller-Nurasyid, M.; Navarro, P.; Perusse, L.; Pervjakova, N.; Sarti, C.; Smith, A.V.; Smith, J.A.; Stancakova, A.; Strawbridge, R.J.; Stringham, H.M.; Sung, Y.J.; Tanaka, T.; Teumer, A.; Trompet, S.; van der Laan, S.W.; van der Most, P.J.; Van Vliet-Ostaptchouk, J.V.; Vedantam, S.L.; Verweij, N.; Vink, J.M.; Vitart, V.; Wu, Y.; Yengo, L.; Zhang, W.; Hua Zhao, J.; Zimmermann, M.E.; Zubair, N.; Abecasis, G.R.; Adair, L.S.; Afaq, S.; Afzal, U.; Bakker, S.J.L.; Bartz, T.M.; Beilby, J.; Bergman, R.N.; Bergmann, S.; Biffar, R.; Blangero, J.; Boerwinkle, E.; Bonnycastle, L.L.; Bottinger, E.; Braga, D.; Buckley, B.M.; Buyske, S.; Campbell, H.; Chambers, J.C.; Collins, F.S.; Curran, J.E.; de Borst, G.J.; de Craen, A.J.M.; de Geus, E.J.C.; Dedoussis, G.; Delgado, G.E.; den Ruijter, H.M.; Eiriksdottir, G.; Eriksson, A.L.; Esko, T.; Faul, J.D.; Ford, I.; Forrester, T.; Gertow, K.; Gigante, B.; Glorioso, N.; Gong, J.; Grallert, H.; Grammer, T.B.; Grarup, N.; Haitjema, S.; Hallmans, G.; Hamsten, A.; Hansen, T.; Harris, T.B.; Hartman, C.A.; Hassinen, M.; Hastie, N.D.; Heath, A.C.; Hernandez, D.; Hindorff, L.; Hocking, L.J.; Hollensted, M.; Holmen, O.L.; Homuth, G.; Jan Hottenga, J.; Huang, J.; Hung, J.; Hutri-Kahonen, N.; Ingelsson, E.; James, A.L.; Jansson, J.-O.; Jarvelin, M.-R.; Jhun, M.A.; Jorgensen, M.E.; Juonala, M.; Kahonen, M.; Karlsson, M.; Koistinen, H.A.; Kolcic, I.; Kolovou, G.; Kooperberg, C.; Kramer, B.K.; Kuusisto, J.; Kvaloy, K.; Lakka, T.A.; Langenberg, C.; Launer, L.J.; Leander, K.; Lee, N.R.; Lind, L.; Lindgren, C.M.; Linneberg, A.; Lobbens, S.; Loh, M.; Lorentzon, M.; Luben, R.; Lubke, G.; Ludolph-Donislawski, A.; Lupoli, S.; Madden, P.A.F.; Mannikko, R.; Marques-Vidal, P.; Martin, N.G.; McKenzie, C.A.; McKnight, B.; Mellstrom, D.; Menni, C.; Montgomery, G.W.; Musk, A.B.; Narisu, N.; Nauck, M.; Nolte, I.M.; Oldehinkel, A.J.; Olden, M.; Ong, K.K.; Padmanabhan, S.; Peyser, P.A.; Pisinger, C.; Porteous, D.J.; Raitakari, O.T.; Rankinen, T.; Rao, D.C.; Rasmussen-Torvik, L.J.; Rawal, R.; Rice, T.; Ridker, P.M.; Rose, L.M.; Bien, S.A.; Rudan, I.; Sanna, S.; Sarzynski, M.A.; Sattar, N.; Savonen, K.; Schlessinger, D.; Scholtens, S.; Schurmann, C.; Scott, R.A.; Sennblad, B.; Siemelink, M.A.; Silbernagel, G.; Slagboom, P.E.; Snieder, H.; Staessen, J.A.; Stott, D.J.; Swertz, M.A.; Swift, A.J.; Taylor, K.D.; Tayo, B.O.; Thorand, B.; Thuillier, D.; Tuomilehto, J.; Uitterlinden, A.G.; Vandenput, L.; Vohl, M.