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Author Asvold, B.O.; Midthjell, K.; Krokstad, S.; Rangul, V.; Bauman, A. url  doi
  Title Prolonged sitting may increase diabetes risk in physically inactive individuals: an 11 year follow-up of the HUNT Study, Norway Type Journal Article
  Year 2017 Publication Diabetologia Abbreviated Journal Diabetologia  
  Volume 60 Issue 5 Pages 830-835  
  Keywords Adult; Body Mass Index; Diabetes Mellitus, Type 2/*epidemiology/metabolism; Exercise/physiology; Female; Humans; Incidence; Leisure Activities; Male; Middle Aged; *Sedentary Lifestyle; Epidemiology; Sedentary lifestyle; Type 2 diabetes mellitus  
  Abstract AIMS/HYPOTHESIS: We examined the association between sitting time and diabetes incidence, overall and by strata of leisure-time physical activity and BMI. METHODS: We followed 28,051 adult participants of the Nord-Trondelag Health Study (the HUNT Study), a population-based study, for diabetes incidence from 1995-1997 to 2006-2008 and estimated HRs of any diabetes by categories of self-reported total daily sitting time at baseline. RESULTS: Of 28,051 participants, 1253 (4.5%) developed diabetes during 11 years of follow-up. Overall, sitting >/=8 h/day was associated with a 17% (95% CI 2, 34) higher risk of developing diabetes compared with sitting </=4 h/day, adjusted for age, sex and education. However, the association was attenuated to a non-significant 9% (95% CI -5, 26) increase in risk after adjustment for leisure-time physical activity and BMI. The association between sitting time and diabetes risk differed by leisure-time physical activity (p Interaction = 0.01). Among participants with low leisure-time physical activity (</=2 h light activity per week and no vigorous activity), sitting 5-7 h/day and >/=8 h/day were associated with a 26% (95% CI 2, 57) and 30% (95% CI 5, 61) higher risk of diabetes, respectively, compared with sitting </=4 h/day. There was no corresponding association among participants with high leisure-time physical activity (>/=3 h light activity or >0 h vigorous activity per week). There was no statistical evidence that the association between sitting time and diabetes risk differed by obesity (p Interaction = 0.65). CONCLUSIONS/INTERPRETATION: Our findings suggest that total sitting time has little association with diabetes risk in the population as a whole, but prolonged sitting may contribute to an increased diabetes risk among physically inactive people.  
  Address School of Public Health, Sydney University, Sydney, NSW, 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 0012-186X ISBN Medium  
  Area Expedition Conference  
  Notes PMID:28054097 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1879  
Permanent link to this record
 

 
Author Dastani, Z.; Hivert, M.-F.; Timpson, N.; Perry, J.R.B.; Yuan, X.; Scott, R.A.; Henneman, P.; Heid, I.M.; Kizer, J.R.; Lyytikainen, L.-P.; Fuchsberger, C.; Tanaka, T.; Morris, A.P.; Small, K.; Isaacs, A.; Beekman, M.; Coassin, S.; Lohman, K.; Qi, L.; Kanoni, S.; Pankow, J.S.; Uh, H.-W.; Wu, Y.; Bidulescu, A.; Rasmussen-Torvik, L.J.; Greenwood, C.M.T.; Ladouceur, M.; Grimsby, J.; Manning, A.K.; Liu, C.-T.; Kooner, J.; Mooser, V.E.; Vollenweider, P.; Kapur, K.A.; Chambers, J.; Wareham, N.J.; Langenberg, C.; Frants, R.; Willems-Vandijk, K.; Oostra, B.A.; Willems, S.M.; Lamina, C.; Winkler, T.W.; Psaty, B.M.; Tracy, R.P.; Brody, J.; Chen, I.; Viikari, J.; Kahonen, M.; Pramstaller, P.P.; Evans, D.M.; St Pourcain, B.; Sattar, N.; Wood, A.R.; Bandinelli, S.; Carlson, O.D.; Egan, J.M.; Bohringer, S.; van Heemst, D.; Kedenko, L.; Kristiansson, K.; Nuotio, M.-L.; Loo, B.-M.; Harris, T.; Garcia, M.; Kanaya, A.; Haun, M.; Klopp, N.; Wichmann, H.-E.; Deloukas, P.; Katsareli, E.; Couper, D.J.; Duncan, B.B.; Kloppenburg, M.; Adair, L.S.; Borja, J.B.; Wilson, J.G.; Musani, S.; Guo, X.; Johnson, T.; Semple, R.; Teslovich, T.M.; Allison, M.A.; Redline, S.; Buxbaum, S.G.; Mohlke, K.L.; Meulenbelt, I.; Ballantyne, C.M.; Dedoussis, G.V.; Hu, F.B.; Liu, Y.; Paulweber, B.; Spector, T.D.; Slagboom, P.E.; Ferrucci, L.; Jula, A.; Perola, M.; Raitakari, O.; Florez, J.C.; Salomaa, V.; Eriksson, J.G.; Frayling, T.M.; Hicks, A.A.; Lehtimaki, T.; Smith, G.D.; Siscovick, D.S.; Kronenberg, F.; van Duijn, C.; Loos, R.J.F.; Waterworth, D.M.; Meigs, J.B.; Dupuis, J.; Richards, J.B.; Voight, B.F.; Scott, L.J.; Steinthorsdottir, V.; Dina, C.; Welch, R.P.; Zeggini, E.; Huth, C.; Aulchenko, Y.S.; Thorleifsson, G.; McCulloch, L.J.; Ferreira, T.; Grallert, H.; Amin, N.; Wu, G.; Willer, C.J.; Raychaudhuri, S.; McCarroll, S.A.; Hofmann, O.M.; Segre, A.V.; van Hoek, M.; Navarro, P.; Ardlie, K.; Balkau, B.; Benediktsson, R.; Bennett, A.J.; Blagieva, R.; Boerwinkle, E.; Bonnycastle, L.L.; Bostrom, K.B.; Bravenboer, B.; Bumpstead, S.; Burtt, N.P.; Charpentier, G.; Chines, P.S.; Cornelis, M.; Crawford, G.; Doney, A.S.F.; Elliott, K.S.; Elliott, A.L.; Erdos, M.R.; Fox, C.S.; Franklin, C.S.; Ganser, M.; Gieger, C.; Grarup, N.; Green, T.; Griffin, S.; Groves, C.J.; Guiducci, C.; Hadjadj, S.; Hassanali, N.; Herder, C.; Isomaa, B.; Jackson, A.U.; Johnson, P.R.V.; Jorgensen, T.; Kao, W.H.L.; Kong, A.; Kraft, P.; Kuusisto, J.; Lauritzen, T.; Li, M.; Lieverse, A.; Lindgren, C.M.; Lyssenko, V.; Marre, M.; Meitinger, T.; Midthjell, K.; Morken, M.A.; Narisu, N.; Nilsson, P.; Owen, K.R.; Payne, F.; Petersen, A.-K.; Platou, C.; Proenca, C.; Prokopenko, I.; Rathmann, W.; Rayner, N.W.; Robertson, N.R.; Rocheleau, G.; Roden, M.; Sampson, M.J.; Saxena, R.; Shields, B.M.; Shrader, P.; Sigurdsson, G.; Sparso, T.; Strassburger, K.; Stringham, H.M.; Sun, Q.; Swift, A.J.; Thorand, B.; Tichet, J.; Tuomi, T.; van Dam, R.M.; van Haeften, T.W.; van Herpt, T.; van Vliet-Ostaptchouk, J.V.; Walters, G.B.; Weedon, M.N.; Wijmenga, C.; Witteman, J.; Bergman, R.N.; Cauchi, S.; Collins, F.S.; Gloyn, A.L.; Gyllensten, U.; Hansen, T.; Hide, W.A.; Hitman, G.A.; Hofman, A.; Hunter, D.J.; Hveem, K.; Laakso, M.; Morris, A.D.; Palmer, C.N.A.; Rudan, I.; Sijbrands, E.; Stein, L.D.; Tuomilehto, J.; Uitterlinden, A.; Walker, M.; Watanabe, R.M.; Abecasis, G.R.; Boehm, B.O.; Campbell, H.; Daly, M.J.; Hattersley, A.T.; Pedersen, O.; Barroso, I.; Groop, L.; Sladek, R.; Thorsteinsdottir, U.; Wilson, J.F.; Illig, T.; Froguel, P.; van Duijn, C.M.; Stefansson, K.; Altshuler, D.; Boehnke, M.; McCarthy, M.I.; Soranzo, N.; Wheeler, E.; Glazer, N.L.; Bouatia-Naji, N.; Magi, R.; Randall, J.; Elliott, P.; Rybin, D.; Dehghan, A.; Hottenga, J.J.; Song, K.; Goel, A.; Lajunen, T.; Doney, A.; Cavalcanti-Proenca, C.; Kumari, M.; Timpson, N.J.; Zabena, C.; Ingelsson, E.; An, P.; O'Connell, J.; Luan, J.'an; Elliott, A.; McCarroll, S.A.; Roccasecca, R.M.; Pattou, F.; Sethupathy, P.; Ariyurek, Y.; Barter, P.; Beilby, J.P.; Ben-Shlomo, Y.; Bergmann, S.; Bochud, M.; Bonnefond, A.; Borch-Johnsen, K.; Bottcher, Y.; Brunner, E.; Bumpstead, S.J.; Chen, Y.