Personality Dimensions as Common and Broadband-Specific Features for Internalizing and Externalizing Disorders

Several researchers have suggested that the nature of the covariation between internalizing and externalizing disorders may be understood better by examining the associations between temperament or personality and these disorders. The present study examined neuroticism as a potential common feature underlying both internalizing and externalizing disorders and novelty seeking as a potential broad-band specific feature influencing externalizing disorders alone. Participants were 12- to 18-year-old twin pairs (635 monozygotic twin pairs and 691 dizygotic twin pairs; 48 % male and 52 % female) recruited from the Colorado Center for Antisocial Drug Dependence. Genetic and nonshared environmental influences shared in common with neuroticism influenced the covariation among distinct internalizing disorders, the covariation among distinct externalizing disorders, and the covariation between internalizing and externalizing disorders. Genetic influences shared in common with novelty seeking influenced the covariation among externalizing disorders and the covariation between major depressive disorder and externalizing disorders, but not the covariation among internalizing disorders or between anxiety disorders and externalizing disorders. Also, after accounting for genetic and environmental influences shared in common with neuroticism and novelty seeking, there were no significant common genetic or environmental influences among the disorders examined, suggesting that the covariance among the disorders is sufficiently explained by neuroticism and novelty seeking. We conclude that neuroticism is a heritable common feature of both internalizing disorders and externalizing disorders, and that novelty seeking is a heritable broad-band specific factor that distinguishes anxiety disorders from externalizing disorders.     

Structure and Etiology of Co-occurring Internalizing and Externalizing Disorders in Adolescents

Several studies suggest that a two-factor model positing internalizing and externalizing factors explains the interrelationships among psychiatric disorders. However, it is unclear whether the covariation between internalizing and externalizing disorders is due to common genetic or environmental influences. We examined whether a model positing two latent factors, internalizing and externalizing, explained the interrelationships among six psychiatric disorders (major depressive disorder, generalized anxiety disorder, separation anxiety disorder, attention-deficit/hyperactivity disorder, oppositional defiant disorder, and conduct disorder) in adolescents, and whether there are common genetic and environmental influences on internalizing and externalizing latent factors. Multivariate behavior genetic analyses of data from 1162 twin pairs and 426 siblings ascertained from the general population via the Colorado Center for Antisocial Drug Dependence (CADD) were conducted. We found support for a model positing two latent factors (internalizing and externalizing). These factors were moderately heritable and influenced by significant common genetic and nonshared environmental influences. These findings suggest that co-occurrence of internalizing and externalizing psychopathology in adolescents results from both genetic and environmental influences.     

Genetics in eating disorders: state of the science

Eating disorders have been viewed as psychiatric illnesses that are strongly influenced by societal pressures towards thinness and attractiveness. Although the environmental context of these disorders must not be neglected, recent research in the area of genetic epidemiology suggests a substantial influence of genetic factors on liability to eating disorders. This review presents a synthesis of current knowledge about genetic factors implicated in the etiology of eating disorders.     

Infectious and immune factors in the pathogenesis of neurodevelopmental disorders: epidemiology, hypotheses, and animal models

Both genetic and environmental factors contribute to the pathogenesis of a wide variety of neurodevelopmental disorders, including autism, mental retardation, and schizophrenia. Some heritable disorders approach 100% penetrance; nonetheless, even in these disorders, subtle aspects of clinical disease expression may be influenced by the environment. In other disorders with genetic influences, exogenous factors, and the timepoint(s) during nervous system development at which they are introduced, modulate expression of disease. Elucidation of the mechanisms guiding this intricate interplay between host response genes, environmental agents, and the neurodevelopmental context within which these interactions occur, is necessary to understand the continuum of clinical outcomes. This chapter will review the evidence that infectious and immune factors may contribute to the pathogenesis of neurodevelopmental disorders, describe an animal model of neurodevelopmental disorders based upon viral infection, identify processes by which neural circuitry may be compromised, and outline areas for future research.     

