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Your search keyword '"Witte, D. R."' showing total 121 results
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121 results on '"Witte, D. R."'

5. Exome sequencing-driven discovery of coding polymorphisms associated with common metabolic phenotypes

Author

Albrechtsen, A., Grarup, N., Li, Y., Sparsø, T., Tian, G., Cao, H., Jiang, T., Kim, S. Y., Korneliussen, T., Li, Q., Nie, C., Wu, R., Skotte, L., Morris, A. P., Ladenvall, C., Cauchi, S., Stančáková, A., Andersen, G., Astrup, A., Banasik, K., Bennett, A. J., Bolund, L., Charpentier, G., Chen, Y., Dekker, J. M., Doney, A. S. F., Dorkhan, M., Forsen, T., Frayling, T. M., Groves, C. J., Gui, Y., Hallmans, G., Hattersley, A. T., He, K., Hitman, G. A., Holmkvist, J., Huang, S., Jiang, H., Jin, X., Justesen, J. M., Kristiansen, K., Kuusisto, J., Lajer, M., Lantieri, O., Li, W., Liang, H., Liao, Q., Liu, X., Ma, T., Ma, X., Manijak, M. P., Marre, M., Mokrosiński, J., Morris, A. D., Mu, B., Nielsen, A. A., Nijpels, G., Nilsson, P., Palmer, C. N. A., Rayner, N. W., Renström, F., Ribel-Madsen, R., Robertson, N., Rolandsson, O., Rossing, P., Schwartz, T. W., Slagboom, P. E., Sterner, M., Tang, M., Tarnow, L., Tuomi, T., van’t Riet, E., van Leeuwen, N., Varga, T. V., Vestmar, M. A., Walker, M., Wang, B., Wang, Y., Wu, H., Xi, F., Yengo, L., Yu, C., Zhang, X., Zhang, J., Zhang, Q., Zhang, W., Zheng, H., Zhou, Y., Altshuler, D., ‘t Hart, L. M., Franks, P. W., Balkau, B., Froguel, P., McCarthy, M. I., Laakso, M., Groop, L., Christensen, C., Brandslund, I., Lauritzen, T., Witte, D. R., Linneberg, A., Jørgensen, T., Hansen, T., Wang, J., Nielsen, R., Pedersen, O., D.E.S.I.R. Study Group, and the DIAGRAM Consortium

Published
2013
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10. Homozygous carriers of the G allele of rs4664447 of the glucagon gene (GCG) are characterised by decreased fasting and stimulated levels of insulin, glucagon and glucagon-like peptide (GLP)-1

Author

Torekov, S. S., Ma, L., Grarup, N., Hartmann, B., Hainerová, I. A., Kielgast, U., Kissow, H., Rosenkilde, M., Lebl, J., Witte, D. R., Jørgensen, T., Sandbaek, A., Lauritzen, T., Madsen, O. D., Wang, J., Linneberg, A., Madsbad, S., Holst, J. J., Hansen, T., Pedersen, O., and GIANT Consortium

Published
2011
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19. Sex-specific effects of naturally occurring variants in the dopamine receptor D2 locus on insulin secretion and Type 2 diabetes susceptibility

Author

Guigas, B., de Leeuw van Weenen, J. E., van Leeuwen, N., Simonis-Bik, A. M., van Haeften, T. W., Nijpels, G., Houwing-Duistermaat, J. J., Beekman, M., Deelen, J., Havekes, L. M., Penninx, B. W. J. H., Vogelzangs, N., van ‘t Riet, E., Dehghan, A., Hofman, A., Witteman, J. C., Uitterlinden, A. G., Grarup, N., Jrgensen, T., Witte, D. R., Lauritzen, T., Hansen, T., Pedersen, O., Hottenga, J., Romijn, J. A., Diamant, M., Kramer, M. H. H., Heine, R. J., Willemsen, G., Dekker, J. M., Eekhoff, E. M., Pijl, H., de Geus, E. J., Slagboom, P. E., and ‘t Hart, L. M.

Published
2014
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20. Research: Educational and psychological aspects Patient-reported outcomes after 10-year follow-up of intensive, multifactorial treatment in individuals with screen-detected type 2 diabetes: the ADDITION-Europe trial

Author

Dalsgaard, E.-M., Sandbæk, A., Griffin, S. J., Rutten, G. E. H. M., Khunti, K., Davies, M. J., Irving, G. J., Vos, R. C., Webb, D. R., Wareham, N. J., and Witte, D. R.

Subjects
Glycated Hemoglobin, Male, Health Status, Blood Pressure, Middle Aged, Article, Patient Care Planning, Cholesterol, Mental Health, Diabetes Mellitus, Type 2, Patient Satisfaction, Quality of Life, Humans, Hypoglycemic Agents, Mass Screening, Female, Patient Reported Outcome Measures, Aged, Follow-Up Studies
Abstract

AIMS: To present the longer-term impact of multifactorial treatment of type 2 diabetes on self-reported health status, diabetes-specific quality of life, and diabetes treatment satisfaction at 10-year follow up of the ADDITION-Europe trial. METHODS: The ADDITION-Europe trial enrolled 3057 individuals with screen-detected type 2 diabetes from four centres [Denmark, the UK (Cambridge and Leicester) and the Netherlands], between 2001 and 2006. Participants were randomized at general practice level to intensive treatment or to routine care . The trial ended in 2009 and a 10-year follow-up was performed at the end of 2014. We measured self-reported health status (36-item Short-Form Health Survey and EQ-5D), diabetes-specific quality of life (Audit of Diabetes-Dependent Quality of Life questionnaire), and diabetes treatment satisfaction (Diabetes Treatment Satisfaction Questionnaire) at different time points during the study period. A mixed-effects model was applied to estimate the effect of intensive treatment (intention-to-treat analyses) on patient-reported outcome measures for each centre. Centre-specific estimates were pooled using a fixed effects meta-analysis. RESULTS: There was no difference in patient-reported outcome measures between the routine care and intensive treatment arms in this 10-year follow-up study [EQ-5D: –0.01 (95% CI – 0.03, 0.01); Physical Composite Score (36-item Short-Form Health Survey): –0.27 (95% CI – 1.11, 0.57), Audit of Diabetes-Dependent Quality of Life questionnaire: –0.01 (95% CI –0.11, 0.10); and Diabetes Treatment Satisfaction Questionnaire: –0.20 (95% CI –0.70, 0.29)]. CONCLUSIONS: Intensive, multifactorial treatment of individuals with screen-detected type 2 diabetes did not affect self-reported health status, diabetes-specific quality of life, or diabetes treatment satisfaction at 10-year follow-up compared to routine care.

