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1. Life expectancy associated with different ages at diagnosis of type 2 diabetes in high-income countries : 23 million person-years of observation

Author: Kaptoge, Stephen, Sun, Luanluan, Walker, Matthew, Spackman, Sarah, Pennells, Lisa, Seshasai, Sreenivasa Rao Kondapally, Bolton, Thomas, Ataklte, Feven, Willeit, Peter, Bell, Steven, Burgess, Steven, Altay, Servet, Assmann, Gerd, Ben-Shlomo, Yoav, Best, Lyle G., Bjorkelund, Cecilia, Blazer, Dan G., Brenner, Hermann, Brunner, Eric J., Dagenais, Gilles R., Cooper, Jackie A., Cooper, Cyrus, Crespo, Carlos J., Cushman, Mary, D'Agostino, Ralph B., Sr., Daimon, Makoto, Daniels, Lori B., Dankner, Rachel, Davidson, Karina W., de Jongh, Renate T., Donfrancesco, Chiara, Ducimetiere, Pierre, Elders, Petra J. M., Engstrom, Gunnar, Ford, Ian, Gallacher, John, Bakker, Stephan J. L., Goldbourt, Uri, de la Camara, Agustin Gomez, Grimsgaard, Sameline, Gudnason, Vilmundur, Hansson, Per-Olof, Imano, Hironori, Jukema, J. Wouter, Kabrhel, Christopher, Kauhanen, Jussi, Kavousi, Maryam, Kiechl, Stefan, Knuiman, Matthew W., Kromhout, Daan, Krumholz, Harlan M., Kuller, Lewis H., Laatikainen, Tiina, Lawlor, Debbie A., Meyer, Haakon E., Mukamal, Kenneth, Nietert, Paul J., Ninomiya, Toshiharu, Nitsch, Dorothea, Nordestgaard, Borge G., Palmieri, Luigi, Price, Jackie F., Ridker, Paul M., Sun, Qi, Rosengren, Annika, Roussel, Ronan, Sakurai, Masaru, Salomaa, Veikko, Schottker, Ben, Shaw, Jonathan E., Strandberg, Timo E., Sundström, Johan, Tolonen, Hanna, Tverdal, Aage, Verschuren, W. M. Monique, Volzke, Henry, Wagenknecht, Lynne, Wallace, Robert B., Wannamethee, S. Goya, Wareham, Nicholas J., Wassertheil-Smoller, Sylvia, Yamagishi, Kazumasa, Yeap, Bu B., Harrison, Seamus, Thompson, Simon G., Inouye, Michael, Griffin, Simon, Butterworth, Adam S., Wood, Angela M., Sattar, Naveed, Danesh, John, Di Angelantonio, Emanuele, Kaptoge, Stephen, Sun, Luanluan, Walker, Matthew, Spackman, Sarah, Pennells, Lisa, Seshasai, Sreenivasa Rao Kondapally, Bolton, Thomas, Ataklte, Feven, Willeit, Peter, Bell, Steven, Burgess, Steven, Altay, Servet, Assmann, Gerd, Ben-Shlomo, Yoav, Best, Lyle G., Bjorkelund, Cecilia, Blazer, Dan G., Brenner, Hermann, Brunner, Eric J., Dagenais, Gilles R., Cooper, Jackie A., Cooper, Cyrus, Crespo, Carlos J., Cushman, Mary, D'Agostino, Ralph B., Sr., Daimon, Makoto, Daniels, Lori B., Dankner, Rachel, Davidson, Karina W., de Jongh, Renate T., Donfrancesco, Chiara, Ducimetiere, Pierre, Elders, Petra J. M., Engstrom, Gunnar, Ford, Ian, Gallacher, John, Bakker, Stephan J. L., Goldbourt, Uri, de la Camara, Agustin Gomez, Grimsgaard, Sameline, Gudnason, Vilmundur, Hansson, Per-Olof, Imano, Hironori, Jukema, J. Wouter, Kabrhel, Christopher, Kauhanen, Jussi, Kavousi, Maryam, Kiechl, Stefan, Knuiman, Matthew W., Kromhout, Daan, Krumholz, Harlan M., Kuller, Lewis H., Laatikainen, Tiina, Lawlor, Debbie A., Meyer, Haakon E., Mukamal, Kenneth, Nietert, Paul J., Ninomiya, Toshiharu, Nitsch, Dorothea, Nordestgaard, Borge G., Palmieri, Luigi, Price, Jackie F., Ridker, Paul M., Sun, Qi, Rosengren, Annika, Roussel, Ronan, Sakurai, Masaru, Salomaa, Veikko, Schottker, Ben, Shaw, Jonathan E., Strandberg, Timo E., Sundström, Johan, Tolonen, Hanna, Tverdal, Aage, Verschuren, W. M. Monique, Volzke, Henry, Wagenknecht, Lynne, Wallace, Robert B., Wannamethee, S. Goya, Wareham, Nicholas J., Wassertheil-Smoller, Sylvia, Yamagishi, Kazumasa, Yeap, Bu B., Harrison, Seamus, Thompson, Simon G., Inouye, Michael, Griffin, Simon, Butterworth, Adam S., Wood, Angela M., Sattar, Naveed, Danesh, John, and Di Angelantonio, Emanuele
Abstract: Background The prevalence of type 2 diabetes is increasing rapidly, particularly among younger age groups. Estimates suggest that people with diabetes die, on average, 6 years earlier than people without diabetes. We aimed to provide reliable estimates of the associations between age at diagnosis of diabetes and all-cause mortality, cause-specific mortality, and reductions in life expectancy. Methods For this observational study, we conducted a combined analysis of individual-participant data from 19 high income countries using two large-scale data sources: the Emerging Risk Factors Collaboration (96 cohorts, median baseline years 1961-2007, median latest follow-up years 1980-2013) and the UK Biobank (median baseline year 2006, median latest follow-up year 2020). We calculated age-adjusted and sex-adjusted hazard ratios (HRs) for all-cause mortality according to age at diagnosis of diabetes using data from 1 515 718 participants, in whom deaths were recorded during 23 center dot 1 million person-years of follow-up. We estimated cumulative survival by applying age-specific HRs to age-specific death rates from 2015 for the USA and the EU. Findings For participants with diabetes, we observed a linear dose-response association between earlier age at diagnosis and higher risk of all-cause mortality compared with participants without diabetes. HRs were 2 center dot 69 (95% CI 2 center dot 43-2 center dot 97) when diagnosed at 30-39 years, 2 center dot 26 (2 center dot 08-2 center dot 45) at 40-49 years, 1 center dot 84 (1 center dot 72-1 center dot 97) at 50-59 years, 1 center dot 57 (1 center dot 47-1 center dot 67) at 60-69 years, and 1 center dot 39 (1 center dot 29-1 center dot 51) at 70 years and older. HRs per decade of earlier diagnosis were similar for men and women. Using death rates from the USA, a 50-year-old individual with diabetes died on average 14 years earlier when diagnosed aged 30 years, 10 years earlier when diagnosed aged 40 years, or 6 years earlier
Published: 2023
Full Text: View/download PDF

2. Circulating insulin-like growth factors and risks of overall, aggressive and early-onset prostate cancer : a collaborative analysis of 20 prospective studies and Mendelian randomization analysis

Author: Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael, V, Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, H. Bas, Cohn, Barbara A., Deschasaux-Tanguy, Melanie, Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Haiman, Christopher A., Hankey, Graham J., Holly, Jeffrey M. P., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Kubo, Tatsuhiko, Le Marchand, Loic, MacInnis, Robert J., Mannisto, Satu, Metter, E. Jeffrey, Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Pollak, Michael N., Roobol, Monique J., Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Touvier, Mathilde, Van Den Eeden, Stephen K., Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., Travis, Ruth C., Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael, V, Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, H. Bas, Cohn, Barbara A., Deschasaux-Tanguy, Melanie, Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Haiman, Christopher A., Hankey, Graham J., Holly, Jeffrey M. P., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Kubo, Tatsuhiko, Le Marchand, Loic, MacInnis, Robert J., Mannisto, Satu, Metter, E. Jeffrey, Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Pollak, Michael N., Roobol, Monique J., Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Touvier, Mathilde, Van Den Eeden, Stephen K., Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., and Travis, Ruth C.
Abstract: Background Previous studies had limited power to assess the associations of circulating insulin-like growth factors (IGFs) and IGF-binding proteins (IGFBPs) with clinically relevant prostate cancer as a primary endpoint, and the association of genetically predicted IGF-I with aggressive prostate cancer is not known. We aimed to investigate the associations of IGF-I, IGF-II, IGFBP-1, IGFBP-2 and IGFBP-3 concentrations with overall, aggressive and early-onset prostate cancer. Methods Prospective analysis of biomarkers using the Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group dataset (up to 20 studies, 17 009 prostate cancer cases, including 2332 aggressive cases). Odds ratios (OR) and 95% confidence intervals (CI) for prostate cancer were estimated using conditional logistic regression. For IGF-I, two-sample Mendelian randomization (MR) analysis was undertaken using instruments identified using UK Biobank (158 444 men) and outcome data from PRACTICAL (up to 85 554 cases, including 15 167 aggressive cases). Additionally, we used colocalization to rule out confounding by linkage disequilibrium. Results In observational analyses, IGF-I was positively associated with risks of overall (OR per 1 SD = 1.09: 95% CI 1.07, 1.11), aggressive (1.09: 1.03, 1.16) and possibly early-onset disease (1.11: 1.00, 1.24); associations were similar in MR analyses (OR per 1 SD = 1.07: 1.00, 1.15; 1.10: 1.01, 1.20; and 1.13; 0.98, 1.30, respectively). Colocalization also indicated a shared signal for IGF-I and prostate cancer (PP4: 99%). Men with higher IGF-II (1.06: 1.02, 1.11) and IGFBP-3 (1.08: 1.04, 1.11) had higher risks of overall prostate cancer, whereas higher IGFBP-1 was associated with a lower risk (0.95: 0.91, 0.99); these associations were attenuated following adjustment for IGF-I. Conclusions These findings support the role of IGF-I in the development of prostate cancer, including for aggressive disease.
Published: 2023
Full Text: View/download PDF

3. Life expectancy associated with different ages at diagnosis of type 2 diabetes in high-income countries : 23 million person-years of observation

Author: Kaptoge, Stephen, Sun, Luanluan, Walker, Matthew, Spackman, Sarah, Pennells, Lisa, Seshasai, Sreenivasa Rao Kondapally, Bolton, Thomas, Ataklte, Feven, Willeit, Peter, Bell, Steven, Burgess, Steven, Altay, Servet, Assmann, Gerd, Ben-Shlomo, Yoav, Best, Lyle G., Bjorkelund, Cecilia, Blazer, Dan G., Brenner, Hermann, Brunner, Eric J., Dagenais, Gilles R., Cooper, Jackie A., Cooper, Cyrus, Crespo, Carlos J., Cushman, Mary, D'Agostino, Ralph B., Sr., Daimon, Makoto, Daniels, Lori B., Dankner, Rachel, Davidson, Karina W., de Jongh, Renate T., Donfrancesco, Chiara, Ducimetiere, Pierre, Elders, Petra J. M., Engstrom, Gunnar, Ford, Ian, Gallacher, John, Bakker, Stephan J. L., Goldbourt, Uri, de la Camara, Agustin Gomez, Grimsgaard, Sameline, Gudnason, Vilmundur, Hansson, Per-Olof, Imano, Hironori, Jukema, J. Wouter, Kabrhel, Christopher, Kauhanen, Jussi, Kavousi, Maryam, Kiechl, Stefan, Knuiman, Matthew W., Kromhout, Daan, Krumholz, Harlan M., Kuller, Lewis H., Laatikainen, Tiina, Lawlor, Debbie A., Meyer, Haakon E., Mukamal, Kenneth, Nietert, Paul J., Ninomiya, Toshiharu, Nitsch, Dorothea, Nordestgaard, Borge G., Palmieri, Luigi, Price, Jackie F., Ridker, Paul M., Sun, Qi, Rosengren, Annika, Roussel, Ronan, Sakurai, Masaru, Salomaa, Veikko, Schottker, Ben, Shaw, Jonathan E., Strandberg, Timo E., Sundström, Johan, Tolonen, Hanna, Tverdal, Aage, Verschuren, W. M. Monique, Volzke, Henry, Wagenknecht, Lynne, Wallace, Robert B., Wannamethee, S. Goya, Wareham, Nicholas J., Wassertheil-Smoller, Sylvia, Yamagishi, Kazumasa, Yeap, Bu B., Harrison, Seamus, Thompson, Simon G., Inouye, Michael, Griffin, Simon, Butterworth, Adam S., Wood, Angela M., Sattar, Naveed, Danesh, John, Di Angelantonio, Emanuele, Kaptoge, Stephen, Sun, Luanluan, Walker, Matthew, Spackman, Sarah, Pennells, Lisa, Seshasai, Sreenivasa Rao Kondapally, Bolton, Thomas, Ataklte, Feven, Willeit, Peter, Bell, Steven, Burgess, Steven, Altay, Servet, Assmann, Gerd, Ben-Shlomo, Yoav, Best, Lyle G., Bjorkelund, Cecilia, Blazer, Dan G., Brenner, Hermann, Brunner, Eric J., Dagenais, Gilles R., Cooper, Jackie A., Cooper, Cyrus, Crespo, Carlos J., Cushman, Mary, D'Agostino, Ralph B., Sr., Daimon, Makoto, Daniels, Lori B., Dankner, Rachel, Davidson, Karina W., de Jongh, Renate T., Donfrancesco, Chiara, Ducimetiere, Pierre, Elders, Petra J. M., Engstrom, Gunnar, Ford, Ian, Gallacher, John, Bakker, Stephan J. L., Goldbourt, Uri, de la Camara, Agustin Gomez, Grimsgaard, Sameline, Gudnason, Vilmundur, Hansson, Per-Olof, Imano, Hironori, Jukema, J. Wouter, Kabrhel, Christopher, Kauhanen, Jussi, Kavousi, Maryam, Kiechl, Stefan, Knuiman, Matthew W., Kromhout, Daan, Krumholz, Harlan M., Kuller, Lewis H., Laatikainen, Tiina, Lawlor, Debbie A., Meyer, Haakon E., Mukamal, Kenneth, Nietert, Paul J., Ninomiya, Toshiharu, Nitsch, Dorothea, Nordestgaard, Borge G., Palmieri, Luigi, Price, Jackie F., Ridker, Paul M., Sun, Qi, Rosengren, Annika, Roussel, Ronan, Sakurai, Masaru, Salomaa, Veikko, Schottker, Ben, Shaw, Jonathan E., Strandberg, Timo E., Sundström, Johan, Tolonen, Hanna, Tverdal, Aage, Verschuren, W. M. Monique, Volzke, Henry, Wagenknecht, Lynne, Wallace, Robert B., Wannamethee, S. Goya, Wareham, Nicholas J., Wassertheil-Smoller, Sylvia, Yamagishi, Kazumasa, Yeap, Bu B., Harrison, Seamus, Thompson, Simon G., Inouye, Michael, Griffin, Simon, Butterworth, Adam S., Wood, Angela M., Sattar, Naveed, Danesh, John, and Di Angelantonio, Emanuele
Abstract: Background The prevalence of type 2 diabetes is increasing rapidly, particularly among younger age groups. Estimates suggest that people with diabetes die, on average, 6 years earlier than people without diabetes. We aimed to provide reliable estimates of the associations between age at diagnosis of diabetes and all-cause mortality, cause-specific mortality, and reductions in life expectancy. Methods For this observational study, we conducted a combined analysis of individual-participant data from 19 high income countries using two large-scale data sources: the Emerging Risk Factors Collaboration (96 cohorts, median baseline years 1961-2007, median latest follow-up years 1980-2013) and the UK Biobank (median baseline year 2006, median latest follow-up year 2020). We calculated age-adjusted and sex-adjusted hazard ratios (HRs) for all-cause mortality according to age at diagnosis of diabetes using data from 1 515 718 participants, in whom deaths were recorded during 23 center dot 1 million person-years of follow-up. We estimated cumulative survival by applying age-specific HRs to age-specific death rates from 2015 for the USA and the EU. Findings For participants with diabetes, we observed a linear dose-response association between earlier age at diagnosis and higher risk of all-cause mortality compared with participants without diabetes. HRs were 2 center dot 69 (95% CI 2 center dot 43-2 center dot 97) when diagnosed at 30-39 years, 2 center dot 26 (2 center dot 08-2 center dot 45) at 40-49 years, 1 center dot 84 (1 center dot 72-1 center dot 97) at 50-59 years, 1 center dot 57 (1 center dot 47-1 center dot 67) at 60-69 years, and 1 center dot 39 (1 center dot 29-1 center dot 51) at 70 years and older. HRs per decade of earlier diagnosis were similar for men and women. Using death rates from the USA, a 50-year-old individual with diabetes died on average 14 years earlier when diagnosed aged 30 years, 10 years earlier when diagnosed aged 40 years, or 6 years earlier
Published: 2023
Full Text: View/download PDF

4. Circulating insulin-like growth factors and risks of overall, aggressive and early-onset prostate cancer : a collaborative analysis of 20 prospective studies and Mendelian randomization analysis

Author: Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael, V, Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, H. Bas, Cohn, Barbara A., Deschasaux-Tanguy, Melanie, Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Haiman, Christopher A., Hankey, Graham J., Holly, Jeffrey M. P., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Kubo, Tatsuhiko, Le Marchand, Loic, MacInnis, Robert J., Mannisto, Satu, Metter, E. Jeffrey, Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Pollak, Michael N., Roobol, Monique J., Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Touvier, Mathilde, Van Den Eeden, Stephen K., Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., Travis, Ruth C., Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael, V, Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, H. Bas, Cohn, Barbara A., Deschasaux-Tanguy, Melanie, Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Haiman, Christopher A., Hankey, Graham J., Holly, Jeffrey M. P., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Kubo, Tatsuhiko, Le Marchand, Loic, MacInnis, Robert J., Mannisto, Satu, Metter, E. Jeffrey, Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Pollak, Michael N., Roobol, Monique J., Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Touvier, Mathilde, Van Den Eeden, Stephen K., Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., and Travis, Ruth C.
Abstract: Background Previous studies had limited power to assess the associations of circulating insulin-like growth factors (IGFs) and IGF-binding proteins (IGFBPs) with clinically relevant prostate cancer as a primary endpoint, and the association of genetically predicted IGF-I with aggressive prostate cancer is not known. We aimed to investigate the associations of IGF-I, IGF-II, IGFBP-1, IGFBP-2 and IGFBP-3 concentrations with overall, aggressive and early-onset prostate cancer. Methods Prospective analysis of biomarkers using the Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group dataset (up to 20 studies, 17 009 prostate cancer cases, including 2332 aggressive cases). Odds ratios (OR) and 95% confidence intervals (CI) for prostate cancer were estimated using conditional logistic regression. For IGF-I, two-sample Mendelian randomization (MR) analysis was undertaken using instruments identified using UK Biobank (158 444 men) and outcome data from PRACTICAL (up to 85 554 cases, including 15 167 aggressive cases). Additionally, we used colocalization to rule out confounding by linkage disequilibrium. Results In observational analyses, IGF-I was positively associated with risks of overall (OR per 1 SD = 1.09: 95% CI 1.07, 1.11), aggressive (1.09: 1.03, 1.16) and possibly early-onset disease (1.11: 1.00, 1.24); associations were similar in MR analyses (OR per 1 SD = 1.07: 1.00, 1.15; 1.10: 1.01, 1.20; and 1.13; 0.98, 1.30, respectively). Colocalization also indicated a shared signal for IGF-I and prostate cancer (PP4: 99%). Men with higher IGF-II (1.06: 1.02, 1.11) and IGFBP-3 (1.08: 1.04, 1.11) had higher risks of overall prostate cancer, whereas higher IGFBP-1 was associated with a lower risk (0.95: 0.91, 0.99); these associations were attenuated following adjustment for IGF-I. Conclusions These findings support the role of IGF-I in the development of prostate cancer, including for aggressive disease.
Published: 2023
Full Text: View/download PDF

5. Life expectancy associated with different ages at diagnosis of type 2 diabetes in high-income countries : 23 million person-years of observation

Author: Kaptoge, Stephen, Sun, Luanluan, Walker, Matthew, Spackman, Sarah, Pennells, Lisa, Seshasai, Sreenivasa Rao Kondapally, Bolton, Thomas, Ataklte, Feven, Willeit, Peter, Bell, Steven, Burgess, Steven, Altay, Servet, Assmann, Gerd, Ben-Shlomo, Yoav, Best, Lyle G., Bjorkelund, Cecilia, Blazer, Dan G., Brenner, Hermann, Brunner, Eric J., Dagenais, Gilles R., Cooper, Jackie A., Cooper, Cyrus, Crespo, Carlos J., Cushman, Mary, D'Agostino, Ralph B., Sr., Daimon, Makoto, Daniels, Lori B., Dankner, Rachel, Davidson, Karina W., de Jongh, Renate T., Donfrancesco, Chiara, Ducimetiere, Pierre, Elders, Petra J. M., Engstrom, Gunnar, Ford, Ian, Gallacher, John, Bakker, Stephan J. L., Goldbourt, Uri, de la Camara, Agustin Gomez, Grimsgaard, Sameline, Gudnason, Vilmundur, Hansson, Per-Olof, Imano, Hironori, Jukema, J. Wouter, Kabrhel, Christopher, Kauhanen, Jussi, Kavousi, Maryam, Kiechl, Stefan, Knuiman, Matthew W., Kromhout, Daan, Krumholz, Harlan M., Kuller, Lewis H., Laatikainen, Tiina, Lawlor, Debbie A., Meyer, Haakon E., Mukamal, Kenneth, Nietert, Paul J., Ninomiya, Toshiharu, Nitsch, Dorothea, Nordestgaard, Borge G., Palmieri, Luigi, Price, Jackie F., Ridker, Paul M., Sun, Qi, Rosengren, Annika, Roussel, Ronan, Sakurai, Masaru, Salomaa, Veikko, Schottker, Ben, Shaw, Jonathan E., Strandberg, Timo E., Sundström, Johan, Tolonen, Hanna, Tverdal, Aage, Verschuren, W. M. Monique, Volzke, Henry, Wagenknecht, Lynne, Wallace, Robert B., Wannamethee, S. Goya, Wareham, Nicholas J., Wassertheil-Smoller, Sylvia, Yamagishi, Kazumasa, Yeap, Bu B., Harrison, Seamus, Thompson, Simon G., Inouye, Michael, Griffin, Simon, Butterworth, Adam S., Wood, Angela M., Sattar, Naveed, Danesh, John, Di Angelantonio, Emanuele, Kaptoge, Stephen, Sun, Luanluan, Walker, Matthew, Spackman, Sarah, Pennells, Lisa, Seshasai, Sreenivasa Rao Kondapally, Bolton, Thomas, Ataklte, Feven, Willeit, Peter, Bell, Steven, Burgess, Steven, Altay, Servet, Assmann, Gerd, Ben-Shlomo, Yoav, Best, Lyle G., Bjorkelund, Cecilia, Blazer, Dan G., Brenner, Hermann, Brunner, Eric J., Dagenais, Gilles R., Cooper, Jackie A., Cooper, Cyrus, Crespo, Carlos J., Cushman, Mary, D'Agostino, Ralph B., Sr., Daimon, Makoto, Daniels, Lori B., Dankner, Rachel, Davidson, Karina W., de Jongh, Renate T., Donfrancesco, Chiara, Ducimetiere, Pierre, Elders, Petra J. M., Engstrom, Gunnar, Ford, Ian, Gallacher, John, Bakker, Stephan J. L., Goldbourt, Uri, de la Camara, Agustin Gomez, Grimsgaard, Sameline, Gudnason, Vilmundur, Hansson, Per-Olof, Imano, Hironori, Jukema, J. Wouter, Kabrhel, Christopher, Kauhanen, Jussi, Kavousi, Maryam, Kiechl, Stefan, Knuiman, Matthew W., Kromhout, Daan, Krumholz, Harlan M., Kuller, Lewis H., Laatikainen, Tiina, Lawlor, Debbie A., Meyer, Haakon E., Mukamal, Kenneth, Nietert, Paul J., Ninomiya, Toshiharu, Nitsch, Dorothea, Nordestgaard, Borge G., Palmieri, Luigi, Price, Jackie F., Ridker, Paul M., Sun, Qi, Rosengren, Annika, Roussel, Ronan, Sakurai, Masaru, Salomaa, Veikko, Schottker, Ben, Shaw, Jonathan E., Strandberg, Timo E., Sundström, Johan, Tolonen, Hanna, Tverdal, Aage, Verschuren, W. M. Monique, Volzke, Henry, Wagenknecht, Lynne, Wallace, Robert B., Wannamethee, S. Goya, Wareham, Nicholas J., Wassertheil-Smoller, Sylvia, Yamagishi, Kazumasa, Yeap, Bu B., Harrison, Seamus, Thompson, Simon G., Inouye, Michael, Griffin, Simon, Butterworth, Adam S., Wood, Angela M., Sattar, Naveed, Danesh, John, and Di Angelantonio, Emanuele
Abstract: Background The prevalence of type 2 diabetes is increasing rapidly, particularly among younger age groups. Estimates suggest that people with diabetes die, on average, 6 years earlier than people without diabetes. We aimed to provide reliable estimates of the associations between age at diagnosis of diabetes and all-cause mortality, cause-specific mortality, and reductions in life expectancy. Methods For this observational study, we conducted a combined analysis of individual-participant data from 19 high income countries using two large-scale data sources: the Emerging Risk Factors Collaboration (96 cohorts, median baseline years 1961-2007, median latest follow-up years 1980-2013) and the UK Biobank (median baseline year 2006, median latest follow-up year 2020). We calculated age-adjusted and sex-adjusted hazard ratios (HRs) for all-cause mortality according to age at diagnosis of diabetes using data from 1 515 718 participants, in whom deaths were recorded during 23 center dot 1 million person-years of follow-up. We estimated cumulative survival by applying age-specific HRs to age-specific death rates from 2015 for the USA and the EU. Findings For participants with diabetes, we observed a linear dose-response association between earlier age at diagnosis and higher risk of all-cause mortality compared with participants without diabetes. HRs were 2 center dot 69 (95% CI 2 center dot 43-2 center dot 97) when diagnosed at 30-39 years, 2 center dot 26 (2 center dot 08-2 center dot 45) at 40-49 years, 1 center dot 84 (1 center dot 72-1 center dot 97) at 50-59 years, 1 center dot 57 (1 center dot 47-1 center dot 67) at 60-69 years, and 1 center dot 39 (1 center dot 29-1 center dot 51) at 70 years and older. HRs per decade of earlier diagnosis were similar for men and women. Using death rates from the USA, a 50-year-old individual with diabetes died on average 14 years earlier when diagnosed aged 30 years, 10 years earlier when diagnosed aged 40 years, or 6 years earlier
Published: 2023
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6. Circulating insulin-like growth factors and risks of overall, aggressive and early-onset prostate cancer : a collaborative analysis of 20 prospective studies and Mendelian randomization analysis

