Nonshared Environment Research Articles

On Sibling Designs

To the Editor: Comparisons of siblings that are discordant for particular exposures or outcomes are increasingly used in epidemiology.1 Frisell et al2 have provided important insight into potential limitations of sibling comparisons. We would like to add three points to their thought provoking discussion. First, given that uncontrolled, unshared environmental factors can bias the results of sibling-matched studies, Frisell et al2 note that these aspects should be measured and controlled when possible. Usually discordant sibling studies do, however, control for systematic unshared aspects of the family environment that can be measured, for example, birth order, maternal and paternal age, and gestational age at birth. Furthermore, population estimates controlled for measured unshared aspects of the family environment often render similar estimates to the discordant sibling estimates. It is the nonsystematic aspects of the unshared environment that are most difficult to measure and that tend to be uncontrolled. But evidence suggests that these nonsystematic factors tend to be events that do not relate in any general way to confounding factors.3 Thus, after taking into account the way that discordant sibling studies are actually done, the extent to which their results will be biased by unshared factors remains unclear. Second, Frisell et al2 note that sibling-matched designs will yield causal estimates when all confounders are perfectly shared between siblings and there are no unshared confounders. Although subject to limitations, biometric models from genetically informative data suggest that some outcomes have a low shared environmental contribution to variance.3 Certainly, the lack of a shared environmental contribution to variation within a population, using these models, is not equivalent to no causal effect of shared environmental factors on health outcomes. Nevertheless, given that uncontrolled systematic factors of the nonshared environment will bias the results from discordant sibling designs, and that the purpose of using the discordant sibling design is to control for the shared environmental factors, one must question the appropriateness of a discordant sibling design when convergent evidence suggests that shared environmental factors contribute little to interindividual variation in the outcome of interest. Third, Frisell et al2 underscore the potential dilution of effects in the sibling design when a proportion of “discordant” pairs are actually concordant misclassified pairs—a point that they expand from previous findings in the economics literature.4 Frisell et al2 discuss random misclassification, however. We suggest that misclassification may not be random. Consider the example of siblings from women discordant for smoking across pregnancies. Misclassification of smoking status may indeed vary systematically by nonshared familial factors such as birth order. For example, few women are likely to take up smoking in their second pregnancy if they did not smoke in the first. Thus, discordant women for whom data indicate smoking in a second but not first pregnancy would be more likely to be “concordant smokers” who were misclassified than women who smoked in a first but not subsequent pregnancies. The impact of this bias may be greater than the bias from random misclassification and may bias toward or away from the null. Discordant sibling studies are increasingly used to help confirm results from population studies or to indicate the potential for bias in them. Also, genetically informative designs to understand developmental contributions to health increasingly inform these and other epidemiological studies. Discussions of potential biases that accompany evolving study designs will continue to improve our science. Frisell et al’s2 thought provoking article should stimulate continued methodological work investigating the practical implications of the types of biases that sibling studies are prone to. Katherine M. Keyes Department of Epidemiology Mailman School of Public Health Columbia University New York State Psychiatric Institute New York, NY [email protected] George Davey Smith MRC Centre for Causal Analyses in Translational Epidemiology School of Social and Community Medicine University of Bristol Oakfield House Oakfield Grove Bristol, United Kingdom Ezra Susser Department of Epidemiology Mailman School of Public Health Columbia University New York State Psychiatric Institute New York, NY

Heritability assessment of cartilage metabolism. A twin study on procollagen II N-terminal propeptide (PIIANP)

Heritability assessment of cartilage metabolism. A twin study on procollagen II N-terminal propeptide (PIIANP)

Marital adjustment as a moderator for genetic and environmental influences on parenting.

Family systems theory proposes that the parent-child relationship is embedded within the broader system of the family, and that other family subsystems can influence the dynamics and quality of the parent-child relationship. The current paper examines marital adjustment as a context for the parent-child relationship during adolescence. Specifically, the extent to which marital adjustment moderates child-based genetic and environmental effects on the parent-child relationship was assessed. Data for this study were from the initial wave of the Nonshared Environment in Adolescent Development (NEAD) study, and included 720 families with same-sex sibling pairs, ages 10-18 years. A range of sibling and family types was sampled, with 93 monozygotic twin pairs, 99 dizygotic twin pairs, and 95 sibling pairs from nondivorced families, and 182 sibling, 109 half-sibling, and 130 unrelated sibling pairs from stepfamilies. Composite measures of marriage (based on parent reports) and parenting (based child and parent reports and observation ratings) were examined. Results indicate that as marital adjustment declines, evocative child effects on parenting increase, while the role of shared family experiences declines. However, the specific impact of marital adjustment on child-based genetic and child-specific nonshared environmental contributions to parenting differed for mothers and fathers. This study identifies a previously unexplored mechanism through which family subsystems influence each other.

