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Author Hjerkind, K.V.; Stenehjem, J.S.; Nilsen, T.I.L. url  doi
  Title Adiposity, physical activity and risk of diabetes mellitus: prospective data from the population-based HUNT study, Norway Type Journal Article
  Year 2017 Publication BMJ Open Abbreviated Journal BMJ Open  
  Volume 7 Issue 1 Pages e013142  
  Keywords *Adiposity; Adult; Aged; Aged, 80 and over; Body Mass Index; Comorbidity; Diabetes Mellitus/*epidemiology; *Exercise; Female; Humans; Longitudinal Studies; Male; Middle Aged; Norway/epidemiology; Odds Ratio; Overweight/*epidemiology; Prospective Studies; Risk Factors; Young Adult; *Epidemiology; *Public Health  
  Abstract BACKGROUND: Physical activity may counteract the adverse effects of adiposity on cardiovascular mortality; however, the evidence of a similar effect on diabetes is sparse. This study examines whether physical activity may compensate for the adverse effect of adiposity on diabetes risk. METHODS: The study population consisted of 38 231 individuals aged 20 years or more who participated in two consecutive waves of the prospective longitudinal Nord-Trondelag Health Study in Norway: in 1984-1986 and in 1995-1997. A Poisson regression model with SEs derived from robust variance was used to estimate adjusted risk ratios of diabetes between categories of body mass index and physical activity. RESULTS: Risk of diabetes increased both with increasing body mass (Ptrend <0.001) and with decreasing physical activity level (Ptrend <0.001 in men and 0.01 in women). Combined analyses showed that men who were both obese and had low activity levels had a risk ratio of 17 (95% CI 9.52 to 30) compared to men who were normal weight and highly active, whereas obese men who reported high activity had a risk ratio of 13 (95% CI 6.92 to 26). Corresponding analysis in obese women produced risk ratios of 15 (95% CI 9.18 to 25) and 13 (95% CI 7.42 to 21) among women reporting low and high activity levels, respectively. CONCLUSIONS: This study shows that overweight and obesity are associated with a substantially increased risk of diabetes, particularly among those who also reported being physically inactive. High levels of physical activity were associated with a lower risk of diabetes within all categories of body mass index, but there was no clear evidence that being physically active could entirely compensate for the adverse effect of adiposity on diabetes risk.  
  Address Cancer Registry of Norway, Institute of Population-based Cancer Research, Oslo, 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 2044-6055 ISBN Medium  
  Area Expedition Conference  
  Notes (up) PMID:28093432; PMCID:PMC5253523 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1929  
Permanent link to this record
 

 
Author Grunseit, A.C.; Chau, J.Y.; Rangul, V.; Holmen, T.L.; Bauman, A. url  doi
  Title Patterns of sitting and mortality in the Nord-Trondelag health study (HUNT) Type Journal Article
  Year 2017 Publication The International Journal of Behavioral Nutrition and Physical Activity Abbreviated Journal Int J Behav Nutr Phys Act  
  Volume 14 Issue 1 Pages 8  
  Keywords Adult; Aged; Cardiovascular Diseases/*mortality; *Cause of Death; *Exercise; Female; Humans; Male; Middle Aged; *Posture; Proportional Hazards Models; Prospective Studies; Risk Factors; *Sedentary Lifestyle; Self Report; Young Adult; *Cardiovascular disease; *Epidemiology; *Mortality; *Sedentary behaviour  
  Abstract BACKGROUND: Current evidence concerning sedentary behaviour and mortality risk has used single time point assessments of sitting. Little is known about how changes in sitting levels over time affect subsequent mortality risk. AIM: To examine the associations between patterns of sitting time assessed at two time points 11 years apart and risk of all-cause and cardio-metabolic disease mortality. METHODS: Participants were 25,651 adults aged > =20 years old from the Nord-Trondelag Health Study with self-reported total sitting time in 1995-1997 (HUNT2) and 2006-2008 (HUNT3). Four categories characterised patterns of sitting: (1) low at HUNT2/ low at HUNT3, 'consistently low sitting'; (2) low at HUNT2/high at HUNT3, 'increased sitting'; (3) high at HUNT2/low at HUNT3, 'reduced sitting'; and (4) high at HUNT2 /high at HUNT3, 'consistently high sitting'. Associations of sitting pattern with all-cause and cardio-metabolic disease mortality were analysed using Cox regression adjusted for confounders. RESULTS: Mean follow-up was 6.2 years (158880 person-years); 1212 participants died. Compared to 'consistently low sitting', adjusted hazard ratios for all-cause mortality were 1.51 (95% CI: 1.28-2.78), 1.03 (95% CI: 0.88-1.20), and 1.26 (95% CI: 1.06-1.51) for 'increased sitting', 'reduced sitting' and 'consistently high sitting' respectively. CONCLUSIONS: Examining patterns of sitting over time augments single time-point analyses of risk exposures associated with high sitting time. Whilst sitting habits can be stable over a long period, life events (e.g., changing jobs, retiring or illness) may influence sitting trajectories and therefore sitting-attributable risk. Reducing sitting may yield mortality risks comparable to a stable low-sitting pattern.  
