Search

Your search keyword '"Richmond, Rebecca C."' showing total 656 results
Start Over Author "Richmond, Rebecca C."
656 results on '"Richmond, Rebecca C."'

104. Associations of device-measured physical activity across adolescence with metabolic traits: Prospective cohort study

Author

Bell, Joshua A., Hamer, Mark, Richmond, Rebecca C., Timpson, Nicholas J., Carslake, David, and Davey Smith, George

Subjects
Adolescence -- Health aspects, Exercise -- Health aspects, Biological sciences
Abstract

Background Multiple occasions of device-measured physical activity have not been previously examined in relation to metabolic traits. We described associations of total activity, moderate-to-vigorous physical activity (MVPA), and sedentary time from three accelerometry measures taken across adolescence with detailed traits related to systemic metabolism. Methods and findings There were 1,826 male and female participants recruited at birth in 1991-1992 via mothers into the Avon Longitudinal Study of Parents and Children offspring cohort who attended clinics in 2003-2005, 2005-2006, and 2006-2008 who were included in [greater than or equal to]1 analysis. Waist-worn uniaxial accelerometers measured total activity (counts/min), MVPA (min/d), and sedentary time (min/d) over [greater than or equal to]3 d at mean age 12y, 14y, and 15y. Current activity (at age 15y), mean activity across occasions, interaction by previous activity, and change in activity were examined in relation to systolic and diastolic blood pressure, insulin, C-reactive protein, and 230 traits from targeted metabolomics (nuclear magnetic resonance spectroscopy), including lipoprotein cholesterol and triglycerides, amino and fatty acids, glycoprotein acetyls, and others, at age 15y. Mean current total activity was 477.5 counts/min (SD = 164.0) while mean MVPA and sedentary time durations were 23.6 min/d (SD = 17.9) and 522.1 min/d (SD = 66.0), respectively. Mean body mass index at age 15y was 21.4 kg/m.sup.2 (SD = 3.5). Correlations between first and last activity measurement occasions were low (e.g., r = 0.40 for counts/min). Current activity was most strongly associated with cholesterol and triglycerides in high-density lipoprotein (HDL) and very low-density lipoprotein (VLDL) particles (e.g., -0.002 mmol/l or -0.18 SD units; 95% CI -0.24--0.11 for triglycerides in chylomicrons and extremely large very low-density lipoprotein [XL VLDL]) and with glycoprotein acetyls (-0.02 mmol/l or -0.16 SD units; 95% CI -0.22--0.10), among others. Associations were similar for mean activity across 3 occasions. Attenuations were modest with adjustment for fat mass index based on dual-energy X-ray absorptiometry (DXA). In mutually adjusted models, higher MVPA and sedentary time were oppositely associated with cholesterol and triglycerides in VLDL and HDL particles (MVPA more strongly with glycoprotein acetyls and sedentary time more strongly with amino acids). Associations appeared less consistent for sedentary time than for MVPA based on longer-term measures and were weak for change in all activity types from age 12y-15y. Evidence was also weak for interaction between activity types at age 15y and previous activity measures in relation to most traits (minimum P = 0.003; median P = 0.26 for counts/min) with interaction coefficients mostly positive. Study limitations include modest sample sizes and relatively short durations of accelerometry measurement on each occasion (3-7 d) and of time lengths between first and last accelerometry occasions ( Conclusions Our results support associations of physical activity with metabolic traits that are small in magnitude and more robust for higher MVPA than lower sedentary time. Activity fluctuates over time, but associations of current activity with most metabolic traits do not differ by previous activity. This suggests that the metabolic effects of physical activity, if causal, depend on most recent engagement., Author(s): Joshua A. Bell 1,2,*, Mark Hamer 3, Rebecca C. Richmond 1,2, Nicholas J. Timpson 1,2, David Carslake 1,2, George Davey Smith 1,2 Introduction Cardiometabolic diseases contribute the most to [...]

Published
2018
Full Text
View/download PDF

105. Influence of puberty timing on adiposity and cardiometabolic traits: A Mendelian randomisation study

Author

Bell, Joshua A., Carslake, David, Wade, Kaitlin H., Richmond, Rebecca C., Langdon, Ryan J., Vincent, Emma E., Holmes, Michael V., Timpson, Nicholas J., and Davey Smith, George

Subjects
Pediatric diseases -- Risk factors, Metabolic diseases -- Risk factors, Medical research, Puberty -- Health aspects, Biological sciences
Abstract

Background Earlier puberty is widely linked with future obesity and cardiometabolic disease. We examined whether age at puberty onset likely influences adiposity and cardiometabolic traits independent of childhood adiposity. Methods and findings One-sample Mendelian randomisation (MR) analyses were conducted on up to 3,611 white-European female and male offspring from the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort recruited at birth via mothers between 1 April 1991 and 31 December 1992. Time-sensitive exposures were age at menarche and age at voice breaking. Outcomes measured at age 18 y were body mass index (BMI), dual-energy X-ray absorptiometry-based fat and lean mass indices, blood pressure, and 230 cardiometabolic traits derived from targeted metabolomics (150 concentrations plus 80 ratios from nuclear magnetic resonance [NMR] spectroscopy covering lipoprotein subclasses of cholesterol and triglycerides, amino acids, inflammatory glycoproteins, and others). Adjustment was made for pre-pubertal BMI measured at age 8 y. For negative control MR analyses, BMI and cardiometabolic trait measures taken at age 8 y (before puberty, and which therefore cannot be an outcome of puberty itself) were used. For replication analyses, 2-sample MR was conducted using summary genome-wide association study data on up to 322,154 adults for post-pubertal BMI, 24,925 adults for post-pubertal NMR cardiometabolic traits, and 13,848 children for pre-pubertal obesity (negative control). Like observational estimates, 1-sample MR estimates in ALSPAC using 351 polymorphisms for age at menarche (explaining 10.6% of variance) among 2,053 females suggested that later age at menarche (per year) was associated with -1.38 kg/m.sup.2 of BMI at age 18 y (or -0.34 SD units, 95% CI -0.46, -0.23; P = 9.77 x 10.sup.-09). This coefficient attenuated 10-fold upon adjustment for BMI at age 8 y, to -0.12 kg/m.sup.2 (or -0.03 SDs, 95% CI -0.13, 0.07; P = 0.55). Associations with blood pressure were similar, but associations across other traits were small and inconsistent. In negative control MR analyses, later age at menarche was associated with -0.77 kg/m.sup.2 of pre-pubertal BMI measured at age 8 y (or -0.39 SDs, 95% CI -0.50, -0.29; P = 6.28 x 10.sup.-13 ), indicating that variants influencing menarche also influence BMI before menarche. Cardiometabolic trait associations were weaker and less consistent among males and both sexes combined. Higher BMI at age 8 y (per 1 kg/m.sup.2 using 95 polymorphisms for BMI explaining 3.4% of variance) was associated with earlier menarche among 2,648 females (by -0.26 y, 95% CI -0.37, -0.16; P = 1.16 x 10.sup.-06 ), likewise among males and both sexes combined. In 2-sample MR analyses using 234 polymorphisms and inverse variance weighted (IVW) regression, each year later age at menarche was associated with -0.81 kg/m.sup.2 of adult BMI (or -0.17 SD units, 95% CI -0.21, -0.12; P = 4.00 x 10.sup.-15). Associations were weaker with cardiometabolic traits. Using 202 polymorphisms, later menarche was associated with lower odds of childhood obesity (IVW-based odds ratio = 0.52 per year later, 95% CI 0.48, 0.57; P = 6.64 x 10.sup.-15). Study limitations include modest sample sizes for 1-sample MR, lack of inference to non-white-European populations, potential selection bias through modest completion rates of puberty questionnaires, and likely disproportionate measurement error of exposures by sex. The cardiometabolic traits examined were heavily lipid-focused and did not include hormone-related traits such as insulin and insulin-like growth factors. Conclusions Our results suggest that puberty timing has a small influence on adiposity and cardiometabolic traits and that preventive interventions should instead focus on reducing childhood adiposity., Author(s): Joshua A. Bell 1,*, David Carslake 1, Kaitlin H. Wade 1, Rebecca C. Richmond 1, Ryan J. Langdon 1, Emma E. Vincent 1,2, Michael V. Holmes 1,3,4,5, Nicholas J. [...]

Published
2018
Full Text
View/download PDF

107. Maternal smoking during pregnancy and autism: using causal inference methods in a birth cohort study

Author

Caramaschi, Doretta, Taylor, Amy E., Richmond, Rebecca C., Havdahl, Karoline Alexandra, Golding, Jean, Relton, Caroline L., Munafò, Marcus R., Davey Smith, George, and Rai, Dheeraj

Subjects
Adult, Male, Genotype, Mothers, Receptors, Nicotinic, Brain and Behaviour, Polymorphism, Single Nucleotide, Article, Cigarette Smoking, Epigenesis, Genetic, lcsh:RC321-571, Young Adult, Pregnancy, mental disorders, Humans, Longitudinal Studies, Prospective Studies, Autistic Disorder, lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry, Tobacco and Alcohol, ALSPAC, Prenatal Exposure Delayed Effects, Physical and Mental Health, Female, Tobacco Smoke Pollution, ICEP
Abstract

An association between maternal smoking in pregnancy and autism may be biologically plausible, but the evidence to date is inconsistent. We aimed to investigate the causal relationship between maternal smoking during pregnancy and offspring autism using conventional analysis and causal inference methods. In the Avon Longitudinal Study of Parents and Children we investigated the association of maternal smoking during pregnancy (exposure) with offspring autism spectrum disorder (ASD) or possible ASD diagnosis (n = 11,946) and high scores on four autism-related traits (outcomes) (n = 7402–9152). Maternal smoking was self-reported and also measured using an epigenetic score (n = 866–964). Partner’s smoking was used as a negative control for intrauterine exposure (n = 6616–10,995). Mendelian randomisation (n = 1002–2037) was carried out using a genetic variant at the CHRNA3 locus in maternal DNA as a proxy for heaviness of smoking. In observational analysis, we observed an association between smoking during pregnancy and impairments in social communication [OR = 1.56, 95% CI = 1.29, 1.87] and repetitive behaviours, but multivariable adjustment suggested evidence for confounding. There was weaker evidence of such association for the other traits or a diagnosis of autism. The magnitude of association for partner’s smoking with impairments in social communication was similar [OR = 1.56, 95% CI = 1.30, 1.87] suggesting potential for shared confounding. There was weak evidence for an association of the epigenetic score or genetic variation at CHRNA3 with ASD or any of the autism-related traits. In conclusion, using several analytic methods, we did not find enough evidence to support a causal association between maternal smoking during pregnancy and offspring autism or related traits.