The role of gene–environment correlations and interactions in middle childhood depressive symptoms

Depression is known to be associated with a wide array of environmental factors. Such associations are due at least in part to genetic influences on both. This issue has been little explored with preadolescent children. Measures of family chaos and parenting style at age 9 and child depressive symptoms at age 12 were completed by 3,258 twin pairs from the Twins Early Development Study and their parents. Quantitative genetic modeling was used to explore common and unique genetic and environmental influences on both family environment and later depressive symptoms. Depressive symptoms at age 12 were significantly heritable. Moderate genetic effects influenced parenting style and family chaos at the age of 9, indicating gene-environment correlation. There were significant genetic correlations between family environment and depressive symptoms. There was some evidence of a Gene × Environment interaction, with stronger genetic effects on depressive symptoms for children with more suboptimal family environment. There was an Environment × Environment interaction, with effects of nonshared environment on depressive symptoms stronger for twins with more adverse parenting experiences. There is some evidence for gene-environment correlation between aspects of family environment in middle childhood and subsequent depressive symptoms. This suggests that one of the mechanisms by which genes lead to depressive symptoms may be by themselves influencing depressogenic environments.

Parenting and risk for mood, anxiety and substance use disorders: a study in population-based male twins.

Previous studies consistently identified a relationship between parenting behavior and psychopathology. In this study, we extended prior analyses performed in female twins to a large sample of twins from male-male pairs. We used interview data on 2,609 adult male twins from a population-based twin registry. We examined the association between three retrospectively reported parenting dimensions (coldness, protectiveness, and authoritarianism) and lifetime history of seven common psychiatric and substance use disorders. Using univariate structural equation modeling, we also examined the influence of the genetic and environmental factors on parenting. Examined individually, coldness was consistently associated with risk for a broad range of adult psychopathology. Averaged odds of psychiatric disorders associated with parenting were increased between 26 and 36 %. When the three parenting dimensions were examined together, coldness remained significant for major depression, phobia, and generalized anxiety disorder. Controlling for other disorders, the associations between the parenting dimensions and psychopathology were non-specific. Twin fitting model demonstrated that modest heritability accounted for parenting, whereas most variance resulted from the non-shared environment. Based on our current and prior findings, there is broad similarity in the impact of parenting on adult psychopathology between men and women.

Genetic and Environmental Influences on the Relationship Between Mastery and Alcohol Dependence

Sense of mastery, a personal resource, is likely to have an inverse association with alcohol dependence. Previous evidence, however, is sparse. In addition, the extent to which an association is due to genetic or environmental factors is unknown. Data were from 3,983 male twins and 2,630 female twins who had ever used alcohol, interviewed in the Virginia Adult Twin Study of Psychiatric and Substance Use Disorders. Mastery was measured by a 6-item scale. Lifetime diagnosis of alcohol dependence was based on DSM-IV criteria assessed in a structured diagnostic interview. Univariate analyses modeled the relative contributions of genetic and environmental factors to mastery and alcohol dependence using Mx software. Bivariate Cholesky models were fit to the mastery and alcohol dependence raw data. In the best-fitting model of mastery, genetic factors accounted for about 33% of the observed variance. Nonshared environmental factors, including random measurement error, accounted for the remaining 67%. Fifty-six percent of the variance in liability to alcohol dependence was genetic, and the other 44% was explained by the nonshared environment. The phenotypic polychoric correlation between mastery and alcohol dependence of -0.18 was primarily (67% in the best-fitting model) explained by genes common to both low mastery and alcohol dependence; the rest was explained by nonshared environmental factors. The findings indicate that genetic risk for alcohol dependence overlaps with genetic factors that influence sense of mastery. Key challenges for future research are to identify the genes that influence mastery and alcohol dependence, as well as the environmental pathways by which they come to be linked.

