Common health conditions in childhood and adolescence, school absence, and educational attainment: Mendelian randomization study

AbstractGood health is positively related to children’s educational outcomes, but relationships may not be causal. Demonstrating a causal influence would strongly support childhood and adolescent health as important for education policy. We applied genetic causal inference methods to assess the causal relationship of common health conditions at age 10 (primary/elementary school) and 13 (mid-secondary/mid-high school) with educational attainment at 16 and school absence at 14–16. Participants were 6113 children from the Avon Longitudinal Study of Parents and Children (ALSPAC). Exposures were symptoms of attention-deficit hyperactivity disorder (ADHD), autism spectrum disorder (ASD), depression, asthma, migraines and BMI. Genetic liability for these conditions and BMI was indexed by polygenic scores. In non-genetic, multivariate-adjusted models, all health conditions except asthma and migraines were associated with poorer attainment and greater school absence. School absence substantially mediated effects of BMI (39.9% for BMI at 13) and migraines (72.0% at 10), on attainment with more modest mediation for emotional and neurodevelopmental conditions. In genetic models, a unit increase in standardized BMI at 10 predicted a 0.19 S.D. decrease (95% CI: 0.11, 0.28) in attainment at 16, equivalent to around a 1/3 grade lower in all subjects, and 8.7% more school absence (95% CI:1.8%,16.1%). Associations were similar at 13. Genetic liability for ADHD predicted lower attainment but not more absence. Triangulation across multiple approaches supports a causal, negative influence on educational outcomes of BMI and ADHD, but not of ASD, depression, asthma or migraine. Higher BMI in childhood and adolescence may causally impair educational outcomes.

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Common health conditions in childhood and adolescence, school absence, and educational attainment: Mendelian randomization study

10.1101/19012906 ◽

2019 ◽

Author(s):

Amanda Hughes ◽

Kaitlin H Wade ◽

Frances Rice ◽

Matt Dickson ◽

Alisha Davies ◽

...

Keyword(s):

Autism Spectrum Disorder ◽

Secondary School ◽

Educational Attainment ◽

Mendelian Randomization ◽

Negative Influence ◽

Autism Spectrum ◽

Health Conditions ◽

Childhood And Adolescence ◽

List Type ◽

School Absence

ABSTRACTObjectivesTo assess the causal relationship of different health conditions in childhood and adolescence with educational attainment and school absence.DesignLongitudinal observational study and Mendelian randomization (MR) analyses.SettingAvon Longitudinal Study of Parents and Children (ALSPAC), a population sample of children from South-West England born in 1991-1992.Participants6113 unrelated children with available GCSE records and genetic data (50% female).ExposuresSix common health conditions with known genetic markers measured at age 10 (primary school) and 13 (mid-secondary school). These were: symptoms of Attention-Deficit Hyperactivity Disorder (ADHD), Autism Spectrum Disorder (ASD), depression, asthma, migraines and BMI. Genetic liability for these conditions and BMI was indexed by polygenic scores.Main outcome measuresEducational attainment at age 16 (total GCSE and equivalents points score), school absence at age 14-16.ResultsIn multivariate-adjusted observational models, all health conditions except asthma and migraines were associated with poorer educational attainment and greater school absence. Substantial mediation by school absence was seen for BMI (e.g. 35.6% for BMI at 13) and migraines (67% at age 10), with more modest mediation for behavioural and neurodevelopmental measures of health. In genetic models, a unit increase in genetically instrumented BMI z-score at age 10 predicted a 0.19 S.D. decrease (95% CI: −0.28 to −0.11) in attainment at 16, equivalent to around a 1/3 grade difference in each subject. It also predicted 8.6% more school absence (95% CI:1.3%, 16.5%). Similar associations were seen for BMI at age 13. Consistent with previous work, genetic liability for ADHD predicted lower educational attainment, but did not clearly increase school absence.ConclusionsTriangulation across multiple approaches supported a causal, negative influence of higher BMI on educational attainment and school absence. Further research is required to understand the mechanisms linking higher BMI with school absence and attainment.What is already known on this topicOn average, children with common health conditions have worse educational attainmentIt is unclear whether all health-attainment and health-absenteeism associations are causal, or reflect confounding by social and economic circumstancesWe do not know how much health-related school absenteeism contributes to these associationsWhat this study addsResults support a negative influence of high BMI in secondary school on educational attainment (GCSEs) and absenteeismAbsenteeism substantially mediated BMI-GCSE associations, suggesting a target for interventionThere was less evidence for causal effects of Autism Spectrum Disorder, depressive symptoms, asthma or migraines on attainment and absenteeismContribution of absenteeism to ADHD-GCSE associations was modest, suggesting interventions should target other mechanisms

