Methodologies for Monitoring Mental Health on Twitter: Systematic Review.

BACKGROUND: The use of social media data to predict mental health outcomes has the potential to allow for the continuous monitoring of mental health and well-being and provide timely information that can supplement traditional clinical assessments. However, it is crucial that the methodologies used to create models for this purpose are of high quality from both a mental health and machine learning perspective. Twitter has been a popular choice of social media because of the accessibility of its data, but access to big data sets is not a guarantee of robust results. OBJECTIVE: This study aims to review the current methodologies used in the literature for predicting mental health outcomes from Twitter data, with a focus on the quality of the underlying mental health data and the machine learning methods used. METHODS: A systematic search was performed across 6 databases, using keywords related to mental health disorders, algorithms, and social media. In total, 2759 records were screened, of which 164 (5.94%) papers were analyzed. Information about methodologies for data acquisition, preprocessing, model creation, and validation was collected, as well as information about replicability and ethical considerations. RESULTS: The 164 studies reviewed used 119 primary data sets. There were an additional 8 data sets identified that were not described in enough detail to include, and 6.1% (10/164) of the papers did not describe their data sets at all. Of these 119 data sets, only 16 (13.4%) had access to ground truth data (ie, known characteristics) about the mental health disorders of social media users. The other 86.6% (103/119) of data sets collected data by searching keywords or phrases, which may not be representative of patterns of Twitter use for those with mental health disorders. The annotation of mental health disorders for classification labels was variable, and 57.1% (68/119) of the data sets had no ground truth or clinical input on this annotation. Despite being a common mental health disorder, anxiety received little attention. CONCLUSIONS: The sharing of high-quality ground truth data sets is crucial for the development of trustworthy algorithms that have clinical and research utility. Further collaboration across disciplines and contexts is encouraged to better understand what types of predictions will be useful in supporting the management and identification of mental health disorders. A series of recommendations for researchers in this field and for the wider research community are made, with the aim of enhancing the quality and utility of future outputs.

Extensions of the causal framework to Mendelian randomisation and gene-environment interaction.

In our commentary we ask whether we should ultimately endeavour to find the deep causes of behaviours? Then we discuss two extensions of the proposed framework: (1) Mendelian randomisation and (2) hypothesis-free gene-environment interaction (leveraging heterogeneity in genetic associations). These complementary methods help move us towards second-generation causal knowledge, ultimately understanding mechanistic pathways and identifying more effective intervention targets.

Changing genetic architecture of body mass index from infancy to early adulthood: an individual based pooled analysis of 25 twin cohorts.

BACKGROUND: Body mass index (BMI) shows strong continuity over childhood and adolescence and high childhood BMI is the strongest predictor of adult obesity. Genetic factors strongly contribute to this continuity, but it is still poorly known how their contribution changes over childhood and adolescence. Thus, we used the genetic twin design to estimate the genetic correlations of BMI from infancy to adulthood and compared them to the genetic correlations of height. METHODS: We pooled individual level data from 25 longitudinal twin cohorts including 38,530 complete twin pairs and having 283,766 longitudinal height and weight measures. The data were analyzed using Cholesky decomposition offering genetic and environmental correlations of BMI and height between all age combinations from 1 to 19 years of age. RESULTS: The genetic correlations of BMI and height were stronger than the trait correlations. For BMI, we found that genetic correlations decreased as the age between the assessments increased, a trend that was especially visible from early to middle childhood. In contrast, for height, the genetic correlations were strong between all ages. Age-to-age correlations between environmental factors shared by co-twins were found for BMI in early childhood but disappeared altogether by middle childhood. For height, shared environmental correlations persisted from infancy to adulthood. CONCLUSIONS: Our results suggest that the genes affecting BMI change over childhood and adolescence leading to decreasing age-to-age genetic correlations. This change is especially visible from early to middle childhood indicating that new genetic factors start to affect BMI in middle childhood. Identifying mediating pathways of these genetic factors can open possibilities for interventions, especially for those children with high genetic predisposition to adult obesity.

A Polygenic Approach to Understanding Resilience to Peer Victimisation.