Published
2020

24. Publisher Correction: Protein-altering variants associated with body mass index implicate pathways that control energy intake and expenditure in obesity (Nature Genetics, (2018), 50, 1, (26-41), 10.1038/s41588-017-0011-x)

Author

Turcot, V., Lu, Y., Highland, H. M., Schurmann, C., Justice, A. E., Fine, R. S., Bradfield, J. P., Esko, T., Giri, A., Graff, M., Guo, X., Hendricks, A. E., Karaderi, T., Lempradl, A., Locke, A. E., Mahajan, A., Marouli, E., Sivapalaratnam, S., Young, K. L., Alfred, T., Feitosa, M. F., Masca, N. G. D., Manning, A. K., Medina-Gomez, C., Mudgal, P., M. C. Y., Ng, Reiner, A. P., Vedantam, S., Willems, S. M., Winkler, T. W., Abecasis, G., Aben, K. K., Alam, D. S., Alharthi, S. E., Marchiori, Allison, Amouyel, P., Asselbergs, F. W., Auer, P. L., Balkau, B., Bang, L. E., Barroso, I., Bastarache, L., Benn, M., Bergmann, S., Bielak, L. F., Bluher, M., Boehnke, M., Boeing, H., Boerwinkle, E., Boger, C. A., Bork-Jensen, J., Bots, M. L., Bottinger, E. P., Bowden, D. W., Brandslund, I., Breen, G., Brilliant, M. H., Broer, L., Brumat, M., Burt, A. A., Butterworth, A. S., Campbell, P. T., Cappellani, S., Carey, D. J., Catamo, E., Caulfield, M. J., Chambers, J. C., Chasman, D. I., Chen, Y. -D. I., Chowdhury, R., Christensen, C., Chu, A. Y., Cocca, M., Collins, F. S., Cook, J. P., Corley, J., Galbany, J. C., Cox, A. J., Crosslin, D. S., Cuellar-Partida, G., D'Eustacchio, A., Danesh, J., Davies, G., Bakker, P. I. W., Groot, M. C. H., Mutsert, R., Deary, I. J., Dedoussis, G., Demerath, E. W., Heijer, M., Hollander, A. I., Ruijter, H. M., Dennis, J. G., Denny, J. C., Di Angelantonio, E., Drenos, F., Du, M., Dube, M. -P., Dunning, A. M., Easton, D. F., Edwards, T. L., Ellinghaus, D., Ellinor, P. T., Elliott, P., Evangelou, E., Farmaki, A. -E., Farooqi, I. S., Faul, J. D., Fauser, S., Feng, S., Ferrannini, E., Ferrieres, J., Florez, J. C., Ford, I., Fornage, M., Franco, O. H., Franke, A., Franks, P. W., Friedrich, N., Frikke-Schmidt, R., Galesloot, T. E., Gan, W., Gandin, I., Gasparini, P., Gibson, J., Giedraitis, V., Gjesing, A. P., Gordon-Larsen, P., Gorski, M., Grabe, H. -J., Grant, S. F. A., Grarup, N., Griffiths, H. L., Grove, M. L., Gudnason, V., Gustafsson, S., Haessler, J., Hakonarson, H., Hammerschlag, A. R., Hansen, T., Harris, K. M., Harris, T. B., Hattersley, A. T., Have, C. T., Hayward, C., He, L., Heard-Costa, N. L., Heath, A. C., Heid, I. M., Helgeland, O., Hernesniemi, J., Hewitt, A. W., Holmen, O. L., Hovingh, G. K., Howson, J. M. M., Hu, Y., Huang, P. L., Huffman, J. E., Ikram, M. A., Ingelsson, E., Jackson, A. U., Jansson, J. -H., Jarvik, G. P., Jensen, G. B., Jia, Y., Johansson, S., Jorgensen, M. E., Jorgensen, T., Jukema, J. W., Kahali, B., Kahn, R. S., Kahonen, M., Kamstrup, P. R., Kanoni, S., Kaprio, J., Karaleftheri, M., Kardia, S. L. R., Karpe, F., Kathiresan, S., Kee, F., Kiemeney, L. A., Kim, E., Kitajima, H., Komulainen, P., Kooner, J. S., Kooperberg, C., Korhonen, T., Kovacs, P., Kuivaniemi, H., Kutalik, Z., Kuulasmaa, K., Kuusisto, J., Laakso, M., Lakka, T. A., Lamparter, D., Lange, E. M., Lange, L. A., Langenberg, C., Larson, E. B., Lee, N. R., Lehtimaki, T., Lewis, C. E., Li, H., Li, J., Li-Gao, R., Lin, H., Lin, K. -H., Lin, L. -A., Lin, X., Lind, L., Lindstrom, J., Linneberg, A., Liu, C. -T., Liu, D. J., Liu, Y., K. S., Lo, Lophatananon, A., Lotery, A. J., Loukola, A., Luan, J., Lubitz, S. A., Lyytikainen, L. -P., Mannisto, S., Marenne, G., Mazul, A. L., Mccarthy, M. I., McKean-Cowdin, R., Medland, S. E., Meidtner, K., Milani, L., Mistry, V., Mitchell, P., Mohlke, K. L., Moilanen, L., Moitry, M., Montgomery, G. W., Mook-Kanamori, D. O., Moore, C., Mori, T. A., Morris, A. D., Morris, A. P., Muller-Nurasyid, M., Munroe, P. B., Nalls, M. A., Narisu, N., Nelson, C. P., Neville, M., Nielsen, S. F., Nikus, K., Njolstad, P. R., Nordestgaard, B. G., Nyholt, D. R., O'Connel, J. R., O'Donoghue, M. L., Loohuis, L. M. O., Ophoff, R. A