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Author Sardahaee, F.S.; Holmen, T.L.; Micali, N.; Kvaloy, K. url  doi
  Title (up) Effects of single genetic variants and polygenic obesity risk scores on disordered eating in adolescents – The HUNT study Type Journal Article
  Year 2017 Publication Appetite Abbreviated Journal Appetite  
  Volume 118 Issue Pages 8-16  
  Keywords Adolescents; Comt; Disordered eating; Eat-12; Hunt; Obesity polygenic risk score  
  Abstract PURPOSE: Improving the understanding of the role of genetic risk on disordered eating (DE). METHODS: A case-control study including 1757 (F: 979, M: 778) adolescents (aged 13-19 years) from the Nord-Trondelag Health Study (HUNT), an ethnically homogenous Norwegian population based study. Cases and controls were defined using a shortened version of the Eating Attitude Test. Logistic regression was employed to test for associations between DE phenotypes and 24 obesity and eating disorder susceptibility SNPs, and the joint effect of a subset of these in a genetic risk score (GRS). RESULTS: COMT was shown to be associated with poor appetite/undereating (OR: 0.6, CI 95%: 0.43-0.83, p = 0.002). Independent of obesity associations, the weighted GRS was associated to overeating in 13-15 year old females (OR: 2.07, CI 95%: 1.14-3.76, p = 0.017). Additionally, a significant association was observed between the GRS and loss of control over eating in the total sample (OR: 1.62, CI 95%: 1.01-2.61, p = 0.046). CONCLUSIONS: The COMT variant (rs4680) was associated with poor appetite/undereating. Our study further confirms prior findings that obesity risk also confers risk for loss of control over eating; and overeating amongst girls.  
  Address HUNT Research Center, Department of Public Health and Nursing, Faculty of Medicine and Health Science, Norwegian University of Science and Technology, Trondheim, Norway; Department of Research and Development, Levanger Hospital, Nord-Trondelag Health Trust, Levanger, Norway. Electronic address: kirsti.kvaloy@ntnu.no  
  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 0195-6663 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:28694222 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1975  
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Author Lu, X.; Peloso, G.M.; Liu, D.J.; Wu, Y.; Zhang, H.; Zhou, W.; Li, J.; Tang, C.S.-M.; Dorajoo, R.; Li, H.; Long, J.; Guo, X.; Xu, M.; Spracklen, C.N.; Chen, Y.; Liu, X.; Zhang, Y.; Khor, C.C.; Liu, J.; Sun, L.; Wang, L.; Gao, Y.-T.; Hu, Y.; Yu, K.; Wang, Y.; Cheung, C.Y.Y.; Wang, F.; Huang, J.; Fan, Q.; Cai, Q.; Chen, S.; Shi, J.; Yang, X.; Zhao, W.; Sheu, W.H.-H.; Cherny, S.S.; He, M.; Feranil, A.B.; Adair, L.S.; Gordon-Larsen, P.; Du, S.; Varma, R.; Chen, Y.-D.I.; Shu, X.-O.; Lam, K.S.L.; Wong, T.Y.; Ganesh, S.K.; Mo, Z.; Hveem, K.; Fritsche, L.G.; Nielsen, J.B.; Tse, H.-F.; Huo, Y.; Cheng, C.-Y.; Chen, Y.E.; Zheng, W.; Tai, E.S.; Gao, W.; Lin, X.; Huang, W.; Abecasis, G.; Kathiresan, S.; Mohlke, K.L.; Wu, T.; Sham, P.C.; Gu, D.; Willer, C.J. url  doi
  Title (up) Exome chip meta-analysis identifies novel loci and East Asian-specific coding variants that contribute to lipid levels and coronary artery disease Type Meta-Analysis
  Year 2017 Publication Nature Genetics Abbreviated Journal Nat Genet  
  Volume 49 Issue 12 Pages 1722-1730  
  Keywords Asian Continental Ancestry Group/genetics; Coronary Artery Disease/ethnology/*genetics; Europe; European Continental Ancestry Group/genetics; Exome/*genetics; Far East; Gene Frequency; Genetic Predisposition to Disease/ethnology/*genetics; *Genetic Variation; Genome-Wide Association Study; Genotype; Humans; Lipid Metabolism/*genetics; Lipids/analysis  
  Abstract Most genome-wide association studies have been of European individuals, even though most genetic variation in humans is seen only in non-European samples. To search for novel loci associated with blood lipid levels and clarify the mechanism of action at previously identified lipid loci, we used an exome array to examine protein-coding genetic variants in 47,532 East Asian individuals. We identified 255 variants at 41 loci that reached chip-wide significance, including 3 novel loci and 14 East Asian-specific coding variant associations. After a meta-analysis including >300,000 European samples, we identified an additional nine novel loci. Sixteen genes were identified by protein-altering variants in both East Asians and Europeans, and thus are likely to be functional genes. Our data demonstrate that most of the low-frequency or rare coding variants associated with lipids are population specific, and that examining genomic data across diverse ancestries may facilitate the identification of functional genes at associated loci.  
