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Article ; Online: Profile-likelihood Bayesian model averaging for two-sample summary data Mendelian randomization in the presence of horizontal pleiotropy.

Shapland, Chin Yang / Zhao, Qingyuan / Bowden, Jack

2022 Volume 41, Issue 6, Page(s) 1100–1119

Abstract: Two-sample summary data Mendelian randomization is a popular method for assessing causality in epidemiology, by using genetic variants as instrumental variables. If genes exert pleiotropic effects on the outcome not entirely through the exposure of ... ...

Abstract	Two-sample summary data Mendelian randomization is a popular method for assessing causality in epidemiology, by using genetic variants as instrumental variables. If genes exert pleiotropic effects on the outcome not entirely through the exposure of interest, this can lead to heterogeneous and (potentially) biased estimates of causal effect. We investigate the use of Bayesian model averaging to preferentially search the space of models with the highest posterior likelihood. We develop a Metropolis-Hasting algorithm to perform the search using the recently developed MR-RAPS as the basis for defining a posterior distribution that efficiently accounts for pleiotropic and weak instrument bias. We demonstrate how our general modeling approach can be extended from a standard one-component causal model to a two-component model, which allows a large proportion of SNPs to violate the InSIDE assumption. We use Monte Carlo simulations to illustrate our methods and compare it to several related approaches. We finish by applying our approach to investigate the causal role of cholesterol on the development age-related macular degeneration.
MeSH term(s)	Bayes Theorem ; Causality ; Genetic Pleiotropy ; Genetic Variation ; Humans ; Mendelian Randomization Analysis/methods ; Polymorphism, Single Nucleotide
Language	English
Publishing date	2022-01-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	843037-8
ISSN	1097-0258 ; 0277-6715
ISSN (online)	1097-0258
ISSN	0277-6715
DOI	10.1002/sim.9320
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Article: Using Mendelian Randomisation to Prioritise Candidate Maternal Metabolic Traits Influencing Offspring Birthweight.

Barry, Ciarrah-Jane Shannon / Lawlor, Deborah A / Shapland, Chin Yang / Sanderson, Eleanor / Borges, Maria Carolina

Metabolites

2022 Volume 12, Issue 6

Abstract: Marked physiological changes in pregnancy are essential to support foetal growth; however, evidence on the role of specific maternal metabolic traits from human studies is limited. We integrated Mendelian randomisation (MR) and metabolomics data to probe ...

Abstract	Marked physiological changes in pregnancy are essential to support foetal growth; however, evidence on the role of specific maternal metabolic traits from human studies is limited. We integrated Mendelian randomisation (MR) and metabolomics data to probe the effect of 46 maternal metabolic traits on offspring birthweight (
Language	English
Publishing date	2022-06-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662251-8
ISSN	2218-1989
ISSN	2218-1989
DOI	10.3390/metabo12060537
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Article ; Online: Structural models of genome-wide covariance identify multiple common dimensions in autism.

de Hoyos, Lucía / Barendse, Maria T / Schlag, Fenja / van Donkelaar, Marjolein M J / Verhoef, Ellen / Shapland, Chin Yang / Klassmann, Alexander / Buitelaar, Jan / Verhulst, Brad / Fisher, Simon E / Rai, Dheeraj / St Pourcain, Beate

Nature communications

2024 Volume 15, Issue 1, Page(s) 1770

Abstract: Common genetic variation has been associated with multiple phenotypic features in Autism Spectrum Disorder (ASD). However, our knowledge of shared genetic factor structures contributing to this highly heterogeneous phenotypic spectrum is limited. Here, ... ...

Abstract	Common genetic variation has been associated with multiple phenotypic features in Autism Spectrum Disorder (ASD). However, our knowledge of shared genetic factor structures contributing to this highly heterogeneous phenotypic spectrum is limited. Here, we developed and implemented a structural equation modelling framework to directly model genomic covariance across core and non-core ASD phenotypes, studying autistic individuals of European descent with a case-only design. We identified three independent genetic factors most strongly linked to language performance, behaviour and developmental motor delay, respectively, studying an autism community sample (N = 5331). The three-factorial structure was largely confirmed in independent ASD-simplex families (N = 1946), although we uncovered, in addition, simplex-specific genetic overlap between behaviour and language phenotypes. Multivariate models across cohorts revealed novel associations, including links between language and early mastering of self-feeding. Thus, the common genetic architecture in ASD is multi-dimensional with overarching genetic factors contributing, in combination with ascertainment-specific patterns, to phenotypic heterogeneity.
MeSH term(s)	Humans ; Autistic Disorder/genetics ; Autism Spectrum Disorder/genetics ; Phenotype ; Language ; Models, Structural
Language	English
Publishing date	2024-02-27
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-024-46128-8
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Article ; Online: The developmental genetic architecture of vocabulary skills during the first three years of life: Capturing emerging associations with later-life reading and cognition.

