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Article ; Online: Letter to the Editor From Richmond et al: "Sleep Duration and Visceral Adipose Tissue: Linear and Nonlinear Mendelian Randomization Analyses".

Richmond, Rebecca C / Hamilton, Fergus W / Davey Smith, George

The Journal of clinical endocrinology and metabolism

2023 Volume 109, Issue 3, Page(s) e1316–e1317

MeSH term(s)	Humans ; Sleep Duration ; Mendelian Randomization Analysis ; Sleep ; Obesity, Abdominal ; Genome-Wide Association Study
Language	English
Publishing date	2023-10-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	3029-6
ISSN	1945-7197 ; 0021-972X
ISSN (online)	1945-7197
ISSN	0021-972X
DOI	10.1210/clinem/dgad598
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Article ; Online: Mendelian Randomization: Concepts and Scope.

Richmond, Rebecca C / Davey Smith, George

Cold Spring Harbor perspectives in medicine

2022 Volume 12, Issue 1

Abstract: Mendelian randomization (MR) is a method of studying the causal effects of modifiable exposures (i.e., potential risk factors) on health, social, and economic outcomes using genetic variants associated with the specific exposures of interest. MR provides ...

Abstract	Mendelian randomization (MR) is a method of studying the causal effects of modifiable exposures (i.e., potential risk factors) on health, social, and economic outcomes using genetic variants associated with the specific exposures of interest. MR provides a more robust understanding of the influence of these exposures on outcomes because germline genetic variants are randomly inherited from parents to offspring and, as a result, should not be related to potential confounding factors that influence exposure-outcome associations. The genetic variant can therefore be used as a tool to link the proposed risk factor and outcome, and to estimate this effect with less confounding and bias than conventional epidemiological approaches. We describe the scope of MR, highlighting the range of applications being made possible as genetic data sets and resources become larger and more freely available. We outline the MR approach in detail, covering concepts, assumptions, and estimation methods. We cover some common misconceptions, provide strategies for overcoming violation of assumptions, and discuss future prospects for extending the clinical applicability, methodological innovations, robustness, and generalizability of MR findings.
MeSH term(s)	Causality ; Mendelian Randomization Analysis ; Risk Factors
Language	English
Publishing date	2022-01-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	2157-1422
ISSN (online)	2157-1422
DOI	10.1101/cshperspect.a040501
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Article ; Online: Sex steroid hormones and risk of breast cancer: a two-sample Mendelian randomization study.

Nounu, Aayah / Kar, Siddhartha P / Relton, Caroline L / Richmond, Rebecca C

Breast cancer research : BCR

2022 Volume 24, Issue 1, Page(s) 66

Abstract: Background: Breast cancer (BC) has the highest cancer incidence and mortality in women worldwide. Observational epidemiological studies suggest a positive association between testosterone, estradiol, dehydroepiandrosterone sulphate (DHEAS) and other sex ...