Genetic and environmental effects on age at menarche, and its relationship with reproductive health in twins

INTRODUCTION:Menarche or first menstrual period is a landmark in reproductive life span and it is the most prominent change of puberty. The timing of menarche can be under the influence of genes as well as individual environmental factors interacting with genetic factors.OBJECTIVE:Our study objectives were (a) to investigate the heritability of age of menarche in twins, (b) to obtain the association between age of menarche and childhood factors, and reproductive events/behavior, (c) to examine whether or not having a male co-twin affects early/late menarche.METHODOLOGY:A group of female-female identical (n = 108, 54 pairs), non-identical twins (n = 68, 34 pairs) and 17 females from opposite-sex twin sets were identified from twin registries of Malaysia and Iran. Genetic analysis was performed via two methods of Falconers’ formula and maximum likelihood.RESULTS:Heritability was found to be 66% using Falconers’ formula and 15% using univariate twin analysis. Model analysis revealed that shared environmental factors have a major contribution in determining the age of menarche (82%) followed by non-shared environment (18%).DISCUSSION:Result of this study is consistent with that of the literature. Timing of menarche could be under the influence of shared and non-shared environmental effects. Hirsutism was found to have a higher frequency among subjects with late menarche. There was no significant difference in age of menarche between females of opposite-sex twins and females of same-sex twins.CONCLUSION:It is concluded that twin models provide a powerful means of examining the total genetic contribution to age of menarche. Longitudinal studies of twins may clarify the type of environmental effects that determine the age of menarche.

The genetic and environmental etiology of decision-making: A longitudinal twin study

The present study examined the genetic and environmental etiology of decision-making (Iowa Gambling Task; Bechara, Damásio, Damásio, & Anderson, 1994), in a sample of twins at ages 11–13, 14–15, and 16–18 years. The variance across five 20-trial blocks could be explained by a latent “decision-making’’ factor within each of the three times of IGT administration. This latent factor was modestly influenced by genetic factors, explaining 35%, 20% and 46% of the variance within each of the three times of IGT administration. The remaining variance was explained by the non-shared environment (65%, 80% and 54%, respectively). Block-specific non-shared environmental influences were also observed. The stability of decision-making was modest across development. Youth showed a trend to choose less risky decks at later ages, suggesting some improvement in task performance across development. These findings contribute to our understanding of decision-making by highlighting the particular importance of each person's unique experiences on individual differences.

The Peri/Postnatal Epigenetic Twins Study (PETS)

The Peri/postnatal Epigenetic Twins Study (PETS) is a longitudinal cohort of 250 pairs of Australian twins and their mothers, who were recruited mid-way through pregnancy from January 2007 to September 2009. The study is centered on the developmental origins of health and disease paradigm (DOHaD) in which an adverse intrauterine environment predisposes the individual to complex disease in later life by reducing growth in utero and adversely altering developmental plasticity. Data concerning diet and lifestyle were collected from mothers during pregnancy, and samples of plasma and serum taken at 28 weeks' gestation. We attended 75% of all births, at which time we collected multiple biological samples including placenta, cord blood, and neonatal cheek cells, the latter from 91% of pairs. Chorionicity was recorded and zygosity was determined by DNA testing where necessary. Approximately 40% of the twins are monozygotic, two-thirds of which are dichorionic. Twins were seen again at 18 months of age and repeat blood and cheek swabs taken where possible. Studies of gene expression and the epigenetic marks of DNA methylation have so far revealed that twins exhibit a wide range of epigenetic discordance at birth, that one-third of the epigenome changes significantly between birth and 18 months; shared (maternal) environment, genetic factors, and non-shared intrauterine environment contribute to an increasing proportion of epigenetic variation at birth, respectively, and affect tissues differently, and that within-pair birth weight discordance correlates with epigenetic discordance in genes associated with lipid metabolism, supporting an epigenetic mechanism for DOHaD.

Indicators of domestic/intimate partner violence are structured by genetic and nonshared environmental influences

One of the most consistent findings to emerge from domestic/intimate partner violence (IPV) research is that IPV tends to “run in the family.” Social learning theories appear to be consistent with empirical data, but almost no attention has been given to alternative explanations, including that genetic factors explain intergenerational transmission of IPV. Data for this study were drawn from wave 4 of the National Longitudinal Study of Adolescent Health (Add Health). Three indicators of IPV were measured and genetic factors accounted for 24% of the variance in hitting one's partner, 54% of the variance in injuring one's partner, and 51% of the variance in forcing sexual activity on one's partner. The shared environment explained none of the variance across all three indicators and the nonshared environment explained the remainder of the variance. These findings point to the importance of genetic factors in the etiology of IPV.