., Owen, K. R., Packard, C. J., Padmanabhan, S., Palmer, C. N. A., Palmer, N. D., Pasterkamp, G., Patel, A. P., Pattie, A., Pedersen, O., Peissig, P. L., Peloso, G. M., Pennell, C. E., Perola, M., Perry, J. A., Perry, J. R. B., Pers, T. H., Person, T. N., Peters, A., Petersen, E. R. B., Peyser, P. A., Pirie, A., Polasek, O., Polderman, T. J., Puolijoki, H., Raitakari, O. T., Rasheed, A., Rauramaa, R., Reilly, D. F., Renstrom, F., Rheinberger, M., Ridker, P. M., Rioux, J. D., Rivas, M. A., Roberts, D. J., Robertson, N. R., Robino, A., Rolandsson, O., Rudan, I., Ruth, K. S., Saleheen, D., Salomaa, V., Samani, N. J., Sapkota, Y., Sattar, N., Schoen, R. E., Schreiner, P. J., Schulze, M. B., Scott, R. A., Segura-Lepe, M. P., Shah, S. H., Sheu, W. H. -H., Sim, X., Slater, A. J., Small, K. S., Smith, A. V., Southam, L., Spector, T. D., Speliotes, E. K., Starr, J. M., Stefansson, K., Steinthorsdottir, V., Stirrups, K. E., Strauch, K., Stringham, H. M., Stumvoll, M., Sun, L., Surendran, P., Swift, A. J., Tada, H., Tansey, K. E., Tardif, J. -C., Taylor, K. D., Teumer, A., Thompson, D. J., Thorleifsson, G., Thorsteinsdottir, U., Thuesen, B. H., Tonjes, A., Tromp, G., Trompet, S., Tsafantakis, E., Tuomilehto, J., Tybjaerg-Hansen, A., Tyrer, J. P., Uher, R., Uitterlinden, A. G., Uusitupa, M., Laan, S. W., Duijn, C. M., Leeuwen, N., van Setten, J., Vanhala, M., Varbo, A., Varga, T. V., Varma, R., Edwards, D. R. V., Vermeulen, S. H., Veronesi, G., Vestergaard, H., Vitart, V., Vogt, T. F., Volker, U., Vuckovic, D., Wagenknecht, L. E., Walker, M., Wallentin, L., Wang, F., Wang, C. A., Wang, S., Wang, Y., Ware, E. B., Wareham, N. J., Warren, H. R., Waterworth, D. M., Wessel, J., White, H. D., Willer, C. J., Wilson, J. G., Witte, D. R., Wood, A. R., Wu, Y., Yaghootkar, H., Yao, J., Yao, P., Yerges-Armstrong, L. M., Young, R., Zeggini, E., Zhan, X., Zhang, W., Zhao, J. H., Zhao, W., Zhou, W., Zondervan, K. T., Rotter, J. I., Pospisilik, J. A., Rivadeneira, F., Borecki, I. B., Deloukas, P., Frayling, T. M., Lettre, G., North, K. E., Lindgren, C. M., Hirschhorn, J. N., Loos, R. J. F., Turcot, V., Lu, Y., Highland, H. M., Schurmann, C., Justice, A. E., Fine, R. S., Bradfield, J. P., Esko, T., Giri, A., Graff, M., Guo, X., Hendricks, A. E., Karaderi, T., Lempradl, A., Locke, A. E., Mahajan, A., Marouli, E., Sivapalaratnam, S., Young, K. L., Alfred, T., Feitosa, M. F., Masca, N. G. D., Manning, A. K., Medina-Gomez, C., Mudgal, P., Ng, M. C. Y., Reiner, A. P., Vedantam, S., Willems, S. M., Winkler, T. W., Abecasis, G., Aben, K. K., Alam, D. S., Alharthi, S. E., Marchiori, Allison, Amouyel, P., Asselbergs, F. W., Auer, P. L., Balkau, B., Bang, L. E., Barroso, I., Bastarache, L., Benn, M., Bergmann, S., Bielak, L. F., Bluher, M., Boehnke, M., Boeing, H., Boerwinkle, E., Boger, C. A., Bork-Jensen, J., Bots, M. L., Bottinger, E. P., Bowden, D. W., Brandslund, I., Breen, G., Brilliant, M. H., Broer, L., Brumat, M., Burt, A. A., Butterworth, A. S., Campbell, P. T., Cappellani, S., Carey, D. J., Catamo, E., Caulfield, M. J., Chambers, J. C., Chasman, D. I., Chen, Y. -D. I., Chowdhury, R., Christensen, C., Chu, A. Y., Cocca, M., Collins, F. S., Cook, J. P., Corley, J., Galbany, J. C., Cox, A. J., Crosslin, D. S., Cuellar-Partida, G., D'Eustacchio, A., Danesh, J., Davies, G., Bakker, P. I. W., Groot, M. C. H., Mutsert, R., Deary, I. J., Dedoussis, G., Demerath, E. W., Heijer, M., Hollander, A. I., Ruijter, H. M., Dennis, J. G., Denny, J. C., Di