Joseph has written what purports to be a refutation of studies of Twins Reared-Apart (TRAs) with a singular focus on the Minnesota Study of Twins Reared-Apart (MISTRA). I show, in detail, that (a) his criticisms of previous TRA studies depend on sources that were discredited prior to MISTRA, as they all failed the test of replicability, (b) the list of biases he uses to invalidate MISTRA do not support his arguments, (c) the accusations of questionable research practices are unsubstantiated, (d) his claim that MISTRA should be evaluated in the context of psychology’s replication crisis is refuted. The TRA studies are constructive replications. Like many other scholars, past and present, he has been misled by the variation introduced by small samples (sampling error) and the distortion created by walking in the garden of forking paths. His endeavor is a concatenation of elision and erroneous statistical/scientific reasoning.

The endowment effect is a well-documented decision phenomenon, referring to a tendency that people price a commodity higher when selling it than when buying it. This phenomenon can be interpreted as a sort of inertia, an unwillingness to make a change, or in other words an attachment to the status-quo. People with autism dislike social interaction, and are thus probably less willing to buy and sell items and more attached to the status quo. Previous research revealed that T-carriers of a single-nucleotide polymorphism (SNP) of the dopamine beta-hydroxylase (DBH) gene, rs1611115 (C-1021T), are associated with autism and difficulty in social interaction. Therefore, rs1611115 may modulate the endowment effect. In the current study, the subjects sold and bought lotteries with various probabilities of winning money and provided saliva for genotyping. We found that T-carriers (people of CT genotype in this study) exhibited greater endowment effects compared to people of CC genotype. We discuss another two possible explanations of our results: empathy and loss aversion. This is the first attempt to research the endowment effect from the perspective of genes. The result indicates that an SNP of genes (an innate factor) can exert an observable effect on human market activities.

Behavioral genetics and cultural evolution have both revolutionized our understanding of human behavior – largely independent of each other. Here, we reconcile these two fields under a dual inheritance framework, offering a more nuanced understanding of the interaction between genes and culture. Going beyond typical analyses of gene–environment interactions, we describe the cultural dynamics that shape these interactions by shaping the environment and population structure. A cultural evolutionary approach can explain, for example, how factors such as rates of innovation and diffusion, density of cultural subgroups, and tolerance for behavioral diversity impact heritability estimates, thus yielding predictions for different social contexts. Moreover, when cumulative culture functionally overlaps with genes, genetic effects become masked, unmasked, or even reversed, and the causal effects of an identified gene become confounded with features of the cultural environment. The manner of confounding is specific to a particular society at a particular time, but a WEIRD (western, educated, industrialized, rich, and democratic) sampling problem obscures this boundedness. Cultural evolutionary dynamics are typically missing from models of gene-to-phenotype causality, hindering generalizability of genetic effects across societies and across time. We lay out a reconciled framework and use it to predict the ways in which heritability should differ between societies, between socioeconomic levels, and other groupings within some societies but not others, and over the life course. An integrated cultural evolutionary behavioral genetic approach cuts through the nature–nurture debate and helps resolve controversies in topics such as IQ.

Nick Martin has had an outsized influence on the field of behavioral genetics. Much of this influence stems from his mentorship of young scientists. I describe Nick’s mentorship, and what makes it special, from a personal perspective.

The author provides a personal perspective on Nick Martin’s contributions to behavioral genetics and his role in the workshops on statistical genetics held annually in Boulder. Highlighted are Prof. Martin’s seminal work on multivariate behavioral genetics, his career-long commitment to the value of the study of twins, and his enthusiastic support of the didactic mission of the ‘Boulder workshops’. These contributions and activities continue unabated as we celebrate Prof. Martin’s 70th birthday.

The Longitudinal Israeli Study of Twins (LIST) focuses on the developmental, genetic and environmental contributions to individual differences in children’s and adolescents’ social behavior. Key variables have been empathy, prosocial behavior, temperament and values. Another major goal of LIST has been to study gene–environment correlations, mainly concerning parenting. LIST includes 1657 families of Hebrew-speaking Israeli twins who have participated at least once in the study. Children’s environment and their development are assessed in a multivariate, multimethod fashion, including observed, parent-reported and self-reported data. The current article summarizes and updates recent findings from LIST. For example, LIST provided evidence for the heritability of human values with the youngest sample to date, and the first genetic investigation of adolescents’ identity formation. Finally, future aims of LIST are discussed.

The Twins Early Development Study (TEDS) is a longitudinal twin study that recruited over 16,000 twin-pairs born between 1994 and 1996 in England and Wales through national birth records. More than 10,000 of these families are still engaged in the study. TEDS was and still is a representative sample of the population in England and Wales. Rich cognitive and emotional/behavioral data have been collected from the twins from infancy to emerging adulthood, with data collection at first contact and at ages 2, 3, 4, 7, 8, 9, 10, 12, 14, 16, 18 and 21, enabling longitudinal genetically sensitive analyses. Data have been collected from the twins themselves, from their parents and teachers, and from the UK National Pupil Database. Genotyped DNA data are available for 10,346 individuals (who are unrelated except for 3320 dizygotic co-twins). TEDS data have contributed to over 400 scientific papers involving more than 140 researchers in 50 research institutions. TEDS offers an outstanding resource for investigating cognitive and behavioral development across childhood and early adulthood and actively fosters scientific collaborations.