-C.; Volzke, H.; Vonk, J.M.; Waeber, G.; Waldenberger, M.; Westendorp, R.G.J.; Wild, S.; Willemsen, G.; Wolffenbuttel, B.H.R.; Wong, A.; Wright, A.F.; Zhao, W.; Zillikens, M.C.; Baldassarre, D.; Balkau, B.; Bandinelli, S.; Boger, C.A.; Boomsma, D.I.; Bouchard, C.; Bruinenberg, M.; Chasman, D.I.; Chen, Y.-D.I.; Chines, P.S.; Cooper, R.S.; Cucca, F.; Cusi, D.; Faire, U. de; Ferrucci, L.; Franks, P.W.; Froguel, P.; Gordon-Larsen, P.; Grabe, H.-J.; Gudnason, V.; Haiman, C.A.; Hayward, C.; Hveem, K.; Johnson, A.D.; Wouter Jukema, J.; Kardia, S.L.R.; Kivimaki, M.; Kooner, J.S.; Kuh, D.; Laakso, M.; Lehtimaki, T.; Marchand, L.L.; Marz, W.; McCarthy, M.I.; Metspalu, A.; Morris, A.P.; Ohlsson, C.; Palmer, L.J.; Pasterkamp, G.; Pedersen, O.; Peters, A.; Peters, U.; Polasek, O.; Psaty, B.M.; Qi, L.; Rauramaa, R.; Smith, B.H.; Sorensen, T.I.A.; Strauch, K.; Tiemeier, H.; Tremoli, E.; van der Harst, P.; Vestergaard, H.; Vollenweider, P.; Wareham, N.J.; Weir, D.R.; Whitfield, J.B.; Wilson, J.F.; Tyrrell, J.; Frayling, T.M.; Barroso, I.; Boehnke, M.; Deloukas, P.; Fox, C.S.; Hirschhorn, J.N.; Hunter, D.J.; Spector, T.D.; Strachan, D.P.; van Duijn, C.M.; Heid, I.M.; Mohlke, K.L.; Marchini, J.; Loos, R.J.F.; Kilpelainen, T.O.; Liu, C.-T.; Borecki, I.B.; North, K.E.; Cupples, L.A. url  doi
  Title Genome-wide meta-analysis of 241,258 adults accounting for smoking behaviour identifies novel loci for obesity traits Type Journal Article
  Year 2017 Publication (up) Nature Communications Abbreviated Journal Nat Commun  
  Volume 8 Issue Pages 14977  
  Keywords  
  Abstract Few genome-wide association studies (GWAS) account for environmental exposures, like smoking, potentially impacting the overall trait variance when investigating the genetic contribution to obesity-related traits. Here, we use GWAS data from 51,080 current smokers and 190,178 nonsmokers (87% European descent) to identify loci influencing BMI and central adiposity, measured as waist circumference and waist-to-hip ratio both adjusted for BMI. We identify 23 novel genetic loci, and 9 loci with convincing evidence of gene-smoking interaction (GxSMK) on obesity-related traits. We show consistent direction of effect for all identified loci and significance for 18 novel and for 5 interaction loci in an independent study sample. These loci highlight novel biological functions, including response to oxidative stress, addictive behaviour, and regulatory functions emphasizing the importance of accounting for environment in genetic analyses. Our results suggest that tobacco smoking may alter the genetic susceptibility to overall adiposity and body fat distribution.  