Angelantonio, E., Drenos, F., Du, M., Dube, M. -P., Dunning, A. M., Easton, D. F., Edwards, T. L., Ellinghaus, D., Ellinor, P. T., Elliott, P., Evangelou, E., Farmaki, A. -E., Farooqi, I. S., Faul, J. D., Fauser, S., Feng, S., Ferrannini, E., Ferrieres, J., Florez, J. C., Ford, I., Fornage, M., Franco, O. H., Franke, A., Franks, P. W., Friedrich, N., Frikke-Schmidt, R., Galesloot, T. E., Gan, W., Gandin, I., Gasparini, P., Gibson, J., Giedraitis, V., Gjesing, A. P., Gordon-Larsen, P., Gorski, M., Grabe, H. -J., Grant, S. F. A., Grarup, N., Griffiths, H. L., Grove, M. L., Gudnason, V., Gustafsson, S., Haessler, J., Hakonarson, H., Hammerschlag, A. R., Hansen, T., Harris, K. M., Harris, T. B., Hattersley, A. T., Have, C. T., Hayward, C., He, L., Heard-Costa, N. L., Heath, A. C., Heid, I. M., Helgeland, O., Hernesniemi, J., Hewitt, A. W., Holmen, O. L., Hovingh, G. K., Howson, J. M. M., Hu, Y., Huang, P. L., Huffman, J. E., Ikram, M. A., Ingelsson, E., Jackson, A. U., Jansson, J. -H., Jarvik, G. P., Jensen, G. B., Jia, Y., Johansson, S., Jorgensen, M. E., Jorgensen, T., Jukema, J. W., Kahali, B., Kahn, R. S., Kahonen, M., Kamstrup, P. R., Kanoni, S., Kaprio, J., Karaleftheri, M., Kardia, S. L. R., Karpe, F., Kathiresan, S., Kee, F., Kiemeney, L. A., Kim, E., Kitajima, H., Komulainen, P., Kooner, J. S., Kooperberg, C., Korhonen, T., Kovacs, P., Kuivaniemi, H., Kutalik, Z., Kuulasmaa, K., Kuusisto, J., Laakso, M., Lakka, T. A., Lamparter, D., Lange, E. M., Lange, L. A., Langenberg, C., Larson, E. B., Lee, N. R., Lehtimaki, T., Lewis, C. E., Li, H., Li, J., Li-Gao, R., Lin, H., Lin, K. -H., Lin, L. -A., Lin, X., Lind, L., Lindstrom, J., Linneberg, A., Liu, C. -T., Liu, D. J., Liu, Y., Lo, K. S., Lophatananon, A., Lotery, A. J., Loukola, A., Luan, J., Lubitz, S. A., Lyytikainen, L. -P., Mannisto, S., Marenne, G., Mazul, A. L., Mccarthy, M. I., McKean-Cowdin, R., Medland, S. E., Meidtner, K., Milani, L., Mistry, V., Mitchell, P., Mohlke, K. L., Moilanen, L., Moitry, M., Montgomery, G. W., Mook-Kanamori, D. O., Moore, C., Mori, T. A., Morris, A. D., Morris, A. P., Muller-Nurasyid, M., Munroe, P. B., Nalls, M. A., Narisu, N., Nelson, C. P., Neville, M., Nielsen, S. F., Nikus, K., Njolstad, P. R., Nordestgaard, B. G., Nyholt, D. R., O'Connel, J. R., O'Donoghue, M. L., Loohuis, L. M. O., Ophoff, R. A., Owen, K. R., Packard, C. J., Padmanabhan, S., Palmer, C. N. A., Palmer, N. D., Pasterkamp, G., Patel, A. P., Pattie, A., Pedersen, O., Peissig, P. L., Peloso, G. M., Pennell, C. E., Perola, M., Perry, J. A., Perry, J. R. B., Pers, T. H., Person, T. N., Peters, A., Petersen, E. R. B., Peyser, P. A., Pirie, A., Polasek, O., Polderman, T. J., Puolijoki, H., Raitakari, O. T., Rasheed, A., Rauramaa, R., Reilly, D. F., Renstrom, F., Rheinberger, M., Ridker, P. M., Rioux, J. D., Rivas, M. A., Roberts, D. J., Robertson, N. R., Robino, A., Rolandsson, O., Rudan, I., Ruth, K. S., Saleheen, D., Salomaa, V., Samani, N. J., Sapkota, Y., Sattar, N., Schoen, R. E., Schreiner, P. J., Schulze, M. B., Scott, R. A., Segura-Lepe, M. P., Shah, S. H., Sheu, W. H. -H., Sim, X., Slater, A. J., Small, K. S., Smith, A. V., Southam, L., Spector, T. D., Speliotes, E. K., Starr, J. M., Stefansson, K., Steinthorsdottir, V., Stirrups, K. E., Strauch, K., Stringham, H. M., Stumvoll, M., Sun, L., Surendran, P., Swift, A. J., Tada, H., Tansey, K. E., Tardif, J. -C., Taylor, K. D., Teumer, A., Thompson, D. J., Thorleifsson, G., Thorsteinsdottir, U., Thuesen, B. H., Tonjes, A., Tromp, G., Trompet, S., Tsafantakis, E., Tuomilehto, J., Tybjaerg-Hansen, A., Tyrer, J. P., Uher, R., Uitterlinden, A. G., Uusitupa, M., Laan, S. W., Duijn, C. M., Leeuwen, N., van Setten, J., Vanhala, M., Varbo, A., Varga, T. V., Varma, R., Edwards, D. R. V., Vermeulen, S. H., Veronesi, G., Vestergaard, H., Vitart, V., Vogt, T. F., Volker, U., Vuckovic, D., Wagenknecht, L. E., Walker, M., Wallentin, L., Wang, F., Wang, C. A., Wang, S., Wang, Y., Ware, E. B., Wareham, N. J., Warren, H. R., Waterworth, D. M., Wessel, J., White, H. D., Willer, C. J., Wilson, J. G., Witte, D. R., Wood, A. R., Wu, Y., Yaghootkar, H., Yao, J., Yao, P., Yerges-Armstrong, L. M., Young, R., Zeggini, E., Zhan, X., Zhang, W., Zhao, J. H., Zhao, W., Zhou, W., Zondervan, K. T., Rotter, J. I., Pospisilik, J. A., Rivadeneira, F., Borecki, I. B., Deloukas, P., Frayling, T. M., Lettre, G., North, K. E., Lindgren, C. M., Hirschhorn, J. N., and Loos, R. J. F.