-D.I.; Chines, P.; Clarke, R.; Coin, L.J.M.; Cooper, M.N.; Crisponi, L.; Day, I.N.M.; de Geus, E.J.C.; Delplanque, J.; Fedson, A.C.; Fischer-Rosinsky, A.; Forouhi, N.G.; Franzosi, M.G.; Galan, P.; Goodarzi, M.O.; Graessler, J.; Grundy, S.; Gwilliam, R.; Hallmans, G.; Hammond, N.; Han, X.; Hartikainen, A.-L.; Hayward, C.; Heath, S.C.; Hercberg, S.; Hillman, D.R.; Hingorani, A.D.; Hui, J.; Hung, J.; Kaakinen, M.; Kaprio, J.; Kesaniemi, Y.A.; Kivimaki, M.; Knight, B.; Koskinen, S.; Kovacs, P.; Kyvik, K.O.; Lathrop, G.M.; Lawlor, D.A.; Le Bacquer, O.; Lecoeur, C.; Li, Y.; Mahley, R.; Mangino, M.; Martinez-Larrad, M.T.; McAteer, J.B.; McPherson, R.; Meisinger, C.; Melzer, D.; Meyre, D.; Mitchell, B.D.; Mukherjee, S.; Naitza, S.; Neville, M.J.; Orru, M.; Pakyz, R.; Paolisso, G.; Pattaro, C.; Pearson, D.; Peden, J.F.; Pedersen, N.L.; Pfeiffer, A.F.H.; Pichler, I.; Polasek, O.; Posthuma, D.; Potter, S.C.; Pouta, A.; Province, M.A.; Rayner, N.W.; Rice, K.; Ripatti, S.; Rivadeneira, F.; Rolandsson, O.; Sandbaek, A.; Sandhu, M.; Sanna, S.; Sayer, A.A.; Scheet, P.; Seedorf, U.; Sharp, S.J.; Shields, B.; Sigurethsson, G.; Sijbrands, E.J.G.; Silveira, A.; Simpson, L.; Singleton, A.; Smith, N.L.; Sovio, U.; Swift, A.; Syddall, H.; Syvanen, A.-C.; Tonjes, A.; Uitterlinden, A.G.; van Dijk, K.W.; Varma, D.; Visvikis-Siest, S.; Vitart, V.; Vogelzangs, N.; Waeber, G.; Wagner, P.J.; Walley, A.; Ward, K.L.; Watkins, H.; Wild, S.H.; Willemsen, G.; Witteman, J.C.M.; Yarnell, J.W.G.; Zelenika, D.; Zethelius, B.; Zhai, G.; Zhao, J.H.; Zillikens, M.C.; Borecki, I.B.; Meneton, P.; Magnusson, P.K.E.; Nathan, D.M.; Williams, G.H.; Silander, K.; Bornstein, S.R.; Schwarz, P.; Spranger, J.; Karpe, F.; Shuldiner, A.R.; Cooper, C.; Serrano-Rios, M.; Lind, L.; Palmer, L.J.; Hu, F.B. 1st; Franks, P.W.; Ebrahim, S.; Marmot, M.; Kao, W.H.L.; Pramstaller, P.P.; Wright, A.F.; Stumvoll, M.; Hamsten, A.; Buchanan, T.A.; Valle, T.T.; Rotter, J.I.; Penninx, B.W.J.H.; Boomsma, D.I.; Cao, A.; Scuteri, A.; Schlessinger, D.; Uda, M.; Ruokonen, A.; Jarvelin, M.-R.; Peltonen, L.; Mooser, V.; Sladek, R.; Musunuru, K.; Smith, A.V.; Edmondson, A.C.; Stylianou, I.M.; Koseki, M.; Pirruccello, J.P.; Chasman, D.I.; Johansen, C.T.; Fouchier, S.W.; Peloso, G.M.; Barbalic, M.; Ricketts, S.L.; Bis, J.C.; Feitosa, M.F.; Orho-Melander, M.; Melander, O.; Li, X.; Li, M.; Cho, Y.S.; Go, M.J.; Kim, Y.J.; Lee, J.-Y.; Park, T.; Kim, K.; Sim, X.; Ong, R.T.-H.; Croteau-Chonka, D.C.; Lange, L.A.; Smith, J.D.; Ziegler, A.; Zhang, W.; Zee, R.Y.L.; Whitfield, J.B.; Thompson, J.R.; Surakka, I.; Spector, T.D.; Smit, J.H.; Sinisalo, J.; Scott, J.; Saharinen, J.; Sabatti, C.; Rose, L.M.; Roberts, R.; Rieder, M.; Parker, A.N.; Pare, G.; O'Donnell, C.J.; Nieminen, M.S.; Nickerson, D.A.; Montgomery, G.W.; McArdle, W.; Masson, D.; Martin, N.G.; Marroni, F.; Lucas, G.; Luben, R.; Lokki, M.-L.; Lettre, G.; Launer, L.J.; Lakatta, E.G.; Laaksonen, R.; Kyvik, K.O.; Konig, I.R.; Khaw, K.-T.; Kaplan, L.M.; Johansson, A.; Janssens, A.C.J.W.; Igl, W.; Hovingh, G.K.; Hengstenberg, C.; Havulinna, A.S.; Hastie, N.D.; Harris, T.B.; Haritunians, T.; Hall, A.S.; Groop, L.C.; Gonzalez, E.; Freimer, N.B.; Erdmann, J.; Ejebe, K.G.; Doring, A.; Dominiczak, A.F.; Demissie, S.; Deloukas, P.; de Faire, U.; Crawford, G.; Chen, Y.-der I.; Caulfield, M.J.; Boekholdt, S.M.; Assimes, T.L.; Quertermous, T.; Seielstad, M.; Wong, T.Y.; Tai, E.-S.; Feranil, A.B.; Kuzawa, C.W.; Taylor, H.A.J.; Gabriel, S.B.; Holm, H.; Gudnason, V.; Krauss, R.M.; Ordovas, J.M.; Munroe, P.B.; Kooner, J.S.; Tall, A.R.; Hegele, R.A.; Kastelein, J.J.P.; Schadt, E.E.; Strachan, D.P.; Reilly, M.P.; Samani, N.J.; Schunkert, H.; Cupples, L.A.; Sandhu, M.S.; Ridker, P.M.; Rader, D.J.; Kathiresan, S. url  doi
  Title Novel loci for adiponectin levels and their influence on type 2 diabetes and metabolic traits: a multi-ethnic meta-analysis of 45,891 individuals Type Journal Article
  Year 2012 Publication PLoS Genetics Abbreviated Journal PLoS Genet  
  Volume 8 Issue 3 Pages e1002607  
  Keywords Adiponectin/*blood/genetics; African Americans; Asian Continental Ancestry Group; Cholesterol, HDL/genetics; Diabetes Mellitus, Type 2/*genetics; European Continental Ancestry Group; Female; Gene Expression; Genetic Predisposition to Disease; *Genome-Wide Association Study; Glucose Tolerance Test; Humans; Insulin Resistance/genetics; Male; Metabolic Networks and Pathways; Polymorphism, Single Nucleotide; Waist-Hip Ratio  
  Abstract Circulating levels of adiponectin, a hormone produced predominantly by adipocytes, are highly heritable and are inversely associated with type 2 diabetes mellitus (T2D) and other metabolic traits. We conducted a meta-analysis of genome-wide association studies in 39,883 individuals of European ancestry to identify genes associated with metabolic disease. We identified 8 novel loci associated with adiponectin levels and confirmed 2 previously reported loci (P = 4.5x10(-8)-1.2x10(-43)). Using a novel method to combine data across ethnicities (N = 4,232 African Americans, N = 1,776 Asians, and N = 29,347 Europeans), we identified two additional novel loci. Expression analyses of 436 human adipocyte samples revealed that mRNA levels of 18 genes at candidate regions were associated with adiponectin concentrations after accounting for multiple testing (p<3x10(-4)). We next developed a multi-SNP genotypic risk score to test the association of adiponectin decreasing risk alleles on metabolic traits and diseases using consortia-level meta-analytic data. This risk score was associated with increased risk of T2D (p = 4.3x10(-3), n = 22,044), increased triglycerides (p = 2.6x10(-14), n = 93,440), increased waist-to-hip ratio (p = 1.8x10(-5), n = 77,167), increased glucose two hours post oral glucose tolerance testing (p = 4.4x10(-3), n = 15,234), increased fasting insulin (p = 0.015, n = 48,238), but with lower in HDL-cholesterol concentrations (p = 4.5x10(-13), n = 96,748) and decreased BMI (p = 1.4x10(-4), n = 121,335). These findings identify novel genetic determinants of adiponectin levels, which, taken together, influence risk of T2D and markers of insulin resistance.  