The neurodevelopmental frontostriatal disorders: evolutionary adaptiveness and anomalous lateralization

The frontostriatal system (dorsolateral prefrontal cortex, lateral orbitofrontal cortex, anterior cingulate, supplementary motor area, and associated basal-ganglia structures) is subject to a range of neurodevelopmental disorders: Tourette's syndrome (TS), obsessive compulsive disorder (OCD), attention deficit hyperactivity disorder (ADHD), schizophrenia (SCZ), autism, and probably depression. The system is responsible for our adaptive responses (initiation, execution, or withholding) to environmental situations, and the above disorders, involving effectively excessive release or withholding of various types of response, are all a consequence of changes in specific frontostriatal regions. The disorders all have a genetic component, and their persistence in the genome indicates that their clinical manifestations may also be associated, perhaps in low levels in close relatives, with certain adaptive advantages in given situations. Thus autism is associated with computational careers, depression with literary creativity, SCZ with lateral thinking and the Odyssean personality, ADHD with an Ice-Age readiness to respond, OCD with a focused range of interests, and TS with competitive sports and jazz improvisation. The disorders are all highly comorbid, and which one predominantly manifests may depend on how the frontostriatal system happens to be compromised as a result of inherited genetic predispositions and environmental contingency. We review the adaptive nature of the various subclinical manifestations and the evidence for concomitant phenomena (possibly epiphenomena): alterations in structural, functional, and behavioral lateralization in each syndrome. Indeed it is not clear that altered lateralization in frontostriatal disorders of a neurodevelopmental origin generally has any adaptive significance; it may often simply serve as a marker for altered regulatory function of the frontostriatal system, alterations which in low genetic dosage or penetrance continue to play an adaptive role in clinically unaffected close relatives of probands, but which, in high dosage or penetrance in the probands themselves, are generally deleterious.     

Genetic and environmental influences on pre‐schizophrenic personality: MAXCOV‐HITMAX and LISREL analyses

Postulating that the predisposition to illness in Claridge's disease model of schizophrenia can be equated with the personality dimensions S or Insensitivity, (low) E or Extraversion, and N or Neuroticism, as measured by Van Kampen's 3DPT, and assuming that the mode of transmission of schizophrenia is basically polygenic, the genetic and environmental etiology of S, E, and N was assessed in a sample of 52 MZ and 76 DZ twin pairs and their parents by means of LISREL. Besides, in a sample of 2118 subjects MAXCOV–HITMAX analyses were conducted for these factors as well as for the personality dimension G or Orderliness, but now assessed by the 4DPT, in order to find out whether a discrete or quasi‐discrete variable might also underlie these dimensions, giving support to the possibility of dominance or epistasis. The results obtained in these investigations favoured a model for all three dimensions, allowing for both additive and non‐additive genetic effects in combination with non‐shared environmental influences. It was not possible to choose between a model involving dominance and a model involving epistatic genetic effects. With the use of scores corrected for sex and age, which were converted to normal scores, the proportion of variance explained by additive genetic factors was 20% for S, 40–41% for E, and 26–29% for N. Dominance or multiple‐gene epistasis accounted for 37–38% (S), 19–20% (E), and 30–31% (N), and unshared environmental influences for 42–43% (S), 41% (E), and 42–43% (N) respectively. Copyright © 1999 John Wiley & Sons, Ltd.     

Essentialist Biases Toward Psychiatric Disorders: Brain Disorders Are Presumed Innate

A large campaign has sought to destigmatize psychiatric disorders by disseminating the view that they are in fact brain disorders. But when psychiatric disorders are associated with neurobiological correlates, laypeople's attitudes toward patients are harsher, and the prognoses seem poorer. Here, we ask whether these misconceptions could result from the essentialist presumption that brain disorders are innate. To this end, we invited laypeople to reason about psychiatric disorders that are diagnosed by either a brain or a behavioral test that were strictly matched for their informative value. Participants viewed disorders as more likely to be innate and immutable when the diagnosis was supported by a brain test as compared to a behavioral test. These results show for the first time that people spontaneously essentialize psychiatric conditions that are linked to the brain, even when the brain probe offers no additional diagnostic or genetic information. This bias suggests that people consider the biological essence of living things as materially embodied.     