Previous studies suggest an individual's risk of depression following adversity may be moderated by their genetic liability. No study, however, has examined peer victimisation, an experience repeatedly associated with mental illness. We explore whether the negative mental health outcomes following victimisation can be partly attributed to genetic factors using polygenic scores for depression and wellbeing. Among participants from the Avon Longitudinal Study of Parents and Children (ALSPAC), we show that polygenic scores and peer victimisation are significant independent predictors of depressive symptoms (n=2268) and wellbeing (n=2299) in early adulthood. When testing for interaction effects, our results lead us to conclude that low mental health and wellbeing following peer victimisation is unlikely to be explained by a moderating effect of genetic factors, as indexed by current polygenic scores. Genetic profiling is therefore unlikely to be effective in identifying those more vulnerable to the effects of victimisation at present. The reasons why some go on to experience mental health problems following victimisation, while others remain resilient, requires further exploration, but our results rule out a major influence of current polygenic scores.

Keeping up with the Wangs: individual and contextual influences on mental wellbeing and depressive symptoms in China.

BACKGROUND: In recent decades, China has experienced dramatic changes to its social and economic environment, which has affected the distribution of wellbeing across its citizens. While several studies have investigated individual level predictors of wellbeing in the Chinese population, less research has been done looking at contextual effects. This cross-sectional study looks at the individual and contextual effects of (regional) education, unemployment and marriage (rate) on individual happiness, life satisfaction and depressive symptomatology. METHODS: Data were collected from over 29,000 individuals (aged 18 to 110, 51.91% female) in the China Family Panel Studies, and merged with county level census data obtained from the 2010 China Population Census and Statistical Yearbook. To explore contextual effects, we used multilevel models accounting for the hierarchical structure of the data. RESULTS: We found that a one-year increase in education was associated with a 0.17% increase in happiness and a 0.16% decrease in depressive symptoms. Unemployed men were 1% less happy, 1% less satisfied with life and reported 0.84% more depressive symptoms than employed men while minimal effects were seen for women. Single, divorced and widowed individuals had worse outcomes than married individuals (ranging from 2.96 to 21% differences). We found interaction effects for education and employment. Less educated individuals had greater happiness and less depressive symptoms in counties with higher average education compared to counterparts in less educated counties. In contrast, more educated individuals were less satisfied with life in more educated counties, an effect that is possibly due to social comparison. Employed individuals had lower life satisfaction in areas of high unemployment, while levels were constant for the unemployed. A 1% increase in county marriage rate was associated with 0.33 and 0.24% increases in happiness and life satisfaction respectively, with no interactions. We speculate that this effect could be due to greater social cohesion in the neighbourhood. CONCLUSIONS: Our results show that policies designed to improve employment and marriage rates will be beneficial for all, while interventions to encourage positive social comparison strategies may help to offset the negative effects of increasing neighbourhood average education on the highly educated.

Social media use and social connectedness among adolescents in the United Kingdom: a qualitative exploration of displacement and stimulation.

BACKGROUND: Connectedness to family and peers is a key determinant of adolescent mental health. Existing research examining associations between social media use and social connectedness has been largely quantitative and has focused primarily on loneliness, or on specific aspects of peer relationships. In this qualitative study we use the displacement hypothesis and the stimulation hypothesis as competing theoretical lenses through which we examine the complex relationship between social media use and feelings of connectedness to family and peers. METHODS: In-depth paired and individual interviews were conducted with twenty-four 13-14-year-olds in two inner-city English secondary schools. Interviews were transcribed verbatim, coded and thematically analysed. RESULTS: Analysis identified four themes: (i) 'Displacement of face-to-face socialising' (ii) 'Social obligations' (iii) '(Mis)Trust' and (iv) 'Personal and group identity'. Results indicated stronger support for the stimulation hypothesis than the displacement hypothesis. We found evidence of a complex set of reciprocal and circular relationships between social media use and connectedness consistent with a 'rich-get-richer' and a 'poor-get-poorer' effect for family and peer connectedness - and a 'poor-get-richer' effect in peer connectedness for those who find face-to-face interactions difficult. CONCLUSION: Our findings suggest that parents should take a measured approach to social media use, providing clear guidance, promoting trust and responsible time management, and acknowledging the role of social media in making connections. Understanding and sharing in online experiences is likely to promote social connectedness. Supporting young people to negotiate breathing space in online interactions and prioritising trust over availability in peer relationships may optimise the role of social media in promoting peer connectedness.

Peer victimisation during adolescence and its impact on wellbeing in adulthood: a prospective cohort study.

