Non-additive Genetic Influences Research Articles

Unraveling the Relation Between Personality and Well-Being in a Genetically Informative Design

In the current study, common and unique genetic and environmental influences on personality and a broad range of well-being measures were investigated. Data on the Big Five, life satisfaction, quality of life, self-rated health, loneliness, and depression from 14,253 twins and their siblings (age M: 31.82, SD: 14.41, range 16–97) from the Netherlands Twin Register were used in multivariate extended twin models. The best-fitting theoretical model indicated that genetic variance in personality and well-being traits can be decomposed into effects due to one general, common factor ( Mdn: 60%, range 15%–89%), due to personality-specific ( Mdn: 2%, range 0%–78%) and well-being-specific ( Mdn: 12%, range 4%–35%) factors, and trait-specific effects ( Mdn: 18%, range 0%–65%). Significant amounts of non-additive genetic influences on the traits’ (co)variances were found, while no evidence was found for quantitative or qualitative sex differences. Taken together, our study paints a fine-grained, complex picture of common and unique genetic and environmental effects on personality and well-being. Implications for the interpretation of shared variance, inflated phenotypic correlations between traits and future gene finding studies are discussed.

Genetic and Environmental Architecture of Five Factor Model and Super-Factors: An Italian Twin Study.

No previous research explored the genetic and environmental structure of Big Five dimensions of personality and higher-order factors in a single twin study, except, in part, for just one study. We used the twin design to estimate the effects of genes and environment on both Five Factor model and related second- and third-order factors (i.e., Alpha [stability], Beta [plasticity], and GFP [general factor of personality]). We analyzed data from 314 adult twins (157 pairs: 83 monozygotic, 74 dizygotic; mean age: 52 years) enrolled in the Italian Twin Register. Participants underwent clinical and instrumental evaluations, and completed a 25-adjective list drawn from the Short Adjectives Checklist to Measure Big Five (SACBIF). We applied quantitative genetic models to unravel the sources of variation and covariation for the Big Five and higher-order factors. We found a similar etiological architecture across the different levels of analysis, with moderate to substantial non-additive genetic and unique environmental influences on all the personality traits, and no shared environmental contribution for any of them. We also detected significant genetic correlations for the Big Five dimensions and the Alpha and Beta super-factors. With some limitations, our results suggest that the etiological architecture of personality may be invariant to the factor level of analysis.

Three Patterns of Inheritance of Quantitative Dermatoglyphic Traits: Kosovo Albanian Twin Study.

Dermatoglyphs are epidermal ridge configurations on the fingers, palms and soles that are formed during fetal development, and therefore only the intrauterine environment can have any influence on their formation. This study aims at investigating the genetic and environmental contribution in determining quantitative dermatoglyphic traits in 32 monozygotic (MZ) and 35 dizygotic (DZ) same-sex twins from the Albanian population of Kosovo. All genetic analyses were run in the statistical program Mx. After assumptions testing, based on the pattern of MZ-DZ correlations, univariate models were fitted to the data in order to estimate additive genetic (A), common (C) and individual (E) environmental influences for all variables. The exception was the atd-angle for which a model with nonadditive genetic (D) influences was tested, since DZ correlations were less than half of MZ correlations. Goodness of fit of the full ACE or ADE model was compared to the saturated model. The fit of nested models (AE, CE, DE or E) was compared to the full models (ACE or ADE). Our results indicate that additive genetic component strongly contributes to individual differences in finger ridge counts (49-81%), and weakly (0-50%) on the formation of the palmar ridge counts between the palmar triradii a, b, c, and d. The specific pattern found for the atd-angle implies the impact of a nonadditive genetic component, possibly the effect of a major gene. Further, more powered studies are needed to confirm this pattern, especially for resolving the issue of the huge difference in MZ and DZ twin similarity for the atd-angle palmar trait.

Twin Study of the Relationship between Childhood Negative Emotionality and Hyperactivity/Inattention Problems.