Verhaltensgenetik

Behavioural genetics has provided ample evidence for the influence of genes on personality traits and psychological disorders. In this review, the methodological strategies of behavioural genetics are described and study results with special relevance for psychotherapists are highlighted.Moreover, some traditional myths and misunderstandings are discussed. In particular, two findings are underscored: While genetic factors substantially contribute to the development of personality traits, environmental influences shared by the members of a family appear to be virtually absent. In contrast, environmental factor specific to an individual seem to play an important role.Second, genes do not only have a direct impact on the development of psychological disorders, but also act in an indirect way by increasing the probability of exposure to stressful life events which in turn function as risk factors for psychological disorders. It is concluded that research should incorporate both genetic and environmental factors to be able to evaluate their relative impact and elucidate the interaction of nature and nurture.     

A Multivariate Genetic Analysis of Specific Phobia, Separation Anxiety and Social Phobia in Early Childhood

BACKGROUND: Comorbidity amongst anxiety disorders is very common in children as in adults and leads to considerable distress and impairment, yet is poorly understood. Multivariate genetic analyses can shed light on the origins of this comorbidity by revealing whether genetic or environmental risks for one disorder also influence another. We examined the genetic and environmental influences on the comorbidity between three common childhood anxiety disorders: Specific Phobia, Separation Anxiety and Social Phobia. METHODS: Using a two-phase design 4,662 twin-pairs were screened in the first phase and 854 pairs were assessed in the second phase by maternal-informant diagnostic interview using DSM-IV criteria. RESULTS: Multivariate genetic analysis revealed significant shared environmental over-lap between Specific Phobia and Separation Anxiety and significant familial and non-shared environmental over-lap between Specific Phobia and Social Phobia. CONCLUSIONS: Familial influences, especially shared environment, are central to the comorbidity between Specific Phobia and both Separation Anxiety and Social Phobia.     

A Common Genetic Factor Explains the Covariation Among ADHD ODD and CD Symptoms in 9–10 Year Old Boys and Girls

Previous studies examining the covariation among Attention Deficit Hyperactivity Disorder (ADHD), Oppositional Defiant Disorder (ODD) and Conduct Disorder (CD) have yielded inconsistent results. Some studies have concluded that the covariation among these symptoms is due to common genetic influences, whereas others have found a common environmental overlap. The present study investigated the genetic and environmental correlations among these three childhood disorders, based on a sample of 1,219 twins, age 9–10 years. A latent externalizing behavior factor was found to explain the covariance among ADHD, ODD and CD symptoms. Genetic influences explained more than half of the variance in this externalizing factor in both boys and girls. There were also unique genetic and environmental influences in each set of symptoms, suggesting some etiological independence of the three disorders. Our findings have implications for molecular genetic studies trying to identify susceptibility genes for these disorders. This study was funded by NIMH (R01 MH58354). Catherine Tuvblad was supported by post-doctoral stipends from the Swedish Council for Working Life and Social Research (Project 2006-1501) and the Sweden-America Foundation. Adrian Raine was supported by NIMH (Independent Scientist Award K02 MH01114-08). We thank the Southern California Twin Project staff for their assistance in collecting data, and the twins and their families for their participation.     

Self‐esteem: a behavioural genetic perspective

Self‐esteem, the affective or evaluative appraisal of one's self, is linked with adaptive personality functioning: high self‐esteem is associated with psychological health benefits (e.g. subjective well‐being, absence of depression and anxiety), effective coping with illness, and satisfactory social relationships. Although several pathways have been hypothesized to effect within‐family transmission of self‐esteem (e.g. parenting style, family relationship patterns), we focus in this article on genetic influences. Genetic studies on both global and domain‐specific self‐esteem and on both level and stability of self‐esteem converge in showing that (i) genetic influences on self‐esteem are substantial, (ii) shared environmental influences are minimal, and (iii) non‐shared environmental influences explain the largest amount of variance in self‐esteem. We advocate that understanding of current issues in self‐esteem research will be enriched by including behavioural genetic approaches. Copyright © 2002 John Wiley & Sons, Ltd.     