  Address Department of Public health and General practice, HUNT Research Centre, Faculty of Medicine, NTNU – Norwegian University of Science and Technology, Levanger, 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 1479-5868 ISBN Medium  
  Area Expedition Conference  
  Notes (up) PMID:28122625; PMCID:PMC5267382 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1918  
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 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 (up) PMID:28146470; PMCID:PMC5302847 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1953  
Permanent link to this record
 

 
Author Brumpton, B.; Mai, X.-M.; Langhammer, A.; Laugsand, L.E.; Janszky, I.; Strand, L.B. url  doi
  Title Prospective study of insomnia and incident asthma in adults: the HUNT study Type Journal Article
  Year 2017 Publication The European Respiratory Journal Abbreviated Journal Eur Respir J  
  Volume 49 Issue 2 Pages  
  Keywords  
  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.  
  Address Dept of Public Health and General Practice, Faculty of Medicine, Norwegian University of Science and Technology, NTNU, 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 0903-1936 ISBN Medium  
  Area Expedition Conference  
  Notes (up) PMID:28153868 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1887  
Permanent link to this record
 

 
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 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  
  Publisher Place of Publication Editor  
  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 (up) PMID:28209224; PMCID:PMC5314135 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 2030  
Permanent link to this record
 

 
Author Alsnes, I.V.; Vatten, L.J.; Fraser, A.; Bjorngaard, J.H.; Rich-Edwards, J.; Romundstad, P.R.; Asvold, B.O. url  doi
  Title Hypertension in Pregnancy and Offspring Cardiovascular Risk in Young Adulthood: Prospective and Sibling Studies in the HUNT Study (Nord-Trondelag Health Study) in Norway Type Multicenter Study
  Year 2017 Publication Hypertension (Dallas, Tex. : 1979) Abbreviated Journal Hypertension  
  Volume 69 Issue 4 Pages 591-598  
  Keywords Adult; Blood Pressure/*physiology; Cardiovascular Diseases/*epidemiology/etiology/physiopathology; Female; Follow-Up Studies; Humans; Hypertension, Pregnancy-Induced/*epidemiology/physiopathology; Incidence; Infant, Newborn; Norway/epidemiology; Pregnancy; *Pregnancy Complications, Cardiovascular; Prospective Studies; *Registries; Risk Factors; Siblings; adolescent; blood pressure; cardiovascular disease; mother; preeclampsia  
  Abstract Women with hypertensive disorders in pregnancy are at increased lifetime risk for cardiovascular disease. We examined the offspring's cardiovascular risk profile in young adulthood and their siblings' cardiovascular risk profile. From the HUNT study (Nord-Trondelag Health Study) in Norway, 15 778 participants (mean age: 29 years), including 210 sibling groups, were linked to information from the Medical Birth Registry of Norway. Blood pressure, anthropometry, serum lipids, and C-reactive protein were assessed. Seven hundred and six participants were born after exposure to maternal hypertension in pregnancy: 336 mothers had gestational hypertension, 343 had term preeclampsia, and 27 had preterm preeclampsia. Offspring whose mothers had hypertension in pregnancy had 2.7 (95% confidence interval, 1.8-3.5) mm Hg higher systolic blood pressure, 1.5 (0.9-2.1) mm Hg higher diastolic blood pressure, 0.66 (0.31-1.01) kg/m2 higher body mass index, and 1.49 (0.65-2.33) cm wider waist circumference, compared with offspring of normotensive pregnancies. Similar differences were observed for gestational hypertension and term preeclampsia. Term preeclampsia was also associated with higher concentrations of non-high-density lipoprotein cholesterol (0.14 mmol/L, 0.03-0.25) and triglycerides (0.13 mmol/L, 0.06-0.21). Siblings born after a normotensive pregnancy had nearly identical risk factor levels as siblings born after maternal hypertension. Offspring born after maternal hypertension in pregnancy have a more adverse cardiovascular risk profile in young adulthood than offspring of normotensive pregnancies. Their siblings, born after a normotensive pregnancy, have a similar risk profile, suggesting that shared genes or lifestyle may account for the association, rather than an intrauterine effect. All children of mothers who have experienced hypertension in pregnancy may be at increased lifetime risk of cardiovascular disease.  
  Address From the Department of Public Health and General Practice, Faculty of Medicine, NTNU, Norwegian University of Science and Technology, Trondheim (I.V.A., L.J.V., J.H.B., J.R.-E., P.R.R., B.O.A.); MRC Integrative Epidemiology Unit at the University of Bristol and School of Social and Community Medicine, University of Bristol, United Kingdom (A.F.); Channing Division of Network Medicine, Department of Medicine, Connors Center for Women's Health and Gender Biology, Brigham and Women's Hospital, Boston, MA (J.R.-E.); Harvard Medical School, Boston, MA (J.R.-E.); Department of Epidemiology, the Harvard T.H. Chan School of Public Health, Boston, MA (L.J.V., J.R.-E.); and Department of Endocrinology, St. Olavs Hospital, Trondheim University Hospital, Norway (B.O.A.)  
