Classical Twin Design Research Articles

Genetic and Neuronal Basis for Facial Emotion Perception in Humans and Macaques

Abstract The ability to rapidly recognize basic facial emotions (e.g., fear) is crucial for social interactions and adaptive functioning. To date, the origin of facial emotion recognition ability remains equivocal. Using a classical twin design in humans, we found a clear dissection of low and high spatial frequencies (LSF and HSF) in facial emotion perception: whereas genetic factors contributed to individual variation in LSF processing, HSF processing is largely shaped by environmental effects. Furthermore, the ability to recognize facial emotion of LSF content genetically correlated with the function of the amygdala. Crucially, single-unit recording of the amygdala in macaques further revealed the dissociation between LSF and HSF processing in facial emotion perception, indicating the existence of an evolutionarily conserved mechanism. This cross-species study enhances insights into the neurobiological dual-route model (subcortical vs. cortical) of emotion perception and illuminates the origin and the functional development of the emotional brain in primates.

Parent-child interaction at age 5 months: genetic and environmental contributions and associations with later socio-communicative development.

Characteristics of parent-child interaction (PCI) early in life have been associated with later development in the child. Twin studies can help to disentangle child contributions to parent-child interaction, for example, by assessing the influence of the child's genetics on his/her social environment, which includes parental behaviour. Infant twins from a community sample [354 monozygotic (MZ), 268 same-sex dizygotic (DZ)] were assessed in terms of PCI at age 5 months. We used the classical twin design to map the aetiology of several parent and child PCI scales and their covariation. We investigated the relations between PCI and later parent-rated child's social communication, language, and autistic traits at ages 2 and 3. Heritability was below 20% for all the included PCI traits. Unique (nonshared) environmental influences substantially overlapped across several PCI scales, suggesting that idiosyncrasies linked to each session shaped the scoring of several traits in a systematic way. Factor analysis revealed three uncorrelated latent factors, which were conceptualized as 'child negative affect', 'positive affective interaction', and 'parent's supportive strategies'. Parents who were rated highly on 'sensitive responsiveness' at 5 months tended to rate their offspring higher in terms of socio-communicative and language development and lower in terms of autistic traits in the second and third years of life. This study maps the phenotypic and aetiological structure of PCI in early infancy and supports the view that parents' sensitive responsiveness towards their infant is associated with later developmental gains in several domains. We did not find strong evidence of any so-called evocative genetic effects on parents' behaviour. We discuss the results considering the general challenge for lab-based observational PCI measures to capture the richness of parent-child interaction.

Migraine heritability and beyond: A scoping review of twin studies.

This scoping review aimed to summarize current knowledge from twin studies on migraine. Migraine heritability, genetic correlations with migraine comorbid disorders, and the use of discordant twin pairs in migraine research are described. Further, the review considers the unused potential of twin studies in migraine research and reflects on future directions. Twin studies can be used to understand how heritable and environmental factors influence human traits and disorders. The classical twin design compares the resemblance of a trait in monozygotic twins to that in dizygotic twins. The classical twin design can be extended to estimate the genetic correlation between disorders, model causality, and describe differences within discordant twin pairs. Studies focusing on migraine and using a twin study design were included. The search was performed on the PubMed-MEDLINE database using the search terms "migraine" AND "twin" OR "twins." It was done in May 2023, rerun in November 2023, and managed with the Covidence software. The search identified 52 twin studies on migraine. In 24 papers, the heritability of migraine was estimated with a classical twin design. Heritability estimates ranged from 0.36 to 0.48 for studies with adults, both men and women, and unspecified migraine. Migraine heritability was predominantly estimated with twin cohorts of North European ancestry, and only two studies examined migraine subtypes. A multilevel classical twin design was used in 11 studies to examine the co-occurrence between migraine and comorbid disorders. The differences within migraine discordant twin pairs were examined in nine studies. The heritability of migraine was estimated with a classical twin design in twin cohorts from seven different countries, with remarkably similar results across studies. Future studies should include migraine subtypes and twin cohorts of non-North European ancestry to better reflect the global population. Beyond heritability estimations, the twin method is a valuable tool for understanding causality and describing differences within discordant twin pairs. Despite more than 80 years of twin studies in migraine research, the twin design has a large unused potential to advance our understanding of migraine.