  Address NHLBI Framingham Heart Study, Framingham, Massachusetts, 01702 USA  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 2041-1723 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:28443625; PMCID:PMC5414044 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1937  
Permanent link to this record
 

 
Author Scelo, G.; Purdue, M.P.; Brown, K.M.; Johansson, M.; Wang, Z.; Eckel-Passow, J.E.; Ye, Y.; Hofmann, J.N.; Choi, J.; Foll, M.; Gaborieau, V.; Machiela, M.J.; Colli, L.M.; Li, P.; Sampson, J.N.; Abedi-Ardekani, B.; Besse, C.; Blanche, H.; Boland, A.; Burdette, L.; Chabrier, A.; Durand, G.; Le Calvez-Kelm, F.; Prokhortchouk, E.; Robinot, N.; Skryabin, K.G.; Wozniak, M.B.; Yeager, M.; Basta-Jovanovic, G.; Dzamic, Z.; 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.; Baglietto, L.; Boeing, H.; Khaw, K.-T.; Weiderpass, E.; Ljungberg, B.; Sitaram, R.T.; Bruinsma, F.; Jordan, S.J.; Severi, G.; Winship, I.; 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.L.; 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.; Michael Gaziano, J.; Sesso, H.D.; Black, A.; Freedman, N.D.; Huang, W.-Y.; Anema, J.G.; Kahnoski, R.J.; Lane, B.R.; Noyes, S.L.; Petillo, D.; Teh, B.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.; Henrion, M.; Larkin, J.; Barman, P.; Leibovich, B.C.; Choueiri, T.K.; Mark Lathrop, G.; Rothman, N.; Deleuze, J.-F.; McKay, J.D.; Parker, A.S.; Wu, X.; Houlston, R.S.; Brennan, P.; Chanock, S.J. url  doi
  Title Genome-wide association study identifies multiple risk loci for renal cell carcinoma Type Journal Article
  Year 2017 Publication (up) Nature Communications Abbreviated Journal Nat Commun  
  Volume 8 Issue Pages 15724  
  Keywords  
  Abstract Previous genome-wide association studies (GWAS) have identified six risk loci for renal cell carcinoma (RCC). We conducted a meta-analysis of two new scans of 5,198 cases and 7,331 controls together with four existing scans, totalling 10,784 cases and 20,406 controls of European ancestry. Twenty-four loci were tested in an additional 3,182 cases and 6,301 controls. We confirm the six known RCC risk loci and identify seven new loci at 1p32.3 (rs4381241, P=3.1 x 10(-10)), 3p22.1 (rs67311347, P=2.5 x 10(-8)), 3q26.2 (rs10936602, P=8.8 x 10(-9)), 8p21.3 (rs2241261, P=5.8 x 10(-9)), 10q24.33-q25.1 (rs11813268, P=3.9 x 10(-8)), 11q22.3 (rs74911261, P=2.1 x 10(-10)) and 14q24.2 (rs4903064, P=2.2 x 10(-24)). Expression quantitative trait analyses suggest plausible candidate genes at these regions that may contribute to RCC susceptibility.  