The present study aimed to determine the genetic and environmental etiology of the association between childhood negative emotionality (NE) and hyperactivity/inattention problems (HIP) using South Korean elementary school twins (mean age = 10.19 years, SD = 1.79 years). Telephone interviews were given to mothers of 919 twins (229 monozygotic males: 112 pairs and 5 individuals; 148 dizygotic males: 73 pairs and 2 individuals; 180 monozygotic females: 87 pairs and 6 individuals; 103 dizygotic females: 50 pairs and 3 individuals; 259 opposite-sex dizygotic twins: 127 pairs and 5 individuals) to assess their children's NE and HIP. Consistent with prior studies, the phenotypic correlation between NE and the HIP was moderate (r = .29; 95% CI = .24, .34). Model-fitting analysis revealed that additive genetic and nonshared environmental influences on NE were .45 (95% CI [.34, .54]) and .55 (95% CI [.46, .66]), respectively, and that additive and nonadditive genetic, and nonshared environmental influences on HIP were .08 (95% CI [.03, .26]), .41 (95% CI [.21, .51]) and .51 (95% CI = .42, .61), respectively. In addition, the additive genetic correlation between NE and HIP was 1.0 (95% CI [.52, 1.00]), indicating that additive genetic factors are entirely shared between the two phenotypes. Nonadditive genetic influences were unique to HIP and not responsible for the NE-HIP association. Nonshared environmental correlation was significant but modest (re = .18, 95% CI [.06, .30]).

An Extended Twin-Pedigree Study of Different Classes of Voluntary Exercise Behavior

We investigated the familial clustering of different classes of voluntary regular exercise behavior in extended twin-family pedigrees. In contrast to the earlier work based on twin data only, this allowed us to estimate the contributions of shared household effects (C), additive (A), and non-additive (D) genetic effects on voluntary exercise behavior. To test whether shared household effects were inflated by assortative mating we examined the causes of spousal resemblance. For adolescent and adult participants (aged 16 to 65) in the Netherlands Twin Register we constructed 19,543 pedigrees which specified all relations among nuclear family members and larger families in the register (N = 50,690 individuals). Data were available on total weekly MET minutes spent on leisure time exercise, and on total weekly MET minutes spent on exercise activities in team-based, solitary, competitive, non-competitive, externally paced and internally paced exercise. We analyzed the data in the Mendel software package (Lange et al. in Bioinformatics 29(12):1568–1570, 2013) under multiple definitions of household sharing and used data from spouses of twins to test phenotypic assortment, social homogamy, and marital interaction as potential sources of spousal resemblance. Results confirmed the influence of genetic factors on the total volume of weekly exercise behavior throughout the life span. Broad sense heritability ranged from 34 to 41% (19–26% A, 12–21% D), and did not depend on the definition for household sharing. Engaging in team-based, competitive, externally paced activities (e.g., soccer) was ~ 13% more heritable than engaging in non-competitive, solitary activities (e.g., jogging). Having shared a household as siblings explained 4–8% of the variance in adult exercise behavior, whereas sharing a household by spouses yielded higher C estimates (20–24%), as it incorporates spousal resemblance. Spousal resemblance was explained by both social homogamy and marital interaction, with little evidence for phenotypic assortment. We conclude that both the amount of voluntary exercise behavior and the preference for specific classes of exercise activities in adults is explained by additive and non-additive genetic factors and unique environmental influences that include correlated exercise behavior of spouses.

The Nature and Nurture of HEXACO Personality Trait Differences

Abstract. This study was designed to provide detailed estimates of genetic and environmental sources of variance in the HEXACO personality traits. For this purpose, we analyzed data from a German extended twin family study including 573 pairs of twins as well as 208 mothers, 119 fathers, 228 spouses, and 143 offspring of twins. All participants provided self-reports on the HEXACO-60. Extended twin family analyses using structural equation modeling (SEM) yielded that additive and nonadditive genetic influences accounted for about 50% of the variance in personality traits. The remaining variance was primarily due to individual-specific environmental sources and random measurement error. Spousal similarity in Openness was attributable to assortative mating, whereas spousal similarity in Honesty-Humility was attributable to environmental circumstances, partly due to a shared social background and spouse-specific effects. Our analyses yielded specifics for different personality traits. However, transmission of trait similarity from one generation to the next was primarily genetic.

WHY DO PEOPLE DIFFER IN THEIR ACHIEVEMENT MOTIVATION? A NUCLEAR TWIN FAMILY STUDY

Although many previous studies have emphasized the role of environmental factors, such as parental home and school environment, on achievement motivation, classical twin studies suggest that both additive genetic influences and non-shared environmental influences explain interindividual differences in achievement motivation. By applying a Nuclear Twin Family Design on the data of the German nationally representative of TwinLife study, we analyzed genetic and environmental influences on achievement motivation in adolescents and young adults. As expected, the results provided evidence for the impact of additive genetic variation, non-additive genetic influences, as well as twin specific shared environmental influences. The largest amount of variance was attributed to non-shared environmental influences, showing the importance of individual experiences in forming differences in achievement motivation. Overall, we suggest a revision of models and theories that explain variation in achievement motivation by differences in familial socialization only.