Overlapping genetic influences between creativity and borderline personality symptoms in a large Dutch sample

Creativity and mental disorders are sometimes seen as intertwined, but research is still unclear on whether, how much, and why. Here we explore the potential role of shared genetic factors behind creativity and symptoms of borderline personality disorder (BPD, characterized by mood swings and randomness of thoughts). Data were collected from 6745 twins (2378 complete pairs) by the Netherlands Twin Register on BPD scores (PAI-BOR questionnaire) and working in a creative profession (proxy for creativity). First, we tested whether there is an association between BPD symptoms and creative professions. Results confirmed that individuals scoring higher on the BPD spectrum are more likely to have a creative profession (Cohen’s d = 0.16). Next, we modeled how much of this association reflects underlying genetic and/or environmental correlations—by using a bivariate classical twin design. We found that creativity and BPD were each influenced by genetic factors (heritability = 0.45 for BPD and 0.67 for creativity) and that these traits are genetically correlated rG = 0.17. Environmental influences were not correlated. This is evidence for a common genetic mechanism between borderline personality scores and creativity which may reflect causal effects and shed light on mechanisms.

Prevalence and heritability of parental-reported speech and/or language difficulties in a Swedish population-based twin sample.

Research on genetic and environmental influences on speech and/or language difficulties (SaLD) is sparse, with inconsistent heritability estimates. We aimed to estimate the prevalence of parental reported SaLD and the relative contributions of genetic and environmental factors for the phenotype using a Swedish population-based twin sample. We hypothesized that there would be a stronger genetic than environmental effect on SaLD. Data were collected from The Child and Adolescent Twin Study in Sweden. The study sample included 16,774 twin pairs (16,946 males, 16,602 females), of which 5141 were monozygotic, 5861 dizygotic (DZ), and 5772 opposite-sex DZ pairs. The language items in the Autism-Tics, Attention-Deficit Hyperactivity Disorder, and other Comorbidities inventory were used to categorize individuals as having parental-reported SaLD. A classical twin design was used to estimate the relative contribution of genetic and environmental factors to the liability of SaLD. The prevalence of SaLD was 7.85% (95% confidence interval (CI) [7.57%-8.15%]) and 7.27% (95% CI [6.99%-7.55%]) when excluding individuals with autism and intellectual disability (ID). We also found that SaLD were significantly more prevalent in males than females with a ratio of 2:1. The heritability was estimated to be 75% (95% CI [67%-83%]) for SaLD. Shared environment played a significant role with an estimated contribution of 22% (95% CI [14%-30%]). The heritability estimate was reduced to 70% but with overlapping CI when excluding individuals with autism and ID. We provide evidence that SaLD is common in the population and under strong genetic influence. Future studies should focus on mapping the genetic architecture of SaLD and related disorders.

Conventional twin studies overestimate the environmental differences between families relevant to educational attainment

Estimates of shared environmental influence on educational attainment (EA) using the Classical Twin Design (CTD) have been enlisted as genetically sensitive measures of unequal opportunity. However, key assumptions of the CTD appear violated for EA. In this study we compared CTD estimates of shared environmental influence on EA with estimates from a Nuclear Twin and Family Design (NTFD) in the same 982 German families. Our CTD model estimated shared environmental influence at 43%. After accounting for assortative mating, our best fitting NTFD model estimated shared environmental influence at 26%, disaggregating this into twin-specific shared environments (16%) and environmental influences shared by all siblings (10%). Only the sibling shared environment captures environmental influences that reliably differ between families, suggesting the CTD substantially overestimates between-family differences in educational opportunity. Moreover, parental education was found to have no environmental effect on offspring education once genetic influences were accounted for.

A twin study of genetic and environmental contributions to attention-deficit/hyperactivity disorder over time.

Attention-deficit/hyperactivity disorder (ADHD) is an increasingly commonly diagnosed neurodevelopmental condition. One possibility is that this reflects a genuine increase in the prevalence of ADHD due to secular environmental changes, yet this hypothesis remains untested. We therefore investigated whether the genetic and environmental variance underlying ADHD, and traits of ADHD, has changed over time. We identified twins born from 1982 to 2008 from the Swedish Twin Registry (STR). We linked the STR with the Swedish National Patient Register and Prescribed Drug Register to identify diagnoses of ADHD and prescriptions of ADHD medication for these twins. We also utilized data collected from participants in the Child and Adolescent Twin Study in Sweden (CATSS), born from 1992 to 2008. Their parents completed a structured ADHD screening tool, which was used to measure traits of ADHD and assign broad screening diagnoses of ADHD. We used the classical twin design to test whether the degree to which variation in these measures was influenced by genetic and environmental variation changed over time. We included 22,678 twin pairs from the STR and 15,036 pairs from CATSS. The heritability of ADHD in the STR ranged from 66% to 86% over time, although these fluctuations were not statistically significant. We observed a modest increase in variance in ADHD traits, from 0.98 to 1.09. This was driven by small increases in the underlying genetic and environmental variance, with heritability estimated as 64%-65%. No statistically significant changes in variance in screening diagnoses were observed. The relative contribution of genetic and environmental factors to ADHD has remained stable over time, despite its increasing prevalence. Thus, changes in the underlying etiology of ADHD over time are unlikely to explain the increase in ADHD diagnoses.

