Erin E. Horn

A Phenotypic Null Hypothesis for the Genetics of Personality

We review the genetically informed literature on the genetics of personality. Over the past century, quantitative genetic studies, using identical and fraternal twins, have demonstrated that differences in human personality are substantially heritable. We focus on more contemporary questions to which that basic observation has led. We examine whether differences in the heritability of personality are replicable across different traits, samples, and studies; how the heritability of personality relates to its reliability; and how behavior genetics can be employed in studies of validity, and we discuss the stability of personality in genetic and environmental variance. The appropriate null hypothesis in behavior genetics is not that genetic or environmental influence on personality is zero. Instead, we offer a phenotypic null hypothesis, which states that genetic variance is not an independent mechanism of individual differences in personality but rather a reflection of processes that are best conceptualized at the phenotypic level.

The General Factor of Personality and Evaluation

According to the proposal of the general factor of personality (GFP), socially desirable personality traits have been selected for throughout evolution because they increase fitness. However, it remains unknown whether people high on this factor actually behave in socially desirable ways or whether they simply endorse traits of positive valence. We separated these two sources of variance by having 619 participants respond to 120 personality adjectives organised into 30 quadruples balanced for content and valence (e.g. unambitious, easy–going, driven and workaholic tapped the trait achievement–striving). An exploratory six–factor solution fit well, and the factors resembled the Big Five. We subsequently extracted a higher–order factor from this solution, which appeared similar to the GFP. A Schmid–Leiman transformation of the higher–order factor, however, revealed that it clustered items of similar valence but opposite content (e.g. at the negative pole, unambitious and workaholic), rendering it an implausible description of evolved adaptive behaviour. Isolating this evaluative factor using exploratory structural equation modelling generated factors consisting of items of similar descriptive content but different valence (e.g. driven and workaholic), and the correlations among these factors were of small magnitude, indicating that the putative GFP capitalises primarily on evaluative rather than descriptive variance. Implications are discussed. Copyright

Do maladaptive behaviors exist at one or both ends of personality traits

In the Diagnostic and Statistical Manual of Mental Disorders (5th ed.; American Psychiatric Association, 2013) personality disorder trait model, maladaptive behavior is located at one end of continuous scales. Widiger and colleagues, however, have argued that maladaptive behavior exists at both ends of trait continua. We propose that the role of evaluative variance differentiates these two perspectives and that once evaluation is isolated, maladaptive behaviors emerge at both ends of nonevaluative trait dimensions. In Study 1, we argue that evaluative variance is worthwhile to measure separately from descriptive content because it clusters items by valence regardless of content (e.g., lazy and workaholic; apathetic and anxious; gullible and paranoid; timid and hostile, etc.), which is unlikely to describe a consistent behavioral style. We isolate evaluation statistically (Study 2) and at the time of measurement (Study 3) to show that factors unrelated to valence evidence maladaptive behavior at both ends. We argue that nonevaluative factors, which display maladaptive behavior at both ends of continua, may better approximate ways in which individuals actually behave.

Interactions Between Socioeconomic Status and Components of Variation in Cognitive Ability

We have proposed that differences in the heritability of cognitive ability as a function of socioeconomic status (SES) be called the Scarr-Rowe interaction, after the investigator who first reported it (Scarr) and the investigator who provided a crucial replication (Rowe). In 2003, a replication by Turkheimer et al. (Psychol Sci 14:623–628, 2003) sparked renewed interest in the subject. Since then, there have been a large number of attempts at replication using a diversity of cultures, ages, and measures of cognitive ability. We review recent studies, and delve more deeply into the nature of the phenomenon itself. Differences in heritability coefficients are necessarily the result of differences in identical (MZ) and fraternal (DZ) twin correlations, which are in turn ratios of variances between and within twin pairs. We review the existing literature with this in mind, reanalyzing the results where possible to examine how between- and within-pair variances change with differences in SES. We also include recent attempts to replicate the interaction using molecular genetic data rather than family relationships. We conclude that with two exceptions, the Scarr-Rowe interaction has replicated in American samples, in both family and molecular genetic studies. The interaction has fared less well in Europe, where more equal access to educational and other economic resources, which are crucial to observing differences in heritability, may limit the severity of poverty, although early reports that the phenomenon was not found in the large British Twins’ Early Development Study (TEDS) sample have been tempered by more recent positive results. Finally, we offer a proposal for the possible mechanism of the effect.

Revisiting the Effect of Marital Support on Depressive Symptoms in Mothers and Fathers: A Genetically Informed Study

This article uses a genetically informed design to evaluate whether (1) the well-documented association between marital support and depressive symptoms is accounted for by genetic and/or shared environmental selection, (2) gender differences are found after controlling for selection effects, and (3) parenthood moderates any nonshared environmental relation between depressive symptoms and marital support. We used a sample of 1,566 pairs of same-sexed, married twins from the Australian Twin Registry to evaluate our hypotheses that (1) the predicted effect of marital support on depressive symptoms is not fully an artifact of selection, (2) the etiological sources accounting for this effect differ between husbands and wives, and (3) parenthood status moderates the effect of marital support on depressive symptoms adjusting for selection effects. The results support the first hypotheses. However, after controlling for selection, the effect of marital support on depressive symptoms was not significantly different for husbands and wives. Parenthood moderated the effect of marital support, such that after controlling for selection, marital support is more strongly associated with depressive symptoms for full-time parents than nonfull-time parents.