  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 0194-911X ISBN Medium  
  Area Expedition Conference  
  Notes (up) PMID:28223467 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1875  
Permanent link to this record
 

 
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 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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  ISSN 1949-8357 ISBN Medium  
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  Notes (up) PMID:28261402; PMCID:PMC5330203 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1904  
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Author Yu, D.; Takata, Y.; Smith-Warner, S.A.; Blot, W.; Sawada, N.; White, E.; Freedman, N.; Robien, K.; Giovannucci, E.; Zhang, X.; Park, Y.; Gao, Y.-T.; Chlebowski, R.T.; Langhammer, A.; Yang, G.; Severi, G.; Manjer, J.; Khaw, K.-T.; Weiderpass, E.; Liao, L.M.; Caporaso, N.; Krokstad, S.; Hveem, K.; Sinha, R.; Ziegler, R.; Tsugane, S.; Xiang, Y.-B.; Johansson, M.; Zheng, W.; Shu, X.-O. url  doi
  Title Prediagnostic Calcium Intake and Lung Cancer Survival: A Pooled Analysis of 12 Cohort Studies Type Journal Article
  Year 2017 Publication Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology Abbreviated Journal Cancer Epidemiol Biomarkers Prev  
  Volume 26 Issue 7 Pages 1060-1070  
  Keywords  
  Abstract Background: Lung cancer is the leading cause of cancer death. Little is known about whether prediagnostic nutritional factors may affect survival. We examined the associations of prediagnostic calcium intake from foods and/or supplements with lung cancer survival.Methods: The present analysis included 23,882 incident, primary lung cancer patients from 12 prospective cohort studies. Dietary calcium intake was assessed using food-frequency questionnaires at baseline in each cohort and standardized to caloric intake of 2,000 kcal/d for women and 2,500 kcal/d for men. Stratified, multivariable-adjusted Cox regression was applied to compute hazard ratios (HR) and 95% confidence intervals (CI).Results: The 5-year survival rates were 56%, 21%, and 5.7% for localized, regional, and distant stage lung cancer, respectively. Low prediagnostic dietary calcium intake (<500-600 mg/d, less than half of the recommendation) was associated with a small increase in risk of death compared with recommended calcium intakes (800-1,200 mg/d); HR (95% CI) was 1.07 (1.01-1.13) after adjusting for age, stage, histology, grade, smoking status, pack-years, and other potential prognostic factors. The association between low calcium intake and higher lung cancer mortality was evident primarily among localized/regional stage patients, with HR (95% CI) of 1.15 (1.04-1.27). No association was found for supplemental calcium with survival in the multivariable-adjusted model.Conclusions: This large pooled analysis is the first, to our knowledge, to indicate that low prediagnostic dietary calcium intake may be associated with poorer survival among early-stage lung cancer patients.Impact: This multinational prospective study linked low calcium intake to lung cancer prognosis. Cancer Epidemiol Biomarkers Prev; 26(7); 1060-70. (c)2017 AACR.  
  Address Vanderbilt Epidemiology Center, Vanderbilt University Medical Center, Nashville, Tennessee. xiao-ou.shu@vanderbilt.edu  
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  ISSN 1055-9965 ISBN Medium  
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  Notes (up) PMID:28264875; PMCID:PMC5500413 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 2025  
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Author Zisko, N.; Skjerve, K.N.; Tari, A.R.; Sandbakk, S.B.; Wisloff, U.; Nes, B.M.; Nauman, J. url  doi
  Title Personal Activity Intelligence (PAI), Sedentary Behavior and Cardiovascular Risk Factor Clustering – the HUNT Study Type Journal Article
  Year 2017 Publication Progress in Cardiovascular Diseases Abbreviated Journal Prog Cardiovasc Dis  
  Volume 60 Issue 1 Pages 89-95  
  Keywords Cardiovascular disease; Cardiovascular disease risk factors; Exercise; Exercise intensity; Physical activity; Sedentary behavior  
  Abstract Prolonged sedentary behavior (SB) positively associates with clustering of risk factors for cardiovascular disease (CVD). The recently developed metric for physical activity (PA) tracking called Personal Activity Intelligence (PAI) takes into account age, sex, resting and maximum heart rate, and a score of >/=100 weekly PAI has been shown to reduce the risk of premature CVD death in healthy as well as individuals with known CVD risk factors, regardless of whether or not the current PA recommendations were met. The aim of the present study was to examine if PAI modifies the associations between SB and CVD risk factor (CV-RF) clustering in a large apparently healthy general population cohort (n=29,950, aged >/=20 years). Logistic regression revealed that in those with >/=100 weekly PAI, the likelihood of CV-RF clustering prevalence associated with prolonged SB was attenuated across age groups. Monitoring weekly PAI-level could be useful to ensure that people perform enough PA to combat SB's deleterious association with CV-RF.  