Genetic and Environmental Overlaps Among Sasang Constitution Types: A Multivariate Twin Study.

According to the Sasang theory, humans can be categorized into one of the four Sasang constitution (SC) types. The four SC types are Tae-Yang (TY), Tae-Eum (TE), So-Yang (SY), and So-Eum (SE), which are determined mainly on the basis of anthropometric characteristics, personality, and the balance of the physiological functions of the major organ systems. There is a growing recognition in the complementary and alternative medicine area that SC types have the potential to be a useful scientific tool for the prevention, diagnosis, and treatment of diseases (Cooper, Evidence Based Complementary and Alternative Medicine, Vol. 6 (Suppl. 1), 2009, pp. 1-3). The main purposes of the present study are to estimate genetic and environmental influences on SC types, and to explore genetic and environmental correlations that affect phenotypic associations among the SC types. In total, 1,742 (365 monozygotic male, 173 dizygotic male, 675 monozygotic female, 271 dizygotic female, and 258 opposite-sex dizygotic) twins (mean age = 19.1 ± 3.1 year) completed a Sasang questionnaire. Univariate and multivariate model-fitting analyses were performed. Total (additive and non-additive) genetic influences were 71% for males and 81% for females in TE, 70% for males and 71% for females in SE, and 47% for both sexes in SY. Non-additive genetic effects were substantial, and shared environmental influences were negligible in most SC types. Multivariate model-fitting analysis revealed that non-additive genetic and individual-specific environmental correlations between TE and SE were -0.92 (95% CI [-0.89, -0.93]) and -0.62 (95% CI [-0.57, -0.68]), respectively. The corresponding estimates were -0.55 (95% CI [-0.48, -0.61]) and -0.44 (95% CI [-0.37, -0.51]) between TE and SY and 0.19 (95% CI [0.09, 0.29]) and -0.40 (95% CI [-0.32, -0.47]) between SE and SY. These results suggest that the phenotypic associations among SC types may be mediated by pleiotropic mechanism of genes.

Estimation of nonadditive genetic influences on standard lactation production (305 days) in upgrading of Serbian-Fleckvieh to Holstein-Friesian cattle breed

Estimation of nonadditive genetic influences on standard lactation production (305 days) in upgrading of Serbian-Fleckvieh to Holstein-Friesian cattle breed

Genetic and Environmental Influences on the Developmental Course of Attention-Deficit/Hyperactivity Disorder Symptoms From Childhood to Adolescence

Attention-deficit/hyperactivity disorder (ADHD) is conceptualized as a neurodevelopmental disorder that is strongly heritable. However, to our knowledge, no study to date has examined the genetic and environmental influences explaining interindividual differences in the developmental course of ADHD symptoms from childhood to adolescence (ie, systematic decreases or increases with age). The reason ADHD symptoms persist in some children but decline in others is an important concern, with implications for prognosis and interventions. To assess the proportional impact of genes and the environment on interindividual differences in the developmental course of ADHD symptom domains of hyperactivity/impulsivity and inattention between ages 8 and 16 years. A prospective sample of 8395 twin pairs from the Twins Early Development Study, recruited from population records of births in England and Wales between January 1, 1994, and December 31, 1996. Data collection at age 8 years took place between November 2002 and November 2004; data collection at age 16 years took place between February 2011 and January 2013. Both DSM-IV ADHD symptom subscales were rated 4 times by participants' mothers. Estimates from latent growth curve models indicated that the developmental course of hyperactivity/impulsivity symptoms followed a sharp linear decrease (mean score of 6.0 at age 8 years to 2.9 at age 16 years). Interindividual differences in the linear change in hyperactivity/impulsivity were under strong additive genetic influences (81%; 95% CI, 73%-88%). More than half of the genetic variation was specific to the developmental course and not shared with the baseline level of hyperactivity/impulsivity. The linear decrease in inattention symptoms was less pronounced (mean score of 5.8 at age 8 years to 4.9 at age 16 years). Nonadditive genetic influences accounted for a substantial amount of variation in the developmental course of inattention symptoms (54%; 95% CI, 8%-76%), with more than half being specific to the developmental course. The large genetic influences on the developmental course of ADHD symptoms are mostly specific and independent of those that account for variation in the baseline level of symptoms. Different sets of genes may be associated with the developmental course vs the baseline level of ADHD symptoms and explain why some children remit from ADHD, whereas others persist. Recent longitudinal imaging data indicate that the maintenance or increase in symptoms is underpinned by atypical trajectories of cortical development. This may reflect a specific genetic liability, distinct from that which contributes to baseline ADHD symptoms, and warrants closer follow-up.

