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1. The role of accelerometer-derived sleep traits on glycated haemoglobin and glucose levels: a Mendelian randomization study

Author

Liu, Junxi, Richmond, Rebecca C., Anderson, Emma L., Bowden, Jack, Barry, Ciarrah-Jane S., Dashti, Hassan S., Daghlas, Iyas S., Lane, Jacqueline M., Kyle, Simon D., Vetter, Céline, Morrison, Claire L., 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, Rutter, Martin K., and Lawlor, Deborah A.

Published
2024
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5. Genomic analysis of diet composition finds novel loci and associations with health and lifestyle

Author

Meddens, S Fleur W, de Vlaming, Ronald, Bowers, Peter, Burik, Casper AP, Linnér, Richard Karlsson, Lee, Chanwook, Okbay, Aysu, Turley, Patrick, Rietveld, Cornelius A, Fontana, Mark Alan, Ghanbari, Mohsen, Imamura, Fumiaki, McMahon, George, van der Most, Peter J, Voortman, Trudy, Wade, Kaitlin H, Anderson, Emma L, Braun, Kim VE, Emmett, Pauline M, Esko, Tonũ, Gonzalez, Juan R, Kiefte-de Jong, Jessica C, Langenberg, Claudia, Luan, Jian’an, Muka, Taulant, Ring, Susan, Rivadeneira, Fernando, Snieder, Harold, van Rooij, Frank JA, Wolffenbuttel, Bruce HR, Smith, George Davey, Franco, Oscar H, Forouhi, Nita G, Ikram, M Arfan, Uitterlinden, Andre G, van Vliet-Ostaptchouk, Jana V, Wareham, Nick J, Cesarini, David, Harden, K Paige, Lee, James J, Benjamin, Daniel J, Chow, Carson C, and Koellinger, Philipp D

Subjects
Biomedical and Clinical Sciences, Nutrition and Dietetics, Prevention, Behavioral and Social Science, Genetics, Obesity, Human Genome, Nutrition, Diabetes, Aetiology, 2.1 Biological and endogenous factors, Cardiovascular, Metabolic and endocrine, Body Mass Index, Diabetes Mellitus, Type 2, Diet, Genome-Wide Association Study, Genomics, Humans, Life Style, 23andMe Research Team, EPIC- InterAct Consortium, Lifelines Cohort Study, Biological Sciences, Medical and Health Sciences, Psychology and Cognitive Sciences, Psychiatry, Clinical sciences, Biological psychology, Clinical and health psychology
Abstract

We conducted genome-wide association studies (GWAS) of relative intake from the macronutrients fat, protein, carbohydrates, and sugar in over 235,000 individuals of European ancestries. We identified 21 unique, approximately independent lead SNPs. Fourteen lead SNPs are uniquely associated with one macronutrient at genome-wide significance (P

Published
2021

7. Efficacy of metformin targets on cardiometabolic health in the general population and non-diabetic individuals: a Mendelian randomization study

Author

Zheng, Jie, Xu, Min, Yang, Qian, Hu, Chunyan, Walker, Venexia, Lu, Jieli, Wang, Jiqiu, Liu, Ruixin, Xu, Yu, Wang, Tiange, Zhao, Zhiyun, Yuan, Jinqiu, Burgess, Stephen, Au Yeung, Shiu Lun, Luo, Shan, Anderson, Emma L., Holmes, Michael V., Smith, George Davey, Ning, Guang, Wang, Weiqing, Gaunt, Tom R., and Bi, Yufang

Published
2023
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13. Deciphering the Influence of Socioeconomic Status on Brain Structure: Insights from Mendelian Randomization

Author

Xia, Charley, primary, Lu, Yuechen, additional, Zhou, Zhuzhuoyu, additional, Marchi, Mattia, additional, Kweon, Hyeokmoon, additional, Ning, Yuchen, additional, Liewald, David C.M., additional, Anderson, Emma L., additional, Koellinger, Philipp D., additional, Cox, Simon R., additional, Boks, Marco P., additional, and Hill, William David, additional

Published
2024
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16. The bidirectional effects between cognitive ability and brain morphology: A life course Mendelian randomization analysis