Environment-by-PGS Interaction in the Classical Twin Design: An Application to Childhood Anxiety and Negative Affect

One type of genotype-environment interaction occurs when genetic effects on a phenotype are moderated by an environment; or when environmental effects on a phenotype are moderated by genes. Here we outline these types of genotype-environment interaction models, and propose a test of genotype-environment interaction based on the classical twin design, which includes observed genetic variables (polygenic scores: PGSs) that account for part of the genetic variance of the phenotype. We introduce environment-by-PGS interaction and the results of a simulation study to address statistical power and parameter recovery. Next, we apply the model to empirical data on anxiety and negative affect in children. The power to detect environment-by-PGS interaction depends on the heritability of the phenotype, and the strength of the PGS. The simulation results indicate that under realistic conditions of sample size, heritability and strength of the interaction, the environment-by-PGS model is a viable approach to detect genotype-environment interaction. In 7-year-old children, we defined two PGS based on the largest genetic association studies for 2 traits that are genetically correlated to childhood anxiety and negative affect, namely major depression (MDD) and intelligence (IQ). We find that common environmental influences on negative affect are amplified for children with a lower IQ-PGS.

Maximizing the value of twin studies in health and behaviour.

In the classical twin design, researchers compare trait resemblance in cohorts of identical and non-identical twins to understand how genetic and environmental factors correlate with resemblance in behaviour and other phenotypes. The twin design is also a valuable tool for studying causality, intergenerational transmission, and gene-environment correlation and interaction. Here we review recent developments in twin studies, recent results from twin studies of new phenotypes and recent insights into twinning. We ask whether the results of existing twin studies are representative of the general population and of global diversity, and we conclude that stronger efforts to increase representativeness are needed. We provide an updated overview of twin concordance and discordance for major diseases and mental disorders, which conveys a crucial message: genetic influences are not as deterministic as many believe. This has important implications for public understanding of genetic risk prediction tools, as the accuracy of genetic predictions can never exceed identical twin concordance rates.

Self-control and grit are associated with school performance mainly because of shared genetic effects.

By combining the classical twin design with regression analysis, we investigated the role of two non-cognitive factors, self-control and grit, in the prediction of school performance. We did so at the phenotypic, genetic, and environmental level. Teachers filled out a survey on the twins' school performance (school grades for reading, literacy, and math), self-control (ASEBA self-control scale), and grit (the perseverance aspect) for 4891 Dutch 12-years-old twin pairs (3837 pairs with data for both and 1054 pairs with data for one of the twins). We employed regression analyses to first assess the contributions of self-control and grit to school performance at the phenotypic level, and next at the genetic and environmental level, while correcting for rater (teacher) effects, parental SES, and sex. Higher SES was associated with better school performance, self-control, and grit. On average, girls had more self-control and grit than boys. Corrected for sex, SES, and teacher rater effects, genetic factors accounted for 74%, 69%, and 58% of the phenotypic variance of school performance, self-control, and grit, respectively. Phenotypically, self-control and grit explained 28.3% of the variance in school performance. We found that this phenotypic result largely reflected genetic influences. Children who have better self-control and are grittier tend to do better in school. Individual differences in these three traits are not correlated because of shared environmental influences, but mainly because of shared genetic factors.