The Children of the Twins Early Development Study (CoTEDS) is a new prospective children-of-twins study in the UK, designed to investigate intergenerational associations across child developmental stages. CoTEDS will enable research on genetic and environmental factors that underpin parent–child associations, with a focus on mental health and cognitive-related traits. Through CoTEDS, we will have a new lens to examine the roles that parents play in influencing child development, as well as the genetic and environmental factors that shape parenting behavior and experiences. Recruitment is ongoing from the sample of approximately 20,000 contactable adult twins who have been enrolled in the Twins Early Development Study (TEDS) since infancy. TEDS twins are invited to register all offspring to CoTEDS at birth, with 554 children registered as of May 2019. By recruiting the second generation of TEDS participants, CoTEDS will include information on adult twins and their offspring from infancy. Parent questionnaire-based data collection is now underway for 1- and 2-year-old CoTEDS infants, with further waves of data collection planned. Current data collection includes the following primary constructs: child mental health, temperament, language and cognitive development; parent mental health and social relationships; parenting behaviors and feelings; and other socioecological factors. Measurement tools have been selected with reference to existing genetically informative cohort studies to ensure overlap in phenotypes measured at corresponding stages of development. This built-in study overlap is intended to enable replication and triangulation of future analyses across samples and research designs. Here, we summarize study protocols and measurement procedures and describe future plans.

Several research teams have previously traced patterns of emerging conduct problems (CP) from early or middle childhood. The current study expands on this previous literature by using a genetically-informed, experimental, and long-term longitudinal design to examine trajectories of early-emerging conduct problems and early childhood discriminators of such patterns from the toddler period to adolescence. The sample represents a cohort of 731 toddlers and diverse families recruited based on socioeconomic, child, and family risk, varying in urbanicity and assessed on nine occasions between ages 2 and 14. In addition to examining child, family, and community level discriminators of patterns of emerging conduct problems, we were able to account for genetic susceptibility using polygenic scores and the study's experimental design to determine whether random assignment to the Family Check-Up (FCU) discriminated trajectory groups. In addition, in accord with differential susceptibility theory, we tested whether the effects of the FCU were stronger for those children with higher genetic susceptibility. Results augmented previous findings documenting the influence of child (inhibitory control [IC], gender) and family (harsh parenting, parental depression, and educational attainment) risk. In addition, children in the FCU were overrepresented in the persistent low versus persistent high CP group, but such direct effects were qualified by an interaction between the intervention and genetic susceptibility that was consistent with differential susceptibility. Implications are discussed for early identification and specifically, prevention efforts addressing early child and family risk.

Depression and anxiety are highly comorbid due to shared genetic risk factors, but less is known about whether burnout shares these risk factors. We aimed to examine whether the covariation between major depressive disorder (MDD), generalized anxiety disorder (GAD), and burnout is explained by common genetic and/or environmental factors. This cross-sectional study included 25,378 Swedish twins responding to a survey in 2005–2006. Structural equation models were used to analyze whether the trait variances and covariances were due to additive genetics, non-additive genetics, shared environment, and unique environment. Univariate analyses tested sex limitation models and multivariate analysis tested Cholesky, independent pathway, and common pathway models. The phenotypic correlations were 0.71 (0.69–0.74) between MDD and GAD, 0.58 (0.56–0.60) between MDD and burnout, and 0.53 (0.50–0.56) between GAD and burnout. Heritabilities were 45% for MDD, 49% for GAD, and 38% for burnout; no statistically significant sex differences were found. A common pathway model was chosen as the final model. The common factor was influenced by genetics (58%) and unique environment (42%), and explained 77% of the variation in MDD, 69% in GAD, and 44% in burnout. GAD and burnout had additive genetic factors unique to the phenotypes (11% each), while MDD did not. Unique environment explained 23% of the variability in MDD, 20% in GAD, and 45% in burnout. In conclusion, the covariation was explained by an underlying common factor, largely influenced by genetics. Burnout was to a large degree influenced by unique environmental factors not shared with MDD and GAD.

We examined developmental trends and sources of stability and change in adolescent personality by using twin data collected from 1981 to 2010 (273 monozygotic (MZ) and 48 dizygotic (DZ) twin pairs) from a secondary school affiliated with the University of Tokyo. Phenotypic analyses showed high rank-order stability and substantial mean-level increases in neuroticism and declines in extraversion over the adolescent years. Longitudinal bivariate genetic analyses revealed that the best-fitting model for adolescent personality includes additive genetic and non-shared environmental influences. Heritability estimates ranged approximately from 0.30 to 0.60. Additionally, three-year stability in adolescent personality was influenced mainly by genetic factors, and there were both genetic and environmental innovations in mid-adolescence. Our findings suggest that both genetic and environmental effects have significant roles in the etiology of personality development across adolescence.

The phenotypic (observed), genetic, and environmental correlations were examined in a sample of adult twins between the four factors and global score of the trait emotional intelligence questionnaire (TEIQue) and the seven vocational interest factors of the Jackson Career Explorer (JCE). Multiple significant correlations were found involving the work style vocational interest factor (consisting of job security, stamina, accountability, planfulness, and interpersonal confidence) and the social vocational interest factor (which included interests in the social sciences, personal services, teaching, social services, and elementary education), both of which correlated significantly with all of the TEIQue variables (well-being, self-control, emotionality, sociability, and global trait EI). Following bivariate genetic analyses, most of the significant phenotypic correlations were found to also have significant genetic correlations as well as significant non-shared (unique) environmental correlations.