  Address K.G. Jebsen Center of Exercise in Medicine at the Department of Circulation and Medical Imaging, Norwegian University of Science and Technology, Faculty of Medicine, Trondheim, Norway; Department of Cardiology, St. Olavs Hospital, Norway  
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  Series Volume Series Issue Edition  
  ISSN 0033-0620 ISBN Medium  
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  Notes (up) PMID:28274818 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 2028  
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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 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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  ISSN 0946-672X ISBN Medium  
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  Notes (up) PMID:28347468 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1979  
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Author Jaremko, J.L.; Azmat, O.; Lambert, R.G.; Bird, P.; Haugen, I.K.; Jans, L.; Weber, U.; Winn, N.; Zubler, V.; Maksymowych, W.P. url  doi
  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
  Year 2017 Publication The Journal of Rheumatology Abbreviated Journal J Rheumatol  
  Volume 44 Issue 11 Pages 1718-1722  
  Keywords Bone Marrow Lesion; Knee Joint; Mri; Omeract; Osteoarthritis; Scoring Methods  
  Abstract 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.  
  Address 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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  ISSN 0315-162X ISBN Medium  
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  Notes (up) PMID:28365581 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1932  
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Author Bjornland, T.; Langaas, M.; Grill, V.; Mostad, I.L. url  doi
  Title Assessing gene-environment interaction effects of FTO, MC4R and lifestyle factors on obesity using an extreme phenotype sampling design: Results from the HUNT study Type Journal Article
  Year 2017 Publication PloS one Abbreviated Journal PLoS One  
  Volume 12 Issue 4 Pages e0175071  
  Keywords Alpha-Ketoglutarate-Dependent Dioxygenase FTO/*genetics; Body Mass Index; *Gene-Environment Interaction; Humans; *Life Style; Obesity/*genetics; *Phenotype; Receptor, Melanocortin, Type 4/*genetics; Waist-Hip Ratio  
  Abstract BACKGROUND: Our aim was to assess the influence of age, gender and lifestyle factors on the effect of the obesity-promoting alleles of FTO and MCR4. METHODS: The HUNT study comprises health information on the population of Nord-Trondelag county, Norway. Extreme phenotype participants (gender-wise lower and upper quartiles of waist-hip-ratio and BMI >/= 35 kg/m2) in the third survey, HUNT3 (2006-08), were genotyped for the single-nucleotide polymorphisms rs9939609 (FTO) and rs17782313 (MC4R); 25686 participants were successfully genotyped. Extreme sampling was chosen to increase power to detect genetic and gene-environment effects on waist-hip-ratio and BMI. Statistical inference was based on linear regression models and a missing-covariate likelihood approach for the extreme phenotype sampling design. Environmental factors were physical activity, diet (artificially sweetened beverages) and smoking. Longitudinal analysis was performed using material from HUNT2 (1995-97). RESULTS: Cross-sectional and longitudinal genetic effects indicated stronger genetic associations with obesity in young than in old, as well as differences between women and men. We observed larger genetic effects among physically inactive compared to active individuals. This interaction was age-dependent and seen mainly in 20-40 year olds. We observed a greater FTO effect among men with a regular intake of artificially sweetened beverages, compared to non-drinkers. Interaction analysis of smoking was mainly inconclusive. CONCLUSIONS: In a large all-adult and area-based population survey the effects of obesity-promoting minor-alleles of FTO and MCR4, and interactions with life style factors are age- and gender-related. These findings appear relevant when designing individualized treatment for and prophylaxis against obesity.  
