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1. Estimating dose-response relationships for vitamin D with coronary heart disease, stroke, and all-cause mortality: observational and Mendelian randomisation analyses

Author

Sofianopoulou, Eleni, Kaptoge, Stephen K, Afzal, Shoaib, Jiang, Tao, Gill, Dipender, Gundersen, Thomas E, Bolton, Thomas R, Allara, Elias, Arnold, Matthew G, Mason, Amy M, Chung, Ryan, Pennells, Lisa A M, Shi, Fanchao, Sun, Luanluan, Willeit, Peter, Forouhi, Nita G, Langenberg, Claudia, Sharp, Stephen J, Panico, Salvatore, Engström, Gunnar, Melander, Olle, Tong, Tammy Y N, Perez-Cornago, Aurora, Norberg, Margareta, Johansson, Ingegerd, Katzke, Verena, Srour, Bernard, Sánchez, María José, Redondo-Sánchez, Daniel, Olsen, Anja, Dahm, Christina C, Overvad, Kim, Brustad, Magritt, Skeie, Guri, Moreno-Iribas, Conchi, Onland-Moret, N Charlotte, van der Schouw, Yvonne T, Tsilidis, Konstantinos K, Heath, Alicia K, Agnoli, Claudia, Krogh, Vittorio, de Boer, Ian H, Kobylecki, Camilla Jannie, Çolak, Yunus, Zittermann, Armin, Sundström, Johan, Welsh, Paul, Weiderpass, Elisabete, Aglago, Elom K, Ferrari, Pietro, Clarke, Robert, Boutron, Marie-Christine, Severi, Gianluca, MacDonald, Conor, Providencia, Rui, Masala, Giovanna, Zamora Ros, Raul, Boer, Jolanda, Verschuren, Wm Monique, Cawthon, Peggy, Schierbeck, Louise L, Cooper, Cyrus, Schulze, Matthias B, Bergmann, Manuela M, Hannemann, Anke, Kiechl, Stefan, Brenner, Hermann, van Schoor, Natasja M, Albertorio, Juan R, Sacerdote, Carlotta, Linneberg, Allan, Kårhus, LineL, Huerta, José María, Imaz, Liher, Joergensen, Christel, Ben-Shlomo, Yoav, Lundqvist, Annamari, Gallacher, John, Sattar, Naveed, Wood, Angela M, Wareham, Nicholas J, Nordestgaard, Børge G, Di Angelantonio, Emanuele, Danesh, John, Butterworth, Adam S, and Burgess, Stephen

Abstract

Randomised trials of vitamin D supplementation for cardiovascular disease and all-cause mortality have generally reported null findings. However, generalisability of results to individuals with low vitamin D status is unclear. We aimed to characterise dose-response relationships between 25-hydroxyvitamin D (25[OH]D) concentrations and risk of coronary heart disease, stroke, and all-cause mortality in observational and Mendelian randomisation frameworks.

Published
2024
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2. Mild-to-Moderate Kidney Dysfunction and Cardiovascular Disease: Observational and Mendelian Randomization Analyses

