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Pubertal timing matters for psychological development. Early maturation in girls is linked to risk for depression and externalizing problems in adolescence and possibly adulthood, and early and late maturation in boys are linked to depression. It is unclear whether pubertal timing uniquely predicts problems; it might instead mediate the continuity of behavior problems from childhood to adolescence or create psychological risk specifically in youth with existing problems, thus moderating the link. We investigated these issues in 534 girls and 550 boys, measuring pubertal timing by a logistic model fit to annual self-report measures of development and, in girls, age at menarche. Prepuberty internalizing and externalizing behavior problems were reported by parents. Adolescent behavior problems were reported by parents and youth. As expected, behavior problems were moderately stable. Pubertal timing was not predicted by childhood problems, so it did not mediate the continuity of behavior problems from childhood to adolescence. Pubertal timing did not moderate links between early and later problems for girls. For boys, early maturation accentuated the link between childhood problems and adolescent substance use. Overall, the replicated links between puberty and behavior problems appear to reflect the unique effects of puberty and child behavior problems on the development of adolescent behavior problems.

The Colorado Twin Registry (CTR) is a population-based registry formed from birth and school records including twins born between 1968 and the present. Two previous reports on the CTR [Rhea et al., (2006). Twin Research and Human Genetics, 9, 941-949; Rhea et al., (2013).Twin Research and Human Genetics, 16, 351-357] covered developments in the CTR through 2012. This report briefly summarizes previously presented material on ascertainment and recruitment and the relationships between samples and studies, discusses developments since 2012 for four previously described twin samples, describes two new samples and their complementary studies and expands on two subjects briefly mentioned in the last report: a history of genotyping efforts involving CTR samples, and a survey of collaborations and consortia in which CTR twins have been included. The CTR remains an active resource for both ongoing, longitudinal research and the recruitment of new twin samples for newly identified research opportunities.

The purpose of this update is to provide the most current information about both the Colorado Adoption Project (CAP) and the Longitudinal Twin Study (LTS) and to introduce the Colorado Adoption/Twin Study of Lifespan behavioral development and cognitive aging (CATSLife), a product of their merger and a unique study of lifespan behavioral development and cognitive aging. The primary objective of CATSLife is to assess the unique saliency of early childhood genetic and environmental factors to adult cognitive maintenance and change, as well as proximal influences and innovations that emerge across development. CATSLife is currently assessing up to 1600 individuals on the cusp of middle age, targeting those between 30 and 40 years of age. The ongoing CATSLife data collection is described as well as the longitudinal data available from the earlier CAP and LTS assessments. We illustrate CATSLife via current projects and publications, highlighting the measurement of genetic, biochemical, social, sociodemographic and environmental indices, including geospatial features, and their impact on cognitive maintenance in middle adulthood. CATSLife provides an unparalleled opportunity to assess prospectively the etiologies of cognitive change and test the saliency of early childhood versus proximal influences on the genesis of cognitive decline.

Because of recent concerns about the replication of published results in the behavioral and biomedical sciences (Ioannidis, PLoS Medicine, Vol. 2, 2005, p. e124; Open Science Collaboration, Science, Vol. 349, 2015, p. 943; Pashler & Wagenmakers, Perspectives on Psychological Science, Vol. 7, 2012, pp. 528-530), we have conducted a replication of our recently published analyses of longitudinal reading performance and attention deficit-hyperactivity disorder data from twin pairs selected for reading difficulties (Wadsworth et al., Twin Research and Human Genetics, Vol. 18, 2015, pp. 755-761). Results obtained from univariate and bivariate (DeFries & Fulker, Behavior Genetics, Vol. 15, 1985, pp. 467-473; Acta Geneticae Medicae et Gemellologiae: Twin Research, Vol. 37, 1988, pp. 205-216) analyses of data from a subset of twin pairs tested in the International Longitudinal Twin Study of Early Reading Development at post-4th grade, and its continuation into high school at post-9th grade, were compared to those from our previous report. Similar measures of reading performance, the same measures of inattention and hyperactivity/impulsivity, and similar selection criteria were used in the two studies. In general, the patterns of results obtained from these two independent studies were highly similar. Thus, these results clearly illustrate the principle that findings from studies in quantitative behavioral genetics often replicate (Plomin et al., Perspectives on Psychological Science, Vol. 11, 2016, pp. 3-23).

Although cross-sectional twin studies have assessed the genetic and environmental etiologies of substance use during adolescence and early adulthood, comparisons of results across different samples, measures, and cohorts are problematic. While several longitudinal twin studies have investigated these issues, few corroborating adoption studies have been conducted. The current study is the first to estimate the magnitude of genetic, shared environmental, and non-shared environmental influences on substance use (cigarettes, alcohol, and marijuana) from ages 14 to 18 years, using a prospective longitudinal adoption design. Adoptive and control sibling correlations provided substantial evidence for early genetic effects on cigarette, alcohol, and marijuana use/no use. Shared environmental effects were relatively modest, except for alcohol use, which showed increases in late adolescence (age 17 to 18 years). Sibling similarity for quantity/frequency of use also support additive genetic influences across adolescence, with some shared environmental influences for all three substances. To test the stability of these influences across time, a series of independent pathway models were run to explore common and age-specific influences. For all substances, there were minimal age-specific additive genetic and shared environmental influences on quantity/frequency of use. Further, there was a trend toward increasing genetic influences on cigarette and alcohol use across ages. Genetic influences on marijuana were important early, but did not contribute substantially at age 17 and 18 years. Overall, the findings indicate that genetic influences make important contributions to the frequency/quantity of substance use in adolescence, and suggest that new genetic influences may emerge in late adolescence for cigarette and alcohol use.