  Address Department of Epidemiology, Biostatistics, and Occupational Health, Jewish General Hospital, Lady Davis Institute, McGill University, Montreal, Canada  
  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 1553-7390 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:22479202; PMC3315470 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1516  
Permanent link to this record
 

 
Author Demirkan, A.; van Duijn, C.M.; Ugocsai, P.; Isaacs, A.; Pramstaller, P.P.; Liebisch, G.; Wilson, J.F.; Johansson, A.; Rudan, I.; Aulchenko, Y.S.; Kirichenko, A.V.; Janssens, A.C.J.W.; Jansen, R.C.; Gnewuch, C.; Domingues, F.S.; Pattaro, C.; Wild, S.H.; Jonasson, I.; Polasek, O.; Zorkoltseva, I.V.; Hofman, A.; Karssen, L.C.; Struchalin, M.; Floyd, J.; Igl, W.; Biloglav, Z.; Broer, L.; Pfeufer, A.; Pichler, I.; Campbell, S.; Zaboli, G.; Kolcic, I.; Rivadeneira, F.; Huffman, J.; Hastie, N.D.; Uitterlinden, A.; Franke, L.; Franklin, C.S.; Vitart, V.; Nelson, C.P.; Preuss, M.; Bis, J.C.; O'Donnell, C.J.; Franceschini, N.; Witteman, J.C.M.; Axenovich, T.; Oostra, B.A.; Meitinger, T.; Hicks, A.A.; Hayward, C.; Wright, A.F.; Gyllensten, U.; Campbell, H.; Schmitz, G. url  doi
  Title Genome-wide association study identifies novel loci associated with circulating phospho- and sphingolipid concentrations Type Journal Article
  Year 2012 Publication PLoS Genetics Abbreviated Journal PLoS Genet  
  Volume 8 Issue 2 Pages e1002490  
  Keywords Carotid Intima-Media Thickness; Databases, Genetic; Diabetes Mellitus, Type 2/blood/genetics; European Continental Ancestry Group/*genetics; Genetic Loci; *Genome, Human; *Genome-Wide Association Study; Humans; *Phospholipids/blood/genetics; Polymorphism, Single Nucleotide; *Sphingolipids/blood/genetics  
  Abstract Phospho- and sphingolipids are crucial cellular and intracellular compounds. These lipids are required for active transport, a number of enzymatic processes, membrane formation, and cell signalling. Disruption of their metabolism leads to several diseases, with diverse neurological, psychiatric, and metabolic consequences. A large number of phospholipid and sphingolipid species can be detected and measured in human plasma. We conducted a meta-analysis of five European family-based genome-wide association studies (N = 4034) on plasma levels of 24 sphingomyelins (SPM), 9 ceramides (CER), 57 phosphatidylcholines (PC), 20 lysophosphatidylcholines (LPC), 27 phosphatidylethanolamines (PE), and 16 PE-based plasmalogens (PLPE), as well as their proportions in each major class. This effort yielded 25 genome-wide significant loci for phospholipids (smallest P-value = 9.88x10(-204)) and 10 loci for sphingolipids (smallest P-value = 3.10x10(-57)). After a correction for multiple comparisons (P-value<2.2x10(-9)), we observed four novel loci significantly associated with phospholipids (PAQR9, AGPAT1, PKD2L1, PDXDC1) and two with sphingolipids (PLD2 and APOE) explaining up to 3.1% of the variance. Further analysis of the top findings with respect to within class molar proportions uncovered three additional loci for phospholipids (PNLIPRP2, PCDH20, and ABDH3) suggesting their involvement in either fatty acid elongation/saturation processes or fatty acid specific turnover mechanisms. Among those, 14 loci (KCNH7, AGPAT1, PNLIPRP2, SYT9, FADS1-2-3, DLG2, APOA1, ELOVL2, CDK17, LIPC, PDXDC1, PLD2, LASS4, and APOE) mapped into the glycerophospholipid and 12 loci (ILKAP, ITGA9, AGPAT1, FADS1-2-3, APOA1, PCDH20, LIPC, PDXDC1, SGPP1, APOE, LASS4, and PLD2) to the sphingolipid pathways. In large meta-analyses, associations between FADS1-2-3 and carotid intima media thickness, AGPAT1 and type 2 diabetes, and APOA1 and coronary artery disease were observed. In conclusion, our study identified nine novel phospho- and sphingolipid loci, substantially increasing our knowledge of the genetic basis for these traits.  
  Address Genetic Epidemiology Unit, Department of Epidemiology, Erasmus University Medical Center, Rotterdam, The Netherlands  
  Corporate Author EUROSPAN 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 PMID:22359512; PMC3280968 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1520  
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Author Engdahl, B.; Aarhus, L.; Lie, A.; Tambs, K. url  doi
  Title Cardiovascular risk factors and hearing loss: The HUNT study Type Journal Article
  Year 2015 Publication Int J Audiol Abbreviated Journal International journal of audiology  
  Volume 54 Issue 12 Pages 958-966  
  Keywords Epidemiology; alcohol; blood lipids; blood pressure; body mass index; diabetes; hearing loss; physical activity; smoking  
  Abstract OBJECTIVE: The purpose of the present paper was to examine the association between prospectively and cross-sectionally assessed cardiovascular risk factors and hearing loss. DESIGN: Hearing was assessed by pure-tone average thresholds at low (0.25-0.5 kHz), middle (1-2 kHz), and high (3-8 kHz) frequencies. Self-reported or measured cardiovascular risk factors were assessed both 11 years before and simultaneously with the audiometric assessment. Cardiovascular risk factors were smoking, alcohol use, physical inactivity, waist circumference, body mass index, resting heart rate, blood pressure, triglycerides, total serum cholesterol, LDL cholesterol, HDL cholesterol, and diabetes. STUDY SAMPLE: A population-based cohort of 31 547 subjects. RESULTS: After adjustment for age, sex, level of education, income, recurrent ear infections, and noise exposure, risk factors associated with poorer hearing sensitivity were smoking, diabetes, physical inactivity, resting heart rate, and waist circumference. Smoking was only associated with hearing loss at high frequencies. The effects were very small, in combination explaining only 0.2-0.4% of the variance in addition to the component explained by age and the other cofactors. CONCLUSION: This cohort study indicates that, although many cardiovascular risk factors are associated with hearing loss, the effects are small and of doubtful clinical relevance.  
  Address  
  Corporate Author Thesis  
  Publisher Place of Publication a Division of Mental Health , Norwegian Institute of Public Health , Nydalen , Oslo , Norway.b Natio Editor  
  Language Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN ISBN Medium  
  Area Expedition Conference  
  Notes 1708-8186Engdahl, BoAarhus, LisaLie, ArveTambs, KristianN01 DC62104/DC/NIDCD NIH HHS/United StatesJournal ArticleResearch Support, N.I.H., ExtramuralEnglandInt J Audiol. 2015;54(12):958-66. doi: 10.3109/14992027.2015.1090631. Epub 2015 Oct 8. Approved no  
  Call Number HUNT @ maria.stuifbergen @ Engdahl2015 Serial 1805  
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Author Ernstsen, L.; Strand, B.H.; Nilsen, S.M.; Espnes, G.A.; Krokstad, S. url  doi
  Title Trends in absolute and relative educational inequalities in four modifiable ischaemic heart disease risk factors: repeated cross-sectional surveys from the Nord-Trondelag Health Study (HUNT) 1984-2008 Type Journal Article
  Year 2012 Publication BMC Public Health Abbreviated Journal BMC Public Health  
  Volume 12 Issue Pages 266  
  Keywords Adult; Cross-Sectional Studies; Diabetes Mellitus/*epidemiology; *Educational Status; Female; Humans; Hypercholesterolemia/*epidemiology; Hypertension/*epidemiology; Male; Middle Aged; Myocardial Ischemia/*epidemiology; Norway/epidemiology; Risk Factors; Smoking/*epidemiology  
  Abstract BACKGROUND: There has been an overall decrease in incident ischaemic heart disease (IHD), but the reduction in IHD risk factors has been greater among those with higher social position. Increased social inequalities in IHD mortality in Scandinavian countries is often referred to as the Scandinavian “public health puzzle”. The objective of this study was to examine trends in absolute and relative educational inequalities in four modifiable ischaemic heart disease risk factors (smoking, diabetes, hypertension and high total cholesterol) over the last three decades among Norwegian middle-aged women and men. METHODS: Population-based, cross-sectional data from The Nord-Trondelag Health Study (HUNT): HUNT 1 (1984-1986), HUNT 2 (1995-1997) and HUNT 3 (2006-2008), women and men 40-59 years old. Educational inequalities were assessed using the Slope Index of Inequality (SII) and The Relative Index of Inequality (RII). RESULTS: Smoking prevalence increased for all education groups among women and decreased in men. Relative and absolute educational inequalities in smoking widened in both genders, with significantly higher absolute inequalities among women than men in the two last surveys. Diabetes prevalence increased in all groups. Relative inequalities in diabetes were stable, while absolute inequalities increased both among women (p = 0.05) and among men (p = 0.01). Hypertension prevalence decreased in all groups. Relative inequalities in hypertension widened over time in both genders. However, absolute inequalities in hypertension decreased among women (p = 0.05) and were stable among men (p = 0.33). For high total cholesterol relative and absolute inequalities remained stable in both genders. CONCLUSION: Widening absolute educational inequalities in smoking and diabetes over the last three decades gives rise to concern. The mechanisms behind these results are less clear, and future studies are needed to assess if educational inequalities in secondary prevention of IHD are larger compared to educational inequalities in primary prevention of IHD. Continued monitoring of IHD risk factors at the population level is therefore warranted. The results emphasise the need for public health efforts to prevent future burdens of life-style-related diseases and to avoid further widening in socioeconomic inequalities in IHD mortality in Norway, especially among women.  
  Address Sor-Trondelag University College, Mauritz Hansens gt 2, 7004, Trondheim, Norway. linda.ernstsen@hist.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 1471-2458 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:22471945; PMC3434116 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1524  
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Author Fleiner, H.F.; Bjoro, T.; Midthjell, K.; Grill, V.; Asvold, B.O. url  doi
  Title Prevalence of Thyroid Dysfunction in Autoimmune and Type 2 Diabetes: The Population-Based HUNT Study in Norway Type Journal Article
  Year 2016 Publication J Clin Endocrinol Metab Abbreviated Journal The Journal of clinical endocrinology and metabolism  
  Volume 101 Issue 2 Pages 669-677  
  Keywords Adult; Age of Onset; Aged; Cross-Sectional Studies; Databases, Factual; Diabetes Mellitus, Type 1/*complications/*epidemiology; Diabetes Mellitus, Type 2/*complications/*epidemiology; Female; Humans; Hyperthyroidism/complications/epidemiology; Hypothyroidism/complications/epidemiology; Iodide Peroxidase/blood/immunology; Male; Middle Aged; Norway/epidemiology; Prevalence; Sex Factors; Thyroid Diseases/*complications/*epidemiology; Thyroid Hormones/blood  
  Abstract CONTEXT: Associations between autoimmune diabetes and autoimmune thyroid disease are known but insufficiently characterized. Some evidence suggests that type 2 diabetes may also be associated with hypothyroidism. OBJECTIVE: The objective of the study was to investigate associations of autoimmune and type 2 diabetes with the prevalence of hypo- and hyperthyroidism. DESIGN AND SETTING: This was a cross-sectional, population-based study of adults in two surveys of the Nord-Trondelag Health (HUNT) Study. PARTICIPANTS: A total of 34 235 participants of HUNT2 (1995-1997) and 48 809 participants of HUNT3 (2006-2008) participated in the study. MAIN OUTCOME MEASURES: Prevalence of hypo- and hyperthyroidism was estimated, assessed by self-report, serum measurements, and linkage with the Norwegian Prescription Database. RESULTS: In HUNT2, autoimmune diabetes was associated with a higher age-adjusted prevalence of hypothyroidism among both women (prevalence ratio 1.79, 95% confidence interval [CI] 1.30-2.47) and men (prevalence ratio 2.71, 95% CI 1.76-4.19), compared with having no diabetes. For hyperthyroidism, the corresponding cumulative prevalence ratios were 2.12 (95% CI 1.36-3.32) in women and 2.54 (95% CI 1.24-5.18) in men with autoimmune diabetes. The age-adjusted excess prevalence of hypothyroidism ( approximately 6 percentage points) and the presence of thyroid peroxidase antibodies (8-10 percentage points) associated with autoimmune diabetes was similar in women and men. Type 2 diabetes was not associated with the prevalence of hypothyroidism. In HUNT3, associations were broadly similar to those in HUNT2. CONCLUSIONS: Autoimmune diabetes, but not type 2 diabetes, was strongly and gender neutrally associated with an increased prevalence of hypo- and hyperthyroidism and the presence of thyroid peroxidase antibodies. Increased surveillance for hypothyroidism appears not necessary in patients with type 2 diabetes.  