  Address Department of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, Michigan, USA  
  Corporate Author GLGC Consortium Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 1061-4036 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:29083407 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1957  
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Author Liu, D.J.; Peloso, G.M.; Yu, H.; Butterworth, A.S.; Wang, X.; Mahajan, A.; Saleheen, D.; Emdin, C.; Alam, D.; Alves, A.C.; Amouyel, P.; Di Angelantonio, E.; Arveiler, D.; Assimes, T.L.; Auer, P.L.; Baber, U.; Ballantyne, C.M.; Bang, L.E.; Benn, M.; Bis, J.C.; Boehnke, M.; Boerwinkle, E.; Bork-Jensen, J.; Bottinger, E.P.; Brandslund, I.; Brown, M.; Busonero, F.; Caulfield, M.J.; Chambers, J.C.; Chasman, D.I.; Chen, Y.E.; Chen, Y.-D.I.; Chowdhury, R.; Christensen, C.; Chu, A.Y.; Connell, J.M.; Cucca, F.; Cupples, L.A.; Damrauer, S.M.; Davies, G.; Deary, I.J.; Dedoussis, G.; Denny, J.C.; Dominiczak, A.; Dube, M.-P.; Ebeling, T.; Eiriksdottir, G.; Esko, T.; Farmaki, A.-E.; Feitosa, M.F.; Ferrario, M.; Ferrieres, J.; Ford, I.; Fornage, M.; Franks, P.W.; Frayling, T.M.; Frikke-Schmidt, R.; Fritsche, L.G.; Frossard, P.; Fuster, V.; Ganesh, S.K.; Gao, W.; Garcia, M.E.; Gieger, C.; Giulianini, F.; Goodarzi, M.O.; Grallert, H.; Grarup, N.; Groop, L.; Grove, M.L.; Gudnason, V.; Hansen, T.; Harris, T.B.; Hayward, C.; Hirschhorn, J.N.; Holmen, O.L.; Huffman, J.; Huo, Y.; Hveem, K.; Jabeen, S.; Jackson, A.U.; Jakobsdottir, J.; Jarvelin, M.-R.; Jensen, G.B.; Jorgensen, M.E.; Jukema, J.W.; Justesen, J.M.; Kamstrup, P.R.; Kanoni, S.; Karpe, F.; Kee, F.; Khera, A.V.; Klarin, D.; Koistinen, H.A.; Kooner, J.S.; Kooperberg, C.; Kuulasmaa, K.; Kuusisto, J.; Laakso, M.; Lakka, T.; Langenberg, C.; Langsted, A.; Launer, L.J.; Lauritzen, T.; Liewald, D.C.M.; Lin, L.A.; Linneberg, A.; Loos, R.J.F.; Lu, Y.; Lu, X.; Magi, R.; Malarstig, A.; Manichaikul, A.; Manning, A.K.; Mantyselka, P.; Marouli, E.; Masca, N.G.D.; Maschio, A.; Meigs, J.B.; Melander, O.; Metspalu, A.; Morris, A.P.; Morrison, A.C.; Mulas, A.; Muller-Nurasyid, M.; Munroe, P.B.; Neville, M.J.; Nielsen, J.B.; Nielsen, S.F.; Nordestgaard, B.G.; Ordovas, J.M.; Mehran, R.; O'Donnell, C.J.; Orho-Melander, M.; Molony, C.M.; Muntendam, P.; Padmanabhan, S.; Palmer, C.N.A.; Pasko, D.; Patel, A.P.; Pedersen, O.; Perola, M.; Peters, A.; Pisinger, C.; Pistis, G.; Polasek, O.; Poulter, N.; Psaty, B.M.; Rader, D.J.; Rasheed, A.; Rauramaa, R.; Reilly, D.F.; Reiner, A.P.; Renstrom, F.; Rich, S.S.; Ridker, P.M.; Rioux, J.D.; Robertson, N.R.; Roden, D.M.; Rotter, J.I.; Rudan, I.; Salomaa, V.; Samani, N.J.; Sanna, S.; Sattar, N.; Schmidt, E.M.; Scott, R.A.; Sever, P.; Sevilla, R.S.; Shaffer, C.M.; Sim, X.; Sivapalaratnam, S.; Small, K.S.; Smith, A.V.; Smith, B.H.; Somayajula, S.; Southam, L.; Spector, T.D.; Speliotes, E.K.; Starr, J.M.; Stirrups, K.E.; Stitziel, N.; Strauch, K.; Stringham, H.M.; Surendran, P.; Tada, H.; Tall, A.R.; Tang, H.; Tardif, J.-C.; Taylor, K.D.; Trompet, S.; Tsao, P.S.; Tuomilehto, J.; Tybjaerg-Hansen, A.; van Zuydam, N.R.; Varbo, A.; Varga, T.V.; Virtamo, J.; Waldenberger, M.; Wang, N.; Wareham, N.J.; Warren, H.R.; Weeke, P.E.; Weinstock, J.; Wessel, J.; Wilson, J.G.; Wilson, P.W.F.; Xu, M.; Yaghootkar, H.; Young, R.; Zeggini, E.; Zhang, H.; Zheng, N.S.; Zhang, W.; Zhang, Y.; Zhou, W.; Zhou, Y.; Zoledziewska, M.; Howson, J.M.M.; Danesh, J.; McCarthy, M.I.; Cowan, C.A.; Abecasis, G.; Deloukas, P.; Musunuru, K.; Willer, C.J.; Kathiresan, S. url  doi
  Title (up) Exome-wide association study of plasma lipids in >300,000 individuals Type Journal Article
  Year 2017 Publication Nature Genetics Abbreviated Journal Nat Genet  
  Volume 49 Issue 12 Pages 1758-1766  
  Keywords Coronary Artery Disease/blood/genetics; Diabetes Mellitus, Type 2/blood/genetics; Exome/*genetics; Genetic Association Studies/*methods; Genetic Predisposition to Disease/genetics; *Genetic Variation; Genotype; Humans; Lipids/*blood; Macular Degeneration/blood/genetics; Phenotype; Risk Factors  
  Abstract We screened variants on an exome-focused genotyping array in >300,000 participants (replication in >280,000 participants) and identified 444 independent variants in 250 loci significantly associated with total cholesterol (TC), high-density-lipoprotein cholesterol (HDL-C), low-density-lipoprotein cholesterol (LDL-C), and/or triglycerides (TG). At two loci (JAK2 and A1CF), experimental analysis in mice showed lipid changes consistent with the human data. We also found that: (i) beta-thalassemia trait carriers displayed lower TC and were protected from coronary artery disease (CAD); (ii) excluding the CETP locus, there was not a predictable relationship between plasma HDL-C and risk for age-related macular degeneration; (iii) only some mechanisms of lowering LDL-C appeared to increase risk for type 2 diabetes (T2D); and (iv) TG-lowering alleles involved in hepatic production of TG-rich lipoproteins (TM6SF2 and PNPLA3) tracked with higher liver fat, higher risk for T2D, and lower risk for CAD, whereas TG-lowering alleles involved in peripheral lipolysis (LPL and ANGPTL4) had no effect on liver fat but decreased risks for both T2D and CAD.  