Published
2018

110. Investigating the effect of sexual behaviour on oropharyngeal cancer risk: a methodological assessment of Mendelian randomization

Author

Gormley, Mark, primary, Dudding, Tom, additional, Kachuri, Linda, additional, Burrows, Kimberley, additional, Chong, Amanda HW, additional, Martin, Richard M, additional, Thomas, Steven, additional, Tyrrell, Jessica, additional, Ness, Andrew R, additional, Brennan, Paul, additional, Munafò, Marcus R, additional, Pring, Miranda, additional, Boccia, Stefania, additional, Olshan, Andrew F, additional, Diergaarde, Brenda, additional, Hung, Rayjean J, additional, Liu, Geoffrey, additional, Tajara, Eloiza, additional, Severino, Patricia, additional, Toporcov, Tatiana N, additional, Lacko, Martin, additional, Waterboer, Tim, additional, Brenner, Nicole, additional, Smith, George Davey, additional, Vincent, Emma E, additional, and Richmond, Rebecca C, additional

Published
2021
Full Text
View/download PDF

113. Additional file 1 of Genome-wide association studies identify 137 genetic loci for DNA methylation biomarkers of aging

Author

McCartney, Daniel L., Min, Josine L., Richmond, Rebecca C., Lu, Ake T., Sobczyk, Maria K., Davies, Gail, Broer, Linda, Guo, Xiuqing, Jeong, Ayoung, Jung, Jeesun, Kasela, Silva, Katrinli, Seyma, Kuo, Pei-Lun, Matias-Garcia, Pamela R., Mishra, Pashupati P., Nygaard, Marianne, Palviainen, Teemu, Patki, Amit, Raffield, Laura M., Ratliff, Scott M., Richardson, Tom G., Robinson, Oliver, Soerensen, Mette, Sun, Dianjianyi, Tsai, Pei-Chien, van der Zee, Matthijs D., Walker, Rosie M., Wang, Xiaochuan, Wang, Yunzhang, Xia, Rui, Xu, Zongli, Yao, Jie, Zhao, Wei, Correa, Adolfo, Boerwinkle, Eric, Dugué, Pierre-Antoine, Durda, Peter, Elliott, Hannah R., Gieger, Christian, de Geus, Eco J. C., Harris, Sarah E., Hemani, Gibran, Imboden, Medea, Kähönen, Mika, Kardia, Sharon L. R., Kresovich, Jacob K., Li, Shengxu, Lunetta, Kathryn L., Mangino, Massimo, Mason, Dan, McIntosh, Andrew M., Mengel-From, Jonas, Moore, Ann Zenobia, Murabito, Joanne M., Ollikainen, Miina, Pankow, James S., Pedersen, Nancy L., Peters, Annette, Polidoro, Silvia, Porteous, David J., Raitakari, Olli, Rich, Stephen S., Sandler, Dale P., Sillanpää, Elina, Smith, Alicia K., Southey, Melissa C., Strauch, Konstantin, Tiwari, Hemant, Tanaka, Toshiko, Tillin, Therese, Uitterlinden, Andre G., Van Den Berg, David J., van Dongen, Jenny, Wilson, James G., Wright, John, Yet, Idil, Arnett, Donna, Bandinelli, Stefania, Bell, Jordana T., Binder, Alexandra M., Boomsma, Dorret I., Chen, Wei, Christensen, Kaare, Conneely, Karen N., Elliott, Paul, Ferrucci, Luigi, Fornage, Myriam, Hägg, Sara, Hayward, Caroline, Irvin, Marguerite, Kaprio, Jaakko, Lawlor, Deborah A., Lehtimäki, Terho, Lohoff, Falk W., Milani, Lili, Milne, Roger L., Probst-Hensch, Nicole, Reiner, Alex P., Ritz, Beate, Rotter, Jerome I., Smith, Jennifer A., Taylor, Jack A., van Meurs, Joyce B. J., Vineis, Paolo, Waldenberger, Melanie, Deary, Ian J., Relton, Caroline L., Horvath, Steve, and Marioni, Riccardo E.

Abstract

Additional file 1. Individual cohort descriptions and acknowledgements.

Published
2021
Full Text
View/download PDF

114. Additional file 5 of Genome-wide association studies identify 137 genetic loci for DNA methylation biomarkers of aging

Author

McCartney, Daniel L., Min, Josine L., Richmond, Rebecca C., Lu, Ake T., Sobczyk, Maria K., Davies, Gail, Broer, Linda, Guo, Xiuqing, Jeong, Ayoung, Jung, Jeesun, Kasela, Silva, Katrinli, Seyma, Kuo, Pei-Lun, Matias-Garcia, Pamela R., Mishra, Pashupati P., Nygaard, Marianne, Palviainen, Teemu, Patki, Amit, Raffield, Laura M., Ratliff, Scott M., Richardson, Tom G., Robinson, Oliver, Soerensen, Mette, Sun, Dianjianyi, Tsai, Pei-Chien, van der Zee, Matthijs D., Walker, Rosie M., Wang, Xiaochuan, Wang, Yunzhang, Xia, Rui, Xu, Zongli, Yao, Jie, Zhao, Wei, Correa, Adolfo, Boerwinkle, Eric, Dugué, Pierre-Antoine, Durda, Peter, Elliott, Hannah R., Gieger, Christian, de Geus, Eco J. C., Harris, Sarah E., Hemani, Gibran, Imboden, Medea, Kähönen, Mika, Kardia, Sharon L. R., Kresovich, Jacob K., Li, Shengxu, Lunetta, Kathryn L., Mangino, Massimo, Mason, Dan, McIntosh, Andrew M., Mengel-From, Jonas, Moore, Ann Zenobia, Murabito, Joanne M., Ollikainen, Miina, Pankow, James S., Pedersen, Nancy L., Peters, Annette, Polidoro, Silvia, Porteous, David J., Raitakari, Olli, Rich, Stephen S., Sandler, Dale P., Sillanpää, Elina, Smith, Alicia K., Southey, Melissa C., Strauch, Konstantin, Tiwari, Hemant, Tanaka, Toshiko, Tillin, Therese, Uitterlinden, Andre G., Van Den Berg, David J., van Dongen, Jenny, Wilson, James G., Wright, John, Yet, Idil, Arnett, Donna, Bandinelli, Stefania, Bell, Jordana T., Binder, Alexandra M., Boomsma, Dorret I., Chen, Wei, Christensen, Kaare, Conneely, Karen N., Elliott, Paul, Ferrucci, Luigi, Fornage, Myriam, Hägg, Sara, Hayward, Caroline, Irvin, Marguerite, Kaprio, Jaakko, Lawlor, Deborah A., Lehtimäki, Terho, Lohoff, Falk W., Milani, Lili, Milne, Roger L., Probst-Hensch, Nicole, Reiner, Alex P., Ritz, Beate, Rotter, Jerome I., Smith, Jennifer A., Taylor, Jack A., van Meurs, Joyce B. J., Vineis, Paolo, Waldenberger, Melanie, Deary, Ian J., Relton, Caroline L., Horvath, Steve, and Marioni, Riccardo E.

Abstract

Additional file 5. Colocalization plots.

Published
2021
Full Text
View/download PDF

115. Additional file 2 of Investigating the relationships between unfavourable habitual sleep and metabolomic traits: evidence from multi-cohort multivariable regression and Mendelian randomization analyses

Author

Bos, Maxime M., Goulding, Neil J., Lee, Matthew A., Hofman, Amy, Bot, Mariska, Pool, René, Vijfhuizen, Lisanne S., Zhang, Xiang, Chihua Li, Mustafa, Rima, Neville, Matt J., Ruifang Li-Gao, Trompet, Stella, Beekman, Marian, Biermasz, Nienke R., Dorret I. Boomsma, Boer, Irene De, Constantinos Christodoulides, Dehghan, Abbas, Dijk, Ko Willems Van, Ford, Ian, Ghanbari, Mohsen, Heijmans, Bastiaan T., M. Arfan Ikram, J. Wouter Jukema, Mook-Kanamori, Dennis O., Karpe, Fredrik, Luik, Annemarie I., L. H. Lumey, Maagdenberg, Arn M. J. M. Van Den, Mooijaart, Simon P., Mutsert, Renée De, Penninx, Brenda W. J. H., Rensen, Patrick C. N., Richmond, Rebecca C., Rosendaal, Frits R., Sattar, Naveed, Schoevers, Robert A., P. Eline Slagboom, Terwindt, Gisela M., Carisha S. Thesing, Wade, Kaitlin H., Wijsman, Carolien A., Willemsen, Gonneke, Aeilko H. Zwinderman, Heemst, Diana Van, Noordam, Raymond, and Lawlor, Deborah A.

Abstract

Additional file 2: Figure S1. IVW Mendelian randomization estimates, and age, sex and BMI-adjusted multivariable regression estimates for the associations between short sleep duration and 113 NMR derived metabolites. Figure S2. Comparison of the point estimates of the IVW Mendelian randomization and age, sex and BMI-adjusted multivariable regression analyses for the associations between short sleep duration and 113 NMR derived metabolites. Figure S3. Mendelian randomization and age, sex and BMI-adjusted multivariable regression analyses results for select associations of short sleep duration with NMR metabolites. Figure S4. IVW Mendelian randomization estimates and age, sex and BMI adjusted multivariable regression estimates for the associations between long sleep duration and 113 NMR derived metabolites. Figure S5. Comparison of the point estimates of the IVW Mendelian randomization and age, sex and BMI-adjusted multivariable regression analyses for the associations between long sleep duration and 113 NMR derived metabolites. Figure S6A. Mendelian randomization and age, sex and BMI-adjusted multivariable regression analyses results for select associations of long sleep duration with NMR metabolites. Figure S6B. Mendelian randomization and age, sex and BMI adjusted multivariable regression analyses results for select associations of long sleep duration with NMR metabolites.