BACKGROUND: Peer victimisation is a common occurrence and has well-established links with a range of psychiatric problems in adulthood. Significantly less is known however, about how victimisation influences positive aspects of mental health such as wellbeing. The purpose of this study was therefore to assess for the first time, whether peer victimisation in adolescence is associated with adult wellbeing. We aimed to understand whether individuals who avoid a diagnosis of depression after victimisation, maintain good wellbeing in later life, and therefore display resilience. METHODS: Longitudinal data was taken from the Avon Longitudinal Study of Parents and Children, a prospective cohort study based in the UK. Peer victimisation was assessed at 13 years using a modified version of the bullying and friendship interview schedule, and wellbeing at age 23 using the Warwick-Edinburgh Mental Well-Being Scale. The presence or absence of depression was diagnosed using the Clinical Interview Schedule-Revised at 18 years. A series of logistic and linear regression analyses were used to explore relationships between peer victimisation, depression, and wellbeing, adjusting for potentially confounding individual and family factors. RESULTS: Just over 15% of victims of frequent bullying had a diagnosis of depression at age 18. Victimisation also had a significant impact on wellbeing, with a one-point increase in frequent victimisation associated with a 2.71-point (SE = 0.46, p < 0.001) decrease in wellbeing scores aged 23. This finding remained after adjustment for the mediating and moderating effects of depression, suggesting that the burden of victimisation extends beyond depression to impact wellbeing. Results therefore show that individuals who remain partially resilient by avoiding a diagnosis of depression after victimisation have significantly poorer wellbeing than their non-victimised counterparts. CONCLUSION: Overall, our study demonstrates for the first time that victimisation during adolescence is a significant risk factor for not only the onset of depression, but also poor wellbeing in adulthood. Such findings highlight the importance of investigating both dimensions of mental health to understand the true burden of victimisation and subsequent resilience. In addition to the need for interventions that reduce the likelihood of depression following adolescent victimisation, efforts should also be made to promote good wellbeing.

Genome-wide association analysis identifies three new susceptibility loci for childhood body mass index.

A large number of genetic loci are associated with adult body mass index. However, the genetics of childhood body mass index are largely unknown. We performed a meta-analysis of genome-wide association studies of childhood body mass index, using sex- and age-adjusted standard deviation scores. We included 35 668 children from 20 studies in the discovery phase and 11 873 children from 13 studies in the replication phase. In total, 15 loci reached genome-wide significance (P-value < 5 × 10(-8)) in the joint discovery and replication analysis, of which 12 are previously identified loci in or close to ADCY3, GNPDA2, TMEM18, SEC16B, FAIM2, FTO, TFAP2B, TNNI3K, MC4R, GPR61, LMX1B and OLFM4 associated with adult body mass index or childhood obesity. We identified three novel loci: rs13253111 near ELP3, rs8092503 near RAB27B and rs13387838 near ADAM23. Per additional risk allele, body mass index increased 0.04 Standard Deviation Score (SDS) [Standard Error (SE) 0.007], 0.05 SDS (SE 0.008) and 0.14 SDS (SE 0.025), for rs13253111, rs8092503 and rs13387838, respectively. A genetic risk score combining all 15 SNPs showed that each additional average risk allele was associated with a 0.073 SDS (SE 0.011, P-value = 3.12 × 10(-10)) increase in childhood body mass index in a population of 1955 children. This risk score explained 2% of the variance in childhood body mass index. This study highlights the shared genetic background between childhood and adult body mass index and adds three novel loci. These loci likely represent age-related differences in strength of the associations with body mass index.

Understanding the genetic and environmental specificity and overlap between well-being and internalizing symptoms in adolescence.

Moderate inverse correlations are typically found between well-being and mental illness. We aimed to investigate the role of genes and environments in explaining the relationships between two aspects of well-being and two measures of internalizing symptoms. Altogether, 4700 pairs of 16-year-old twins contributed data on subjective happiness and life satisfaction, as well as symptoms of depression and emotional problems. Well-being was moderately correlated with internalizing symptoms (range = -0.45, -0.58). Multivariate twin model-fitting indicated both genetic and environmental overlap. Life satisfaction and happiness demonstrated different patterns of overlap, with stronger genetic links between life satisfaction and depression. Non-shared environmental influences were largely specific to each trait. This study supports the theory of mental health and illness being partly (but not entirely) correlated dimensions. There are also significant genetic and environmental factors to identify for well-being that go beyond the absence of mental illness. It is therefore possible that different interventions are needed for treating mental illness and promoting mental health.

Genetic and environmental correlations between subjective wellbeing and experience of life events in adolescence.