Subjects
Publisher correction
Abstract

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Published
2019

30. Discovery of rare variants associated with blood pressure regulation through meta-analysis of 1.3 million individuals

Author

Surendran, P., Feofanova, E. V., Lahrouchi, N., Ntalla, I., Karthikeyan, S., Cook, J., Chen, L., Mifsud, B., Yao, C., Kraja, A. T., Cartwright, J. H., Hellwege, J. N., Giri, A., Tragante, V., Thorleifsson, G., Liu, D. J., Prins, B. P., Stewart, I. D., Cabrera, C. P., Eales, J. M., Akbarov, A., Auer, P. L., Bielak, L. F., Bis, J. C., Braithwaite, V. S., Brody, J. A., Daw, E. W., Warren, H. R., Drenos, F., Nielsen, S. F., Faul, J. D., Fauman, E. B., Fava, C., Ferreira, T., Foley, C. N., Franceschini, N., Gao, H., Giannakopoulou, O., Giulianini, F., Gudbjartsson, D. F., Guo, X., Harris, S. E., Havulinna, A. S., Helgadottir, A., Huffman, J. E., Hwang, S. -J., Kanoni, S., Kontto, J., Larson, M. G., Li-Gao, R., Lindstrom, J., Lotta, L. A., Lu, Y., Luan, J., Mahajan, A., Malerba, G., Masca, N. G. D., Mei, H., Menni, C., Mook-Kanamori, D. O., Mosen-Ansorena, D., Muller-Nurasyid, M., Pare, G., Paul, D. S., Perola, M., Poveda, A., Rauramaa, R., Richard, M., Richardson, T. G., Sepulveda, N., Sim, X., Smith, A. V., Smith, J. A., Staley, J. R., Stanakova, A., Sulem, P., Theriault, S., Thorsteinsdottir, U., Trompet, S., Varga, T. V., Velez Edwards, D. R., Veronesi, G., Weiss, S., Willems, S. M., Yao, J., Young, R., Yu, B., Zhang, W., Zhao, J. -H., Zhao, W., Evangelou, E., Aeschbacher, S., Asllanaj, E., Blankenberg, S., Bonnycastle, L. L., Bork-Jensen, J., Brandslund, I., Braund, P. S., Burgess, S., Cho, K., Christensen, C., Connell, J., Mutsert, R., Dominiczak, A. F., Dorr, M., Eiriksdottir, G., Farmaki, A. -E., Gaziano, J. M., Grarup, N., Grove, M. L., Hallmans, G., Hansen, T., Have, C. T., Heiss, G., Jorgensen, M. E., Jousilahti, P., Kajantie, E., Kamat, M., Karajamaki, A. M., Karpe, F., Koistinen, H. A., Kovesdy, C. P., Kuulasmaa, K., Laatikainen, T., Lannfelt, L., Lee, I. -T., Lee, W. -J., de Boer, R. A., van der Harst, P., van der Meer, P., Verweij, N., Linneberg, A., Martin, L. W., Moitry, M., Nadkarni, G., Neville, M. J., Palmer, C. N. A., Papanicolaou, G. J., Pedersen, O., Peters, J., Poulter, N., Rasheed, A., Rasmussen, K. L., Rayner, N. W., Magi, R., Renstrom, F., Rettig, R., Rossouw, J., Schreiner, P. J., Sever, P. S., Sigurdsson, E. L., Skaaby, T., Sun, Y. V., Sundstrom, J., Thorgeirsson, G., Esko, T., Trabetti, E., Tsao, P. S., Tuomi, T., Turner, S. T., Tzoulaki, I., Vaartjes, I., Vergnaud, A. -C., Willer, C. J., Wilson, P. W. F., Witte, D. R., Yonova-Doing, E., Zhang, H., Aliya, N., Almgren, P., Amouyel, P., Asselbergs, F. W., Barnes, M. R., Blakemore, A. I., Boehnke, M., Bots, M. L., Bottinger, E. P., Buring, J. E., Chambers, J. C., Chen, Y. -D. I., Chowdhury, R., Conen, D., Correa, A., Davey Smith, G., Boer, R. A., Deary, I. J., Dedoussis, G., Deloukas, P., Di Angelantonio, E., Elliott, P., Butterworth, A. S., Danesh, J., Langenberg, C., Mccarthy, M. I., Franks, P. W., Rolandsson, O., Wareham, N. J., Felix, S. B., Ferrieres, J., Ford, I., Fornage, M., Franks, S., Frossard, P., Gambaro, G., Gaunt, T. R., Groop, L., Gudnason, V., Harris, T. B., Hayward, C., Hennig, B. J., Herzig, K. -H., Ingelsson, E., Tuomilehto, J., Jarvelin, M. -R., Jukema, J. W., Kardia, S. L. R., Kee, F., Kooner, J. S., Kooperberg, C., Launer, L. J., Lind, L., Loos, R. J. F., Majumder, A. S., Laakso, M., Melander, O., Mohlke, K. L., Murray, A. D., Nordestgaard, B. G., Orho-Melander, M., Packard, C. J., Padmanabhan, S., Palmas, W., Polasek, O., Porteous, D. J., Prentice, A. M., Province, M. A., Relton, C. L., Rice, K., Ridker, P. M., Rosendaal, F. R., Rotter, J. I., Rudan, I., Salomaa, V., Samani, N. J., Sattar, N., Sheu, W. H. -H., Smith, B. H., Soranzo, N., Spector, T. D., Starr, J. M., Sebert, S., Taylor, K. D., Lakka, T. A., Timpson, N. J., Tobin, M. D., Zeggini, E., Ramachandran, V. S., Virtamo, J., Volker, U., Weir, D. R., Charchar, F. J., Edwards, D. R. V., Edwards, T. L., Hung, A. M., O'Donnell, C. J., Tomaszewski, M., Caulfield, M. J., Holm, H., Lindgren, C. M., Liu, C., Manning, A. K., Morris, A. P., Morrison, A. C., Psaty, B. M., Saleheen, D., Stefansson, K., Boerwinkle, E., Chasman, D. I., Levy, D., Newton-Cheh, C., Munroe, P. B., Howson, J. M. M., Home Office, Imperial College Healthcare NHS Trust- BRC Funding, Medical Research Council (MRC), UNIVERSITY OF OULU, Epidemiology, Complex Disease Genetics, Research Programs Unit, CAMM - Research Program for Clinical and Molecular Metabolism, Faculty of Medicine, University of Helsinki, HUS Children and Adolescents, Lastentautien yksikkö, Clinicum, Children's Hospital, Helsinki University Hospital Area, HUS Internal Medicine and Rehabilitation, Department of Medicine, Department of Biochemistry and Developmental Biology, Centre of Excellence in Complex Disease Genetics, HUS Abdominal Center, Institute for Molecular Medicine Finland, Endokrinologian yksikkö, Department of Public Health, Cardiovascular Centre (CVC), Restoring Organ Function by Means of Regenerative Medicine (REGENERATE), Feofanova, Elena V [0000-0003-1428-7199], Chasman, Daniel I [0000-0003-3357-0862], Munroe, Patricia B [0000-0002-4176-2947], Howson, Joanna MM [0000-0001-7618-0050], Apollo - University of Cambridge Repository, Cardiology, and ACS - Heart failure & arrhythmias

Subjects
Candidate gene, Blood Pressure, GATA5 Transcription Factor, Gene Frequency, Genetic Predisposition to Disease, Genome-Wide Association Study, Genotype, Humans, Hypertension, Mutation, Phospholipase C beta, Polymorphism, Single Nucleotide, LOCI, Genome-wide association study, 0302 clinical medicine, Polymorphism (computer science), genetics, GENOME-WIDE ASSOCIATION, MENDELIAN RANDOMIZATION, COMMON VARIANTS, IDENTIFIES COMMON, RISK, FREQUENCY, TRAITS, HYPERTENSION, GENETICS, EPIC-CVD, 11 Medical and Health Sciences, health care economics and organizations, Genetics & Heredity, Genetics, 0303 health sciences, Million Veteran Program, 1184 Genetics, developmental biology, physiology, Single Nucleotide, humanities, 3. Good health, genetic association study, EPIC-InterAct, epidemiology, Life Sciences & Biomedicine, Understanding Society Scientific Group, hypertension, education, Biology, Article, 03 medical and health sciences, Mendelian randomization, Polymorphism, Allele frequency, Gene, 030304 developmental biology, Science & Technology, 06 Biological Sciences, meta-analysis, Minor allele frequency, genome-wide association studies, 3111 Biomedicine, 030217 neurology & neurosurgery, LifeLines Cohort Study, Developmental Biology
Abstract

Genetic studies of blood pressure (BP) to date have mainly analyzed common variants (minor allele frequency > 0.05). In a meta-analysis of up to ~1.3 million participants, we discovered 106 new BP-associated genomic regions and 87 rare (minor allele frequency ≤ 0.01) variant BP associations (P

Published
2020
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38. Patient‐reported outcomes after 10‐year follow‐up of intensive, multifactorial treatment in individuals with screen‐detected type 2 diabetes: the ADDITION‐Europe trial.

Author

Dalsgaard, E.‐M., Sandbæk, A., Griffin, S. J., Rutten, G. E. H. M., Khunti, K., Davies, M. J., Irving, G. J., Vos, R. C., Webb, D. R., Wareham, N. J., and Witte, D. R.