DNA damage response in monozygotic twins discordant for smoking habits

Previous studies in twins indicate that non-shared environment, beyond genetic factors, contributes substantially to individual variation in mutagen sensitivity; however, the role of specific causative factors (e.g. tobacco smoke, diet) was not elucidated. In this investigation, a population of 22 couples of monozygotic twins with discordant smoking habits was selected with the aim of evaluating the influence of tobacco smoke on individual response to DNA damage. The study design virtually eliminated the contribution of genetic heterogeneity to the intra-pair variation in DNA damage response, and thus any difference in the end-points investigated could directly be attributed to the non-shared environment experienced by co-twins, which included as main factor cigarette smoke exposure. Peripheral lymphocytes of study subjects were challenged ex vivo with γ-rays, and the induction, processing, fixation of DNA damage evaluated through multiple approaches. Folate status of study subjects was considered significant covariate since it is affected by smoking habits and can influence radiosensitivity. Similar responses were elicited by γ-rays in co-twins for all the end-points analysed, despite their discordant smoking habits. Folate status did not modify DNA damage response, even though a combined effect of smoking habits, low-plasma folic acid level, and ionising radiation was observed on apoptosis. A possible modulation of DNA damage response by duration and intensity of tobacco smoke exposure was suggested by Comet assay and micronucleus data, but the effect was quantitatively limited. Overall, the results obtained indicate that differences in smoking habits do not contribute to a large extent to inter-individual variability in the response to radiation-induced DNA damage observed in healthy human populations.

Challenging gender practices: Intersectional narratives of sibling relations and parent–child engagements in transnational serial migration

This article aims to contribute to the currently sparse literature on transnational families and gender. It focuses on the retrospective accounts of Caribbean-born adults who as children were serial migrants, joining their parents in the UK following a period of separation. It considers aspects of their relationships with their siblings and with their mothers and fathers. The article illuminates what the serial migrants viewed as contradictory everyday practices that produced ‘non-shared environments’. It discusses three ways in which transnationalism appeared to be a central part of the serial migrants’ family lives. First, it was embodied. Second, it was lived as cultural difference between Caribbean-born and UK-born siblings. Third, it was reported to be evident in parental practices. The article illustrates the importance of viewing gendered narratives in a psychosocial intersectional perspective.

Qualitative dermatoglyphic traits in monozygotic and dizygotic twins of Albanian population in Kosovo

Dermatoglyphs are polygenetically determined epidermal ridge configurations on the fingers, palms and soles. An analysis of the digito-palmar dermatoglyphics obtained from 69 pairs of same-sex twins (32 monozygotic and 37 dizygotic) was performed in the population of Kosovo. Qualitative traits on the fingers (whorls, arches, radial and ulnar loops) and palms (pattern frequencies in the thenar/I, II, III and IV interdigital areas and hypothenar, the frequencies of positions of axial triradius) of both hands were analysed. The homolateral and heterolateral concordance of dermatoglyphic patterns between twin pairs were calculated for the monozygotic and dizygotic twins separately. The estimates of heritability for qualitative dermatoglyphic traits and the impacts of twin's shared (c2) and non-shared (individual) environments (e2) were presented. According to our results, the heritability patterns sharply distinguish highly heritable dermatoglyphic traits (patterns on the thenar and I interdigital area, II interdigital area and all the digits) and the traits with weak genetic component (patterns on the III and IV interdigital area, the hypothenar and the axial triradius position). In addition, the concordance and the heritability estimates in twins correspond to the embryonic growth of fingers (from the first to the fifth finger) and palm patterns (the II interdigital area). Based on findings presented here, we expect that the noxious environmental factors (possibly causing diseases later in life) would leave traces on the dermatoglyphs, which could be recognized as the increased dissimilarity of the twins (and other relatives) in the III and IV interdigital area, hypothenar, and in axial triradius position.