Some life events appear heritable due to the genetic influence on related behaviours. Shared genetic influence between negative behaviours and negative life events has previously been established. This study investigated whether subjective wellbeing and positive life events were genetically associated. Participants in the Twins Early Development Study (aged 16.32 ± .68 years) completed subjective wellbeing and life events assessments via two separate studies (overlapping N for wellbeing and life events measures ranged from 3527 to 9350). We conducted bivariate twin models between both positive and negative life events with subjective wellbeing and related positive psychological traits including subjective happiness, life satisfaction, optimism, hopefulness and gratitude measured at 16 years. Results suggested that the heritability of life events can partially be explained by shared genetic influences with the wellbeing indicators. Wellbeing traits were positively genetically correlated with positive life events and negatively correlated with negative life events (except curiosity where there was no correlation). Those positive traits that drive behaviour (grit and ambition) showed the highest genetic correlation with life events, whereas the reflective trait gratitude was less correlated. This suggests that gene-environment correlations might explain the observed genetic association between life events and wellbeing. Inheriting propensity for positive traits might cause you to seek environments that lead to positive life events and avoid environments which make negative life events more likely.

Association between stressful life events and psychotic experiences in adolescence: evidence for gene-environment correlations.

BACKGROUND: Stressful life events (SLEs) are associated with psychotic experiences. SLEs might act as an environmental risk factor, but may also share a genetic propensity with psychotic experiences. AIMS: To estimate the extent to which genetic and environmental factors influence the relationship between SLEs and psychotic experiences. METHOD: Self- and parent reports from a community-based twin sample (4830 16-year-old pairs) were analysed using structural equation model fitting. RESULTS: SLEs correlated with positive psychotic experiences (r = 0.12-0.14, all P<0.001). Modest heritability was shown for psychotic experiences (25-57%) and dependent SLEs (32%). Genetic influences explained the majority of the modest covariation between dependent SLEs and paranoia and cognitive disorganisation (bivariate heritabilities 74-86%). The relationship between SLEs and hallucinations and grandiosity was explained by both genetic and common environmental effects. CONCLUSIONS: Further to dependent SLEs being an environmental risk factor, individuals may have an underlying genetic propensity increasing their risk of dependent SLEs and positive psychotic experiences.

The opposite end of the attention deficit hyperactivity disorder continuum: genetic and environmental aetiologies of extremely low ADHD traits.

BACKGROUND: Although attention deficit hyperactivity disorder (ADHD) is thought to reflect a continuously distributed quantitative trait, it is assessed through binary diagnosis or skewed measures biased towards its high, symptomatic extreme. A growing trend is to study the positive tail of normally distributed traits, a promising avenue, for example, to study high intelligence to increase power for gene-hunting for intelligence. However, the emergence of such a 'positive genetics' model has been tempered for ADHD due to poor phenotypic resolution at the low extreme. Overcoming this methodological limitation, we conduct the first study to assess the aetiologies of low extreme ADHD traits. METHODS: In a population-representative sample of 2,143 twins, the Strength and Weaknesses of ADHD Symptoms and Normal behaviour (SWAN) questionnaire was used to assess ADHD traits on a continuum from low to high. Aetiological influences on extreme ADHD traits were estimated using DeFries-Fulker extremes analysis. ADHD traits were related to behavioural, cognitive and home environmental outcomes using regression. RESULTS: Low extreme ADHD traits were significantly influenced by shared environmental factors (23-35%) but were not significantly heritable. In contrast, high-extreme ADHD traits showed significant heritability (39-51%) but no shared environmental influences. Compared to individuals with high extreme or with average levels of ADHD traits, individuals with low extreme ADHD traits showed fewer internalizing and externalizing behaviour problems, better cognitive performance and more positive behaviours and positive home environmental outcomes. CONCLUSIONS: Shared environmental influences on low extreme ADHD traits may reflect passive gene-environment correlation, which arises because parents provide environments as well as passing on genes. Studying the low extreme opens new avenues to study mechanisms underlying previously neglected positive behaviours. This is different from the current deficit-based model of intervention, but congruent with a population-level approach to improving youth wellbeing.

Exploring the Genetic Etiology of Trust in Adolescents: Combined Twin and DNA Analyses.