Published
2021
Full Text
View/download PDF

116. Additional file 6 of Genome-wide association studies identify 137 genetic loci for DNA methylation biomarkers of aging

Author

McCartney, Daniel L., Min, Josine L., Richmond, Rebecca C., Lu, Ake T., Sobczyk, Maria K., Davies, Gail, Broer, Linda, Guo, Xiuqing, Jeong, Ayoung, Jung, Jeesun, Kasela, Silva, Katrinli, Seyma, Kuo, Pei-Lun, Matias-Garcia, Pamela R., Mishra, Pashupati P., Nygaard, Marianne, Palviainen, Teemu, Patki, Amit, Raffield, Laura M., Ratliff, Scott M., Richardson, Tom G., Robinson, Oliver, Soerensen, Mette, Sun, Dianjianyi, Tsai, Pei-Chien, van der Zee, Matthijs D., Walker, Rosie M., Wang, Xiaochuan, Wang, Yunzhang, Xia, Rui, Xu, Zongli, Yao, Jie, Zhao, Wei, Correa, Adolfo, Boerwinkle, Eric, Dugué, Pierre-Antoine, Durda, Peter, Elliott, Hannah R., Gieger, Christian, de Geus, Eco J. C., Harris, Sarah E., Hemani, Gibran, Imboden, Medea, Kähönen, Mika, Kardia, Sharon L. R., Kresovich, Jacob K., Li, Shengxu, Lunetta, Kathryn L., Mangino, Massimo, Mason, Dan, McIntosh, Andrew M., Mengel-From, Jonas, Moore, Ann Zenobia, Murabito, Joanne M., Ollikainen, Miina, Pankow, James S., Pedersen, Nancy L., Peters, Annette, Polidoro, Silvia, Porteous, David J., Raitakari, Olli, Rich, Stephen S., Sandler, Dale P., Sillanpää, Elina, Smith, Alicia K., Southey, Melissa C., Strauch, Konstantin, Tiwari, Hemant, Tanaka, Toshiko, Tillin, Therese, Uitterlinden, Andre G., Van Den Berg, David J., van Dongen, Jenny, Wilson, James G., Wright, John, Yet, Idil, Arnett, Donna, Bandinelli, Stefania, Bell, Jordana T., Binder, Alexandra M., Boomsma, Dorret I., Chen, Wei, Christensen, Kaare, Conneely, Karen N., Elliott, Paul, Ferrucci, Luigi, Fornage, Myriam, Hägg, Sara, Hayward, Caroline, Irvin, Marguerite, Kaprio, Jaakko, Lawlor, Deborah A., Lehtimäki, Terho, Lohoff, Falk W., Milani, Lili, Milne, Roger L., Probst-Hensch, Nicole, Reiner, Alex P., Ritz, Beate, Rotter, Jerome I., Smith, Jennifer A., Taylor, Jack A., van Meurs, Joyce B. J., Vineis, Paolo, Waldenberger, Melanie, Deary, Ian J., Relton, Caroline L., Horvath, Steve, and Marioni, Riccardo E.

Abstract

Additional file 6. Review history.

Published
2021
Full Text
View/download PDF

117. Additional file 4 of Genome-wide association studies identify 137 genetic loci for DNA methylation biomarkers of aging

Author

McCartney, Daniel L., Min, Josine L., Richmond, Rebecca C., Lu, Ake T., Sobczyk, Maria K., Davies, Gail, Broer, Linda, Guo, Xiuqing, Jeong, Ayoung, Jung, Jeesun, Kasela, Silva, Katrinli, Seyma, Kuo, Pei-Lun, Matias-Garcia, Pamela R., Mishra, Pashupati P., Nygaard, Marianne, Palviainen, Teemu, Patki, Amit, Raffield, Laura M., Ratliff, Scott M., Richardson, Tom G., Robinson, Oliver, Soerensen, Mette, Sun, Dianjianyi, Tsai, Pei-Chien, van der Zee, Matthijs D., Walker, Rosie M., Wang, Xiaochuan, Wang, Yunzhang, Xia, Rui, Xu, Zongli, Yao, Jie, Zhao, Wei, Correa, Adolfo, Boerwinkle, Eric, Dugué, Pierre-Antoine, Durda, Peter, Elliott, Hannah R., Gieger, Christian, de Geus, Eco J. C., Harris, Sarah E., Hemani, Gibran, Imboden, Medea, Kähönen, Mika, Kardia, Sharon L. R., Kresovich, Jacob K., Li, Shengxu, Lunetta, Kathryn L., Mangino, Massimo, Mason, Dan, McIntosh, Andrew M., Mengel-From, Jonas, Moore, Ann Zenobia, Murabito, Joanne M., Ollikainen, Miina, Pankow, James S., Pedersen, Nancy L., Peters, Annette, Polidoro, Silvia, Porteous, David J., Raitakari, Olli, Rich, Stephen S., Sandler, Dale P., Sillanpää, Elina, Smith, Alicia K., Southey, Melissa C., Strauch, Konstantin, Tiwari, Hemant, Tanaka, Toshiko, Tillin, Therese, Uitterlinden, Andre G., Van Den Berg, David J., van Dongen, Jenny, Wilson, James G., Wright, John, Yet, Idil, Arnett, Donna, Bandinelli, Stefania, Bell, Jordana T., Binder, Alexandra M., Boomsma, Dorret I., Chen, Wei, Christensen, Kaare, Conneely, Karen N., Elliott, Paul, Ferrucci, Luigi, Fornage, Myriam, Hägg, Sara, Hayward, Caroline, Irvin, Marguerite, Kaprio, Jaakko, Lawlor, Deborah A., Lehtimäki, Terho, Lohoff, Falk W., Milani, Lili, Milne, Roger L., Probst-Hensch, Nicole, Reiner, Alex P., Ritz, Beate, Rotter, Jerome I., Smith, Jennifer A., Taylor, Jack A., van Meurs, Joyce B. J., Vineis, Paolo, Waldenberger, Melanie, Deary, Ian J., Relton, Caroline L., Horvath, Steve, and Marioni, Riccardo E.

Abstract

Additional file 4. Assessment of genomic inflation and heterogeneity.

Published
2021
Full Text
View/download PDF

118. Additional file 3 of Genome-wide association studies identify 137 genetic loci for DNA methylation biomarkers of aging

Author

McCartney, Daniel L., Min, Josine L., Richmond, Rebecca C., Lu, Ake T., Sobczyk, Maria K., Davies, Gail, Broer, Linda, Guo, Xiuqing, Jeong, Ayoung, Jung, Jeesun, Kasela, Silva, Katrinli, Seyma, Kuo, Pei-Lun, Matias-Garcia, Pamela R., Mishra, Pashupati P., Nygaard, Marianne, Palviainen, Teemu, Patki, Amit, Raffield, Laura M., Ratliff, Scott M., Richardson, Tom G., Robinson, Oliver, Soerensen, Mette, Sun, Dianjianyi, Tsai, Pei-Chien, van der Zee, Matthijs D., Walker, Rosie M., Wang, Xiaochuan, Wang, Yunzhang, Xia, Rui, Xu, Zongli, Yao, Jie, Zhao, Wei, Correa, Adolfo, Boerwinkle, Eric, Dugué, Pierre-Antoine, Durda, Peter, Elliott, Hannah R., Gieger, Christian, de Geus, Eco J. C., Harris, Sarah E., Hemani, Gibran, Imboden, Medea, Kähönen, Mika, Kardia, Sharon L. R., Kresovich, Jacob K., Li, Shengxu, Lunetta, Kathryn L., Mangino, Massimo, Mason, Dan, McIntosh, Andrew M., Mengel-From, Jonas, Moore, Ann Zenobia, Murabito, Joanne M., Ollikainen, Miina, Pankow, James S., Pedersen, Nancy L., Peters, Annette, Polidoro, Silvia, Porteous, David J., Raitakari, Olli, Rich, Stephen S., Sandler, Dale P., Sillanpää, Elina, Smith, Alicia K., Southey, Melissa C., Strauch, Konstantin, Tiwari, Hemant, Tanaka, Toshiko, Tillin, Therese, Uitterlinden, Andre G., Van Den Berg, David J., van Dongen, Jenny, Wilson, James G., Wright, John, Yet, Idil, Arnett, Donna, Bandinelli, Stefania, Bell, Jordana T., Binder, Alexandra M., Boomsma, Dorret I., Chen, Wei, Christensen, Kaare, Conneely, Karen N., Elliott, Paul, Ferrucci, Luigi, Fornage, Myriam, Hägg, Sara, Hayward, Caroline, Irvin, Marguerite, Kaprio, Jaakko, Lawlor, Deborah A., Lehtimäki, Terho, Lohoff, Falk W., Milani, Lili, Milne, Roger L., Probst-Hensch, Nicole, Reiner, Alex P., Ritz, Beate, Rotter, Jerome I., Smith, Jennifer A., Taylor, Jack A., van Meurs, Joyce B. J., Vineis, Paolo, Waldenberger, Melanie, Deary, Ian J., Relton, Caroline L., Horvath, Steve, and Marioni, Riccardo E.

Abstract

Additional file 3. Supplementary Figures - Figures S1-S31.