  Address Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department Health and Human Services, Bethesda, Maryland 20892, USA  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 2041-1723 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:28598434; PMCID:PMC5472706 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1976  
Permanent link to this record
 

 
Author Ferreira, M.A.; Vonk, J.M.; Baurecht, H.; Marenholz, I.; Tian, C.; Hoffman, J.D.; Helmer, Q.; Tillander, A.; Ullemar, V.; van Dongen, J.; Lu, Y.; Ruschendorf, F.; Esparza-Gordillo, J.; Medway, C.W.; Mountjoy, E.; Burrows, K.; Hummel, O.; Grosche, S.; Brumpton, B.M.; Witte, J.S.; Hottenga, J.-J.; Willemsen, G.; Zheng, J.; Rodriguez, E.; Hotze, M.; Franke, A.; Revez, J.A.; Beesley, J.; Matheson, M.C.; Dharmage, S.C.; Bain, L.M.; Fritsche, L.G.; Gabrielsen, M.E.; Balliu, B.; Nielsen, J.B.; Zhou, W.; Hveem, K.; Langhammer, A.; Holmen, O.L.; Loset, M.; Abecasis, G.R.; Willer, C.J.; Arnold, A.; Homuth, G.; Schmidt, C.O.; Thompson, P.J.; Martin, N.G.; Duffy, D.L.; Novak, N.; Schulz, H.; Karrasch, S.; Gieger, C.; Strauch, K.; Melles, R.B.; Hinds, D.A.; Hubner, N.; Weidinger, S.; Magnusson, P.K.E.; Jansen, R.; Jorgenson, E.; Lee, Y.-A.; Boomsma, D.I.; Almqvist, C.; Karlsson, R.; Koppelman, G.H.; Paternoster, L. url  doi
  Title Shared genetic origin of asthma, hay fever and eczema elucidates allergic disease biology Type Meta-Analysis
  Year 2017 Publication (up) Nature Genetics Abbreviated Journal Nat Genet  
  Volume 49 Issue 12 Pages 1752-1757  
  Keywords Asthma/*genetics; Eczema/*genetics; Genetic Predisposition to Disease/*genetics; Genome-Wide Association Study/methods; Humans; Hypersensitivity/*genetics; Phenotype; Polymorphism, Single Nucleotide; Rhinitis, Allergic, Seasonal/*genetics; Risk Factors  
  Abstract Asthma, hay fever (or allergic rhinitis) and eczema (or atopic dermatitis) often coexist in the same individuals, partly because of a shared genetic origin. To identify shared risk variants, we performed a genome-wide association study (GWAS; n = 360,838) of a broad allergic disease phenotype that considers the presence of any one of these three diseases. We identified 136 independent risk variants (P < 3 x 10(-8)), including 73 not previously reported, which implicate 132 nearby genes in allergic disease pathophysiology. Disease-specific effects were detected for only six variants, confirming that most represent shared risk factors. Tissue-specific heritability and biological process enrichment analyses suggest that shared risk variants influence lymphocyte-mediated immunity. Six target genes provide an opportunity for drug repositioning, while for 36 genes CpG methylation was found to influence transcription independently of genetic effects. Asthma, hay fever and eczema partly coexist because they share many genetic risk variants that dysregulate the expression of immune-related genes.  
  Address MRC Integrative Epidemiology Unit, School of Social and Community Medicine, University of Bristol, Bristol, UK  
  Corporate Author LifeLines Cohort Study Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 1061-4036 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:29083406 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1903  
Permanent link to this record
 

 