Abstract	Background: Breast cancer (BC) has the highest cancer incidence and mortality in women worldwide. Observational epidemiological studies suggest a positive association between testosterone, estradiol, dehydroepiandrosterone sulphate (DHEAS) and other sex steroid hormones with postmenopausal BC. We used a two-sample Mendelian randomization analysis to investigate this association. Methods: Genetic instruments for nine sex steroid hormones and sex hormone-binding globulin (SHBG) were obtained from genome-wide association studies (GWAS) of UK Biobank (total testosterone (TT) N: 230,454, bioavailable testosterone (BT) N: 188,507 and SHBG N: 189,473), The United Kingdom Household Longitudinal Study (DHEAS N: 9722), the LIFE-Adult and LIFE-Heart cohorts (estradiol N: 2607, androstenedione N: 711, aldosterone N: 685, progesterone N: 1259 and 17-hydroxyprogesterone N: 711) and the CORtisol NETwork (CORNET) consortium (cortisol N: 25,314). Outcome GWAS summary statistics were obtained from the Breast Cancer Association Consortium (BCAC) for overall BC risk (N: 122,977 cases and 105,974 controls) and subtype-specific analyses. Results: We found that a standard deviation (SD) increase in TT, BT and estradiol increased the risk of overall BC (OR 1.14, 95% CI 1.09-1.21, OR 1.19, 95% CI 1.07-1.33 and OR 1.03, 95% CI 1.01-1.06, respectively) and ER + BC (OR 1.19, 95% CI 1.12-1.27, OR 1.25, 95% CI 1.11-1.40 and OR 1.06, 95% CI 1.03-1.09, respectively). An SD increase in DHEAS also increased ER + BC risk (OR 1.09, 95% CI 1.03-1.16). Subtype-specific analyses showed similar associations with ER+ expressing subtypes: luminal A-like BC, luminal B-like BC and luminal B/HER2-negative-like BC. Conclusions: TT, BT, DHEAS and estradiol increase the risk of ER+ type BCs similar to observational studies. Understanding the role of sex steroid hormones in BC risk, particularly subtype-specific risks, highlights the potential importance of attempts to modify and/or monitor hormone levels in order to prevent BC.
MeSH term(s)	17-alpha-Hydroxyprogesterone ; Adult ; Aldosterone ; Androstenedione ; Breast Neoplasms/epidemiology ; Breast Neoplasms/genetics ; Dehydroepiandrosterone Sulfate ; Estradiol ; Female ; Genome-Wide Association Study ; Gonadal Steroid Hormones ; Humans ; Hydrocortisone ; Longitudinal Studies ; Mendelian Randomization Analysis ; Progesterone ; Sex Hormone-Binding Globulin ; Testosterone
Chemical Substances	Gonadal Steroid Hormones ; Sex Hormone-Binding Globulin ; Testosterone (3XMK78S47O) ; Androstenedione (409J2J96VR) ; Aldosterone (4964P6T9RB) ; Progesterone (4G7DS2Q64Y) ; Estradiol (4TI98Z838E) ; Dehydroepiandrosterone Sulfate (57B09Q7FJR) ; 17-alpha-Hydroxyprogesterone (68-96-2) ; Hydrocortisone (WI4X0X7BPJ)
Language	English
Publishing date	2022-10-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2015059-3
ISSN	1465-542X ; 1465-5411
ISSN (online)	1465-542X
ISSN	1465-5411
DOI	10.1186/s13058-022-01553-9
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Article ; Online: Letter regarding, "Association between the use of aspirin and risk of lung cancer: results from pooled cohorts and Mendelian randomization analyses".

Nounu, Aayah / Walker, Venexia / Richmond, Rebecca C

Journal of cancer research and clinical oncology

2021 Volume 147, Issue 7, Page(s) 2171–2173

MeSH term(s)	Aspirin/adverse effects ; Genome-Wide Association Study ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/epidemiology ; Lung Neoplasms/genetics ; Mendelian Randomization Analysis
Chemical Substances	Aspirin (R16CO5Y76E)
Language	English
Publishing date	2021-01-12
Publishing country	Germany
Document type	Letter ; Comment
ZDB-ID	134792-5
ISSN	1432-1335 ; 0171-5216 ; 0084-5353 ; 0943-9382
ISSN (online)	1432-1335
ISSN	0171-5216 ; 0084-5353 ; 0943-9382
DOI	10.1007/s00432-020-03508-z
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Article ; Online: Correction to: Letter regarding, "Association between the use of aspirin and risk of lung cancer: results from pooled cohorts and Mendelian randomization analyses".

Nounu, Aayah / Walker, Venexia / Richmond, Rebecca C

Journal of cancer research and clinical oncology

2021 Volume 147, Issue 7, Page(s) 2175

Language	English
Publishing date	2021-02-27
Publishing country	Germany
Document type	Published Erratum
ZDB-ID	134792-5
ISSN	1432-1335 ; 0171-5216 ; 0084-5353 ; 0943-9382
ISSN (online)	1432-1335
ISSN	0171-5216 ; 0084-5353 ; 0943-9382
DOI	10.1007/s00432-021-03636-0
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Article ; Online: Estimating the health impact of nicotine exposure by dissecting the effects of nicotine versus non-nicotine constituents of tobacco smoke: A multivariable Mendelian randomisation study.

Khouja, Jasmine N / Sanderson, Eleanor / Wootton, Robyn E / Taylor, Amy E / Church, Billy A / Richmond, Rebecca C / Munafò, Marcus R

PLoS genetics

2024 Volume 20, Issue 2, Page(s) e1011157

Abstract: The detrimental health effects of smoking are well-known, but the impact of regular nicotine use without exposure to the other constituents of tobacco is less clear. Given the increasing daily use of alternative nicotine delivery systems, such as e- ... ...