Published
2021
Full Text
View/download PDF

119. Salicylic Acid and Risk of Colorectal Cancer : A Two-Sample Mendelian Randomization Study

Author

Nounu, Aayah, Richmond, Rebecca C., Stewart, Isobel D., Surendran, Praveen, Wareham, Nicholas J., Butterworth, Adam, Weinstein, Stephanie J., Albanes, Demetrius, Baron, John A., Hopper, John L., Figueiredo, Jane C., Newcomb, Polly A., Lindor, Noralane M., Casey, Graham, Platz, Elizabeth A., Marchand, Loic Le, Ulrich, Cornelia M., Li, Christopher I., van Dujinhoven, Fraenzel J. B., Gsur, Andrea, Campbell, Peter T., Moreno, Victor, Vodicka, Pavel, Vodickova, Ludmila, Amitay, Efrat, Alwers, Elizabeth, Chang-Claude, Jenny, Sakoda, Lori C., Slattery, Martha L., Schoen, Robert E., Gunter, Marc J., Castellvi-Bel, Sergi, Kim, Hyeong-Rok, Kweon, Sun-Seog, Chan, Andrew T., Li, Li, Zheng, Wei, Bishop, D. Timothy, Buchanan, Daniel D., Giles, Graham G., Gruber, Stephen B., Rennert, Gad, Stadler, Zsofia K., Harrison, Tabitha A., Lin, Yi, Keku, Temitope O., Woods, Michael O., Schafmayer, Clemens, Van Guelpen, Bethany, Gallinger, Steven, Hampel, Heather, Berndt, Sonja I., Pharoah, Paul D. P., Lindblom, Annika, Wolk, Alicja, Wu, Anna H., White, Emily, Peters, Ulrike, Drew, David A., Scherer, Dominique, Bermejo, Justo Lorenzo, Brenner, Hermann, Hoffmeister, Michael, Williams, Ann C., Relton, Caroline L., Nounu, Aayah, Richmond, Rebecca C., Stewart, Isobel D., Surendran, Praveen, Wareham, Nicholas J., Butterworth, Adam, Weinstein, Stephanie J., Albanes, Demetrius, Baron, John A., Hopper, John L., Figueiredo, Jane C., Newcomb, Polly A., Lindor, Noralane M., Casey, Graham, Platz, Elizabeth A., Marchand, Loic Le, Ulrich, Cornelia M., Li, Christopher I., van Dujinhoven, Fraenzel J. B., Gsur, Andrea, Campbell, Peter T., Moreno, Victor, Vodicka, Pavel, Vodickova, Ludmila, Amitay, Efrat, Alwers, Elizabeth, Chang-Claude, Jenny, Sakoda, Lori C., Slattery, Martha L., Schoen, Robert E., Gunter, Marc J., Castellvi-Bel, Sergi, Kim, Hyeong-Rok, Kweon, Sun-Seog, Chan, Andrew T., Li, Li, Zheng, Wei, Bishop, D. Timothy, Buchanan, Daniel D., Giles, Graham G., Gruber, Stephen B., Rennert, Gad, Stadler, Zsofia K., Harrison, Tabitha A., Lin, Yi, Keku, Temitope O., Woods, Michael O., Schafmayer, Clemens, Van Guelpen, Bethany, Gallinger, Steven, Hampel, Heather, Berndt, Sonja I., Pharoah, Paul D. P., Lindblom, Annika, Wolk, Alicja, Wu, Anna H., White, Emily, Peters, Ulrike, Drew, David A., Scherer, Dominique, Bermejo, Justo Lorenzo, Brenner, Hermann, Hoffmeister, Michael, Williams, Ann C., and Relton, Caroline L.

Abstract

Salicylic acid (SA) has observationally been shown to decrease colorectal cancer (CRC) risk. Aspirin (acetylsalicylic acid, that rapidly deacetylates to SA) is an effective primary and secondary chemopreventive agent. Through a Mendelian randomization (MR) approach, we aimed to address whether levels of SA affected CRC risk, stratifying by aspirin use. A two-sample MR analysis was performed using GWAS summary statistics of SA (INTERVAL and EPIC-Norfolk, N = 14,149) and CRC (CCFR, CORECT, GECCO and UK Biobank, 55,168 cases and 65,160 controls). The DACHS study (4410 cases and 3441 controls) was used for replication and stratification of aspirin-use. SNPs proxying SA were selected via three methods: (1) functional SNPs that influence the activity of aspirin-metabolising enzymes; (2) pathway SNPs present in enzymes' coding regions; and (3) genome-wide significant SNPs. We found no association between functional SNPs and SA levels. The pathway and genome-wide SNPs showed no association between SA and CRC risk (OR: 1.03, 95% CI: 0.84-1.27 and OR: 1.08, 95% CI: 0.86-1.34, respectively). Results remained unchanged upon aspirin use stratification. We found little evidence to suggest that an SD increase in genetically predicted SA protects against CRC risk in the general population and upon stratification by aspirin use.

Published
2021
Full Text
View/download PDF

120. A Combined Proteomics and Mendelian Randomization Approach to Investigate the Effects of Aspirin-Targeted Proteins on Colorectal Cancer

Author

Nounu, Aayah, Greenhough, Alexander, Heesom, Kate J., Richmond, Rebecca C., Zheng, Jie, Weinstein, Stephanie J., Albanes, Demetrius, Baron, John A., Hopper, John L., Figueiredo, Jane C., Newcomb, Polly A., Lindor, Noralane M., Casey, Graham, Platz, Elizabeth A., Le Marchand, Loic, Ulrich, Cornelia M., Li, Christopher, I, van Duijnhoven, Franzel J. B., Gsur, Andrea, Campbell, Peter T., Moreno, Victor, Vodicka, Pavel, Vodickova, Ludmila, Brenner, Hermann, Chang-Claude, Jenny, Hoffmeister, Michael, Sakoda, Lori C., Slattery, Martha L., Schoen, Robert E., Gunter, Marc J., Castellvi-Bel, Sergi, Kim, Hyeong Rok, Kweon, Sun-Seog, Chan, Andrew T., Li, Li, Zheng, Wei, Bishop, D. Timothy, Buchanan, Daniel D., Giles, Graham G., Gruber, Stephen B., Rennert, Gad, Stadler, Zsofia K., Harrison, Tabitha A., Lin, Yi, Keku, Temitope O., Woods, Michael O., Schafmayer, Clemens, Van Guelpen, Bethany, Gallinger, Steven, Hampel, Heather, Berndt, Sonja, I, Pharoah, Paul D. P., Lindblom, Annika, Wolk, Alicja, Wu, Anna H., White, Emily, Peters, Ulrike, Drew, David A., Scherer, Dominique, Bermejo, Justo Lorenzo, Williams, Ann C., Relton, Caroline L., Nounu, Aayah, Greenhough, Alexander, Heesom, Kate J., Richmond, Rebecca C., Zheng, Jie, Weinstein, Stephanie J., Albanes, Demetrius, Baron, John A., Hopper, John L., Figueiredo, Jane C., Newcomb, Polly A., Lindor, Noralane M., Casey, Graham, Platz, Elizabeth A., Le Marchand, Loic, Ulrich, Cornelia M., Li, Christopher, I, van Duijnhoven, Franzel J. B., Gsur, Andrea, Campbell, Peter T., Moreno, Victor, Vodicka, Pavel, Vodickova, Ludmila, Brenner, Hermann, Chang-Claude, Jenny, Hoffmeister, Michael, Sakoda, Lori C., Slattery, Martha L., Schoen, Robert E., Gunter, Marc J., Castellvi-Bel, Sergi, Kim, Hyeong Rok, Kweon, Sun-Seog, Chan, Andrew T., Li, Li, Zheng, Wei, Bishop, D. Timothy, Buchanan, Daniel D., Giles, Graham G., Gruber, Stephen B., Rennert, Gad, Stadler, Zsofia K., Harrison, Tabitha A., Lin, Yi, Keku, Temitope O., Woods, Michael O., Schafmayer, Clemens, Van Guelpen, Bethany, Gallinger, Steven, Hampel, Heather, Berndt, Sonja, I, Pharoah, Paul D. P., Lindblom, Annika, Wolk, Alicja, Wu, Anna H., White, Emily, Peters, Ulrike, Drew, David A., Scherer, Dominique, Bermejo, Justo Lorenzo, Williams, Ann C., and Relton, Caroline L.

Abstract

Background: Evidence for aspirin's chemopreventative properties on colorectal cancer (CRC) is substantial, but its mechanism of action is not well-understood. We combined a proteomic approach with Mendelian randomization (MR) to identify possible new aspirin targets that decrease CRC risk. Methods: Human colorectal adenoma cells (RG/C2) were treated with aspirin (24 hours) and a stable isotope labeling with amino acids in cell culture (SILAC) based proteomics approach identified altered protein expression. Protein quantitative trait loci (pQTLs) from INTERVAL (N = 3,301) and expression QTLs (eQTLs) from the eQTLGen Consortium (N = 31,684) were used as genetic proxies for protein and mRNA expression levels. Two-sample MR of mRNA/protein expression on CRC risk was performed using eQTL/pQTL data combined with CRC genetic summary data from the Colon Cancer Family Registry (CCFR), Colorectal Transdisciplinary (CORECT), Genetics and Epidemiology of Colorectal Cancer (GECCO) consortia and UK Biobank (55,168 cases and 65,160 controls). Results: Altered expression was detected for 125/5886 proteins. Of these, aspirin decreased MCM6, RRM2, and ARFIP2 expression, and MR analysis showed that a standard deviation increase in mRNA/protein expression was associated with increased CRC risk (OR: 1.08, 95% CI, 1.03-1.13; OR: 3.33, 95% CI, 2.46-4.50; and OR: 1.15, 95% CI, 1.02-1.29, respectively). Conclusions: MCM6 and RRM2 are involved in DNA repair whereby reduced expression may lead to increased DNA aberrations and ultimately cancer cell death, whereas ARFIP2 is involved in actin cytoskeletal regulation, indicating a possible role in aspirin's reduction of metastasis. Impact: Our approach has shown how laboratory experiments and population-based approaches can combine to identify aspirin-targeted proteins possibly affecting CRC risk.