Author: Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael, V, Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, H. Bas, Cohn, Barbara A., Deschasaux-Tanguy, Melanie, Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Haiman, Christopher A., Hankey, Graham J., Holly, Jeffrey M. P., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Kubo, Tatsuhiko, Le Marchand, Loic, MacInnis, Robert J., Mannisto, Satu, Metter, E. Jeffrey, Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Pollak, Michael N., Roobol, Monique J., Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Touvier, Mathilde, Van Den Eeden, Stephen K., Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., Travis, Ruth C., Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael, V, Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, H. Bas, Cohn, Barbara A., Deschasaux-Tanguy, Melanie, Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Haiman, Christopher A., Hankey, Graham J., Holly, Jeffrey M. P., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Kubo, Tatsuhiko, Le Marchand, Loic, MacInnis, Robert J., Mannisto, Satu, Metter, E. Jeffrey, Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Pollak, Michael N., Roobol, Monique J., Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Touvier, Mathilde, Van Den Eeden, Stephen K., Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., and Travis, Ruth C.
Abstract: Background Previous studies had limited power to assess the associations of circulating insulin-like growth factors (IGFs) and IGF-binding proteins (IGFBPs) with clinically relevant prostate cancer as a primary endpoint, and the association of genetically predicted IGF-I with aggressive prostate cancer is not known. We aimed to investigate the associations of IGF-I, IGF-II, IGFBP-1, IGFBP-2 and IGFBP-3 concentrations with overall, aggressive and early-onset prostate cancer. Methods Prospective analysis of biomarkers using the Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group dataset (up to 20 studies, 17 009 prostate cancer cases, including 2332 aggressive cases). Odds ratios (OR) and 95% confidence intervals (CI) for prostate cancer were estimated using conditional logistic regression. For IGF-I, two-sample Mendelian randomization (MR) analysis was undertaken using instruments identified using UK Biobank (158 444 men) and outcome data from PRACTICAL (up to 85 554 cases, including 15 167 aggressive cases). Additionally, we used colocalization to rule out confounding by linkage disequilibrium. Results In observational analyses, IGF-I was positively associated with risks of overall (OR per 1 SD = 1.09: 95% CI 1.07, 1.11), aggressive (1.09: 1.03, 1.16) and possibly early-onset disease (1.11: 1.00, 1.24); associations were similar in MR analyses (OR per 1 SD = 1.07: 1.00, 1.15; 1.10: 1.01, 1.20; and 1.13; 0.98, 1.30, respectively). Colocalization also indicated a shared signal for IGF-I and prostate cancer (PP4: 99%). Men with higher IGF-II (1.06: 1.02, 1.11) and IGFBP-3 (1.08: 1.04, 1.11) had higher risks of overall prostate cancer, whereas higher IGFBP-1 was associated with a lower risk (0.95: 0.91, 0.99); these associations were attenuated following adjustment for IGF-I. Conclusions These findings support the role of IGF-I in the development of prostate cancer, including for aggressive disease.
Published: 2023
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7. Life expectancy associated with different ages at diagnosis of type 2 diabetes in high-income countries : 23 million person-years of observation

Author: Kaptoge, Stephen, Sun, Luanluan, Walker, Matthew, Spackman, Sarah, Pennells, Lisa, Seshasai, Sreenivasa Rao Kondapally, Bolton, Thomas, Ataklte, Feven, Willeit, Peter, Bell, Steven, Burgess, Steven, Altay, Servet, Assmann, Gerd, Ben-Shlomo, Yoav, Best, Lyle G., Bjorkelund, Cecilia, Blazer, Dan G., Brenner, Hermann, Brunner, Eric J., Dagenais, Gilles R., Cooper, Jackie A., Cooper, Cyrus, Crespo, Carlos J., Cushman, Mary, D'Agostino, Ralph B., Sr., Daimon, Makoto, Daniels, Lori B., Dankner, Rachel, Davidson, Karina W., de Jongh, Renate T., Donfrancesco, Chiara, Ducimetiere, Pierre, Elders, Petra J. M., Engstrom, Gunnar, Ford, Ian, Gallacher, John, Bakker, Stephan J. L., Goldbourt, Uri, de la Camara, Agustin Gomez, Grimsgaard, Sameline, Gudnason, Vilmundur, Hansson, Per-Olof, Imano, Hironori, Jukema, J. Wouter, Kabrhel, Christopher, Kauhanen, Jussi, Kavousi, Maryam, Kiechl, Stefan, Knuiman, Matthew W., Kromhout, Daan, Krumholz, Harlan M., Kuller, Lewis H., Laatikainen, Tiina, Lawlor, Debbie A., Meyer, Haakon E., Mukamal, Kenneth, Nietert, Paul J., Ninomiya, Toshiharu, Nitsch, Dorothea, Nordestgaard, Borge G., Palmieri, Luigi, Price, Jackie F., Ridker, Paul M., Sun, Qi, Rosengren, Annika, Roussel, Ronan, Sakurai, Masaru, Salomaa, Veikko, Schottker, Ben, Shaw, Jonathan E., Strandberg, Timo E., Sundström, Johan, Tolonen, Hanna, Tverdal, Aage, Verschuren, W. M. Monique, Volzke, Henry, Wagenknecht, Lynne, Wallace, Robert B., Wannamethee, S. Goya, Wareham, Nicholas J., Wassertheil-Smoller, Sylvia, Yamagishi, Kazumasa, Yeap, Bu B., Harrison, Seamus, Thompson, Simon G., Inouye, Michael, Griffin, Simon, Butterworth, Adam S., Wood, Angela M., Sattar, Naveed, Danesh, John, Di Angelantonio, Emanuele, Kaptoge, Stephen, Sun, Luanluan, Walker, Matthew, Spackman, Sarah, Pennells, Lisa, Seshasai, Sreenivasa Rao Kondapally, Bolton, Thomas, Ataklte, Feven, Willeit, Peter, Bell, Steven, Burgess, Steven, Altay, Servet, Assmann, Gerd, Ben-Shlomo, Yoav, Best, Lyle G., Bjorkelund, Cecilia, Blazer, Dan G., Brenner, Hermann, Brunner, Eric J., Dagenais, Gilles R., Cooper, Jackie A., Cooper, Cyrus, Crespo, Carlos J., Cushman, Mary, D'Agostino, Ralph B., Sr., Daimon, Makoto, Daniels, Lori B., Dankner, Rachel, Davidson, Karina W., de Jongh, Renate T., Donfrancesco, Chiara, Ducimetiere, Pierre, Elders, Petra J. M., Engstrom, Gunnar, Ford, Ian, Gallacher, John, Bakker, Stephan J. L., Goldbourt, Uri, de la Camara, Agustin Gomez, Grimsgaard, Sameline, Gudnason, Vilmundur, Hansson, Per-Olof, Imano, Hironori, Jukema, J. Wouter, Kabrhel, Christopher, Kauhanen, Jussi, Kavousi, Maryam, Kiechl, Stefan, Knuiman, Matthew W., Kromhout, Daan, Krumholz, Harlan M., Kuller, Lewis H., Laatikainen, Tiina, Lawlor, Debbie A., Meyer, Haakon E., Mukamal, Kenneth, Nietert, Paul J., Ninomiya, Toshiharu, Nitsch, Dorothea, Nordestgaard, Borge G., Palmieri, Luigi, Price, Jackie F., Ridker, Paul M., Sun, Qi, Rosengren, Annika, Roussel, Ronan, Sakurai, Masaru, Salomaa, Veikko, Schottker, Ben, Shaw, Jonathan E., Strandberg, Timo E., Sundström, Johan, Tolonen, Hanna, Tverdal, Aage, Verschuren, W. M. Monique, Volzke, Henry, Wagenknecht, Lynne, Wallace, Robert B., Wannamethee, S. Goya, Wareham, Nicholas J., Wassertheil-Smoller, Sylvia, Yamagishi, Kazumasa, Yeap, Bu B., Harrison, Seamus, Thompson, Simon G., Inouye, Michael, Griffin, Simon, Butterworth, Adam S., Wood, Angela M., Sattar, Naveed, Danesh, John, and Di Angelantonio, Emanuele
Abstract: Background The prevalence of type 2 diabetes is increasing rapidly, particularly among younger age groups. Estimates suggest that people with diabetes die, on average, 6 years earlier than people without diabetes. We aimed to provide reliable estimates of the associations between age at diagnosis of diabetes and all-cause mortality, cause-specific mortality, and reductions in life expectancy. Methods For this observational study, we conducted a combined analysis of individual-participant data from 19 high income countries using two large-scale data sources: the Emerging Risk Factors Collaboration (96 cohorts, median baseline years 1961-2007, median latest follow-up years 1980-2013) and the UK Biobank (median baseline year 2006, median latest follow-up year 2020). We calculated age-adjusted and sex-adjusted hazard ratios (HRs) for all-cause mortality according to age at diagnosis of diabetes using data from 1 515 718 participants, in whom deaths were recorded during 23 center dot 1 million person-years of follow-up. We estimated cumulative survival by applying age-specific HRs to age-specific death rates from 2015 for the USA and the EU. Findings For participants with diabetes, we observed a linear dose-response association between earlier age at diagnosis and higher risk of all-cause mortality compared with participants without diabetes. HRs were 2 center dot 69 (95% CI 2 center dot 43-2 center dot 97) when diagnosed at 30-39 years, 2 center dot 26 (2 center dot 08-2 center dot 45) at 40-49 years, 1 center dot 84 (1 center dot 72-1 center dot 97) at 50-59 years, 1 center dot 57 (1 center dot 47-1 center dot 67) at 60-69 years, and 1 center dot 39 (1 center dot 29-1 center dot 51) at 70 years and older. HRs per decade of earlier diagnosis were similar for men and women. Using death rates from the USA, a 50-year-old individual with diabetes died on average 14 years earlier when diagnosed aged 30 years, 10 years earlier when diagnosed aged 40 years, or 6 years earlier
Published: 2023
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8. Circulating insulin-like growth factors and risks of overall, aggressive and early-onset prostate cancer : a collaborative analysis of 20 prospective studies and Mendelian randomization analysis

Author: Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael, V, Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, H. Bas, Cohn, Barbara A., Deschasaux-Tanguy, Melanie, Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Haiman, Christopher A., Hankey, Graham J., Holly, Jeffrey M. P., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Kubo, Tatsuhiko, Le Marchand, Loic, MacInnis, Robert J., Mannisto, Satu, Metter, E. Jeffrey, Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Pollak, Michael N., Roobol, Monique J., Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Touvier, Mathilde, Van Den Eeden, Stephen K., Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., Travis, Ruth C., Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael, V, Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, H. Bas, Cohn, Barbara A., Deschasaux-Tanguy, Melanie, Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Haiman, Christopher A., Hankey, Graham J., Holly, Jeffrey M. P., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Kubo, Tatsuhiko, Le Marchand, Loic, MacInnis, Robert J., Mannisto, Satu, Metter, E. Jeffrey, Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Pollak, Michael N., Roobol, Monique J., Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Touvier, Mathilde, Van Den Eeden, Stephen K., Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., and Travis, Ruth C.
Abstract: Background Previous studies had limited power to assess the associations of circulating insulin-like growth factors (IGFs) and IGF-binding proteins (IGFBPs) with clinically relevant prostate cancer as a primary endpoint, and the association of genetically predicted IGF-I with aggressive prostate cancer is not known. We aimed to investigate the associations of IGF-I, IGF-II, IGFBP-1, IGFBP-2 and IGFBP-3 concentrations with overall, aggressive and early-onset prostate cancer. Methods Prospective analysis of biomarkers using the Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group dataset (up to 20 studies, 17 009 prostate cancer cases, including 2332 aggressive cases). Odds ratios (OR) and 95% confidence intervals (CI) for prostate cancer were estimated using conditional logistic regression. For IGF-I, two-sample Mendelian randomization (MR) analysis was undertaken using instruments identified using UK Biobank (158 444 men) and outcome data from PRACTICAL (up to 85 554 cases, including 15 167 aggressive cases). Additionally, we used colocalization to rule out confounding by linkage disequilibrium. Results In observational analyses, IGF-I was positively associated with risks of overall (OR per 1 SD = 1.09: 95% CI 1.07, 1.11), aggressive (1.09: 1.03, 1.16) and possibly early-onset disease (1.11: 1.00, 1.24); associations were similar in MR analyses (OR per 1 SD = 1.07: 1.00, 1.15; 1.10: 1.01, 1.20; and 1.13; 0.98, 1.30, respectively). Colocalization also indicated a shared signal for IGF-I and prostate cancer (PP4: 99%). Men with higher IGF-II (1.06: 1.02, 1.11) and IGFBP-3 (1.08: 1.04, 1.11) had higher risks of overall prostate cancer, whereas higher IGFBP-1 was associated with a lower risk (0.95: 0.91, 0.99); these associations were attenuated following adjustment for IGF-I. Conclusions These findings support the role of IGF-I in the development of prostate cancer, including for aggressive disease.
Published: 2023
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9. The optimal healthy ranges of thyroid function defined by the risk of cardiovascular disease and mortality:systematic review and individual participant data meta-analysis

Author: Xu, Yanning, Derakhshan, Arash, Hysaj, Ola, Wildisen, Lea, Ittermann, Till, Pingitore, Alessandro, Abolhassani, Nazanin, Medici, Marco, Kiemeney, Lambertus A.L.M., Riksen, Niels P., Dullaart, Robin P.F., Trompet, Stella, Dörr, Marcus, Brown, Suzanne J., Schmidt, Börge, Führer-Sakel, Dagmar, Vanderpump, Mark P.J., Muendlein, Axel, Drexel, Heinz, Fink, Howard A., Ikram, M. Kamran, Kavousi, Maryam, Rhee, Connie M., Bensenor, Isabela M., Azizi, Fereidoun, Hankey, Graeme J., Iacoviello, Massimo, Imaizumi, Misa, Ceresini, Graziano, Ferrucci, Luigi, Sgarbi, José A., Bauer, Douglas C., Wareham, Nick, Boelaert, Kristien, Bakker, Stephan J.L., Jukema, J. Wouter, Vaes, Bert, Iervasi, Giorgio, Yeap, Bu B., Westendorp, Rudi G.J., Korevaar, Tim I.M., Völzke, Henry, Razvi, Salman, Gussekloo, Jacobijn, Walsh, John P., Cappola, Anne R., Rodondi, Nicolas, Peeters, Robin P., Chaker, Layal, Xu, Yanning, Derakhshan, Arash, Hysaj, Ola, Wildisen, Lea, Ittermann, Till, Pingitore, Alessandro, Abolhassani, Nazanin, Medici, Marco, Kiemeney, Lambertus A.L.M., Riksen, Niels P., Dullaart, Robin P.F., Trompet, Stella, Dörr, Marcus, Brown, Suzanne J., Schmidt, Börge, Führer-Sakel, Dagmar, Vanderpump, Mark P.J., Muendlein, Axel, Drexel, Heinz, Fink, Howard A., Ikram, M. Kamran, Kavousi, Maryam, Rhee, Connie M., Bensenor, Isabela M., Azizi, Fereidoun, Hankey, Graeme J., Iacoviello, Massimo, Imaizumi, Misa, Ceresini, Graziano, Ferrucci, Luigi, Sgarbi, José A., Bauer, Douglas C., Wareham, Nick, Boelaert, Kristien, Bakker, Stephan J.L., Jukema, J. Wouter, Vaes, Bert, Iervasi, Giorgio, Yeap, Bu B., Westendorp, Rudi G.J., Korevaar, Tim I.M., Völzke, Henry, Razvi, Salman, Gussekloo, Jacobijn, Walsh, John P., Cappola, Anne R., Rodondi, Nicolas, Peeters, Robin P., and Chaker, Layal
Abstract: Background: Reference intervals of thyroid-stimulating hormone (TSH) and free thyroxine (FT4) are statistically defined by the 2·5–97·5th percentiles, without accounting for potential risk of clinical outcomes. We aimed to define the optimal healthy ranges of TSH and FT4 based on the risk of cardiovascular disease and mortality. Methods:This systematic review and individual participant data (IPD) meta-analysis identified eligible prospective cohorts through the Thyroid Studies Collaboration, supplemented with a systematic search via Embase, MEDLINE (Ovid), Web of science, the Cochrane Central Register of Controlled Trials, and Google Scholar from Jan 1, 2011, to Feb 12, 2017 with an updated search to Oct 13, 2022 (cohorts found in the second search were not included in the IPD). We included cohorts that collected TSH or FT4, and cardiovascular outcomes or mortality for adults (aged ≥18 years). We excluded cohorts that included solely pregnant women, individuals with overt thyroid diseases, and individuals with cardiovascular disease. We contacted the study investigators of eligible cohorts to provide IPD on demographics, TSH, FT4, thyroid peroxidase antibodies, history of cardiovascular disease and risk factors, medication use, cardiovascular disease events, cardiovascular disease mortality, and all-cause mortality. The primary outcome was a composite outcome including cardiovascular disease events (coronary heart disease, stroke, and heart failure) and all-cause mortality. Secondary outcomes were the separate assessment of cardiovascular disease events, all-cause mortality, and cardiovascular disease mortality. We performed one-step (cohort-stratified Cox models) and two-step (random-effects models) meta-analyses adjusting for age, sex, smoking, systolic blood pressure, diabetes, and total cholesterol. The study was registered with PROSPERO, CRD42017057576.Findings
Published: 2023

10. Circulating insulin-like growth factors and risks of overall, aggressive and early-onset prostate cancer : a collaborative analysis of 20 prospective studies and Mendelian randomization analysis

Author: Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael V., Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-De-Mesquita, H. Bas, Cohn, Barbara A., Deschasaux-Tanguy, Melanie, Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Haiman, Christopher A., Hankey, Graham J., Holly, Jeffrey M. P., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Kubo, Tatsuhiko, Le Marchand, Loic, Macinnis, Robert J., Männistö, Satu, Metter, E. Jeffrey, Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Pollak, Michael N., Roobol, Monique J., Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Touvier, Mathilde, Van Den Eeden, Stephen K., Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., Travis, Ruth C., The PRACTICAL Consortium, CRUK, BPC3, CAPS, PEGASUS, Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael V., Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-De-Mesquita, H. Bas, Cohn, Barbara A., Deschasaux-Tanguy, Melanie, Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Haiman, Christopher A., Hankey, Graham J., Holly, Jeffrey M. P., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Kubo, Tatsuhiko, Le Marchand, Loic, Macinnis, Robert J., Männistö, Satu, Metter, E. Jeffrey, Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Pollak, Michael N., Roobol, Monique J., Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Touvier, Mathilde, Van Den Eeden, Stephen K., Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., Travis, Ruth C., and The PRACTICAL Consortium, CRUK, BPC3, CAPS, PEGASUS
Abstract: Background: Previous studies had limited power to assess the associations of circulating insulin-like growth factors (IGFs) and IGF-binding proteins (IGFBPs) with clinically relevant prostate cancer as a primary endpoint, and the association of genetically predicted IGF-I with aggressive prostate cancer is not known. We aimed to investigate the associations of IGF-I, IGF-II, IGFBP-1, IGFBP-2 and IGFBP-3 concentrations with overall, aggressive and early-onset prostate cancer. Methods: Prospective analysis of biomarkers using the Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group dataset (up to 20 studies, 17 009 prostate cancer cases, including 2332 aggressive cases). Odds ratios (OR) and 95% confidence intervals (CI) for prostate cancer were estimated using conditional logistic regression. For IGF-I, two-sample Mendelian randomization (MR) analysis was undertaken using instruments identified using UK Biobank (158 444 men) and outcome data from PRACTICAL (up to 85 554 cases, including 15 167 aggressive cases). Additionally, we used colocalization to rule out confounding by linkage disequilibrium. Results: In observational analyses, IGF-I was positively associated with risks of overall (OR per 1 SD = 1.09: 95% CI 1.07, 1.11), aggressive (1.09: 1.03, 1.16) and possibly early-onset disease (1.11: 1.00, 1.24); associations were similar in MR analyses (OR per 1 SD = 1.07: 1.00, 1.15; 1.10: 1.01, 1.20; and 1.13; 0.98, 1.30, respectively). Colocalization also indicated a shared signal for IGF-I and prostate cancer (PP4: 99%). Men with higher IGF-II (1.06: 1.02, 1.11) and IGFBP-3 (1.08: 1.04, 1.11) had higher risks of overall prostate cancer, whereas higher IGFBP-1 was associated with a lower risk (0.95: 0.91, 0.99); these associations were attenuated following adjustment for IGF-I. Conclusions: These findings support the role of IGF-I in the development of prostate cancer, including for aggressive disease.
Published: 2023
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11. Circulating insulin-like growth factors and risks of overall, aggressive and early-onset prostate cancer : a collaborative analysis of 20 prospective studies and Mendelian randomization analysis