Author Liu, D.J.; Peloso, G.M.; Yu, H.; Butterworth, A.S.; Wang, X.; Mahajan, A.; Saleheen, D.; Emdin, C.; Alam, D.; Alves, A.C.; Amouyel, P.; Di Angelantonio, E.; Arveiler, D.; Assimes, T.L.; Auer, P.L.; Baber, U.; Ballantyne, C.M.; Bang, L.E.; Benn, M.; Bis, J.C.; Boehnke, M.; Boerwinkle, E.; Bork-Jensen, J.; Bottinger, E.P.; Brandslund, I.; Brown, M.; Busonero, F.; Caulfield, M.J.; Chambers, J.C.; Chasman, D.I.; Chen, Y.E.; Chen, Y.-D.I.; Chowdhury, R.; Christensen, C.; Chu, A.Y.; Connell, J.M.; Cucca, F.; Cupples, L.A.; Damrauer, S.M.; Davies, G.; Deary, I.J.; Dedoussis, G.; Denny, J.C.; Dominiczak, A.; Dube, M.-P.; Ebeling, T.; Eiriksdottir, G.; Esko, T.; Farmaki, A.-E.; Feitosa, M.F.; Ferrario, M.; Ferrieres, J.; Ford, I.; Fornage, M.; Franks, P.W.; Frayling, T.M.; Frikke-Schmidt, R.; Fritsche, L.G.; Frossard, P.; Fuster, V.; Ganesh, S.K.; Gao, W.; Garcia, M.E.; Gieger, C.; Giulianini, F.; Goodarzi, M.O.; Grallert, H.; Grarup, N.; Groop, L.; Grove, M.L.; Gudnason, V.; Hansen, T.; Harris, T.B.; Hayward, C.; Hirschhorn, J.N.; Holmen, O.L.; Huffman, J.; Huo, Y.; Hveem, K.; Jabeen, S.; Jackson, A.U.; Jakobsdottir, J.; Jarvelin, M.-R.; Jensen, G.B.; Jorgensen, M.E.; Jukema, J.W.; Justesen, J.M.; Kamstrup, P.R.; Kanoni, S.; Karpe, F.; Kee, F.; Khera, A.V.; Klarin, D.; Koistinen, H.A.; Kooner, J.S.; Kooperberg, C.; Kuulasmaa, K.; Kuusisto, J.; Laakso, M.; Lakka, T.; Langenberg, C.; Langsted, A.; Launer, L.J.; Lauritzen, T.; Liewald, D.C.M.; Lin, L.A.; Linneberg, A.; Loos, R.J.F.; Lu, Y.; Lu, X.; Magi, R.; Malarstig, A.; Manichaikul, A.; Manning, A.K.; Mantyselka, P.; Marouli, E.; Masca, N.G.D.; Maschio, A.; Meigs, J.B.; Melander, O.; Metspalu, A.; Morris, A.P.; Morrison, A.C.; Mulas, A.; Muller-Nurasyid, M.; Munroe, P.B.; Neville, M.J.; Nielsen, J.B.; Nielsen, S.F.; Nordestgaard, B.G.; Ordovas, J.M.; Mehran, R.; O'Donnell, C.J.; Orho-Melander, M.; Molony, C.M.; Muntendam, P.; Padmanabhan, S.; Palmer, C.N.A.; Pasko, D.; Patel, A.P.; Pedersen, O.; Perola, M.; Peters, A.; Pisinger, C.; Pistis, G.; Polasek, O.; Poulter, N.; Psaty, B.M.; Rader, D.J.; Rasheed, A.; Rauramaa, R.; Reilly, D.F.; Reiner, A.P.; Renstrom, F.; Rich, S.S.; Ridker, P.M.; Rioux, J.D.; Robertson, N.R.; Roden, D.M.; Rotter, J.I.; Rudan, I.; Salomaa, V.; Samani, N.J.; Sanna, S.; Sattar, N.; Schmidt, E.M.; Scott, R.A.; Sever, P.; Sevilla, R.S.; Shaffer, C.M.; Sim, X.; Sivapalaratnam, S.; Small, K.S.; Smith, A.V.; Smith, B.H.; Somayajula, S.; Southam, L.; Spector, T.D.; Speliotes, E.K.; Starr, J.M.; Stirrups, K.E.; Stitziel, N.; Strauch, K.; Stringham, H.M.; Surendran, P.; Tada, H.; Tall, A.R.; Tang, H.; Tardif, J.-C.; Taylor, K.D.; Trompet, S.; Tsao, P.S.; Tuomilehto, J.; Tybjaerg-Hansen, A.; van Zuydam, N.R.; Varbo, A.; Varga, T.V.; Virtamo, J.; Waldenberger, M.; Wang, N.; Wareham, N.J.; Warren, H.R.; Weeke, P.E.; Weinstock, J.; Wessel, J.; Wilson, J.G.; Wilson, P.W.F.; Xu, M.; Yaghootkar, H.; Young, R.; Zeggini, E.; Zhang, H.; Zheng, N.S.; Zhang, W.; Zhang, Y.; Zhou, W.; Zhou, Y.; Zoledziewska, M.; Howson, J.M.M.; Danesh, J.; McCarthy, M.I.; Cowan, C.A.; Abecasis, G.; Deloukas, P.; Musunuru, K.; Willer, C.J.; Kathiresan, S. url  doi
  Title Exome-wide association study of plasma lipids in >300,000 individuals Type Journal Article
  Year 2017 Publication (up) Nature Genetics Abbreviated Journal Nat Genet  
  Volume 49 Issue 12 Pages 1758-1766  
  Keywords Coronary Artery Disease/blood/genetics; Diabetes Mellitus, Type 2/blood/genetics; Exome/*genetics; Genetic Association Studies/*methods; Genetic Predisposition to Disease/genetics; *Genetic Variation; Genotype; Humans; Lipids/*blood; Macular Degeneration/blood/genetics; Phenotype; Risk Factors  