As the Twig Is Bent? The Myth of Child-Rearing Influences on Personality Development

Social scientists and laypersons alike believe that child-rearing styles and family environments are formative of personality traits such as shyness and activity level, intellectual traits such as IQ, and psychopathology. After 100 years of behavioral genetic research, however, including new studies of twins raised apart and together, little factual support for this “common sense” proposition can be found. Nonintellectual traits seem to be determined instead by genetic influences and by relatively specific environmental influences, most of which are not particularly tied to the family or parental treatments. Intellectual traits show modest family environmental influence, but that influence may diminish in importance after childhood. I conclude that parents should be given less credit for children who turn out well and should take less blame for children who turn out poorly. Counselors who blame parents less for children's behavioral outcomes—especially extreme traits and psychopathology—may find those parents to be more willing helpers in those intervention processes that have been shown to work.     

Fluency disorders in genetic syndromes

The characteristics of various genetic syndromes have included “stuttering” as a primary symptom associated with that syndrome. Specifically, Down syndrome, fragile X syndrome, Prader-Willi syndrome, Tourette syndrome, Neurofibromatosis type I, and Turner syndrome all list “stuttering” as a characteristic of that syndrome. An extensive review of these syndromes indicated clients diagnosed with these syndromes do show evidence of nonfluency patterns, but not all would be considered stuttering. Many of the syndromes are marked by degrees of mental retardation that probably contribute to a higher than average prevalence of stuttering, as well as a higher than average prevalence of other fluency disorders (when compared to the population at large).

An in-depth analysis of the available data indicates that some of these genetic syndromes show patterns of stuttering that may be indicative of only that syndrome (or similar syndromes) that can be differentially diagnosed from developmental stuttering. Among these patterns are the word-final nonfluencies noted in Prader-Willi syndrome; the presence of stuttering in the absence of secondary behaviors noted in Prader-Willi syndrome and; the presence of palilalia, word-final and word-medial nonfluencies, and word-medial and word-final nonfluencies in Tourette syndrome. Implications for future research are discussed in light of these findings.

Educational objectives: The reader will be able to: (1) describe the various different genetic syndromes that are associated with fluency disorders; (2) describe the types of nonfluencies that are associated with the major types of genetic syndromes that have fluency disorders; (3) describe the behaviors that may assist in differentially diagnosing different types of speech characteristics associated with various genetic syndromes.     

Can we fight stigma with science? The effect of aetiological framing on attitudes towards anorexia nervosa and the impact on volitional stigma

The present study experimentally investigated the way in which exposure to various aetiological explanations of anorexia nervosa (AN) differentially affected stigmatisation and behavioural intention outcomes. University students (N = 161) were randomly assigned to read one of four aetiological vignettes presenting the causes of AN as biological/genetic, socio‐cultural, environmental, or multifactorial. Results indicate that those who received a socio‐cultural explanation made stronger socio‐cultural causal attributions, fewer biological/genetic causal attributions, and were significantly less willing to sign a health insurance petition for AN. Unexpectedly, the multifactorial group considered individuals with AN as more responsible and blameworthy for their condition. Overall, findings were comparative with previous research and partially support the propositions of attribution theory. Results also suggest that by conceptualising the aetiology of AN as biological or genetic, or at least increasing one's knowledge of these contributing factors, it may be possible to decrease the level of blame‐based stigma associated with AN.     

Identifying environmental contributions to autism: provocative clues and false leads

The potential role of environmental factors in autism spectrum disorders (ASD) is an area of emerging interest within the public and scientific communities. The high degree of heritability of ASD suggests that environmental influences are likely to operate through their interaction with genetic susceptibility during vulnerable periods of development. Evaluation of the plausibility of specific neurotoxicants as etiological agents in ASD should be guided by toxicological principles, including dose-effect dependency and pharmacokinetic parameters. Clinical and epidemiological investigations require the use of sufficiently powered study designs with appropriate control groups and unbiased case ascertainment and exposure assessment. Although much of the existing data that have been used to implicate environmental agents in ASD are limited by methodological shortcomings, a number of efforts are underway that will allow more rigorous evaluation of the role of environmental exposures in the etiology and/or phenotypic expression of the disorder. Surveillance systems are now in place that will provide reliable prevalence estimates going forward in time. Anticipated discoveries in genetics, brain pathology, and the molecular/cellular basis of functional impairment in ASD are likely to provide new opportunities to explore environmental aspects of this disorder.     