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Developmental milestones in early childhood and genetic liability to neurodevelopmental disorders

10.31234/osf.io/x8wst ◽

2020 ◽

Author(s):

Laurie John Hannigan ◽

Ragna Bugge Askeland ◽

Helga Ask ◽

Martin Tesli ◽

Elizabeth Corfield ◽

...

Keyword(s):

Language Development ◽

Motor Development ◽

Neurodevelopmental Disorders ◽

Autism Spectrum ◽

Probit Regression ◽

Developmental Milestones ◽

Genetic Liability ◽

Polygenic Scores ◽

Walking Age ◽

Children First

BackgroundEarly developmental milestones, such as the age at first walking or talking, are associated with later diagnoses of neurodevelopmental disorders, but the relationship to genetic risk for neurodevelopmental disorders are unknown. Here, we investigate associations between genetic liability to autism spectrum disorder (autism), attention deficit hyperactivity disorder (ADHD), and schizophrenia and attainment of early-life language and motor development milestones.MethodsWe use data from a genotyped sub-set (N = 15 205) of children in the Norwegian Mother, Father and Child Cohort Study (MoBa). In this sample, we calculate polygenic scores for autism; ADHD and schizophrenia and predict maternal reports of children’s age at first walking and talking, motor delays at 18 months, language delays at 3 years, and a generalized measure of concerns about development. We use linear and probit regression models in a multi-group framework to test for sex differences.ResultsADHD polygenic scores predicted earlier walking age in both males and females (β=-0.037, pFDR=0.001), and earlier first use of sentences (β=-0.087, pFDR=0.032) but delayed language development at 3 years in females only (β=0.194, pFDR=0.001). Additionally, we found evidence that autism polygenic scores were associated with later walking (β=0.027, pFDR=0.024) and motor delays at 18 months (β = 0.065, pFDR=0.028). Schizophrenia polygenic scores were associated with a measure of general concerns about development at 3 years in females only (β=0.132, pFDR=0.024).ConclusionsGenetic liabilities for neurodevelopmental disorders show some specific associations with measures of early motor and language development in the general population, including the age at which children first walk and talk. Associations are generally small and occasionally in unexpected directions. Sex differences are evident in some instances, but clear patterns across different polygenic scores and outcomes are hard to discern. These findings suggest that genetic susceptibility for neurodevelopmental disorders is manifested in the timing of developmental milestones in infancy.

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Life course and work ability among older adults

Revista de Saúde Pública ◽

10.11606/s1518-8787.2018052000648 ◽

2019 ◽

Vol 52 (Suppl 2) ◽

pp. 11s ◽

Cited By ~ 1

Author(s):

Camila Menezes Sabino de Castro ◽

Maria Fernanda Lima-Costa ◽

Cibele Comini César ◽

Jorge Alexandre Barbosa Neves ◽

Fabíola Bof de Andrade ◽

...

Keyword(s):