Abstract	The detrimental health effects of smoking are well-known, but the impact of regular nicotine use without exposure to the other constituents of tobacco is less clear. Given the increasing daily use of alternative nicotine delivery systems, such as e-cigarettes, it is increasingly important to understand and separate the effects of nicotine use from the impact of tobacco smoke exposure. Using a multivariable Mendelian randomisation framework, we explored the direct effects of nicotine compared with the non-nicotine constituents of tobacco smoke on health outcomes (lung cancer, chronic obstructive pulmonary disease [COPD], forced expiratory volume in one second [FEV-1], forced vital capacity [FVC], coronary heart disease [CHD], and heart rate [HR]). We used Genome-Wide Association Study (GWAS) summary statistics from Buchwald and colleagues, the GWAS and Sequencing Consortium of Alcohol and Nicotine, the International Lung Cancer Consortium, and UK Biobank. Increased nicotine metabolism increased the risk of COPD, lung cancer, and lung function in the univariable analysis. However, when accounting for smoking heaviness in the multivariable analysis, we found that increased nicotine metabolite ratio (indicative of decreased nicotine exposure per cigarette smoked) decreases heart rate (b = -0.30, 95% CI -0.50 to -0.10) and lung function (b = -33.33, 95% CI -41.76 to -24.90). There was no clear evidence of an effect on the remaining outcomes. The results suggest that these smoking-related outcomes are not due to nicotine exposure but are caused by the other components of tobacco smoke; however, there are multiple potential sources of bias, and the results should be triangulated using evidence from a range of methodologies.
MeSH term(s)	Humans ; Electronic Nicotine Delivery Systems ; Genome-Wide Association Study ; Lung Neoplasms/genetics ; Nicotine/adverse effects ; Nicotine/analysis ; Pulmonary Disease, Chronic Obstructive/genetics ; Smoking/adverse effects ; Smoking/genetics ; Tobacco Products ; Tobacco Smoke Pollution ; Mendelian Randomization Analysis
Chemical Substances	Nicotine (6M3C89ZY6R) ; Tobacco Smoke Pollution
Language	English
Publishing date	2024-02-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	2186725-2
ISSN	1553-7404 ; 1553-7390
ISSN (online)	1553-7404
ISSN	1553-7390
DOI	10.1371/journal.pgen.1011157
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Article: An observational analysis of risk factors associated with symptomatic third molar teeth.

Bruce, Douglas / Dudding, Tom / Gormley, Mark / Richmond, Rebecca C / Haworth, Simon

Wellcome open research

2023 Volume 7, Page(s) 71

Abstract: Background: Third molar teeth (wisdom teeth) are a common cause of pain and infection in young adults. The study aimed to describe the prevalence of symptomatic third molar teeth and identify factors which predispose to third molar symptoms in a birth ... ...

Abstract	Background: Third molar teeth (wisdom teeth) are a common cause of pain and infection in young adults. The study aimed to describe the prevalence of symptomatic third molar teeth and identify factors which predispose to third molar symptoms in a birth cohort. Methods: An observational study was undertaken nested in the Avon Longitudinal Study of Parents and Children (ALSPAC), a birth cohort based in south west England. The main outcomes were self-reported third molar pain, swelling and treatment for third molar problems, taken from questionnaires completed at age 23 years. The exposures including sex, dental history, socioeconomic status, diet, and genetic factors were obtained from earlier ALSPAC data. Results: In total 4,222 ALSPAC participants responded to one or more questions about third molar teeth. The final sample included more female participants than male participants. The majority of participants (56.6%) reported at least one episode of pain associated with their third molars. Females had greater odds than males of reporting swelling (adjusted odds ratio (OR) 1.97; 95%confidence interval (CI) 1.56, 2.51), pain (adjusted OR=1.96; 95%CI 1.56, 2.51) and receiving both non-surgical and surgical treatment (adjusted OR=2.30; 95%CI 1.62, 3.35, adjusted OR=1.54; 95%CI 1.17, 2.06 respectively). Participants with previously filled teeth had greater odds of third molar extraction. There were no strong associations between index of multiple deprivation (IMD) score or sugar intake and the third molar outcomes. There was weak evidence for a genetic contribution to third molar pain. Conclusions: Symptomatic third molars are common in this age group, with over half of the participants reporting pain or other symptoms. Female participants had greater odds for third molar pain, swelling and treatment.
Language	English
Publishing date	2023-07-17
Publishing country	England
Document type	Journal Article
ISSN	2398-502X
ISSN	2398-502X
DOI	10.12688/wellcomeopenres.17673.2
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Article ; Online: Establishing the relationships between adiposity and reproductive factors: a multivariable Mendelian randomization analysis.