  Address Cardiovascular Research Center, Massachusetts General Hospital, Boston, Massachusetts, USA  
  Corporate Author VA Million Veteran Program Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 1061-4036 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:29083408; PMCID:PMC5709146 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1943  
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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 (up) 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  
  Corporate Author Thesis  
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  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 2047-4873 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:28429960 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1999  
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Author Li, J.; Wu, B.; Selbaek, G.; Krokstad, S.; Helvik, A.-S. url  doi
  Title (up) Factors associated with consumption of alcohol in older adults – a comparison between two cultures, China and Norway: the CLHLS and the HUNT-study Type Journal Article
  Year 2017 Publication BMC Geriatrics Abbreviated Journal BMC Geriatr  
  Volume 17 Issue 1 Pages 172  
  Keywords Abstainers; Alcohol consumption; China; Elderly; Norway; Older adults  
  Abstract BACKGROUND: There is little knowledge about the consumption of alcohol among Chinese and Norwegian older adults aged 65 years and over. The aim of this study was to investigate the prevalence and factors related to alcohol consumption among older adults in China and Norway. METHODS: The Chinese Longitudinal Healthy Longevity Survey (CLHLS) data in 2008-2009 conducted in China and The Nord-Trondelag Health Study data in 2006-2008 (HUNT3) conducted in Norway were used. Mulitvariable logistic regression was used to test the factors related to alcohol consumption. RESULTS: The prevalence of participants who drink alcohol in the Chinese and Norwegian sample were 19.88% and 46.2%, respectively. The weighted prevalence of participants with consumption of alcohol in the Chinese sample of women and men were 7.20% and 34.14%, respectively. In the Norwegian sample, the prevalence of consumption of alcohol were 43.31% and 65.35% for women and men, respectively. Factors such as younger age, higher level of education, living in urban areas, living with spouse or partner, and better health status were related to higher likelihood of alcohol consumption among Norwegian older women and men; while reported better health status and poorer life satisfaction were related to higher likelihood of alcohol consumption among Chinese. In addition, rural males and older females with higher level of education were more likely to consume alcohol. CONCLUSION: The alcohol consumption patterns were quite different between China and Norway. Besides economic development levels and cultures in the two different countries, demographic characteristics, socioeconomic status, overall health status, and life satisfaction were associated with alcohol consumption as well.  
  Address St. Olav's 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 1471-2318 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:28760157; PMCID:PMC5537928 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1947  
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Author Machiela, M.J.; Hofmann, J.N.; Carreras-Torres, R.; Brown, K.M.; Johansson, M.; Wang, Z.; Foll, M.; Li, P.; Rothman, N.; Savage, S.A.; Gaborieau, V.; McKay, J.D.; Ye, Y.; Henrion, M.; Bruinsma, F.; Jordan, S.; Severi, G.; Hveem, K.; Vatten, L.J.; Fletcher, T.; Koppova, K.; Larsson, S.C.; Wolk, A.; Banks, R.E.; Selby, P.J.; Easton, D.F.; Pharoah, P.; Andreotti, G.; Freeman, L.E.B.; Koutros, S.; Albanes, D.; Mannisto, S.; Weinstein, S.; Clark, P.E.; Edwards, T.E.; Lipworth, L.; Gapstur, S.M.; Stevens, V.L.; Carol, H.; Freedman, M.L.; Pomerantz, M.M.; Cho, E.; Kraft, P.; Preston, M.A.; Wilson, K.M.; Gaziano, J.M.; Sesso, H.S.; Black, A.; Freedman, N.D.; Huang, W.-Y.; Anema, J.G.; Kahnoski, R.J.; Lane, B.R.; Noyes, S.L.; Petillo, D.; Colli, L.M.; Sampson, J.N.; Besse, C.; Blanche, H.; Boland, A.; Burdette, L.; Prokhortchouk, E.; Skryabin, K.G.; Yeager, M.; Mijuskovic, M.; Ognjanovic, M.; Foretova, L.; Holcatova, I.; Janout, V.; Mates, D.; Mukeriya, A.; Rascu, S.; Zaridze, D.; Bencko, V.; Cybulski, C.; Fabianova, E.; Jinga, V.; Lissowska, J.; Lubinski, J.; Navratilova, M.; Rudnai, P.; Szeszenia-Dabrowska, N.; Benhamou, S.; Cancel-Tassin, G.; Cussenot, O.; Bueno-de-Mesquita, H.B.; Canzian, F.; Duell, E.J.; Ljungberg, B.; Sitaram, R.T.; Peters, U.; White, E.; Anderson, G.L.; Johnson, L.; Luo, J.; Buring, J.; Lee, I.-M.; Chow, W.-H.; Moore, L.E.; Wood, C.; Eisen, T.; Larkin, J.; Choueiri, T.K.; Lathrop, G.M.; Teh, B.T.; Deleuze, J.-F.; Wu, X.; Houlston, R.S.; Brennan, P.; Chanock, S.J.; Scelo, G.; Purdue, M.P. url  doi
  Title (up) Genetic Variants Related to Longer Telomere Length are Associated with Increased Risk of Renal Cell Carcinoma Type Journal Article
  Year 2017 Publication European Urology Abbreviated Journal Eur Urol  
  Volume 72 Issue 5 Pages 747-754  
  Keywords Genetic variants; Mendelian randomization; Renal cell carcinoma; Risk; Telomere length  