Published
2021
Full Text
View/download PDF

121. Strengthening the Reporting of Observational Studies in Epidemiology Using Mendelian Randomization:The STROBE-MR Statement

Author

Skrivankova, Veronika W., Richmond, Rebecca C., Woolf, Benjamin A.R., Yarmolinsky, James, Davies, Neil M., Swanson, Sonja A., Vanderweele, Tyler J., Higgins, Julian P.T., Timpson, Nicholas J., Dimou, Niki, Langenberg, Claudia, Golub, Robert M., Loder, Elizabeth W., Gallo, Valentina, Tybjaerg-Hansen, Anne, Davey Smith, George, Egger, Matthias, Richards, J. Brent, Skrivankova, Veronika W., Richmond, Rebecca C., Woolf, Benjamin A.R., Yarmolinsky, James, Davies, Neil M., Swanson, Sonja A., Vanderweele, Tyler J., Higgins, Julian P.T., Timpson, Nicholas J., Dimou, Niki, Langenberg, Claudia, Golub, Robert M., Loder, Elizabeth W., Gallo, Valentina, Tybjaerg-Hansen, Anne, Davey Smith, George, Egger, Matthias, and Richards, J. Brent

Abstract

Importance: Mendelian randomization (MR) studies use genetic variation associated with modifiable exposures to assess their possible causal relationship with outcomes and aim to reduce potential bias from confounding and reverse causation. Objective: To develop the STROBE-MR Statement as a stand-alone extension to the STROBE (Strengthening the Reporting of Observational Studies in Epidemiology) guideline for the reporting of MR studies. Design, Setting, and Participants: The development of the STROBE-MR Statement followed the Enhancing the Quality and Transparency of Health Research (EQUATOR) framework guidance and used the STROBE Statement as a starting point to draft a checklist tailored to MR studies. The project was initiated in 2018 by reviewing the literature on the reporting of instrumental variable and MR studies. A group of 17 experts, including MR methodologists, MR study design users, developers of previous reporting guidelines, and journal editors, participated in a workshop in May 2019 to define the scope of the Statement and draft the checklist. The draft checklist was published as a preprint in July 2019 and discussed on the preprint platform, in social media, and at the 4th Mendelian Randomization Conference. The checklist was then revised based on comments, further refined through 2020, and finalized in July 2021. Findings: The STROBE-MR checklist is organized into 6 sections (Title and Abstract, Introduction, Methods, Results, Discussion, and Other Information) and includes 20 main items and 30 subitems. It covers both 1-sample and 2-sample MR studies that assess 1 or multiple exposures and outcomes, and addresses MR studies that follow a genome-wide association study and are reported in the same article. The checklist asks authors to justify why MR is a helpful method to address the study question and state prespecified causal hypotheses. The measurement, quality, and selection of genetic variants must be described and attempts to assess validi

Published
2021

122. Strengthening the reporting of observational studies in epidemiology using mendelian randomisation (STROBE-MR):Explanation and elaboration

Author

Skrivankova, Veronika W., Richmond, Rebecca C., Woolf, Benjamin A.R., Davies, Neil M., Swanson, Sonja A., Vanderweele, Tyler J., Timpson, Nicholas J., Higgins, Julian P.T., Dimou, Niki, Langenberg, Claudia, Loder, Elizabeth W., Golub, Robert M., Egger, Matthias, Smith, George Davey, Richards, J. Brent, Skrivankova, Veronika W., Richmond, Rebecca C., Woolf, Benjamin A.R., Davies, Neil M., Swanson, Sonja A., Vanderweele, Tyler J., Timpson, Nicholas J., Higgins, Julian P.T., Dimou, Niki, Langenberg, Claudia, Loder, Elizabeth W., Golub, Robert M., Egger, Matthias, Smith, George Davey, and Richards, J. Brent

Abstract

Mendelian randomisation (MR) studies allow a better understanding of the causal effects of modifiable exposures on health outcomes, but the published evidence is often hampered by inadequate reporting. Reporting guidelines help authors effectively communicate all critical information about what was done and what was found. STROBE-MR (strengthening the reporting of observational studies in epidemiology using mendelian randomisation) assists authors in reporting their MR research clearly and transparently. Adopting STROBE-MR should help readers, reviewers, and journal editors evaluate the quality of published MR studies. This article explains the 20 items of the STROBE-MR checklist, along with their meaning and rationale, using terms defined in a glossary. Examples of transparent reporting are used for each item to illustrate best practices.

Published
2021

124. Reporting and methodological quality of studies that use Mendelian randomisation in UK Biobank: a meta-epidemiological study

Author

Gibson, Mark J, Spiga, Francesca, Campbell, Amy, Khouja, Jasmine N, Richmond, Rebecca C, and Munafò, Marcus R

Abstract

ObjectivesTo identify whether Mendelian randomisation (MR) studies are appropriately conducted and reported in enough detail for other researchers to accurately replicate and interpret them.DesignCross-sectional meta-epidemiological study.Data sourcesWeb of Science, EMBASE, PubMed and PsycINFO were searched on 15 July 2022 for literature.Eligibility criteriaFull research articles that conducted an MR analysis exclusively using individual-level UK Biobank data to obtain a causal estimate of the exposure–outcome relationship (for no more than ten exposures or outcomes).Methods and analysisData were extracted using a 25-item checklist relating to reporting and methodological quality (based on the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE)-MR reporting guidelines and the guidelines for performing MR investigations). Article characteristics, such as 2021 Journal Impact Factor, publication year, journal word limit/recommendation, whether the MR analysis was the primary analysis, open access status and whether reporting guidelines were followed, were also extracted. Descriptive statistics were calculated for each item, and whether article characteristics predicted overall article completeness was investigated with linear regression.Results116 articles were included in this review. The proportion of articles which reported complete information/adequate methodology ranged from 3% to 100% across the different items. Palindromic variants, variant replication, missing data, associations of the instrumental variable with the exposure or outcome and bias introduced by two-sample methods used on a single sample were often not completely addressed (<11%). There was no clear evidence that article characteristics predicted overall completeness except for primary analysis status.ConclusionsThe results identify areas in which the reporting and conducting of MR studies needs to be improved and also suggest researchers do not make use of supplementary materials to sufficiently report secondary analyses. Future research should focus on the quality of code and analyses, attempt direct replications and investigate the impact of the STROBE-MR specifically.Study registrationhttps://osf.io/nwrdj

Published
2023
Full Text
View/download PDF

126. Using genetic variants to evaluate the causal effect of cholesterol lowering on head and neck cancer risk: A Mendelian randomization study

Author

Gormley, Mark, primary, Yarmolinsky, James, additional, Dudding, Tom, additional, Burrows, Kimberley, additional, Martin, Richard M., additional, Thomas, Steven, additional, Tyrrell, Jessica, additional, Brennan, Paul, additional, Pring, Miranda, additional, Boccia, Stefania, additional, Olshan, Andrew F., additional, Diergaarde, Brenda, additional, Hung, Rayjean J., additional, Liu, Geoffrey, additional, Legge, Danny, additional, Tajara, Eloiza H., additional, Severino, Patricia, additional, Lacko, Martin, additional, Ness, Andrew R., additional, Davey Smith, George, additional, Vincent, Emma E., additional, and Richmond, Rebecca C., additional

Published
2021
Full Text
View/download PDF

128. Exploring the causal effect of maternal pregnancy adiposity on offspring adiposity: Mendelian randomization using polygenic risk scores

Author

Bond, Tom A, primary, Richmond, Rebecca C, additional, Karhunen, Ville, additional, Cuellar-Partida, Gabriel, additional, Borges, Maria Carolina, additional, Zuber, Verena, additional, Alves, Alexessander Couto, additional, Mason, Dan, additional, Yang, Tiffany C, additional, Gunter, Marc J, additional, Dehghan, Abbas, additional, Tzoulaki, Ioanna, additional, Sebert, Sylvain, additional, Evans, David M, additional, Lewin, Alex M, additional, O’Reilly, Paul F, additional, Lawlor, Deborah A, additional, and Järvelin, Marjo-Riitta, additional

Published
2021
Full Text
View/download PDF

129. Assessing the role of genome-wide DNA methylation between smoking and risk of lung cancer using repeated measurements: the HUNT study

Author

Sun, Yi-Qian, primary, Richmond, Rebecca C, additional, Suderman, Matthew, additional, Min, Josine L, additional, Battram, Thomas, additional, Flatberg, Arnar, additional, Beisvag, Vidar, additional, Nøst, Therese Haugdahl, additional, Guida, Florence, additional, Jiang, Lin, additional, Wahl, Sissel Gyrid Freim, additional, Langhammer, Arnulf, additional, Skorpen, Frank, additional, Walker, Rosie M, additional, Bretherick, Andrew D, additional, Zeng, Yanni, additional, Chen, Yue, additional, Johansson, Mattias, additional, Sandanger, Torkjel M, additional, Relton, Caroline L, additional, and Mai, Xiao-Mei, additional

Published
2021
Full Text
View/download PDF

131. A Combined Proteomics and Mendelian Randomization Approach to Investigate the Effects of Aspirin-Targeted Proteins on Colorectal Cancer