Author

Korologou-Linden, Roxanna, primary, Schuurmans, Isabel K., additional, Cecil, Charlotte A.M., additional, White, Tonya, additional, Banaschewski, Tobias, additional, Bokde, Arun L.W., additional, Desrivières, Sylvane, additional, Grigis, Antoine, additional, Garavan, Hugh, additional, Gowland, Penny, additional, Heinz, Andreas, additional, Brühl, Rüdiger, additional, Martinot, Jean-Luc, additional, Martinot, Marie-Laure Paillère, additional, Artiges, Eric, additional, Nees, Frauke, additional, Orfanos, Dimitri Papadopoulos, additional, Paus, Tomáš, additional, Poustka, Luise, additional, Holz, Nathalie, additional, Fröhner, Juliane H., additional, Smolka, M, additional, Walter, Henrik, additional, Winterer, Jeanne, additional, Whelan, Robert, additional, Schumann, Gunter, additional, Howe, Laura D, additional, Ben-Shlomo, Yoav, additional, Davies, Neil M, additional, and Anderson, Emma L, additional

Published
2023
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21. Hypertensive disorders of pregnancy and midlife maternal cognition in a prospective cohort study.

Author

Birnie, Kate, Catov, Janet, Anderson, Emma L., Lapidaire, Winok, Kilpi, Fanny, Lawlor, Deborah A., and Fraser, Abigail

Abstract

Hypertensive disorders of pregnancy (HDP) are associated with an increased risk of cardiovascular disorders, with recent evidence linking pre‐eclampsia with vascular dementia. We examined associations of HDP with cognitive performance measured in midlife, in a prospective cohort study, the Avon Longitudinal Study of Parents and Children. Six cognitive function domains were measured 20 years after pregnancy at a mean age of 51 years. The cognition tests were repeated at clinics in the following two years. Cognitive function domains measured were immediate and delayed verbal episodic memory, working memory, processing speed, verbal intelligence, and verbal fluency. Exposures were pre‐eclampsia, gestational hypertension (GH), and a combined category of any HDP, all compared to normotensive pregnancy. Of 3393 pregnancies included in the analysis, GH was experienced by 417 (12.3%) and pre‐eclampsia by 57 (1.7%). GH was associated with lower verbal episodic memory, in the delayed logic memory test (‐0.16 SDs; 95% CI ‐0.30, ‐0.03; p =.015) and there was weak evidence of an association with the immediate logic memory test (‐0.13 SDs; ‐0.27, 0.001; p =.058). However, we did not see steeper declines by age for women with GH and there was no evidence of associations with other cognitive domains or for pre‐eclampsia with any domains. Results were not substantially changed after controlling for midlife blood pressure. Our findings suggest that a history of GH is associated with slightly reduced episodic memory 20 years after pregnancy, but we found no evidence of a quicker age‐related decline compared to women with normotensive pregnancies. [ABSTRACT FROM AUTHOR]

Published
2024
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23. The causal role of accelerometer-derived sleep traits on glycated haemoglobin: a Mendelian randomization study

Author

Liu, Junxi, primary, Richmond, Rebecca C, additional, Anderson, Emma L, additional, Bowden, Jack, additional, Barry, Ciarrah-Jane S, additional, Dashti, Hassan S, additional, Daghlas, Iyas S, additional, Lane, Jacqueline M, additional, Kyle, Simon D, additional, Vetter, Céline, additional, Morrison, Claire L, 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 A, additional, Ray, David W, additional, Weedon, Michael N, additional, Saxena, Richa, additional, Rutter, Martin K, additional, and Lawlor, Deborah A, additional

Published
2022
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29. Exposure to multiple childhood social risk factors and adult body mass index trajectories from ages 20 to 64 years

Author

Caleyachetty, Rishi, Stafford, Mai, Cooper, Rachel, Anderson, Emma L, Howe, Laura D, Cosco, Theodore D, Kuh, Diana, Hardy, Rebecca, Caleyachetty, Rishi, Stafford, Mai, Cooper, Rachel, Anderson, Emma L, Howe, Laura D, Cosco, Theodore D, Kuh, Diana, and Hardy, Rebecca