  Abstract BACKGROUND: Relative telomere length in peripheral blood leukocytes has been evaluated as a potential biomarker for renal cell carcinoma (RCC) risk in several studies, with conflicting findings. OBJECTIVE: We performed an analysis of genetic variants associated with leukocyte telomere length to assess the relationship between telomere length and RCC risk using Mendelian randomization, an approach unaffected by biases from temporal variability and reverse causation that might have affected earlier investigations. DESIGN, SETTING, AND PARTICIPANTS: Genotypes from nine telomere length-associated variants for 10 784 cases and 20 406 cancer-free controls from six genome-wide association studies (GWAS) of RCC were aggregated into a weighted genetic risk score (GRS) predictive of leukocyte telomere length. OUTCOME MEASUREMENTS AND STATISTICAL ANALYSIS: Odds ratios (ORs) relating the GRS and RCC risk were computed in individual GWAS datasets and combined by meta-analysis. RESULTS AND LIMITATIONS: Longer genetically inferred telomere length was associated with an increased risk of RCC (OR=2.07 per predicted kilobase increase, 95% confidence interval [CI]:=1.70-2.53, p<0.0001). As a sensitivity analysis, we excluded two telomere length variants in linkage disequilibrium (R(2)>0.5) with GWAS-identified RCC risk variants (rs10936599 and rs9420907) from the telomere length GRS; despite this exclusion, a statistically significant association between the GRS and RCC risk persisted (OR=1.73, 95% CI=1.36-2.21, p<0.0001). Exploratory analyses for individual histologic subtypes suggested comparable associations with the telomere length GRS for clear cell (N=5573, OR=1.93, 95% CI=1.50-2.49, p<0.0001), papillary (N=573, OR=1.96, 95% CI=1.01-3.81, p=0.046), and chromophobe RCC (N=203, OR=2.37, 95% CI=0.78-7.17, p=0.13). CONCLUSIONS: Our investigation adds to the growing body of evidence indicating some aspect of longer telomere length is important for RCC risk. PATIENT SUMMARY: Telomeres are segments of DNA at chromosome ends that maintain chromosomal stability. Our study investigated the relationship between genetic variants associated with telomere length and renal cell carcinoma risk. We found evidence suggesting individuals with inherited predisposition to longer telomere length are at increased risk of developing renal cell carcinoma.  
  Address Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department Health and Human Services, Bethesda, MS, USA. Electronic address: purduem@mail.nih.gov  
  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 0302-2838 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:28797570; PMCID:PMC5641242 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1959  
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Author Scelo, G.; Purdue, M.P.; Brown, K.M.; Johansson, M.; Wang, Z.; Eckel-Passow, J.E.; Ye, Y.; Hofmann, J.N.; Choi, J.; Foll, M.; Gaborieau, V.; Machiela, M.J.; Colli, L.M.; Li, P.; Sampson, J.N.; Abedi-Ardekani, B.; Besse, C.; Blanche, H.; Boland, A.; Burdette, L.; Chabrier, A.; Durand, G.; Le Calvez-Kelm, F.; Prokhortchouk, E.; Robinot, N.; Skryabin, K.G.; Wozniak, M.B.; Yeager, M.; Basta-Jovanovic, G.; Dzamic, Z.; Foretova, L.; Holcatova, I.; Janout, V.; Mates, D.; Mukeriya, A.; Rascu, S.; Zaridze, D.; Bencko, V.; Cybulski, C.; Fabianova, E.; Jinga, V.; Lissowska, J.; Lubinski, J.; Navratilova, M.; Rudnai, P.; Szeszenia-Dabrowska, N.; Benhamou, S.; Cancel-Tassin, G.; Cussenot, O.; Baglietto, L.; Boeing, H.; Khaw, K.-T.; Weiderpass, E.; Ljungberg, B.; Sitaram, R.T.; Bruinsma, F.; Jordan, S.J.; Severi, G.; Winship, I.; Hveem, K.; Vatten, L.J.; Fletcher, T.; Koppova, K.; Larsson, S.C.; Wolk, A.; Banks, R.E.; Selby, P.J.; Easton, D.F.; Pharoah, P.; Andreotti, G.; Freeman, L.E.B.; Koutros, S.; Albanes, D.; Mannisto, S.; Weinstein, S.; Clark, P.E.; Edwards, T.L.; Lipworth, L.; Gapstur, S.M.; Stevens, V.L.; Carol, H.; Freedman, M.L.; Pomerantz, M.M.; Cho, E.; Kraft, P.; Preston, M.A.; Wilson, K.M.; Michael Gaziano, J.; Sesso, H.D.; Black, A.; Freedman, N.D.; Huang, W.-Y.; Anema, J.G.; Kahnoski, R.J.; Lane, B.R.; Noyes, S.L.; Petillo, D.; Teh, B.T.; Peters, U.; White, E.; Anderson, G.L.; Johnson, L.; Luo, J.; Buring, J.; Lee, I.-M.; Chow, W.-H.; Moore, L.E.; Wood, C.; Eisen, T.; Henrion, M.; Larkin, J.; Barman, P.; Leibovich, B.C.; Choueiri, T.K.; Mark Lathrop, G.; Rothman, N.; Deleuze, J.-F.; McKay, J.D.; Parker, A.S.; Wu, X.; Houlston, R.S.; Brennan, P.; Chanock, S.J. url  doi
  Title (up) Genome-wide association study identifies multiple risk loci for renal cell carcinoma Type Journal Article
  Year 2017 Publication Nature Communications Abbreviated Journal Nat Commun  
  Volume 8 Issue Pages 15724  
  Keywords  
  Abstract Previous genome-wide association studies (GWAS) have identified six risk loci for renal cell carcinoma (RCC). We conducted a meta-analysis of two new scans of 5,198 cases and 7,331 controls together with four existing scans, totalling 10,784 cases and 20,406 controls of European ancestry. Twenty-four loci were tested in an additional 3,182 cases and 6,301 controls. We confirm the six known RCC risk loci and identify seven new loci at 1p32.3 (rs4381241, P=3.1 x 10(-10)), 3p22.1 (rs67311347, P=2.5 x 10(-8)), 3q26.2 (rs10936602, P=8.8 x 10(-9)), 8p21.3 (rs2241261, P=5.8 x 10(-9)), 10q24.33-q25.1 (rs11813268, P=3.9 x 10(-8)), 11q22.3 (rs74911261, P=2.1 x 10(-10)) and 14q24.2 (rs4903064, P=2.2 x 10(-24)). Expression quantitative trait analyses suggest plausible candidate genes at these regions that may contribute to RCC susceptibility.  