Verhoef, Ellen / Shapland, Chin Yang / Fisher, Simon E / Dale, Philip S / St Pourcain, Beate

PLoS genetics

2021 Volume 17, Issue 2, Page(s) e1009144

Abstract: Individual differences in early-life vocabulary measures are heritable and associated with subsequent reading and cognitive abilities, although the underlying mechanisms are little understood. Here, we (i) investigate the developmental genetic ... ...

Abstract	Individual differences in early-life vocabulary measures are heritable and associated with subsequent reading and cognitive abilities, although the underlying mechanisms are little understood. Here, we (i) investigate the developmental genetic architecture of expressive and receptive vocabulary in early-life and (ii) assess timing of emerging genetic associations with mid-childhood verbal and non-verbal skills. We studied longitudinally assessed early-life vocabulary measures (15-38 months) and later-life verbal and non-verbal skills (7-8 years) in up to 6,524 unrelated children from the population-based Avon Longitudinal Study of Parents and Children (ALSPAC) cohort. We dissected the phenotypic variance of rank-transformed scores into genetic and residual components by fitting multivariate structural equation models to genome-wide genetic-relationship matrices. Our findings show that the genetic architecture of early-life vocabulary involves multiple distinct genetic factors. Two of these genetic factors are developmentally stable and also contribute to genetic variation in mid-childhood skills: One genetic factor emerging with expressive vocabulary at 24 months (path coefficient: 0.32(SE = 0.06)) was also related to later-life reading (path coefficient: 0.25(SE = 0.12)) and verbal intelligence (path coefficient: 0.42(SE = 0.13)), explaining up to 17.9% of the phenotypic variation. A second, independent genetic factor emerging with receptive vocabulary at 38 months (path coefficient: 0.15(SE = 0.07)), was more generally linked to verbal and non-verbal cognitive abilities in mid-childhood (reading path coefficient: 0.57(SE = 0.07); verbal intelligence path coefficient: 0.60(0.10); performance intelligence path coefficient: 0.50(SE = 0.08)), accounting for up to 36.1% of the phenotypic variation and the majority of genetic variance in these later-life traits (≥66.4%). Thus, the genetic foundations of mid-childhood reading and cognitive abilities are diverse. They involve at least two independent genetic factors that emerge at different developmental stages during early language development and may implicate differences in cognitive processes that are already detectable during toddlerhood.
MeSH term(s)	Child ; Child, Preschool ; Cognition ; Cohort Studies ; Correlation of Data ; Female ; Genome-Wide Association Study ; Genotype ; Humans ; Infant ; Intelligence/genetics ; Language Development ; Longitudinal Studies ; Male ; Multivariate Analysis ; Phenotype ; Polymorphism, Single Nucleotide ; Reading ; Software ; Vocabulary
Language	English
Publishing date	2021-02-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2186725-2
ISSN	1553-7404 ; 1553-7390
ISSN (online)	1553-7404
ISSN	1553-7390
DOI	10.1371/journal.pgen.1009144
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Article ; Online: A Bayesian approach to Mendelian randomisation with dependent instruments.

Shapland, Chin Yang / Thompson, John R / Sheehan, Nuala A

Statistics in medicine

2018 Volume 38, Issue 6, Page(s) 985–1001

Abstract: Mendelian randomisation (MR) is a method for establishing causality between a risk factor and an outcome by using genetic variants as instrumental variables. In practice, the association between individual genetic variants and the risk factor is often ... ...

Abstract	Mendelian randomisation (MR) is a method for establishing causality between a risk factor and an outcome by using genetic variants as instrumental variables. In practice, the association between individual genetic variants and the risk factor is often weak, which may lead to a lack of precision in the MR and even biased MR estimates. Usually, the most significant variant within a genetic region is selected to represent the association with the risk factor, but there is no guarantee that this variant will be causal or that it will capture all of the genetic association within the region. It may be advantageous to use extra variants selected from the same region in the MR. The problem is to decide which variants to select. Rather than selecting a specific set of variants, we investigate the use of Bayesian model averaging (BMA) to average the MR over all possible combinations of genetic variants. Our simulations demonstrate that the BMA version of MR outperforms classical estimation with many dependent variants and performs much better than an MR based on variants selected by penalised regression. In further simulations, we investigate robustness to violations in the model assumptions and demonstrate sensitivity to the inclusion of invalid instruments. The method is illustrated by applying it to an MR of the effect of body mass index on blood pressure using SNPs in the FTO gene.
MeSH term(s)	Bayes Theorem ; Causality ; Computer Simulation ; Humans ; Linkage Disequilibrium/genetics ; Mendelian Randomization Analysis/methods ; Models, Statistical ; Polymorphism, Single Nucleotide/genetics ; Risk Factors
Language	English
Publishing date	2018-11-28
Publishing country	England
Document type	Journal Article
ZDB-ID	843037-8
ISSN	1097-0258 ; 0277-6715
ISSN (online)	1097-0258
ISSN	0277-6715
DOI	10.1002/sim.8029
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Article ; Online: Harnessing tissue-specific genetic variation to dissect putative causal pathways between body mass index and cardiometabolic phenotypes.