Prince, Claire / Howe, Laura D / Sharp, Gemma C / Fraser, Abigail / Richmond, Rebecca C

BMC medicine

2023 Volume 21, Issue 1, Page(s) 350

Abstract: Background: Few studies have investigated associations between adiposity and reproductive factors using causal methods, both of which have a number of consequences on women's health. Here we assess whether adiposity at different points in the lifecourse ...

Abstract	Background: Few studies have investigated associations between adiposity and reproductive factors using causal methods, both of which have a number of consequences on women's health. Here we assess whether adiposity at different points in the lifecourse affects reproductive factors differently and independently, and the plausibility of the impact of reproductive factors on adiposity. Methods: We used genetic data from UK Biobank (273,238 women) and other consortia (EGG, GIANT, ReproGen and SSGAC) for eight reproductive factors: age at menarche, age at menopause, age at first birth, age at last birth, number of births, being parous, age first had sexual intercourse and lifetime number of sexual partners, and two adiposity traits: childhood and adulthood body size. We applied multivariable Mendelian randomization to account for genetic correlation and to estimate the causal effects of childhood and adulthood adiposity, independently of each other, on reproductive factors. Additionally, we estimated the effects of reproductive factors, independently of other relevant reproductive factors, on adulthood adiposity. Results: We found a higher childhood body size leads to an earlier age at menarche, and an earlier age at menarche leads to a higher adulthood body size. Furthermore, we find contrasting and independent effects of childhood and adulthood body size on age at first birth (beta 0.22 SD (95% confidence interval: 0.14, 0.31) vs - 2.49 (- 2.93, - 2.06) per 1 SD increase), age at last birth (0.13 (0.06,0.21) vs - 1.86 (- 2.23, - 1.48) per 1 SD increase), age at menopause (0.17 (0.09, 0.25) vs - 0.99 (- 1.39, - 0.59) per 1 SD increase), and likelihood of having children (Odds ratio 0.97 (0.95, 1.00) vs 1.20 (1.06, 1.37) per 1 SD increase). Conclusions: Our findings demonstrate the importance of considering a lifecourse approach when investigating the inter-relationships between adiposity measures and reproductive events, as well as the use of 'age specific' genetic instruments when evaluating lifecourse hypotheses in a Mendelian randomization framework.
MeSH term(s)	Female ; Humans ; Adiposity/genetics ; Menarche/genetics ; Mendelian Randomization Analysis ; Menopause/genetics ; Obesity
Language	English
Publishing date	2023-09-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2131669-7
ISSN	1741-7015 ; 1741-7015
ISSN (online)	1741-7015
ISSN	1741-7015
DOI	10.1186/s12916-023-03051-x
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Article ; Online: Establishing causal relationships between sleep and adiposity traits using Mendelian randomization.

Hayes, Bryony L / Vabistsevits, Marina / Martin, Richard M / Lawlor, Deborah A / Richmond, Rebecca C / Robinson, Timothy

Obesity (Silver Spring, Md.)

2023 Volume 31, Issue 3, Page(s) 861–870

Abstract: Objective: The aim of this study was to systematically evaluate the direction of any potential causal effect between sleep and adiposity traits.: Methods: Two-sample Mendelian randomization was used to assess the association of genetically predicted ... ...