Approximately 60% of children with reading difficulties (RD) meet criteria for at least one co-occurring disorder. The most common of these, attention deficit-hyperactivity disorder (ADHD), occurs in 20-40% of individuals with RD. Recent studies have suggested that genetic influences are responsible. To assess the genetic etiologies of RD and the comorbidity of RD and two ADHD symptom dimensions -- inattention (IN) and hyperactivity/impulsivity (H/I) -- we are conducting the first longitudinal twin study of RD and ADHD. Data from twin pairs in which at least one member of the pair met criteria for proband status for RD at initial assessment, and were reassessed 5 years later, were subjected to DeFries-Fulker (DF) analysis. Analyses of reading composite data indicated that over 60% of the proband deficit at initial assessment was due to genetic influences, and that reading deficits at follow-up were due substantially to the same genetic influences. When a bivariate DF model was fitted to reading performance and IN data, genetic influences accounted for 60% of contemporaneous comorbidity and over 60% of the longitudinal relationship. In contrast, analysis of the comorbidity between reading performance and H/I indicated that common genetic influences accounted for only about 20% of the contemporaneous and about 10% of the longitudinal relationships. Results indicate that (1) genetic influences on RD are substantial and highly stable; (2) the comorbidity between RD and IN is due largely to genetic influences, both contemporaneously and longitudinally; and (3) genetic influences contribute significantly less to the comorbidity between RD and H/I.

This paper describes the Colorado Adoption Project (CAP), an ongoing genetically informative longitudinal study of behavioral development. We describe the features of the adoption design used in CAP, and discuss how this type of design uses data from both parent-offspring and related- versus unrelated-sibling comparisons to estimate the importance of genetic and shared environmental influences for resemblance among family members. The paper provides an overview of CAP's history, how subjects were ascertained, recruited, and retained, and the domains of assessment that have been explored since the CAP's initiation in 1975. Findings from some representative papers that make use of data from CAP participants illustrate the study's multifaceted nature as a parent-offspring and sibling behavioral genetic study, a study that parallels a complimentary twin study, a longitudinal study of development, a source of subjects for molecular genetic investigation, and a study of the outcomes of the adoption process itself. As subjects assessed first at age 1 approach age 40, we hope the CAP will establish itself as the first prospective adoption study of lifespan development.

The augmented multiple regression model for the analysis of data from selected twin pairs was extended to facilitate analyses of data from twin pairs and nontwin siblings. Fitting this extended model to data from both selected twin pairs and siblings yields direct estimates of heritability (h2) and the difference between environmental influences shared by members of twin pairs and those of sib or twin-sib pairs (i.e., c2(t) - c2 (s)). When this model was fitted to reading performance data from 293 monozygotic and 436 dizygotic pairs selected for reading difficulties, and 291 of their nontwin siblings, h2 = .48 ± .22, p = .03, and c2 (t) - c2 (s) = .22 ± .12, p = .06. Although the test for differential shared environmental influences is only marginally significant, the results of this analysis suggest that environmental influences on reading performance that are shared by members of twin pairs (.36) may be substantially greater than those for less contemporaneous twin-sibling pairs (.14).

Results obtained from previous longitudinal studies of reading difficulties indicate that reading deficits are generally stable. However, little is known about the etiology of this stability. Thus, the primary objective of this first longitudinal twin study of reading difficulties is to provide an initial assessment of genetic and environmental influences on the stability of reading deficits. Data were analyzed from a sample of 56 twin pairs, 18 identical (monozygotic, MZ) and 38 fraternal (dizygotic, DZ), in which at least one member of each pair was classified as reading-disabled in the Colorado Learning Disabilities Research Center, and on whom follow-up data were available. The twins were tested at two time points (average age of 10.3 years at initial assessment and 16.1 years at follow-up). A composite measure of reading performance (PIAT Reading Recognition, Reading Comprehension and Spelling) was highly stable, with a stability correlation of .84. Data from the initial time point were first subjected to univariate DeFries-Fulker multiple regression analysis and the resulting estimate of the heritability of the group deficit (h2g) was .84 (+/-.26). When the initial and follow-up data were then fitted to a bivariate extension of the basic DF model, bivariate heritability was estimated at .65, indicating that common genetic influences account for approximately 75% of the stability between reading measures at the two time points.

Although it has been suggested that genetic influences on reading difficulties may differ in boys and girls, results obtained from previous analyses of data from same-sex twin pairs have failed to provide evidence for a differential genetic etiology of reading disability (RD) as a function of gender. However, results of a recent study in which data from both same-sex and opposite-sex twin pairs were analyzed indicated a higher heritability for reading difficulties in boys (Harlaar et al., 2005). Because the current sample of twin pairs tested in the Colorado Learning Disabilities Research Center is substantially larger than that analyzed for our previous report (Wadsworth et al., 2000), this hypothesis was tested more rigorously using data from both same-sex and opposite-sex twin pairs in our current augmented sample. Composite reading scores from 634 twin pairs were subjected to DeFries-Fulker sex-limitation analysis using the model-fitting approach of Purcell and Sham (2003). Analysis of data from the combined sample of male and female twins indicated that genetic influences account for more than half the proband reading deficit (h2g = .58). When this model was extended to test for gender differences in the magnitude of genetic influences on RD, h2g estimates were somewhat higher for females than for males (.63 and .53, respectively), but the difference was nonsignificant (p > .3). A test for qualitative gender differences was also nonsignificant. Thus, these results provide little evidence for a differential genetic etiology of RD in boys and girls.