Common genetic and nonshared environmental factors contribute to the association between socioemotional dispositions and the externalizing factor in children

Childhood behavioral disorders including conduct disorder (CD), oppositional defiant disorder (ODD), and attention-deficit/hyperactivity disorder (ADHD) often co-occur. Prior twin research shows that common sets of genetic and environmental factors are associated with these various disorders and they form a latent factor called Externalizing. The developmental propensity model posits that CD develops in part from socioemotional dispositions of prosociality, negative emotionality, and daring; and recent research has supported the expected genetic and environmental associations between these dispositions and CD. This study examined the developmental propensity model in relation to the broader Externalizing factor that represents the covariance among behavior disorders in children. Parents of 686 six- to twelve-year-old twin pairs rated them on symptoms of CD, ADHD, and ODD using the disruptive behavior disorder scale and on prosociality, negative emotionality, and daring using the child and adolescent dispositions scale. A latent factor multivariate Cholesky model was used with each disposition latent factor comprised of respective questionnaire items and the Externalizing factor comprised of symptom dimensions of CD, ADHD inattention, ADHD hyperactivity/impulsivity, and ODD. Results supported the hypothesis that the socioemotional dispositions and the Externalizing factor have genetic factors in common, but there was not a single genetic factor associated with all of the constructs. As expected, nonshared environment factors were shared by the dispositions and externalizing factor but, again, no single nonshared environmental factor was common to all constructs. A shared environmental factor was associated with both negative emotionality and externalizing. The developmental propensity model was supported and appears to extend to the broader externalizing spectrum of childhood disorders. Socioemotional dispositions of prosociality, negative emotionality, and (to a lesser extent) daring may contribute to the covariation among behavioral disorders and perhaps to their comorbid expression through common sets of primarily genetic but also environmental factors.

Heritability of Ambulatory and Beat-to-Beat Office Blood Pressure in Large Multigenerational Arab Pedigrees: The ‘Oman Family Study’

To estimate the heritability of ambulatory blood pressure (BP), heart rate (HR), and beat-to-beat office BP and HR in an isolated, environmentally and genetically homogeneous Omani Arab population. Ambulatory BP measurements were recorded in 1,124 subjects with a mean age of 33.8 ± 16.2 years, using the auscultatory mode of the validated Schiller ambulatory BP Monitor. Beat-to-beat BP and HR were recorded by the Task Force Monitor. Heritability was estimated using quantitative genetic analysis. This was achieved by applying the maximum-likelihood-based variance decomposition method implemented in SOLAR software. We detected statistically significant heritability estimates for office beat-to-beat, 24-hour, daytime, and sleep HR of 0.31, 0.21, 0.20, and 0.07, respectively. Heritability estimates in the above mentioned conditions for systolic BP (SBP)/diastolic BP (DBP)/mean BP (MBP)were all significant and estimated at 0.19/0.19/0.19, 0.30/0.44/0.41, 0.28/0.38/0.39, and 0.21/0.18/0.20,respectively. Heritability estimates for 24-hour and daytime ambulatory SBP, DBP, and MBP ranged from 0.28 to 0.44, and were higher than the heritability estimates for beat-to-beat recordings and sleep periods,which were estimated within a narrow range of 0.18-0.21. In this cohort, because shared environments are common to all, the environmental influence that occurs is primarily due to the variation in non-shared environment that is unique to the individual. We demonstrated significant heritability estimates for both beat-to-beat office and ambulatory BP and HR recordings, but 24-hour and daytime ambulatory heritabilities are higher than those from beat-to-beat resting levels and ambulatory night-time recordings.

Learning preference among monozygotic twins: An exploratory study

Students have preferences for how they receive information. The goal of this pilot study was to discover whether there are differences in learning preferences among monozygotic twins doing similar course work while living together. The Visual, Auditory, Reading/writing, Kinesthetic (VARK) scale was used to evaluate learning preference. It was found that there is a marked difference in the learning preference among monozygotic twins. This difference can be attributed to the non-shared environment. An extensive study of this type using a larger sample of monozygotic twins is recommended.

