Co-recovery of physical size and cognitive ability from infancy to adolescence: A twin study.

This study tested phenotypic and biometric associations between physical and cognitive catch-up growth in a community sample of twins (n = 1285, 51.8% female, 89.3% White). Height and weight were measured at up to 17 time points between birth and 15 years, and cognitive ability was assessed at up to 16 time points between 3 months and 15 years. Weight and length at birth were positively associated with cognitive abilities in infancy and adolescence (r's = .16-.51). More rapid weight catch-up growth was associated with slower, steadier cognitive catch-up growth. Shared and nonshared environmental factors accounted for positive associations between physical size at birth and cognitive outcomes. Findings highlight the role of prenatal environmental experiences in physical and cognitive co-development.

On the big list of causes.

The methodological shift from twin studies to genome-wide association studies (GWASs) diminished estimates of true genetic causation underlying statistical heritability of behavioral differences. The sum total of causal genetic influence on behavior is not zero, but, (a) no one cited in the target article ever thought this was the case, and (b) there is still little known about concrete instances of genetic causation.

Nonlinear Catch-Up Growth in Height, Weight, and Head Circumference from Birth to Adolescence: A Longitudinal Twin Study.

Owing to high rates of prenatal complications, twins are, on average, substantially smaller than population norms on physical measurements including height, weight, and head circumference at birth. By early childhood, twins are physically average. This study is the first to explore the process of catch-up growth by fitting asymptotic growth models to age-standardized height, weight, and head circumference measurements in a community sample of twins (n = 1281, 52.3% female) followed at up to 17 time points from birth to 15 years. Catch-up growth was rapid over the first year and plateaued around the population mean by early childhood. Shared environmental factors accounted for the majority of individual differences in initial physical size (57.7-65.5%), whereas additive genetic factors accounted for the majority of individual differences in the upper asymptotes of height, weight, and head circumference (73.4-92.6%). Both additive genetic and shared environmental factors were associated with variance in how quickly twins caught up. Gestational age and family SES emerged as important environmental correlates of physical catch-up growth.

A Longitudinal Analysis of Gene x Environment Interaction on Verbal Intelligence Across Adolescence and Early Adulthood.

The Scarr-Rowe hypothesis proposes that the heritability of intelligence is higher in more advantaged socioeconomic contexts. An early demonstration of this hypothesis was Rowe and colleagues (Rowe et al., Child Dev 70:1151-1162, 1999), where an interaction between the heritability of verbal intelligence and parental education was identified in adolescent siblings in Wave I of the National Longitudinal Study of Adolescent to Adult Health. The present study repeated their original analysis at Wave I using contemporary methods, replicated the finding during young adulthood at Wave III, and analyzed the interaction longitudinally utilizing multiple measurements. We examined parental education, family income, and peer academic environment as potential moderators. Results indicated increased heritability and decreased shared environmental variance of verbal intelligence at higher levels of parental education and peer academic environment in adolescence. Moreover, moderation by peer academic environment persisted into adulthood with its effect partially attributable to novel gene-environment interactions that arose in the process of cognitive development.

Wrestling with Social and Behavioral Genomics: Risks, Potential Benefits, and Ethical Responsibility.

In this consensus report by a diverse group of academics who conduct and/or are concerned about social and behavioral genomics (SBG) research, the authors recount the often-ugly history of scientific attempts to understand the genetic contributions to human behaviors and social outcomes. They then describe what the current science-including genomewide association studies and polygenic indexes-can and cannot tell us, as well as its risks and potential benefits. They conclude with a discussion of responsible behavior in the context of SBG research. SBG research that compares individuals within a group according to a "sensitive" phenotype requires extra attention to responsible conduct and to responsible communication about the research and its findings. SBG research (1) on sensitive phenotypes that (2) compares two or more groups defined by (a) race, (b) ethnicity, or (c) genetic ancestry (where genetic ancestry could easily be misunderstood as race or ethnicity) requires a compelling justification to be conducted, funded, or published. All authors agree that this justification at least requires a convincing argument that a study's design could yield scientifically valid results; some authors would additionally require the study to have a socially favorable risk-benefit profile.

Quasi-causal associations between chronotype and post-traumatic stress disorder symptoms: A twin study.