  Address Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department Health and Human Services, Bethesda, Maryland 20892, USA  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 2041-1723 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:28598434; PMCID:PMC5472706 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1976  
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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 (up) 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 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 (up) 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 PMID:28448500; PMCID:PMC5407576 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1909  
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Author Bjorngaard, J.H.; Nordestgaard, A.T.; Taylor, A.E.; Treur, J.L.; Gabrielsen, M.E.; Munafo, M.R.; Nordestgaard, B.G.; Asvold, B.O.; Romundstad, P.; Davey Smith, G. url  doi
  Title (up) Heavier smoking increases coffee consumption: findings from a Mendelian randomization analysis Type Journal Article
  Year 2017 Publication International Journal of Epidemiology Abbreviated Journal Int J Epidemiol  
  Volume Issue Pages  
  Keywords Coffee, tea, smoking, Mendelian randomization  
  Abstract Background: There is evidence for a positive relationship between cigarette and coffee consumption in smokers. Cigarette smoke increases metabolism of caffeine, so this may represent a causal effect of smoking on caffeine intake. Methods: We performed Mendelian randomization analyses in the UK Biobank ( N = 114 029), the Norwegian HUNT study ( N = 56 664) and the Copenhagen General Population Study (CGPS) ( N = 78 650). We used the rs16969968 genetic variant as a proxy for smoking heaviness in all studies and rs4410790 and rs2472297 as proxies for coffee consumption in UK Biobank and CGPS. Analyses were conducted using linear regression and meta-analysed across studies. Results: Each additional cigarette per day consumed by current smokers was associated with higher coffee consumption (0.10 cups per day, 95% CI: 0.03, 0.17). There was weak evidence for an increase in tea consumption per additional cigarette smoked per day (0.04 cups per day, 95% CI: -0.002, 0.07). There was strong evidence that each additional copy of the minor allele of rs16969968 (which increases daily cigarette consumption) in current smokers was associated with higher coffee consumption (0.16 cups per day, 95% CI: 0.11, 0.20), but only weak evidence for an association with tea consumption (0.04 cups per day, 95% CI: -0.01, 0.09). There was no clear evidence that rs16969968 was associated with coffee or tea consumption in never or former smokers or that the coffee-related variants were associated with cigarette consumption. Conclusions: Higher cigarette consumption causally increases coffee intake. This is consistent with faster metabolism of caffeine by smokers, but could also reflect a behavioural effect of smoking on coffee drinking.  