Author: Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael V., Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-De-Mesquita, H. Bas, Cohn, Barbara A., Deschasaux-Tanguy, Melanie, Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Haiman, Christopher A., Hankey, Graham J., Holly, Jeffrey M. P., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Kubo, Tatsuhiko, Le Marchand, Loic, Macinnis, Robert J., Männistö, Satu, Metter, E. Jeffrey, Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Pollak, Michael N., Roobol, Monique J., Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Touvier, Mathilde, Van Den Eeden, Stephen K., Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., Travis, Ruth C., The PRACTICAL Consortium, CRUK, BPC3, CAPS, PEGASUS, Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael V., Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-De-Mesquita, H. Bas, Cohn, Barbara A., Deschasaux-Tanguy, Melanie, Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Haiman, Christopher A., Hankey, Graham J., Holly, Jeffrey M. P., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Kubo, Tatsuhiko, Le Marchand, Loic, Macinnis, Robert J., Männistö, Satu, Metter, E. Jeffrey, Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Pollak, Michael N., Roobol, Monique J., Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Touvier, Mathilde, Van Den Eeden, Stephen K., Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., Travis, Ruth C., and The PRACTICAL Consortium, CRUK, BPC3, CAPS, PEGASUS
Abstract: Background: Previous studies had limited power to assess the associations of circulating insulin-like growth factors (IGFs) and IGF-binding proteins (IGFBPs) with clinically relevant prostate cancer as a primary endpoint, and the association of genetically predicted IGF-I with aggressive prostate cancer is not known. We aimed to investigate the associations of IGF-I, IGF-II, IGFBP-1, IGFBP-2 and IGFBP-3 concentrations with overall, aggressive and early-onset prostate cancer. Methods: Prospective analysis of biomarkers using the Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group dataset (up to 20 studies, 17 009 prostate cancer cases, including 2332 aggressive cases). Odds ratios (OR) and 95% confidence intervals (CI) for prostate cancer were estimated using conditional logistic regression. For IGF-I, two-sample Mendelian randomization (MR) analysis was undertaken using instruments identified using UK Biobank (158 444 men) and outcome data from PRACTICAL (up to 85 554 cases, including 15 167 aggressive cases). Additionally, we used colocalization to rule out confounding by linkage disequilibrium. Results: In observational analyses, IGF-I was positively associated with risks of overall (OR per 1 SD = 1.09: 95% CI 1.07, 1.11), aggressive (1.09: 1.03, 1.16) and possibly early-onset disease (1.11: 1.00, 1.24); associations were similar in MR analyses (OR per 1 SD = 1.07: 1.00, 1.15; 1.10: 1.01, 1.20; and 1.13; 0.98, 1.30, respectively). Colocalization also indicated a shared signal for IGF-I and prostate cancer (PP4: 99%). Men with higher IGF-II (1.06: 1.02, 1.11) and IGFBP-3 (1.08: 1.04, 1.11) had higher risks of overall prostate cancer, whereas higher IGFBP-1 was associated with a lower risk (0.95: 0.91, 0.99); these associations were attenuated following adjustment for IGF-I. Conclusions: These findings support the role of IGF-I in the development of prostate cancer, including for aggressive disease.
Published: 2023
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12. Circulating insulin-like growth factors and risks of overall, aggressive and early-onset prostate cancer : a collaborative analysis of 20 prospective studies and Mendelian randomization analysis

Author: Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael V., Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-De-Mesquita, H. Bas, Cohn, Barbara A., Deschasaux-Tanguy, Melanie, Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Haiman, Christopher A., Hankey, Graham J., Holly, Jeffrey M. P., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Kubo, Tatsuhiko, Le Marchand, Loic, Macinnis, Robert J., Männistö, Satu, Metter, E. Jeffrey, Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Pollak, Michael N., Roobol, Monique J., Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Touvier, Mathilde, Van Den Eeden, Stephen K., Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., Travis, Ruth C., The PRACTICAL Consortium, CRUK, BPC3, CAPS, PEGASUS, Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael V., Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-De-Mesquita, H. Bas, Cohn, Barbara A., Deschasaux-Tanguy, Melanie, Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Haiman, Christopher A., Hankey, Graham J., Holly, Jeffrey M. P., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Kubo, Tatsuhiko, Le Marchand, Loic, Macinnis, Robert J., Männistö, Satu, Metter, E. Jeffrey, Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Pollak, Michael N., Roobol, Monique J., Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Touvier, Mathilde, Van Den Eeden, Stephen K., Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., Travis, Ruth C., and The PRACTICAL Consortium, CRUK, BPC3, CAPS, PEGASUS
Abstract: Background: Previous studies had limited power to assess the associations of circulating insulin-like growth factors (IGFs) and IGF-binding proteins (IGFBPs) with clinically relevant prostate cancer as a primary endpoint, and the association of genetically predicted IGF-I with aggressive prostate cancer is not known. We aimed to investigate the associations of IGF-I, IGF-II, IGFBP-1, IGFBP-2 and IGFBP-3 concentrations with overall, aggressive and early-onset prostate cancer. Methods: Prospective analysis of biomarkers using the Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group dataset (up to 20 studies, 17 009 prostate cancer cases, including 2332 aggressive cases). Odds ratios (OR) and 95% confidence intervals (CI) for prostate cancer were estimated using conditional logistic regression. For IGF-I, two-sample Mendelian randomization (MR) analysis was undertaken using instruments identified using UK Biobank (158 444 men) and outcome data from PRACTICAL (up to 85 554 cases, including 15 167 aggressive cases). Additionally, we used colocalization to rule out confounding by linkage disequilibrium. Results: In observational analyses, IGF-I was positively associated with risks of overall (OR per 1 SD = 1.09: 95% CI 1.07, 1.11), aggressive (1.09: 1.03, 1.16) and possibly early-onset disease (1.11: 1.00, 1.24); associations were similar in MR analyses (OR per 1 SD = 1.07: 1.00, 1.15; 1.10: 1.01, 1.20; and 1.13; 0.98, 1.30, respectively). Colocalization also indicated a shared signal for IGF-I and prostate cancer (PP4: 99%). Men with higher IGF-II (1.06: 1.02, 1.11) and IGFBP-3 (1.08: 1.04, 1.11) had higher risks of overall prostate cancer, whereas higher IGFBP-1 was associated with a lower risk (0.95: 0.91, 0.99); these associations were attenuated following adjustment for IGF-I. Conclusions: These findings support the role of IGF-I in the development of prostate cancer, including for aggressive disease.
Published: 2023
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13. Life expectancy associated with different ages at diagnosis of type 2 diabetes in high-income countries : 23 million person-years of observation

Author: Kaptoge, Stephen, Sun, Luanluan, Walker, Matthew, Spackman, Sarah, Pennells, Lisa, Seshasai, Sreenivasa Rao Kondapally, Bolton, Thomas, Ataklte, Feven, Willeit, Peter, Bell, Steven, Burgess, Steven, Altay, Servet, Assmann, Gerd, Ben-Shlomo, Yoav, Best, Lyle G., Bjorkelund, Cecilia, Blazer, Dan G., Brenner, Hermann, Brunner, Eric J., Dagenais, Gilles R., Cooper, Jackie A., Cooper, Cyrus, Crespo, Carlos J., Cushman, Mary, D'Agostino, Ralph B., Sr., Daimon, Makoto, Daniels, Lori B., Dankner, Rachel, Davidson, Karina W., de Jongh, Renate T., Donfrancesco, Chiara, Ducimetiere, Pierre, Elders, Petra J. M., Engstrom, Gunnar, Ford, Ian, Gallacher, John, Bakker, Stephan J. L., Goldbourt, Uri, de la Camara, Agustin Gomez, Grimsgaard, Sameline, Gudnason, Vilmundur, Hansson, Per-Olof, Imano, Hironori, Jukema, J. Wouter, Kabrhel, Christopher, Kauhanen, Jussi, Kavousi, Maryam, Kiechl, Stefan, Knuiman, Matthew W., Kromhout, Daan, Krumholz, Harlan M., Kuller, Lewis H., Laatikainen, Tiina, Lawlor, Debbie A., Meyer, Haakon E., Mukamal, Kenneth, Nietert, Paul J., Ninomiya, Toshiharu, Nitsch, Dorothea, Nordestgaard, Borge G., Palmieri, Luigi, Price, Jackie F., Ridker, Paul M., Sun, Qi, Rosengren, Annika, Roussel, Ronan, Sakurai, Masaru, Salomaa, Veikko, Schottker, Ben, Shaw, Jonathan E., Strandberg, Timo E., Sundström, Johan, Tolonen, Hanna, Tverdal, Aage, Verschuren, W. M. Monique, Volzke, Henry, Wagenknecht, Lynne, Wallace, Robert B., Wannamethee, S. Goya, Wareham, Nicholas J., Wassertheil-Smoller, Sylvia, Yamagishi, Kazumasa, Yeap, Bu B., Harrison, Seamus, Thompson, Simon G., Inouye, Michael, Griffin, Simon, Butterworth, Adam S., Wood, Angela M., Sattar, Naveed, Danesh, John, Di Angelantonio, Emanuele, Kaptoge, Stephen, Sun, Luanluan, Walker, Matthew, Spackman, Sarah, Pennells, Lisa, Seshasai, Sreenivasa Rao Kondapally, Bolton, Thomas, Ataklte, Feven, Willeit, Peter, Bell, Steven, Burgess, Steven, Altay, Servet, Assmann, Gerd, Ben-Shlomo, Yoav, Best, Lyle G., Bjorkelund, Cecilia, Blazer, Dan G., Brenner, Hermann, Brunner, Eric J., Dagenais, Gilles R., Cooper, Jackie A., Cooper, Cyrus, Crespo, Carlos J., Cushman, Mary, D'Agostino, Ralph B., Sr., Daimon, Makoto, Daniels, Lori B., Dankner, Rachel, Davidson, Karina W., de Jongh, Renate T., Donfrancesco, Chiara, Ducimetiere, Pierre, Elders, Petra J. M., Engstrom, Gunnar, Ford, Ian, Gallacher, John, Bakker, Stephan J. L., Goldbourt, Uri, de la Camara, Agustin Gomez, Grimsgaard, Sameline, Gudnason, Vilmundur, Hansson, Per-Olof, Imano, Hironori, Jukema, J. Wouter, Kabrhel, Christopher, Kauhanen, Jussi, Kavousi, Maryam, Kiechl, Stefan, Knuiman, Matthew W., Kromhout, Daan, Krumholz, Harlan M., Kuller, Lewis H., Laatikainen, Tiina, Lawlor, Debbie A., Meyer, Haakon E., Mukamal, Kenneth, Nietert, Paul J., Ninomiya, Toshiharu, Nitsch, Dorothea, Nordestgaard, Borge G., Palmieri, Luigi, Price, Jackie F., Ridker, Paul M., Sun, Qi, Rosengren, Annika, Roussel, Ronan, Sakurai, Masaru, Salomaa, Veikko, Schottker, Ben, Shaw, Jonathan E., Strandberg, Timo E., Sundström, Johan, Tolonen, Hanna, Tverdal, Aage, Verschuren, W. M. Monique, Volzke, Henry, Wagenknecht, Lynne, Wallace, Robert B., Wannamethee, S. Goya, Wareham, Nicholas J., Wassertheil-Smoller, Sylvia, Yamagishi, Kazumasa, Yeap, Bu B., Harrison, Seamus, Thompson, Simon G., Inouye, Michael, Griffin, Simon, Butterworth, Adam S., Wood, Angela M., Sattar, Naveed, Danesh, John, and Di Angelantonio, Emanuele
Abstract: Background The prevalence of type 2 diabetes is increasing rapidly, particularly among younger age groups. Estimates suggest that people with diabetes die, on average, 6 years earlier than people without diabetes. We aimed to provide reliable estimates of the associations between age at diagnosis of diabetes and all-cause mortality, cause-specific mortality, and reductions in life expectancy. Methods For this observational study, we conducted a combined analysis of individual-participant data from 19 high income countries using two large-scale data sources: the Emerging Risk Factors Collaboration (96 cohorts, median baseline years 1961-2007, median latest follow-up years 1980-2013) and the UK Biobank (median baseline year 2006, median latest follow-up year 2020). We calculated age-adjusted and sex-adjusted hazard ratios (HRs) for all-cause mortality according to age at diagnosis of diabetes using data from 1 515 718 participants, in whom deaths were recorded during 23 center dot 1 million person-years of follow-up. We estimated cumulative survival by applying age-specific HRs to age-specific death rates from 2015 for the USA and the EU. Findings For participants with diabetes, we observed a linear dose-response association between earlier age at diagnosis and higher risk of all-cause mortality compared with participants without diabetes. HRs were 2 center dot 69 (95% CI 2 center dot 43-2 center dot 97) when diagnosed at 30-39 years, 2 center dot 26 (2 center dot 08-2 center dot 45) at 40-49 years, 1 center dot 84 (1 center dot 72-1 center dot 97) at 50-59 years, 1 center dot 57 (1 center dot 47-1 center dot 67) at 60-69 years, and 1 center dot 39 (1 center dot 29-1 center dot 51) at 70 years and older. HRs per decade of earlier diagnosis were similar for men and women. Using death rates from the USA, a 50-year-old individual with diabetes died on average 14 years earlier when diagnosed aged 30 years, 10 years earlier when diagnosed aged 40 years, or 6 years earlier
Published: 2023
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14. Vitamin K1 Intake and Incident Diabetes in the Danish Diet, Cancer, and Health Study

Author: Pokharel, Pratik, Bellinge, Jamie W, Dalgaard, Frederik, Murray, Kevin, Sim, Marc, Yeap, Bu B, Connolly, Emma, Blekkenhorst, Lauren C, Bondonno, Catherine P, Lewis, Joshua R, Gislason, Gunnar, Tjønneland, Anne, Overvad, Kim, Hodgson, Jonathan M, Schultz, Carl, Bondonno, Nicola P, Pokharel, Pratik, Bellinge, Jamie W, Dalgaard, Frederik, Murray, Kevin, Sim, Marc, Yeap, Bu B, Connolly, Emma, Blekkenhorst, Lauren C, Bondonno, Catherine P, Lewis, Joshua R, Gislason, Gunnar, Tjønneland, Anne, Overvad, Kim, Hodgson, Jonathan M, Schultz, Carl, and Bondonno, Nicola P
Abstract: Context Observational studies have reported lower risks of type 2 diabetes with higher vitamin K1 intake, but these studies overlook effect modification due to known diabetes risk factors. Objective To identify subgroups that might benefit from vitamin K1 intake, we examined associations between vitamin K1 intake and incident diabetes overall and in subpopulations at risk of diabetes. Methods Participants from the prospective cohort, the Danish Diet, Cancer, and Health Study, with no history of diabetes were followed up for diabetes incidence. The association between intake of vitamin K1, estimated from a food frequency questionnaire completed at baseline, and incident diabetes was determined using multivariable-adjusted Cox proportional-hazards models. Results In 54 787 Danish residents with a median (interquartile range) age of 56 (52-60) years at baseline, 6700 individuals were diagnosed with diabetes during 20.8 (17.3-21.6) years of follow-up. Vitamin K1 intake was inversely and linearly associated with incident diabetes (P < .0001). Compared to participants with the lowest vitamin K1 intake (median:57 µg/d), participants with the highest intakes (median:191 µg/d) had a 31% lower risk of diabetes (HR; 95% CI, 0.69; 0.64-0.74) after multivariable adjustments. The inverse association between vitamin K1 intake and incident diabetes was present in all subgroups (namely, men and women, ever and never smokers, low and high physical activity groups, and in participants who were normal to overweight and obese), with differences in absolute risk between subgroups. Conclusion Higher intake of foods rich in vitamin K1 was associated with a lower risk of diabetes. If the associations observed are causal, our results indicate that more cases of diabetes would be prevented in subgroups at higher risk (men, smokers, participants with obesity, and those with low physical activity). diet, non–insulin-dependent d
Published: 2023

15. Circulating insulin-like growth factors and risks of overall, aggressive and early-onset prostate cancer : a collaborative analysis of 20 prospective studies and Mendelian randomization analysis

Author: Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael V., Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-De-Mesquita, H. Bas, Cohn, Barbara A., Deschasaux-Tanguy, Melanie, Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Haiman, Christopher A., Hankey, Graham J., Holly, Jeffrey M. P., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Kubo, Tatsuhiko, Le Marchand, Loic, Macinnis, Robert J., Männistö, Satu, Metter, E. Jeffrey, Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Pollak, Michael N., Roobol, Monique J., Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Touvier, Mathilde, Van Den Eeden, Stephen K., Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., Travis, Ruth C., The PRACTICAL Consortium, CRUK, BPC3, CAPS, PEGASUS, Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael V., Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-De-Mesquita, H. Bas, Cohn, Barbara A., Deschasaux-Tanguy, Melanie, Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Haiman, Christopher A., Hankey, Graham J., Holly, Jeffrey M. P., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Kubo, Tatsuhiko, Le Marchand, Loic, Macinnis, Robert J., Männistö, Satu, Metter, E. Jeffrey, Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Pollak, Michael N., Roobol, Monique J., Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Touvier, Mathilde, Van Den Eeden, Stephen K., Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., Travis, Ruth C., and The PRACTICAL Consortium, CRUK, BPC3, CAPS, PEGASUS
Abstract: Background: Previous studies had limited power to assess the associations of circulating insulin-like growth factors (IGFs) and IGF-binding proteins (IGFBPs) with clinically relevant prostate cancer as a primary endpoint, and the association of genetically predicted IGF-I with aggressive prostate cancer is not known. We aimed to investigate the associations of IGF-I, IGF-II, IGFBP-1, IGFBP-2 and IGFBP-3 concentrations with overall, aggressive and early-onset prostate cancer. Methods: Prospective analysis of biomarkers using the Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group dataset (up to 20 studies, 17 009 prostate cancer cases, including 2332 aggressive cases). Odds ratios (OR) and 95% confidence intervals (CI) for prostate cancer were estimated using conditional logistic regression. For IGF-I, two-sample Mendelian randomization (MR) analysis was undertaken using instruments identified using UK Biobank (158 444 men) and outcome data from PRACTICAL (up to 85 554 cases, including 15 167 aggressive cases). Additionally, we used colocalization to rule out confounding by linkage disequilibrium. Results: In observational analyses, IGF-I was positively associated with risks of overall (OR per 1 SD = 1.09: 95% CI 1.07, 1.11), aggressive (1.09: 1.03, 1.16) and possibly early-onset disease (1.11: 1.00, 1.24); associations were similar in MR analyses (OR per 1 SD = 1.07: 1.00, 1.15; 1.10: 1.01, 1.20; and 1.13; 0.98, 1.30, respectively). Colocalization also indicated a shared signal for IGF-I and prostate cancer (PP4: 99%). Men with higher IGF-II (1.06: 1.02, 1.11) and IGFBP-3 (1.08: 1.04, 1.11) had higher risks of overall prostate cancer, whereas higher IGFBP-1 was associated with a lower risk (0.95: 0.91, 0.99); these associations were attenuated following adjustment for IGF-I. Conclusions: These findings support the role of IGF-I in the development of prostate cancer, including for aggressive disease.
Published: 2023
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16. Circulating insulin-like growth factors and risks of overall, aggressive and early-onset prostate cancer : a collaborative analysis of 20 prospective studies and Mendelian randomization analysis

Author: Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael V., Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-De-Mesquita, H. Bas, Cohn, Barbara A., Deschasaux-Tanguy, Melanie, Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Haiman, Christopher A., Hankey, Graham J., Holly, Jeffrey M. P., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Kubo, Tatsuhiko, Le Marchand, Loic, Macinnis, Robert J., Männistö, Satu, Metter, E. Jeffrey, Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Pollak, Michael N., Roobol, Monique J., Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Touvier, Mathilde, Van Den Eeden, Stephen K., Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., Travis, Ruth C., The PRACTICAL Consortium, CRUK, BPC3, CAPS, PEGASUS, Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael V., Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-De-Mesquita, H. Bas, Cohn, Barbara A., Deschasaux-Tanguy, Melanie, Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Haiman, Christopher A., Hankey, Graham J., Holly, Jeffrey M. P., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Kubo, Tatsuhiko, Le Marchand, Loic, Macinnis, Robert J., Männistö, Satu, Metter, E. Jeffrey, Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Pollak, Michael N., Roobol, Monique J., Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Touvier, Mathilde, Van Den Eeden, Stephen K., Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., Travis, Ruth C., and The PRACTICAL Consortium, CRUK, BPC3, CAPS, PEGASUS
Abstract: Background: Previous studies had limited power to assess the associations of circulating insulin-like growth factors (IGFs) and IGF-binding proteins (IGFBPs) with clinically relevant prostate cancer as a primary endpoint, and the association of genetically predicted IGF-I with aggressive prostate cancer is not known. We aimed to investigate the associations of IGF-I, IGF-II, IGFBP-1, IGFBP-2 and IGFBP-3 concentrations with overall, aggressive and early-onset prostate cancer. Methods: Prospective analysis of biomarkers using the Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group dataset (up to 20 studies, 17 009 prostate cancer cases, including 2332 aggressive cases). Odds ratios (OR) and 95% confidence intervals (CI) for prostate cancer were estimated using conditional logistic regression. For IGF-I, two-sample Mendelian randomization (MR) analysis was undertaken using instruments identified using UK Biobank (158 444 men) and outcome data from PRACTICAL (up to 85 554 cases, including 15 167 aggressive cases). Additionally, we used colocalization to rule out confounding by linkage disequilibrium. Results: In observational analyses, IGF-I was positively associated with risks of overall (OR per 1 SD = 1.09: 95% CI 1.07, 1.11), aggressive (1.09: 1.03, 1.16) and possibly early-onset disease (1.11: 1.00, 1.24); associations were similar in MR analyses (OR per 1 SD = 1.07: 1.00, 1.15; 1.10: 1.01, 1.20; and 1.13; 0.98, 1.30, respectively). Colocalization also indicated a shared signal for IGF-I and prostate cancer (PP4: 99%). Men with higher IGF-II (1.06: 1.02, 1.11) and IGFBP-3 (1.08: 1.04, 1.11) had higher risks of overall prostate cancer, whereas higher IGFBP-1 was associated with a lower risk (0.95: 0.91, 0.99); these associations were attenuated following adjustment for IGF-I. Conclusions: These findings support the role of IGF-I in the development of prostate cancer, including for aggressive disease.
Published: 2023
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17. Vitamin k-1 intake and incident diabetes in the Danish diet, cancer, and health study

Author: Pokharel, Pratik, Bellinge, Jamie W., Dalgaard, Frederik, Murray, Kevin, Sim, Marc, Yeap, Bu B., Connolly, Emma, Blekkenhorst, Lauren C., Bondonno, Catherine P., Lewis, Joshua R., Gislason, Gunnar, Tjønneland, Anne, Overvad, Kim, Hodgson, Jonathan M., Schultz, Carl, Bondonno, Nicola P., Pokharel, Pratik, Bellinge, Jamie W., Dalgaard, Frederik, Murray, Kevin, Sim, Marc, Yeap, Bu B., Connolly, Emma, Blekkenhorst, Lauren C., Bondonno, Catherine P., Lewis, Joshua R., Gislason, Gunnar, Tjønneland, Anne, Overvad, Kim, Hodgson, Jonathan M., Schultz, Carl, and Bondonno, Nicola P.
Abstract: Context: Observational studies have reported lower risks of type 2 diabetes with higher vitamin K1 intake, but these studies overlook effect modification due to known diabetes risk factors. Objective: To identify subgroups that might benefit from vitamin K1 intake, we examined associations between vitamin K1 intake and incident diabetes overall and in subpopulations at risk of diabetes. Methods: Participants from the prospective cohort, the Danish Diet, Cancer, and Health Study, with no history of diabetes were followed up for diabetes incidence. The association between intake of vitamin K1, estimated from a food frequency questionnaire completed at baseline, and incident diabetes was determined using multivariable-adjusted Cox proportional-hazards models. Results: In 54 787 Danish residents with a median (interquartile range) age of 56 (52-60) years at baseline, 6700 individuals were diagnosed with diabetes during 20.8 (17.3-21.6) years of follow-up. Vitamin K1 intake was inversely and linearly associated with incident diabetes (P < .0001). Compared to participants with the lowest vitamin K1 intake (median:57 g/d), participants with the highest intakes (median:191 g/d) had a 31% lower risk of diabetes (HR; 95% CI, 0.69; 0.64-0.74) after multivariable adjustments. The inverse association between vitamin K1 intake and incident diabetes was present in all subgroups (namely, men and women, ever and never smokers, low and high physical activity groups, and in participants who were normal to overweight and obese), with differences in absolute risk between subgroups. Conclusion: Higher intake of foods rich in vitamin K1 was associated with a lower risk of diabetes. If the associations observed are causal, our results indicate that more cases of diabetes would be prevented in subgroups at higher risk (men, smokers, participants with obesity, and those with low physical activity).
Published: 2023