  Address  
  Corporate Author Thesis  
  Publisher Place of Publication Department of Cancer Research and Molecular Medicine (H.F.F., V.G.), Norwegian University of Science Editor  
  Language Summary Language Original Title  
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  ISSN ISBN Medium  
  Area Expedition Conference  
  Notes Fleiner, Hanne FBjoro, TrineMidthjell, KristianGrill, ValdemarAsvold, Bjorn OengResearch Support, Non-U.S. Gov't2015/11/20 06:00J Clin Endocrinol Metab. 2016 Feb;101(2):669-77. doi: 10.1210/jc.2015-3235. Epub 2015 Nov 19. Approved no  
  Call Number HUNT @ maria.stuifbergen @ Fleiner2016 Serial 1738  
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Author Folling, I.S.; Kulseng, B.; Midthjell, K.; Rangul, V.; Helvik, A.-S. url  doi
  Title Individuals at high risk for type 2 diabetes invited to a lifestyle program: characteristics of participants versus non-participants (the HUNT Study) and 24-month follow-up of participants (the VEND-RISK Study) Type Journal Article
  Year 2017 Publication BMJ Open Diabetes Research & Care Abbreviated Journal BMJ Open Diabetes Res Care  
  Volume 5 Issue 1 Pages e000368  
  Keywords Findrisc; lifestyle programme; non-participants; primary health care; type 2 diabetes  
  Abstract OBJECTIVE: Prevention of type 2 diabetes mellitus is possible through lifestyle programs, but the effect depends on the program's content, resources, and setting. Lifestyle programs are often confronted with high rates of non-participation and attrition. This study invited individuals at high risk for type 2 diabetes to a lifestyle program in the Norwegian primary healthcare setting. The aims were to investigate possible differences in characteristics between participants and non-participants and to study the effect of the lifestyle program at 24-month follow-up for participants. RESEARCH DESIGN AND METHODS: Individuals identified at high risk for type 2 diabetes during the third survey of the Nord-Trondelag Health Study (HUNT3) from two municipalities (n=332) were invited to a lifestyle program (the VEND-RISK Study). A cross-sectional design was used to explore if the participants' characteristics differed from non-participants. A non-randomized, single-arm, pre-post examination was used to examine the effect of the lifestyle program on participants' characteristics at 24-month follow-up. RESULTS: Of all individuals at high risk for type 2 diabetes invited to the lifestyle program, 86% (287/332) declined to participate. Non-participating women had fewer years of education (p<0.001), compared with participating women. For men, no differences were seen between non-participants and participants. Among all participants (n=45) at 24-month follow-up, none had developed type 2 diabetes, and HbA1c (p<0.001) had decreased significantly. There was a small reduction in mean body mass index from baseline to 24 months that was not statistically significant. For women, waist circumference (-4.0 cm, p<0.001) decreased significantly. CONCLUSIONS: Future research regarding individuals at high risk for type 2 diabetes in the primary healthcare lifestyle program should focus on how to promote recruitment of women with low education. Participants attending this study's lifestyle program improved their cardiometabolic markers. CLINICAL TRIALS REGISTRATION: NCT01135901; Results.  
  Address St. Olavs University Hospital, 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 2052-4897 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:28878932; PMCID:PMC5574427 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1899  
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Author Gaulton, K.J.; Ferreira, T.; Lee, Y.; Raimondo, A.; Magi, R.; Reschen, M.E.; Mahajan, A.; Locke, A.; William Rayner, N.; Robertson, N.; Scott, R.A.; Prokopenko, I.; Scott, L.J.; Green, T.; Sparso, T.; Thuillier, D.; Yengo, L.; Grallert, H.; Wahl, S.; Franberg, M.; Strawbridge, R.J.; Kestler, H.; Chheda, H.; Eisele, L.; Gustafsson, S.; Steinthorsdottir, V.; Thorleifsson, G.; Qi, L.; Karssen, L.C.; van Leeuwen, E.M.; Willems, S.M.; Li, M.; Chen, H.; Fuchsberger, C.; Kwan, P.; Ma, C.; Linderman, M.; Lu, Y.; Thomsen, S.K.; Rundle, J.K.; Beer, N.L.; van de Bunt, M.; Chalisey, A.; Kang, H.M.; Voight, B.F.; Abecasis, G.R.; Almgren, P.; Baldassarre, D.; Balkau, B.; Benediktsson, R.; Bluher, M.; Boeing, H.; Bonnycastle, L.L.; Bottinger, E.P.; Burtt, N.P.; Carey, J.; Charpentier, G.; Chines, P.S.; Cornelis, M.C.; Couper, D.J.; Crenshaw, A.T.; van Dam, R.M.; Doney, A.S.; Dorkhan, M.; Edkins, S.; Eriksson, J.G.; Esko, T.; Eury, E.; Fadista, J.; Flannick, J.; Fontanillas, P.; Fox, C.; Franks, P.W.; Gertow, K.; Gieger, C.; Gigante, B.; Gottesman, O.; Grant, G.B.; Grarup, N.; Groves, C.J.; Hassinen, M.; Have, C.T.; Herder, C.; Holmen, O.L.; Hreidarsson, A.B.; Humphries, S.E.; Hunter, D.J.; Jackson, A.U.; Jonsson, A.; Jorgensen, M.E.; Jorgensen, T.; Kao, W.H.; Kerrison, N.D.; Kinnunen, L.; Klopp, N.; Kong, A.; Kovacs, P.; Kraft, P.; Kravic, J.; Langford, C.; Leander, K.; Liang, L.; Lichtner, P.; Lindgren, C.M.; Lindholm, E.; Linneberg, A.; Liu, C.T.; Lobbens, S.; Luan, J.; Lyssenko, V.; Mannisto, S.; McLeod, O.; Meyer, J.; Mihailov, E.; Mirza, G.; Muhleisen, T.W.; Muller-Nurasyid, M.; Navarro, C.; Nothen, M.M.; Oskolkov, N.N.; Owen, K.R.; Palli, D.; Pechlivanis, S.; Peltonen, L.; Perry, J.R.; Platou, C.G.; Roden, M.; Ruderfer, D.; Rybin, D.; van der Schouw, Y.T.; Sennblad, B.; Sigurethsson, G.; Stancakova, A.; Steinbach, G.; Storm, P.; Strauch, K.; Stringham, H.M.; Sun, Q.; Thorand, B.; Tikkanen, E.; Tonjes, A.; Trakalo, J.; Tremoli, E.; Tuomi, T.; Wennauer, R.; Wiltshire, S.; Wood, A.R.; Zeggini, E.; Dunham, I.; Birney, E.; Pasquali, L.; Ferrer, J.; Loos, R.J.; Dupuis, J.; Florez, J.C.; Boerwinkle, E.; Pankow, J.S.; van Duijn, C.; Sijbrands, E.; Meigs, J.B.; Hu, F.B.; Thorsteinsdottir, U.; Stefansson, K.; Lakka, T.A.; Rauramaa, R.; Stumvoll, M.; Pedersen, N.L.; Lind, L.; Keinanen-Kiukaanniemi, S.M.; Korpi-Hyovalti, E.; Saaristo, T.E.; Saltevo, J.; Kuusisto, J.; Laakso, M.; Metspalu, A.; Erbel, R.; Jocke, K.H.; Moebus, S.; Ripatti, S.; Salomaa, V.; Ingelsson, E.; Boehm, B.O.; Bergman, R.N.; Collins, F.S.; Mohlke, K.L.; Koistinen, H.; Tuomilehto, J.; Hveem, K.; Njolstad, I.; Deloukas, P.; Donnelly, P.J.; Frayling, T.M.; Hattersley, A.T.; de Faire, U.; Hamsten, A.; Illig, T.; Peters, A.; Cauchi, S.; Sladek, R.; Froguel, P.; Hansen, T.; Pedersen, O.; Morris, A.D.; Palmer, C.N.; Kathiresan, S.; Melander, O.; Nilsson, P.M.; Groop, L.C.; Barroso, I.; Langenberg, C.; Wareham, N.J.; O'Callaghan, C.A.; Gloyn, A.L.; Altshuler, D.; Boehnke, M.; Teslovich, T.M.; McCarthy, M.I.; Morris, A.P.; Replication, D.I.A.G.; Meta-analysis, C. url  doi
  Title Genetic fine mapping and genomic annotation defines causal mechanisms at type 2 diabetes susceptibility loci Type Journal Article
  Year 2015 Publication Nat Genet Abbreviated Journal Nature genetics  
  Volume 47 Issue 12 Pages 1415-1425  
  Keywords HUNT2; metabochip; Binding Sites; Case-Control Studies; Chromatin Immunoprecipitation; *Chromosome Mapping; Diabetes Mellitus, Type 2/*genetics; Gene Expression Regulation; *Genetic Loci; *Genetic Predisposition to Disease; Genome-Wide Association Study; Genomics; Hepatocyte Nuclear Factor 3-beta/*genetics/metabolism; Humans; Islets of Langerhans/metabolism/pathology; Liver/metabolism/pathology; Molecular Sequence Annotation; Polymorphism, Single Nucleotide/*genetics; Receptor, Melatonin, MT2/*genetics/metabolism  
  Abstract We performed fine mapping of 39 established type 2 diabetes (T2D) loci in 27,206 cases and 57,574 controls of European ancestry. We identified 49 distinct association signals at these loci, including five mapping in or near KCNQ1. 'Credible sets' of the variants most likely to drive each distinct signal mapped predominantly to noncoding sequence, implying that association with T2D is mediated through gene regulation. Credible set variants were enriched for overlap with FOXA2 chromatin immunoprecipitation binding sites in human islet and liver cells, including at MTNR1B, where fine mapping implicated rs10830963 as driving T2D association. We confirmed that the T2D risk allele for this SNP increases FOXA2-bound enhancer activity in islet- and liver-derived cells. We observed allele-specific differences in NEUROD1 binding in islet-derived cells, consistent with evidence that the T2D risk allele increases islet MTNR1B expression. Our study demonstrates how integration of genetic and genomic information can define molecular mechanisms through which variants underlying association signals exert their effects on disease.  