Author

Gaziano, Liam, Sun, Luanluan, Arnold, Matthew, Bell, Steven, Cho, Kelly, Kaptoge, Stephen K., Song, Rebecca J., Burgess, Stephen, Posner, Daniel C., Mosconi, Katja, Robinson-Cohen, Cassianne, Mason, Amy M., Bolton, Thomas R., Tao, Ran, Allara, Elias, Schubert, Petra, Chen, Lingyan, Staley, James R., Staplin, Natalie, Altay, Servet, Amiano, Pilar, Arndt, Volker, Ärnlöv, Johan, Barr, Elizabeth L.M., Björkelund, Cecilia, Boer, Jolanda M.A., Brenner, Hermann, Casiglia, Edoardo, Chiodini, Paolo, Cooper, Jackie A., Coresh, Josef, Cushman, Mary, Dankner, Rachel, Davidson, Karina W., de Jongh, Renate T., Donfrancesco, Chiara, Engström, Gunnar, Freisling, Heinz, de la Cámara, Agustín Gómez, Gudnason, Vilmundur, Hankey, Graeme J., Hansson, Per-Olof, Heath, Alicia K., Hoorn, Ewout J., Imano, Hironori, Jassal, Simerjot K., Kaaks, Rudolf, Katzke, Verena, Kauhanen, Jussi, Kiechl, Stefan, Koenig, Wolfgang, Kronmal, Richard A., Kyrø, Cecilie, Lawlor, Deborah A., Ljungberg, Börje, MacDonald, Conor, Masala, Giovanna, Meisinger, Christa, Melander, Olle, Moreno Iribas, Conchi, Ninomiya, Toshiharu, Nitsch, Dorothea, Nordestgaard, Børge G., Onland-Moret, Charlotte, Palmieri, Luigi, Petrova, Dafina, Garcia, Jose Ramón Quirós, Rosengren, Annika, Sacerdote, Carlotta, Sakurai, Masaru, Santiuste, Carmen, Schulze, Matthias B., Sieri, Sabina, Sundström, Johan, Tikhonoff, Valérie, Tjønneland, Anne, Tong, Tammy, Tumino, Rosario, Tzoulaki, Ioanna, van der Schouw, Yvonne T., Monique Verschuren, W.M., Völzke, Henry, Wallace, Robert B., Wannamethee, S. Goya, Weiderpass, Elisabete, Willeit, Peter, Woodward, Mark, Yamagishi, Kazumasa, Zamora-Ros, Raul, Akwo, Elvis A., Pyarajan, Saiju, Gagnon, David R., Tsao, Philip S., Muralidhar, Sumitra, Edwards, Todd L., Damrauer, Scott M., Joseph, Jacob, Pennells, Lisa, Wilson, Peter W.F., Harrison, Seamus, Gaziano, Thomas A., Inouye, Michael, Baigent, Colin, Casas, Juan P., Langenberg, Claudia, Wareham, Nick, Riboli, Elio, Gaziano, J.Michael, Danesh, John, Hung, Adriana M., Butterworth, Adam S., Wood, Angela M., Di Angelantonio, Emanuele, Koettgen, Anna, Shaw, Jonathan, Atkins, Robert, Zimmet, Paul, Whincup, Peter, Willeit, Peter, Willeit, Johann, Leitner, Christoph, Casiglia, Edoardo, Tikhonoff, Valérie, Tybjaerg-Hansen, Anne, Schnohr, Peter, Afzal, Shoaib, Pablos, David Lora, Arriscado, Cristina Martin, Ferreiro, Carmen Romero, Wallace, Robert B., Stocker, Hannah, Schöttker, Ben, Holleczek, Bernd, Chetrit, Angela, Welin, Lennart, Svärdsudd, Kurt, Welin, Lennart, Svärdsudd, Kurt, Lissner, Lauren, Hange, Dominique, Mehlig, Kirsten, Nagel, Dorothea, Norman, Paul E., Almeida, Osvaldo, Flicker, Leon, Hata, Jun, Honda, Takanori, Furuta, Yoshihiko, Iso, Hiroyasu, Kitamura, Akihiko, Muraki, Isao, Salonen, Jukka T., Tuomainen, Tomi-Pekka, van Zutphen, E. M., van Schoor, N. M., Donfrancesco, Chiara, Lo Noce, Cinzia, Palmieri, Luigi, Cushman, Mary, Kronmal, Richard, Koenig, Wolfgang, Meisinger, Christa, Lappas, Georg, Nilsson, Peter M., Melander, Olle, Hedblad, Bo, Nitsch, Dorothea, Cooper, Jackie A., Shaffer, Jonathan, Schwartz, Joseph, Shimbo, Daichi, Sato, Shinichi, Iso, Hiroyasu, Hayama-Terada, Mina, Jassal, Simerjot, Aspelund, Thor, Thorsson, Bolli, Sigurdsson, Gunnar, Chaker, Layal, Ikram, Kamran M., Kavousi, Maryam, Tunstall-Pedoe, Hugh, Woodward, Mark, Völzke, Henry, Can, Günay, Yüksel, Hüsniye, Özkan, Uğur, Nakagawa, Hideaki, Morikawa, Yuko, Ishizaki, Masao, Ärnlöv, Johan, Arndt, Volker, Feskens, Edith, Geleijnse, Johanna M, and Kromhout, Daan

Published
2022
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3. RETRACTED: Estimating dose-response relationships for vitamin D with coronary heart disease, stroke, and all-cause mortality: observational and Mendelian randomisation analyses