OBJECTIVE: The evening ("night owl") chronotype is associated with greater severity and lifetime prevalence of post-traumatic stress disorder (PTSD) symptoms compared to morning or intermediate chronotypes. This twin study investigated the gene-environment relationships between chronotype, recent PTSD symptoms, and lifetime intrusive symptoms. METHODS: We used the reduced Horne-Östberg Morningness-Eveningness Questionnaire (rMEQ) to assess chronotype in a sample of 3777 same-sex adult twin pairs raised together (70.4% monozygotic, 29.6% dizygotic) in the community-based Washington State Twin Registry. PTSD symptoms were reported on the Impact of Events Scale (IES) and a single item for lifetime experience of intrusive symptoms after a stressful or traumatic event. RESULTS: Genetic influences accounted for 50% of chronotype variance, 30% of IES score variance, and 14% of lifetime intrusive symptom variance. Bivariate twin models showed a phenotypic association (bp) between evening chronotype and more severe PTSD symptoms (bp = -0.16, SE = 0.02, p < .001) that remained significant even after adjusting for shared genetic and environmental influences (bp = -0.10, SE = 0.04, p = .009), as well as age, sex, and self-reported sleep duration (bp = -0.11, SE = 0.04, p = .004). An association was found between evening chronotype and lifetime intrusive symptoms (bp = -0.11, SE = 0.03, p < .001) that was no longer significant after adjusting for shared genetic and environmental influences (bp = 0.04, SE = 0.06, p = .558). CONCLUSIONS: Our results suggest a "quasi-causal" relationship between evening chronotype and PTSD symptoms that is not purely attributable to genetic or shared environmental factors. Evening chronotype may increase vulnerability to pathologic stress responses in the setting of circadian misalignment, providing potential avenues of prevention and treatment using chronobiological strategies.

Nonlinear Catch-Up Growth in Height, Weight, and Head Circumference from Birth to Adolescence: A Longitudinal Twin Study.

Owing to high rates of prenatal complications, twins are, on average, substantially smaller than population norms on physical measurements including height, weight, and head circumference at birth. By early childhood, twins are physically average. This study is the first to explore the process of catch-up growth by fitting asymptotic growth models to age-standardized height, weight, and head circumference measurements in a community sample of twins ( n = 1,281, 52.3% female) followed at up to 17 time points from birth to 15 years. Catch-up growth was rapid over the first year and plateaued around the population mean by early childhood. Shared environmental factors accounted for the majority of individual differences in initial physical size (57.7%-65.5%), whereas additive genetic factors accounted for the majority of individual differences in the upper asymptotes of height, weight, and head circumference (73.4%-92.6%). Both additive genetic and shared environmental factors were associated with variance in how quickly twins caught up. Gestational age and family SES emerged as important environmental correlates of physical catch-up growth.

Simulated nonlinear genetic and environmental dynamics of complex traits.

Genetic studies of complex traits often show disparities in estimated heritability depending on the method used, whether by genomic associations or twin and family studies. We present a simulation of individual genomes with dynamic environmental conditions to consider how linear and nonlinear effects, gene-by-environment interactions, and gene-by-environment correlations may work together to govern the long-term development of complex traits and affect estimates of heritability from common methods. Our simulation studies demonstrate that the genetic effects estimated by genome wide association studies in unrelated individuals are inadequate to characterize gene-by-environment interaction, while including related individuals in genome-wide complex trait analysis (GCTA) allows gene-by-environment interactions to be recovered in the heritability. These theoretical findings provide an explanation for the "missing heritability" problem and bridge the conceptual gap between the most common findings of GCTA and twin studies. Future studies may use the simulation model to test hypotheses about phenotypic complexity either in an exploratory way or by replicating well-established observations of specific phenotypes.

This time I mean it: The nature-nurture debate is over.

The target article is skeptical of the heritability concept while maintaining an old-fashioned point of view about it. As a descriptive statistic, it is to be expected that heritability goes up and down in different circumstances, but the relationship between heritability coefficients and the biological processes that underlie them is difficult to specify, and may be impossible in humans.

The pillars of health: influence of multiple lifestyle behaviors on body mass index and depressive symptoms in adult twins.