  Address Department of Clinical Nutrition and Speech-Language Therapy, Clinic of Clinical Services, St. Olavs Hospital, Trondheim University Hospital, Trondheim, Norway  
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  ISSN 1932-6203 ISBN Medium  
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  Notes (up) PMID:28384342; PMCID:PMC5383228 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1884  
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Author Borte, S.; Winsvold, B.S.; Stensland, S.O.; Smastuen, M.C.; Zwart, J.-A. url  doi
  Title The effect of foetal growth restriction on the development of migraine and tension-type headache in adulthood. The HUNT Study Type Journal Article
  Year 2017 Publication PloS one Abbreviated Journal PLoS One  
  Volume 12 Issue 4 Pages e0175908  
  Keywords Adult; Birth Weight; Female; Fetal Growth Retardation/epidemiology/*etiology; Gestational Age; Health Surveys; Humans; Infant, Newborn; Logistic Models; Male; Migraine Disorders/complications/*diagnosis/epidemiology; Norway/epidemiology; Odds Ratio; Pregnancy; Registries; Risk Factors; Tension-Type Headache/complications/*diagnosis/epidemiology; Young Adult  
  Abstract BACKGROUND: There is little knowledge about how factors early in life affect the development of migraine and tension-type headache. We aimed to examine whether growth restriction in utero is associated with development of migraine and frequent tension-type headache in adults. METHODS: The population-based Nord-Trondelag Health Study (HUNT 3) contained a validated headache questionnaire, which differentiated between migraine and tension-type headache. These data were linked to information on weight and gestational age at birth from the Norwegian Medical Birth Registry. In total 4557 females and 2789 males, aged 19-41 years, were included in this registry-based study. Participants were categorized as appropriate for gestational age (AGA, 10th-90th percentile), small for gestational age (SGA, 3rd-10th percentile) or very small for gestational age (VSGA, < 3rd percentile). Logistic regression was used to calculate odds ratios (OR) with 95% confidence intervals (CI) for migraine and tension-type headache, with exposure being growth restriction at birth. RESULTS: The effect of growth restriction on migraine was modified by sex, with a significant association in males (p<0.001), but not in females (p = 0.20). In particular, males born VSGA were at increased risk of developing migraine (OR 2.73, 95% CI 1.63-4.58, p<0.001), with an intermediate risk among those born SGA (OR 1.50, 95% CI 0.96-2.35, p = 0.08) compared to those born AGA. There was no significant association between growth restriction and frequent TTH (p = 0.051). CONCLUSION: Growth restriction was associated with increased risk of migraine in adulthood among males, but not among females. This suggests that migraine might, in part, be influenced by early life events, and that males seem to be particularly vulnerable.  
  Address Department of Neurology, Oslo University Hospital, Oslo, Norway  
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  ISSN 1932-6203 ISBN Medium  
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  Notes (up) PMID:28410431; PMCID:PMC5391957 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1885  
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Author Videm, V.; Thomas, R.; Brown, M.A.; Hoff, M. url  doi
  Title Self-reported Diagnosis of Rheumatoid Arthritis or Ankylosing Spondylitis Has Low Accuracy: Data from the Nord-Trondelag Health Study Type Journal Article
  Year 2017 Publication The Journal of Rheumatology Abbreviated Journal J Rheumatol  
  Volume 44 Issue 8 Pages 1134-1141  
  Keywords Ankylosing Spondylitis; Epidemiology; Rheumatoid Arthritis  
  Abstract 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.  
  Address 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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  ISSN 0315-162X ISBN Medium  
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  Notes (up) PMID:28412703 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 2001  
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Author Ueland, T.; Laugsand, L.E.; Vatten, L.J.; Janszky, I.; Platou, C.; Michelsen, A.E.; Damas, J.K.; Aukrust, P.; Asvold, B.O. url  doi
  Title Extracellular matrix markers and risk of myocardial infarction: The HUNT Study in Norway Type Journal Article
  Year 2017 Publication European Journal of Preventive Cardiology Abbreviated Journal Eur J Prev Cardiol  
  Volume 24 Issue 11 Pages 1161-1167  
  Keywords Extracellular matrix; Ykl-40; case-control; myocardial infarction  
  Abstract Aims Extracellular matrix remodelling may influence atherosclerotic progression and plaque stability. We hypothesized that evaluation of extracellular matrix markers, with potentially different roles during atherogenesis, could provide information on underlying mechanisms and risk of myocardial infarction (MI) in apparently healthy individuals. Methods We conducted a case-control study nested within the population-based HUNT2 cohort in Norway. A total of 58,761 men and women, free of known cardiovascular disease, were followed for a first MI. During 11.3 years of follow-up, 1587 incident MIs were registered, and these cases were compared with 3959 age- and sex-matched controls. Circulating levels of the ECM proteins CD147 (ECM metalloproteinase inducer; EMMPRIN), cartilage oligomeric matrix protein (COMP: thrombospondin-5) and YKL-40 (chitinase-3-like-1) were measured by enzyme immunoassays. Results We found an inverse association between COMP (quartile (Q) 4 vs. Q1: hazard ratio 0.81 (95% confidence interval: 0.67-0.98)) and YKL-40 (Q4 vs. Q1: hazard ratio 0.77 (0.62-0.95)) with incidence of MI after full multivariable adjustment. Serum CD147 was not associated with MI risk in adjusted analysis. Conclusion High levels of COMP and YKL-40 were associated with lower risk of incident MI, suggesting a potential beneficial role in promoting plaque stability in individuals without incident cardiovascular disease.  