Subjects
ATTITUDE (Psychology), CONFIDENCE intervals, HEALTH status indicators, HEALTH surveys, META-analysis, TYPE 2 diabetes, HEALTH outcome assessment, PATIENT satisfaction, QUALITY of life, QUESTIONNAIRES, SELF-evaluation, THERAPEUTICS, TREATMENT effectiveness, DESCRIPTIVE statistics
Abstract

Aims: To present the longer‐term impact of multifactorial treatment of type 2 diabetes on self‐reported health status, diabetes‐specific quality of life, and diabetes treatment satisfaction at 10‐year follow up of the ADDITION‐Europe trial. Methods: The ADDITION‐Europe trial enrolled 3057 individuals with screen‐detected type 2 diabetes from four centres [Denmark, the UK (Cambridge and Leicester) and the Netherlands], between 2001 and 2006. Participants were randomized at general practice level to intensive treatment or to routine care. The trial ended in 2009 and a 10‐year follow‐up was performed at the end of 2014. We measured self‐reported health status (36‐item Short‐Form Health Survey and EQ‐5D), diabetes‐specific quality of life (Audit of Diabetes‐Dependent Quality of Life questionnaire), and diabetes treatment satisfaction (Diabetes Treatment Satisfaction Questionnaire) at different time points during the study period. A mixed‐effects model was applied to estimate the effect of intensive treatment (intention‐to‐treat analyses) on patient‐reported outcome measures for each centre. Centre‐specific estimates were pooled using a fixed effects meta‐analysis. Results: There was no difference in patient‐reported outcome measures between the routine care and intensive treatment arms in this 10‐year follow‐up study [EQ‐5D: –0.01 (95% CI –0.03, 0.01); Physical Composite Score (36‐item Short‐Form Health Survey): –0.27 (95% CI –1.11, 0.57), Audit of Diabetes‐Dependent Quality of Life questionnaire: –0.01 (95% CI –0.11, 0.10); and Diabetes Treatment Satisfaction Questionnaire: –0.20 (95% CI –0.70, 0.29)]. Conclusions: Intensive, multifactorial treatment of individuals with screen‐detected type 2 diabetes did not affect self‐reported health status, diabetes‐specific quality of life, or diabetes treatment satisfaction at 10‐year follow‐up compared to routine care. What's new?: The burden of diabetes and its treatment may cause psychosocial stress.Good metabolic control improves psychosocial well‐being.Identifying people early in the disease course through screening and introducing long‐term intensive treatment does not cause psychosocial harm.Clinicians and public health systems implementing early detection and intensive treatment protocols for type 2 diabetes do not need to worry that these may have a long‐term adverse impact on peoples' psychosocial well‐being. [ABSTRACT FROM AUTHOR]

Published
2020
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41. Predictive ability of 35 frailty scores for cardiovascular events in the general population

Author

Aguayo, G A, Schritz, A, Donneau, A F, Vaillant, M T, Stranges, S, Malissoux, L, Guillaume, M, Muller, M, Witte, D R, APH - Aging & Later Life, ACS - Atherosclerosis & ischemic syndromes, and Internal medicine

Abstract

Introduction: Frailty is a state of vulnerability in elderly people linked to higher mortality risk. Cardiovascular disease (CVD) is highly prevalent in aged populations and associated with frailty. Thus, frailty state could predict higher risk of CVD. Many frailty scores (FS) have been developed, but none of them is considered the gold standard. We aimed to compare predictive and discriminative ability of an extensive list of FS with regard to incidence of CVD in a sample of the general elderly population in England. We assessed the hypothesis that some FS will have better predictive ability than others, depending on their characteristics. Methods: We performed a prospective analysis of the association between 35 FS in participants free of CVD at baseline wave 2 of the English Longitudinal Study of Ageing (2004-2005), and incident CVD assessed until February 2012. The sample consisted of 4,177 participants (43.0 % men). Hazard ratios (HR) and 95% confidence intervals (95% CI) were calculated for each FS using Cox proportional hazards model, adjusted for demographic, lifestyle and comorbidity variables. FS were analyzed on a continuous scale and using original cutoffs. The added predictive ability of FS beyond a basic model consisting of sex and age was studied using Harrel's C statistic (the higher the better). Results: The median follow-up was 5.8 years, the incidence rate of CVD events was 301.2/10,000 person-years and CVD represented 28% of the total cause of death. The mean age was 70.5 (SD: +/-7.8) years. In fully-adjusted models with demographics, lifestyles and comorbidity, HRs ranged from: 1.0 (0.7; 1.6) to 12.7 (5.5; 29.3). Using cutoffs, HRs ranged from 0.7 (0.2; 1.9) to 1.8 (1.3; 2.5). Adjusted for sex and age, delta Harrel's C statistic ranged from-0.8 (-3.4; 1.8) to 3.0 (-0.4; 6.4). The best CVD predictive ability was found for the Frailty Index with 70 variables and the Comprehensive Geriatric Assessment screening FS for continuous and cutoff analyses respectively. In conclusion, there is high variability in the association between different published FS and incident CVD. FS have better predictive ability used as continuous variable. Although most of the analyzed FS have good predictive ability with regard to incident CVD, they do not significantly improve on the discriminative capacity of a basic model. Our results will help to guide clinicians, researchers and public health practitioners in choosing the most informative frailty assessment tool.

Published
2017
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42. Prospective association between late evening food consumption and risk of prediabetes and diabetes: the Whitehall II cohort study.

Author

Færch, K., Quist, J. S., Hulman, A., Witte, D. R., Tabak, A. G., Brunner, E. J., Kivimäki, M., Jørgensen, M. E., Panda, S., and Vistisen, D.

Subjects
TYPE 2 diabetes risk factors, PREDIABETIC state, CONFIDENCE intervals, FOOD habits, GLYCOSYLATED hemoglobin, INGESTION, LONGITUDINAL method, SCIENTIFIC observation, RISK assessment, SEX distribution, TIME, EFFECT sizes (Statistics), ODDS ratio, GLYCEMIC control, DISEASE risk factors
Abstract

Aims: We examined whether late evening food consumption was prospectively associated with the risk of developing prediabetes or diabetes in a large observational study of individuals with normoglycaemia. Methods: Participants were 2642 men and women with normoglycaemia (HbA1c < 39 mmol/mol; < 5.7%) from the Whitehall II study. Time of last eating episode (TLEE) before the examination day was assessed at baseline. We studied the associations of TLEE with 5‐year changes in HbA1c and risk of developing prediabetes or diabetes (HbA1c ≥ 39 mmol/mol; ≥ 5.7%). Potential heterogeneity in the association between TLEE and prediabetes or diabetes was examined using recursive partitioning modelling for time‐to‐event outcomes. Results: There was a tendency of an overall association of TLEE with change in HbA1c but with little effect size [β per 1‐h increase in TLEE = 0.2 mmol/mol, 95% CI −0.0 to 0.3 (0.01%, −0.00 to 0.03); P = 0.055] and no association with the risk of developing prediabetes/diabetes (risk ratio per 1‐h increase in TLEE = 1.03, 95% CI 0.94 to 1.13; P = 0.511). According to the recursive partitioning modelling, women with HbA1c ≤ 36 mmol/mol and TLEE after 21:00 had a 1.51 times (95% CI 1.16 to 1.93) higher 5‐year risk of developing prediabetes or diabetes than those having their TLEE between 16:00 and 21:00 (35.4% vs. 23.5%; P = 0.003). Conclusions: There was no overall association of TLEE with the development of prediabetes or diabetes in the Whitehall II population. However, explorative analyses suggested that eating late in the evening was associated with increased risk of developing prediabetes/diabetes among women with good glycaemic control. Whether restricting late evening food consumption is effective and feasible for the prevention of Type 2 diabetes needs testing in randomized controlled trials. What's new?: Eating within a specific time window each day, i.e. time‐restricted eating, reduces cardiometabolic risk in rodents.In humans, timing of meal intake has acute effects on glucose regulation, but the long‐term effects of meal timing on diabetes risk are less clear.In 2642 men and women from the Whitehall II study, we found no associations between timing of last eating episode and 5‐year development of prediabetes or diabetes.However, explorative analyses suggested that late evening food consumption was associated with increased 5‐year risk of developing prediabetes or diabetes among women with good glycaemic control.Whether restricting late evening food consumption is effective and feasible for the prevention of Type 2 diabetes needs testing in randomized controlled trials. [ABSTRACT FROM AUTHOR]