18. Vitamin K1 intake and incident diabetes in the Danish Diet Cancer and Health Study: Supplemental information

Author: Pokharel, Pratik, Bellinge, Jamie W., Dalgaard, Frederik, Murray, Kevin, Sim, Marc, Yeap, Bu B., Connolly, Emma, Blekkenhorst, Lauren C., Bondonno, Catherine P., Lewis, Joshua, Gislason, Gunnar, Tjønneland, Anne, Overvad, Kim, Hodgson, Jonathan M., Schulz, Carl, Bondonno, Nicola P., Pokharel, Pratik, Bellinge, Jamie W., Dalgaard, Frederik, Murray, Kevin, Sim, Marc, Yeap, Bu B., Connolly, Emma, Blekkenhorst, Lauren C., Bondonno, Catherine P., Lewis, Joshua, Gislason, Gunnar, Tjønneland, Anne, Overvad, Kim, Hodgson, Jonathan M., Schulz, Carl, and Bondonno, Nicola P.
Published: 2023

19. Vitamin K1 Intake and Incident Diabetes in the Danish Diet, Cancer, and Health Study

Author: Pokharel, Pratik, Bellinge, Jamie W, Dalgaard, Frederik, Murray, Kevin, Sim, Marc, Yeap, Bu B, Connolly, Emma, Blekkenhorst, Lauren C, Bondonno, Catherine P, Lewis, Joshua R, Gislason, Gunnar, Tjønneland, Anne, Overvad, Kim, Hodgson, Jonathan M, Schultz, Carl, Bondonno, Nicola P, Pokharel, Pratik, Bellinge, Jamie W, Dalgaard, Frederik, Murray, Kevin, Sim, Marc, Yeap, Bu B, Connolly, Emma, Blekkenhorst, Lauren C, Bondonno, Catherine P, Lewis, Joshua R, Gislason, Gunnar, Tjønneland, Anne, Overvad, Kim, Hodgson, Jonathan M, Schultz, Carl, and Bondonno, Nicola P
Abstract: Context Observational studies have reported lower risks of type 2 diabetes with higher vitamin K1 intake, but these studies overlook effect modification due to known diabetes risk factors. Objective To identify subgroups that might benefit from vitamin K1 intake, we examined associations between vitamin K1 intake and incident diabetes overall and in subpopulations at risk of diabetes. Methods Participants from the prospective cohort, the Danish Diet, Cancer, and Health Study, with no history of diabetes were followed up for diabetes incidence. The association between intake of vitamin K1, estimated from a food frequency questionnaire completed at baseline, and incident diabetes was determined using multivariable-adjusted Cox proportional-hazards models. Results In 54 787 Danish residents with a median (interquartile range) age of 56 (52-60) years at baseline, 6700 individuals were diagnosed with diabetes during 20.8 (17.3-21.6) years of follow-up. Vitamin K1 intake was inversely and linearly associated with incident diabetes (P < .0001). Compared to participants with the lowest vitamin K1 intake (median:57 µg/d), participants with the highest intakes (median:191 µg/d) had a 31% lower risk of diabetes (HR; 95% CI, 0.69; 0.64-0.74) after multivariable adjustments. The inverse association between vitamin K1 intake and incident diabetes was present in all subgroups (namely, men and women, ever and never smokers, low and high physical activity groups, and in participants who were normal to overweight and obese), with differences in absolute risk between subgroups. Conclusion Higher intake of foods rich in vitamin K1 was associated with a lower risk of diabetes. If the associations observed are causal, our results indicate that more cases of diabetes would be prevented in subgroups at higher risk (men, smokers, participants with obesity, and those with low physical activity). diet, non–insulin-dependent d
Published: 2023

20. Circulating insulin-like growth factors and risks of overall, aggressive and early-onset prostate cancer : a collaborative analysis of 20 prospective studies and Mendelian randomization analysis

Author: Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael, V, Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, H. Bas, Cohn, Barbara A., Deschasaux-Tanguy, Melanie, Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Haiman, Christopher A., Hankey, Graham J., Holly, Jeffrey M. P., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Kubo, Tatsuhiko, Le Marchand, Loic, MacInnis, Robert J., Mannisto, Satu, Metter, E. Jeffrey, Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Pollak, Michael N., Roobol, Monique J., Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Touvier, Mathilde, Van Den Eeden, Stephen K., Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., Travis, Ruth C., Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael, V, Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, H. Bas, Cohn, Barbara A., Deschasaux-Tanguy, Melanie, Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Haiman, Christopher A., Hankey, Graham J., Holly, Jeffrey M. P., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Kubo, Tatsuhiko, Le Marchand, Loic, MacInnis, Robert J., Mannisto, Satu, Metter, E. Jeffrey, Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Pollak, Michael N., Roobol, Monique J., Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Touvier, Mathilde, Van Den Eeden, Stephen K., Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., and Travis, Ruth C.
Abstract: Background Previous studies had limited power to assess the associations of circulating insulin-like growth factors (IGFs) and IGF-binding proteins (IGFBPs) with clinically relevant prostate cancer as a primary endpoint, and the association of genetically predicted IGF-I with aggressive prostate cancer is not known. We aimed to investigate the associations of IGF-I, IGF-II, IGFBP-1, IGFBP-2 and IGFBP-3 concentrations with overall, aggressive and early-onset prostate cancer. Methods Prospective analysis of biomarkers using the Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group dataset (up to 20 studies, 17 009 prostate cancer cases, including 2332 aggressive cases). Odds ratios (OR) and 95% confidence intervals (CI) for prostate cancer were estimated using conditional logistic regression. For IGF-I, two-sample Mendelian randomization (MR) analysis was undertaken using instruments identified using UK Biobank (158 444 men) and outcome data from PRACTICAL (up to 85 554 cases, including 15 167 aggressive cases). Additionally, we used colocalization to rule out confounding by linkage disequilibrium. Results In observational analyses, IGF-I was positively associated with risks of overall (OR per 1 SD = 1.09: 95% CI 1.07, 1.11), aggressive (1.09: 1.03, 1.16) and possibly early-onset disease (1.11: 1.00, 1.24); associations were similar in MR analyses (OR per 1 SD = 1.07: 1.00, 1.15; 1.10: 1.01, 1.20; and 1.13; 0.98, 1.30, respectively). Colocalization also indicated a shared signal for IGF-I and prostate cancer (PP4: 99%). Men with higher IGF-II (1.06: 1.02, 1.11) and IGFBP-3 (1.08: 1.04, 1.11) had higher risks of overall prostate cancer, whereas higher IGFBP-1 was associated with a lower risk (0.95: 0.91, 0.99); these associations were attenuated following adjustment for IGF-I. Conclusions These findings support the role of IGF-I in the development of prostate cancer, including for aggressive disease.
Published: 2023
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21. Circulating free testosterone and risk of aggressive prostate cancer : Prospective and Mendelian randomisation analyses in international consortia

Author: Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael, V, Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, Bas, Chen, Chu, Cohn, Barbara A., Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Goodman, Gary E., Haiman, Christopher A., Hankey, Graeme J., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Knekt, Paul, Kubo, Tatsuhiko, Langseth, Hilde, Laughlin, Gail, Le Marchand, Loic, Luostarinen, Tapio, MacInnis, Robert J., Maenpaa, Hanna O., Mannisto, Satu, Metter, Jeffrey E., Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Rissanen, Harri, Sawada, Norie, Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Tsugane, Shoichiro, Vatten, Lars, Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., Travis, Ruth C., Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael, V, Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, Bas, Chen, Chu, Cohn, Barbara A., Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Goodman, Gary E., Haiman, Christopher A., Hankey, Graeme J., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Knekt, Paul, Kubo, Tatsuhiko, Langseth, Hilde, Laughlin, Gail, Le Marchand, Loic, Luostarinen, Tapio, MacInnis, Robert J., Maenpaa, Hanna O., Mannisto, Satu, Metter, Jeffrey E., Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Rissanen, Harri, Sawada, Norie, Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Tsugane, Shoichiro, Vatten, Lars, Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., and Travis, Ruth C.
Abstract: Previous studies had limited power to assess the associations of testosterone with aggressive disease as a primary endpoint. Further, the association of genetically predicted testosterone with aggressive disease is not known. We investigated the associations of calculated free and measured total testosterone and sex hormone-binding globulin (SHBG) with aggressive, overall and early-onset prostate cancer. In blood-based analyses, odds ratios (OR) and 95% confidence intervals (CI) for prostate cancer were estimated using conditional logistic regression from prospective analysis of biomarker concentrations in the Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group (up to 25 studies, 14 944 cases and 36 752 controls, including 1870 aggressive prostate cancers). In Mendelian randomisation (MR) analyses, using instruments identified using UK Biobank (up to 194 453 men) and outcome data from PRACTICAL (up to 79 148 cases and 61 106 controls, including 15 167 aggressive cancers), ORs were estimated using the inverse-variance weighted method. Free testosterone was associated with aggressive disease in MR analyses (OR per 1 SD = 1.23, 95% CI = 1.08-1.40). In blood-based analyses there was no association with aggressive disease overall, but there was heterogeneity by age at blood collection (OR for men aged <60 years 1.14, CI = 1.02-1.28; P-het = .0003: inverse association for older ages). Associations for free testosterone were positive for overall prostate cancer (MR: 1.20, 1.08-1.34; blood-based: 1.03, 1.01-1.05) and early-onset prostate cancer (MR: 1.37, 1.09-1.73; blood-based: 1.08, 0.98-1.19). SHBG and total testosterone were inversely associated with overall prostate cancer in blood-based analyses, with null associations in MR analysis. Our results support free testosterone, rather than total testosterone, in the development of prostate cancer, including aggressive subgroups.
Published: 2022
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22. Circulating free testosterone and risk of aggressive prostate cancer : Prospective and Mendelian randomisation analyses in international consortia

Author: Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael, V, Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, Bas, Chen, Chu, Cohn, Barbara A., Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Goodman, Gary E., Haiman, Christopher A., Hankey, Graeme J., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Knekt, Paul, Kubo, Tatsuhiko, Langseth, Hilde, Laughlin, Gail, Le Marchand, Loic, Luostarinen, Tapio, MacInnis, Robert J., Maenpaa, Hanna O., Mannisto, Satu, Metter, Jeffrey E., Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Rissanen, Harri, Sawada, Norie, Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Tsugane, Shoichiro, Vatten, Lars, Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., Travis, Ruth C., Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael, V, Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, Bas, Chen, Chu, Cohn, Barbara A., Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Goodman, Gary E., Haiman, Christopher A., Hankey, Graeme J., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Knekt, Paul, Kubo, Tatsuhiko, Langseth, Hilde, Laughlin, Gail, Le Marchand, Loic, Luostarinen, Tapio, MacInnis, Robert J., Maenpaa, Hanna O., Mannisto, Satu, Metter, Jeffrey E., Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Rissanen, Harri, Sawada, Norie, Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Tsugane, Shoichiro, Vatten, Lars, Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., and Travis, Ruth C.
Abstract: Previous studies had limited power to assess the associations of testosterone with aggressive disease as a primary endpoint. Further, the association of genetically predicted testosterone with aggressive disease is not known. We investigated the associations of calculated free and measured total testosterone and sex hormone-binding globulin (SHBG) with aggressive, overall and early-onset prostate cancer. In blood-based analyses, odds ratios (OR) and 95% confidence intervals (CI) for prostate cancer were estimated using conditional logistic regression from prospective analysis of biomarker concentrations in the Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group (up to 25 studies, 14 944 cases and 36 752 controls, including 1870 aggressive prostate cancers). In Mendelian randomisation (MR) analyses, using instruments identified using UK Biobank (up to 194 453 men) and outcome data from PRACTICAL (up to 79 148 cases and 61 106 controls, including 15 167 aggressive cancers), ORs were estimated using the inverse-variance weighted method. Free testosterone was associated with aggressive disease in MR analyses (OR per 1 SD = 1.23, 95% CI = 1.08-1.40). In blood-based analyses there was no association with aggressive disease overall, but there was heterogeneity by age at blood collection (OR for men aged <60 years 1.14, CI = 1.02-1.28; P-het = .0003: inverse association for older ages). Associations for free testosterone were positive for overall prostate cancer (MR: 1.20, 1.08-1.34; blood-based: 1.03, 1.01-1.05) and early-onset prostate cancer (MR: 1.37, 1.09-1.73; blood-based: 1.08, 0.98-1.19). SHBG and total testosterone were inversely associated with overall prostate cancer in blood-based analyses, with null associations in MR analysis. Our results support free testosterone, rather than total testosterone, in the development of prostate cancer, including aggressive subgroups.
Published: 2022
Full Text: View/download PDF

23. Circulating free testosterone and risk of aggressive prostate cancer : Prospective and Mendelian randomisation analyses in international consortia

Author: Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael V., Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, Bas, Chen, Chu, Cohn, Barbara A., Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Goodman, Gary E., Haiman, Christopher A., Hankey, Graeme J., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Knekt, Paul, Kubo, Tatsuhiko, Langseth, Hilde, Laughlin, Gail, Le Marchand, Loic, Luostarinen, Tapio, MacInnis, Robert J., Mäenpää, Hanna O., Männistö, Satu, Metter, Jeffrey E., Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Rissanen, Harri, Sawada, Norie, Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Tsugane, Shoichiro, Vatten, Lars, Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., Travis, Ruth C., Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael V., Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, Bas, Chen, Chu, Cohn, Barbara A., Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Goodman, Gary E., Haiman, Christopher A., Hankey, Graeme J., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Knekt, Paul, Kubo, Tatsuhiko, Langseth, Hilde, Laughlin, Gail, Le Marchand, Loic, Luostarinen, Tapio, MacInnis, Robert J., Mäenpää, Hanna O., Männistö, Satu, Metter, Jeffrey E., Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Rissanen, Harri, Sawada, Norie, Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Tsugane, Shoichiro, Vatten, Lars, Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., and Travis, Ruth C.
Abstract: Previous studies had limited power to assess the associations of testosterone with aggressive disease as a primary endpoint. Further, the association of genetically predicted testosterone with aggressive disease is not known. We investigated the associations of calculated free and measured total testosterone and sex hormone-binding globulin (SHBG) with aggressive, overall and early-onset prostate cancer. In blood-based analyses, odds ratios (OR) and 95% confidence intervals (CI) for prostate cancer were estimated using conditional logistic regression from prospective analysis of biomarker concentrations in the Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group (up to 25 studies, 14 944 cases and 36 752 controls, including 1870 aggressive prostate cancers). In Mendelian randomisation (MR) analyses, using instruments identified using UK Biobank (up to 194 453 men) and outcome data from PRACTICAL (up to 79 148 cases and 61 106 controls, including 15 167 aggressive cancers), ORs were estimated using the inverse-variance weighted method. Free testosterone was associated with aggressive disease in MR analyses (OR per 1 SD = 1.23, 95% CI = 1.08-1.40). In blood-based analyses there was no association with aggressive disease overall, but there was heterogeneity by age at blood collection (OR for men aged <60 years 1.14, CI = 1.02-1.28; Phet =.0003: inverse association for older ages). Associations for free testosterone were positive for overall prostate cancer (MR: 1.20, 1.08-1.34; blood-based: 1.03, 1.01-1.05) and early-onset prostate cancer (MR: 1.37, 1.09-1.73; blood-based: 1.08, 0.98-1.19). SHBG and total testosterone were inversely associated with overall prostate cancer in blood-based analyses, with null associations in MR analysis. Our results support free testosterone, rather than total testosterone, in the development of prostate cancer, including aggressive subgroups.
Published: 2022
Full Text: View/download PDF

24. Circulating free testosterone and risk of aggressive prostate cancer : Prospective and Mendelian randomisation analyses in international consortia

Author: Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael V., Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, Bas, Chen, Chu, Cohn, Barbara A., Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Goodman, Gary E., Haiman, Christopher A., Hankey, Graeme J., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Knekt, Paul, Kubo, Tatsuhiko, Langseth, Hilde, Laughlin, Gail, Le Marchand, Loic, Luostarinen, Tapio, MacInnis, Robert J., Mäenpää, Hanna O., Männistö, Satu, Metter, Jeffrey E., Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Rissanen, Harri, Sawada, Norie, Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Tsugane, Shoichiro, Vatten, Lars, Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., Travis, Ruth C., Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael V., Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, Bas, Chen, Chu, Cohn, Barbara A., Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Goodman, Gary E., Haiman, Christopher A., Hankey, Graeme J., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Knekt, Paul, Kubo, Tatsuhiko, Langseth, Hilde, Laughlin, Gail, Le Marchand, Loic, Luostarinen, Tapio, MacInnis, Robert J., Mäenpää, Hanna O., Männistö, Satu, Metter, Jeffrey E., Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Rissanen, Harri, Sawada, Norie, Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Tsugane, Shoichiro, Vatten, Lars, Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., and Travis, Ruth C.
Abstract: Previous studies had limited power to assess the associations of testosterone with aggressive disease as a primary endpoint. Further, the association of genetically predicted testosterone with aggressive disease is not known. We investigated the associations of calculated free and measured total testosterone and sex hormone-binding globulin (SHBG) with aggressive, overall and early-onset prostate cancer. In blood-based analyses, odds ratios (OR) and 95% confidence intervals (CI) for prostate cancer were estimated using conditional logistic regression from prospective analysis of biomarker concentrations in the Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group (up to 25 studies, 14 944 cases and 36 752 controls, including 1870 aggressive prostate cancers). In Mendelian randomisation (MR) analyses, using instruments identified using UK Biobank (up to 194 453 men) and outcome data from PRACTICAL (up to 79 148 cases and 61 106 controls, including 15 167 aggressive cancers), ORs were estimated using the inverse-variance weighted method. Free testosterone was associated with aggressive disease in MR analyses (OR per 1 SD = 1.23, 95% CI = 1.08-1.40). In blood-based analyses there was no association with aggressive disease overall, but there was heterogeneity by age at blood collection (OR for men aged <60 years 1.14, CI = 1.02-1.28; Phet =.0003: inverse association for older ages). Associations for free testosterone were positive for overall prostate cancer (MR: 1.20, 1.08-1.34; blood-based: 1.03, 1.01-1.05) and early-onset prostate cancer (MR: 1.37, 1.09-1.73; blood-based: 1.08, 0.98-1.19). SHBG and total testosterone were inversely associated with overall prostate cancer in blood-based analyses, with null associations in MR analysis. Our results support free testosterone, rather than total testosterone, in the development of prostate cancer, including aggressive subgroups.
Published: 2022
Full Text: View/download PDF

25. Circulating free testosterone and risk of aggressive prostate cancer : Prospective and Mendelian randomisation analyses in international consortia

Author: Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael, V, Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, Bas, Chen, Chu, Cohn, Barbara A., Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Goodman, Gary E., Haiman, Christopher A., Hankey, Graeme J., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Knekt, Paul, Kubo, Tatsuhiko, Langseth, Hilde, Laughlin, Gail, Le Marchand, Loic, Luostarinen, Tapio, MacInnis, Robert J., Maenpaa, Hanna O., Mannisto, Satu, Metter, Jeffrey E., Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Rissanen, Harri, Sawada, Norie, Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Tsugane, Shoichiro, Vatten, Lars, Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., Travis, Ruth C., Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael, V, Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, Bas, Chen, Chu, Cohn, Barbara A., Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Goodman, Gary E., Haiman, Christopher A., Hankey, Graeme J., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Knekt, Paul, Kubo, Tatsuhiko, Langseth, Hilde, Laughlin, Gail, Le Marchand, Loic, Luostarinen, Tapio, MacInnis, Robert J., Maenpaa, Hanna O., Mannisto, Satu, Metter, Jeffrey E., Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Rissanen, Harri, Sawada, Norie, Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Tsugane, Shoichiro, Vatten, Lars, Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., and Travis, Ruth C.
Abstract: Previous studies had limited power to assess the associations of testosterone with aggressive disease as a primary endpoint. Further, the association of genetically predicted testosterone with aggressive disease is not known. We investigated the associations of calculated free and measured total testosterone and sex hormone-binding globulin (SHBG) with aggressive, overall and early-onset prostate cancer. In blood-based analyses, odds ratios (OR) and 95% confidence intervals (CI) for prostate cancer were estimated using conditional logistic regression from prospective analysis of biomarker concentrations in the Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group (up to 25 studies, 14 944 cases and 36 752 controls, including 1870 aggressive prostate cancers). In Mendelian randomisation (MR) analyses, using instruments identified using UK Biobank (up to 194 453 men) and outcome data from PRACTICAL (up to 79 148 cases and 61 106 controls, including 15 167 aggressive cancers), ORs were estimated using the inverse-variance weighted method. Free testosterone was associated with aggressive disease in MR analyses (OR per 1 SD = 1.23, 95% CI = 1.08-1.40). In blood-based analyses there was no association with aggressive disease overall, but there was heterogeneity by age at blood collection (OR for men aged <60 years 1.14, CI = 1.02-1.28; P-het = .0003: inverse association for older ages). Associations for free testosterone were positive for overall prostate cancer (MR: 1.20, 1.08-1.34; blood-based: 1.03, 1.01-1.05) and early-onset prostate cancer (MR: 1.37, 1.09-1.73; blood-based: 1.08, 0.98-1.19). SHBG and total testosterone were inversely associated with overall prostate cancer in blood-based analyses, with null associations in MR analysis. Our results support free testosterone, rather than total testosterone, in the development of prostate cancer, including aggressive subgroups.
Published: 2022
Full Text: View/download PDF

26. Circulating free testosterone and risk of aggressive prostate cancer : Prospective and Mendelian randomisation analyses in international consortia

Author: Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael V., Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, Bas, Chen, Chu, Cohn, Barbara A., Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Goodman, Gary E., Haiman, Christopher A., Hankey, Graeme J., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Knekt, Paul, Kubo, Tatsuhiko, Langseth, Hilde, Laughlin, Gail, Le Marchand, Loic, Luostarinen, Tapio, MacInnis, Robert J., Mäenpää, Hanna O., Männistö, Satu, Metter, Jeffrey E., Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Rissanen, Harri, Sawada, Norie, Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Tsugane, Shoichiro, Vatten, Lars, Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., Travis, Ruth C., Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael V., Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, Bas, Chen, Chu, Cohn, Barbara A., Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Goodman, Gary E., Haiman, Christopher A., Hankey, Graeme J., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Knekt, Paul, Kubo, Tatsuhiko, Langseth, Hilde, Laughlin, Gail, Le Marchand, Loic, Luostarinen, Tapio, MacInnis, Robert J., Mäenpää, Hanna O., Männistö, Satu, Metter, Jeffrey E., Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Rissanen, Harri, Sawada, Norie, Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Tsugane, Shoichiro, Vatten, Lars, Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., and Travis, Ruth C.
Abstract: Previous studies had limited power to assess the associations of testosterone with aggressive disease as a primary endpoint. Further, the association of genetically predicted testosterone with aggressive disease is not known. We investigated the associations of calculated free and measured total testosterone and sex hormone-binding globulin (SHBG) with aggressive, overall and early-onset prostate cancer. In blood-based analyses, odds ratios (OR) and 95% confidence intervals (CI) for prostate cancer were estimated using conditional logistic regression from prospective analysis of biomarker concentrations in the Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group (up to 25 studies, 14 944 cases and 36 752 controls, including 1870 aggressive prostate cancers). In Mendelian randomisation (MR) analyses, using instruments identified using UK Biobank (up to 194 453 men) and outcome data from PRACTICAL (up to 79 148 cases and 61 106 controls, including 15 167 aggressive cancers), ORs were estimated using the inverse-variance weighted method. Free testosterone was associated with aggressive disease in MR analyses (OR per 1 SD = 1.23, 95% CI = 1.08-1.40). In blood-based analyses there was no association with aggressive disease overall, but there was heterogeneity by age at blood collection (OR for men aged <60 years 1.14, CI = 1.02-1.28; Phet =.0003: inverse association for older ages). Associations for free testosterone were positive for overall prostate cancer (MR: 1.20, 1.08-1.34; blood-based: 1.03, 1.01-1.05) and early-onset prostate cancer (MR: 1.37, 1.09-1.73; blood-based: 1.08, 0.98-1.19). SHBG and total testosterone were inversely associated with overall prostate cancer in blood-based analyses, with null associations in MR analysis. Our results support free testosterone, rather than total testosterone, in the development of prostate cancer, including aggressive subgroups.
Published: 2022
Full Text: View/download PDF