Multivariate Analysis ◽

Life Course ◽

Work Ability ◽

Educational Level ◽

Good Health ◽

Health Conditions ◽

Baseline Survey ◽

Good Work ◽

Childhood And Adolescence ◽

Men And Women

OBJECTIVE: To examine factors associated with perception of work ability in a nationally representative sample of Brazilians aged 50 years and over. METHODS: We used data from 8,903 participants of the baseline survey of the Brazilian Longitudinal Study of Aging (ELSI-Brazil). The dependent variable was self-rated work ability (good or very good versus fair, poor, or very poor). Independent variables included factors that operate at the beginning, middle, and current stage of life. Multivariate analysis was based on prevalence ratios (PR) and 95% confidence intervals (95%CI) estimated by Poisson regression. RESULTS: Good work ability was reported by 49% of \ participants (49.4% among men and 48.6% among women). Results of the multivariate analysis showed that, for both men and women, good work ability showed positive and statistically significant associations (p < 0.05) with good health up to 15 years of age (PR = 1.22 and 1.18 , respectively), educational level ≥ 8 years (PR = 1.19 and 1.21, respectively), and current good self-rated health (PR = 1.88 and 1.94, respectively). Negative associations were observed for current age (PR = 0.99 for each increase of one year among men and women), medical diagnosis of depression (PR = 0.70 for men and PR = 0.87 for women), and having one or more at least chronic diseases (PR = 0.88 for men and 0.91 for women). Only for men, positive associations for the age at which they started working (PR = 1.14 and 1.12 for 11–17 and ≥ 18 years, respectively) and living with a spouse (PR = 1.09) were found. CONCLUSIONS: Work ability in older ages is built over the life course, particularly by the health conditions in childhood and adolescence, age at which men begin working, educational level, and health conditions in older ages. Policies aimed at increasing longevity in the labor market must take these factors into account.

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Exploring the causal effects of genetic liability to ADHD and Autism on Alzheimer’s disease

10.1101/2020.04.15.043380 ◽

2020 ◽

Author(s):

Panagiota Pagoni ◽

Christina Dardani ◽

Beate Leppert ◽

Roxanna Korologou-Linden ◽

George Davey Smith ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Educational Attainment ◽

Mendelian Randomization ◽

Causal Effect ◽

Autism Spectrum ◽

Causal Effects ◽

Direct Effects ◽

Limited Evidence ◽

Genetic Liability

ABSTRACTBackgroundThere are very few studies investigating possible links between Attention Deficit Hyperactivity Disorder (ADHD), Autism Spectrum Disorder (ASD) and Alzheimer’s disease and these have been limited by small sample sizes, diagnostic and recall bias. However, neurocognitive deficits affecting educational attainment in individuals with ADHD could be risk factors for Alzheimer’s later in life while hyper plasticity of the brain in ASD and strong positive genetic correlations of ASD with IQ and educational attainment could be protective against Alzheimer’s.MethodsWe estimated the bidirectional total causal effects of genetic liability to ADHD and ASD on Alzheimer’s disease through two-sample Mendelian randomization. We investigated their direct effects, independent of educational attainment and IQ, through Multivariable Mendelian randomization.ResultsThere was limited evidence to suggest that genetic liability to ADHD (OR=1.00, 95% CI: 0.98 to 1.02, p=0.39) or ASD (OR=0.99, 95% CI: 0.97 to 1.01, p=0.70) was associated with risk of Alzheimer’s disease. Similar causal effect estimates were identified when the direct effects, independent of educational attainment (ADHD: OR=1.00, 95% CI: 0.99 to 1.01, p=0.07; ASD: OR=0.99, 95% CI: 0.98 to 1.00, p=0.28) and IQ (ADHD: OR=1.00, 95% CI: 0.99 to 1.02. p=0.29; ASD: OR=0.99, 95% CI: 0.98 to 1.01, p=0.99), were assessed. Finally, genetic liability to Alzheimer’s disease was not found to have a causal effect on risk of ADHD or ASD (ADHD: OR=1.12, 95% CI: 0.86 to 1.44, p=0.37; ASD: OR=1.19, 95% CI: 0.94 to 1.51, p=0.14).ConclusionsIn the first study to date investigating the causal associations between genetic liability to ADHD, ASD and Alzheimer’s, within an MR framework, we found limited evidence to suggest a causal effect. It is important to encourage future research using ADHD and ASD specific subtype data, as well as longitudinal data in order to further elucidate any associations between these conditions.

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Identifying intergenerational risk factors for ADHD symptoms using polygenic scores in the Norwegian Mother, Father and Child Cohort

10.1101/2021.02.16.21251737 ◽

2021 ◽

Author(s):

Jean-Baptiste Pingault ◽

Wikus Barkhuizen ◽

Biyao Wang ◽

Laurie J. Hannigan ◽

Espen Moen Eilertsen ◽

...