  Abstract We screened variants on an exome-focused genotyping array in >300,000 participants (replication in >280,000 participants) and identified 444 independent variants in 250 loci significantly associated with total cholesterol (TC), high-density-lipoprotein cholesterol (HDL-C), low-density-lipoprotein cholesterol (LDL-C), and/or triglycerides (TG). At two loci (JAK2 and A1CF), experimental analysis in mice showed lipid changes consistent with the human data. We also found that: (i) beta-thalassemia trait carriers displayed lower TC and were protected from coronary artery disease (CAD); (ii) excluding the CETP locus, there was not a predictable relationship between plasma HDL-C and risk for age-related macular degeneration; (iii) only some mechanisms of lowering LDL-C appeared to increase risk for type 2 diabetes (T2D); and (iv) TG-lowering alleles involved in hepatic production of TG-rich lipoproteins (TM6SF2 and PNPLA3) tracked with higher liver fat, higher risk for T2D, and lower risk for CAD, whereas TG-lowering alleles involved in peripheral lipolysis (LPL and ANGPTL4) had no effect on liver fat but decreased risks for both T2D and CAD.  
  Address Cardiovascular Research Center, Massachusetts General Hospital, Boston, Massachusetts, USA  
  Corporate Author VA Million Veteran Program Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 1061-4036 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:29083408; PMCID:PMC5709146 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1943  
Permanent link to this record
 

 
Author Lu, X.; Peloso, G.M.; Liu, D.J.; Wu, Y.; Zhang, H.; Zhou, W.; Li, J.; Tang, C.S.-M.; Dorajoo, R.; Li, H.; Long, J.; Guo, X.; Xu, M.; Spracklen, C.N.; Chen, Y.; Liu, X.; Zhang, Y.; Khor, C.C.; Liu, J.; Sun, L.; Wang, L.; Gao, Y.-T.; Hu, Y.; Yu, K.; Wang, Y.; Cheung, C.Y.Y.; Wang, F.; Huang, J.; Fan, Q.; Cai, Q.; Chen, S.; Shi, J.; Yang, X.; Zhao, W.; Sheu, W.H.-H.; Cherny, S.S.; He, M.; Feranil, A.B.; Adair, L.S.; Gordon-Larsen, P.; Du, S.; Varma, R.; Chen, Y.-D.I.; Shu, X.-O.; Lam, K.S.L.; Wong, T.Y.; Ganesh, S.K.; Mo, Z.; Hveem, K.; Fritsche, L.G.; Nielsen, J.B.; Tse, H.-F.; Huo, Y.; Cheng, C.-Y.; Chen, Y.E.; Zheng, W.; Tai, E.S.; Gao, W.; Lin, X.; Huang, W.; Abecasis, G.; Kathiresan, S.; Mohlke, K.L.; Wu, T.; Sham, P.C.; Gu, D.; Willer, C.J. url  doi
  Title Exome chip meta-analysis identifies novel loci and East Asian-specific coding variants that contribute to lipid levels and coronary artery disease Type Meta-Analysis
  Year 2017 Publication (up) Nature Genetics Abbreviated Journal Nat Genet  
  Volume 49 Issue 12 Pages 1722-1730  
  Keywords Asian Continental Ancestry Group/genetics; Coronary Artery Disease/ethnology/*genetics; Europe; European Continental Ancestry Group/genetics; Exome/*genetics; Far East; Gene Frequency; Genetic Predisposition to Disease/ethnology/*genetics; *Genetic Variation; Genome-Wide Association Study; Genotype; Humans; Lipid Metabolism/*genetics; Lipids/analysis  
  Abstract Most genome-wide association studies have been of European individuals, even though most genetic variation in humans is seen only in non-European samples. To search for novel loci associated with blood lipid levels and clarify the mechanism of action at previously identified lipid loci, we used an exome array to examine protein-coding genetic variants in 47,532 East Asian individuals. We identified 255 variants at 41 loci that reached chip-wide significance, including 3 novel loci and 14 East Asian-specific coding variant associations. After a meta-analysis including >300,000 European samples, we identified an additional nine novel loci. Sixteen genes were identified by protein-altering variants in both East Asians and Europeans, and thus are likely to be functional genes. Our data demonstrate that most of the low-frequency or rare coding variants associated with lipids are population specific, and that examining genomic data across diverse ancestries may facilitate the identification of functional genes at associated loci.  