Socioeconomic Modifiers of Genetic and Environmental Influences on Body Mass Index in Adult Twins

OBJECTIVE Individual measures of socioeconomic status (SES) suppress genetic variance in body mass index (BMI). Our objective was to examine the influence of both individual-level (i.e., educational attainment, household income) and macrolevel (i.e., neighborhood socioeconomic advantage) SES indicators on genetic contributions to BMI. METHOD The study used education level data from 4,162 monozygotic (MZ) and 1,900 dizygotic (DZ) same-sex twin pairs (64% female), income level data from 3,498 MZ and 1,534 DZ pairs (65% female), and neighborhood-level socioeconomic deprivation data from 2,327 MZ and 948 DZ pairs (65% female). Covariates included age (M = 40.4 ± 17.5 years), sex, and ethnicity. The cotwin control model was used to evaluate the mechanisms through which SES influences BMI (e.g., through genetic vs. environmental pathways), and a gene-by-environment interaction model was used to test whether residual variance in BMI, after controlling for the main effects of SES, was moderated by socioeconomic measures. RESULTS SES significantly predicted BMI. The association was noncausal, however, and instead was driven primarily through a common underlying genetic background that tended to grow less influential as SES increased. After controlling for the main effect of SES, both genetic and nonshared environmental variance decreased with increasing SES. CONCLUSIONS The impact of individual and macrolevel SES on BMI extends beyond its main effects. The influence of genes on BMI is moderated by individual and macrolevel measures of SES, such that when SES is higher, genetic factors become less influential.

Sleep Duration and Area-Level Deprivation in Twins

STUDY OBJECTIVES We used quantitative genetic models to assess whether area-level deprivation as indicated by the Singh Index predicts shorter sleep duration and modifies its underlying genetic and environmental contributions. METHODS Participants were 4,218 adult twin pairs (2,377 monozygotic and 1,841 dizygotic) from the University of Washington Twin Registry. Participants self-reported habitual sleep duration. The Singh Index was determined by linking geocoding addresses to 17 indicators at the census-tract level using data from Census of Washington State and Census Tract Cartographic Boundary Files from 2000 and 2010. Data were analyzed using univariate and bivariate genetic decomposition and quantitative genetic interaction models that assessed A (additive genetics), C (common environment), and E (unique environment) main effects of the Singh Index on sleep duration and allowed the magnitude of residual ACE variance components in sleep duration to vary with the Index. RESULTS The sample had a mean age of 38.2 y (standard deviation [SD] = 18), and was predominantly female (62%) and Caucasian (91%). Mean sleep duration was 7.38 h (SD = 1.20) and the mean Singh Index score was 0.00 (SD = 0.89). The heritability of sleep duration was 39% and the Singh Index was 12%. The uncontrolled phenotypic regression of sleep duration on the Singh Index showed a significant negative relationship between area-level deprivation and sleep length (b = -0.080, P < 0.001). Every 1 SD in Singh Index was associated with a ∼4.5 min change in sleep duration. For the quasi-causal bivariate model, there was a significant main effect of E (b(0E) = -0.063; standard error [SE] = 0.30; P < 0.05). Residual variance components unique to sleep duration were significant for both A (b(0Au) = 0.734; SE = 0.020; P < 0.001) and E (b(0Eu) = 0.934; SE = 0.013; P < 0.001). CONCLUSIONS Area-level deprivation has a quasi-causal association with sleep duration, with greater deprivation being related to shorter sleep. As area-level deprivation increases, unique genetic and nonshared environmental residual variance in sleep duration increases.

Quasi-causal associations of physical activity and neighborhood walkability with body mass index: A twin study

OBJECTIVE Physical activity, neighborhood walkability, and body mass index (BMI, kg/m(2)) associations were tested using quasi-experimental twin methods. We hypothesized that physical activity and walkability were independently associated with BMI within twin pairs, controlling for genetic and environmental background shared between them. METHODS Data were from 6376 (64% female; 58% identical) same-sex pairs, University of Washington Twin Registry, 2008-2013. Neighborhood walking, moderate-to-vigorous physical activity (MVPA), and BMI were self-reported. Residential address was used to calculate walkability. Phenotypic (non-genetically informed) and biometric (genetically informed) regression was employed, controlling for age, sex, and race. RESULTS Walking and MVPA were associated with BMI in phenotypic analyses; associations were attenuated but significant in biometric analyses (Ps<0.05). Walkability was not associated with BMI, however, was associated with walking (but not MVPA) in both phenotypic and biometric analyses (Ps<0.05), with no attenuation accounting for shared genetic and environmental background. CONCLUSIONS The association between activity and BMI is largely due to shared genetic and environmental factors, but a significant causal relationship remains accounting for shared background. Although walkability is not associated with BMI, it is associated with neighborhood walking (but not MVPA) accounting for shared background, suggesting a causal relationship between them.

Abstract: Psychological Distress and Recurrent Herpetic Disease: A Dynamic Study of Lesion Recurrence and Viral Shedding Episodes in Adults

Psychological Distress and Recurrent Herpetic Disease: A Dynamic Study of Lesion Recurrence and Viral Shedding Episodes in Adults