Neonatal DNA methylation profile in human twins is specified by a complex interplay between intrauterine environmental and genetic factors, subject to tissue-specific influence

Comparison between groups of monozygotic (MZ) and dizygotic (DZ) twins enables an estimation of the relative contribution of genetic and shared and nonshared environmental factors to phenotypic variability. Using DNA methylation profiling of ∼20,000 CpG sites as a phenotype, we have examined discordance levels in three neonatal tissues from 22 MZ and 12 DZ twin pairs. MZ twins exhibit a wide range of within-pair differences at birth, but show discordance levels generally lower than DZ pairs. Within-pair methylation discordance was lowest in CpG islands in all twins and increased as a function of distance from islands. Variance component decomposition analysis of DNA methylation in MZ and DZ pairs revealed a low mean heritability across all tissues, although a wide range of heritabilities was detected for specific genomic CpG sites. The largest component of variation was attributed to the combined effects of nonshared intrauterine environment and stochastic factors. Regression analysis of methylation on birth weight revealed a general association between methylation of genes involved in metabolism and biosynthesis, providing further support for epigenetic change in the previously described link between low birth weight and increasing risk for cardiovascular, metabolic, and other complex diseases. Finally, comparison of our data with that of several older twins revealed little evidence for genome-wide epigenetic drift with increasing age. This is the first study to analyze DNA methylation on a genome scale in twins at birth, further highlighting the importance of the intrauterine environment on shaping the neonatal epigenome.

Gene-by-preschool interaction on the development of early externalizing problems.

Preschool involves an array of new social experiences that may impact the development of early externalizing behavior problems over the transition to grade school. Using longitudinal data from a nationally representative sample of over 600 pairs of US twins, we tested whether the genetic and environmental influences on externalizing problems differed between children who did versus did not attend preschool. At age 4, the genetic and environmental etiology of externalizing did not differ by preschool attendance. In contrast, by age 5 years (kindergarten age), the genetic and environmental etiology of externalizing significantly differed by preschool attendance. Among children who did not attend preschool, externalizing at age 5 was predominantly due to environmental influences (52% shared environment, 34% non-shared environment) rather than genetic differences (13%), whereas among children who had attended preschool, externalizing at age 5 was primarily due to genes (67%), and shared environmental influences were negligible (0%). These interactions represented the differential longitudinal persistence of genes and environments that contributed to externalizing at age 4. Sensitivity analyses ruled out confounding due to early mental ability, socioeconomic status, minority status, child age, and prior history of childcare. These results indicate that preschool enrollment is associated with increased genetic and decreased shared environmental influences on the development of early externalizing behavior problems.

Genetic and nonshared environmental factors affect the likelihood of being charged with driving under the influence (DUI) and driving while intoxicated (DWI)

Driving under the influence (DUI) and driving while intoxicated (DWI) are related to a range of serious health, legal, and financial costs. Given the costs to society of DUIs and DWIs, there has been interest in identifying the causes of DUIs and DWIs. The current study added to this existing knowledge base by estimating genetic and environmental effects on DUIs and DWIs in a sample of twins drawn from the National Longitudinal Study of Adolescent Health (Add Health). The results of the analyses revealed that genetic factors explained 53% of the variance in DUIs/DWIs and the nonshared environment explained 47% of the variance. Shared environmental factors explained none of the variance in DUIs/DWIs. We conclude with a discussion of the results, the limitations of the study, and how the findings might be compatible with policies designed to reduce DUIs and DWIs.

Broad Bandwidth or High Fidelity? Evidence from the Structure of Genetic and Environmental Effects on the Facets of the Five Factor Model

The Five Factor Model of personality is well-established at the phenotypic level, but much less is known about the coherence of the genetic and environmental influences within each personality domain. Univariate behavioral genetic analyses have consistently found the influence of additive genes and nonshared environment on multiple personality facets, but the extent to which genetic and environmental influences on specific facets reflect more general influences on higher order factors is less clear. We applied a multivariate quantitative-genetic approach to scores on the CPI-Big Five facets for 490 monozygotic and 317 dizygotic twins who took part in the National Merit Twin Study. Our results revealed a complex genetic structure for facets composing all five factors, with both domain-general and facet-specific genetic and environmental influences. For three of the Big Five domains, models that required common genetic and environmental influences on each facet to occur by way of effects on a higher order trait did not fit as well as models allowing for common genetic and environmental effects to act directly on the facets. These results add to the growing body of literature indicating that important variation in personality occurs at the facet level which may be overshadowed by aggregating to the trait level. Research at the facet level, rather than the factor level, is likely to have pragmatic advantages in future research on the genetics of personality.