Leyden, Genevieve M / Shapland, Chin Yang / Davey Smith, George / Sanderson, Eleanor / Greenwood, Michael P / Murphy, David / Richardson, Tom G

American journal of human genetics

2022 Volume 109, Issue 2, Page(s) 240–252

Abstract: Body mass index (BMI) is a complex disease risk factor known to be influenced by genes acting via both metabolic pathways and appetite regulation. In this study, we aimed to gain insight into the phenotypic consequences of BMI-associated genetic variants, ...

Abstract	Body mass index (BMI) is a complex disease risk factor known to be influenced by genes acting via both metabolic pathways and appetite regulation. In this study, we aimed to gain insight into the phenotypic consequences of BMI-associated genetic variants, which may be mediated by their expression in different tissues. First, we harnessed meta-analyzed gene expression datasets derived from subcutaneous adipose (n = 1257) and brain (n = 1194) tissue to identify 86 and 140 loci, respectively, which provided evidence of genetic colocalization with BMI. These two sets of tissue-partitioned loci had differential effects with respect to waist-to-hip ratio, suggesting that the way they influence fat distribution might vary despite their having very similar average magnitudes of effect on BMI itself (adipose = 0.0148 and brain = 0.0149 standard deviation change in BMI per effect allele). For instance, BMI-associated variants colocalized with TBX15 expression in adipose tissue (posterior probability [PPA] = 0.97), but not when we used TBX15 expression data derived from brain tissue (PPA = 0.04) This gene putatively influences BMI via its role in skeletal development. Conversely, there were loci where BMI-associated variants provided evidence of colocalization with gene expression in brain tissue (e.g., NEGR1, PPA = 0.93), but not when we used data derived from adipose tissue, suggesting that these genes might be more likely to influence BMI via energy balance. Leveraging these tissue-partitioned variant sets through a multivariable Mendelian randomization framework provided strong evidence that the brain-tissue-derived variants are predominantly responsible for driving the genetically predicted effects of BMI on cardiovascular-disease endpoints (e.g., coronary artery disease: odds ratio = 1.05, 95% confidence interval = 1.04-1.07, p = 4.67 × 10
MeSH term(s)	Adipose Tissue/metabolism ; Adipose Tissue/pathology ; Body Mass Index ; Brain/metabolism ; Brain/pathology ; Cell Adhesion Molecules, Neuronal/genetics ; Cell Adhesion Molecules, Neuronal/metabolism ; Coronary Artery Disease/genetics ; Coronary Artery Disease/metabolism ; Coronary Artery Disease/pathology ; Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/metabolism ; Diabetes Mellitus, Type 2/pathology ; GPI-Linked Proteins/genetics ; GPI-Linked Proteins/metabolism ; Gene Expression Profiling ; Gene Expression Regulation ; Genetic Loci ; Genetic Variation ; Genome, Human ; Genome-Wide Association Study ; Humans ; Mendelian Randomization Analysis ; Metabolic Networks and Pathways/genetics ; Obesity/genetics ; Obesity/metabolism ; Obesity/pathology ; Stroke Volume/physiology ; T-Box Domain Proteins/genetics ; T-Box Domain Proteins/metabolism ; Waist-Hip Ratio
Chemical Substances	Cell Adhesion Molecules, Neuronal ; GPI-Linked Proteins ; NEGR1 protein, human ; T-Box Domain Proteins ; TBX15 protein, human
Language	English
Publishing date	2022-01-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	219384-x
ISSN	1537-6605 ; 0002-9297
ISSN (online)	1537-6605
ISSN	0002-9297
DOI	10.1016/j.ajhg.2021.12.013
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Article ; Online: The developmental origins of genetic factors influencing language and literacy: Associations with early-childhood vocabulary.