Behavioral traits generally show moderate to strong genetic influence, with heritability estimates of around 50%. Some recent research has suggested that trust may be an exception because it is more strongly influenced by social interactions. In a sample of over 7,000 adolescent twins from the United Kingdom's Twins Early Development Study, we found broad sense heritability estimates of 57% for generalized trust and 51% for trust in friends. Genomic-relatedness-matrix restricted maximum likelihood (GREML) estimates in the same sample indicate that 21% of the narrow sense genetic variance can be explained by common single nucleotide polymorphisms for generalized trust and 43% for trust in friends. As expected, this implies a large amount of unexplained heritability, although power is low for estimating DNA-based heritability. The missing heritability may be accounted for by interactions between DNA and the social environment during development or via gene-environment correlations with rare variants. How these genes and environments correlate seem especially important for the development of trust.

Common disorders are quantitative traits.

After drifting apart for 100 years, the two worlds of genetics - quantitative genetics and molecular genetics - are finally coming together in genome-wide association (GWA) research, which shows that the heritability of complex traits and common disorders is due to multiple genes of small effect size. We highlight a polygenic framework, supported by recent GWA research, in which qualitative disorders can be interpreted simply as being the extremes of quantitative dimensions. Research that focuses on quantitative traits - including the low and high ends of normal distributions - could have far-reaching implications for the diagnosis, treatment and prevention of the problematic extremes of these traits.

Zygosity Differences in Height and Body Mass Index of Twins From Infancy to Old Age: A Study of the CODATwins Project.

A trend toward greater body size in dizygotic (DZ) than in monozygotic (MZ) twins has been suggested by some but not all studies, and this difference may also vary by age. We analyzed zygosity differences in mean values and variances of height and body mass index (BMI) among male and female twins from infancy to old age. Data were derived from an international database of 54 twin cohorts participating in the COllaborative project of Development of Anthropometrical measures in Twins (CODATwins), and included 842,951 height and BMI measurements from twins aged 1 to 102 years. The results showed that DZ twins were consistently taller than MZ twins, with differences of up to 2.0 cm in childhood and adolescence and up to 0.9 cm in adulthood. Similarly, a greater mean BMI of up to 0.3 kg/m2 in childhood and adolescence and up to 0.2 kg/m2 in adulthood was observed in DZ twins, although the pattern was less consistent. DZ twins presented up to 1.7% greater height and 1.9% greater BMI than MZ twins; these percentage differences were largest in middle and late childhood and decreased with age in both sexes. The variance of height was similar in MZ and DZ twins at most ages. In contrast, the variance of BMI was significantly higher in DZ than in MZ twins, particularly in childhood. In conclusion, DZ twins were generally taller and had greater BMI than MZ twins, but the differences decreased with age in both sexes.

The CODATwins Project: The Cohort Description of Collaborative Project of Development of Anthropometrical Measures in Twins to Study Macro-Environmental Variation in Genetic and Environmental Effects on Anthropometric Traits.

For over 100 years, the genetics of human anthropometric traits has attracted scientific interest. In particular, height and body mass index (BMI, calculated as kg/m2) have been under intensive genetic research. However, it is still largely unknown whether and how heritability estimates vary between human populations. Opportunities to address this question have increased recently because of the establishment of many new twin cohorts and the increasing accumulation of data in established twin cohorts. We started a new research project to analyze systematically (1) the variation of heritability estimates of height, BMI and their trajectories over the life course between birth cohorts, ethnicities and countries, and (2) to study the effects of birth-related factors, education and smoking on these anthropometric traits and whether these effects vary between twin cohorts. We identified 67 twin projects, including both monozygotic (MZ) and dizygotic (DZ) twins, using various sources. We asked for individual level data on height and weight including repeated measurements, birth related traits, background variables, education and smoking. By the end of 2014, 48 projects participated. Together, we have 893,458 height and weight measures (52% females) from 434,723 twin individuals, including 201,192 complete twin pairs (40% monozygotic, 40% same-sex dizygotic and 20% opposite-sex dizygotic) representing 22 countries. This project demonstrates that large-scale international twin studies are feasible and can promote the use of existing data for novel research purposes.

Identical genetic influences underpin behavior problems in adolescence and basic traits of personality.