Environmental effects on brain functional networks in a juvenile twin population

The brain’s intrinsic organization into large-scale functional networks, the resting state networks (RSN), shows complex inter-individual variability, consolidated during development. Nevertheless, the role of gene and environment on developmental brain functional connectivity (FC) remains largely unknown. Twin design represents an optimal platform to shed light on these effects acting on RSN characteristics. In this study, we applied statistical twin methods to resting-state functional magnetic resonance imaging (rs-fMRI) scans from 50 young twin pairs (aged 10–30 years) to preliminarily explore developmental determinants of brain FC. Multi-scale FC features were extracted and tested for applicability of classical ACE and ADE twin designs. Epistatic genetic effects were also assessed. In our sample, genetic and environmental effects on the brain functional connections largely varied between brain regions and FC features, showing good consistency at multiple spatial scales. Although we found selective contributions of common environment on temporo-occipital connections and of genetics on frontotemporal connections, the unique environment showed a predominant effect on FC link- and node-level features. Despite the lack of accurate genetic modeling, our preliminary results showed complex relationships between genes, environment, and functional brain connections during development. A predominant role of the unique environment on multi-scale RSN characteristics was suggested, which needs replications on independent samples. Future investigations should especially focus on nonadditive genetic effects, which remain largely unexplored.

Heritability of the glycan clock of biological age.

Immunoglobulin G is posttranslationally modified by the addition of complex N-glycans affecting its function and mediating inflammation at multiple levels. IgG glycome composition changes with age and health in a predictive pattern, presumably due to inflammaging. As a result, a novel biological aging biomarker, glycan clock of age, was developed. Glycan clock of age is the first of biological aging clocks for which multiple studies showed a possibility of clock reversal even with simple lifestyle interventions. However, none of the previous studies determined to which extent the glycan clock can be turned, and how much is fixed by genetic predisposition. To determine the contribution of genetic and environmental factors to phenotypic variation of the glycan clock, we performed heritability analysis on two TwinsUK female cohorts. IgG glycans from monozygotic and dizygotic twin pairs were analyzed by UHPLC and glycan age was calculated using the glycan clock. In order to determine additive genetic, shared, and unique environmental contributions, a classical twin design was applied. Heritability of the glycan clock was calculated for participants of one cross-sectional and one longitudinal cohort with three time points to assess the reliability of measurements. Heritability estimate for the glycan clock was 39% on average, suggesting a moderate contribution of additive genetic factors (A) to glycan clock variation. Remarkably, heritability estimates remained approximately the same in all time points of the longitudinal study, even though IgG glycome composition changed substantially. Most environmental contributions came from shared environmental factors (C), with unique environmental factors (E) having a minor role. Interestingly, heritability estimates nearly doubled, to an average of 71%, when we included age as a covariant. This intervention also inflated the estimates of unique environmental factors contributing to glycan clock variation. A complex interplay between genetic and environmental factors defines alternative IgG glycosylation during aging and, consequently, dictates the glycan clock's ticking. Apparently, environmental factors (including lifestyle choices) have a strong impact on the biological age measured with the glycan clock, which additionally clarifies why this aging clock is one of the most potent biomarkers of biological aging.

A Trait‐like Component of Subjective Memory Concern in Men from Average Age 38 to 67 Years

AbstractBackgroundSubjective memory concern is a risk factor for dementia in older adults, yet it also appears to be stable over time. Few studies examine memory concern starting in midlife in cognitively normal adults or the role of genetic influences on memory concern. We focused on the stability of subjective memory concern from early midlife into older adulthood and its association with objectively assessed episodic memory and depressive symptoms. Using a classical twin design, we assessed genetic and environmental influences on longitudinally‐assessed subjective concern and its overlap with episodic memory and depressive symptoms.MethodWe examined 1,334 community‐dwelling men assessed in the Survey of Health and the Vietnam Era Twin Study of Aging, who were assessed for subjective memory concern at average ages 38, 56, 62, and 67. Objective episodic memory and depressive symptoms were assessed at 56, 62, and 67. Biometric twin models were used to estimate genetic and environmental influences over time, and correlated genetic and environmental influences between measures.ResultSubjective memory concern was highly stable after average age 38 and not significantly associated with age. Phenotypic models showed that subjective memory concern was more related to depressive symptoms (β = .46) than with episodic memory (β = ‐.12) within timepoint, as shown by non‐overlapping confidence intervals. There were no significant lagged associations of subjective memory concern with episodic memory or depressive symptoms. Heritability of subjective memory concern was 51% and remained stable over time; 49% of the variation was attributed to unshared environmental influences. There were also significant genetic correlations between subjective memory concern and both episodic memory and depressive symptoms.ConclusionSubjective memory concern was stable from age 38 to age 67, and over half of the variance was explained by genetic influences. There was also significant genetic overlap with depressive symptoms and episodic memory. The stability and heritability results provide strong support for a trait‐like component of subjective memory concern. To be most useful as an indicator of imminent cognitive decline and increased risk for dementia, it will be important to differentiate dynamic aspects of subjective concern from its trait‐related dimension.

