Schizotypal personality (schizotypy) has been considered an endophenotype for schizophrenia, in that it shares neurological, psychophysiological, and behavioral characteristics associated with disorders of the schizophrenia spectrum (Gottesman and Gould 2003
; Lenzenweger 2006
; Linney et al. 2003
). Behavioral genetic studies have demonstrated heritable factors are important for schizotypal personality in adults (Linney et al. 2003
). Despite the fact that self-report screening has been found to aid in the detection of liable individuals in the adult population (MacDonald et al. 2001
), there is currently no instrument to assess schizotypal traits in child or adolescent samples. Additionally, no studies to date have investigated the influence of genetic and environmental factors that contribute to the stability of schizotypal traits in adolescence using a measure designed to assess traits during this developmental period. It has been argued that schizotypal personality traits are qualitatively similar to the characteristic symptoms of schizophrenia, albeit quantitatively less severe. As such, it behooves us to understand the development and etiology of schizotypal personality traits, in order to aid our understanding of the wider schizophrenia spectrum. The aim of the present study was thus to investigate the genetic and environmental influences and their stability from ages 11–16 years old in a longitudinal twin study.
Given that the age of onset for schizophrenia occurs in late adolescence or early adulthood [American Psychiatric Association Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR), 2004], investigating schizotypal traits, especially during development, offers a promising way to identify individuals with schizophrenia latent liability (Claridge 1987
; Meehl 1989
). The validity of this approach is suggested by an increase in liability for categorically defined Schizotypal Personality Disorder (SPD) and schizotypal personality in the relatives of patients with schizophrenia (Kendler 1985
), as well as elevated probability of psychotic episodes in individuals who present with high levels of schizotypy (Chapman et al. 1994
; Linney et al. 2003
). Psychometrically measured schizotypy has been found to be elevated among schizophrenia patients (Chapman et al. 1978
) and their relatives (Chen et al. 1998
), and those with higher schizotypal scores have more relatives with schizophrenia (Chapman et al. 1994
). Moreover, twin studies have shown schizotypal personality disorder is genetically related to schizophrenia and therefore may reflect some facets of genetic predisposition to schizophrenia (Chang et al. 2002
; Kendler et al. 1993
Significant genetic influences have been found in studies of adult twins from the general population using many different self-report schizotypy scales (heritabilities ranging from 29 to 67%; for review, see Linney et al. 2003
), although one study failed to report genetic influences on a specific scale measuring perceptual aberrations (Kendler and Hewitt 1992
). In addition, the shared environment (i.e., non-genetic factors that contribute to twin similarity) has been found to influence both the positive symptoms (Kendler and Hewitt 1992
; MacDonald et al. 2001
), as well as the negative symptoms of schizotypy in adults (Miller 1993
The dimensional structure of schizotypal traits has also been investigated, both phenotypically and genetically. Schizotypal personality has been shown to have a highly analogous dimensional structure in the general population, with latent factors resembling the classical schizophrenia positive, negative, and disorganization symptom dimensions (Raine et al. 1994
; Raine 1991
; Vollema and Van den Bosch 1995
; Claridge et al. 1996
; Mason et al. 2005
). The majority of evidence supports three symptom clusters: (1) Cognitive-Perceptual deficits (comprised of Ideas of Reference, Magical Thinking, Unusual Perceptual Experiences, and Paranoid Ideation), (2) Interpersonal-Affective deficits (Social Anxiety, No Close Friends, Blunted Affect, Paranoid Ideation), and (3) Disorganized behavior (Odd Behavior and Odd Speech).
Factor analytic studies of adults have reported two or three phenotypic factors, depending on the number and item content of scales. For example, a three-factor model was found to fit the data better than a single or a two-factor model; these three schizotypal factors paralleled the three reported schizophrenia symptom dimensions (Mata et al. 2000
). Further, using the Schizotypal Personality Questionnaire (SPQ; Raine 1991
) a three-factor model, comprised of Cognitive–Perceptual deficits, Interpersonal Deficits, and Disorganization, was found to underlie individual differences in both schizophrenic and normal samples (Rossi and Daneluzzo 2002
). This demonstrates some parallel aspects between schizotypal traits and schizophrenia symptoms, at least phenotypically.