27. Circulating free testosterone and risk of aggressive prostate cancer : Prospective and Mendelian randomisation analyses in international consortia

Author: Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael, V, Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, Bas, Chen, Chu, Cohn, Barbara A., Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Goodman, Gary E., Haiman, Christopher A., Hankey, Graeme J., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Knekt, Paul, Kubo, Tatsuhiko, Langseth, Hilde, Laughlin, Gail, Le Marchand, Loic, Luostarinen, Tapio, MacInnis, Robert J., Maenpaa, Hanna O., Mannisto, Satu, Metter, Jeffrey E., Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Rissanen, Harri, Sawada, Norie, Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Tsugane, Shoichiro, Vatten, Lars, Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., Travis, Ruth C., Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael, V, Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, Bas, Chen, Chu, Cohn, Barbara A., Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Goodman, Gary E., Haiman, Christopher A., Hankey, Graeme J., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Knekt, Paul, Kubo, Tatsuhiko, Langseth, Hilde, Laughlin, Gail, Le Marchand, Loic, Luostarinen, Tapio, MacInnis, Robert J., Maenpaa, Hanna O., Mannisto, Satu, Metter, Jeffrey E., Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Rissanen, Harri, Sawada, Norie, Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Tsugane, Shoichiro, Vatten, Lars, Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., and Travis, Ruth C.
Abstract: Previous studies had limited power to assess the associations of testosterone with aggressive disease as a primary endpoint. Further, the association of genetically predicted testosterone with aggressive disease is not known. We investigated the associations of calculated free and measured total testosterone and sex hormone-binding globulin (SHBG) with aggressive, overall and early-onset prostate cancer. In blood-based analyses, odds ratios (OR) and 95% confidence intervals (CI) for prostate cancer were estimated using conditional logistic regression from prospective analysis of biomarker concentrations in the Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group (up to 25 studies, 14 944 cases and 36 752 controls, including 1870 aggressive prostate cancers). In Mendelian randomisation (MR) analyses, using instruments identified using UK Biobank (up to 194 453 men) and outcome data from PRACTICAL (up to 79 148 cases and 61 106 controls, including 15 167 aggressive cancers), ORs were estimated using the inverse-variance weighted method. Free testosterone was associated with aggressive disease in MR analyses (OR per 1 SD = 1.23, 95% CI = 1.08-1.40). In blood-based analyses there was no association with aggressive disease overall, but there was heterogeneity by age at blood collection (OR for men aged <60 years 1.14, CI = 1.02-1.28; P-het = .0003: inverse association for older ages). Associations for free testosterone were positive for overall prostate cancer (MR: 1.20, 1.08-1.34; blood-based: 1.03, 1.01-1.05) and early-onset prostate cancer (MR: 1.37, 1.09-1.73; blood-based: 1.08, 0.98-1.19). SHBG and total testosterone were inversely associated with overall prostate cancer in blood-based analyses, with null associations in MR analysis. Our results support free testosterone, rather than total testosterone, in the development of prostate cancer, including aggressive subgroups.
Published: 2022
Full Text: View/download PDF

28. Subclinical thyroid dysfunction and incident diabetes: a systematic review and an individual participant data analysis of prospective cohort studies.

Author: Alwan, Heba, Alwan, Heba, Villoz, Fanny, Feller, Martin, Dullaart, Robin PF, Bakker, Stephan JL, Peeters, Robin P, Kavousi, Maryam, Bauer, Douglas C, Cappola, Anne R, Yeap, Bu B, Walsh, John P, Brown, Suzanne J, Ceresini, Graziano, Ferrucci, Luigi, Gussekloo, Jacobijn, Trompet, Stella, Iacoviello, Massimo, Moon, Jae Hoon, Razvi, Salman, Bensenor, Isabela M, Azizi, Fereidoun, Amouzegar, Atieh, Valdés, Sergio, Colomo, Natalia, Wareham, Nick J, Jukema, J Wouter, Westendorp, Rudi GJ, Kim, Ki Woong, Rodondi, Nicolas, Del Giovane, Cinzia, Alwan, Heba, Alwan, Heba, Villoz, Fanny, Feller, Martin, Dullaart, Robin PF, Bakker, Stephan JL, Peeters, Robin P, Kavousi, Maryam, Bauer, Douglas C, Cappola, Anne R, Yeap, Bu B, Walsh, John P, Brown, Suzanne J, Ceresini, Graziano, Ferrucci, Luigi, Gussekloo, Jacobijn, Trompet, Stella, Iacoviello, Massimo, Moon, Jae Hoon, Razvi, Salman, Bensenor, Isabela M, Azizi, Fereidoun, Amouzegar, Atieh, Valdés, Sergio, Colomo, Natalia, Wareham, Nick J, Jukema, J Wouter, Westendorp, Rudi GJ, Kim, Ki Woong, Rodondi, Nicolas, and Del Giovane, Cinzia
Abstract: ObjectiveFew prospective studies have assessed whether individuals with subclinical thyroid dysfunction are more likely to develop diabetes, with conflicting results. In this study, we conducted a systematic review of the literature and an individual participant data analysis of multiple prospective cohorts to investigate the association between subclinical thyroid dysfunction and incident diabetes.MethodsWe performed a systematic review of the literature in Medline, Embase, and the Cochrane Library from inception to February 11, 2022. A two-stage individual participant data analysis was conducted to compare participants with subclinical hypothyroidism and subclinical hyperthyroidism vs euthyroidism at baseline and the adjusted risk of developing diabetes at follow-up.ResultsAmong 61 178 adults from 18 studies, 49% were females, mean age was 58 years, and mean follow-up time was 8.2 years. At the last available follow-up, there was no association between subclinical hypothyroidism and incidence of diabetes (odds ratio (OR) = 1.02, 95% CI: 0.88-1.17, I2 = 0%) or subclinical hyperthyroidism and incidence of diabetes (OR = 1.03, 95% CI: 0.82-1.30, I2 = 0%), in age- and sex-adjusted analyses. Time-to-event analysis showed similar results (hazard ratio for subclinical hypothyroidism: 0.98, 95% CI: 0.87-1.11; hazard ratio for subclinical hyperthyroidism: 1.07, 95% CI: 0.88-1.29). The results were robust in all sub-group and sensitivity analyses.ConclusionsThis is the largest systematic review and individual participant data analysis to date investigating the prospective association between subclinical thyroid dysfunction and diabetes. We did not find an association between subclinical thyroid dysfunction and incident diabetes. Our results do not support screening patients with subclinical thyroid dysfunction for diabetes.Significance statementEvidence is conflicting regarding whether an association exists between subclinical thyroid dysfunction and incident diabetes. We t
Published: 2022

29. Subclinical thyroid dysfunction and incident diabetes:a systematic review and an individual participant data analysis of prospective cohort studies

Author: Alwan, Heba, Villoz, Fanny, Feller, Martin, Dullaart, Robin P.F., Bakker, Stephan J.L., Peeters, Robin P., Kavousi, Maryam, Bauer, Douglas C., Cappola, Anne R., Yeap, Bu B., Walsh, John P., Brown, Suzanne J., Ceresini, Graziano, Ferrucci, Luigi, Gussekloo, Jacobijn, Trompet, Stella, Iacoviello, Massimo, Moon, Jae Hoon, Razvi, Salman, Bensenor, Isabela M., Azizi, Fereidoun, Amouzegar, Atieh, Valdés, Sergio, Colomo, Natalia, Wareham, Nick J., Jukema, J. Wouter, Westendorp, Rudi G.J., Kim, Ki Woong, Rodondi, Nicolas, Del Giovane, Cinzia, Alwan, Heba, Villoz, Fanny, Feller, Martin, Dullaart, Robin P.F., Bakker, Stephan J.L., Peeters, Robin P., Kavousi, Maryam, Bauer, Douglas C., Cappola, Anne R., Yeap, Bu B., Walsh, John P., Brown, Suzanne J., Ceresini, Graziano, Ferrucci, Luigi, Gussekloo, Jacobijn, Trompet, Stella, Iacoviello, Massimo, Moon, Jae Hoon, Razvi, Salman, Bensenor, Isabela M., Azizi, Fereidoun, Amouzegar, Atieh, Valdés, Sergio, Colomo, Natalia, Wareham, Nick J., Jukema, J. Wouter, Westendorp, Rudi G.J., Kim, Ki Woong, Rodondi, Nicolas, and Del Giovane, Cinzia
Abstract: Objective Few prospective studies have assessed whether individuals with subclinical thyroid dysfunction are more likely to develop diabetes, with conflicting results. In this study, we conducted a systematic review of the literature and an individual participant data analysis of multiple prospective cohorts to investigate the association between subclinical thyroid dysfunction and incident diabetes. Methods We performed a systematic review of the literature in Medline, Embase, and the Cochrane Library from inception to February 11, 2022. A two-stage individual participant data analysis was conducted to compare participants with subclinical hypothyroidism and subclinical hyperthyroidism vs euthyroidism at baseline and the adjusted risk of developing diabetes at follow-up. Results Among 61 178 adults from 18 studies, 49% were females, mean age was 58 years, and mean follow-up time was 8.2 years. At the last available follow-up, there was no association between subclinical hypothyroidism and incidence of diabetes (odds ratio (OR) = 1.02, 95% CI: 0.88–1.17, I2 = 0%) or subclinical hyperthyroidism and incidence of diabetes (OR = 1.03, 95% CI: 0.82–1.30, I2 = 0%), in age- and sex-adjusted analyses. Time-to-event analysis showed similar results (hazard ratio for subclinical hypothyroidism: 0.98, 95% CI: 0.87–1.11; hazard ratio for subclinical hyperthyroidism: 1.07, 95% CI: 0.88–1.29). The results were robust in all sub-group and sensitivity analyses. Conclusions This is the largest systematic review and individual participant data analysis to date investigating the prospective association between subclinical thyroid dysfunction and diabetes. We did not find an association between subclinical thyroid dysfunction and incident diabetes. Our results do not support screening patients with subclinical thyroid dysfunction for diabetes. Significance statement Evidence is conflicting regarding whether an association exists be, Objective: Few prospective studies have assessed whether individuals with subclinical thyroid dysfunction are more likely to develop diabetes, with conflicting results. In this study, we conducted a systematic review of the literature and an individual participant data analysis of multiple prospective cohorts to investigate the association between subclinical thyroid dysfunction and incident diabetes. Methods: We performed a systematic review of the literature in Medline, Embase, and the Cochrane Library from inception to February 11, 2022. A two-stage individual participant data analysis was conducted to compare participants with subclinical hypothyroidism and subclinical hyperthyroidism vs euthyroidism at baseline and the adjusted risk of developing diabetes at follow-up. Results: Among 61 178 adults from 18 studies, 49% were females, mean age was 58 years, and mean follow-up time was 8.2 years. At the last available follow-up, there was no association between subclinical hypothyroidism and incidence of diabetes (odds ratio (OR) = 1.02, 95% CI: 0.88-1.17, I2 = 0%) or subclinical hyperthyroidism and incidence of diabetes (OR = 1.03, 95% CI: 0.82-1.30, I2 = 0%), in age- and sex-adjusted analyses. Time-to-event analysis showed similar results (hazard ratio for subclinical hypothyroidism: 0.98, 95% CI: 0.87-1.11; hazard ratio for subclinical hyperthyroidism: 1.07, 95% CI: 0.88-1.29). The results were robust in all sub-group and sensitivity analyses. Conclusions: This is the largest systematic review and individual participant data analysis to date investigating the prospective association between subclinical thyroid dysfunction and diabetes. We did not find an association between subclinical thyroid dysfunction and incident diabetes. Our results do not support screening patients with subclinical thyroid dysfunction for diabetes. Significance statement: Evidence is conflicting regarding whether an association exists between subclinical thyroid dysfunction and incide
Published: 2022

30. Subclinical thyroid dysfunction and incident diabetes:a systematic review and an individual participant data analysis of prospective cohort studies

Author: Alwan, Heba, Villoz, Fanny, Feller, Martin, Dullaart, Robin P.F., Bakker, Stephan J.L., Peeters, Robin P., Kavousi, Maryam, Bauer, Douglas C., Cappola, Anne R., Yeap, Bu B., Walsh, John P., Brown, Suzanne J., Ceresini, Graziano, Ferrucci, Luigi, Gussekloo, Jacobijn, Trompet, Stella, Iacoviello, Massimo, Moon, Jae Hoon, Razvi, Salman, Bensenor, Isabela M., Azizi, Fereidoun, Amouzegar, Atieh, Valdés, Sergio, Colomo, Natalia, Wareham, Nick J., Jukema, J. Wouter, Westendorp, Rudi G.J., Kim, Ki Woong, Rodondi, Nicolas, Del Giovane, Cinzia, Alwan, Heba, Villoz, Fanny, Feller, Martin, Dullaart, Robin P.F., Bakker, Stephan J.L., Peeters, Robin P., Kavousi, Maryam, Bauer, Douglas C., Cappola, Anne R., Yeap, Bu B., Walsh, John P., Brown, Suzanne J., Ceresini, Graziano, Ferrucci, Luigi, Gussekloo, Jacobijn, Trompet, Stella, Iacoviello, Massimo, Moon, Jae Hoon, Razvi, Salman, Bensenor, Isabela M., Azizi, Fereidoun, Amouzegar, Atieh, Valdés, Sergio, Colomo, Natalia, Wareham, Nick J., Jukema, J. Wouter, Westendorp, Rudi G.J., Kim, Ki Woong, Rodondi, Nicolas, and Del Giovane, Cinzia
Abstract: Objective Few prospective studies have assessed whether individuals with subclinical thyroid dysfunction are more likely to develop diabetes, with conflicting results. In this study, we conducted a systematic review of the literature and an individual participant data analysis of multiple prospective cohorts to investigate the association between subclinical thyroid dysfunction and incident diabetes. Methods We performed a systematic review of the literature in Medline, Embase, and the Cochrane Library from inception to February 11, 2022. A two-stage individual participant data analysis was conducted to compare participants with subclinical hypothyroidism and subclinical hyperthyroidism vs euthyroidism at baseline and the adjusted risk of developing diabetes at follow-up. Results Among 61 178 adults from 18 studies, 49% were females, mean age was 58 years, and mean follow-up time was 8.2 years. At the last available follow-up, there was no association between subclinical hypothyroidism and incidence of diabetes (odds ratio (OR) = 1.02, 95% CI: 0.88–1.17, I2 = 0%) or subclinical hyperthyroidism and incidence of diabetes (OR = 1.03, 95% CI: 0.82–1.30, I2 = 0%), in age- and sex-adjusted analyses. Time-to-event analysis showed similar results (hazard ratio for subclinical hypothyroidism: 0.98, 95% CI: 0.87–1.11; hazard ratio for subclinical hyperthyroidism: 1.07, 95% CI: 0.88–1.29). The results were robust in all sub-group and sensitivity analyses. Conclusions This is the largest systematic review and individual participant data analysis to date investigating the prospective association between subclinical thyroid dysfunction and diabetes. We did not find an association between subclinical thyroid dysfunction and incident diabetes. Our results do not support screening patients with subclinical thyroid dysfunction for diabetes. Significance statement Evidence is conflicting regarding whether an association exists be, Objective: Few prospective studies have assessed whether individuals with subclinical thyroid dysfunction are more likely to develop diabetes, with conflicting results. In this study, we conducted a systematic review of the literature and an individual participant data analysis of multiple prospective cohorts to investigate the association between subclinical thyroid dysfunction and incident diabetes. Methods: We performed a systematic review of the literature in Medline, Embase, and the Cochrane Library from inception to February 11, 2022. A two-stage individual participant data analysis was conducted to compare participants with subclinical hypothyroidism and subclinical hyperthyroidism vs euthyroidism at baseline and the adjusted risk of developing diabetes at follow-up. Results: Among 61 178 adults from 18 studies, 49% were females, mean age was 58 years, and mean follow-up time was 8.2 years. At the last available follow-up, there was no association between subclinical hypothyroidism and incidence of diabetes (odds ratio (OR) = 1.02, 95% CI: 0.88-1.17, I2 = 0%) or subclinical hyperthyroidism and incidence of diabetes (OR = 1.03, 95% CI: 0.82-1.30, I2 = 0%), in age- and sex-adjusted analyses. Time-to-event analysis showed similar results (hazard ratio for subclinical hypothyroidism: 0.98, 95% CI: 0.87-1.11; hazard ratio for subclinical hyperthyroidism: 1.07, 95% CI: 0.88-1.29). The results were robust in all sub-group and sensitivity analyses. Conclusions: This is the largest systematic review and individual participant data analysis to date investigating the prospective association between subclinical thyroid dysfunction and diabetes. We did not find an association between subclinical thyroid dysfunction and incident diabetes. Our results do not support screening patients with subclinical thyroid dysfunction for diabetes. Significance statement: Evidence is conflicting regarding whether an association exists between subclinical thyroid dysfunction and incide
Published: 2022

31. Circulating free testosterone and risk of aggressive prostate cancer : Prospective and Mendelian randomisation analyses in international consortia

Author: Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael V., Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, Bas, Chen, Chu, Cohn, Barbara A., Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Goodman, Gary E., Haiman, Christopher A., Hankey, Graeme J., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Knekt, Paul, Kubo, Tatsuhiko, Langseth, Hilde, Laughlin, Gail, Le Marchand, Loic, Luostarinen, Tapio, MacInnis, Robert J., Mäenpää, Hanna O., Männistö, Satu, Metter, Jeffrey E., Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Rissanen, Harri, Sawada, Norie, Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Tsugane, Shoichiro, Vatten, Lars, Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., Travis, Ruth C., Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael V., Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, Bas, Chen, Chu, Cohn, Barbara A., Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Goodman, Gary E., Haiman, Christopher A., Hankey, Graeme J., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Knekt, Paul, Kubo, Tatsuhiko, Langseth, Hilde, Laughlin, Gail, Le Marchand, Loic, Luostarinen, Tapio, MacInnis, Robert J., Mäenpää, Hanna O., Männistö, Satu, Metter, Jeffrey E., Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Rissanen, Harri, Sawada, Norie, Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Tsugane, Shoichiro, Vatten, Lars, Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., and Travis, Ruth C.
Abstract: Previous studies had limited power to assess the associations of testosterone with aggressive disease as a primary endpoint. Further, the association of genetically predicted testosterone with aggressive disease is not known. We investigated the associations of calculated free and measured total testosterone and sex hormone-binding globulin (SHBG) with aggressive, overall and early-onset prostate cancer. In blood-based analyses, odds ratios (OR) and 95% confidence intervals (CI) for prostate cancer were estimated using conditional logistic regression from prospective analysis of biomarker concentrations in the Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group (up to 25 studies, 14 944 cases and 36 752 controls, including 1870 aggressive prostate cancers). In Mendelian randomisation (MR) analyses, using instruments identified using UK Biobank (up to 194 453 men) and outcome data from PRACTICAL (up to 79 148 cases and 61 106 controls, including 15 167 aggressive cancers), ORs were estimated using the inverse-variance weighted method. Free testosterone was associated with aggressive disease in MR analyses (OR per 1 SD = 1.23, 95% CI = 1.08-1.40). In blood-based analyses there was no association with aggressive disease overall, but there was heterogeneity by age at blood collection (OR for men aged <60 years 1.14, CI = 1.02-1.28; Phet =.0003: inverse association for older ages). Associations for free testosterone were positive for overall prostate cancer (MR: 1.20, 1.08-1.34; blood-based: 1.03, 1.01-1.05) and early-onset prostate cancer (MR: 1.37, 1.09-1.73; blood-based: 1.08, 0.98-1.19). SHBG and total testosterone were inversely associated with overall prostate cancer in blood-based analyses, with null associations in MR analysis. Our results support free testosterone, rather than total testosterone, in the development of prostate cancer, including aggressive subgroups.
Published: 2022
Full Text: View/download PDF

32. Circulating free testosterone and risk of aggressive prostate cancer : Prospective and Mendelian randomisation analyses in international consortia

Author: Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael, V, Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, Bas, Chen, Chu, Cohn, Barbara A., Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Goodman, Gary E., Haiman, Christopher A., Hankey, Graeme J., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Knekt, Paul, Kubo, Tatsuhiko, Langseth, Hilde, Laughlin, Gail, Le Marchand, Loic, Luostarinen, Tapio, MacInnis, Robert J., Maenpaa, Hanna O., Mannisto, Satu, Metter, Jeffrey E., Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Rissanen, Harri, Sawada, Norie, Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Tsugane, Shoichiro, Vatten, Lars, Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., Travis, Ruth C., Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael, V, Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, Bas, Chen, Chu, Cohn, Barbara A., Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Goodman, Gary E., Haiman, Christopher A., Hankey, Graeme J., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Knekt, Paul, Kubo, Tatsuhiko, Langseth, Hilde, Laughlin, Gail, Le Marchand, Loic, Luostarinen, Tapio, MacInnis, Robert J., Maenpaa, Hanna O., Mannisto, Satu, Metter, Jeffrey E., Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Rissanen, Harri, Sawada, Norie, Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Tsugane, Shoichiro, Vatten, Lars, Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., and Travis, Ruth C.
Abstract: Previous studies had limited power to assess the associations of testosterone with aggressive disease as a primary endpoint. Further, the association of genetically predicted testosterone with aggressive disease is not known. We investigated the associations of calculated free and measured total testosterone and sex hormone-binding globulin (SHBG) with aggressive, overall and early-onset prostate cancer. In blood-based analyses, odds ratios (OR) and 95% confidence intervals (CI) for prostate cancer were estimated using conditional logistic regression from prospective analysis of biomarker concentrations in the Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group (up to 25 studies, 14 944 cases and 36 752 controls, including 1870 aggressive prostate cancers). In Mendelian randomisation (MR) analyses, using instruments identified using UK Biobank (up to 194 453 men) and outcome data from PRACTICAL (up to 79 148 cases and 61 106 controls, including 15 167 aggressive cancers), ORs were estimated using the inverse-variance weighted method. Free testosterone was associated with aggressive disease in MR analyses (OR per 1 SD = 1.23, 95% CI = 1.08-1.40). In blood-based analyses there was no association with aggressive disease overall, but there was heterogeneity by age at blood collection (OR for men aged <60 years 1.14, CI = 1.02-1.28; P-het = .0003: inverse association for older ages). Associations for free testosterone were positive for overall prostate cancer (MR: 1.20, 1.08-1.34; blood-based: 1.03, 1.01-1.05) and early-onset prostate cancer (MR: 1.37, 1.09-1.73; blood-based: 1.08, 0.98-1.19). SHBG and total testosterone were inversely associated with overall prostate cancer in blood-based analyses, with null associations in MR analysis. Our results support free testosterone, rather than total testosterone, in the development of prostate cancer, including aggressive subgroups.
Published: 2022
Full Text: View/download PDF

33. Circulating free testosterone and risk of aggressive prostate cancer : Prospective and Mendelian randomisation analyses in international consortia