  Address 12 Department of Endocrinology, St Olavs Hospital, Trondheim, Norway  
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  ISSN 2047-4873 ISBN Medium  
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  Notes (up) PMID:28429960 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1999  
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Author Osthus, I.B.O.; Lydersen, S.; Dalen, H.; Nauman, J.; Wisloff, U. url  doi
  Title Association of Telomere Length With Myocardial Infarction: A Prospective Cohort From the Population Based HUNT 2 Study Type Journal Article
  Year 2017 Publication Progress in Cardiovascular Diseases Abbreviated Journal Prog Cardiovasc Dis  
  Volume 59 Issue 6 Pages 649-655  
  Keywords Age Factors; Aged; Aged, 80 and over; Female; Genetic Markers; Humans; Incidence; Linear Models; Male; Multivariate Analysis; Myocardial Infarction/diagnosis/epidemiology/*genetics; Norway/epidemiology; Polymerase Chain Reaction; Predictive Value of Tests; Prognosis; Proportional Hazards Models; Prospective Studies; Risk Factors; Sex Factors; Telomere/*genetics; *Telomere Homeostasis; Time Factors; Cardiovascular diseases; Myocardial infarction; Prevention; Risk factors; Telomeres  
  Abstract As possible markers of biological age, telomere length (TL) has been associated with age-related diseases such as myocardial infarction (MI) with conflicting findings. We sought to assess the relationship between TL and risk of future MI in 915 healthy participants (51.7% women) 65 years or older from a population-based prospective cohort (the HUNT 2 study, Norway). Mean TL was measured by quantitative PCR expressed as relative T (telomere repeat copy number) to S (single copy gene number) ratio, and log-transformed. During a mean follow up of 13.0 (SD, 3.2) years and 11,923 person-years, 82 participants were diagnosed with MI. We used Cox proportional hazard regressions to estimate hazard ratios (HR) and 95% confidence interval (CI). Relative TL was associated with age in women (P=0.01), but not in men (P=0.43). Using relative TL as a continuous variable, we observed a higher risk of MI in participants with longer telomeres with HRs of 2.46 (95% CI; 1.13 to 4.54) in men, and 2.93 (95% CI; 1.41 to 6.10) in women. Each 1-SD change in relative TL was associated with an HR of 1.54 (95% CI; 1.15 to 2.06) and 1.67 (95% CI; 1.18 to 2.37) in men and women, respectively. Compared with the bottom tertile of relative TL, HR of incident MI in top tertile was 2.71 (95% CI; 1.25 to 5.89) in men, and 3.65 (95% CI; 1.35 to 9.90) in women. Longer telomeres in healthy participants 65 years or older are associated with a high risk of incident MI. Future large scale prospective studies are needed to confirm these findings and explore the potential association between TL and MI.  
  Address K. G. Jebsen Center of Exercise in Medicine at the Department of Circulation and Medical Imaging, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway; School of Human Movement & Nutrition Sciences, University of Queensland, Australia  
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  ISSN 0033-0620 ISBN Medium  
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  Notes (up) PMID:28442329 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1968  
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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 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 (up) PMID:28443625; PMCID:PMC5414044 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1937  
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Author Graff, M.; Scott, R.A.; Justice, A.E.; Young, K.L.; Feitosa, M.F.; Barata, L.; Winkler, T.W.; Chu, A.Y.; Mahajan, A.; Hadley, D.; Xue, L.; Workalemahu, T.; Heard-Costa, N.L.; den Hoed, M.; Ahluwalia, T.S.; Qi, Q.; Ngwa, J.S.; Renstrom, F.; Quaye, L.; Eicher, J.D.; Hayes, J.E.; Cornelis, M.; Kutalik, Z.; Lim, E.; Luan, J.'an; Huffman, J.E.; Zhang, W.; Zhao, W.; Griffin, P.J.; Haller, T.; Ahmad, S.; Marques-Vidal, P.M.; Bien, S.; Yengo, L.; Teumer, A.; Smith, A.V.; Kumari, M.; Harder, M.N.; Justesen, J.M.; Kleber, M.E.; Hollensted, M.; Lohman, K.; Rivera, N.V.; Whitfield, J.B.; Zhao, J.H.; Stringham, H.M.; Lyytikainen, L.-P.; Huppertz, C.; Willemsen, G.; Peyrot, W.J.; Wu, Y.; Kristiansson, K.; Demirkan, A.; Fornage, M.; Hassinen, M.; Bielak, L.F.; Cadby, G.; Tanaka, T.; Magi, R.; van der Most, P.J.; Jackson, A.U.; Bragg-Gresham, J.L.; Vitart, V.; Marten, J.; Navarro, P.; Bellis, C.; Pasko, D.; Johansson, A.; Snitker, S.; Cheng, Y.