  Address  
  Corporate Author Thesis  
  Publisher Place of Publication Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK.Department of Genetics, S Editor  
  Language Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN ISBN Medium  
  Area Expedition Conference  
  Notes Gaulton, Kyle JFerreira, TeresaLee, YejiRaimondo, AnneMagi, ReedikReschen, Michael EMahajan, AnubhaLocke, AdamWilliam Rayner, NRobertson, NeilScott, Robert AProkopenko, IngaScott, Laura JGreen, ToddSparso, ThomasThuillier, DorotheeYengo, LoicGrallert, HaraldWahl, SimoneFranberg, MattiasStrawbridge, Rona JKestler, HansChheda, HimanshuEisele, LewinGustafsson, StefanSteinthorsdottir, ValgerdurThorleifsson, GudmarQi, LuKarssen, Lennart Cvan Leeuwen, Elisabeth MWillems, Sara MLi, ManChen, HanFuchsberger, ChristianKwan, PhoenixMa, ClementLinderman, MichaelLu, YingchangThomsen, Soren KRundle, Jana KBeer, Nicola Lvan de Bunt, MartijnChalisey, AnilKang, Hyun MinVoight, Benjamin FAbecasis, Goncalo RAlmgren, PeterBaldassarre, DamianoBalkau, BeverleyBenediktsson, RafnBluher, MatthiasBoeing, HeinerBonnycastle, Lori LBottinger, Erwin PBurtt, Noel PCarey, JasonCharpentier, GuillaumeChines, Peter SCornelis, Marilyn CCouper, David JCrenshaw, Andrew Tvan Dam, Rob MDoney, Alex S FDorkhan, MozhganEdkins, SarahEriksson, Johan GEsko, TonuEury, ElodieFadista, JoaoFlannick, JasonFontanillas, PierreFox, CarolineFranks, Paul WGertow, KarlGieger, ChristianGigante, BrunaGottesman, OmriGrant, George BGrarup, NielsGroves, Christopher JHassinen, MaijaHave, Christian THerder, ChristianHolmen, Oddgeir LHreidarsson, Astradur BHumphries, Steve EHunter, David JJackson, Anne UJonsson, AnnaJorgensen, Marit EJorgensen, TorbenKao, Wen-Hong LKerrison, Nicola DKinnunen, LeenaKlopp, NormanKong, AugustineKovacs, PeterKraft, PeterKravic, JasminaLangford, CordeliaLeander, KarinLiang, LimingLichtner, PeterLindgren, Cecilia MLindholm, EeroLinneberg, AllanLiu, Ching-TiLobbens, StephaneLuan, Jian'anLyssenko, ValeriyaMannisto, SatuMcLeod, OlgaMeyer, JuliaMihailov, EvelinMirza, GhazalaMuhleisen, Thomas WMuller-Nurasyid, MartinaNavarro, CarmenNothen, Markus MOskolkov, Nikolay NOwen, Katharine RPalli, DomenicoPechlivanis, SonaliPeltonen, LeenaPerry, John R BPlatou, Carl G PRoden, MichaelRuderfer, DouglasRybin, Denisvan der Schouw, Yvonne TSennblad, BengtSigurethsson, GunnarStancakova, AlenaSteinbach, GeraldStorm, PetterStrauch, KonstantinStringham, Heather MSun, QiThorand, BarbaraTikkanen, EmmiTonjes, AnkeTrakalo, JosephTremoli, ElenaTuomi, TiinamaijaWennauer, RomanWiltshire, StevenWood, Andrew RZeggini, EleftheriaDunham, IanBirney, EwanPasquali, LorenzoFerrer, JorgeLoos, Ruth J FDupuis, JoseeFlorez, Jose CBoerwinkle, EricPankow, James Svan Duijn, CorneliaSijbrands, EricMeigs, James BHu, Frank BThorsteinsdottir, UnnurStefansson, KariLakka, Timo ARauramaa, RainerStumvoll, MichaelPedersen, Nancy LLind, LarsKeinanen-Kiukaanniemi, Sirkka MKorpi-Hyovalti, EevaSaaristo, Timo ESaltevo, JuhaKuusisto, JohannaLaakso, MarkkuMetspalu, AndresErbel, RaimundJocke, Karl-HeinzMoebus, SusanneRipatti, SamuliSalomaa, VeikkoIngelsson, ErikBoehm, Bernhard OBergman, Richard NCollins, Francis SMohlke, Karen LKoistinen, HeikkiTuomilehto, JaakkoHveem, KristianNjolstad, IngerDeloukas, PanagiotisDonnelly, Peter JFrayling, Timothy MHattersley, Andrew Tde Faire, UlfHamsten, AndersIllig, ThomasPeters, AnnetteCauchi, StephaneSladek, RobFroguel, PhilippeHansen, TorbenPedersen, OlufMorris, Andrew DPalmer, Collin N AKathiresan, SekarMelander, OlleNilsson, Peter MGroop, Leif CBarroso, InesLangenberg, ClaudiaWareham, Nicholas JO'Callaghan, Christopher AGloyn, Anna LAltshuler, DavidBoehnke, MichaelTeslovich, Tanya MMcCarthy, Mark IMorris, Andrew P(DIAGRAM)eng098395/Wellcome Trust/United KingdomHHSN268201100005C/HL/NHLBI NIH HHS/HHSN268201100006C/HL/NHLBI NIH HHS/HHSN268201100007C/HL/NHLBI NIH HHS/HHSN268201100008C/HL/NHLBI NIH HHS/HHSN268201100009C/HL/NHLBI NIH HHS/HHSN268201100010C/HL/NHLBI NIH HHS/HHSN268201100011C/HL/NHLBI NIH HHS/HHSN268201100012C/HL/NHLBI NIH HHS/K24 DK080140/DK/NIDDK NIH HHS/N01 HC025195/HC/NHLBI NIH HHS/N01 HG065403/HG/NHGRI NIH HHS/N02 HL64278/HL/NHLBI NIH HHS/R01 AG010175/AG/NIA NIH HHS/R01 DK062370/DK/NIDDK NIH HHS/R01 DK072193/DK/NIDDK NIH HHS/R01 DK073490/DK/NIDDK NIH HHS/R01 DK078616/DK/NIDDK NIH HHS/R01 DK098032/DK/NIDDK NIH HHS/R01 HL059367/HL/NHLBI NIH HHS/R01 HL086694/HL/NHLBI NIH HHS/R01 HL087641/HL/NHLBI NIH HHS/U01 DK085526/DK/NIDDK NIH HHS/U01 DK085545/DK/NIDDK NIH HHS/U01 HG004399/HG/NHGRI NIH HHS/U01 HG004402/HG/NHGRI NIH HHS/UL1 RR025005/RR/NCRR NIH HHS/Z01 HG000024-13/Intramural NIH HHS/2015/11/10 06:00Nat Genet. 2015 Dec;47(12):1415-25. doi: 10.1038/ng.3437. Epub 2015 Nov 9. Approved no  
  Call Number HUNT @ maria.stuifbergen @ Gaulton2015 Serial 1810  
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Author Gusarova, V.; O'Dushlaine, C.; Teslovich, T.M.; Benotti, P.N.; Mirshahi, T.; Gottesman, O.; Van Hout, C.V.; Murray, M.F.; Mahajan, A.; Nielsen, J.B.; Fritsche, L.; Wulff, A.B.; Gudbjartsson, D.F.; Sjogren, M.; Emdin, C.A.; Scott, R.A.; Lee, W.-J.; Small, A.; Kwee, L.C.; Dwivedi, O.P.; Prasad, R.B.; Bruse, S.; Lopez, A.E.; Penn, J.; Marcketta, A.; Leader, J.B.; Still, C.D.; Kirchner, H.L.; Mirshahi, U.L.; Wardeh, A.H.; Hartle, C.M.; Habegger, L.; Fetterolf, S.N.; Tusie-Luna, T.; Morris, A.P.; Holm, H.; Steinthorsdottir, V.; Sulem, P.; Thorsteinsdottir, U.; Rotter, J.I.; Chuang, L.-M.; Damrauer, S.; Birtwell, D.; Brummett, C.M.; Khera, A.V.; Natarajan, P.; Orho-Melander, M.; Flannick, J.; Lotta, L.A.; Willer, C.J.; Holmen, O.L.; Ritchie, M.D.; Ledbetter, D.H.; Murphy, A.J.; Borecki, I.B.; Reid, J.G.; Overton, J.D.; Hansson, O.; Groop, L.; Shah, S.H.; Kraus, W.E.; Rader, D.J.; Chen, Y.-D.I.; Hveem, K.; Wareham, N.J.; Kathiresan, S.; Melander, O.; Stefansson, K.; Nordestgaard, B.G.; Tybjaerg-Hansen, A.; Abecasis, G.R.; Altshuler, D.; Florez, J.C.; Boehnke, M.; McCarthy, M.I.; Yancopoulos, G.D.; Carey, D.J.; Shuldiner, A.R.; Baras, A.; Dewey, F.E.; Gromada, J. url  doi
  Title Genetic inactivation of ANGPTL4 improves glucose homeostasis and is associated with reduced risk of diabetes Type Journal Article
  Year 2018 Publication Nature Communications Abbreviated Journal Nat Commun  
  Volume 9 Issue 1 Pages 2252  
  Keywords Amino Acid Substitution; Angiopoietin-like 4 Protein/*deficiency/*genetics/metabolism; Animals; Blood Glucose/metabolism; Case-Control Studies; Diabetes Mellitus, Type 2/etiology/*genetics/*metabolism; Female; Gene Silencing; Genetic Association Studies; Genetic Variation; Heterozygote; Homeostasis; Humans; Insulin Resistance/genetics; Lipoprotein Lipase/metabolism; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Risk Factors; Whole Exome Sequencing  
  Abstract Angiopoietin-like 4 (ANGPTL4) is an endogenous inhibitor of lipoprotein lipase that modulates lipid levels, coronary atherosclerosis risk, and nutrient partitioning. We hypothesize that loss of ANGPTL4 function might improve glucose homeostasis and decrease risk of type 2 diabetes (T2D). We investigate protein-altering variants in ANGPTL4 among 58,124 participants in the DiscovEHR human genetics study, with follow-up studies in 82,766 T2D cases and 498,761 controls. Carriers of p.E40K, a variant that abolishes ANGPTL4 ability to inhibit lipoprotein lipase, have lower odds of T2D (odds ratio 0.89, 95% confidence interval 0.85-0.92, p = 6.3 x 10(-10)), lower fasting glucose, and greater insulin sensitivity. Predicted loss-of-function variants are associated with lower odds of T2D among 32,015 cases and 84,006 controls (odds ratio 0.71, 95% confidence interval 0.49-0.99, p = 0.041). Functional studies in Angptl4-deficient mice confirm improved insulin sensitivity and glucose homeostasis. In conclusion, genetic inactivation of ANGPTL4 is associated with improved glucose homeostasis and reduced risk of T2D.  