Author

Nounu, Aayah, primary, Greenhough, Alexander, additional, Heesom, Kate J., additional, Richmond, Rebecca C., additional, Zheng, Jie, additional, Weinstein, Stephanie J., additional, Albanes, Demetrius, additional, Baron, John A., additional, Hopper, John L., additional, Figueiredo, Jane C., additional, Newcomb, Polly A., additional, Lindor, Noralane M., additional, Casey, Graham, additional, Platz, Elizabeth A., additional, Le Marchand, Loïc, additional, Ulrich, Cornelia M., additional, Li, Christopher I., additional, van Duijnhoven, Fränzel J.B., additional, Gsur, Andrea, additional, Campbell, Peter T., additional, Moreno, Víctor, additional, Vodicka, Pavel, additional, Vodickova, Ludmila, additional, Brenner, Hermann, additional, Chang-Claude, Jenny, additional, Hoffmeister, Michael, additional, Sakoda, Lori C., additional, Slattery, Martha L., additional, Schoen, Robert E., additional, Gunter, Marc J., additional, Castellví-Bel, Sergi, additional, Kim, Hyeong Rok, additional, Kweon, Sun-Seog, additional, Chan, Andrew T., additional, Li, Li, additional, Zheng, Wei, additional, Bishop, D. Timothy, additional, Buchanan, Daniel D., additional, Giles, Graham G., additional, Gruber, Stephen B., additional, Rennert, Gad, additional, Stadler, Zsofia K., additional, Harrison, Tabitha A., additional, Lin, Yi, additional, Keku, Temitope O., additional, Woods, Michael O., additional, Schafmayer, Clemens, additional, Van Guelpen, Bethany, additional, Gallinger, Steven, additional, Hampel, Heather, additional, Berndt, Sonja I., additional, Pharoah, Paul D.P., additional, Lindblom, Annika, additional, Wolk, Alicja, additional, Wu, Anna H., additional, White, Emily, additional, Peters, Ulrike, additional, Drew, David A., additional, Scherer, Dominique, additional, Bermejo, Justo Lorenzo, additional, Williams, Ann C., additional, and Relton, Caroline L., additional

Published
2021
Full Text
View/download PDF

132. The Role of Gallstones in Gallbladder Cancer in India: A Mendelian Randomization Study

Author

Mhatre, Sharayu, primary, Richmond, Rebecca C., additional, Chatterjee, Nilanjan, additional, Rajaraman, Preetha, additional, Wang, Zhaoming, additional, Zhang, Haoyu, additional, Badwe, Rajendra, additional, Goel, Mahesh, additional, Patkar, Shraddha, additional, Shrikhande, Shailesh V., additional, Patil, Prachi S., additional, Davey Smith, George, additional, Relton, Caroline L., additional, and Dikshit, Rajesh P., additional

Published
2021
Full Text
View/download PDF

133. Additional file 1 of Epigenetic prediction of complex traits and mortality in a cohort of individuals with oropharyngeal cancer

Author

Langdon, Ryan J., Beynon, Rhona A., Ingarfield, Kate, Marioni, Riccardo E., McCartney, Daniel L., Martin, Richard M., Ness, Andy R., Pawlita, Michael, Waterboer, Tim, Relton, Caroline, Thomas, Steven J., and Richmond, Rebecca C.

Abstract

Additional file 1: Supplementary Table 1: Baseline descriptive characteristics of included participants, stratified by HPV status. Supplementary Table 2: Multivariable Cox proportional hazards results for model 2 (clinical) and model 3 (respective phenotype). Supplementary Table 3: Baseline descriptive characteristics of participants included in the sensitivity analysis (n=248). Supplementary Table 4: Results of the sensitivity analysis restricted to participants with data available for BMI. Supplementary Table 5: A comparison of minimally adjusted and fully adjusted Cox proportional hazards models results, using the imputed dataset (n=408). Supplementary Table 6: Details of array type and sample size for studies used to derive DNAm scores in this analysis. Supplementary Table 7: Proportion of missing data (n=408).

Published
2020
Full Text
View/download PDF

134. Using Genetic Variation to Explore the Causal Effect of Maternal Pregnancy Adiposity on Future Offspring Adiposity: A Mendelian Randomisation Study

Author

Richmond, Rebecca C., Timpson, Nicholas J., Felix, Janine F., Palmer, Tom, Gaillard, Romy, McMahon, George, Davey Smith, George, Jaddoe, Vincent W., and Lawlor, Debbie A.

Subjects
Obesity -- Risk factors -- Genetic aspects, Body mass index -- Measurement -- Genetic aspects, Genetic variation -- Identification and classification -- Genetic aspects, Pregnant women -- Genetic aspects -- Health aspects, Biological sciences
Abstract

Background It has been suggested that greater maternal adiposity during pregnancy affects lifelong risk of offspring fatness via intrauterine mechanisms. Our aim was to use Mendelian randomisation (MR) to investigate the causal effect of intrauterine exposure to greater maternal body mass index (BMI) on offspring BMI and fat mass from childhood to early adulthood. Methods and Findings We used maternal genetic variants as instrumental variables (IVs) to test the causal effect of maternal BMI in pregnancy on offspring fatness (BMI and dual-energy X-ray absorptiometry [DXA] determined fat mass index [FMI]) in a MR approach. This was investigated, with repeat measurements, from ages 7 to 18 in the Avon Longitudinal Study of Parents and Children (ALSPAC; n = 2,521 to 3,720 for different ages). We then sought to replicate findings with results for BMI at age 6 in Generation R (n = 2,337 for replication sample; n = 6,057 for total pooled sample). In confounder-adjusted multivariable regression in ALSPAC, a 1 standard deviation (SD, equivalent of 3.7 kg/m2) increase in maternal BMI was associated with a 0.25 SD (95% CI 0.21-0.29) increase in offspring BMI at age 7, with similar results at later ages and when FMI was used as the outcome. A weighted genetic risk score was generated from 32 genetic variants robustly associated with BMI (minimum F-statistic = 45 in ALSPAC). The MR results using this genetic risk score as an IV in ALSPAC were close to the null at all ages (e.g., 0.04 SD (95% CI -0.21-0.30) at age 7 and 0.03 SD (95% CI -0.26-0.32) at age 18 per SD increase in maternal BMI), which was similar when a 97 variant generic risk score was used in ALSPAC. When findings from age 7 in ALSPAC were meta-analysed with those from age 6 in Generation R, the pooled confounder-adjusted multivariable regression association was 0.22 SD (95% CI 0.19-0.25) per SD increase in maternal BMI and the pooled MR effect (pooling the 97 variant score results from ALSPAC with the 32 variant score results from Generation R) was 0.05 SD (95%CI -0.11-0.21) per SD increase in maternal BMI (p-value for difference between the two results = 0.05). A number of sensitivity analyses exploring violation of the MR results supported our main findings. However, power was limited for some of the sensitivity tests and further studies with relevant data on maternal, offspring, and paternal genotype are required to obtain more precise (and unbiased) causal estimates. Conclusions Our findings provide little evidence to support a strong causal intrauterine effect of incrementally greater maternal BMI resulting in greater offspring adiposity., Author(s): Rebecca C. Richmond 1,2,*, Nicholas J. Timpson 1,2, Janine F. Felix 3,4,5, Tom Palmer 6, Romy Gaillard 3,4,5, George McMahon 2, George Davey Smith 1,2, Vincent W. Jaddoe 3,4,5, [...]

Published
2017
Full Text
View/download PDF

135. Genome-wide association study of offspring birth weight in 86,577 women identifies five novel loci and highlights maternal genetic effects that are independent of fetal genetics

Author

Beaumont, Robin N, Warrington, Nicole M, Cavadino, Alana, Tyrrell, Jessica, Nodzenski, Michael, Horikoshi, Momoko, Geller, Frank, Myhre, Ronny, Richmond, Rebecca C, Paternoster, Lavinia, Bradfield, Jonathan P, Kreiner-Møller, Eskil, Huikari, Ville, Metrustry, Sarah, Lunetta, Kathryn L, Painter, Jodie N, Hottenga, Jouke-Jan, Allard, Catherine, Barton, Sheila J, Espinosa, Ana, Marsh, Julie A, Potter, Catherine, Zhang, Ge, Ang, Wei, Berry, Diane J, Bouchard, Luigi, Das, Shikta, Hakonarson, Hakon, Heikkinen, Jani, Helgeland, Øyvind, Hocher, Berthold, Hofman, Albert, Inskip, Hazel M, Jones, Samuel E, Kogevinas, Manolis, Lind, Penelope A, Marullo, Letizia, Medland, Sarah E, Murray, Anna, Murray, Jeffrey C, Njølstad, Pål R, Nohr, Ellen A, Reichetzeder, Christoph, Ring, Susan M, Ruth, Katherine S, Santa-Marina, Loreto, Scholtens, Denise M, Willemsen, Gonneke, Bartels, Meike, Boomsma, Dorret I, Biological Psychology, APH - Health Behaviors & Chronic Diseases, APH - Personalized Medicine, Amsterdam Neuroscience - Mood, Anxiety, Psychosis, Stress & Sleep, APH - Mental Health, and APH - Methodology

Subjects
Netherlands Twin Register (NTR), Genotype, Protein-Serine-Threonine Kinases/genetics, Actins/genetics, Birth Weight/genetics, Receptor, Melatonin, MT2/genetics, Gestational Age, Polymorphism, Single Nucleotide/genetics, Transcription Factor 7-Like 2 Protein/genetics, HMGA2 Protein/genetics, Kv1.3 Potassium Channel/genetics, Trans-Activators/genetics, Cytochrome P-450 CYP3A/genetics, Genetic Variation/genetics, SDG 3 - Good Health and Well-being, Proteins/genetics, Genome-Wide Association Study/methods, Journal Article, Humans, Female, Alleles, DNA-Binding Proteins/genetics
Abstract

Genome-wide association studies of birth weight have focused on fetal genetics, whereas relatively little is known about the role of maternal genetic variation. We aimed to identify maternal genetic variants associated with birth weight that could highlight potentially relevant maternal determinants of fetal growth. We meta-analysed data on up to 8.7 million SNPs in up to 86 577 women of European descent from the Early Growth Genetics (EGG) Consortium and the UK Biobank. We used structural equation modelling (SEM) and analyses of mother-child pairs to quantify the separate maternal and fetal genetic effects. Maternal SNPs at 10 loci (MTNR1B, HMGA2, SH2B3, KCNAB1, L3MBTL3, GCK, EBF1, TCF7L2, ACTL9, CYP3A7) were associated with offspring birth weight at P

Published
2018

136. Investigating the DNA methylation profile of e-cigarette use

Author

Richmond, Rebecca C, primary, Rejon, Carlos Sillero, additional, Khouja, Jasmine N, additional, Prince, Claire, additional, Board, Alexander, additional, Sharp, Gemma, additional, Suderman, Matthew, additional, Relton, Caroline L, additional, Munafò, Marcus, additional, and Gage, Suzanne H, additional