Abstract	Objective: The aim of this study was to systematically evaluate the direction of any potential causal effect between sleep and adiposity traits. Methods: Two-sample Mendelian randomization was used to assess the association of genetically predicted sleep traits with adiposity and vice versa. Using data from UK Biobank and 23andMe, the sleep traits explored were morning preference (chronotype; N = 697,828), insomnia (N = 1,331,010), sleep duration (N = 446,118), napping (N = 452,633), and daytime sleepiness (N = 452,071). Using data from the Genetic Investigation of ANthropometric Traits (GIANT) and Early Growth Genetics (EGG) consortia, the adiposity traits explored were adult BMI, hip circumference (HC), waist circumference (WC), waist-hip ratio (WHR; N = 322,154), and childhood BMI (N = 35,668). Results: This study found evidence that insomnia symptoms increased mean WC, BMI, and WHR (difference in means, WC = 0.39 SD [95% CI: 0.13-0.64], BMI = 0.47 SD [95% CI: 0.22-0.73], and WHR = 0.34 SD [95% CI: 0.16-0.52]). Napping increased mean WHR (0.23 SD [95% CI: 0.08-0.39]). Higher HC, WC, and adult BMI increased odds of daytime sleepiness (HC = 0.02 SD [95% CI: 0.01-0.04], WC = 0.04 SD [95% CI: 0.01-0.06], and BMI 0.02 SD [95% CI: 0.00-0.04]). This study also found that higher mean childhood BMI resulted in lower odds of napping (-0.01 SD [95% CI: 0.02-0.00]). Conclusions: The effects of insomnia on adiposity and of adiposity on daytime sleepiness suggest that poor sleep and weight gain may contribute to a feedback loop that could be detrimental to overall health.
MeSH term(s)	Adult ; Child ; Humans ; Adiposity/genetics ; Body Mass Index ; Disorders of Excessive Somnolence ; Mendelian Randomization Analysis ; Obesity/genetics ; Risk Factors ; Sleep ; Sleep Initiation and Maintenance Disorders ; Waist-Hip Ratio
Language	English
Publishing date	2023-02-15
Publishing country	United States
Document type	Journal Article ; Meta-Analysis ; Research Support, Non-U.S. Gov't
ZDB-ID	2230457-5
ISSN	1930-739X ; 1071-7323 ; 1930-7381
ISSN (online)	1930-739X
ISSN	1071-7323 ; 1930-7381
DOI	10.1002/oby.23668
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Article ; Online: Mendelian randomization analysis of the causal impact of body mass index and waist-hip ratio on rates of hospital admission.

Hazewinkel, Audinga-Dea / Richmond, Rebecca C / Wade, Kaitlin H / Dixon, Padraig

Economics and human biology

2021 Volume 44, Page(s) 101088

Abstract: We analyze how measures of adiposity - body mass index (BMI) and waist hip ratio (WHR) - causally influence rates of hospital admission. Conventional analyses of this relationship are susceptible to omitted variable bias from variables that jointly ... ...

Abstract	We analyze how measures of adiposity - body mass index (BMI) and waist hip ratio (WHR) - causally influence rates of hospital admission. Conventional analyses of this relationship are susceptible to omitted variable bias from variables that jointly influence both hospital admission and adipose status. We implement a novel quasi-Poisson instrumental variable model in a Mendelian randomization framework, identifying causal effects from random perturbations to germline genetic variation. We estimate the individual and joint effects of BMI, WHR, and WHR adjusted for BMI. We also implement multivariable instrumental variable methods in which the causal effect of one exposure is estimated conditionally on the causal effect of another exposure. Data on 310,471 participants and over 550,000 inpatient admissions in the UK Biobank were used to perform one-sample and two-sample Mendelian randomization analyses. The results supported a causal role of adiposity on hospital admissions, with consistency across all estimates and sensitivity analyses. Point estimates were generally larger than estimates from comparable observational specifications. We observed an attenuation of the BMI effect when adjusting for WHR in the multivariable Mendelian randomization analyses, suggesting that an adverse fat distribution, rather than a higher BMI itself, may drive the relationship between adiposity and risk of hospital admission.
MeSH term(s)	Adiposity/genetics ; Body Mass Index ; Hospitals ; Humans ; Mendelian Randomization Analysis ; Polymorphism, Single Nucleotide ; Waist-Hip Ratio
Language	English
Publishing date	2021-11-26
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2099749-8
ISSN	1873-6130 ; 1570-677X
ISSN (online)	1873-6130
ISSN	1570-677X
DOI	10.1016/j.ehb.2021.101088
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