  Address Regeneron Pharmaceuticals, Tarrytown, 10591, NY, USA. jesper.gromada@regeneron.com  
  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:29899519; PMCID:PMC5997992 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 2086  
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Author Hagen, K.; Asvold, B.O.; Midthjell, K.; Stovner, L.J.; Zwart, J.-A.; Linde, M. url  doi
  Title Inverse relationship between type 1 diabetes mellitus and migraine. Data from the Nord-Trondelag Health Surveys 1995-1997 and 2006-2008 Type Journal Article
  Year 2018 Publication Cephalalgia : an International Journal of Headache Abbreviated Journal Cephalalgia  
  Volume 38 Issue 3 Pages 417-426  
  Keywords *Epidemiology; *diabetes mellitus; *headache; *migraine  
  Abstract Aims The aim of this cross-sectional population-based study was to investigate the associations between migraine and type 1 and type 2 diabetes mellitus (DM). Methods We used data from the second (1995-1997) and third survey (2006-2008) in the Nord-Trondelag Health Study. Analyses were made for the 26,121 participants (30-97 years of age, median 58.3 years) with known headache and DM status in both surveys, and for the 39,584 participants in the third survey (20-97 years, median 54.1 years). The diagnosis of migraine was given to those who fulfilled the questionnaire-based migraine diagnosis in the second and/or third survey. Associations were assessed using multiple logistic regression, estimating prevalence odds ratio (OR) with 95% confidence intervals (CIs). Results In the multivariate analysis of the 26,121 participants in both surveys, adjusting for age, gender, years of education, and smoking, classical type 1 DM (n = 81) was associated with a lower prevalence of any headache (OR = 0.55, 95% CI 0.34-0.88),and migraine (OR = 0.47, 95% CI 0.26-0.96) compared to those without DM (n = 24,779). Correspondingly, the merged group of classical type 1 DM and latent autoimmune diabetes of adults (LADA) (n = 153) were less likely to have migraine (OR = 0.53, 95% CI 0.31-0.91). Similarly, an inverse relationship between type 1 DM and migraine was found in analyses of 39,584 participants in the third survey. No clear association was found between headache and type 2 DM. Conclusions In this cross-sectional population-based study of mainly middle-aged participants, type 1 DM was inversely associated with headache, in particular migraine.  
  Address 2 Norwegian Advisory Unit on Headache, St. Olavs Hospital, 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 0333-1024 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:28114807 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 2087  
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Author Heuch, I.; Heuch, I.; Hagen, K.; Sorgjerd, E.P.; Asvold, B.O.; Zwart, J.-A. url  doi
  Title Is chronic low back pain a risk factor for diabetes? The Nord-Trondelag Health Study Type Journal Article
  Year 2018 Publication BMJ Open Diabetes Research & Care Abbreviated Journal BMJ Open Diabetes Res Care  
  Volume 6 Issue 1 Pages e000569  
  Keywords Hunt; cohort; diabetes; low back pain; musculoskeletal disorder  
  Abstract Objective: The purpose of this study was to examine the risk of diabetes associated with the presence or absence of chronic low back pain, considering both cross-sectional and cohort data. Research design and methods: Analyses were based on the Norwegian HUNT2 and HUNT3 surveys of Nord-Trondelag County. The prevalence of diabetes was compared in groups with and without chronic low back pain among 45 157 participants aged 30-69 years. Associations between low back pain at baseline and risk of diabetes were examined in an 11-year follow-up of 30 380 individuals with no baseline diagnosis of diabetes. The comorbidity between diabetes and low back pain was assessed at the end of follow-up. All analyses were carried out considering generalized linear models incorporating adjustment for other relevant risk factors. Results: Cross-sectional analyses did not reveal any association between low back pain and diabetes. With adjustment for age, body mass index, physical activity and smoking, the cohort study of women showed a significant association between low back pain at baseline and risk of diabetes (RR 1.30; 95% CI 1.09 to 1.54, p=0.003). The association differed between age groups (p=0.015), with a stronger association in relatively young women. In men, no association was found in the whole age range (RR 1.02; 95% CI 0.86 to 1.21, p=0.82). No association was observed between diabetes and chronic low back pain at the end of follow-up. Conclusion: Among younger women, those with chronic low back pain may have an increased risk of diabetes.  
  Address Faculty of Medicine, University of Oslo, 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 2052-4897 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:30397493; PMCID:PMC6203062 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 2097  
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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 PMID:28093432; PMCID:PMC5253523 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1929  
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Author Hjort, R.; Ahlqvist, E.; Carlsson, P.-O.; Grill, V.; Groop, L.; Martinell, M.; Rasouli, B.; Rosengren, A.; Tuomi, T.; Asvold, B.O.; Carlsson, S. url  doi
  Title Overweight, obesity and the risk of LADA: results from a Swedish case-control study and the Norwegian HUNT Study Type Journal Article
  Year 2018 Publication Diabetologia Abbreviated Journal Diabetologia  
  Volume 61 Issue 6 Pages 1333-1343  
  Keywords Adult; Aged; Autoantibodies/blood; Body Mass Index; Case-Control Studies; Diabetes Mellitus, Type 2/*epidemiology; Female; Humans; Insulin Resistance; Insulin-Secreting Cells/metabolism; Latent Autoimmune Diabetes in Adults/*complications/*diagnosis/*epidemiology; Male; Middle Aged; Norway/epidemiology; Obesity/*complications/epidemiology; Odds Ratio; Overweight/*complications/epidemiology; Prospective Studies; Risk Factors; Sweden; Young Adult; *Andis; *ANDiU; *Body mass index; *Case-control study; *Estrid; *HUNT Study; *Lada; *Latent autoimmune diabetes in adults; *Prospective study; *Type 2 diabetes  
  Abstract AIMS/HYPOTHESIS: Excessive weight is a risk factor for type 2 diabetes, but its role in the promotion of autoimmune diabetes is not clear. We investigated the risk of latent autoimmune diabetes in adults (LADA) in relation to overweight/obesity in two large population-based studies. METHODS: Analyses were based on incident cases of LADA (n = 425) and type 2 diabetes (n = 1420), and 1704 randomly selected control participants from a Swedish case-control study and prospective data from the Norwegian HUNT Study including 147 people with LADA and 1,012,957 person-years of follow-up (1984-2008). We present adjusted ORs and HRs with 95% CI. RESULTS: In the Swedish data, obesity was associated with an increased risk of LADA (OR 2.93, 95% CI 2.17, 3.97), which was even stronger for type 2 diabetes (OR 18.88, 95% CI 14.29, 24.94). The association was stronger in LADA with low GAD antibody (GADA; <median) (OR 4.25; 95% CI 2.76, 6.52) but present also in LADA with high GADA (OR 2.14; 95% CI 1.42, 3.24). In the Swedish data, obese vs normal weight LADA patients had lower GADA levels, better beta cell function, and were more likely to have low-risk HLA-genotypes. The combination of overweight and family history of diabetes (FHD) conferred an OR of 4.57 (95% CI 3.27, 6.39) for LADA and 24.51 (95% CI 17.82, 33.71) for type 2 diabetes. Prospective data from HUNT indicated even stronger associations; HR for LADA was 6.07 (95% CI 3.76, 9.78) for obesity and 7.45 (95% CI 4.02, 13.82) for overweight and FHD. CONCLUSIONS/INTERPRETATION: Overweight/obesity is associated with increased risk of LADA, particularly when in combination with FHD. These findings support the hypothesis that, even in the presence of autoimmunity, factors linked to insulin resistance, such as excessive weight, could promote onset of diabetes.  