Author

Sofianopoulou, Eleni, Kaptoge, Stephen K, Afzal, Shoaib, Jiang, Tao, Gill, Dipender, Gundersen, Thomas E, Bolton, Thomas R, Allara, Elias, Arnold, Matthew G, Mason, Amy M, Chung, Ryan, Pennells, Lisa A M, Shi, Fanchao, Sun, Luanluan, Willeit, Peter, Forouhi, Nita G, Langenberg, Claudia, Sharp, Stephen J, Panico, Salvatore, Engström, Gunnar, Melander, Olle, Tong, Tammy Y N, Perez-Cornago, Aurora, Norberg, Margareta, Johansson, Ingegerd, Katzke, Verena, Srour, Bernard, José Sánchez, María, Redondo-Sánchez, Daniel, Olsen, Anja, Dahm, Christina C, Overvad, Kim, Brustad, Magritt, Skeie, Guri, Moreno-Iribas, Conchi, Onland-Moret, N Charlotte, van der Schouw, Yvonne T, Tsilidis, Konstantinos K, Heath, Alicia K, Agnoli, Claudia, Krogh, Vittorio, de Boer, Ian H, Kobylecki, Camilla Jannie, Çolak, Yunus, Zittermann, Armin, Sundström, Johan, Welsh, Paul, Weiderpass, Elisabete, Aglago, Elom K, Ferrari, Pietro, Clarke, Robert, Boutron, Marie-Christine, Severi, Gianluca, MacDonald, Conor, Providencia, Rui, Masala, Giovanna, Zamora Ros, Raul, Boer, Jolanda, Verschuren, WM Monique, Cawthon, Peggy, Schierbeck, Louise L, Cooper, Cyrus, Schulze, Matthias B, Bergmann, Manuela M, Hannemann, Anke, Kiechl, Stefan, Brenner, Hermann, van Schoor, Natasja M, Albertorio, Juan R, Sacerdote, Carlotta, Linneberg, Allan, Kårhus, Line L, Huerta, José María, Imaz, Liher, Joergensen, Christel, Ben-Shlomo, Yoav, Lundqvist, Annamari, Gallacher, John, Sattar, Naveed, Wood, Angela M, Wareham, Nicholas J, Nordestgaard, Børge G, Di Angelantonio, Emanuele, Danesh, John, Butterworth, Adam S, and Burgess, Stephen

Abstract

Randomised trials of vitamin D supplementation for cardiovascular disease and all-cause mortality have generally reported null findings. However, generalisability of results to individuals with low vitamin D status is unclear. We aimed to characterise dose-response relationships between 25-hydroxyvitamin D (25[OH]D) concentrations and risk of coronary heart disease, stroke, and all-cause mortality in observational and Mendelian randomisation frameworks.

Published
2021
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4. Association of LPA Variants With Risk of Coronary Disease and the Implications for Lipoprotein(a)-Lowering Therapies: A Mendelian Randomization Analysis

Author

Burgess, Stephen, Ference, Brian A., Staley, James R., Freitag, Daniel F., Mason, Amy M., Nielsen, Sune F., Willeit, Peter, Young, Robin, Surendran, Praveen, Karthikeyan, Savita, Bolton, Thomas R., Peters, James E., Kamstrup, Pia R., Tybjærg-Hansen, Anne, Benn, Marianne, Langsted, Anne, Schnohr, Peter, Vedel-Krogh, Signe, Kobylecki, Camilla J., Ford, Ian, Packard, Chris, Trompet, Stella, Jukema, J. Wouter, Sattar, Naveed, Di Angelantonio, Emanuele, Saleheen, Danish, Howson, Joanna M. M., Nordestgaard, Børge G., Butterworth, Adam S., and Danesh, John