  Address School of Social and Community Medicine, University of Bristol, Bristol, UK  
  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 0300-5771 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:29025033 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1881  
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Author Alsnes, I.V.; Vatten, L.J.; Fraser, A.; Bjorngaard, J.H.; Rich-Edwards, J.; Romundstad, P.R.; Asvold, B.O. url  doi
  Title (up) 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 PMID:28223467 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1875  
Permanent link to this record
 

 
Author Theofylaktopoulou, D.; Midttun, O.; Ueland, P.M.; Meyer, K.; Fanidi, A.; Zheng, W.; Shu, X.-O.; Xiang, Y.-B.; Prentice, R.; Pettinger, M.; Thomson, C.A.; Giles, G.G.; Hodge, A.; Cai, Q.; Blot, W.J.; Wu, J.; Johansson, M.; Hultdin, J.; Grankvist, K.; Stevens, V.L.; McCullough, M.M.; Weinstein, S.J.; Albanes, D.; Ziegler, R.; Freedman, N.D.; Langhammer, A.; Hveem, K.; Naess, M.; Sesso, H.D.; Gaziano, J.M.; Buring, J.E.; Lee, I.-M.; Severi, G.; Zhang, X.; Stampfer, M.J.; Han, J.; Smith-Warner, S.A.; Zeleniuch-Jacquotte, A.; Le Marchand, L.; Yuan, J.-M.; Wang, R.; Butler, L.M.; Koh, W.-P.; Gao, Y.-T.; Rothman, N.; Ericson, U.; Sonestedt, E.; Visvanathan, K.; Jones, M.R.; Relton, C.; Brennan, P.; Johansson, M.; Ulvik, A. url  doi
  Title (up) Impaired functional vitamin B6 status is associated with increased risk of lung cancer Type Journal Article
  Year 2017 Publication International Journal of Cancer Abbreviated Journal Int J Cancer  
  Volume Issue Pages  
  Keywords 3-hydroxykynurenine:xanthurenic acid; Lung Cancer Cohort Consortium; functional vitamin B6 marker; pyridoxal 5'-phosphate  
  Abstract Circulating vitamin B6 levels have been found to be inversely associated with lung cancer. Most studies have focused on the B6 form pyridoxal 5'-phosphate (PLP), a direct biomarker influenced by inflammation and other factors. Using a functional B6 marker allows further investigation of the potential role of vitamin B6 status in the pathogenesis of lung cancer. We prospectively evaluated the association of the functional marker of vitamin B6 status, the 3-hydroxykynurenine:xanthurenic acid (HK:XA) ratio, with risk of lung cancer in a nested case-control study consisting of 5,364 matched case-control pairs from the Lung Cancer Cohort Consortium (LC3). We used conditional logistic regression to evaluate the association between HK:XA and lung cancer, and random effect models to combine results from different cohorts and regions. High levels of HK:XA, indicating impaired functional B6 status, were associated with an increased risk of lung cancer, the odds ratio comparing the fourth and the first quartiles (OR4thvs.1st ) was 1.25 (95% confidence interval, 1.10-1.41). Stratified analyses indicated that this association was primarily driven by cases diagnosed with squamous cell carcinoma. Notably, the risk associated with HK:XA was approximately 50% higher in groups with a high relative frequency of squamous cell carcinoma, i.e., men, former and current smokers. This risk of squamous cell carcinoma was present in both men and women regardless of smoking status.  
  Address Bevital AS, 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 0020-7136 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:29238985 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 2011  
Permanent link to this record
 

 
Author Zhou, W.; Fritsche, L.G.; Das, S.; Zhang, H.; Nielsen, J.B.; Holmen, O.L.; Chen, J.; Lin, M.; Elvestad, M.B.; Hveem, K.; Abecasis, G.R.; Kang, H.M.; Willer, C.J. url  doi
  Title (up) Improving power of association tests using multiple sets of imputed genotypes from distributed reference panels Type Journal Article
  Year 2017 Publication Genetic Epidemiology Abbreviated Journal Genet Epidemiol  
  Volume 41 Issue 8 Pages 744-755  
  Keywords Gwas; genotype imputation; multiple reference panels; population-specific; study power  
  Abstract The accuracy of genotype imputation depends upon two factors: the sample size of the reference panel and the genetic similarity between the reference panel and the target samples. When multiple reference panels are not consented to combine together, it is unclear how to combine the imputation results to optimize the power of genetic association studies. We compared the accuracy of 9,265 Norwegian genomes imputed from three reference panels-1000 Genomes phase 3 (1000G), Haplotype Reference Consortium (HRC), and a reference panel containing 2,201 Norwegian participants from the population-based Nord Trondelag Health Study (HUNT) from low-pass genome sequencing. We observed that the population-matched reference panel allowed for imputation of more population-specific variants with lower frequency (minor allele frequency (MAF) between 0.05% and 0.5%). The overall imputation accuracy from the population-specific panel was substantially higher than 1000G and was comparable with HRC, despite HRC being 15-fold larger. These results recapitulate the value of population-specific reference panels for genotype imputation. We also evaluated different strategies to utilize multiple sets of imputed genotypes to increase the power of association studies. We observed that testing association for all variants imputed from any panel results in higher power to detect association than the alternative strategy of including only one version of each genetic variant, selected for having the highest imputation quality metric. This was particularly true for lower frequency variants (MAF < 1%), even after adjusting for the additional multiple testing burden.  
  Address Department of Human Genetics, University of Michigan Medical School, Ann Arbor, Michigan, United States of America  
  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 0741-0395 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:28861891 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 2026  
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Author Mauseth, S.A.; Skurtveit, S.; Langhammer, A.; Spigset, O. url  doi
  Title (up) Incidence of and factors associated with anticholinergic drug use among Norwegian women with urinary incontinence Type Journal Article
  Year 2017 Publication International Urogynecology Journal Abbreviated Journal Int Urogynecol J  
  Volume Issue Pages  
  Keywords Anticholinergic drugs; Drug treatment; Epidemiology; Health survey; Prescription patterns; Urinary incontinence  
  Abstract INTRODUCTION AND HYPOTHESIS: The aims of this study were to investigate patterns of prescribing anticholinergic drugs among women with urinary incontinence (UI) and to identify factors associated with prescription of these drugs. METHODS: We analysed questionnaire data on UI from 21,735 women older than 20 years who participated in a cross-sectional population-based study in Nord-Trondelag county, Norway (the HUNT study). These data were linked at the individual level to a national prescription database, and analysed using a multivariate logistic regression model. RESULTS: Among the women with UI, 4.5% had been prescribed an anticholinergic drug during the previous 12 months. Prescription was most frequent in women with urge UI (10.5%) and mixed UI (7.0%). Of women with UI without treatment with an anticholinergic drug, 1.8% obtained such a prescription during the subsequent 12 months, corresponding to 3.1% of women with urge UI and 3.0% of women with mixed UI. Characteristics significantly associated with starting treatment were age above 50 years, urge or mixed UI, severe or very severe symptoms, consumption of four or more cups of coffee per day, and having visited a doctor for UI. No association was found with marital status, parity, smoking, alcohol, body mass index or anxiety/depression. CONCLUSIONS: In this population-based study, 4.5% of women with UI were prescribed an anticholinergic drug, and the 12-month incidence of starting treatment was 1.8%. Age above 50 years, urge or mixed UI, severe symptoms, high coffee consumption and having visited a doctor for UI were factors associated with first-time drug prescription.  