Author: Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael V., Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, Bas, Chen, Chu, Cohn, Barbara A., Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Goodman, Gary E., Haiman, Christopher A., Hankey, Graeme J., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Knekt, Paul, Kubo, Tatsuhiko, Langseth, Hilde, Laughlin, Gail, Le Marchand, Loic, Luostarinen, Tapio, MacInnis, Robert J., Mäenpää, Hanna O., Männistö, Satu, Metter, Jeffrey E., Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Rissanen, Harri, Sawada, Norie, Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Tsugane, Shoichiro, Vatten, Lars, Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., Travis, Ruth C., Watts, Eleanor L., Perez-Cornago, Aurora, Fensom, Georgina K., Smith-Byrne, Karl, Noor, Urwah, Andrews, Colm D., Gunter, Marc J., Holmes, Michael V., Martin, Richard M., Tsilidis, Konstantinos K., Albanes, Demetrius, Barricarte, Aurelio, Bueno-de-Mesquita, Bas, Chen, Chu, Cohn, Barbara A., Dimou, Niki L., Ferrucci, Luigi, Flicker, Leon, Freedman, Neal D., Giles, Graham G., Giovannucci, Edward L., Goodman, Gary E., Haiman, Christopher A., Hankey, Graeme J., Huang, Jiaqi, Huang, Wen-Yi, Hurwitz, Lauren M., Kaaks, Rudolf, Knekt, Paul, Kubo, Tatsuhiko, Langseth, Hilde, Laughlin, Gail, Le Marchand, Loic, Luostarinen, Tapio, MacInnis, Robert J., Mäenpää, Hanna O., Männistö, Satu, Metter, Jeffrey E., Mikami, Kazuya, Mucci, Lorelei A., Olsen, Anja W., Ozasa, Kotaro, Palli, Domenico, Penney, Kathryn L., Platz, Elizabeth A., Rissanen, Harri, Sawada, Norie, Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Tsai, Chiaojung Jillian, Tsugane, Shoichiro, Vatten, Lars, Weiderpass, Elisabete, Weinstein, Stephanie J., Wilkens, Lynne R., Yeap, Bu B., Allen, Naomi E., Key, Timothy J., and Travis, Ruth C.
Abstract: Previous studies had limited power to assess the associations of testosterone with aggressive disease as a primary endpoint. Further, the association of genetically predicted testosterone with aggressive disease is not known. We investigated the associations of calculated free and measured total testosterone and sex hormone-binding globulin (SHBG) with aggressive, overall and early-onset prostate cancer. In blood-based analyses, odds ratios (OR) and 95% confidence intervals (CI) for prostate cancer were estimated using conditional logistic regression from prospective analysis of biomarker concentrations in the Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group (up to 25 studies, 14 944 cases and 36 752 controls, including 1870 aggressive prostate cancers). In Mendelian randomisation (MR) analyses, using instruments identified using UK Biobank (up to 194 453 men) and outcome data from PRACTICAL (up to 79 148 cases and 61 106 controls, including 15 167 aggressive cancers), ORs were estimated using the inverse-variance weighted method. Free testosterone was associated with aggressive disease in MR analyses (OR per 1 SD = 1.23, 95% CI = 1.08-1.40). In blood-based analyses there was no association with aggressive disease overall, but there was heterogeneity by age at blood collection (OR for men aged <60 years 1.14, CI = 1.02-1.28; Phet =.0003: inverse association for older ages). Associations for free testosterone were positive for overall prostate cancer (MR: 1.20, 1.08-1.34; blood-based: 1.03, 1.01-1.05) and early-onset prostate cancer (MR: 1.37, 1.09-1.73; blood-based: 1.08, 0.98-1.19). SHBG and total testosterone were inversely associated with overall prostate cancer in blood-based analyses, with null associations in MR analysis. Our results support free testosterone, rather than total testosterone, in the development of prostate cancer, including aggressive subgroups.
Published: 2022
Full Text: View/download PDF

34. Association of Thyroid Dysfunction with Cognitive Function

Author: Nicolien A. Van Vliet, Diana van Heemst, Osvaldo P. Almeida, Bjørn O. Åsvold, Carole E. Aubert, Jong Bin Bae, Linda E. Barnes, Douglas C. Bauer, Gerard J. Blauw, Carol Brayne, Anne R. Cappola, Graziano Ceresini, Hannie C Comijs, Jean Francois Dartigues, Jean Marie Degryse, Robin P.F. Dullaart, Marlise E.A. Van Eersel, Wendy P.J. Den Elzen, Luigi Ferrucci, Howard A. Fink, Leon Flicker, Hans J. Grabe, Ji Won Han, Catherine Helmer, Martijn Huisman, M.A. (Arfan) Ikram, Misa Imaizumi, Renate T. De Jongh, J. Wouter Jukema, Ki Woong Kim, Lewis H. Kuller, Oscar L. Lopez, Simon P. Mooijaart, Jae Hoon Moon, Elisavet Moutzouri, Matthias Nauck, Jim Parle, R.P. (Robin) Peeters, Mary H. Samuels, Carsten O. Schmidt, Ulf Schminke, PE (Eline) Slagboom, Eystein Stordal, Bert Vaes, Henry Völzke, Rudi G.J. Westendorp, Michiko Yamada, Bu B. Yeap, Nicolas Rodondi, Jacobijn Gussekloo, Stella Trompet, Nicolien A. Van Vliet, Diana van Heemst, Osvaldo P. Almeida, Bjørn O. Åsvold, Carole E. Aubert, Jong Bin Bae, Linda E. Barnes, Douglas C. Bauer, Gerard J. Blauw, Carol Brayne, Anne R. Cappola, Graziano Ceresini, Hannie C Comijs, Jean Francois Dartigues, Jean Marie Degryse, Robin P.F. Dullaart, Marlise E.A. Van Eersel, Wendy P.J. Den Elzen, Luigi Ferrucci, Howard A. Fink, Leon Flicker, Hans J. Grabe, Ji Won Han, Catherine Helmer, Martijn Huisman, M.A. (Arfan) Ikram, Misa Imaizumi, Renate T. De Jongh, J. Wouter Jukema, Ki Woong Kim, Lewis H. Kuller, Oscar L. Lopez, Simon P. Mooijaart, Jae Hoon Moon, Elisavet Moutzouri, Matthias Nauck, Jim Parle, R.P. (Robin) Peeters, Mary H. Samuels, Carsten O. Schmidt, Ulf Schminke, PE (Eline) Slagboom, Eystein Stordal, Bert Vaes, Henry Völzke, Rudi G.J. Westendorp, Michiko Yamada, Bu B. Yeap, Nicolas Rodondi, Jacobijn Gussekloo, and Stella Trompet
Abstract: Importance: In clinical guidelines, overt and subclinical thyroid dysfunction are mentioned as causal and treatable factors for cognitive decline. However, the scientific literature on these associations shows inconsistent findings. Objective: To assess cross-sectional and longitudinal associations of baseline thyroid dysfunction with cognitive function and dementia. Design, Setting, and Participants: This multicohort individual participant data analysis assessed 114267 person-years (median, 1.7-11.3 years) of follow-up for cognitive function and 525222
Published: 2021
Full Text: View/download PDF

35. Association of Thyroid Dysfunction with Cognitive Function

Author: Nicolien A. Van Vliet, Diana van Heemst, Osvaldo P. Almeida, Bjørn O. Åsvold, Carole E. Aubert, Jong Bin Bae, Linda E. Barnes, Douglas C. Bauer, Gerard J. Blauw, Carol Brayne, Anne R. Cappola, Graziano Ceresini, Hannie C Comijs, Jean Francois Dartigues, Jean Marie Degryse, Robin P.F. Dullaart, Marlise E.A. Van Eersel, Wendy P.J. Den Elzen, Luigi Ferrucci, Howard A. Fink, Leon Flicker, Hans J. Grabe, Ji Won Han, Catherine Helmer, Martijn Huisman, M.A. (Arfan) Ikram, Misa Imaizumi, Renate T. De Jongh, J. Wouter Jukema, Ki Woong Kim, Lewis H. Kuller, Oscar L. Lopez, Simon P. Mooijaart, Jae Hoon Moon, Elisavet Moutzouri, Matthias Nauck, Jim Parle, R.P. (Robin) Peeters, Mary H. Samuels, Carsten O. Schmidt, Ulf Schminke, PE (Eline) Slagboom, Eystein Stordal, Bert Vaes, Henry Völzke, Rudi G.J. Westendorp, Michiko Yamada, Bu B. Yeap, Nicolas Rodondi, Jacobijn Gussekloo, Stella Trompet, Nicolien A. Van Vliet, Diana van Heemst, Osvaldo P. Almeida, Bjørn O. Åsvold, Carole E. Aubert, Jong Bin Bae, Linda E. Barnes, Douglas C. Bauer, Gerard J. Blauw, Carol Brayne, Anne R. Cappola, Graziano Ceresini, Hannie C Comijs, Jean Francois Dartigues, Jean Marie Degryse, Robin P.F. Dullaart, Marlise E.A. Van Eersel, Wendy P.J. Den Elzen, Luigi Ferrucci, Howard A. Fink, Leon Flicker, Hans J. Grabe, Ji Won Han, Catherine Helmer, Martijn Huisman, M.A. (Arfan) Ikram, Misa Imaizumi, Renate T. De Jongh, J. Wouter Jukema, Ki Woong Kim, Lewis H. Kuller, Oscar L. Lopez, Simon P. Mooijaart, Jae Hoon Moon, Elisavet Moutzouri, Matthias Nauck, Jim Parle, R.P. (Robin) Peeters, Mary H. Samuels, Carsten O. Schmidt, Ulf Schminke, PE (Eline) Slagboom, Eystein Stordal, Bert Vaes, Henry Völzke, Rudi G.J. Westendorp, Michiko Yamada, Bu B. Yeap, Nicolas Rodondi, Jacobijn Gussekloo, and Stella Trompet
Abstract: Importance: In clinical guidelines, overt and subclinical thyroid dysfunction are mentioned as causal and treatable factors for cognitive decline. However, the scientific literature on these associations shows inconsistent findings. Objective: To assess cross-sectional and longitudinal associations of baseline thyroid dysfunction with cognitive function and dementia. Design, Setting, and Participants: This multicohort individual participant data analysis assessed 114267 person-years (median, 1.7-11.3 years) of follow-up for cognitive function and 525222
Published: 2021
Full Text: View/download PDF

36. Association of Thyroid Dysfunction With Cognitive Function : An Individual Participant Data Analysis

Author: UCL - SSS/IRSS - Institut de recherche santé et société, van Vliet, Nicolien A., van Heemst, Diana, Almeida, Osvaldo P., Åsvold, Bjørn O., Aubert, Carole E., Bae, Jong Bin, Barnes, Linda E., Bauer, Douglas C., Blauw, Gerard J., Brayne, Carol, Cappola, Anne R., Ceresini, Graziano, Comijs, Hannie C., Dartigues, Jean-Francois, Degryse, Jean-Marie, Dullaart, Robin P. F., van Eersel, Marlise E. A., den Elzen, Wendy P. J., Ferrucci, Luigi, Fink, Howard A., Flicker, Leon, Grabe, Hans J., Han, Ji Won, Helmer, Catherine, Huisman, Martijn, Ikram, M. Arfan, Imaizumi, Misa, de Jongh, Renate T., Jukema, J. Wouter, Kim, Ki Woong, Kuller, Lewis H., Lopez, Oscar L., Mooijaart, Simon P., Moon, Jae Hoon, Moutzouri, Elisavet, Nauck, Matthias, Parle, Jim, Peeters, Robin P., Samuels, Mary H., Schmidt, Carsten O., Schminke, Ulf, Slagboom, P. Eline, Stordal, Eystein, Vaes, Bert, Völzke, Henry, Westendorp, Rudi G. J., Yamada, Michiko, Yeap, Bu B., Rodondi, Nicolas, Gussekloo, Jacobijn, Trompet, Stella, UCL - SSS/IRSS - Institut de recherche santé et société, van Vliet, Nicolien A., van Heemst, Diana, Almeida, Osvaldo P., Åsvold, Bjørn O., Aubert, Carole E., Bae, Jong Bin, Barnes, Linda E., Bauer, Douglas C., Blauw, Gerard J., Brayne, Carol, Cappola, Anne R., Ceresini, Graziano, Comijs, Hannie C., Dartigues, Jean-Francois, Degryse, Jean-Marie, Dullaart, Robin P. F., van Eersel, Marlise E. A., den Elzen, Wendy P. J., Ferrucci, Luigi, Fink, Howard A., Flicker, Leon, Grabe, Hans J., Han, Ji Won, Helmer, Catherine, Huisman, Martijn, Ikram, M. Arfan, Imaizumi, Misa, de Jongh, Renate T., Jukema, J. Wouter, Kim, Ki Woong, Kuller, Lewis H., Lopez, Oscar L., Mooijaart, Simon P., Moon, Jae Hoon, Moutzouri, Elisavet, Nauck, Matthias, Parle, Jim, Peeters, Robin P., Samuels, Mary H., Schmidt, Carsten O., Schminke, Ulf, Slagboom, P. Eline, Stordal, Eystein, Vaes, Bert, Völzke, Henry, Westendorp, Rudi G. J., Yamada, Michiko, Yeap, Bu B., Rodondi, Nicolas, Gussekloo, Jacobijn, and Trompet, Stella
Abstract: IMPORTANCE In clinical guidelines, overt and subclinical thyroid dysfunction are mentioned as causal and treatable factors for cognitive decline. However, the scientific literature on these associations shows inconsistent findings. OBJECTIVE To assess cross-sectional and longitudinal associations of baseline thyroid dysfunction with cognitive function and dementia. DESIGN, SETTING, AND PARTICIPANTS This multicohort individual participant data analysis assessed 114 267 person-years (median, 1.7-11.3 years) of follow-up for cognitive function and 525 222 person-years (median, 3.8-15.3 years) for dementia between 1989 and 2017. Analyses on cognitive function included 21 cohorts comprising 38 144 participants. Analyses on dementia included eight cohorts with a total of 2033 cases with dementia and 44 573 controls. Data analysis was performed from December 2016 to January 2021. EXPOSURES Thyroid function was classified as overt hyperthyroidism, subclinical hyperthyroidism, euthyroidism, subclinical hypothyroidism, and overt hypothyroidism based on uniform thyrotropin cutoff values and study-specific free thyroxine values. MAIN OUTCOMES AND MEASURES The primary outcomewas global cognitive function, mostly measured using the Mini-Mental State Examination. Executive function, memory, and dementia were secondary outcomes. Analyses were first performed at study level using multivariable linear regression and multivariable Cox regression, respectively. The studies were combined with restricted maximum likelihood meta-analysis. To overcome the use of different scales, results were transformed to standardized mean differences. For incident dementia, hazard ratios were calculated. RESULTS Among 74 565 total participants, 66 567 (89.3%) participants had normal thyroid function, 577 (0.8%) had overt hyperthyroidism, 2557 (3.4%) had subclinical hyperthyroidism, 4167 (5.6%) had subclinical hypothyroidism, and 697 (0.9%) had overt hypothyroidism. The study-specific median age at basel
Published: 2021

37. Association of Thyroid Dysfunction With Cognitive Function An Individual Participant Data Analysis

Author: van Vliet, Nicolien A., van Heemst, Diana, Almeida, Osvaldo P., Asvold, Bjorn O., Aubert, Carole E., Bin Bae, Jong, Barnes, Linda E., Bauer, Douglas C., Blauw, Gerard J., Brayne, Carol, Cappola, Anne R., Ceresini, Graziano, Comijs, Hannie C., Dartigues, Jean-Francois, Degryse, Jean-Marie, Dullaart, Robin P. F., van Eersel, Marlise E. A., den Elzen, Wendy P. J., Ferrucci, Luigi, Fink, Howard A., Flicker, Leon, Grabe, Hans J., Han, Ji Won, Helmer, Catherine, Huisman, Martijn, Ikram, M. Arfan, Imaizumi, Misa, de Jongh, Renate T., Jukema, J. Wouter, Kim, Ki Woong, Kuller, Lewis H., Lopez, Oscar L., Mooijaart, Simon P., Moon, Jae Hoon, Moutzouri, Elisavet, Nauck, Matthias, Parle, Jim, Peeters, Robin P., Samuels, Mary H., Schmidt, Carsten O., Schminke, Ulf, Slagboom, P. Eline, Stordal, Eystein, Vaes, Bert, Volzke, Henry, Westendorp, Rudi G. J., Yamada, Michiko, Yeap, Bu B., Rodondi, Nicolas, Gussekloo, Jacobijn, van Vliet, Nicolien A., van Heemst, Diana, Almeida, Osvaldo P., Asvold, Bjorn O., Aubert, Carole E., Bin Bae, Jong, Barnes, Linda E., Bauer, Douglas C., Blauw, Gerard J., Brayne, Carol, Cappola, Anne R., Ceresini, Graziano, Comijs, Hannie C., Dartigues, Jean-Francois, Degryse, Jean-Marie, Dullaart, Robin P. F., van Eersel, Marlise E. A., den Elzen, Wendy P. J., Ferrucci, Luigi, Fink, Howard A., Flicker, Leon, Grabe, Hans J., Han, Ji Won, Helmer, Catherine, Huisman, Martijn, Ikram, M. Arfan, Imaizumi, Misa, de Jongh, Renate T., Jukema, J. Wouter, Kim, Ki Woong, Kuller, Lewis H., Lopez, Oscar L., Mooijaart, Simon P., Moon, Jae Hoon, Moutzouri, Elisavet, Nauck, Matthias, Parle, Jim, Peeters, Robin P., Samuels, Mary H., Schmidt, Carsten O., Schminke, Ulf, Slagboom, P. Eline, Stordal, Eystein, Vaes, Bert, Volzke, Henry, Westendorp, Rudi G. J., Yamada, Michiko, Yeap, Bu B., Rodondi, Nicolas, and Gussekloo, Jacobijn
Abstract: IMPORTANCE In clinical guidelines, overt and subclinical thyroid dysfunction are mentioned as causal and treatable factors for cognitive decline. However, the scientific literature on these associations shows inconsistent findings.OBJECTIVE To assess cross-sectional and longitudinal associations of baseline thyroid dysfunction with cognitive function and dementia.DESIGN, SETTING, AND PARTICIPANTS This multicohort individual participant data analysis assessed 114 267 person-years (median, 1.7-11.3 years) of follow-up for cognitive function and 525 222 person-years (median, 3.8-15.3 years) for dementia between 1989 and 2017. Analyses on cognitive function included 21 cohorts comprising 38 144 participants. Analyses on dementia included eight cohorts with a total of 2033 cases with dementia and 44 573 controls. Data analysis was performed from December 2016 to January 2021.EXPOSURES Thyroid function was classified as overt hyperthyroidism, subclinical hyperthyroidism, euthyroidism, subclinical hypothyroidism, and overt hypothyroidism based on uniform thyrotropin cutoff values and study-specific free thyroxine values.MAIN OUTCOMES AND MEASURES The primary outcome was global cognitive function, mostly measured using the Mini-Mental State Examination. Executive function, memory, and dementia were secondary outcomes. Analyses were first performed at study level using multivariable linear regression and multivariable Cox regression, respectively. The studies were combined with restricted maximum likelihood meta-analysis. To overcome the use of different scales, results were transformed to standardized mean differences. For incident dementia, hazard ratios were calculated.RESULTS Among 74 565 total participants, 66 567 (89.3%) participants had normal thyroid function, 577 (0.8%) had overt hyperthyroidism, 2557 (3.4%) had subclinical hyperthyroidism, 4167 (5.6%) had subclinical hypothyroidism, and 697 (0.9%) had overt hypothyroidism. The
Published: 2021

38. Association of Thyroid Dysfunction With Cognitive Function An Individual Participant Data Analysis

Author: van Vliet, Nicolien A., van Heemst, Diana, Almeida, Osvaldo P., Asvold, Bjorn O., Aubert, Carole E., Bin Bae, Jong, Barnes, Linda E., Bauer, Douglas C., Blauw, Gerard J., Brayne, Carol, Cappola, Anne R., Ceresini, Graziano, Comijs, Hannie C., Dartigues, Jean-Francois, Degryse, Jean-Marie, Dullaart, Robin P. F., van Eersel, Marlise E. A., den Elzen, Wendy P. J., Ferrucci, Luigi, Fink, Howard A., Flicker, Leon, Grabe, Hans J., Han, Ji Won, Helmer, Catherine, Huisman, Martijn, Ikram, M. Arfan, Imaizumi, Misa, de Jongh, Renate T., Jukema, J. Wouter, Kim, Ki Woong, Kuller, Lewis H., Lopez, Oscar L., Mooijaart, Simon P., Moon, Jae Hoon, Moutzouri, Elisavet, Nauck, Matthias, Parle, Jim, Peeters, Robin P., Samuels, Mary H., Schmidt, Carsten O., Schminke, Ulf, Slagboom, P. Eline, Stordal, Eystein, Vaes, Bert, Volzke, Henry, Westendorp, Rudi G. J., Yamada, Michiko, Yeap, Bu B., Rodondi, Nicolas, Gussekloo, Jacobijn, van Vliet, Nicolien A., van Heemst, Diana, Almeida, Osvaldo P., Asvold, Bjorn O., Aubert, Carole E., Bin Bae, Jong, Barnes, Linda E., Bauer, Douglas C., Blauw, Gerard J., Brayne, Carol, Cappola, Anne R., Ceresini, Graziano, Comijs, Hannie C., Dartigues, Jean-Francois, Degryse, Jean-Marie, Dullaart, Robin P. F., van Eersel, Marlise E. A., den Elzen, Wendy P. J., Ferrucci, Luigi, Fink, Howard A., Flicker, Leon, Grabe, Hans J., Han, Ji Won, Helmer, Catherine, Huisman, Martijn, Ikram, M. Arfan, Imaizumi, Misa, de Jongh, Renate T., Jukema, J. Wouter, Kim, Ki Woong, Kuller, Lewis H., Lopez, Oscar L., Mooijaart, Simon P., Moon, Jae Hoon, Moutzouri, Elisavet, Nauck, Matthias, Parle, Jim, Peeters, Robin P., Samuels, Mary H., Schmidt, Carsten O., Schminke, Ulf, Slagboom, P. Eline, Stordal, Eystein, Vaes, Bert, Volzke, Henry, Westendorp, Rudi G. J., Yamada, Michiko, Yeap, Bu B., Rodondi, Nicolas, and Gussekloo, Jacobijn
Abstract: IMPORTANCE In clinical guidelines, overt and subclinical thyroid dysfunction are mentioned as causal and treatable factors for cognitive decline. However, the scientific literature on these associations shows inconsistent findings.OBJECTIVE To assess cross-sectional and longitudinal associations of baseline thyroid dysfunction with cognitive function and dementia.DESIGN, SETTING, AND PARTICIPANTS This multicohort individual participant data analysis assessed 114 267 person-years (median, 1.7-11.3 years) of follow-up for cognitive function and 525 222 person-years (median, 3.8-15.3 years) for dementia between 1989 and 2017. Analyses on cognitive function included 21 cohorts comprising 38 144 participants. Analyses on dementia included eight cohorts with a total of 2033 cases with dementia and 44 573 controls. Data analysis was performed from December 2016 to January 2021.EXPOSURES Thyroid function was classified as overt hyperthyroidism, subclinical hyperthyroidism, euthyroidism, subclinical hypothyroidism, and overt hypothyroidism based on uniform thyrotropin cutoff values and study-specific free thyroxine values.MAIN OUTCOMES AND MEASURES The primary outcome was global cognitive function, mostly measured using the Mini-Mental State Examination. Executive function, memory, and dementia were secondary outcomes. Analyses were first performed at study level using multivariable linear regression and multivariable Cox regression, respectively. The studies were combined with restricted maximum likelihood meta-analysis. To overcome the use of different scales, results were transformed to standardized mean differences. For incident dementia, hazard ratios were calculated.RESULTS Among 74 565 total participants, 66 567 (89.3%) participants had normal thyroid function, 577 (0.8%) had overt hyperthyroidism, 2557 (3.4%) had subclinical hyperthyroidism, 4167 (5.6%) had subclinical hypothyroidism, and 697 (0.9%) had overt hypothyroidism. The
Published: 2021