Published
2021
Full Text
View/download PDF

138. Assessing the causal role of sleep traits on glycated haemoglobin: a Mendelian randomization study

Author

Liu, Junxi, primary, Richmond, Rebecca C, additional, Bowden, Jack, additional, Barry, Ciarrah, additional, Dashti, Hassan S, additional, Daghlas, Iyas, additional, Lane, Jacqueline M, additional, Jones, Samuel E, additional, Wood, Andrew R, additional, Frayling, Timothy M, additional, Wright, Alison K, additional, Carr, Matthew J, additional, Anderson, Simon G, additional, Emsley, Richard, additional, Ray, David, additional, Weedon, Michael N, additional, Saxena, Richa, additional, Lawlor, Deborah A, additional, and Rutter, Martin K, additional

Published
2020
Full Text
View/download PDF

140. Genome-wide association analyses of physical activity and sedentary behavior provide insights into underlying mechanisms and roles in disease prevention

Author

Wang, Zhe, Emmerich, Andrew, Pillon, Nicolas J., Moore, Tim, Hemerich, Daiane, Cornelis, Marilyn C., Mazzaferro, Eugenia, Broos, Siacia, Ahluwalia, Tarunveer S., Bartz, Traci M., Bentley, Amy R., Bielak, Lawrence F., Chong, Mike, Chu, Audrey Y., Berry, Diane, Dorajoo, Rajkumar, Dueker, Nicole D., Kasbohm, Elisa, Feenstra, Bjarke, Feitosa, Mary F., Gieger, Christian, Graff, Mariaelisa, Hall, Leanne M., Haller, Toomas, Hartwig, Fernando P., Hillis, David A., Huikari, Ville, Heard-Costa, Nancy, Holzapfel, Christina, Jackson, Anne U., Johansson, Åsa, Jørgensen, Anja Moltke, Kaakinen, Marika A., Karlsson, Robert, Kerr, Kathleen F., Kim, Boram, Koolhaas, Chantal M., Kutalik, Zoltan, Lagou, Vasiliki, Lind, Penelope A., Lorentzon, Mattias, Lyytikäinen, Leo-Pekka, Mangino, Massimo, Metzendorf, Christoph, Monroe, Kristine R., Pacolet, Alexander, Pérusse, Louis, Pool, Rene, Richmond, Rebecca C., Rivera, Natalia V., Robiou-du-Pont, Sebastien, Schraut, Katharina E., Schulz, Christina-Alexandra, Stringham, Heather M., Tanaka, Toshiko, Teumer, Alexander, Turman, Constance, van der Most, Peter J., Vanmunster, Mathias, van Rooij, Frank J. A., van Vliet-Ostaptchouk, Jana V., Zhang, Xiaoshuai, Zhao, Jing-Hua, Zhao, Wei, Balkhiyarova, Zhanna, Balslev-Harder, Marie N., Baumeister, Sebastian E., Beilby, John, Blangero, John, Boomsma, Dorret I., Brage, Soren, Braund, Peter S., Brody, Jennifer A., Bruinenberg, Marcel, Ekelund, Ulf, Liu, Ching-Ti, Cole, John W., Collins, Francis S., Cupples, L. Adrienne, Esko, Tõnu, Enroth, Stefan, Faul, Jessica D., Fernandez-Rhodes, Lindsay, Fohner, Alison E., Franco, Oscar H., Galesloot, Tessel E., Gordon, Scott D., Grarup, Niels, Hartman, Catharina A., Heiss, Gerardo, Hui, Jennie, Illig, Thomas, Jago, Russell, James, Alan, Joshi, Peter K., Jung, Taeyeong, Kähönen, Mika, Kilpeläinen, Tuomas O., Koh, Woon-Puay, Kolcic, Ivana, Kraft, Peter P., Kuusisto, Johanna, Launer, Lenore J., Li, Aihua, Linneberg, Allan, Luan, Jian’an, Vidal, Pedro Marques, Medland, Sarah E., Milaneschi, Yuri, Moscati, Arden, Musk, Bill, Nelson, Christopher P., Nolte, Ilja M., Pedersen, Nancy L., Peters, Annette, Peyser, Patricia A., Power, Christine, Raitakari, Olli T., Reedik, Mägi, Reiner, Alex P., Ridker, Paul M., Rudan, Igor, Ryan, Kathy, Sarzynski, Mark A., Scott, Laura J., Scott, Robert A., Sidney, Stephen, Siggeirsdottir, Kristin, Smith, Albert V., Smith, Jennifer A., Sonestedt, Emily, Strøm, Marin, Tai, E. Shyong, Teo, Koon K., Thorand, Barbara, Tönjes, Anke, Tremblay, Angelo, Uitterlinden, Andre G., Vangipurapu, Jagadish, van Schoor, Natasja, Völker, Uwe, Willemsen, Gonneke, Williams, Kayleen, Wong, Quenna, Xu, Huichun, Young, Kristin L., Yuan, Jian Min, Zillikens, M. Carola, Zonderman, Alan B., Ameur, Adam, Bandinelli, Stefania, Bis, Joshua C., Boehnke, Michael, Bouchard, Claude, Chasman, Daniel I., Smith, George Davey, de Geus, Eco J. C., Deldicque, Louise, Dörr, Marcus, Evans, Michele K., Ferrucci, Luigi, Fornage, Myriam, Fox, Caroline, Garland, Theodore, Gudnason, Vilmundur, Gyllensten, Ulf, Hansen, Torben, Hayward, Caroline, Horta, Bernardo L., Hyppönen, Elina, Jarvelin, Marjo-Riitta, Johnson, W. Craig, Kardia, Sharon L. R., Kiemeney, Lambertus A., Laakso, Markku, Langenberg, Claudia, Lehtimäki, Terho, Marchand, Loic Le, Magnusson, Patrik K. E., Martin, Nicholas G., Melbye, Mads, Metspalu, Andres, Meyre, David, North, Kari E., Ohlsson, Claes, Oldehinkel, Albertine J., Orho-Melander, Marju, Pare, Guillaume, Park, Taesung, Pedersen, Oluf, Penninx, Brenda W. J. H., Pers, Tune H., Polasek, Ozren, Prokopenko, Inga, Rotimi, Charles N., Samani, Nilesh J., Sim, Xueling, Snieder, Harold, Sørensen, Thorkild I. A., Spector, Tim D., Timpson, Nicholas J., van Dam, Rob M., van der Velde, Nathalie, van Duijn, Cornelia M., Vollenweider, Peter, Völzke, Henry, Voortman, Trudy, Waeber, Gérard, Wareham, Nicholas J., Weir, David R., Wichmann, Heinz-Erich, Wilson, James F., Hevener, Andrea L., Krook, Anna, Zierath, Juleen R., Thomis, Martine A. I., Loos, Ruth J. F., and Hoed, Marcel den

Abstract

Although physical activity and sedentary behavior are moderately heritable, little is known about the mechanisms that influence these traits. Combining data for up to 703,901 individuals from 51 studies in a multi-ancestry meta-analysis of genome-wide association studies yields 99 loci that associate with self-reported moderate-to-vigorous intensity physical activity during leisure time (MVPA), leisure screen time (LST) and/or sedentary behavior at work. Loci associated with LST are enriched for genes whose expression in skeletal muscle is altered by resistance training. A missense variant in ACTN3makes the alpha-actinin-3 filaments more flexible, resulting in lower maximal force in isolated type IIAmuscle fibers, and possibly protection from exercise-induced muscle damage. Finally, Mendelian randomization analyses show that beneficial effects of lower LST and higher MVPA on several risk factors and diseases are mediated or confounded by body mass index (BMI). Our results provide insights into physical activity mechanisms and its role in disease prevention.

Published
2022
Full Text
View/download PDF

141. An update on oral cavity cancer: epidemiological trends, prevention strategies and novel approaches in diagnosis and prognosis.

Author

Gormley, Mark, Gray, Emily, Richards, Charlotte, Gormley, Alex, Richmond, Rebecca C., Vincent, Emma E., Dudding, Tom, Ness, Andrew R., and Thomas, Steven J.

Abstract

In the UK, the incidence of oral cavity cancer continues to rise, with an increase of around 60% over the past 10 years. Many patients still present with advanced disease, often resulting in locoregional recurrence and poor outcomes, which has not changed significantly for over four decades. Changes in aetiology may also be emerging, given the decline of smoking in developed countries. Therefore, new methods to better target prevention, improve screening and detect recurrence are needed. High-throughput 'omics' technologies appear promising for future individual-level diagnosis and prognosis. However, given this is a relatively rare cancer with significant intra-tumour heterogeneity and variation in patient response, reliable biomarkers have been difficult to elucidate. From a public health perspective, implementing these novel technologies into current services would require substantial practical, financial and ethical considerations. This may be difficult to justify and implement at present, therefore focus remains on early detection using new patient-led follow-up strategies. This paper reviews the latest evidence on epidemiological trends in oral cavity cancer to help identify at risk groups, population-based approaches for prevention, in addition to potential cutting-edge approaches in the diagnosis and prognosis of this disease. [ABSTRACT FROM AUTHOR]

Published
2022
Full Text
View/download PDF

142. Assessing the causal role of epigenetic clocks in the development of multiple cancers: a Mendelian randomization study.

Author

Berstein, Fernanda Morales, McCartney, Daniel L., Lu, Ake T., Tsilidis, Konstantinos K., Bouras, Emmanouil, Haycock, Philip, Burrows, Kimberley, Phipps, Amanda I., Buchanan, Daniel D., Cheng, Iona, Martin, Richard M., Smith, George Davey, Relton, Caroline L., Horvath, Steve, Marioni, Riccardo E., Richardson, Tom G., and Richmond, Rebecca C.