Heritability and environmental influences on the onset of aortic valve sclerosis: a twin population study

Abstract Background Aortic valve sclerosis (AVSc) is the earliest manifestation of a life-threatening cardiovascular disorder, namely aortic valve stenosis (AS). AVSc is also recognized as a red flag linked to worse cardiovascular outcomes in high-risk coronary artery disease patients. However, the genetic background of AVSc is still unknown. Purpose To examine whether the heritability and environmental contributions play a role in the onset of AVSc using a sample of Italian twins. Methods The present study is based on the classical twin design. Twins, aged 50 to 70 years, already enrolled in the Italian Twin Register, were contacted and invited to undergo a clinical, echocardiographic, and complete carotid artery ultrasound examination at the our Center, between July 2017 and December 2021. The presence of AVSc was recognized as non-uniform thickening with or without spotty calcified areas of the aortic valve leaflets without a significant transvalvular gradient (maximum aortic velocity <2.5 m/s). Twin zygosity was assessed through a questionnaire on physical similarity during childhood, known to be ∼95% accurate. Tetrachoric twin correlations by zygosity were estimated with Mx Software using liability threshold saturated models and incorporating age as a covariate. Liability-threshold structural equation modelling was performed to decompose the phenotypic variance into contributions due to additive genetic (A), common environmental (C), and unique environmental (E) effects. Results A total of 216 adult twins (66 monozygotic, MZ and 42 dizygotic pairs, DZ; mean age 59.9±6.2) were enrolled in the study. The estimated prevalence rate of AVSc in the total sample was 29.2%. As significant sex differences were detected (males 45.2% and females 22.7%, p<0.01), the additional twin analyses were performed as intra-sex analyses. Females showed a greater tetrachoric correlation in MZ twins (r=0.37) compared to DZ twins (r=0.23), suggesting the existence of a genetic influence. Genetic factors, under the best (AE) model, accounted for 38% of the variance in liability to AVSc with the remaining contribution due to unique environmental influences (E = 62%). The contribution of the common environment (C) to the goodness of fit was negligible. The male group was too small for statistical calculation. Conclusion To our knowledge, the present study is the first to document the involvement of genetic factors in the development of AVSc. Our data also warrant further studies to both validate the findings obtained and to better explore the heritability of AVSc. Furthermore, our results provide a first evidence that an echocardiographic screening in individuals with relatives affected by AVSc has a scientific rational basis. Funding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): The Italian Ministry of Health

Heritability of Psychological Traits and Developmental Milestones in Infancy

Although infancy is the most rapid period of postnatal growth and development, factors associated with variation in infant traits are not well understood. To synthesize the large twin study literature partitioning phenotypic variance in psychological traits and developmental milestones in infancy into estimates of heritability and shared and nonshared environment. PubMed, PsycINFO, and references of included publications were searched up to February 11, 2021. Peer-reviewed publications using the classical twin design to study psychological traits and developmental milestones from birth to 2 years old were included. Data were extracted in line with Preferred Reporting Items for Systematic Reviews and Meta-Analyses and categorized using the International Classification of Functioning, Disability and Health: Children and Youth Version. Data were pooled in 3-level random effects models, incorporating within-cohort variance in outcome measurement and between-cohort variance. Data were analyzed from March 2021 through September 2021. The primary outcomes were monozygotic and dizygotic twin correlations. These were used to calculate genetic and shared and nonshared environment estimates. Among 139 publications that were systematically retrieved, data were available on 79 044 twin pairs (31 053 monozygotic and 47 991 dizygotic pairs), 52 independent samples, and 21 countries. Meta-analyses were conducted on psychological traits and developmental milestones from 106 publications organized into 10 categories of functioning, disability, and health. Moderate to high genetic estimates for 8 categories were found, the highest of which was psychomotor functions (pooled h2, 0.59; 95% CI, 0.25-0.79; P < .001). Several categories of traits had substantial shared environment estimates, the highest being mental functions of language (pooled c2, 0.59; 95% CI, 0.24-0.86; P = .001). All examined categories of traits had moderate or high nonshared environment estimates, the highest of which were emotional functions (pooled e2, 0.42; 95% CI, 0.33-0.50; P < .001) and family relationships (pooled e2, 0.42; 95% CI, 0.30-0.55; P < .001). These findings may be an important source of information to guide future gene discovery research, public perspectives on nature and nurture, and clinical insights into the degree to which family history and environments may estimate major domains of infant functioning, disability, and health in psychological traits and developmental milestones.