Keyword(s):

Risk Factors ◽

Cohort Study ◽

Educational Attainment ◽

Intergenerational Transmission ◽

Rating Scale ◽

Autism Spectrum ◽

Intellectual Ability ◽

Adhd Symptoms ◽

Genetic Transmission ◽

Polygenic Scores

AbstractImportanceKnowledge of the mechanisms underlying the intergenerational transmission of risk for attention-deficit/hyperactivity disorder (ADHD) symptoms can inform psychosocial interventions.ObjectiveTo investigate whether parental genetic risk factors associate with their children’s ADHD symptoms due to genetic transmission of risk or due to parental genetic liability that influences offspring ADHD via parenting environments (genetic nurture).Design and participantsThis study is based on the Norwegian Mother, Father and Child Cohort Study and uses data from the Medical Birth Registry of Norway. This prospective cohort study consisted of 5,405 mother-father-offspring trios recruited between 1999 – 2008.ExposuresWe calculated polygenic scores for parental traits previously associated with ADHD, including psychopathology, substance use, neuroticism, educational attainment and intellectual ability.Main outcomes and measuresMothers reported on their 8-year-old children’s ADHD symptoms using the Parent/Teacher Rating Scale for Disruptive Behavior Disorders.ResultsMaternal polygenic scores for ADHD, autism spectrum disorder (ASD), neuroticism and smoking predicted child ADHD symptoms in bivariate analyses. After jointly modelling maternal, paternal and child polygenic scores, ADHD symptoms were predicted by children’s polygenic scores for ADHD (β = 0.10; 95% CI 0.07 to 0.14), smoking (β = 0.07; 95% CI 0.03 to 0.10) and educational attainment (β = −0.09; 95% CI −0.13 to −0.05), indicating direct genetic transmission of risk. Mothers’ polygenic scores for ASD (β = 0.05; 95% CI 0.02 to 0.08) and neuroticism (β = 0.05; 95% CI 0.01 to 0.08) predicted children’s ADHD symptoms conditional on fathers’ and children’s scores, implicating genetic nurture, or effects due to population stratification or assortative mating.ConclusionsThese results suggest that associations between some parental traits and offspring ADHD symptoms likely reflect a nuanced mix of direct genetic transmission (ADHD, smoking and educational attainment) and genetic nurture (ASD and neuroticism). If confirmed, these findings support previous evidence that maternal ASD or neuroticism may be possible targets for intervention to help break the chain of the intergenerational transmission of ADHD risk.

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Genomic prediction of cognitive traits in childhood and adolescence

10.1101/418210 ◽

2018 ◽

Cited By ~ 4

Author(s):

A.G. Allegrini ◽

S. Selzam ◽

K. Rimfeld ◽

S. von Stumm ◽

J.B. Pingault ◽

...

Keyword(s):

Educational Attainment ◽

Complex Traits ◽

Predictive Power ◽

Prediction Models ◽

Educational Achievement ◽

Association Studies ◽

Occupational Status ◽

Childhood And Adolescence ◽

Genome Wide Association Studies ◽

Polygenic Scores

AbstractRecent advances in genomics are producing powerful DNA predictors of complex traits, especially cognitive abilities. Here, we leveraged summary statistics from the most recent genome-wide association studies of intelligence and educational attainment to build prediction models of general cognitive ability and educational achievement. To this end, we compared the performances of multi-trait genomic and polygenic scoring methods. In a representative UK sample of 7,026 children at age 12 and 16, we show that we can now predict up to 11 percent of the variance in intelligence and 16 percent in educational achievement. We also show that predictive power increases from age 12 to age 16 and that genomic predictions do not differ for girls and boys. Multivariate genomic methods were effective in boosting predictive power and, even though prediction accuracy varied across polygenic scores approaches, results were similar using different multivariate and polygenic score methods. Polygenic scores for educational attainment and intelligence are the most powerful predictors in the behavioural sciences and exceed predictions that can be made from parental phenotypes such as educational attainment and occupational status.

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Better to stay or go? A longitudinal study of mobility over the educational life course

International Journal for Population Data Science ◽

10.23889/ijpds.v3i2.568 ◽

2018 ◽

Vol 3 (2) ◽

Author(s):

Amy Sweet ◽

Richard Harris ◽

David Manley

Keyword(s):