Abstract

Background While childhood social risk factors appear to be associated with adult obesity, it is unclear whether exposure to multiple childhood social risk factors is associated with accelerated weight gain during adulthood. Methods We used the Medical Research Council National Survey of Health and Development, a British population-based birth cohort study of participants born in 1946, height and weight were measured by nurses at ages 36, 43, 53 and 60–64 and self-reported at 20 and 26 years. The 9 childhood socioeconomic risk factors and 8 binary childhood psychosocial risk factors were measured, with 13 prospectively measured at age 4 years (or at 7 or 11 years if missing) and 3 were recalled when participants were age 43. Multilevel modelling was used to examine the association between the number of childhood social risk factors and changes in body mass index (BMI) with age. Results Increasing exposure to a higher number of childhood socioeconomic risk factors was associated with higher mean BMI across adulthood for both sexes and with a faster increase in BMI from 20 to 64 years, among women but not men. Associations remained after adjustment for adult social class. There was no evidence of an association between exposure to childhood psychosocial risk factors and mean BMI in either sex at any age. Conclusions Strategies for the prevention and management of weight gain across adulthood may need to tailor interventions in consideration of past exposure to multiple socioeconomic disadvantages experienced during childhood.

Published
2021

30. The bidirectional causal effects of brain morphology across the life course and risk of Alzheimer’s disease: A cross-cohort comparison and Mendelian randomization meta-analysis

Author

Korologou-Linden, Roxanna, primary, Xu, Bing, additional, Coulthard, Elizabeth, additional, Walton, Esther, additional, Wearn, Alfie, additional, Hemani, Gibran, additional, White, Tonya, additional, Cecil, Charlotte, additional, Sharp, Tamsin, additional, Tiemeier, Henning, additional, Banaschewski, Tobias, additional, Bokde, Arun L.W., additional, Quinlan, Erin Burke, additional, Desrivières, Sylvane, additional, Flor, Herta, additional, Grigis, Antoine, additional, Garavan, Hugh, additional, Gowland, Penny, additional, Heinz, Andreas, additional, Brühl, Rüdiger, additional, Martinot, Jean-Luc, additional, Martinot, Marie-Laure Paillère, additional, Artiges, Eric, additional, Nees, Frauke, additional, Orfanos, Dimitri Papadopoulos, additional, Paus, Tomáš, additional, Poustka, Luise, additional, Millenet, Sabina, additional, Fröhner, Juliane H., additional, Smolka, M, additional, Walter, Henrik, additional, Whelan, Robert, additional, Schumann, Gunter, additional, Howe, Laura D, additional, Ben-Shlomo, Yoav, additional, Davies, Neil M, additional, and Anderson, Emma L, additional

Published
2021
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37. 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
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39. Education, intelligence and Alzheimer’s disease: evidence from a multivariable two-sample Mendelian randomization study

Author

Anderson, Emma L, primary, Howe, Laura D, additional, Wade, Kaitlin H, additional, Ben-Shlomo, Yoav, additional, Hill, W David, additional, Deary, Ian J, additional, Sanderson, Eleanor C, additional, Zheng, Jie, additional, Korologou-Linden, Roxanna, additional, Stergiakouli, Evie, additional, Davey Smith, George, additional, Davies, Neil M, additional, and Hemani, Gibran, additional

Published
2020
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41. Investigating causal relations between sleep traits and risk of breast cancer in women: mendelian randomisation study

Author

Richmond, Rebecca C, Anderson, Emma L, Dashti, Hassan S, Jones, Samuel E, Lane, Jacqueline M, Strand, Linn Beate, Brumpton, Ben, Rutter, Martin K, Wood, Andrew R, Straif, Kurt, Relton, Caroline L, Munafò, Marcus, Frayling, Timothy M, Martin, Richard M, Saxena, Richa, Weedon, Michael N, Lawlor, Debbie A, and Smith, George Davey

Subjects
Medicine(all), Adult, Time Factors, Research, Incidence, Breast Neoplasms, Confounding Factors, Epidemiologic, Comorbidity, Mendelian Randomization Analysis, Middle Aged, United Kingdom, Circadian Rhythm, Risk Factors, Case-Control Studies, Sleep Initiation and Maintenance Disorders, Multivariate Analysis, Humans, Female, Prospective Studies, Sleep, Aged, Genome-Wide Association Study
Abstract