  Address Department of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, Michigan, USA  
  Corporate Author GLGC Consortium Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 1061-4036 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:29083407 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1957  
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Author Felde, G.; Ebbesen, M.H.; Hunskaar, S. url  doi
  Title Anxiety and depression associated with urinary incontinence. A 10-year follow-up study from the Norwegian HUNT study (EPINCONT) Type Journal Article
  Year 2017 Publication (up) Neurourology and Urodynamics Abbreviated Journal Neurourol Urodyn  
  Volume 36 Issue 2 Pages 322-328  
  Keywords 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  
  Abstract 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.  
  Address National Centre for Emergency Primary Health Care, Uni Research Health, Bergen, Norway  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0733-2467 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:26584597 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1902  
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Author Hellevik, A.I.; Nordsletten, L.; Johnsen, M.B.; Fenstad, A.M.; Furnes, O.; Storheim, K.; Zwart, J.A.; Flugsrud, G.; Langhammer, A. url  doi
  Title Age of menarche is associated with knee joint replacement due to primary osteoarthritis (The HUNT Study and the Norwegian Arthroplasty Register) Type Journal Article
  Year 2017 Publication (up) Osteoarthritis and Cartilage Abbreviated Journal Osteoarthritis Cartilage  
  Volume 25 Issue 10 Pages 1654-1662  
  Keywords Hip joint replacement; Hormonal therapies; Knee joint replacement; Osteoarthritis; Reproductive history  
  Abstract OBJECTIVE: To investigate whether parity, age at menarche, menopausal status, age at menopause, use of oral contraceptives (OC) or use of hormone replacement therapy (HRT) were associated with total knee replacement (TKR) or total hip replacement (THR) due to primary osteoarthritis. METHOD: In a prospective cohort study of 30,289 women from the second and third surveys of the Nord-Trondelag Health Study, data were linked to the Norwegian Arthroplasty Register (NAR) in order to identify TKR or THR due to primary osteoarthritis. Cox proportional hazards models were used to estimate the hazard ratios (HRs). RESULTS: We observed 430 TKRs and 675 THRs during a mean follow-up time of 8.3 years. Increasing age at menarche was inversely associated with the risk of TKR (P-trend < 0.001). Past users and users of systemic HRT were at higher risk of TKR compared to never users (HR 1.42 (95% confidence interval (CI) 1.06-1.90) and HR 1.40 (95% CI 1.03-1.90), respectively). No association was found between parity, age at menarche, menopausal status, age at menopause, oral contraceptive use or HRT use and THR. CONCLUSION: We found that increasing age at menarche reduced the risk of TKR. Past users and users of systemic HRT were at higher risk of TKR compared to never users. Parity did not increase the risk of THR or TKR.  