A meta-analysis of heritability of cognitive aging: minding the "missing heritability" gap.

The etiologies underlying variation in adult cognitive performance and cognitive aging have enjoyed much attention in the literature, but much of that attention has focused on broad factors, principally general cognitive ability. The current review provides meta-analyses of age trends in heritability of specific cognitive abilities and considers the profile of genetic and environmental factors contributing to cognitive aging to address the 'missing heritability' issue. Our findings, based upon evaluating 27 reports in the literature, indicate that verbal ability demonstrated declining heritability, after about age 60, as did spatial ability and perceptual speed more modestly. Trends for general memory, working memory, and spatial ability generally indicated stability, or small increases in heritability in mid-life. Equivocal results were found for executive function. A second meta-analysis then considered the gap between twin-based versus SNP-based heritability derived from population-based GWAS studies. Specifically, we considered twin correlation ratios to agnostically re-evaluate biometrical models across age and by cognitive domain. Results modestly suggest that nonadditive genetic variance may become increasingly important with age, especially for verbal ability. If so, this would support arguments that lower SNP-based heritability estimates result in part from uncaptured non-additive influences (e.g., dominance, gene-gene interactions), and possibly gene-environment (GE) correlations. Moreover, consistent with longitudinal twin studies of aging, as rearing environment becomes a distal factor, increasing genetic variance may result in part from nonadditive genetic influences or possible GE correlations. Sensitivity to life course dynamics is crucial to understanding etiological contributions to adult cognitive performance and cognitive aging.

Causes of individual differences in adolescent optimism: a study in Dutch twins and their siblings.

The aim of this study was to investigate the degree to which genetic and environmental influences affect variation in adolescent optimism. Optimism (3 items and 6 items approach) and pessimism were assessed by the Life Orientation Test-Revised (LOT-R) in 5,187 adolescent twins and 999 of their non-twin siblings from the Netherlands Twin Register (NTR). Males reported significantly higher optimism scores than females, while females score higher on pessimism. Genetic structural equation modeling revealed that about one-third of the variance in optimism and pessimism was due to additive genetic effects, with the remaining variance being explained by non-shared environmental effects. A bivariate correlated factor model revealed two dimensions with a genetic correlation of −.57 (CI −.67, −.47), while the non-shared environmental correlation was estimated to be −.21 (CI −.25, −.16). Neither an effect of shared environment, non-additive genetic influences, nor quantitative sex differences was found for both dimensions. This result indicates that individual differences in adolescent optimism are mainly accounted for by non-shared environmental factors. These environmental factors do not contribute to the similarity of family members, but to differences between them. Familial resemblance in optimism and pessimism assessed in adolescents is fully accounted for by genetic overlap between family members.

Sleep duration and personality in Croatian twins

The objective of this study was to examine which genetic and environmental influences contribute to individual differences in sleep duration in a sample of Croatian adolescent/early adult twins, as well as to investigate the relationship between personality and sleep duration. Participants included 339 twin pairs (105 monozygotic and 234 dizygotic) aged between 15 and 22 years. They reported on their average sleep duration and personality. The broad heritability estimate (additive and non-additive genetic influences) for sleep duration was 0.63, while personality estimates ranged between 0.47 and 0.62. Significant negative phenotypic associations with neuroticism and openness were mainly genetically mediated 100 and 80%, respectively. Only 6% of the sleep duration variance was explained by genetic influences shared with neuroticism and openness. In regression analysis, age, gender and five personality traits explained 5% of sleep duration variance, with neuroticism and openness as significant predictors. Comparison of short, moderate and long sleepers showed that participants in the short sleepers group had significantly higher neuroticism scores than groups of moderate and long sleepers, as well as a significantly higher openness score than the group of long sleepers. This indicates that personality traits of neuroticism and openness contribute to the prediction of sleep duration due to overlapping genetic influences that contribute to both these personality traits and sleep duration. However, as phenotypic overlap of personality and sleep duration is relatively weak, heritability of sleep duration is not only related to individual differences in personality traits, so future research needs to examine other phenotypic correlates of sleep duration.