A Note on Jöreskog’s ACDE Twin Model: A Solution, Not the Solution

The classical twin design is used to decompose phenotypic variance into genetic and environmental variance components. In practice, for reasons of identification, either an ADE or an ACE twin model is fitted, i.e., models with three variance components. Jöreskog proposed to use the Moore-Penrose inverse to estimate the four genetic and environmental variance components in the ACDE twin model. We demonstrate that the variance components thus obtained do not equal the true genetic and environmental variance components. Given a ACDE model, resorting to an ADE or ACE model or applying Jöreskog’s method will not produce correct results. However, it is possible that Jöreskog’s method will produce a better approximation to the true variance components under certain configurations of A, D, C, and E variance components.

Multivariate Genetic Structure of Externalizing Behavior and Structural Brain Development in a Longitudinal Adolescent Twin Sample.

Externalizing behavior in its more extreme form is often considered a problem to the individual, their families, teachers, and society as a whole. Several brain structures have been linked to externalizing behavior and such associations may arise if the (co)development of externalizing behavior and brain structures share the same genetic and/or environmental factor(s). We assessed externalizing behavior with the Child Behavior Checklist and Youth Self Report, and the brain volumes and white matter integrity (fractional anisotropy [FA] and mean diffusivity [MD]) with magnetic resonance imaging in the BrainSCALE cohort, which consisted of twins and their older siblings from 112 families measured longitudinally at ages 10, 13, and 18 years for the twins. Genetic covariance modeling based on the classical twin design, extended to also include siblings of twins, showed that genes influence externalizing behavior and changes therein (h2 up to 88%). More pronounced externalizing behavior was associated with higher FA (observed correlation rph up to +0.20) and lower MD (rph up to −0.20), with sizeable genetic correlations (FA ra up to +0.42; MD ra up to −0.33). The cortical gray matter (CGM; rph up to −0.20) and cerebral white matter (CWM; rph up to +0.20) volume were phenotypically but not genetically associated with externalizing behavior. These results suggest a potential mediating role for global brain structures in the display of externalizing behavior during adolescence that are both partially explained by the influence of the same genetic factor.

Genetic influences on central and peripheral nervous system activity during fear conditioning

Fear conditioning is an evolutionarily conserved type of learning serving as a model for the acquisition of situationally induced anxiety. Brain function supporting fear conditioning may be genetically influenced, which in part could explain genetic susceptibility for anxiety following stress exposure. Using a classical twin design and functional magnetic resonance imaging, we evaluated genetic influences (h2) on brain activity and standard autonomic measures during fear conditioning. We found an additive genetic influence on mean brain activation (h2 = 0.34) and autonomic responses (h2 = 0.24) during fear learning. The experiment also allowed estimation of the genetic influence on brain activation during safety learning (h2 = 0.55). The mean safety, but not fear, related brain activation was genetically correlated with autonomic responses. We conclude that fear and safety learning processes, both involved in anxiety development, are moderately genetically influenced as expressed both in the brain and the body.

Exploring the foundational origins of public service motivation through the lens of behavioral genetics

AbstractDespite the proliferation of research on public service motivation (PSM), fundamental questions about its origins continue to evade scholars: Is PSM driven by genetics, socialized through experiences, or both? If PSM is socialized, when does socialization occur? Answering these questions is critical for reconciling the state versus trait debate, and for assessing the validity of practical implications prescribed by PSM studies. Utilizing “nature's own experiment,” we adopt a classical twin design with 1035 twin pairs to identify how genetic heritability, a common environment, or unique environment and experiences can explain variation in PSM. Results show that PSM is heavily influenced by individuals' unique environments and experiences; not by genetics. This lends strong evidence to PSM's uniqueness as a motivational construct as related “other‐regarding” concepts show sizeable genetic components. Finally, our results corroborate that PSM is a human resource with dynamic properties organizations can cultivate to enhance productivity in public service workforces.

Heritability in friendship networks

There is considerable evidence nowadays that friendship networks account for a large part of an individual’s success or failure in life. Little, however, is known about the extent to which friendship networks are associated with an individual’s genotype. Using data from the German TwinLife study, we explore, within a classical twin design, whether friendship networks are related to genes. We find a substantial heritability component in twins’ network sizes and network homophily, but not in twins’ network closeness. The genetic influence on network characteristics may be attributable to traits which are themselves influenced by genetic factors. Addressing indirect ways in which genes could influence network characteristics, we do not find evidence that shared hobbies, education, or Big Five personality traits affect networks.