Objective To examine whether sleep traits have a causal effect on risk of breast cancer. Design Mendelian randomisation study. Setting UK Biobank prospective cohort study and Breast Cancer Association Consortium (BCAC) case-control genome-wide association study. Participants 156 848 women in the multivariable regression and one sample mendelian randomisation (MR) analysis in UK Biobank (7784 with a breast cancer diagnosis) and 122 977 breast cancer cases and 105 974 controls from BCAC in the two sample MR analysis. Exposures Self reported chronotype (morning or evening preference), insomnia symptoms, and sleep duration in multivariable regression, and genetic variants robustly associated with these sleep traits. Main outcome measure Breast cancer diagnosis. Results In multivariable regression analysis using UK Biobank data on breast cancer incidence, morning preference was inversely associated with breast cancer (hazard ratio 0.95, 95% confidence interval 0.93 to 0.98 per category increase), whereas there was little evidence for an association between sleep duration and insomnia symptoms. Using 341 single nucleotide polymorphisms (SNPs) associated with chronotype, 91 SNPs associated with sleep duration, and 57 SNPs associated with insomnia symptoms, one sample MR analysis in UK Biobank provided some supportive evidence for a protective effect of morning preference on breast cancer risk (0.85, 0.70, 1.03 per category increase) but imprecise estimates for sleep duration and insomnia symptoms. Two sample MR using data from BCAC supported findings for a protective effect of morning preference (inverse variance weighted odds ratio 0.88, 95% confidence interval 0.82 to 0.93 per category increase) and adverse effect of increased sleep duration (1.19, 1.02 to 1.39 per hour increase) on breast cancer risk (both oestrogen receptor positive and oestrogen receptor negative), whereas evidence for insomnia symptoms was inconsistent. Results were largely robust to sensitivity analyses accounting for horizontal pleiotropy. Conclusions Findings showed consistent evidence for a protective effect of morning preference and suggestive evidence for an adverse effect of increased sleep duration on breast cancer risk.

Published
2019

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

Author

Anderson, Emma L, Richmond, Rebecca C, Jones, Samuel E, Hemani, Gibran, Wade, Kaitlin H, Dashti, Hassan S, Lane, Jacqueline M, Wang, Heming, Saxena, Richa, Brumpton, Ben, Korologou-Linden, Roxanna, Nielsen, Jonas B, Åsvold, Bjørn Olav, Abecasis, Gonçalo, Coulthard, Elizabeth, Kyle, Simon D, Beaumont, Robin N, Tyrrell, Jessica, Frayling, Timothy M, and Munafò, Marcus R

Subjects
*DROWSINESS, *ALZHEIMER'S disease, *GENOME-wide association studies, *SLEEP, *RESEARCH, *SEQUENCE analysis, *RESEARCH methodology, *MEDICAL cooperation, *EVALUATION research, *COMPARATIVE studies, *RESEARCH funding
Abstract

Background: It is established that Alzheimer's disease (AD) patients experience sleep disruption. However, it remains unknown whether disruption in the quantity, quality or timing of sleep is a risk factor for the onset of AD.Methods: We used the largest published genome-wide association studies of self-reported and accelerometer-measured sleep traits (chronotype, duration, fragmentation, insomnia, daytime napping and daytime sleepiness), and AD. Mendelian randomization (MR) was used to estimate the causal effect of self-reported and accelerometer-measured sleep parameters on AD risk.Results: Overall, there was little evidence to support a causal effect of sleep traits on AD risk. There was some suggestive evidence that self-reported daytime napping was associated with lower AD risk [odds ratio (OR): 0.70, 95% confidence interval (CI): 0.50-0.99). Some other sleep traits (accelerometer-measured 'eveningness' and sleep duration, and self-reported daytime sleepiness) had ORs of a similar magnitude to daytime napping, but were less precisely estimated.Conclusions: Overall, we found very limited evidence to support a causal effect of sleep traits on AD risk. Our findings provide tentative evidence that daytime napping may reduce AD risk. Given that this is the first MR study of multiple self-report and objective sleep traits on AD risk, findings should be replicated using independent samples when such data become available. [ABSTRACT FROM AUTHOR]

Published
2021
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47. 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, Nielson, Jonas B, additional, Olav Åsvold, Bjørn, 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, Debbie A, additional, Weedon, Michael N, additional, and Davey Smith, George, additional

Published
2019
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