  Address The HUNT Research Centre, Department of Public Health and Nursing, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology (NTNU), Levanger, Norway. Electronic address: arnulf.langhammer@ntnu.no  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 1063-4584 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:28705605 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1925  
Permanent link to this record
 

 
Author Hellevik, A.I.; Nordsletten, L.; Johnsen, M.B.; Fenstad, A.M.; Furnes, O.; Storheim, K.; Zwart, J.A.; Flugsrud, G.; Langhammer, A. url  doi
  Title Corrigendum to “Age of menarche is associated with knee joint replacement due to primary osteoarthritis (The HUNT Study and the Norwegian Arthroplasty Register)” [Osteoarthr Cartil 25 (2017) 1654-1662] Type Published Erratum
  Year 2017 Publication (up) Osteoarthritis and Cartilage Abbreviated Journal Osteoarthritis Cartilage  
  Volume 25 Issue 12 Pages 2148-2149  
  Keywords  
  Abstract  
  Address The HUNT Research Centre, Department of Public Health and Nursing, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology (NTNU), Levanger, Norway. Electronic address: arnulf.langhammer@ntnu.no  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 1063-4584 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:29066295 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1926  
Permanent link to this record
 

 
Author Johnsen, M.B.; Vie, G.A.; Winsvold, B.S.; Bjorngaard, J.H.; Asvold, B.O.; Gabrielsen, M.E.; Pedersen, L.M.; Hellevik, A.I.; Langhammer, A.; Furnes, O.; Flugsrud, G.B.; Skorpen, F.; Romundstad, P.R.; Storheim, K.; Nordsletten, L.; Zwart, J.A. url  doi
  Title The causal role of smoking on the risk of hip or knee replacement due to primary osteoarthritis: a Mendelian randomisation analysis of the HUNT study Type Journal Article
  Year 2017 Publication (up) Osteoarthritis and Cartilage Abbreviated Journal Osteoarthritis Cartilage  
  Volume 25 Issue 6 Pages 817-823  
  Keywords Epidemiology; Genetic variants; Osteoarthritis; Smoking  
  Abstract OBJECTIVE: Smoking has been associated with a reduced risk of hip and knee osteoarthritis (OA) and subsequent joint replacement. The aim of the present study was to assess whether the observed association is likely to be causal. METHOD: 55,745 participants of a population-based cohort were genotyped for the rs1051730 C > T single-nucleotide polymorphism (SNP), a proxy for smoking quantity among smokers. A Mendelian randomization analysis was performed using rs1051730 as an instrument to evaluate the causal role of smoking on the risk of hip or knee replacement (combined as total joint replacement (TJR)). Association between rs1051730 T alleles and TJR was estimated by hazard ratios (HRs) and 95% confidence intervals (CIs). All analyses were adjusted for age and sex. RESULTS: Smoking quantity (no. of cigarettes) was inversely associated with TJR (HR 0.97, 95% CI 0.97-0.98). In the Mendelian randomization analysis, rs1051730 T alleles were associated with reduced risk of TJR among current smokers (HR 0.84, 95% CI 0.76-0.98, per T allele), however we found no evidence of association among former (HR 0.97, 95% CI 0.88-1.07) and never smokers (HR 0.97, 95% CI 0.89-1.06). Neither adjusting for body mass index (BMI), cardiovascular disease (CVD) nor accounting for the competing risk of mortality substantially changed the results. CONCLUSION: This study suggests that smoking may be causally associated with the reduced risk of TJR. Our findings add support to the inverse association found in previous observational studies. More research is needed to further elucidate the underlying mechanisms of this causal association.  
  Address Communication and Research Unit for Musculoskeletal Disorders, Oslo University Hospital, Oslo, Norway; Faculty of Medicine, University of Oslo, Oslo, Norway. Electronic address: j.a.zwart@medisin.uio.no  
  Corporate Author