BACKGROUND: Guidelines promoting healthy lifestyles are cornerstones of chronic disease prevention and treatment. The purpose of this study is to investigate independent and joint associations of five key health behaviors with health outcomes (body mass index (BMI kg/m2) and depressive symptoms) in adult twins. METHODS: We included 6,048 twin pairs from a community-based registry. Five key health behaviors were: (1) ≥ 8 h of sleep per night, (2) ≥ 5 servings of fruits and vegetables daily, (3) ≤ 2 h sedentary time per day, (4) ≥ 150 min of moderate-to-vigorous physical activity (MVPA) per week, and (5) no smoking. We analyzed phenotypic associations between behaviors and outcomes; whether phenotypic associations were confounded by additive genetic and shared environmental factors within twin pairs ("quasi-causal" associations); and which behaviors, considered simultaneously, had the largest associations with outcomes. RESULTS: We found negative phenotypic associations between number of behaviors achieved with BMI and depressive symptoms score (ps < 0.05). Associations remained significant, though attenuated, when controlling for genetic and shared environmental factors, and demographics, for depressive symptoms score but not BMI (p < 0.05). Quantitative variable importance measures derived from regression tree models showed sedentary time and MVPA were the most important variables in partitioning twins with different BMI, and smoking and sedentary time for partitioning twins with different depressive symptoms score. CONCLUSIONS: Achievement of commonly endorsed health behaviors is associated with lower BMI (especially sedentary and MVPA targets) and depressive symptoms score (especially sedentary and smoking targets). This provides further support of health behavior promotion to improve health outcomes.

Three legs of the missing heritability problem.

The so-called 'missing heritability problem' is often characterized by behavior geneticists as a numerical discrepancy between alternative kinds of heritability. For example, while 'traditional heritability' derived from twin and family studies indicates that approximately ∼50% of variation in intelligence is attributable to genetics, 'SNP heritability' derived from genome-wide association studies indicates that only ∼10% of variation in intelligence is attributable to genetics. This 40% gap in variance accounted for by alternative kinds of heritability is frequently referred to as what's "missing." Philosophers have picked up on this reading, suggesting that "dissolving" the missing heritability problem is merely a matter of closing the numerical gap between traditional and molecular kinds of heritability. We argue that this framing of the problem undervalues the severity of the many challenges to scientific understanding of the "heritability" of human behavior. On our view, resolving the numerical discrepancies between alternative kinds of heritability will do little to advance scientific explanation and understanding of behavior genetics. Thus, we propose a new conceptual framework of the missing heritability problem that comprises three independent methodological and explanatory challenges: the numerical gap, the prediction gap, and the mechanism gap.

What Do We Know About the Genetic Architecture of Psychopathology?

In the second half of the twentieth century, twin and family studies established beyond a reasonable doubt that all forms of psychopathology are substantially heritable and highly polygenic. These conclusions were simultaneously an important theoretical advance and a difficult methodological obstacle, as it became clear that heritability is universal and undifferentiated across forms of psychopathology, and the radical polygenicity of genetic effects limits the biological insight provided by genetically informed studies at the phenotypic level. The paradigm-shifting revolution brought on by the Human Genome Project has recapitulated the great methodological promise and the profound theoretical difficulties of the twin study era. We review these issues using the rubric of genetic architecture, which we define as a search for specific genetic insight that adds to the general conclusion that psychopathology is heritable and polygenic. Although significant problems remain, we see many promising avenues for progress.

Socioeconomic status impacts genetic influences on the longitudinal dynamic relationship between temperament and general cognitive ability in childhood: The Louisville Twin Study.

The current analysis investigates genetic and environmental influences on the bidirectional relationships between temperament and general cognitive ability (GCA). Measures of GCA and three temperament factors (persistence, approach, and reactivity) were collected from 486 children ages 4-9 years (80% white, 50% female) from the Louisville Twin Study from 1976 to 1998. The results indicated a bidirectional dynamic model of temperament influencing subsequent GCA and GCA influencing subsequent temperament. The dynamic relationship between temperament and GCA arose primarily from shared genetic variance, particularly in families with higher socioeconomic status, where input from temperament contributed on average 20% to genetic variance in GCA versus 0% in lower SES families.

Race, Ethnicity, and the Scarr-Rowe Hypothesis: A Cautionary Example of Fringe Science Entering the Mainstream.