  Address Department of Clinical Pharmacology, St. Olav 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 0937-3462 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:29103164 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1954  
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Author Hellevik, A.I.; Johnsen, M.B.; Langhammer, A.; Fenstad, A.M.; Furnes, O.; Storheim, K.; Zwart, J.A.; Flugsrud, G.; Nordsletten, L. url  doi
  Title (up) Incidence of total hip or knee replacement due to osteoarthritis in relation to thyroid function: a prospective cohort study (The Nord-Trondelag Health Study) Type Journal Article
  Year 2017 Publication BMC Musculoskeletal Disorders Abbreviated Journal BMC Musculoskelet Disord  
  Volume 18 Issue 1 Pages 201  
  Keywords Hip joint replacement; Knee joint replacement; Osteoarthritis; Thyroid function; Thyroid stimulating hormone  
  Abstract BACKGROUND: To study whether thyroid function was associated with risk of hip or knee replacement due to primary osteoarthritis. METHODS: In a prospective cohort study, data from the second and third survey of the Nord-Trondelag Health Study were linked to the Norwegian Arthroplasty Register in order to identify total hip or knee replacement as a result of primary osteoarthritis. RESULTS: Among 37 891 participants without previously known thyroid disease we recorded 978 total hip replacements (THRs) and 538 total knee replacements (TKRs) during a median follow-up time of 15.7 years. The analyses were adjusted for sex, age, BMI (body mass index), smoking, physical activity and diabetes. We did not find any association between TSH (thyroid stimulating hormone) and THR or TKR due to osteoarthritis. Neither were changes in TSH over time, or overt hypo- or hyperthyroidism, associated with incidence of THR or TKR. CONCLUSION: No association was found between thyroid function and hip or knee joint replacement due to osteoarthritis.  
  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 1471-2474 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:28521834; PMCID:PMC5437592 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1924  
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Author Folling, I.S.; Kulseng, B.; Midthjell, K.; Rangul, V.; Helvik, A.-S. url  doi
  Title (up) 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 Sen, A.; Opdahl, S.; Strand, L.B.; Vatten, L.J.; Laugsand, L.E.; Janszky, I. url  doi
  Title (up) Insomnia and the Risk of Breast Cancer: The HUNT Study Type Journal Article
  Year 2017 Publication Psychosomatic Medicine Abbreviated Journal Psychosom Med  
  Volume 79 Issue 4 Pages 461-468  
  Keywords  
  Abstract OBJECTIVE: The association of insomnia with subsequent breast cancer risk is largely unknown. Therefore, we assessed whether different symptoms of insomnia and their combination are associated with incident breast cancer in a large population-based study. METHODS: In a prospective cohort study, 33,332 women were followed to monitor the occurrence of their first invasive breast cancer identified by the Cancer Registry of Norway. Insomnia symptoms including () nonrestorative sleep and () difficulty initiating and () maintaining sleep were self-reported using a study specific measure reflecting the current Diagnostic and Statistical Manual of Mental Disorders criteria. Hazard ratios and 95% confidence intervals were calculated using multiadjusted Cox proportional hazards models. RESULTS: A total of 862 incident breast cancer cases occurred during a mean follow-up of 14.7 years. No consistent association was observed between the individual insomnia symptoms and breast cancer risk. However, compared to women reporting no insomnia complaints, those who reported having all three aspects of insomnia simultaneously were at increased risk (hazard ratio, 2.38; 95% confidence interval = 1.11-5.09). CONCLUSION: Our results suggest that having only some aspects of insomnia may not predispose someone to breast cancer. In contrast, experiencing all insomnia symptoms simultaneously might confer considerable excess risk.  
  Address From the Department of Public Health and General Practice (Sen, Opdahl, Strand, Vatten, Laugsand, Janszky), Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway; Department of Internal Medicine (Laugsand), St. Olav's hospital, Trondheim, Norway; and Department of Public Health Sciences (Janszky), Karolinska Institutet, 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 0033-3174 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:27763987 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1978  
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Author Skaaby, T.; Taylor, A.E.; Jacobsen, R.K.; Paternoster, L.; Thuesen, B.H.; Ahluwalia, T.S.; Larsen, S.C.; Zhou, A.; Wong, A.; Gabrielsen, M.E.; Bjorngaard, J.H.; Flexeder, C.; Mannisto, S.; Hardy, R.; Kuh, D.; Barry, S.J.; Tang Mollehave, L.; Cerqueira, C.; Friedrich, N.; Bonten, T.N.; Noordam, R.; Mook-Kanamori, D.O.; Taube, C.; Jessen, L.E.; McConnachie, A.; Sattar, N.; Upton, M.N.; McSharry, C.; Bonnelykke, K.; Bisgaard, H.; Schulz, H.; Strauch, K.; Meitinger, T.; Peters, A.; Grallert, H.; Nohr, E.A.; Kivimaki, M.; Kumari, M.; Volker, U.; Nauck, M.; Volzke, H.; Power, C.; Hypponen, E.; Hansen, T.; Jorgensen, T.; Pedersen, O.; Salomaa, V.; Grarup, N.; Langhammer, A.; Romundstad, P.R.; Skorpen, F.; Kaprio, J.; R Munafo, M.; Linneberg, A. url  doi
  Title (up) Investigating the causal effect of smoking on hay fever and asthma: a Mendelian randomization meta-analysis in the CARTA consortium Type Journal Article
  Year 2017 Publication Scientific Reports Abbreviated Journal Sci Rep  
  Volume 7 Issue 1 Pages 2224  
  Keywords  
  Abstract Observational studies on smoking and risk of hay fever and asthma have shown inconsistent results. However, observational studies may be biased by confounding and reverse causation. Mendelian randomization uses genetic variants as markers of exposures to examine causal effects. We examined the causal effect of smoking on hay fever and asthma by using the smoking-associated single nucleotide polymorphism (SNP) rs16969968/rs1051730. We included 231,020 participants from 22 population-based studies. Observational analyses showed that current vs never smokers had lower risk of hay fever (odds ratio (OR) = 0.68, 95% confidence interval (CI): 0.61, 0.76; P < 0.001) and allergic sensitization (OR = 0.74, 95% CI: 0.64, 0.86; P < 0.001), but similar asthma risk (OR = 1.00, 95% CI: 0.91, 1.09; P = 0.967). Mendelian randomization analyses in current smokers showed a slightly lower risk of hay fever (OR = 0.958, 95% CI: 0.920, 0.998; P = 0.041), a lower risk of allergic sensitization (OR = 0.92, 95% CI: 0.84, 1.02; P = 0.117), but higher risk of asthma (OR = 1.06, 95% CI: 1.01, 1.11; P = 0.020) per smoking-increasing allele. Our results suggest that smoking may be causally related to a higher risk of asthma and a slightly lower risk of hay fever. However, the adverse events associated with smoking limit its clinical significance.  