No Genetic Influence for Childhood Behavior Problems From DNA Analysis

ObjectiveTwin studies of behavior problems in childhood point to substantial genetic influence. It is now possible to estimate genetic influence using DNA alone in samples of unrelated individuals, not relying on family-based designs such as twins. A linear mixed model, which incorporates DNA microarray data, has confirmed twin results by showing substantial genetic influence for diverse traits in adults. Here we present direct comparisons between twin and DNA heritability estimates for childhood behavior problems as rated by parents, teachers, and children themselves.MethodBehavior problem data from 2,500 UK-representative 12-year-old twin pairs were used in twin analyses; DNA analyses were based on 1 member of the twin pair with genotype data for 1.7 million DNA markers. Diverse behavior problems were assessed, including autistic, depressive, and hyperactive symptoms. Genetic influence from DNA was estimated using genome-wide complex trait analysis (GCTA), and the twin estimates of heritability were based on standard twin model fitting.ResultsBehavior problems in childhood—whether rated by parents, teachers, or children themselves—show no significant genetic influence using GCTA, even though twin study estimates of heritability are substantial in the same sample, and even though both GCTA and twin study estimates of genetic influence are substantial for cognitive and anthropometric traits.ConclusionsWe suggest that this new type of “missing heritability,” that is, the gap between GCTA and twin study estimates for behavior problems in childhood, is due to nonadditive genetic influence, which will make it more difficult to identify genes responsible for heritability.

Beyond the heritability of life satisfaction – The roles of personality and twin-specific influences

In a behavior genetic design, we investigated individual differences in life satisfaction and its relation to personality with respect to both internal and external influences. We questioned the absence of shared environment and examined the specific contribution of additive and non-additive genetic influences. We also tested for twin-specific environmental influences in a total sample of 1308 dyads including identical and fraternal twins, siblings, mother–child and grandparent–child pairs. The results showed substantial shared environmental influences on life satisfaction that varied between twins and non-twins, supporting twin-specific environmental influences. Additive and non-additive genetic influences on life satisfaction were completely shared with personality. The remaining variance could be explained by unique non-shared environmental influences for life satisfaction independent of personality.

Evidence for Heritability of Adult Men's Sexual Interest in Youth Under Age 16 from a Population-Based Extended Twin Design

Sexual interest in children resembles sexual gender orientation in terms of early onset and stability across the life span. Although a genetic component to sexual interest in children seems possible, no research has addressed this question to date. Prior research showing familial transmission of pedophilia remains inconclusive about shared environmental or genetic factors. Studies from the domains of sexual orientation and sexually problematic behavior among children pointed toward genetic components. Adult men's sexual interest in youthfulness-related cues may be genetically influenced. The aim of the present study was to test whether male sexual interest in children and youth under age 16 involves a heritable component. The main outcome measure was responses in a confidential survey concerning sexual interest, fantasies, or activity pertaining to children under the age of 16 years during the previous 12 months. The present study used an extended family design within behavioral genetic modeling to estimate the contributions of genetic and environmental factors in the occurrence of adult men's sexual interest in children and youth under age 16. Participants were male twins and their male siblings from a population-based Finnish cohort sample aged 21-43 years (N = 3,967). The incidence of sexual interest in children under age was 3%. Twin correlations were higher for monozygotic than for dizygotic twins. Behavioral genetic model fitting indicated that a model including genetic effects as well as nonshared environmental influences (including measurement error), but not common environmental influences, fits the data best. The amount of variance attributable to nonadditive genetic influences (heritability) was estimated at 14.6%. The present study provides the first indication that genetic influences may play a role in shaping sexual interest toward children and adolescents among adult men. Compared with the variance attributable to nonshared environmental effects (plus measurement error), the contribution of any genetic factors seems comparatively weak. Future research should address the possible interplay of genetic with environmental risk factors, such as own sexual victimization in childhood.

Genetic and environmental influences on the relationship between flow proneness, locus of control and behavioral inhibition.

Flow is a psychological state of high but subjectively effortless attention that typically occurs during active performance of challenging tasks and is accompanied by a sense of automaticity, high control, low self-awareness, and enjoyment. Flow proneness is associated with traits and behaviors related to low neuroticism such as emotional stability, conscientiousness, active coping, self-esteem and life satisfaction. Little is known about the genetic architecture of flow proneness, behavioral inhibition and locus of control – traits also associated with neuroticism – and their interrelation. Here, we hypothesized that individuals low in behavioral inhibition and with an internal locus of control would be more likely to experience flow and explored the genetic and environmental architecture of the relationship between the three variables. Behavioral inhibition and locus of control was measured in a large population sample of 3,375 full twin pairs and 4,527 single twins, about 26% of whom also scored the flow proneness questionnaire. Findings revealed significant but relatively low correlations between the three traits and moderate heritability estimates of .41, .45, and .30 for flow proneness, behavioral inhibition, and locus of control, respectively, with some indication of non-additive genetic influences. For behavioral inhibition we found significant sex differences in heritability, with females showing a higher estimate including significant non-additive genetic influences, while in males the entire heritability was due to additive genetic variance. We also found a mainly genetically mediated relationship between the three traits, suggesting that individuals who are genetically predisposed to experience flow, show less behavioral inhibition (less anxious) and feel that they are in control of their own destiny (internal locus of control). We discuss that some of the genes underlying this relationship may include those influencing the function of dopaminergic neural systems.