In 2020, Pesta et al. published an article entitled "Racial and Ethnic Group Differences in the Heritability of Intelligence: A Systematic Review and Meta-Analysis" in the journal Intelligence. The authors framed their analysis as an examination of the Scarr-Rowe hypothesis, which holds that the heritability of intelligence varies as a function of socioeconomic status. Pesta et al. concluded that the heritability of intelligence does not differ across racial and ethnic groups in the United States. They claimed their results challenge the Scarr-Rowe hypothesis and support the hereditarian position that mean differences in IQ among racial and ethnic groups are attributable to genetic differences rather than environmental disparities. In this commentary, we outline severe theoretical, methodological, and rhetorical flaws in every step of Pesta et al.'s meta-analysis. The most reliable finding from Pesta et al. is consistent with the Scarr-Rowe hypothesis and directly contradicts a hereditarian understanding of group differences in intelligence. Finally, we suggest that Pesta et al. serves as an example of how racially motivated and poorly executed work can find its way into a mainstream scientific journal, underscoring the importance of robust peer review and rigorous editorial judgment in the open-science era.

Genetically informed, multilevel analysis of the Flynn Effect across four decades and three WISC versions.

This study investigated the systematic rise in cognitive ability scores over generations, known as the Flynn Effect, across middle childhood and early adolescence (7-15 years; 291 monozygotic pairs, 298 dizygotic pairs; 89% White). Leveraging the unique structure of the Louisville Twin Study (longitudinal data collected continuously from 1957 to 1999 using the Wechsler Intelligence Scale for Children [WISC], WISC-R, and WISC-III ed.), multilevel analyses revealed between-subjects Flynn Effects-as both decrease in mean scores upon test re-standardization and increase in mean scores across cohorts-as well as within-child Flynn Effects on cognitive growth across age. Overall gains equaled approximately three IQ points per decade. Novel genetically informed analyses suggested that individual sensitivity to the Flynn Effect was moderated by an interplay of genetic and environmental factors.

Genetic and environmental correlates of the nonlinear recovery of cognitive ability in Twins.

Twins regularly score nearly a standard deviation below the population mean on standardized measures of cognitive development in infancy but recover to the population mean by early childhood, making rapid gains through the toddler years. To date, only polynomial growth models have been fit to model cognitive recovery across childhood, limiting the applicability of the growth parameters to later developmental periods. We fit a nonlinear asymptotic Gompertz growth model to prospective cognitive scores from 1,153 individual twins from 578 families (47.9% male, 91.5% White, 61.6% monozygotic) measured at 16 time points between 3 months and 15 years. Twins displayed a lower asymptote of 86.47 (.90 SD below the population mean) and gained on average 17.01 points, achieving an upper asymptote of 103.48. Growth was observed to be most rapid at 3.26 years, highlighting the importance of the toddler years in cognitive development. Biometric analyses revealed that shared environmental factors accounted for the majority of the variance in initial cognitive ability as well as asymptotic growth in cognitive ability. Gestational age and family socioeconomic status (SES) were robust predictors of cognitive growth. Results from the present study provide insight into the growth processes underlying the recovery of cognitive ability to the population mean for children evincing slight delays in their initial cognitive ability. In particular, findings highlight prenatal factors and family economic resources as important aspects of the environment in the recovery of cognitive ability. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Galton's Quincunx: Probabilistic causation in developmental behavior genetics.

In what sense are associations between particular markers and complex behaviors made by genome-wide association studies (GWAS) and related techniques discoveries of, or entries into the study of, the causes of those behaviors? In this paper, we argue that when applied to individuals, the kinds of probabilistic 'causes' of complex traits that GWAS-style studies can point towards do not provide the kind of causal information that is useful for generating explanations; they do not, in other words, point towards useful explanations of why particular individuals have the traits that they do. We develop an analogy centered around Galton's "Quincunx" machine; while each pin might be associated with outcomes of a certain sort, in any particular trial, that pin might be entirely bypassed even if the ball eventually comes to rest in the box most strongly associated with that pin. Indeed, in any particular trial, the actual outcome of a ball hitting a pin might be the opposite of what is usually expected. While we might find particular pins associated with outcomes in the aggregate, these associations will not provide causally relevant information for understanding individual outcomes. In a similar way, the complexities of development likely render impossible any moves from population-level statistical associations between genetic markers and complex behaviors to an understanding of the causal processes by which individuals come to have the traits that they in fact have.

Psychometric and Classification Properties of the Peas in a Pod Questionnaire.