  Address Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark  
  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 2045-2322 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:28533558; PMCID:PMC5440386 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1980  
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Author Thorstensen, K.; Kvitland, M.A.; Irgens, W.O.; Asberg, A.; Borch-Iohnsen, B.; Moen, T.; Hveem, K. url  doi
  Title (up) Iron loading in HFE p.C282Y homozygotes found by population screening: relationships to HLA-type and T-lymphocyte subsets Type Journal Article
  Year 2017 Publication Scandinavian Journal of Clinical and Laboratory Investigation Abbreviated Journal Scand J Clin Lab Invest  
  Volume 77 Issue 7 Pages 477-485  
  Keywords Hla-A*03; Haplotypes; Mhc; homozygote; iron overload  
  Abstract Iron loading in p.C282Y homozygous HFE hemochromatosis subjects is highly variable, and it is unclear what factors cause this variability. Finding such factors could aid in predicting which patients are at highest risk and require closest follow-up. The degree of iron loading has previously been associated with certain HLA-types and with abnormally low CD8 + cell counts in peripheral blood. In 183 Norwegian, p.C282Y homozygotes (104 men, 79 women) originally found through population screening we determined HLA type and measured total T-lymphocytes, CD4 + and CD8 + cells, and compared this with data on iron loading. In p.C282Y homozygous men, but not in homozygous women, we found that the presence of two HLA-A*03 alleles increased the iron load on average by approximately 2-fold compared to p.C282Y homozygous men carrying zero or one A*03 allele. On the other hand, the presence of two HLA-A*01 alleles, in male subjects, apparently reduced the iron loading. In p.C282Y homozygous individuals, the iron loading was increased if the CD8 + cell number was below the 25 percentile or if the CD4 + cell number was above the 75 percentile. This effect appeared to be additive to the effect of the number of HLA-A*03 alleles. Our data indicate that homozygosity for the HLA-A*03 allele significantly increases the risk of excessive iron loading in Norwegian p.C282Y homozygous male patients. In addition, low CD8 + cell number or high CD4 + cell number further increases the risk of excessive iron loading.  
  Address d HUNT Research Centre, Department of Public Health and General Practice, Faculty of Medicine , Norwegian University of Science and Technology , Trondheim , Norway  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0036-5513 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:28678636 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 2013  
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Author Andre, B.; Canhao, H.; Espnes, G.A.; Ferreira Rodrigues, A.M.; Gregorio, M.J.; Nguyen, C.; Sousa, R.; Gronning, K. url  doi
  Title (up) Is there an association between food patterns and life satisfaction among Norway's inhabitants ages 65 years and older? Type Journal Article
  Year 2017 Publication Appetite Abbreviated Journal Appetite  
  Volume 110 Issue Pages 108-115  
  Keywords Anxiety; Depression; Elderly adults; Food patterns; Life satisfaction  
  Abstract The lack of information regarding older adults' health and lifestyles makes it difficult to design suitable interventions for people at risk of developing unhealth lifestyles. Therefore, there is a need to increase knowledge about older adults' food patterns and quality of life. Our aim was to determine associations among food patterns, anxiety, depression, and life satisfaction in Norwegian inhabitants ages 65+. The Nord-Trondelag Health Study (The HUNT Study) is a large, population-based cohort study that includes data for 125 000 Norwegian participants. The cohort used for this study is wave three of the study, consisting of 11 619 participants age 65 and over. Cluster analysis was used to categorize the participants based on similarities in food consumption; two clusters were identified based on similarities regarding food consumption among participants. Significant differences between the clusters were found, as participants in the healthy food-patterns cluster had higher life satisfaction and lower anxiety and depression than those in the unhealthy food-patterns cluster. The associations among food patterns, anxiety, depression, and life satisfaction among older adults show the need for increased focus on interactions among food patterns, food consumption, and life satisfaction among the elderly in order to explore how society can influence these patterns.  
  Address Faculty of Medicine and Health Sciences, Department of Public Health and Nursing, Norwegian University of Science and Technology (NTNU), Norway; NTNU Center for Health Promotion Research, Norway  
  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 0195-6663 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:27988367 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1878  
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Author Heuch, I.; Heuch, I.; Hagen, K.; Mai, X.-M.; Langhammer, A.; Zwart, J.-A. url  doi