39. Association of Thyroid Dysfunction with Cognitive Function:An Individual Participant Data Analysis

Author: Van Vliet, Nicolien A., Van Heemst, Diana, Almeida, Osvaldo P., Åsvold, Bjørn O., Aubert, Carole E., Bae, Jong Bin, Barnes, Linda E., Bauer, Douglas C., Blauw, Gerard J., Brayne, Carol, Cappola, Anne R., Ceresini, Graziano, Comijs, Hannie C., Dartigues, Jean Francois, Degryse, Jean Marie, Dullaart, Robin P.F., Van Eersel, Marlise E.A., Den Elzen, Wendy P.J., Ferrucci, Luigi, Fink, Howard A., Flicker, Leon, Grabe, Hans J., Han, Ji Won, Helmer, Catherine, Huisman, Martijn, Ikram, M. Arfan, Imaizumi, Misa, De Jongh, Renate T., Jukema, J. Wouter, Kim, Ki Woong, Kuller, Lewis H., Lopez, Oscar L., Mooijaart, Simon P., Moon, Jae Hoon, Moutzouri, Elisavet, Nauck, Matthias, Parle, Jim, Peeters, Robin P., Samuels, Mary H., Schmidt, Carsten O., Schminke, Ulf, Slagboom, P. Eline, Stordal, Eystein, Vaes, Bert, Völzke, Henry, Westendorp, Rudi G.J., Yamada, Michiko, Yeap, Bu B., Rodondi, Nicolas, Gussekloo, Jacobijn, Trompet, Stella, Van Vliet, Nicolien A., Van Heemst, Diana, Almeida, Osvaldo P., Åsvold, Bjørn O., Aubert, Carole E., Bae, Jong Bin, Barnes, Linda E., Bauer, Douglas C., Blauw, Gerard J., Brayne, Carol, Cappola, Anne R., Ceresini, Graziano, Comijs, Hannie C., Dartigues, Jean Francois, Degryse, Jean Marie, Dullaart, Robin P.F., Van Eersel, Marlise E.A., Den Elzen, Wendy P.J., Ferrucci, Luigi, Fink, Howard A., Flicker, Leon, Grabe, Hans J., Han, Ji Won, Helmer, Catherine, Huisman, Martijn, Ikram, M. Arfan, Imaizumi, Misa, De Jongh, Renate T., Jukema, J. Wouter, Kim, Ki Woong, Kuller, Lewis H., Lopez, Oscar L., Mooijaart, Simon P., Moon, Jae Hoon, Moutzouri, Elisavet, Nauck, Matthias, Parle, Jim, Peeters, Robin P., Samuels, Mary H., Schmidt, Carsten O., Schminke, Ulf, Slagboom, P. Eline, Stordal, Eystein, Vaes, Bert, Völzke, Henry, Westendorp, Rudi G.J., Yamada, Michiko, Yeap, Bu B., Rodondi, Nicolas, Gussekloo, Jacobijn, and Trompet, Stella
Abstract: Importance: In clinical guidelines, overt and subclinical thyroid dysfunction are mentioned as causal and treatable factors for cognitive decline. However, the scientific literature on these associations shows inconsistent findings. Objective: To assess cross-sectional and longitudinal associations of baseline thyroid dysfunction with cognitive function and dementia. Design, Setting, and Participants: This multicohort individual participant data analysis assessed 114267 person-years (median, 1.7-11.3 years) of follow-up for cognitive function and 525222 person-years (median, 3.8-15.3 years) for dementia between 1989 and 2017. Analyses on cognitive function included 21 cohorts comprising 38144 participants. Analyses on dementia included eight cohorts with a total of 2033 cases with dementia and 44573 controls. Data analysis was performed from December 2016 to January 2021. Exposures: Thyroid function was classified as overt hyperthyroidism, subclinical hyperthyroidism, euthyroidism, subclinical hypothyroidism, and overt hypothyroidism based on uniform thyrotropin cutoff values and study-specific free thyroxine values. Main Outcomes and Measures: The primary outcome was global cognitive function, mostly measured using the Mini-Mental State Examination. Executive function, memory, and dementia were secondary outcomes. Analyses were first performed at study level using multivariable linear regression and multivariable Cox regression, respectively. The studies were combined with restricted maximum likelihood meta-analysis. To overcome the use of different scales, results were transformed to standardized mean differences. For incident dementia, hazard ratios were calculated. Results: Among 74565 total participants, 66567 (89.3%) participants had normal thyroid function, 577 (0.8%) had overt hyperthyroidism, 2557 (3.4%) had subclinical hyperthyroidism, 4167 (5.6%) had subclinical hypothyroidism, and 697 (0.9%) had overt hypothyroidism. The study-specific median age at b
Published: 2021

40. An individual participant data analysis of prospective cohort studies on the association between subclinical thyroid dysfunction and depressive symptoms.

Author: Wildisen, Lea, Wildisen, Lea, Del Giovane, Cinzia, Moutzouri, Elisavet, Beglinger, Shanthi, Syrogiannouli, Lamprini, Collet, Tinh-Hai, Cappola, Anne R, Åsvold, Bjørn O, Bakker, Stephan JL, Yeap, Bu B, Almeida, Osvaldo P, Ceresini, Graziano, Dullaart, Robin PF, Ferrucci, Luigi, Grabe, Hans, Jukema, J Wouter, Nauck, Matthias, Trompet, Stella, Völzke, Henry, Westendorp, Rudi, Gussekloo, Jacobijn, Klöppel, Stefan, Aujesky, Drahomir, Bauer, Douglas, Peeters, Robin, Feller, Martin, Rodondi, Nicolas, Wildisen, Lea, Wildisen, Lea, Del Giovane, Cinzia, Moutzouri, Elisavet, Beglinger, Shanthi, Syrogiannouli, Lamprini, Collet, Tinh-Hai, Cappola, Anne R, Åsvold, Bjørn O, Bakker, Stephan JL, Yeap, Bu B, Almeida, Osvaldo P, Ceresini, Graziano, Dullaart, Robin PF, Ferrucci, Luigi, Grabe, Hans, Jukema, J Wouter, Nauck, Matthias, Trompet, Stella, Völzke, Henry, Westendorp, Rudi, Gussekloo, Jacobijn, Klöppel, Stefan, Aujesky, Drahomir, Bauer, Douglas, Peeters, Robin, Feller, Martin, and Rodondi, Nicolas
Abstract: In subclinical hypothyroidism, the presence of depressive symptoms is often a reason for starting levothyroxine treatment. However, data are conflicting on the association between subclinical thyroid dysfunction and depressive symptoms. We aimed to examine the association between subclinical thyroid dysfunction and depressive symptoms in all prospective cohorts with relevant data available. We performed a systematic review of the literature from Medline, Embase, Cumulative Index to Nursing and Allied Health Literature, and the Cochrane Library from inception to 10th May 2019. We included prospective cohorts with data on thyroid status at baseline and depressive symptoms during follow-up. The primary outcome was depressive symptoms measured at first available follow-up, expressed on the Beck's Depression Inventory (BDI) scale (range 0-63, higher values indicate more depressive symptoms, minimal clinically important difference: 5 points). We performed a two-stage individual participant data (IPD) analysis comparing participants with subclinical hypo- or hyperthyroidism versus euthyroidism, adjusting for depressive symptoms at baseline, age, sex, education, and income (PROSPERO CRD42018091627). Six cohorts met the inclusion criteria, with IPD on 23,038 participants. Their mean age was 60 years, 65% were female, 21,025 were euthyroid, 1342 had subclinical hypothyroidism and 671 subclinical hyperthyroidism. At first available follow-up [mean 8.2 (± 4.3) years], BDI scores did not differ between participants with subclinical hypothyroidism (mean difference = 0.29, 95% confidence interval = - 0.17 to 0.76, I2 = 15.6) or subclinical hyperthyroidism (- 0.10, 95% confidence interval = - 0.67 to 0.48, I2 = 3.2) compared to euthyroidism. This systematic review and IPD analysis of six prospective cohort studies found no clinically relevant association between subclinical thyroid dysfunction at baseline and depressive symptoms during follow-up. The results were robust in all se
Published: 2020

41. Osteocalcin and its forms across the lifespan in adult men

Author: Smith, Cassandra, Voisin, Sarah, Al Saedi, Ahmed, Phu, Steven, Brennan-Speranza, Tara, Parker, Lewan, Eynon, Nir, Hiam, Danielle, Yan, Xu, Scott, David, Blekkenhorst, Lauren C., Lewis, Joshua R., Seeman, Ego, Byrnes, Elizabeth, Flicker, Leon, Duque, Gustavo, Yeap, Bu B., Levinger, Itamar, Smith, Cassandra, Voisin, Sarah, Al Saedi, Ahmed, Phu, Steven, Brennan-Speranza, Tara, Parker, Lewan, Eynon, Nir, Hiam, Danielle, Yan, Xu, Scott, David, Blekkenhorst, Lauren C., Lewis, Joshua R., Seeman, Ego, Byrnes, Elizabeth, Flicker, Leon, Duque, Gustavo, Yeap, Bu B., and Levinger, Itamar
Abstract: Purpose: Osteocalcin (OC), an osteoblast-specific secreted protein expressed by mature osteoblasts, is used in clinical practice and in research as a marker of bone turnover. The carboxylated (cOC) and undercarboxylated (ucOC) forms may have a different biological function but age-specific reference ranges for these components are not established. Given the different physiological roles, development of reference ranges may help to identify people at risk for bone disease. Methods: Blood was collected in the morning after an overnight fast from 236 adult men (18 to 92 years old) free of diabetes, antiresorptive, warfarin or glucocorticoid use. Serum was analyzed for total osteocalcin (tOC) and the ucOC fraction using the hydroxyapatite binding method. cOC, ucOC/tOC and cOC/tOC ratios were calculated. Reference intervals were established by polynomial quantile regression analysis. Results: The normal ranges for young men (≤30 years) were: tOC 17.9–56.8 ng/mL, ucOC 7.1–22.0 ng/mL, cOC 8.51–40.3 ng/mL (2.5th to 97.5th quantiles). Aging was associated with a “U” shaped pattern for tOC, cOC and ucOC levels. ucOC/tOC ratio was higher, while cOC/tOC ratio was lower in men of advanced age. Age explained ∼31%, while body mass index explained ∼4%, of the variance in the ratios. Conclusions: We have defined normal reference ranges for the OC forms in Australian men and demonstrated that the OC ratios may be better measures, than the absolute values, to identify the age-related changes on OC in men. These ratios may be incorporated into future research and clinical trials, and their associations with prediction of events, such as fracture or diabetes risk, should be determined.
Published: 2020

42. An individual participant data analysis of prospective cohort studies on the association between subclinical thyroid dysfunction and depressive symptoms.

Author: Wildisen, Lea, Wildisen, Lea, Del Giovane, Cinzia, Moutzouri, Elisavet, Beglinger, Shanthi, Syrogiannouli, Lamprini, Collet, Tinh-Hai, Cappola, Anne R, Åsvold, Bjørn O, Bakker, Stephan JL, Yeap, Bu B, Almeida, Osvaldo P, Ceresini, Graziano, Dullaart, Robin PF, Ferrucci, Luigi, Grabe, Hans, Jukema, J Wouter, Nauck, Matthias, Trompet, Stella, Völzke, Henry, Westendorp, Rudi, Gussekloo, Jacobijn, Klöppel, Stefan, Aujesky, Drahomir, Bauer, Douglas, Peeters, Robin, Feller, Martin, Rodondi, Nicolas, Wildisen, Lea, Wildisen, Lea, Del Giovane, Cinzia, Moutzouri, Elisavet, Beglinger, Shanthi, Syrogiannouli, Lamprini, Collet, Tinh-Hai, Cappola, Anne R, Åsvold, Bjørn O, Bakker, Stephan JL, Yeap, Bu B, Almeida, Osvaldo P, Ceresini, Graziano, Dullaart, Robin PF, Ferrucci, Luigi, Grabe, Hans, Jukema, J Wouter, Nauck, Matthias, Trompet, Stella, Völzke, Henry, Westendorp, Rudi, Gussekloo, Jacobijn, Klöppel, Stefan, Aujesky, Drahomir, Bauer, Douglas, Peeters, Robin, Feller, Martin, and Rodondi, Nicolas
Abstract: In subclinical hypothyroidism, the presence of depressive symptoms is often a reason for starting levothyroxine treatment. However, data are conflicting on the association between subclinical thyroid dysfunction and depressive symptoms. We aimed to examine the association between subclinical thyroid dysfunction and depressive symptoms in all prospective cohorts with relevant data available. We performed a systematic review of the literature from Medline, Embase, Cumulative Index to Nursing and Allied Health Literature, and the Cochrane Library from inception to 10th May 2019. We included prospective cohorts with data on thyroid status at baseline and depressive symptoms during follow-up. The primary outcome was depressive symptoms measured at first available follow-up, expressed on the Beck's Depression Inventory (BDI) scale (range 0-63, higher values indicate more depressive symptoms, minimal clinically important difference: 5 points). We performed a two-stage individual participant data (IPD) analysis comparing participants with subclinical hypo- or hyperthyroidism versus euthyroidism, adjusting for depressive symptoms at baseline, age, sex, education, and income (PROSPERO CRD42018091627). Six cohorts met the inclusion criteria, with IPD on 23,038 participants. Their mean age was 60 years, 65% were female, 21,025 were euthyroid, 1342 had subclinical hypothyroidism and 671 subclinical hyperthyroidism. At first available follow-up [mean 8.2 (± 4.3) years], BDI scores did not differ between participants with subclinical hypothyroidism (mean difference = 0.29, 95% confidence interval = - 0.17 to 0.76, I2 = 15.6) or subclinical hyperthyroidism (- 0.10, 95% confidence interval = - 0.67 to 0.48, I2 = 3.2) compared to euthyroidism. This systematic review and IPD analysis of six prospective cohort studies found no clinically relevant association between subclinical thyroid dysfunction at baseline and depressive symptoms during follow-up. The results were robust in a
Published: 2020

43. Osteocalcin and its forms across the lifespan in adult men

Author: Smith, Cassandra, Voisin, Sarah, Al Saedi, Ahmed, Phu, Steven, Brennan-Speranza, Tara, Parker, Lewan, Eynon, Nir, Hiam, Danielle, Yan, Xu, Scott, David, Blekkenhorst, Lauren C., Lewis, Joshua R., Seeman, Ego, Byrnes, Elizabeth, Flicker, Leon, Duque, Gustavo, Yeap, Bu B., Levinger, Itamar, Smith, Cassandra, Voisin, Sarah, Al Saedi, Ahmed, Phu, Steven, Brennan-Speranza, Tara, Parker, Lewan, Eynon, Nir, Hiam, Danielle, Yan, Xu, Scott, David, Blekkenhorst, Lauren C., Lewis, Joshua R., Seeman, Ego, Byrnes, Elizabeth, Flicker, Leon, Duque, Gustavo, Yeap, Bu B., and Levinger, Itamar
Abstract: Purpose: Osteocalcin (OC), an osteoblast-specific secreted protein expressed by mature osteoblasts, is used in clinical practice and in research as a marker of bone turnover. The carboxylated (cOC) and undercarboxylated (ucOC) forms may have a different biological function but age-specific reference ranges for these components are not established. Given the different physiological roles, development of reference ranges may help to identify people at risk for bone disease. Methods: Blood was collected in the morning after an overnight fast from 236 adult men (18 to 92 years old) free of diabetes, antiresorptive, warfarin or glucocorticoid use. Serum was analyzed for total osteocalcin (tOC) and the ucOC fraction using the hydroxyapatite binding method. cOC, ucOC/tOC and cOC/tOC ratios were calculated. Reference intervals were established by polynomial quantile regression analysis. Results: The normal ranges for young men (≤30 years) were: tOC 17.9–56.8 ng/mL, ucOC 7.1–22.0 ng/mL, cOC 8.51–40.3 ng/mL (2.5th to 97.5th quantiles). Aging was associated with a “U” shaped pattern for tOC, cOC and ucOC levels. ucOC/tOC ratio was higher, while cOC/tOC ratio was lower in men of advanced age. Age explained ∼31%, while body mass index explained ∼4%, of the variance in the ratios. Conclusions: We have defined normal reference ranges for the OC forms in Australian men and demonstrated that the OC ratios may be better measures, than the absolute values, to identify the age-related changes on OC in men. These ratios may be incorporated into future research and clinical trials, and their associations with prediction of events, such as fracture or diabetes risk, should be determined.
Published: 2020

44. An individual participant data analysis of prospective cohort studies on the association between subclinical thyroid dysfunction and depressive symptoms

Author: Wildisen, Lea, Del Giovane, Cinzia, Moutzouri, Elisavet, Beglinger, Shanthi, Syrogiannouli, Lamprini, Collet, Tinh-Hai, Cappola, Anne R., Asvold, Bjørn O., Bakker, Stephan J. L., Yeap, Bu B., Almeida, Osvaldo P., Ceresini, Graziano, Dullaart, Robin P. F., Ferrucci, Luigi, Grabe, Hans, Jukema, J. Wouter, Nauck, Matthias, Trompet, Stella, Voelzke, Henry, Westendorp, Rudi, Gussekloo, Jacobijn, Kloppel, Stefan, Aujesky, Drahomir, Bauer, Douglas, Peeters, Robin, Feller, Martin, Rodondi, Nicolas, Wildisen, Lea, Del Giovane, Cinzia, Moutzouri, Elisavet, Beglinger, Shanthi, Syrogiannouli, Lamprini, Collet, Tinh-Hai, Cappola, Anne R., Asvold, Bjørn O., Bakker, Stephan J. L., Yeap, Bu B., Almeida, Osvaldo P., Ceresini, Graziano, Dullaart, Robin P. F., Ferrucci, Luigi, Grabe, Hans, Jukema, J. Wouter, Nauck, Matthias, Trompet, Stella, Voelzke, Henry, Westendorp, Rudi, Gussekloo, Jacobijn, Kloppel, Stefan, Aujesky, Drahomir, Bauer, Douglas, Peeters, Robin, Feller, Martin, and Rodondi, Nicolas
Abstract: In subclinical hypothyroidism, the presence of depressive symptoms is often a reason for starting levothyroxine treatment. However, data are conflicting on the association between subclinical thyroid dysfunction and depressive symptoms. We aimed to examine the association between subclinical thyroid dysfunction and depressive symptoms in all prospective cohorts with relevant data available. We performed a systematic review of the literature from Medline, Embase, Cumulative Index to Nursing and Allied Health Literature, and the Cochrane Library from inception to 10th May 2019. We included prospective cohorts with data on thyroid status at baseline and depressive symptoms during follow-up. The primary outcome was depressive symptoms measured at first available follow-up, expressed on the Beck's Depression Inventory (BDI) scale (range 0-63, higher values indicate more depressive symptoms, minimal clinically important difference: 5 points). We performed a two-stage individual participant data (IPD) analysis comparing participants with subclinical hypo- or hyperthyroidism versus euthyroidism, adjusting for depressive symptoms at baseline, age, sex, education, and income (PROSPERO CRD42018091627). Six cohorts met the inclusion criteria, with IPD on 23,038 participants. Their mean age was 60 years, 65% were female, 21,025 were euthyroid, 1342 had subclinical hypothyroidism and 671 subclinical hyperthyroidism. At first available follow-up [mean 8.2 (+/- 4.3) years], BDI scores did not differ between participants with subclinical hypothyroidism (mean difference = 0.29, 95% confidence interval = - 0.17 to 0.76, I-2 = 15.6) or subclinical hyperthyroidism (- 0.10, 95% confidence interval = - 0.67 to 0.48, I-2 = 3.2) compared to euthyroidism. This systematic review and IPD analysis of six prospective cohort studies found no clinically relevant association between subclinical thyroid dysfunction at baseline and depressive symptoms during follow-up. The results were robust in a
Published: 2020

45. An individual participant data analysis of prospective cohort studies on the association between subclinical thyroid dysfunction and depressive symptoms

Author: Wildisen, Lea, Del Giovane, Cinzia, Moutzouri, Elisavet, Beglinger, Shanthi, Syrogiannouli, Lamprini, Collet, Tinh-Hai, Cappola, Anne R., Asvold, Bjørn O., Bakker, Stephan J. L., Yeap, Bu B., Almeida, Osvaldo P., Ceresini, Graziano, Dullaart, Robin P. F., Ferrucci, Luigi, Grabe, Hans, Jukema, J. Wouter, Nauck, Matthias, Trompet, Stella, Voelzke, Henry, Westendorp, Rudi, Gussekloo, Jacobijn, Kloppel, Stefan, Aujesky, Drahomir, Bauer, Douglas, Peeters, Robin, Feller, Martin, Rodondi, Nicolas, Wildisen, Lea, Del Giovane, Cinzia, Moutzouri, Elisavet, Beglinger, Shanthi, Syrogiannouli, Lamprini, Collet, Tinh-Hai, Cappola, Anne R., Asvold, Bjørn O., Bakker, Stephan J. L., Yeap, Bu B., Almeida, Osvaldo P., Ceresini, Graziano, Dullaart, Robin P. F., Ferrucci, Luigi, Grabe, Hans, Jukema, J. Wouter, Nauck, Matthias, Trompet, Stella, Voelzke, Henry, Westendorp, Rudi, Gussekloo, Jacobijn, Kloppel, Stefan, Aujesky, Drahomir, Bauer, Douglas, Peeters, Robin, Feller, Martin, and Rodondi, Nicolas
Abstract: In subclinical hypothyroidism, the presence of depressive symptoms is often a reason for starting levothyroxine treatment. However, data are conflicting on the association between subclinical thyroid dysfunction and depressive symptoms. We aimed to examine the association between subclinical thyroid dysfunction and depressive symptoms in all prospective cohorts with relevant data available. We performed a systematic review of the literature from Medline, Embase, Cumulative Index to Nursing and Allied Health Literature, and the Cochrane Library from inception to 10th May 2019. We included prospective cohorts with data on thyroid status at baseline and depressive symptoms during follow-up. The primary outcome was depressive symptoms measured at first available follow-up, expressed on the Beck's Depression Inventory (BDI) scale (range 0-63, higher values indicate more depressive symptoms, minimal clinically important difference: 5 points). We performed a two-stage individual participant data (IPD) analysis comparing participants with subclinical hypo- or hyperthyroidism versus euthyroidism, adjusting for depressive symptoms at baseline, age, sex, education, and income (PROSPERO CRD42018091627). Six cohorts met the inclusion criteria, with IPD on 23,038 participants. Their mean age was 60 years, 65% were female, 21,025 were euthyroid, 1342 had subclinical hypothyroidism and 671 subclinical hyperthyroidism. At first available follow-up [mean 8.2 (+/- 4.3) years], BDI scores did not differ between participants with subclinical hypothyroidism (mean difference = 0.29, 95% confidence interval = - 0.17 to 0.76, I-2 = 15.6) or subclinical hyperthyroidism (- 0.10, 95% confidence interval = - 0.67 to 0.48, I-2 = 3.2) compared to euthyroidism. This systematic review and IPD analysis of six prospective cohort studies found no clinically relevant association between subclinical thyroid dysfunction at baseline and depressive symptoms during follow-up. The results were robust in a
Published: 2020

46. The associations of anthropometric, behavioural and sociodemographic factors with circulating concentrations of IGF-I, IGF-II, IGFBP-1, IGFBP-2 and IGFBP-3 in a pooled analysis of 16,024 men from 22 studies