-C.; Eriksson, J.; Lim, U.; Aadahl, M.; Adair, L.S.; Amin, N.; Balkau, B.; Auvinen, J.; Beilby, J.; Bergman, R.N.; Bergmann, S.; Bertoni, A.G.; Blangero, J.; Bonnefond, A.; Bonnycastle, L.L.; Borja, J.B.; Brage, S.; Busonero, F.; Buyske, S.; Campbell, H.; Chines, P.S.; Collins, F.S.; Corre, T.; Smith, G.D.; Delgado, G.E.; Dueker, N.; Dorr, M.; Ebeling, T.; Eiriksdottir, G.; Esko, T.; Faul, J.D.; Fu, M.; Faerch, K.; Gieger, C.; Glaser, S.; Gong, J.; Gordon-Larsen, P.; Grallert, H.; Grammer, T.B.; Grarup, N.; van Grootheest, G.; Harald, K.; Hastie, N.D.; Havulinna, A.S.; Hernandez, D.; Hindorff, L.; Hocking, L.J.; Holmens, O.L.; Holzapfel, C.; Hottenga, J.J.; Huang, J.; Huang, T.; Hui, J.; Huth, C.; Hutri-Kahonen, N.; James, A.L.; Jansson, J.-O.; Jhun, M.A.; Juonala, M.; Kinnunen, L.; Koistinen, H.A.; Kolcic, I.; Komulainen, P.; Kuusisto, J.; Kvaloy, K.; Kahonen, M.; Lakka, T.A.; Launer, L.J.; Lehne, B.; Lindgren, C.M.; Lorentzon, M.; Luben, R.; Marre, M.; Milaneschi, Y.; Monda, K.L.; Montgomery, G.W.; De Moor, M.H.M.; Mulas, A.; Muller-Nurasyid, M.; Musk, A.W.; Mannikko, R.; Mannisto, S.; Narisu, N.; Nauck, M.; Nettleton, J.A.; Nolte, I.M.; Oldehinkel, A.J.; Olden, M.; Ong, K.K.; Padmanabhan, S.; Paternoster, L.; Perez, J.; Perola, M.; Peters, A.; Peters, U.; Peyser, P.A.; Prokopenko, I.; Puolijoki, H.; Raitakari, O.T.; Rankinen, T.; Rasmussen-Torvik, L.J.; Rawal, R.; Ridker, P.M.; Rose, L.M.; Rudan, I.; Sarti, C.; Sarzynski, M.A.; Savonen, K.; Scott, W.R.; Sanna, S.; Shuldiner, A.R.; Sidney, S.; Silbernagel, G.; Smith, B.H.; Smith, J.A.; Snieder, H.; Stancakova, A.; Sternfeld, B.; Swift, A.J.; Tammelin, T.; Tan, S.-T.; Thorand, B.; Thuillier, D.; Vandenput, L.; Vestergaard, H.; van Vliet-Ostaptchouk, J.V.; Vohl, M.-C.; Volker, U.; Waeber, G.; Walker, M.; Wild, S.; Wong, A.; Wright, A.F.; Zillikens, M.C.; Zubair, N.; Haiman, C.A.; Lemarchand, L.; Gyllensten, U.; Ohlsson, C.; Hofman, A.; Rivadeneira, F.; Uitterlinden, A.G.; Perusse, L.; Wilson, J.F.; Hayward, C.; Polasek, O.; Cucca, F.; Hveem, K.; Hartman, C.A.; Tonjes, A.; Bandinelli, S.; Palmer, L.J.; Kardia, S.L.R.; Rauramaa, R.; Sorensen, T.I.A.; Tuomilehto, J.; Salomaa, V.; Penninx, B.W.J.H.; de Geus, E.J.C.; Boomsma, D.I.; Lehtimaki, T.; Mangino, M.; Laakso, M.; Bouchard, C.; Martin, N.G.; Kuh, D.; Liu, Y.; Linneberg, A.; Marz, W.; Strauch, K.; Kivimaki, M.; Harris, T.B.; Gudnason, V.; Volzke, H.; Qi, L.; Jarvelin, M.-R.; Chambers, J.C.; Kooner, J.S.; Froguel, P.; Kooperberg, C.; Vollenweider, P.; Hallmans, G.; Hansen, T.; Pedersen, O.; Metspalu, A.; Wareham, N.J.; Langenberg, C.; Weir, D.R.; Porteous, D.J.; Boerwinkle, E.; Chasman, D.I.; Abecasis, G.R.; Barroso, I.; McCarthy, M.I.; Frayling, T.M.; O'Connell, J.R.; van Duijn, C.M.; Boehnke, M.; Heid, I.M.; Mohlke, K.L.; Strachan, D.P.; Fox, C.S.; Liu, C.-T.; Hirschhorn, J.N.; Klein, R.J.; Johnson, A.D.; Borecki, I.B.; Franks, P.W.; North, K.E.; Cupples, L.A.; Loos, R.J.F.; Kilpelainen, T.O. url  doi
  Title Genome-wide physical activity interactions in adiposity – A meta-analysis of 200,452 adults Type Meta-Analysis
  Year 2017 Publication PLoS Genetics Abbreviated Journal PLoS Genet  
  Volume 13 Issue 4 Pages e1006528  
  Keywords Adiposity/*genetics/physiology; Alpha-Ketoglutarate-Dependent Dioxygenase FTO/*genetics; Body Mass Index; Epigenomics; *Exercise; Female; Genetic Predisposition to Disease; Genome-Wide Association Study; Genotype; Humans; Male; Obesity/*genetics/physiopathology; Waist Circumference; Waist-Hip Ratio  
  Abstract Physical activity (PA) may modify the genetic effects that give rise to increased risk of obesity. To identify adiposity loci whose effects are modified by PA, we performed genome-wide interaction meta-analyses of BMI and BMI-adjusted waist circumference and waist-hip ratio from up to 200,452 adults of European (n = 180,423) or other ancestry (n = 20,029). We standardized PA by categorizing it into a dichotomous variable where, on average, 23% of participants were categorized as inactive and 77% as physically active. While we replicate the interaction with PA for the strongest known obesity-risk locus in the FTO gene, of which the effect is attenuated by ~30% in physically active individuals compared to inactive individuals, we do not identify additional loci that are sensitive to PA. In additional genome-wide meta-analyses adjusting for PA and interaction with PA, we identify 11 novel adiposity loci, suggesting that accounting for PA or other environmental factors that contribute to variation in adiposity may facilitate gene discovery.  