Educational Attainment ◽

Educational Outcomes ◽

Negative Impact ◽

Later Life ◽

Individual Characteristics ◽

Childhood And Adolescence ◽

Clear Understanding ◽

Time Period ◽

The Impact

BackgroundThere has been substantial discussion in the literature about where you grow up and if whether or not you experience social and spatial mobility during childhood has substantial bearing upon later life achievement (Pribesh and Downey, 1999; Gasper et al, 2010; Sharkey and Elwert, 2011). ObjectivesThis paper utilises data from the National Pupil Database (NPD) and a quantitative framework to explore the impact of residential mobility on educational outcomes. Many previous studies of neighbourhood mobility have used point in time measures when studying inequality, which means that an individual’s neighbourhood trajectory is overlooked. Data/MethodsWe follow a single cohort of pupils’ over an eleven year time period to analyse their mobility along with their individual characteristics to provide a clear understanding of who is moving and the impact this has on them in terms of educational attainment. We also use the index of multiple deprivation as a measure of neighbourhood wealth to determine to what extent children are able to ’trade up’ in terms of neighbourhood. FindingsOur findings show that moving home has a negative impact on educational attainment compared to those that stay in the same location throughout the educational life cycle. Those that ‘trade up’ in terms of quality of neighbourhood still do not achieve the same educational outcomes as their peers who live in a lower deprived neighbourhood throughout their schooling. ConclusionResidential mobility between deprived areas, as shown in this paper, has more of an impact than just being ‘stuck in place’. It is not purely a case of where you live determining your outcomes, but also how often you move home in childhood and adolescence.

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Genetic liability to schizophrenia is associated with exposure to traumatic events in childhood

Psychological Medicine ◽

10.1017/s0033291720000537 ◽

2020 ◽

pp. 1-8 ◽

Cited By ~ 1

Author(s):

Hannah M. Sallis ◽

Jazz Croft ◽

Alexandra Havdahl ◽

Hannah J. Jones ◽

Erin C. Dunn ◽

...

Keyword(s):

Childhood Trauma ◽

Genome Wide Association Study ◽

Trauma Exposure ◽

Positive Association ◽

Childhood And Adolescence ◽

Birth Cohorts ◽

Genetic Liability ◽

Healthy Environment ◽

Parents And Children ◽

Polygenic Scores

Abstract Background There is a wealth of literature on the observed association between childhood trauma and psychotic illness. However, the relationship between childhood trauma and psychosis is complex and could be explained, in part, by gene–environment correlation. Methods The association between schizophrenia polygenic scores (PGS) and experiencing childhood trauma was investigated using data from the Avon Longitudinal Study of Parents and Children (ALSPAC) and the Norwegian Mother, Father and Child Cohort Study (MoBa). Schizophrenia PGS were derived in each cohort for children, mothers, and fathers where genetic data were available. Measures of trauma exposure were derived based on data collected throughout childhood and adolescence (0–17 years; ALSPAC) and at age 8 years (MoBa). Results Within ALSPAC, we found a positive association between schizophrenia PGS and exposure to trauma across childhood and adolescence; effect sizes were consistent for both child or maternal PGS. We found evidence of an association between the schizophrenia PGS and the majority of trauma subtypes investigated, with the exception of bullying. These results were comparable with those of MoBa. Within ALSPAC, genetic liability to a range of additional psychiatric traits was also associated with a greater trauma exposure. Conclusions Results from two international birth cohorts indicate that genetic liability for a range of psychiatric traits is associated with experiencing childhood trauma. Genome-wide association study of psychiatric phenotypes may also reflect risk factors for these phenotypes. Our findings also suggest that youth at higher genetic risk might require greater resources/support to ensure they grow-up in a healthy environment.

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Is genetic liability to ADHD and ASD causally linked to educational attainment?

10.1101/2020.02.11.944041 ◽

2020 ◽

Cited By ~ 2

Author(s):

Christina Dardani ◽

Beate Leppert ◽

Lucy Riglin ◽

Dheeraj Rai ◽

Laura D Howe ◽

...

Keyword(s):