Published
2019
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44. Trajectories of obesity by spousal diabetes status in the English Longitudinal Study of Ageing.

Author

Silverman‐Retana, O., Hulman, A., Simmons, R. K., Nielsen, J., and Witte, D. R.

Subjects
DIABETES complications, PREVENTION of obesity, OBESITY risk factors, AGE distribution, AGING, HEALTH status indicators, LONGITUDINAL method, PUBLIC health, SEX distribution, SMOKING, PSYCHOLOGY of Spouses, EDUCATIONAL attainment, BODY mass index, DISEASE prevalence, COUPLES therapy, WAIST circumference
Abstract

Aims: To examine whether the development of obesity with age was different for individuals with and without a spouse with diabetes. Methods: We analysed data from the English Longitudinal Study of Ageing [n= 7123, median (interquartile range) age 59 (53–67) years, 51% men], which included four clinical examination waves between 1998 and 2012. The main exposure was having a spouse with diabetes. Outcomes of interest were BMI and waist circumference. We fitted quadratic age‐related trajectories using mixed‐effect models stratified by sex and adjusted for education, smoking and the corresponding interaction terms between age and spousal diabetes status. Results: The baseline spousal diabetes prevalence was 4.4%. Men with a wife with diabetes experienced a steeper increase in BMI (1.6 kg/m2) between ages 50 to 65 years than men with a wife without diabetes (0.9 kg/m2). Women with a husband with diabetes had a similarly shaped BMI trajectory to women with a husband without diabetes, but their average BMI levels were higher between ages 55 and 65 years. Waist circumference trajectories showed a similar shape by spousal diabetes status for men and women, although individuals with a spouse with diabetes had higher waist circumference values throughout follow‐up. Conclusions: We found a positive association between spousal diabetes status and obesity development, which differed by sex among middle‐aged individuals. Evidence from couple‐based interventions is needed to test whether the latter could improve the current individual‐focused public health strategies for obesity prevention. What's new?: The risk of becoming obese is increased among people whose spouses are obese; however, less is known about the BMI trajectories in individuals after their spouse is diagnosed with diabetes.We used prospective data to examine age‐related trajectories of obesity indicators by spousal diabetes status. Having a spouse with diabetes was associated with higher levels of obesity during middle and late adulthood in both sexes.We found a positive association between spousal diabetes status and obesity development, which differed by sex among middle‐aged individuals. [ABSTRACT FROM AUTHOR]

Published
2019
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45. Diabetes in Greenland and its relationship with urbanization

Author

Jørgensen, M E, Borch-Johnsen, K, Witte, D R, and Bjerregaard, P

Abstract

Background and aim: Most studies show that diabetes increases with migration and urbanization. Previous studies from Greenland have shown inconsistent associations between cardiovascular risk and urbanization. Thus, the aim was to study the association between diabetes and urbanization among Greenland Inuit. Methods: A total of 3089 adult Inuit aged 18 years and older participated in a geographically representative, population-based study 'Inuit Health in Transition Study'. The examination included a 75 g oral glucose tolerance test and anthropometric measurements. Information on socio-demographic characteristic and health behaviour was obtained by interview or questionnaire. The participants were categorized according to degree of urbanization into three groups based on current place of residence: (1) participants living in towns (> 2000 inhabitants), (2) participants living in small towns (

Published
2012
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47. Methylglyoxal is associated with changes in kidney function among individuals with screen-detected Type 2 diabetes mellitus.

Author

Jensen, T. M., Vistisen, D., Fleming, T., Nawroth, P. P., Rossing, P., Jørgensen, M. E., Lauritzen, T., Sandbæk, A., and Witte, D. R.

Subjects
DIABETIC nephropathies, KIDNEY physiology, TYPE 2 diabetes diagnosis, HYPERGLYCEMIA, ALBUMINURIA, TYPE 2 diabetes complications, CALCIUM antagonists, BIOMARKERS, BLOOD testing, BLOOD pressure, BLOOD pressure measurement, C-reactive protein, CREATININE, PEOPLE with diabetes, DIURETICS, FASTING, GLOMERULAR filtration rate, GLYCOLYSIS, GLYCOSYLATED hemoglobin, HIGH density lipoproteins, PATIENT aftercare, LOW density lipoproteins, MEDICAL screening, ORGANIC compounds, RESEARCH funding, SMOKING, TRIGLYCERIDES, URINALYSIS, DATA analysis, ALBUMINS, METFORMIN, CROSS-sectional method, WAIST circumference, DIAGNOSIS, DISEASE risk factors
Abstract

Aims The glycolysis-derived metabolite methylglyoxal has been linked to clinical microvascular complications, including diabetic nephropathy. We aimed to further investigate the hypothesis that methylglyoxal is involved in decline in renal function by assessing the associations between measures of renal function during a 6-year follow-up in 1481 people with screen-detected Type 2 diabetes, as part of the Danish arm of the ADDITION-Europe trial ( ADDITION- DK). Methods Biobank serum samples collected at ADDITION- DK baseline (2001-2006) and follow-up (2009-2010) were used in the current analysis of methylglyoxal. We assessed cross-sectional baseline and longitudinal associations between methylglyoxal and urinary albumin-to-creatinine ratio ( ACR) or estimated GFR ( eGFR), and between methylglyoxal and categories of albuminuria or reduced eGFR. Results Baseline methylglyoxal was positively associated with ACR at baseline (12% higher ACR per doubling in methylglyoxal levels), and change in methylglyoxal during 6 years of follow-up was inversely associated with change in eGFR (-1.6 ml/min/1.73 m2 per doubling in methylglyoxal change), in models adjusted for age, sex, HbA1c, systolic blood pressure, anti-hypertensive treatment, LDL-cholesterol, lipid-lowering treatment, C-reactive protein and smoking. Conclusions In a population of people with screen-detected Type 2 diabetes, we observed associations between methylglyoxal and markers of renal function: 6-year change in methylglyoxal was inversely associated with 6-year change in eGFR. Also, methylglyoxal at baseline was positively associated with ACR at baseline. Our study lends further support to a role for methylglyoxal in the pathogenesis of diabetic nephropathy. [ABSTRACT FROM AUTHOR]

Published
2016
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48. Risk scores for diabetes and impaired glycaemia in the Middle East and North Africa.