We examined the item properties of the Two Peas Questionnaire (TPQ) among a sample of same-sex twin pairs from the Washington State Twin Registry. With the exception of the 'two peas' item, three of the mistakenness items showed differential item functioning. Results showed that the monozygotic (MZ) and dizygotic (DZ) pairs may differ in their responses on these items, even among those with similar latent traits of similarity and confusability. Upon comparing three classification methods to determine the zygosity of same-sex twins, the overall classification accuracy rate was over 90% using the unit-weighted pair zygosity sum score, providing an efficient and sufficiently accurate zygosity classification. Given the inherent nature of twin-pair similarity, the TPQ is more accurate in the identification of MZ than DZ pairs. We conclude that the TPQ is a generally accurate, but by no means infallible, method of determining zygosity in twins who have not been genotyped.

Association between low back pain and body mass index in adult twins: an analysis of monozygotic and dizygotic twins of the Washington State Twin Registry.

BACKGROUND CONTEXT: Low back pain (LBP) is a common and significant cause of disability worldwide, however; questions about cause still remain. PURPOSE: To investigate the association between LBP, body mass index (BMI), and moderate to vigorous physical activity (MVPA) in a twin sample. STUDY DESIGN: Cross sectional study of monozygotic (MZ) and dizygotic (DZ) twins from the Washington State Twin Registry. PATIENT SAMPLE: Monozygotic and dizygotic twins from the Washington State Twin Registry. OUTCOME MEASURES: Self-report measures: Low back pain, body mass index, duration and intensity of exercise. METHODS: The sample included 5,183 same-sex pairs (69% MZ). The outcome was self-reported diagnosis of LBP from a health care provider. A phenotypic model tested the association between BMI and LBP without including genetic or shared environmental confounds. We then re-estimated the association using a quasi-causal model which controls for those confounds. Finally, we used a mediation model to investigate if the association between LBP and MVPA was mediated by BMI. RESULTS: In the phenotypic regression of LBP on BMI, there was a ~4-fold increase in the odds of having LBP with every one-unit increase in BMI (odds ratio [OR] =3.83; 95% confidence interval =3.28, 4.46). However, quasi-causal regression of LBP on BMI was reduced to zero (OR =0.95; 95% confidence interval =0.60, 1.49). A significant genetic background to BMI and LBP was present (bA =1.66; p<.001), even after controlling for confounders. In another analysis there was a significant direct effect between MVPA and LBP (bp=-0.092, standard error [SE] =0.017, p<.001). In mediation analysis, the effect of MVPA on LBP was partially mediated through MVPA effects on BMI ( [Formula: see text] =-0.043, SE=0.003, p<.001) and BMI effects on LBP ( [Formula: see text] =1.281, SE=0.079, OR=3.6, p<.001), however shared environmental factors confounded this relationship. CONCLUSIONS: BMI was not associated with LBP, despite sharing a phenotypic association, but they may share a genetic influence. The effect of MVPA on LBP is, in part, mediated by BMI but shared environment confounds this relationship. LEVEL OF EVIDENCE: Level 3.

Midlife Study of the Louisville Twins: Connecting Cognitive Development to Biological and Cognitive Aging.

The Louisville Twin Study (LTS) began in 1958 and became a premier longitudinal twin study of cognitive development. The LTS continuously collected data from twins through 2000 after which the study closed indefinitely due to lack of funding. Now that the majority of the sample is age 40 or older (61.36%, N = 1770), the LTS childhood data can be linked to midlife cognitive functioning, among other physical, biological, social, and psychiatric outcomes. We report results from two pilot studies in anticipation of beginning the midlife phase of the LTS. The first pilot study was a participant tracking study, in which we showed that approximately 90% of the Louisville families randomly sampled (N = 203) for the study could be found. The second pilot study consisted of 40 in-person interviews in which twins completed cognitive, memory, biometric, and functional ability measures. The main purpose of the second study was to correlate midlife measures of cognitive functioning to a measure of biological age, which is an alternative index to chronological age that quantifies age as a function of the breakdown of structural and functional physiological systems, and then to relate both of these measures to twins' cognitive developmental trajectories. Midlife IQ was uncorrelated with biological age (- .01) while better scores on episodic memory more strongly correlated with lower biological age (- .19 to - .31). As expected, midlife IQ positively correlated with IQ measures collected throughout childhood and adolescence. Additionally, positive linear rates of change in FSIQ scores in childhood significantly correlated with biological age (- .68), physical functioning (.71), and functional ability (- .55), suggesting that cognitive development predicts lower biological age, better physical functioning, and better functional ability. In sum, the Louisville twins can be relocated to investigate whether and how early and midlife cognitive and physical health factors contribute to cognitive aging.