Examining cognitive development from a conceptual change point of view: The framework theory approach

Sexual socialization refers to how, through social interaction, an individual acquires and internalizes culture-specific knowledge, values and attitudes about sexuality. Little, however, is known about how an individual's genetic characteristics modify this process, or if individuals gravitate towards specific environments according to their genetic characteristics. The aim was to explore whether adolescents' genetic predispositions modify environmental influences on peer-group sexual attitudes. Using a Finnish population-based sample of twins and their siblings (n = 9534), it was found that genetic effects influenced peer-group sexual attitudes in men (52%) and women (46%), thus offering evidence for gene–environment correlation. Men showed less restricted peer-group sexual attitudes than women. Some indications of different genes influencing environmental exposure in men and women were found.     

Understanding the Covariation Among Childhood Externalizing Symptoms: Genetic and Environmental Influences on Conduct Disorder,Attention Deficit Hyperactivity Disorder,and Oppositional Defiant Disorder Symptoms

Conduct disorder (CD), attention deficit hyperactivity disorder (ADHD), and oppositional defiant disorder (ODD) are common childhood externalizing disorders that frequently co-occur. However, the causes of their comorbidity are not well understood. To address that question, we analyzed data from > 600 Finnish twin pairs, who completed standardized interviews at age 14. Behavior genetic methods were used to examine how genetic/environmental factors contribute to each disorders symptoms and to their covariation. We found significant genetic effects on each disorder with only modest evidence of shared environmental influences. Our data suggest the comorbidity among CD, ADHD, and ODD is primarily explained by shared genetic influences; however, each disorder was also under unique genetic influence, supporting the distinction of each disorder.     

Multivariate analysis of cognitive and temperament measures in 24-month-old adoptive and nonadoptive sibling pairs

The genetic and environmental etiologies of covariation among measures of temperament (the Bayley Infant Behavior Record's Affect and Task Orientation Scales and the first principal component from the New York Longitudinal Study's difficult temperament items) and cognition (the Bayley Mental Development Index [MDI] and the total score on the Sequenced Inventory of Communication Development [SICD] were assessed at 24 months of age in 70 biologically related and 66 unrelated pairs of siblings in the Colorado Adoption Project. Between- and within-pair mean cross products were equated to expectations using the LISREL multiple-group specification (Fulker, Baker and Bock, 1983) to obtain maximum-likelihood estimates of genetic and environmental factor loadings and specific variances. The full one-factor model, with one general factor and five specific factors, provides a satisfactory fit to the data (χ² = 27.8, df = 30, P = 0.58). Genetic influences are important for the Bayley MDI and SICD languages measures, but not for temperament measures. Little or no evidence was found for shared-sibling environmental influences for any of the measures. Various hypotheses regarding genetic and environmental correlation structures were also tested.     

Genetic and environmental influences and covariance among meaning in life,religiousness, and spirituality

Meaning in life, spirituality, and religiousness have been empirically linked in previous research. This study aimed to advance knowledge of the interrelations among these variables by examining their heritable and non-heritable sources of influence, as well as the genetic and environmental contributions to their inter-relations. A sample of 343 middle-aged twins drawn from the Minnesota Twin Registry completed measures of meaning in life and spirituality. There was evidence that religiousness, spirituality, and meaning in life shared common genetic and environmental influences, suggesting that these people's attitudes concerning these variables may arise from shared factors. These results provide novel evidence of a shared genetic substrate for meaning in life, religiousness, and spirituality, and support the possibility that people's basic attitudes about the meaning of existence are commonly rooted in evolved biological factors and conjointly influenced through people's experiences with life.