Educational Attainment ◽

Causal Effect ◽

Educational Interventions ◽

Autism Spectrum ◽

Causal Effects ◽

Sensitivity Analyses ◽

Reverse Direction ◽

Genetic Liability ◽

Higher Educational ◽

Higher Educational Attainment

ABSTRACTBackgroundIndividuals with Attention Deficit Hyperactivity Disorder (ADHD) or Autism Spectrum Disorder (ASD) are at risk of poor educational outcomes. Parental educational attainment has also been associated with risk of ADHD/ASD in the offspring. Despite evidence that ADHD and ASD show genetic links to educational attainment, less is known on the causal nature of the associations and the possible role of IQ.MethodsWe assessed the total causal effects of genetic liability to ADHD/ASD on educational attainment using two-sample Mendelian randomization (MR). We assessed the possible contribution of IQ to the identified causal effects by estimating the “direct” effects of ADHD/ASD on educational attainment, independent of IQ, using Multivariable MR (MVMR). Reverse direction analyses were performed. The latest GWAS meta-analyses of ADHD, ASD, educational attainment and IQ were used. Causal effect estimates were generated using inverse variance weighted models (IVW). Sensitivity analyses were performed to assess the robustness of the estimates and the presence of pleiotropy.ResultsGenetic liability to ADHD had a total (MRIVW:-3.3 months per doubling of liability to ADHD; 95%CI: -4.8 to -1.9; pval= 5*10−6) and direct negative causal effect on educational attainment (MVMRIVW:-1.6 months per doubling of liability to ADHD; 95%CI: -2.5 to -0.6; pval= 4*10−4). There was little evidence of a total causal effect of genetic liability to ASD on educational attainment (MRIVW: 4 days, per doubling of liability to ASD; 95%CI: -4.9 months to 5.6 months; pval= 0.9) but some evidence of a direct effect not via IQ (MVMRIVW:29 days per doubling the genetic liability to ASD; 95%CI: 2 to 48; pval= 0.03). Reverse direction analyses suggested that genetic liability to higher educational attainment was associated with lower risk of ADHD (MRIVWOR: 0.3 per standard deviation (SD) increase; 95%CI: 0.26 to 0.36; pval= 6*10−51), even after IQ was entered in the models (MVMRIVWOR: 0.33 per SD increase; 95%CI: 0.26 to 0.43; pval= 6*10−17). On the contrary, there was evidence consistent with a positive causal effect of genetic liability to higher educational attainment on risk of ASD (MRIVWOR: 1.51 per SD increase; 95%CI: 1.29 to 1.77; pval= 4*10−7), which was found to be largely explained by IQ (MVMRIVWOR per SD increase: 1.24; 95%CI: 0.96 to 1.60; pval= 0.09).ConclusionsOur findings suggest that despite the genetic and phenotypic overlap between ADHD and ASD, they present highly differentiated causal associations with educational attainment. This highlights the necessity for specialized educational interventions for children with ADHD and ASD. Further research is needed in order to decipher whether the identified causal effects reflect parentally transmitted effects, diagnostic masking, or selection bias.

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The Positive End of the Polygenic Score Distribution for ADHD: A Low Risk or a Protective Factor?

10.1101/611897 ◽

2019 ◽

Author(s):

James J. Li

Keyword(s):

Educational Attainment ◽

Functional Outcomes ◽

Protective Factor ◽

Genome Wide Association Study ◽

Add Health ◽

Later Life ◽

Low Risk ◽

Score Distribution ◽

Genetic Liability ◽

Polygenic Scores

AbstractBackgroundPolygenic scores (PGS) are widely used to characterize genetic liability for heritable mental disorders, including attention-deficit/hyperactivity disorder (ADHD). However, little is known about the effects of a low burden of genetic liability for ADHD, including whether this functions as a low risk or protective factor for ADHD and related functional outcomes in later life. The current study examines the association of low ADHD PGS and functional outcomes in adulthood.MethodsParticipants were from Wave IV of the National Longitudinal Study of Adolescent to Adult Health (Add Health) (N=7,088; mean age=29, s.d.=1.74). ADHD PGS was computed from an existing genome-wide association study, and adult functional outcomes, including cognition, educational attainment, mental health and physical health were assessed during in-home interviews.ResultsIndividuals at the lowest end of the ADHD PGS distribution (i.e., lowest 20th percentile) had the lowest probabilities of ADHD, exhibiting a 17-19% reduction in risk for ADHD relative to the observed 8.3% prevalence rate of ADHD in Add Health. Furthermore, individuals with low ADHD PGS had higher cognitive performance, greater levels of educational attainment, and lower BMI relative to individuals representing the rest of the ADHD PGS distribution, including those who were in the medium and high PGS groups.ConclusionsFindings indicate that psychiatric PGS likely capture far more than just the risk and the absence of risk for a psychiatric outcome; where one lies along the PGS distribution may predict diverging functional consequences, for better and for worse.

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