Verhoef, Ellen / Shapland, Chin Yang / Fisher, Simon E / Dale, Philip S / St Pourcain, Beate

Journal of child psychology and psychiatry, and allied disciplines

2020 Volume 62, Issue 6, Page(s) 728–738

Abstract: Background: The heritability of language and literacy skills increases from early-childhood to adolescence. The underlying mechanisms are little understood and may involve (a) the amplification of genetic influences contributing to early language ... ...

Abstract	Background: The heritability of language and literacy skills increases from early-childhood to adolescence. The underlying mechanisms are little understood and may involve (a) the amplification of genetic influences contributing to early language abilities, and/or (b) the emergence of novel genetic factors (innovation). Here, we investigate the developmental origins of genetic factors influencing mid-childhood/early-adolescent language and literacy. We evaluate evidence for the amplification of early-childhood genetic factors for vocabulary, in addition to genetic innovation processes. Methods: Expressive and receptive vocabulary scores at 38 months, thirteen language- and literacy-related abilities and nonverbal cognition (7-13 years) were assessed in unrelated children from the Avon Longitudinal Study of Parents and Children (ALSPAC, N Results: We observed little support for the emergence of novel genetic sources for language, literacy or cognitive abilities during mid-childhood or early adolescence. Instead, genetic factors of early-childhood vocabulary, especially those unique to receptive skills, were amplified and represented the majority of genetic variance underlying many of these later complex skills (≤99%). The most predictive early genetic factor accounted for 29.4%(SE = 12.9%) to 45.1%(SE = 7.6%) of the phenotypic variation in verbal intelligence and literacy skills, but also for 25.7%(SE = 6.4%) in performance intelligence, while explaining only a fraction of the phenotypic variation in receptive vocabulary (3.9%(SE = 1.8%)). Conclusions: Genetic factors contributing to many complex skills during mid-childhood and early adolescence, including literacy, verbal cognition and nonverbal cognition, originate developmentally in early-childhood and are captured by receptive vocabulary. This suggests developmental genetic stability and overarching aetiological mechanisms.
MeSH term(s)	Adolescent ; Child ; Humans ; Language ; Language Development ; Literacy ; Longitudinal Studies ; Vocabulary
Language	English
Publishing date	2020-09-14
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218136-8
ISSN	1469-7610 ; 0021-9630 ; 0373-8086
ISSN (online)	1469-7610
ISSN	0021-9630 ; 0373-8086
DOI	10.1111/jcpp.13327
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Article ; Online: Discordant associations of educational attainment with ASD and ADHD implicate a polygenic form of pleiotropy.

Verhoef, Ellen / Grove, Jakob / Shapland, Chin Yang / Demontis, Ditte / Burgess, Stephen / Rai, Dheeraj / Børglum, Anders D / St Pourcain, Beate

Nature communications

2021 Volume 12, Issue 1, Page(s) 6534

Abstract: Autism Spectrum Disorder (ASD) and Attention-Deficit/Hyperactivity Disorder (ADHD) are complex co-occurring neurodevelopmental conditions. Their genetic architectures reveal striking similarities but also differences, including strong, discordant ... ...

Abstract	Autism Spectrum Disorder (ASD) and Attention-Deficit/Hyperactivity Disorder (ADHD) are complex co-occurring neurodevelopmental conditions. Their genetic architectures reveal striking similarities but also differences, including strong, discordant polygenic associations with educational attainment (EA). To study genetic mechanisms that present as ASD-related positive and ADHD-related negative genetic correlations with EA, we carry out multivariable regression analyses using genome-wide summary statistics (N = 10,610-766,345). Our results show that EA-related genetic variation is shared across ASD and ADHD architectures, involving identical marker alleles. However, the polygenic association profile with EA, across shared marker alleles, is discordant for ASD versus ADHD risk, indicating independent effects. At the single-variant level, our results suggest either biological pleiotropy or co-localisation of different risk variants, implicating MIR19A/19B microRNA mechanisms. At the polygenic level, they point to a polygenic form of pleiotropy that contributes to the detectable genome-wide correlation between ASD and ADHD and is consistent with effect cancellation across EA-related regions.
MeSH term(s)	Attention Deficit Disorder with Hyperactivity/genetics ; Attention Deficit Disorder with Hyperactivity/pathology ; Autism Spectrum Disorder/genetics ; Autism Spectrum Disorder/pathology ; Female ; Genetic Predisposition to Disease/genetics ; Genome-Wide Association Study ; Humans ; Male ; Polymorphism, Single Nucleotide/genetics ; Regression Analysis
Language	English
Publishing date	2021-11-11
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-021-26755-1
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Article: Multivariate genome-wide covariance analyses of literacy, language and working memory skills reveal distinct etiologies.