Heritability of proneness for psychological flow experiences

Flow is a subjective experience of high but effortless attention, loss of self-awareness, control, and enjoyment that can occur during active performance of challenging tasks. Proneness to experience flow is associated with personality, specifically with low neuroticism and high conscientiousness. We investigated genetic and non-genetic influences on flow proneness in 444 adult twin pairs. Data were collected using an on-line administration of the Swedish Flow Proneness Questionnaire, which includes separate scales for flow proneness in three major domains of life: work, maintenance, and leisure. We found moderate (.29–.35) heritabilities for the flow scales. Twin correlations as well as multivariate modeling suggested non-additive genetic influences. Genetic influences were almost entirely shared for the three flow scales and genetic correlations between the scales were very high (.81–.97), suggesting that the same genes influence flow proneness independently of domain. Non-shared environmental influences, in contrast, were largely specific to each flow scale. We conclude that an individual’s general proneness to experience flow is influenced by the same genetic factors regardless of domain, and these may be associated with personality traits that are conducive to flow. In addition, specific environmental factors appear to be of importance for within-individual differences in flow proneness in different domains.

MAINTENANCE OF GENETIC VARIATION IN HUMAN PERSONALITY: TESTING EVOLUTIONARY MODELS BY ESTIMATING HERITABILITY DUE TO COMMON CAUSAL VARIANTS AND INVESTIGATING THE EFFECT OF DISTANT INBREEDING

Personality traits are basic dimensions of behavioral variation, and twin, family, and adoption studies show that around 30% of the between-individual variation is due to genetic variation. There is rapidly growing interest in understanding the evolutionary basis of this genetic variation. Several evolutionary mechanisms could explain how genetic variation is maintained in traits, and each of these makes predictions in terms of the relative contribution of rare and common genetic variants to personality variation, the magnitude of nonadditive genetic influences, and whether personality is affected by inbreeding. Using genome-wide single nucleotide polymorphism (SNP) data from > 8000 individuals, we estimated that little variation in the Cloninger personality dimensions (7.2% on average) is due to the combined effect of common, additive genetic variants across the genome, suggesting that most heritable variation in personality is due to rare variant effects and/or a combination of dominance and epistasis. Furthermore, higher levels of inbreeding were associated with less socially desirable personality trait levels in three of the four personality dimensions. These findings are consistent with genetic variation in personality traits having been maintained by mutation-selection balance.

Affective intensity and lability: Heritability in adult male twins

Inability to monitor and self-regulate heightened levels of affect lability and affect intensity is associated with a range of mood, anxiety, and personality disorders, psychosomatic symptoms and socially maladaptive behaviors. Despite the importance of these aspects of affective regulation, there are no twin study data to shed light on the genetic and environmental components of these constructs. Affective Lability Scale (ALS) and Affect Intensity Measure (AIM) questionnaires were administered to 796 male twins in the Vietnam Era Twin Registry and subjected to twin and model-fitting analyses. Complete data were available from 182 monozygotic and 119 dizygotic twin pairs. Biometrical genetic model-fitting estimates indicated that additive genetic influence accounted for 40% of the variance in affect intensity and 25% of the variance in the ALS subscale assessing anxiety-depression mood shifts. Nonadditive genetic influence was indicated for ALS subscales measuring shifts between normal mood and depression (29%) and anger (27%), respectively. There was negligible evidence of shared environmental influence on affect measures. In contrast, estimates of nonshared environmental influences ranged from 52% to 74%. Female were not included in this study due to the nature of the twin cohort. Data from subjects in a population cohort may not generalize to clinical populations. Measures of environment were not included. These results provide evidence for moderate heritability of affect intensity and specific measures of affect lability. Individual differences in mood regulation may represent phenotypic variation in a core psychobiologic vulnerability (e.g., neurotransmitter systems).