  Address Unit of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Box 210, 171 77, Stockholm, Sweden  
  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 0012-186X ISBN Medium  
  Area Expedition Conference  
  Notes PMID:29589073 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 2098  
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Author Iversen, M.M.; Nefs, G.; Tell, G.S.; Espehaug, B.; Midthjell, K.; Graue, M.; Pouwer, F. url  doi
  Title Anxiety, depression and timing of insulin treatment among people with type 2 diabetes: Nine-year follow-up of the Nord-Trondelag Health Study, Norway Type Journal Article
  Year 2015 Publication J Psychosom Res Abbreviated Journal Journal of psychosomatic research  
  Volume 79 Issue 4 Pages 309-315  
  Keywords HUNT2; Adult; Aged; Aged, 80 and over; Anxiety/*etiology; Cohort Studies; Depression/diagnosis/*etiology; Diabetes Mellitus, Type 2/*complications/drug therapy; Female; Humans; Insulin/administration & dosage/*therapeutic use; Male; Middle Aged; Norway; Prospective Studies; Young Adult  
  Abstract BACKGROUND: Depression and anxiety have been found to be predictors of poor health outcomes in diabetes, but mechanisms are still unclear. AIMS: To examine whether symptoms of anxiety and depression were associated with timing of initiating insulin therapy. METHODS: A cohort study of insulin-naive particpants with type 2 dabetes completed the Hospital Anxiey and Depression Scale, HADS-A (n = 731) and/or the HADS-D (n = 768) in the communy-based Nord-Trondelag Health Study (1995-1997). Information on insulin initiation was retrieved from the Norwegian Prescription Database from January 1, 2004 to November 21, 2012. Cox regression analyses were used to estimate the association between symptoms of anxiety, depression and time to insulin initiation. RESULTS: At baseline, 19% reported anxiety symptoms (score>/=8) and 18% depressive symptoms (score>/=8). After a mean follow-up of 4.4 (SD 3.6) years, 337 (40%) participants had started insulin therapy. After adjustment for sociodemographic and clinical variables, anxiety symptoms were associated with later initiation of insulin therapy (HR 0.70, 95% CI 0.49-0.99), while depressive symptoms were not. Considering groups simultaneously, having both elevated depressive and elevated anxiety symptoms was associated with later time to insulin initiation (HR 0.62, 95% CI 0.39-0.99), while having only anxiety symptoms (without depressive) HR 0.81, 95% CI 0.50-1.32) or only depressive symptoms (without anxiety) (HR 1.08, 95% CI 0.68-1.72) were not. CONCLUSIONS: Anxiety was associated with a later initiation of insulin, while depressive symptoms were not. Persons with both elevated levels of anxiety and depression were also less likely to start insulin therapy. These results need further testing in other prospective studies.  
  Address  
  Corporate Author Thesis  
  Publisher Place of Publication Centre for Evidence-Based Practice, Bergen University College, Norway; Department of Endocrinology, Editor  
  Language Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
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  ISSN ISBN Medium  
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  Notes Iversen, M MNefs, GTell, G SEspehaug, BMidthjell, KGraue, MPouwer, FengEngland2015/07/26 06:00J Psychosom Res. 2015 Oct;79(4):309-15. doi: 10.1016/j.jpsychores.2015.07.004. Epub 2015 Jul 16. Approved no  
  Call Number HUNT @ maria.stuifbergen @ Iversen2015b Serial 1825  
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Author Iversen, M.M.; Tell, G.S.; Espehaug, B.; Midthjell, K.; Graue, M.; Rokne, B.; Berge, L.I.; Ostbye, T. url  doi
  Title Is depression a risk factor for diabetic foot ulcers? 11-years follow-up of the Nord-Trondelag Health Study (HUNT) Type Journal Article
  Year 2014 Publication Journal of Diabetes and its Complications Abbreviated Journal J Diabetes Complications  
  Volume Issue Pages  
  Keywords HUNT2; Cohort study; Depression; Diabetes; Foot ulcer; Norway; Risk factor  
  Abstract AIM: To prospectively examine whether depressive symptoms increase the risk of diabetes and a diabetic foot ulcer. METHODS: The Nord-Trondelag Health Study (HUNT) is a community-based longitudinal study. The Hospital Anxiety and Depression Scale (HADS-D subscale) assessed depressive symptoms. We followed individuals with complete HADS-D data from HUNT2 (1995-97) and assessed whether they reported diabetes with or without a history of diabetic foot ulcer (DFU) in HUNT3 (2006-08) (n=36,031). Logistic regression was used to investigate the effect of depressive symptoms on subsequent development of diabetes and of DFU. RESULTS: Unadjusted odds for reporting diabetes at follow-up was higher among individuals who reported a HADS-D score>/=8 at baseline (OR 1.30 95% CI, 1.07-1.57) than among those reporting a lower score. After adjusting for age, gender and BMI, this association was no longer significant. The odds of developing a DFU was almost two-fold (OR=1.95 95% CI, 1.02-3.74) for those reporting a HADS-D score of 8-10, and 3-fold (OR=3.06 95% CI, 1.24-7.54) for HADS-D scores>/=11, compared to HADS-D scores<8, after adjusting for age, gender and serum glucose. CONCLUSIONS: Symptoms of depression at baseline are associated with an increased risk of a diabetic foot ulcer in a dose response manner during this 11-year follow-up.  
  Address Duke Global Health Institute, Duke University, Box 90519 Durham, NC 27708, 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 1056-8727 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:25283486 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1648  
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Author Jolle, A.; Asvold, B.O.; Holmen, J.; Carlsen, S.M.; Tuomilehto, J.; Bjorngaard, J.H.; Midthjell, K. url  doi
  Title Basic lifestyle advice to individuals at high risk of type 2 diabetes: a 2-year population-based diabetes prevention study. The DE-PLAN intervention in the HUNT Study, Norway Type Journal Article
  Year 2018 Publication BMJ Open Diabetes Research & Care Abbreviated Journal BMJ Open Diabetes Res Care  
  Volume 6 Issue 1 Pages e000509  
  Keywords lifestyle change(s); prevention; screening; type 2 diabetes  
  Abstract Objective: Among individuals at high risk for diabetes identified through a population survey, we performed an intervention study with basic lifestyle advice aiming to prevent diabetes. Research design and methods: Among 50 806 participants in the HUNT3 Survey (2006-2008), 5297 individuals with Finnish Diabetes Risc Score (FINDRISC >/=15 were invited to an oral glucose tolerance test (OGTT) and an education session with lifestyle advice, and 2634 (49.7%) attended. Among them, 2380 people without diabetes were included in the prevention study with repeated examinations and education sessions after 6, 12, and 24 months. We examined participation, diabetes incidence, glycemia, and adiposity during follow-up. Results: Of 2380 participants, 1212 (50.9%) participated in >/=3 of the four examinations. Diabetes was detected in 3.5%, 3.1%, and 4.0% of individuals at the 6-month, 12-month, and 24-month examinations, respectively, indicating a 10.3% 2-year diabetes incidence. Mean (95% CI) increases from baseline to 2-year follow-up were 0.30 (0.29 to 0.32) percentage points (3.3 (3.2 to 3.5) mmol/mol) for Hemoglobin A1c, 0.13 (0.10 to 0.16) mmol/L for fasting serum-glucose, 0.46 (0.36 to 0.56) mmol/L for 2-hour OGTT s-glucose, 0.30 (0.19 to 0.40) kg/m(2) forbody mass index (BMI) (all p<0.001) and -0.5 (-0.9 to -0.2) cm for waist circumference (p=0.004), with broadly similar estimates by baseline age, sex, education, depressive symptoms, BMI, physical activity, and family history of diabetes. Only 206 (8.7%) participants had evidence of >5% weight loss during follow-up; their fasting and 2-hour s-glucose did not increase, and HbA1c increased less than in other participants. Conclusion: Basic lifestyle advice given to high-risk individuals during three group sessions with 6-month intervals was not effective in reducing 2-year diabetes risk.  
  Address HUNT Research Centre, Department of Public Health and Nursing, 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 2052-4897 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:29765613; PMCID:PMC5950645 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 2107  
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Author Jorgensen, P.; Langhammer, A.; Krokstad, S.; Forsmo, S. url  doi
  Title Diagnostic labelling influences self-rated health. A prospective cohort study: the HUNT Study, Norway Type Journal Article
  Year 2015 Publication Fam Pract Abbreviated Journal Family practice  
  Volume 32 Issue 5 Pages 492-499  
  Keywords HUNT2; HUNT3; Adult; Aged; Diabetes Mellitus/*psychology; *Diagnostic Self Evaluation; Female; Follow-Up Studies; *Health Knowledge, Attitudes, Practice; *Health Status; Health Surveys; Humans; Hypertension/*psychology; Hypothyroidism/*psychology; Male; Middle Aged; Norway; Prospective Studies; Young Adult  
  Abstract BACKGROUND: Studies have shown an independent association between poor self-rated health (SRH) and increased mortality. Few studies, however, have investigated any possible impact on SRH of diagnostic labelling. OBJECTIVE: To test whether SRH differed in persons with known and unknown hypothyroidism, diabetes mellitus (DM) or hypertension, opposed to persons without these conditions, after 11-year follow-up. METHODS: Prospective population-based cohort study in North-Trondelag County, Norway, HUNT2 (1995-97) to HUNT3 (2006-08). All inhabitants aged 20 years and older were invited. The response rate was 69.5% in HUNT2 and 54.1% in HUNT3. In total, 34144 persons aged 20-70 years were included in the study population. The outcome was poor SRH. RESULTS: Persons with known disease had an increased odds ratio (OR) to report poor SRH at follow-up; figures ranging from 1.11 (0.68-1.79) to 2.52 (1.46-4.34) (men with hypothyroidism kept out owing to too few numbers). However, in persons not reporting, but having laboratory results indicating these diseases (unknown disease), no corresponding associations with SRH were found. Contrary, the OR for poor SRH in women with unknown hypothyroidism and unknown hypertension was 0.64 (0.38-1.06) and 0.89 (0.79-1.01), respectively. CONCLUSIONS: Awareness opposed to ignorance of hypothyroidism, DM and hypertension seemed to be associated with poor perceived health, suggesting that diagnostic labelling could have a negative effect on SRH. This relationship needs to be tested more thoroughly in future research but should be kept in mind regarding the benefits of early diagnosing of diseases.  