Shapland, Chin Yang / Verhoef, Ellen / Davey Smith, George / Fisher, Simon E / Verhulst, Brad / Dale, Philip S / St Pourcain, Beate

NPJ science of learning

2021 Volume 6, Issue 1, Page(s) 23

Abstract: Several abilities outside literacy proper are associated with reading and spelling, both phenotypically and genetically, though our knowledge of multivariate genomic covariance structures is incomplete. Here, we introduce structural models describing ... ...

Abstract	Several abilities outside literacy proper are associated with reading and spelling, both phenotypically and genetically, though our knowledge of multivariate genomic covariance structures is incomplete. Here, we introduce structural models describing genetic and residual influences between traits to study multivariate links across measures of literacy, phonological awareness, oral language, and phonological working memory (PWM) in unrelated UK youth (8-13 years, N = 6453). We find that all phenotypes share a large proportion of underlying genetic variation, although especially oral language and PWM reveal substantial differences in their genetic variance composition with substantial trait-specific genetic influences. Multivariate genetic and residual trait covariance showed concordant patterns, except for marked differences between oral language and literacy/phonological awareness, where strong genetic links contrasted near-zero residual overlap. These findings suggest differences in etiological mechanisms, acting beyond a pleiotropic set of genetic variants, and implicate variation in trait modifiability even among phenotypes that have high genetic correlations.
Language	English
Publishing date	2021-08-19
Publishing country	England
Document type	Journal Article
ISSN	2056-7936
ISSN	2056-7936
DOI	10.1038/s41539-021-00101-y
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Article ; Online: Genome-Wide Analyses of Vocabulary Size in Infancy and Toddlerhood: Associations With Attention-Deficit/Hyperactivity Disorder, Literacy, and Cognition-Related Traits.

Verhoef, Ellen / Allegrini, Andrea G / Jansen, Philip R / Lange, Katherine / Wang, Carol A / Morgan, Angela T / Ahluwalia, Tarunveer S / Symeonides, Christos / Eising, Else / Franken, Marie-Christine / Hypponen, Elina / Mansell, Toby / Olislagers, Mitchell / Omerovic, Emina / Rimfeld, Kaili / Schlag, Fenja / Selzam, Saskia / Shapland, Chin Yang / Tiemeier, Henning /

Whitehouse, Andrew J O / Saffery, Richard / Bønnelykke, Klaus / Reilly, Sheena / Pennell, Craig E / Wake, Melissa / Cecil, Charlotte A M / Plomin, Robert / Fisher, Simon E / St Pourcain, Beate

Biological psychiatry

2023 Volume 95, Issue 9, Page(s) 859–869

Abstract: Background: The number of words children produce (expressive vocabulary) and understand (receptive vocabulary) changes rapidly during early development, partially due to genetic factors. Here, we performed a meta-genome-wide association study of ... ...

Abstract	Background: The number of words children produce (expressive vocabulary) and understand (receptive vocabulary) changes rapidly during early development, partially due to genetic factors. Here, we performed a meta-genome-wide association study of vocabulary acquisition and investigated polygenic overlap with literacy, cognition, developmental phenotypes, and neurodevelopmental conditions, including attention-deficit/hyperactivity disorder (ADHD). Methods: We studied 37,913 parent-reported vocabulary size measures (English, Dutch, Danish) for 17,298 children of European descent. Meta-analyses were performed for early-phase expressive (infancy, 15-18 months), late-phase expressive (toddlerhood, 24-38 months), and late-phase receptive (toddlerhood, 24-38 months) vocabulary. Subsequently, we estimated single nucleotide polymorphism-based heritability (SNP-h Results: Early-life vocabulary size was modestly heritable (SNP-h Conclusions: The genetic architecture of early-life vocabulary changes during development, shaping polygenic association patterns with later-life ADHD, literacy, and cognition-related traits.
MeSH term(s)	Adolescent ; Humans ; Infant ; Attention Deficit Disorder with Hyperactivity/genetics ; Attention Deficit Disorder with Hyperactivity/diagnosis ; Cognition ; Genome-Wide Association Study ; Literacy ; Longitudinal Studies ; Phenotype ; Vocabulary
Language	English
Publishing date	2023-12-07
Publishing country	United States
Document type	Journal Article ; Meta-Analysis
ZDB-ID	209434-4
ISSN	1873-2402 ; 0006-3223
ISSN (online)	1873-2402
ISSN	0006-3223
DOI	10.1016/j.biopsych.2023.11.025
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