BACKGROUND: Understanding the etiology of adolescent problem behavior has been of enduring interest. Only relatively recently, however, has this issue been examined within a normal personality trait framework. Research suggests that problem behaviors in adolescence and beyond may be adequately explained by the taxonomy provided by the basic dimensions of normal personality: Such problem behaviors are suggested to be extreme points on a distribution of the full range of the underlying traits. We extend work in this field examining the extent to which genetic factors underlying the five-factor model of personality are common with genetic influences on adolescent behavior problems (namely, anxiety, peer problems, conduct, hyperactivity, and low prosociality). METHOD: A nationally representative twin sample (Twins Early Development Study) from the general population of England and Wales, including 2031 pairs of twins aged 16 years old, was used to decompose variation into genetic and environmental components. Behavioral problems in adolescence were assessed by self-report with the Strengths and Difficulties Questionnaire. RESULTS: Adolescent behavior problems were moderately associated with normal personality: Specifically, a fifth to a third of phenotypic variance in problem behaviors was accounted for by five-factor model personality traits. Of central importance here, genetic influences underpinning personality were entirely overlapping with those genetic factors underlying adolescent behavior problems. CONCLUSIONS: These findings suggest that adolescent behavior problems can be understood, at least in part, within a model of normal personality trait variation, with the genetic bases of these behavior problems the same as those genetic influences underpinning normal personality.

Why do spatial abilities predict mathematical performance?

Spatial ability predicts performance in mathematics and eventual expertise in science, technology and engineering. Spatial skills have also been shown to rely on neuronal networks partially shared with mathematics. Understanding the nature of this association can inform educational practices and intervention for mathematical underperformance. Using data on two aspects of spatial ability and three domains of mathematical ability from 4174 pairs of 12-year-old twins, we examined the relative genetic and environmental contributions to variation in spatial ability and to its relationship with different aspects of mathematics. Environmental effects explained most of the variation in spatial ability (~70%) and in mathematical ability (~60%) at this age, and the effects were the same for boys and girls. Genetic factors explained about 60% of the observed relationship between spatial ability and mathematics, with a substantial portion of the relationship explained by common environmental influences (26% and 14% by shared and non-shared environments respectively). These findings call for further research aimed at identifying specific environmental mediators of the spatial-mathematics relationship.

Investigating changes in student mental health and help-seeking behaviour after the introduction of new well-being support services at a UK university.

BACKGROUND: Growing numbers of students now seek mental health support from their higher education providers. In response, a number of universities have invested in non-clinical well-being services, but there have been few evaluations of these. This research addresses a critical gap in the existing literature. AIMS: This study examined the impact of introducing non-clinical well-being advisers on student mental health and help-seeking behaviour at a large UK university. METHOD: Survey data collected pre-post service introduction in 2018 (n = 5562) and 2019 (n = 2637) measured prevalence of depression (Patient Health Questionnaire-9), anxiety (Generalised Anxiety Disorder-7), and low mental well-being (Warwick-Edinburgh Mental Wellbeing Scale), alongside student support-seeking behaviour. Logistic regression models investigated changes in outcome measures. Administrative data (2014-2020) were used to investigate corresponding trends in antidepressant prescribing at the onsite health service, student counselling referrals and course withdrawal rates. RESULTS: Adjusted models suggested reductions in students' levels of anxiety (odds ratio 0.86, 95% CI 0.77-0.96) and low well-being (odds ratio 0.84, 95% CI 0.75-0.94) in 2019, but not depression symptoms (odds ratio 1.05, 95% CI 0.93-1.17). Statistical evidence showed reduced student counselling referrals, with antidepressant prescribing and course withdrawal rates levelling off. Student perception of the availability and accessibility of university support improved. CONCLUSIONS: Our findings suggest a non-clinical well-being service model may improve student perception of support, influence overall levels of anxiety and low well-being, and reduce clinical need. The current study was only able to examine changes over the short term, and a longer follow-up is needed.

Common DNA markers can account for more than half of the genetic influence on cognitive abilities.

For nearly a century, twin and adoption studies have yielded substantial estimates of heritability for cognitive abilities, although it has proved difficult for genomewide-association studies to identify the genetic variants that account for this heritability (i.e., the missing-heritability problem). However, a new approach, genomewide complex-trait analysis (GCTA), forgoes the identification of individual variants to estimate the total heritability captured by common DNA markers on genotyping arrays. In the same sample of 3,154 pairs of 12-year-old twins, we directly compared twin-study heritability estimates for cognitive abilities (language, verbal, nonverbal, and general) with GCTA estimates captured by 1.7 million DNA markers. We found that DNA markers tagged by the array accounted for .66 of the estimated heritability, reaffirming that cognitive abilities are heritable. Larger sample sizes alone will be sufficient to identify many of the genetic variants that influence cognitive abilities.