  Address The Department of Preventive Medicine, The Icahn School of Medicine at Mount Sinai, New York, New York, United States of America  
  Corporate Author PAGE 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 1553-7390 ISBN Medium  
  Area Expedition Conference  
  Notes (up) PMID:28448500; PMCID:PMC5407576 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1909  
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Author Islam, M.K.; Folland, S.; Kaarboe, O.M. url  doi
  Title Social capital and cigarette smoking: New empirics featuring the Norwegian HUNT data Type Journal Article
  Year 2017 Publication Economics and Human Biology Abbreviated Journal Econ Hum Biol  
  Volume 26 Issue Pages 174-185  
  Keywords *Cigarette smoking; *Instrumental variables; *Longitudinal data; *Social capital  
  Abstract Using a rich Norwegian longitudinal data set, this study explores the effects of different social capital variables on the probability of cigarette smoking. There are four social capital variables available in two waves of our data set. Our results based on probit (and OLS) analyses (with municipality fixed-effects) show that the likelihood of smoking participation is negatively and significantly associated with social capital attributes, namely, community trust (-0.017), participation in organizational activities (-0.032), and cohabitation (-0.045). Significant negative associations were also observed in panel data, pooled OLS, and random effects models for community trust (-0.024; -0.010) and cohabitation (-0.040; -0.032). Fixed-effects models also showed significant negative effects for cohabitation (-0.018). Estimates of alternative instrumental variables (IV) based on recursive bivariate probit and IV-GMM models also confirmed negative and significant effects for three of its characteristics: cohabitation (-0.030; -0.046), community trust (-0.065; -0.075), and participation in organizational activities (-0.035; -0.046). The limitations of our conclusions are discussed, and the significance of our study for the field of social capital and health is described, along with suggested avenues for future research.  
  Address Department of Health Management and Health Economics, University of Oslo, 0373 Oslo, 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 1570-677X ISBN Medium  
  Area Expedition Conference  
  Notes (up) PMID:28448881 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1931  
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Author Vindenes, H.K.; Svanes, C.; Lygre, S.H.L.; Hollund, B.-E.; Langhammer, A.; Bertelsen, R.J. url  doi
  Title Prevalence of, and work-related risk factors for, hand eczema in a Norwegian general population (The HUNT Study) Type Journal Article
  Year 2017 Publication Contact Dermatitis Abbreviated Journal Contact Dermatitis  
  Volume 77 Issue 4 Pages 214-223  
  Keywords Hunt; atopic dermatitis; epidemiology; hand eczema; occupational  
  Abstract BACKGROUND: Chemical exposures at work and at home may cause hand eczema. However, this has been scarcely described for Norway. OBJECTIVES: To investigate the prevalence of, and occupational risk factors for, hand eczema in Norway. METHODS: Among 50 805 respondents (aged >/=20 years) to the third Nord-Trondelag Health Study (HUNT3), 5757 persons reported ever having hand eczema, and 4206 answered a hand eczema questionnaire. RESULTS: The lifetime prevalences of hand eczema were 8.4% in men and 13.8% in women (p < 0.001), with onset at age </=10 years in 24% (men) and 20% (women), and onset at age >/=30 years in 37% (men) and 25% (women) (p < 0.001). Work-related hand eczema affected 4.8% of the population, and was most frequently associated with health/social work (29%) and occupational cleaning (20%) in women, and with farming (26%) and industrial occupations (27%) in men. Cleaning detergents (75%) and other chemicals (36%) were the most common exacerbating factors. CONCLUSIONS: The prevalence of hand eczema was 11.3%, and that of work-related hand eczema was 4.8%. Hand eczema was more common in women than in men, but with a later onset in men. Cleaning detergents were the most common aggravating factors. A large proportion of the Nord-Trondelag population is employed in farming, providing the possibility to identify farming as an important risk factor for hand eczema.  
  Address Department of Clinical Science, University of Bergen, 5021, 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 0105-1873 ISBN Medium  
  Area Expedition Conference  
  Notes (up) PMID:28449354