There are only a few studies that have investigated genetic and environmental influences on the symptom dimensions of schizotypal traits. One adult twin study suggested a latent common schizotypy factor in both males and females (MacDonald et al. 2001
). This latent factor—influenced by additive genetic (15%), shared-environmental (45%) and unique environmental effects (i.e., environmental factors not shared by twins, but which serve to make co-twins different from one another) (40%)—was mainly characterized by positive symptoms (e.g., perceptual aberration, magical ideation). Moreover, scores on the positive symptom dimension of SPQ administered to relatives of patients with psychotic disorders were found to relate most strongly to their genetic risk of psychosis (Vollema et al. 2002
). However, in another study that only included female twins (Linney et al. 2003
), one core dimension could not sufficiently account for the genetic covariation among the various schizotypy components of the Oxford-Liverpool Inventory of Feelings and Experiences (Mason et al. 1995
) and the Peters Delusions Inventory (PDI; Peters et al. 1996
). Two latent factors were required—each influenced by genetic and non-shared environmental effects—such that one factor was essentially comprised of the positive symptom scales and the second factor was based on negative dimension scales. Both latent factors had loadings from the cognitive scale, suggesting that while schizotypy traits may be phenotypically multidimensional, both positive and negative aspects may be genetically related to the cognitive disorganization dimension. Although phenotypic studies in adults consistently suggest as many as two or three underlying dimensions may characterize schizotypal traits, the dimensional structure of the genetic and environmental influences remains unclear.
Only one study to date has investigated the genetic and environmental etiology of schizotypal traits during adolescence (Lin et al. 2007
). Using the SPQ (Raine 1991
) and the Perceptual Aberration Scale (PAS; Chapman et al. 1978
) in 12–16 year old Taiwanese twins, 41–49% of the variance of the PAS and the three SPQ subscales were accounted for by genetic factors. While genetic factors were additive for the PAS and the Disorganization subscale of the SPQ, they were non-additive (i.e., including dominance and/or epistasis) on the Cognitive-Perceptual and Interpersonal subscales. The remaining variance of each subscale was accounted for by non-shared environmental factors. Though significant genetic covariation was found among these scales (bivariate heritability amongst the various traits and scales ranged from 50 to 65%), neither a single common factor nor an independent pathway model fit the data, suggesting that genetic and environmental influences underling the various schizotypal traits may be multidimensional (Lin et al. 2007
). Overall, findings regarding the genetic and environmental etiologies and their underlying factor structures have yet to be replicated across different age groups and in other populations.
It must be noted that the Lin et al. study utilized a measure (SPQ) that had been validated for use in adults, in spite of the fact that sample was comprised of children and adolescents; thus, these results must be interpreted with caution. The present study utilized a newly created SPQ-Child version developed specifically for use in child and adolescent samples, with wording changes from the original SPQ-B items in order to make them more age appropriate.
It is well known that an increase in the rate of psychotic symptoms (e.g., hallucinations and delusions) and adjustment problems occurs in adolescence (Erlenmeyer-Kimling 2001
; Laurens et al. 2007
; Walker et al. 1996
; Walker 2001
), and the initial manifestation of poor adjustment generally follows the onset of puberty (Walker and Bollini 2002
). Additionally, hallucinatory experiences and delusional beliefs at age 11 are both strong and specific indices of a schizophrenia spectrum disorder (SSD) diagnosis by age 26 (Poulton et al. 2000
). Despite these findings, there is currently no instrument to assess schizotypal traits in child or adolescent samples.
The present study attempted to clarify further the genetic and environmental etiology of schizotypy using an unselected sample of adolescent twins assessed on two occasions. The aims of the study were fourfold: (1) to investigate the phenotypic factor structure of the SPQ-C, with the expectation that a factor structure similar to that found for the SPQ-B in adults—three symptom dimensions—will emerge and that these dimensions will share a common genetic and environmental etiology; (2) to examine the relative contributions of genetic and environmental effects on self-reported schizotypal traits during adolescence; (3) to investigate whether a common latent factor accounts for genetic and environmental covariation among the three symptom dimensions of schizotypal traits; and (4) to examine the longitudinal genetic and environmental stability of schizotypal traits between the ages of 11 and 16 years old.