Author

Handlos, L. N., Witte, D. R., Almdal, T. P., Nielsen, L. B., Badawi, S. E., Sheikh, A. R. A., Belhadj, M., Nadir, D., Zinai, S., and Vistisen, D.

Subjects
*DIABETES risk factors, *CARDIOVASCULAR disease diagnosis, *HYPERTENSION, *DIABETES, *ETHNIC groups, *GLYCOSYLATED hemoglobin, *MEDICAL screening, *METABOLIC regulation, *RISK assessment, *COMORBIDITY, *DATA analysis, *BODY mass index, *ACQUISITION of data
Abstract

Aims To develop risk scores for diabetes and diabetes or impaired glycaemia for individuals living in the Middle East and North Africa region. In addition, to derive national risk scores for Algeria, Saudi Arabia and the United Arab Emirates and to compare the performance of the regional risk scores with the national risk scores. Methods An opportunistic sample of 6588 individuals aged 30-75 years was screened. Screening consisted of a questionnaire and a clinical examination including measurement of HbA1c. Two regional risk scores and national risk scores for each of the three countries were derived separately by stepwise backwards multiple logistic regression with diabetes [HbA1c ≥ 48 mmol/mol (≥ 6.5%)] and diabetes or impaired glycaemia [HbA1c ≥ 42 mmol/mol (≥ 6.0%)] as outcome. The performance of the regional and national risk scores was compared in data from each country by receiver operating characteristic analysis. Results The eight risk scores all included age and BMI, while additional variables differed between the scores. The areas under the receiver operating characteristic curves were between 0.67 and 0.70, and for sensitivities approximately 75%; specificities varied between 50% and 57%. The regional and the national risk scores performed equally well in the three national samples. Conclusions Two regional risk scores for diabetes and diabetes or impaired glycaemia applicable to the Middle East and North Africa region were identified. The regional risk scores performed as well as the national risk scores derived in the same manner. [ABSTRACT FROM AUTHOR]

Published
2013
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49. Diabetes in Greenland and its relationship with urbanization.

Author

Jørgensen, M. E., Borch-Johnsen, K., Witte, D. R., and Bjerregaard, P.

Subjects
GLUCOSE intolerance, ANTHROPOMETRY, CHI-squared test, DIABETES, EMIGRATION & immigration, EPIDEMIOLOGY, FASTING, INTERVIEWING, METABOLIC regulation, METROPOLITAN areas, QUESTIONNAIRES, SCALES (Weighing instruments), LOGISTIC regression analysis, DATA analysis, BODY mass index, ACQUISITION of data, PATIENT selection, DATA analysis software, DIAGNOSIS
Abstract

Diabet. Med. 29, 755-760 (2012) Abstract Background and aim Most studies show that diabetes increases with migration and urbanization. Previous studies from Greenland have shown inconsistent associations between cardiovascular risk and urbanization. Thus, the aim was to study the association between diabetes and urbanization among Greenland Inuit. Methods A total of 3089 adult Inuit aged 18 years and older participated in a geographically representative, population-based study 'Inuit Health in Transition Study'. The examination included a 75 g oral glucose tolerance test and anthropometric measurements. Information on socio-demographic characteristic and health behaviour was obtained by interview or questionnaire. The participants were categorized according to degree of urbanization into three groups based on current place of residence: (1) participants living in towns (> 2000 inhabitants), (2) participants living in small towns (< 2000 inhabitants) and (3) participants living in villages (< 500 inhabitants). Results The total prevalence of diabetes was 9% of which 79% were previously unknown. Nine per cent had impaired glucose tolerance and 19% had impaired fasting glycaemia (IFG). Compared with towns, odds rations (ORs) for diabetes and impaired fasting glycaemia were higher in small towns [ORdiabetes = 1.5 (1.0-2.3), ORIFG = 1.9 (1.2-2.3)] and villages [ORdiabetes = 1.2 (0.8-1.9), ORIFG = 1.3 (0.9-2.0)], whereas no association was seen for impaired glucose tolerance. The inverse association between urbanization and diabetes and impaired fasting glycaemia persisted after adjustment for relevant confounders. Conclusion Diabetes and impaired fasting glycaemia decreased with urbanization contrary to the results of most studies. It appears that Greenland Inuit follow the pattern usually observed in industrialized countries with the highest risk of diabetes in the lower socio-economic groups. [ABSTRACT FROM AUTHOR]

Published
2012
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50. Comparing risk profiles of individuals diagnosed with diabetes by OGTT and HbA1cThe Danish Inter99 study.

Author

Borg, R., Vistisen, D., Witte, D. R., and Borch-Johnsen, K.

Subjects
GLUCOSE tolerance tests, TYPE 2 diabetes risk factors, DIAGNOSIS of diabetes, HEART disease risk factors, BLOOD pressure
Abstract

Diabet. Med. 27, 906–910 (2010) Aims Glycated haemoglobin (HbA1c) has been proposed as an alternative to the oral glucose tolerance test for diagnosing diabetes. We compared the cardiovascular risk profile of individuals identified by these two alternative methods. Methods We assessed the prevalence of cardiovascular risk factors in individuals with undiagnosed diabetes according to the World Health Organization classification or by the newly proposed HbA1c level ≥ 6.5% among 6258 participants of the Danish Inter99 study. Receiver operating curve analysis assessed the ability of fasting: 2-h plasma glucose and HbA1c to distinguish between individuals at high and low risk of ischemic heart disease, predicted by the PRECARD program. Results Prevalence of undiagnosed diabetes was 4.1% [95% confidence interval (CI) 3.7–4.7%] by the current oral glucose tolerance test definition, whereas 6.6% (95% CI 6.0–7.2%) had diabetes by HbA1c levels. HbA1c-defined individuals were relatively older with higher proportions of men, smokers, lipid abnormalities and macro-albuminuria, but they were leaner and had lower blood pressure. HbA1c was better than fasting- and 2-h plasma glucose at distinguishing between individuals of high and low predicted risk of ischaemic heart disease; however, the difference between HbA1c and fasting- and 2-h plasma glucose was not statistically significant. Conclusions Compared with the current oral glucose tolerance test definition, more individuals were classified as having diabetes based on the HbA1c criteria. This group had as unfavourable a risk profile as those identified by the oral glucose tolerance test. [ABSTRACT FROM AUTHOR]

Published
2010
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