Abstract

IMPORTANCE: Human genetic studies have indicated that plasma lipoprotein(a) (Lp[a]) is causally associated with the risk of coronary heart disease (CHD), but randomized trials of several therapies that reduce Lp(a) levels by 25% to 35% have not provided any evidence that lowering Lp(a) level reduces CHD risk. OBJECTIVE: To estimate the magnitude of the change in plasma Lp(a) levels needed to have the same evidence of an association with CHD risk as a 38.67-mg/dL (ie, 1-mmol/L) change in low-density lipoprotein cholesterol (LDL-C) level, a change that has been shown to produce a clinically meaningful reduction in the risk of CHD. DESIGN, SETTING, AND PARTICIPANTS: A mendelian randomization analysis was conducted using individual participant data from 5 studies and with external validation using summarized data from 48 studies. Population-based prospective cohort and case-control studies featured 20 793 individuals with CHD and 27 540 controls with individual participant data, whereas summarized data included 62 240 patients with CHD and 127 299 controls. Data were analyzed from November 2016 to March 2018. EXPOSURES: Genetic LPA score and plasma Lp(a) mass concentration. MAIN OUTCOMES AND MEASURES: Coronary heart disease. RESULTS: Of the included study participants, 53% were men, all were of white European ancestry, and the mean age was 57.5 years. The association of genetically predicted Lp(a) with CHD risk was linearly proportional to the absolute change in Lp(a) concentration. A 10-mg/dL lower genetically predicted Lp(a) concentration was associated with a 5.8% lower CHD risk (odds ratio [OR], 0.942; 95% CI, 0.933-0.951; P = 3 × 10−37), whereas a 10-mg/dL lower genetically predicted LDL-C level estimated using an LDL-C genetic score was associated with a 14.5% lower CHD risk (OR, 0.855; 95% CI, 0.818-0.893; P = 2 × 10−12). Thus, a 101.5-mg/dL change (95% CI, 71.0-137.0) in Lp(a) concentration had the same association with CHD risk as a 38.67-mg/dL change in LDL-C level. The association of genetically predicted Lp(a) concentration with CHD risk appeared to be independent of changes in LDL-C level owing to genetic variants that mimic the relationship of statins, PCSK9 inhibitors, and ezetimibe with CHD risk. CONCLUSIONS AND RELEVANCE: The clinical benefit of lowering Lp(a) is likely to be proportional to the absolute reduction in Lp(a) concentration. Large absolute reductions in Lp(a) of approximately 100 mg/dL may be required to produce a clinically meaningful reduction in the risk of CHD similar in magnitude to what can be achieved by lowering LDL-C level by 38.67 mg/dL (ie, 1 mmol/L).

Published
2018
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5. Body mass index and all cause mortality in HUNT and UK Biobank studies: linear and non-linear mendelian randomisation analyses

Author

Sun, Yi-Qian, Burgess, Stephen, Staley, James R, Wood, Angela M, Bell, Steven, Kaptoge, Stephen K, Guo, Qi, Bolton, Thomas R, Mason, Amy M, Butterworth, Adam S, Di Angelantonio, Emanuele, Vie, Gunnhild Å, Bjørngaard, Johan H, Kinge, Jonas Minet, Chen, Yue, and Mai, Xiao-Mei

Abstract

ObjectiveTo investigate the shape of the causal relation between body mass index (BMI) and mortality.DesignLinear and non-linear mendelian randomisation analyses.SettingNord-Trøndelag Health (HUNT) Study (Norway) and UK Biobank (United Kingdom).ParticipantsMiddle to early late aged participants of European descent: 56 150 from the HUNT Study and 366 385 from UK Biobank.Main outcome measuresAll cause and cause specific (cardiovascular, cancer, and non-cardiovascular non-cancer) mortality.Results12 015 and 10 344 participants died during a median of 18.5 and 7.0 years of follow-up in the HUNT Study and UK Biobank, respectively. Linear mendelian randomisation analyses indicated an overall positive association between genetically predicted BMI and the risk of all cause mortality. An increase of 1 unit in genetically predicted BMI led to a 5% (95% confidence interval 1% to 8%) higher risk of mortality in overweight participants (BMI 25.0-29.9) and a 9% (4% to 14%) higher risk of mortality in obese participants (BMI ≥30.0) but a 34% (16% to 48%) lower risk in underweight (BMI <18.5) and a 14% (−1% to 27%) lower risk in low normal weight participants (BMI 18.5-19.9). Non-linear mendelian randomisation indicated a J shaped relation between genetically predicted BMI and the risk of all cause mortality, with the lowest risk at a BMI of around 22-25 for the overall sample. Subgroup analyses by smoking status, however, suggested an always-increasing relation of BMI with mortality in never smokers and a J shaped relation in ever smokers.ConclusionsThe previously observed J shaped relation between BMI and risk of all cause mortality appears to have a causal basis, but subgroup analyses by smoking status revealed that the BMI-mortality relation is likely comprised of at least two distinct curves, rather than one J shaped relation. An increased risk of mortality for being underweight was only evident in ever smokers.

Published
2019
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