  Address  
  Corporate Author Thesis  
  Publisher Place of Publication Department of Public Health and General Practice, Norwegian University of Science and Technology, 74 Editor  
  Language Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN ISBN Medium  
  Area Expedition Conference  
  Notes Jorgensen, PalLanghammer, ArnulfKrokstad, SteinarForsmo, SiriengEngland2015/08/05 06:00Fam Pract. 2015 Oct;32(5):492-9. doi: 10.1093/fampra/cmv065. Epub 2015 Aug 3. Approved no  
  Call Number HUNT @ maria.stuifbergen @ Jorgensen2015 Serial 1828  
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Author Jorgensen, P.; Langhammer, A.; Krokstad, S.; Forsmo, S. url  doi
  Title Mortality in persons with undetected and diagnosed hypertension, type 2 diabetes, and hypothyroidism, compared with persons without corresponding disease – a prospective cohort study; The HUNT Study, Norway Type Journal Article
  Year 2017 Publication BMC Family Practice Abbreviated Journal BMC Fam Pract  
  Volume 18 Issue 1 Pages 98  
  Keywords Chronic disease; Diabetes; Hypertension; Primary care; Public health; Thyroid disorders  
  Abstract BACKGROUND: Suggested strategies in reducing the impact of non-communicable diseases (NCD) are early diagnosing and screening. We have limited proof of benefit of population screening for NCD. Increased mortality in persons with diagnosed NCD has been shown for decades. However, mortality in undetected NCD has barely been studied. This paper explores whether all-cause mortality differed between persons with diagnosed hypothyroidism, type 2 diabetes (T2DM), and hypertension, compared with persons with undetected-, and with persons without the corresponding disease. METHODS: A prospective cohort study of the general population in Nord-Trondelag, Norway. Persons >/=20 years at baseline 1995-97 were followed until death or June 15, 2016. Cox proportional hazards models were used to compute age and multiple adjusted hazard ratios (HR) with 95% confidence intervals (CI) for the association between disease status and all-cause mortality. The number of participants in the hypothyroidism study was 31,960, in the T2DM study 37,957, and in the hypertension study 63,371. RESULTS: Mortality was increased in persons with diagnosed type 2 diabetes and hypertension, compared to persons without corresponding disease; HR 1.69 (95% CI 1.55-1.84) and HR 1.23 (95% CI 1.09-1.39), respectively. Among persons with undetected T2DM, the HR was 1.21 (95% CI 1.08-1.37), whilst among undetected hypothyroidism and hypertension, mortality was not increased compared with persons without the diseases. Further, the association with mortality was stronger in persons with long duration of T2DM (HR 1.96 (95% CI 1.57-2.44)) and hypertension (HR 1.32 (95% CI 1.17-1.49)), compared with persons with short duration (HR 1.29 (1.09-1.53) and HR 1.16 (1.03-1-30) respectively). CONCLUSIONS: Mortality was increased in persons with diagnosed T2DM and hypertension, and in undetected T2DM, compared with persons without the diseases. The strength of the association with mortality in undetected T2DM was however lower compared with persons with diagnosed T2DM, and mortality was not increased in persons with undetected hypothyroidism and hypertension, compared with persons without the diseases. Thus, future research needs to test more thoroughly if early diagnosing of these diseases, such as general population screening, is beneficial for health.  
  Address Department of Public Health and Nursing, NTNU, Norwegian University of Science and Technology, Postbox 8905, 7491, 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 1471-2296 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:29212453; PMCID:PMC5719734 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1935  
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Author Kelly, M.A.; Rees, S.D.; Hydrie, M.Z.I.; Shera, A.S.; Bellary, S.; O'Hare, J.P.; Kumar, S.; Taheri, S.; Basit, A.; Barnett, A.H. url  doi
  Title Circadian gene variants and susceptibility to type 2 diabetes: a pilot study Type Journal Article
  Year 2012 Publication PloS one Abbreviated Journal PLoS One  
  Volume 7 Issue 4 Pages e32670  
  Keywords Circadian Rhythm Signaling Peptides and Proteins/*genetics; Diabetes Mellitus, Type 2/*genetics; Female; Gene Frequency; Genetic Association Studies; *Genetic Predisposition to Disease; Genotyping Techniques; Humans; Male; Pilot Projects; *Polymorphism, Single Nucleotide; Risk Factors  
  Abstract BACKGROUND: Disruption of endogenous circadian rhythms has been shown to increase the risk of developing type 2 diabetes, suggesting that circadian genes might play a role in determining disease susceptibility. We present the results of a pilot study investigating the association between type 2 diabetes and selected single nucleotide polymorphisms (SNPs) in/near nine circadian genes. The variants were chosen based on their previously reported association with prostate cancer, a disease that has been suggested to have a genetic link with type 2 diabetes through a number of shared inherited risk determinants. METHODOLOGY/PRINCIPAL FINDINGS: The pilot study was performed using two genetically homogeneous Punjabi cohorts, one resident in the United Kingdom and one indigenous to Pakistan. Subjects with (N = 1732) and without (N = 1780) type 2 diabetes were genotyped for thirteen circadian variants using a competitive allele-specific polymerase chain reaction method. Associations between the SNPs and type 2 diabetes were investigated using logistic regression. The results were also combined with in silico data from other South Asian datasets (SAT2D consortium) and white European cohorts (DIAGRAM+) using meta-analysis. The rs7602358G allele near PER2 was negatively associated with type 2 diabetes in our Punjabi cohorts (combined odds ratio [OR] = 0.75 [0.66-0.86], p = 3.18 x 10(-5)), while the BMAL1 rs11022775T allele was associated with an increased risk of the disease (combined OR = 1.22 [1.07-1.39], p = 0.003). Neither of these associations was replicated in the SAT2D or DIAGRAM+ datasets, however. Meta-analysis of all the cohorts identified disease associations with two variants, rs2292912 in CRY2 and rs12315175 near CRY1, although statistical significance was nominal (combined OR = 1.05 [1.01-1.08], p = 0.008 and OR = 0.95 [0.91-0.99], p = 0.015 respectively). CONCLUSIONS/SIGNIFICANCE: None of the selected circadian gene variants was associated with type 2 diabetes with study-wide significance after meta-analysis. The nominal association observed with the CRY2 SNP, however, complements previous findings and confirms a role for this locus in disease susceptibility.  
  Address College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom. m.a.kelly@bham.ac.uk  
  Corporate Author SAT2D 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 1932-6203 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:22485135; PMC3317653 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1536  
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Author Lindberg, M.; Midthjell, K.; Bjerve, K.S. url  doi
  Title Long-term tracking of plasma phospholipid fatty acid concentrations and their correlation with the dietary intake of marine foods in newly diagnosed diabetic patients: results from a follow-up of the HUNT Study, Norway Type Journal Article
  Year 2013 Publication The British Journal of Nutrition Abbreviated Journal Br J Nutr  
  Volume 109 Issue 6 Pages 1123-1134  
  Keywords Adult; Aged; Aged, 80 and over; Animals; Diabetes Mellitus, Type 2/*blood; *Diet; Docosahexaenoic Acids/blood; Eicosapentaenoic Acid/blood; Fatty Acids/*blood; Fatty Acids, Omega-3/administration & dosage/blood; Fatty Acids, Omega-6/blood; Female; Fishes; Humans; Male; Middle Aged; Norway; Phospholipids/*blood; *Seafood  
  Abstract Analysis of long-chain n-3 and n-6 fatty acid (FA) concentrations is used to evaluate their potential health effects in epidemiological studies, and, recently, also to counsel patients with a suboptimal intake of n-3 FA. Data on the method's ability to track and detect differences within and between individuals in appropriate populations are, however, lacking. The present study provides such data for twenty-nine plasma phospholipid (PL) FA concentrations and indices measured in 214 newly diagnosed type 2 diabetic patients at baseline and after 3 years. 20 : 3n-6 and the 20 : 4n-6:20 : 3n-6 ratio showed the highest tracking coefficients (Spearman's r 0.68), while DHA, EPA and PLN3-index (EPA+DHA) coefficients were 0.60, 0.47 and 0.55, respectively. Fish consumption measured simultaneously with EPA, DHA, sum n-3 and PLN3 index showed Spearman's correlation coefficients of 0.47, 0.44, 0.48 and 0.49, respectively, decreasing to 0.20, 0.19, 0.22 and 0.21 when measured 3 years apart. The within-subject CV of EPA, DHA and PLN3 index were 39.9, 14.3 and 18.0 %, respectively. The corresponding between-subject CV were 33.6, 16.5 and 18.7 %, while the reference change values were 112, 41 and 52 %. In conclusion, PL n-3 FA concentrations showed a significant long-term tracking and were positively correlated with marine food intake. Analytical precision, biological variability, reference change value and the index of individuality of EPA, DHA and PLN3 index are similar to commonly used clinical biomarkers, supporting their validity as dietary markers in clinical and epidemiological work.  
  Address Department of Medical Biochemistry, St. Olavs Hospital, Trondheim University Hospital, 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 0007-1145 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:22846205 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1428  
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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.;