Author: Watts, Eleanor L., Perez-Cornago, Aurora, Appleby, Paul N., Albanes, Demetrius, Ardanaz, Eva, Black, Amanda, Bueno-de-Mesquita, H. Bas, Chan, June M., Chen, Chu, Chubb, S. A. Paul, Cook, Michael B., Deschasaux, Melanie, Donovan, Jenny L., English, Dallas R., Flicker, Leon, Freedman, Neal D., Galan, Pilar, Giles, Graham G., Giovannucci, Edward L., Gunter, Marc J., Habel, Laurel A., Häggström, Christel, Haiman, Christopher, Hamdy, Freddie C., Hercberg, Serge, Holly, Jeff M., Huang, Jiaqi, Huang, Wen-Yi, Johansson, Mattias, Kaaks, Rudolf, Kubo, Tatsuhiko, Lane, J. Athene, Layne, Tracy M., Le Marchand, Loic, Martin, Richard M., Metter, E. Jeffrey, Mikami, Kazuya, Milne, Roger L., Morris, Howard A., Mucci, Lorelei A., Neal, David E., Neuhouser, Marian L., Oliver, Steven E., Overvad, Kim, Ozasa, Kotaro, Pala, Valeria, Pernar, Claire H., Pollak, Michael, Rowlands, Mari-Anne, Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Touvier, Mathilde, Trichopoulou, Antonia, Tsilidis, Konstantinos K., Van Den Eeden, Stephen K., Weinstein, Stephanie J., Wilkens, Lynne, Yeap, Bu B., Key, Timothy J., Allen, Naomi E., Travis, Ruth C., Watts, Eleanor L., Perez-Cornago, Aurora, Appleby, Paul N., Albanes, Demetrius, Ardanaz, Eva, Black, Amanda, Bueno-de-Mesquita, H. Bas, Chan, June M., Chen, Chu, Chubb, S. A. Paul, Cook, Michael B., Deschasaux, Melanie, Donovan, Jenny L., English, Dallas R., Flicker, Leon, Freedman, Neal D., Galan, Pilar, Giles, Graham G., Giovannucci, Edward L., Gunter, Marc J., Habel, Laurel A., Häggström, Christel, Haiman, Christopher, Hamdy, Freddie C., Hercberg, Serge, Holly, Jeff M., Huang, Jiaqi, Huang, Wen-Yi, Johansson, Mattias, Kaaks, Rudolf, Kubo, Tatsuhiko, Lane, J. Athene, Layne, Tracy M., Le Marchand, Loic, Martin, Richard M., Metter, E. Jeffrey, Mikami, Kazuya, Milne, Roger L., Morris, Howard A., Mucci, Lorelei A., Neal, David E., Neuhouser, Marian L., Oliver, Steven E., Overvad, Kim, Ozasa, Kotaro, Pala, Valeria, Pernar, Claire H., Pollak, Michael, Rowlands, Mari-Anne, Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Touvier, Mathilde, Trichopoulou, Antonia, Tsilidis, Konstantinos K., Van Den Eeden, Stephen K., Weinstein, Stephanie J., Wilkens, Lynne, Yeap, Bu B., Key, Timothy J., Allen, Naomi E., and Travis, Ruth C.
Abstract: Insulin-like growth factors (IGFs) and insulin-like growth factor binding proteins (IGFBPs) have been implicated in the aetiology of several cancers. To better understand whether anthropometric, behavioural and sociodemographic factors may play a role in cancer risk via IGF signalling, we examined the cross-sectional associations of these exposures with circulating concentrations of IGFs (IGF-I and IGF-II) and IGFBPs (IGFBP-1, IGFBP-2 and IGFBP-3). The Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group dataset includes individual participant data from 16,024 male controls (i.e. without prostate cancer) aged 22-89 years from 22 prospective studies. Geometric means of protein concentrations were estimated using analysis of variance, adjusted for relevant covariates. Older age was associated with higher concentrations of IGFBP-1 and IGFBP-2 and lower concentrations of IGF-I, IGF-II and IGFBP-3. Higher body mass index was associated with lower concentrations of IGFBP-1 and IGFBP-2. Taller height was associated with higher concentrations of IGF-I and IGFBP-3 and lower concentrations of IGFBP-1. Smokers had higher concentrations of IGFBP-1 and IGFBP-2 and lower concentrations of IGFBP-3 than nonsmokers. Higher alcohol consumption was associated with higher concentrations of IGF-II and lower concentrations of IGF-I and IGFBP-2. African Americans had lower concentrations of IGF-II, IGFBP-1, IGFBP-2 and IGFBP-3 and Hispanics had lower IGF-I, IGF-II and IGFBP-3 than non-Hispanic whites. These findings indicate that a range of anthropometric, behavioural and sociodemographic factors are associated with circulating concentrations of IGFs and IGFBPs in men, which will lead to a greater understanding of the mechanisms through which these factors influence cancer risk.
Published: 2019
Full Text: View/download PDF

47. The associations of anthropometric, behavioural and sociodemographic factors with circulating concentrations of IGF‐I, IGF‐II, IGFBP‐1, IGFBP‐2 and IGFBP‐3 in a pooled analysis of 16,024 men from 22 studies

Author: Watts, Eleanor L., Perez-Cornago, Aurora, Appleby, Paul N., Albanes, Demetrius, Ardanaz, Eva, Black, Amanda, Bueno-de-Mesquita, H. Bas, Chan, June M., Chen, Chu, Chubb, S. A. Paul, Cook, Michael B., Deschasaux, Mélanie, Donovan, Jenny L., English, Dallas R., Flicker, Leon, Freedman, Neal D., Galan, Pilar, Giles, Graham G., Giovannucci, Edward L., Gunter, Marc J., Habel, Laurel A., Häggström, Christel, Haiman, Christopher, Hamdy, Freddie C., Hercberg, Serge, Holly, Jeff M., Huang, Jiaqi, Huang, Wen-Yi, Johansson, Mattias, Kaaks, Rudolf, Kubo, Tatsuhiko, Lane, J. Athene, Layne, Tracy M., Le Marchand, Loic, Martin, Richard M., Metter, E. Jeffrey, Mikami, Kazuya, Milne, Roger L., Morris, Howard A, Mucci, Lorelei A., Neal, David E., Neuhouser, Marian L., Oliver, Steven E, Overvad, Kim, Ozasa, Kotaro, Pala, Valeria, Pernar, Claire H., Pollak, Michael, Rowlands, Mari-Anne, Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Touvier, Mathilde, Trichopoulou, Antonia, Tsilidis, Konstantinos K., Van Den Eeden, Stephen K., Weinstein, Stephanie J., Wilkens, Lynne, Yeap, Bu B., Key, Timothy J., Allen, Naomi E., Travis, Ruth C., Watts, Eleanor L., Perez-Cornago, Aurora, Appleby, Paul N., Albanes, Demetrius, Ardanaz, Eva, Black, Amanda, Bueno-de-Mesquita, H. Bas, Chan, June M., Chen, Chu, Chubb, S. A. Paul, Cook, Michael B., Deschasaux, Mélanie, Donovan, Jenny L., English, Dallas R., Flicker, Leon, Freedman, Neal D., Galan, Pilar, Giles, Graham G., Giovannucci, Edward L., Gunter, Marc J., Habel, Laurel A., Häggström, Christel, Haiman, Christopher, Hamdy, Freddie C., Hercberg, Serge, Holly, Jeff M., Huang, Jiaqi, Huang, Wen-Yi, Johansson, Mattias, Kaaks, Rudolf, Kubo, Tatsuhiko, Lane, J. Athene, Layne, Tracy M., Le Marchand, Loic, Martin, Richard M., Metter, E. Jeffrey, Mikami, Kazuya, Milne, Roger L., Morris, Howard A, Mucci, Lorelei A., Neal, David E., Neuhouser, Marian L., Oliver, Steven E, Overvad, Kim, Ozasa, Kotaro, Pala, Valeria, Pernar, Claire H., Pollak, Michael, Rowlands, Mari-Anne, Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Touvier, Mathilde, Trichopoulou, Antonia, Tsilidis, Konstantinos K., Van Den Eeden, Stephen K., Weinstein, Stephanie J., Wilkens, Lynne, Yeap, Bu B., Key, Timothy J., Allen, Naomi E., and Travis, Ruth C.
Abstract: Insulin‐like growth factors (IGFs) and insulin‐like growth factor binding proteins (IGFBPs) have been implicated in the aetiology of several cancers. To better understand whether anthropometric, behavioural and sociodemographic factors may play a role in cancer risk via IGF signalling, we examined the cross‐sectional associations of these exposures with circulating concentrations of IGFs (IGF‐I and IGF‐II) and IGFBPs (IGFBP‐1, IGFBP‐2 and IGFBP‐3). The Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group dataset includes individual participant data from 16,024 male controls (i.e. without prostate cancer) aged 22–89 years from 22 prospective studies. Geometric means of protein concentrations were estimated using analysis of variance, adjusted for relevant covariates. Older age was associated with higher concentrations of IGFBP‐1 and IGFBP‐2 and lower concentrations of IGF‐I, IGF‐II and IGFBP‐3. Higher body mass index was associated with lower concentrations of IGFBP‐1 and IGFBP‐2. Taller height was associated with higher concentrations of IGF‐I and IGFBP‐3 and lower concentrations of IGFBP‐1. Smokers had higher concentrations of IGFBP‐1 and IGFBP‐2 and lower concentrations of IGFBP‐3 than nonsmokers. Higher alcohol consumption was associated with higher concentrations of IGF‐II and lower concentrations of IGF‐I and IGFBP‐2. African Americans had lower concentrations of IGF‐II, IGFBP‐1, IGFBP‐2 and IGFBP‐3 and Hispanics had lower IGF‐I, IGF‐II and IGFBP‐3 than non‐Hispanic whites. These findings indicate that a range of anthropometric, behavioural and sociodemographic factors are associated with circulating concentrations of IGFs and IGFBPs in men, which will lead to a greater understanding of the mechanisms through which these factors influence cancer risk.
Published: 2019
Full Text: View/download PDF

48. The associations of anthropometric, behavioural and sociodemographic factors with circulating concentrations of IGF‐I, IGF‐II, IGFBP‐1, IGFBP‐2 and IGFBP‐3 in a pooled analysis of 16,024 men from 22 studies

Author: Watts, Eleanor L., Perez-Cornago, Aurora, Appleby, Paul N., Albanes, Demetrius, Ardanaz, Eva, Black, Amanda, Bueno-de-Mesquita, H. Bas, Chan, June M., Chen, Chu, Chubb, S. A. Paul, Cook, Michael B., Deschasaux, Mélanie, Donovan, Jenny L., English, Dallas R., Flicker, Leon, Freedman, Neal D., Galan, Pilar, Giles, Graham G., Giovannucci, Edward L., Gunter, Marc J., Habel, Laurel A., Häggström, Christel, Haiman, Christopher, Hamdy, Freddie C., Hercberg, Serge, Holly, Jeff M., Huang, Jiaqi, Huang, Wen-Yi, Johansson, Mattias, Kaaks, Rudolf, Kubo, Tatsuhiko, Lane, J. Athene, Layne, Tracy M., Le Marchand, Loic, Martin, Richard M., Metter, E. Jeffrey, Mikami, Kazuya, Milne, Roger L., Morris, Howard A, Mucci, Lorelei A., Neal, David E., Neuhouser, Marian L., Oliver, Steven E, Overvad, Kim, Ozasa, Kotaro, Pala, Valeria, Pernar, Claire H., Pollak, Michael, Rowlands, Mari-Anne, Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Touvier, Mathilde, Trichopoulou, Antonia, Tsilidis, Konstantinos K., Van Den Eeden, Stephen K., Weinstein, Stephanie J., Wilkens, Lynne, Yeap, Bu B., Key, Timothy J., Allen, Naomi E., Travis, Ruth C., Watts, Eleanor L., Perez-Cornago, Aurora, Appleby, Paul N., Albanes, Demetrius, Ardanaz, Eva, Black, Amanda, Bueno-de-Mesquita, H. Bas, Chan, June M., Chen, Chu, Chubb, S. A. Paul, Cook, Michael B., Deschasaux, Mélanie, Donovan, Jenny L., English, Dallas R., Flicker, Leon, Freedman, Neal D., Galan, Pilar, Giles, Graham G., Giovannucci, Edward L., Gunter, Marc J., Habel, Laurel A., Häggström, Christel, Haiman, Christopher, Hamdy, Freddie C., Hercberg, Serge, Holly, Jeff M., Huang, Jiaqi, Huang, Wen-Yi, Johansson, Mattias, Kaaks, Rudolf, Kubo, Tatsuhiko, Lane, J. Athene, Layne, Tracy M., Le Marchand, Loic, Martin, Richard M., Metter, E. Jeffrey, Mikami, Kazuya, Milne, Roger L., Morris, Howard A, Mucci, Lorelei A., Neal, David E., Neuhouser, Marian L., Oliver, Steven E, Overvad, Kim, Ozasa, Kotaro, Pala, Valeria, Pernar, Claire H., Pollak, Michael, Rowlands, Mari-Anne, Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Touvier, Mathilde, Trichopoulou, Antonia, Tsilidis, Konstantinos K., Van Den Eeden, Stephen K., Weinstein, Stephanie J., Wilkens, Lynne, Yeap, Bu B., Key, Timothy J., Allen, Naomi E., and Travis, Ruth C.
Abstract: Insulin‐like growth factors (IGFs) and insulin‐like growth factor binding proteins (IGFBPs) have been implicated in the aetiology of several cancers. To better understand whether anthropometric, behavioural and sociodemographic factors may play a role in cancer risk via IGF signalling, we examined the cross‐sectional associations of these exposures with circulating concentrations of IGFs (IGF‐I and IGF‐II) and IGFBPs (IGFBP‐1, IGFBP‐2 and IGFBP‐3). The Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group dataset includes individual participant data from 16,024 male controls (i.e. without prostate cancer) aged 22–89 years from 22 prospective studies. Geometric means of protein concentrations were estimated using analysis of variance, adjusted for relevant covariates. Older age was associated with higher concentrations of IGFBP‐1 and IGFBP‐2 and lower concentrations of IGF‐I, IGF‐II and IGFBP‐3. Higher body mass index was associated with lower concentrations of IGFBP‐1 and IGFBP‐2. Taller height was associated with higher concentrations of IGF‐I and IGFBP‐3 and lower concentrations of IGFBP‐1. Smokers had higher concentrations of IGFBP‐1 and IGFBP‐2 and lower concentrations of IGFBP‐3 than nonsmokers. Higher alcohol consumption was associated with higher concentrations of IGF‐II and lower concentrations of IGF‐I and IGFBP‐2. African Americans had lower concentrations of IGF‐II, IGFBP‐1, IGFBP‐2 and IGFBP‐3 and Hispanics had lower IGF‐I, IGF‐II and IGFBP‐3 than non‐Hispanic whites. These findings indicate that a range of anthropometric, behavioural and sociodemographic factors are associated with circulating concentrations of IGFs and IGFBPs in men, which will lead to a greater understanding of the mechanisms through which these factors influence cancer risk.
Published: 2019
Full Text: View/download PDF

49. The associations of anthropometric, behavioural and sociodemographic factors with circulating concentrations of IGF-I, IGF-II, IGFBP-1, IGFBP-2 and IGFBP-3 in a pooled analysis of 16,024 men from 22 studies

Author: Watts, Eleanor L., Perez-Cornago, Aurora, Appleby, Paul N., Albanes, Demetrius, Ardanaz, Eva, Black, Amanda, Bueno-de-Mesquita, H. Bas, Chan, June M., Chen, Chu, Chubb, S. A. Paul, Cook, Michael B., Deschasaux, Melanie, Donovan, Jenny L., English, Dallas R., Flicker, Leon, Freedman, Neal D., Galan, Pilar, Giles, Graham G., Giovannucci, Edward L., Gunter, Marc J., Habel, Laurel A., Häggström, Christel, Haiman, Christopher, Hamdy, Freddie C., Hercberg, Serge, Holly, Jeff M., Huang, Jiaqi, Huang, Wen-Yi, Johansson, Mattias, Kaaks, Rudolf, Kubo, Tatsuhiko, Lane, J. Athene, Layne, Tracy M., Le Marchand, Loic, Martin, Richard M., Metter, E. Jeffrey, Mikami, Kazuya, Milne, Roger L., Morris, Howard A., Mucci, Lorelei A., Neal, David E., Neuhouser, Marian L., Oliver, Steven E., Overvad, Kim, Ozasa, Kotaro, Pala, Valeria, Pernar, Claire H., Pollak, Michael, Rowlands, Mari-Anne, Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Touvier, Mathilde, Trichopoulou, Antonia, Tsilidis, Konstantinos K., Van Den Eeden, Stephen K., Weinstein, Stephanie J., Wilkens, Lynne, Yeap, Bu B., Key, Timothy J., Allen, Naomi E., Travis, Ruth C., Watts, Eleanor L., Perez-Cornago, Aurora, Appleby, Paul N., Albanes, Demetrius, Ardanaz, Eva, Black, Amanda, Bueno-de-Mesquita, H. Bas, Chan, June M., Chen, Chu, Chubb, S. A. Paul, Cook, Michael B., Deschasaux, Melanie, Donovan, Jenny L., English, Dallas R., Flicker, Leon, Freedman, Neal D., Galan, Pilar, Giles, Graham G., Giovannucci, Edward L., Gunter, Marc J., Habel, Laurel A., Häggström, Christel, Haiman, Christopher, Hamdy, Freddie C., Hercberg, Serge, Holly, Jeff M., Huang, Jiaqi, Huang, Wen-Yi, Johansson, Mattias, Kaaks, Rudolf, Kubo, Tatsuhiko, Lane, J. Athene, Layne, Tracy M., Le Marchand, Loic, Martin, Richard M., Metter, E. Jeffrey, Mikami, Kazuya, Milne, Roger L., Morris, Howard A., Mucci, Lorelei A., Neal, David E., Neuhouser, Marian L., Oliver, Steven E., Overvad, Kim, Ozasa, Kotaro, Pala, Valeria, Pernar, Claire H., Pollak, Michael, Rowlands, Mari-Anne, Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Touvier, Mathilde, Trichopoulou, Antonia, Tsilidis, Konstantinos K., Van Den Eeden, Stephen K., Weinstein, Stephanie J., Wilkens, Lynne, Yeap, Bu B., Key, Timothy J., Allen, Naomi E., and Travis, Ruth C.
Abstract: Insulin-like growth factors (IGFs) and insulin-like growth factor binding proteins (IGFBPs) have been implicated in the aetiology of several cancers. To better understand whether anthropometric, behavioural and sociodemographic factors may play a role in cancer risk via IGF signalling, we examined the cross-sectional associations of these exposures with circulating concentrations of IGFs (IGF-I and IGF-II) and IGFBPs (IGFBP-1, IGFBP-2 and IGFBP-3). The Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group dataset includes individual participant data from 16,024 male controls (i.e. without prostate cancer) aged 22-89 years from 22 prospective studies. Geometric means of protein concentrations were estimated using analysis of variance, adjusted for relevant covariates. Older age was associated with higher concentrations of IGFBP-1 and IGFBP-2 and lower concentrations of IGF-I, IGF-II and IGFBP-3. Higher body mass index was associated with lower concentrations of IGFBP-1 and IGFBP-2. Taller height was associated with higher concentrations of IGF-I and IGFBP-3 and lower concentrations of IGFBP-1. Smokers had higher concentrations of IGFBP-1 and IGFBP-2 and lower concentrations of IGFBP-3 than nonsmokers. Higher alcohol consumption was associated with higher concentrations of IGF-II and lower concentrations of IGF-I and IGFBP-2. African Americans had lower concentrations of IGF-II, IGFBP-1, IGFBP-2 and IGFBP-3 and Hispanics had lower IGF-I, IGF-II and IGFBP-3 than non-Hispanic whites. These findings indicate that a range of anthropometric, behavioural and sociodemographic factors are associated with circulating concentrations of IGFs and IGFBPs in men, which will lead to a greater understanding of the mechanisms through which these factors influence cancer risk.
Published: 2019
Full Text: View/download PDF

50. The associations of anthropometric, behavioural and sociodemographic factors with circulating concentrations of IGF‐I, IGF‐II, IGFBP‐1, IGFBP‐2 and IGFBP‐3 in a pooled analysis of 16,024 men from 22 studies

Author: Watts, Eleanor L., Perez-Cornago, Aurora, Appleby, Paul N., Albanes, Demetrius, Ardanaz, Eva, Black, Amanda, Bueno-de-Mesquita, H. Bas, Chan, June M., Chen, Chu, Chubb, S. A. Paul, Cook, Michael B., Deschasaux, Mélanie, Donovan, Jenny L., English, Dallas R., Flicker, Leon, Freedman, Neal D., Galan, Pilar, Giles, Graham G., Giovannucci, Edward L., Gunter, Marc J., Habel, Laurel A., Häggström, Christel, Haiman, Christopher, Hamdy, Freddie C., Hercberg, Serge, Holly, Jeff M., Huang, Jiaqi, Huang, Wen-Yi, Johansson, Mattias, Kaaks, Rudolf, Kubo, Tatsuhiko, Lane, J. Athene, Layne, Tracy M., Le Marchand, Loic, Martin, Richard M., Metter, E. Jeffrey, Mikami, Kazuya, Milne, Roger L., Morris, Howard A, Mucci, Lorelei A., Neal, David E., Neuhouser, Marian L., Oliver, Steven E, Overvad, Kim, Ozasa, Kotaro, Pala, Valeria, Pernar, Claire H., Pollak, Michael, Rowlands, Mari-Anne, Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Touvier, Mathilde, Trichopoulou, Antonia, Tsilidis, Konstantinos K., Van Den Eeden, Stephen K., Weinstein, Stephanie J., Wilkens, Lynne, Yeap, Bu B., Key, Timothy J., Allen, Naomi E., Travis, Ruth C., Watts, Eleanor L., Perez-Cornago, Aurora, Appleby, Paul N., Albanes, Demetrius, Ardanaz, Eva, Black, Amanda, Bueno-de-Mesquita, H. Bas, Chan, June M., Chen, Chu, Chubb, S. A. Paul, Cook, Michael B., Deschasaux, Mélanie, Donovan, Jenny L., English, Dallas R., Flicker, Leon, Freedman, Neal D., Galan, Pilar, Giles, Graham G., Giovannucci, Edward L., Gunter, Marc J., Habel, Laurel A., Häggström, Christel, Haiman, Christopher, Hamdy, Freddie C., Hercberg, Serge, Holly, Jeff M., Huang, Jiaqi, Huang, Wen-Yi, Johansson, Mattias, Kaaks, Rudolf, Kubo, Tatsuhiko, Lane, J. Athene, Layne, Tracy M., Le Marchand, Loic, Martin, Richard M., Metter, E. Jeffrey, Mikami, Kazuya, Milne, Roger L., Morris, Howard A, Mucci, Lorelei A., Neal, David E., Neuhouser, Marian L., Oliver, Steven E, Overvad, Kim, Ozasa, Kotaro, Pala, Valeria, Pernar, Claire H., Pollak, Michael, Rowlands, Mari-Anne, Schaefer, Catherine A., Schenk, Jeannette M., Stattin, Pär, Tamakoshi, Akiko, Thysell, Elin, Touvier, Mathilde, Trichopoulou, Antonia, Tsilidis, Konstantinos K., Van Den Eeden, Stephen K., Weinstein, Stephanie J., Wilkens, Lynne, Yeap, Bu B., Key, Timothy J., Allen, Naomi E., and Travis, Ruth C.
Abstract: Insulin‐like growth factors (IGFs) and insulin‐like growth factor binding proteins (IGFBPs) have been implicated in the aetiology of several cancers. To better understand whether anthropometric, behavioural and sociodemographic factors may play a role in cancer risk via IGF signalling, we examined the cross‐sectional associations of these exposures with circulating concentrations of IGFs (IGF‐I and IGF‐II) and IGFBPs (IGFBP‐1, IGFBP‐2 and IGFBP‐3). The Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group dataset includes individual participant data from 16,024 male controls (i.e. without prostate cancer) aged 22–89 years from 22 prospective studies. Geometric means of protein concentrations were estimated using analysis of variance, adjusted for relevant covariates. Older age was associated with higher concentrations of IGFBP‐1 and IGFBP‐2 and lower concentrations of IGF‐I, IGF‐II and IGFBP‐3. Higher body mass index was associated with lower concentrations of IGFBP‐1 and IGFBP‐2. Taller height was associated with higher concentrations of IGF‐I and IGFBP‐3 and lower concentrations of IGFBP‐1. Smokers had higher concentrations of IGFBP‐1 and IGFBP‐2 and lower concentrations of IGFBP‐3 than nonsmokers. Higher alcohol consumption was associated with higher concentrations of IGF‐II and lower concentrations of IGF‐I and IGFBP‐2. African Americans had lower concentrations of IGF‐II, IGFBP‐1, IGFBP‐2 and IGFBP‐3 and Hispanics had lower IGF‐I, IGF‐II and IGFBP‐3 than non‐Hispanic whites. These findings indicate that a range of anthropometric, behavioural and sociodemographic factors are associated with circulating concentrations of IGFs and IGFBPs in men, which will lead to a greater understanding of the mechanisms through which these factors influence cancer risk.
Published: 2019
Full Text: View/download PDF

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