Published
2022
Full Text
View/download PDF

143. Assessing the Causal Role of Sleep Traits on Glycated Hemoglobin: A Mendelian Randomization Study.

Author

Junxi Liu, Richmond, Rebecca C., Bowden, Jack, Barry, Ciarrah, Dashti, Hassan S., Daghlas, Iyas, Lane, Jacqueline M., Jones, Samuel E., Wood, Andrew R., Frayling, Timothy M., Wright, Alison K., Carr, Matthew J., Anderson, Simon G., Emsley, Richard A., Ray, David W., Weedon, Michael N., Saxena, Richa, Lawlor, Deborah A., Rutter, Martin K., and Liu, Junxi

Subjects
*SEQUENCE analysis, *TYPE 2 diabetes, *SLEEP, *RESEARCH funding, *INSOMNIA
Abstract

Objective: To examine the effects of sleep traits on glycated hemoglobin (HbA1c).Research Design and Methods: This study triangulated evidence across multivariable regression (MVR) and one- (1SMR) and two-sample Mendelian randomization (2SMR) including sensitivity analyses on the effects of five self-reported sleep traits (i.e., insomnia symptoms [difficulty initiating or maintaining sleep], sleep duration, daytime sleepiness, napping, and chronotype) on HbA1c (in SD units) in adults of European ancestry from the UK Biobank (for MVR and 1SMR analyses) (n = 336,999; mean [SD] age 57 [8] years; 54% female) and in the genome-wide association studies from the Meta-Analyses of Glucose and Insulin-Related Traits Consortium (MAGIC) (for 2SMR analysis) (n = 46,368; 53 [11] years; 52% female).Results: Across MVR, 1SMR, 2SMR, and their sensitivity analyses, we found a higher frequency of insomnia symptoms (usually vs. sometimes or rarely/never) was associated with higher HbA1c (MVR 0.05 SD units [95% CI 0.04-0.06]; 1SMR 0.52 [0.42-0.63]; 2SMR 0.24 [0.11-0.36]). Associations remained, but point estimates were somewhat attenuated after excluding participants with diabetes. For other sleep traits, there was less consistency across methods, with some but not all providing evidence of an effect.Conclusions: Our results suggest that frequent insomnia symptoms cause higher HbA1c levels and, by implication, that insomnia has a causal role in type 2 diabetes. These findings could have important implications for developing and evaluating strategies that improve sleep habits to reduce hyperglycemia and prevent diabetes. [ABSTRACT FROM AUTHOR]

Published
2022
Full Text
View/download PDF

144. Workplace interventions that aim to improve employee health and well-being in male-dominated industries: a systematic review.

Author

Hulls, Paige M., Richmond, Rebecca C., Martin, Richard M., Chavez-Ugalde, Yanaina, and de Vocht, Frank

Abstract

The published evidence on whether workplace health and well-being interventions are as effective in male-dominated industries compared with mixed-gender environments has not been synthesised. We performed a systematic review of workplace interventions aimed at improving employee health and well-being in male-dominated industries. We searched Web of Knowledge, PubMed, Medline, Cochrane Database and Web of Science for articles describing workplace interventions in male-dominated industries that address employee health and well-being. The primary outcome was to determine the effectiveness of the intervention and the process evaluation (intervention delivery and adherence). To assess the quality of evidence, Cochrane Collaboration's Risk of Bias Tool was used. Due to the heterogeneity of reported outcomes, meta-analysis was performed for only some outcomes and a narrative synthesis with albatross plots was presented. After full-text screening, 35 studies met the eligibility criteria. Thirty-two studies delivered the intervention face-to-face, while two were delivered via internet and one using postal mail. Intervention adherence ranged from 50% to 97%, dependent on mode of delivery and industry. 17 studies were considered low risk of bias. Albatross plots indicated some evidence of positive associations, particularly for interventions focusing on musculoskeletal disorders. There was little evidence of intervention effect on body mass index and systolic or diastolic blood pressure. Limited to moderate evidence of beneficial effects was found for workplace health and well-being interventions conducted within male-dominated industries. Such interventions in the workplace can be effective, despite a different culture in male-dominated compared with mixed industries, but are dependent on delivery, industry and outcome. CRD42019161283. [ABSTRACT FROM AUTHOR]

Published
2022
Full Text
View/download PDF

145. Using genetic variants to evaluate the causal effect of cholesterol lowering on head and neck cancer risk: a Mendelian randomization study

Author

Gormley, Mark, primary, Yarmolinsky, James, additional, Dudding, Tom, additional, Burrows, Kimberley, additional, Martin, Richard M, additional, Thomas, Steven, additional, Tyrrell, Jessica, additional, Brennan, Paul, additional, Pring, Miranda, additional, Boccia, Stefania, additional, Olshan, Andrew F, additional, Diergaarde, Brenda, additional, Hung, Rayjean J., additional, Liu, Geoffrey, additional, Legge, Danny, additional, Tajara, Eloiza H, additional, Severino, Patricia, additional, Lacko, Martin, additional, Ness, Andrew R, additional, Smith, George Davey, additional, Vincent, Emma E, additional, and Richmond, Rebecca C, additional

Published
2020
Full Text
View/download PDF

146. Investigating the relationships between unfavorable sleep and metabolomic traits: evidence from multi-cohort multivariable regression and Mendelian randomization analyses

Author

Bos, Maxime M, primary, Goulding, Neil J, additional, Lee, Matthew A, additional, Hofman, Amy, additional, Bot, Mariska, additional, Pool, René, additional, Vijfhuizen, Lisanne S, additional, Zhang, Xiang, additional, Li, Chihua, additional, Mustafa, Rima, additional, Neville, Matt J, additional, Li-Gao, Ruifang, additional, Trompet, Stella, additional, Beekman, Marian, additional, Biermasz, Nienke R, additional, Boomsma, Dorret I, additional, Boer, Irene de, additional, Christodoulides, Constantinos, additional, Dehghan, Abbas, additional, Dijk, Ko Willems van, additional, Ford, Ian, additional, Gao, He, additional, Ghanbari, Mohsen, additional, Heijmans, Bastiaan T, additional, Ikram, M Arfan, additional, Jukema, J Wouter, additional, Mook-Kanamori, Dennis O, additional, Karpe, Fredrik, additional, Luik, Annemarie I, additional, Lumey, L.H., additional, van den Maagdenberg, Arn M.J.M., additional, Mooijaart, Simon P, additional, Mutsert, Renée de, additional, Penninx, Brenda W.J.H., additional, Rensen, Patrick CN, additional, Richmond, Rebecca C, additional, Rosendaal, Frits R, additional, Sattar, Naveed, additional, Schoevers, Robert A, additional, Slagboom, P Eline, additional, Terwindt, Gisela M, additional, Thesing, Carisha S, additional, Wade, Kaitlin H, additional, Wijsman, Carolien A, additional, Willemsen, Gonneke, additional, Zwinderman, Aeilko H., additional, Heemst, Diana van, additional, Noordam, Raymond, additional, and Lawlor, Deborah A, additional

Published
2020
Full Text
View/download PDF

147. A combined proteomics and Mendelian randomization approach to investigate the effects of aspirin-targeted proteins on colorectal cancer

Author

Nounu, Aayah, primary, Greenhough, Alexander, additional, Heesom, Kate J, additional, Richmond, Rebecca C, additional, Zheng, Jie, additional, Weinstein, Stephanie J, additional, Albanes, Demetrius, additional, Baron, John A, additional, Hopper, John L, additional, Figueiredo, Jane C, additional, Newcomb, Polly A, additional, Lindor, Noralane M, additional, Casey, Graham, additional, Platz, Elizabeth A, additional, Le Marchand, Loïc, additional, Ulrich, Cornelia M, additional, Li, Christopher I, additional, van Duijnhoven, Fränzel JB, additional, Gsur, Andrea, additional, Campbell, Peter T, additional, Moreno, Víctor, additional, Vodicka, Pavel, additional, Vodickova, Ludmila, additional, Brenner, Hermann, additional, Chang-Claude, Jenny, additional, Hoffmeister, Michael, additional, Sakoda, Lori C, additional, Slattery, Martha L, additional, Schoen, Robert E, additional, Gunter, Marc J, additional, Castellví-Bel, Sergi, additional, Kim, Hyeong Rok, additional, Kweon, Sun-Seog, additional, Chan, Andrew T, additional, Li, Li, additional, Zheng, Wei, additional, Bishop, D Timothy, additional, Buchanan, Daniel D, additional, Giles, Graham G, additional, Gruber, Stephen B, additional, Rennert, Gad, additional, Stadler, Zsofia K, additional, Harrison, Tabitha A, additional, Lin, Yi, additional, Keku, Temitope O, additional, Woods, Michael O, additional, Schafmayer, Clemens, additional, Van Guelpen, Bethany, additional, Gallinger, Steven J, additional, Hampel, Heather, additional, Berndt, Sonja I, additional, Pharoah, Paul D P, additional, Lindblom, Annika, additional, Wolk, Alicja, additional, Wu, Anna H, additional, White, Emily, additional, Peters, Ulrike, additional, Drew, David A, additional, Scherer, Dominique, additional, Bermejo, Justo Lorenzo, additional, Williams, Ann C, additional, and Relton, Caroline L, additional

Published
2020
Full Text
View/download PDF

150. Is disrupted sleep a risk factor for Alzheimer’s disease? Evidence from a two-sample Mendelian randomization analysis

Author

Anderson, Emma L, primary, Richmond, Rebecca C, additional, Jones, Samuel E, additional, Hemani, Gibran, additional, Wade, Kaitlin H, additional, Dashti, Hassan S, additional, Lane, Jacqueline M, additional, Wang, Heming, additional, Saxena, Richa, additional, Brumpton, Ben, additional, Korologou-Linden, Roxanna, additional, Nielsen, Jonas B, additional, Åsvold, Bjørn Olav, additional, Abecasis, Gonçalo, additional, Coulthard, Elizabeth, additional, Kyle, Simon D, additional, Beaumont, Robin N, additional, Tyrrell, Jessica, additional, Frayling, Timothy M, additional, Munafò, Marcus R, additional, Wood, Andrew R, additional, Ben-Shlomo, Yoav, additional, Howe, Laura D, additional, Lawlor, Deborah A, additional, Weedon, Michael N, additional, and Davey Smith, George, additional

Published
2020
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results