Developmental Instability and Markers of Schizotypy in University Students

Evolutionary Psychology
www.epjournal.net – 2008. 6(4): 586-594
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Original Article
Developmental Instability and Markers of Schizotypy in University Students
Robert J. Thoma, Departments of Psychiatry and Psychology, University of New Mexico, Albuquerque, New
Mexico, USA rjthoma@salud.unm.edu (corresponding author)

Steven W. Gangestad, Department of Psychology, University of New Mexico, Albuquerque, New Mexico,
USA

Matthew J. Euler, Department of Psychology, University of New Mexico, Albuquerque, New Mexico, USA


Per A. Lysne, Department of Psychology, University of New Mexico, Albuquerque, New Mexico, USA


Mollie Monnig, Department of Psychology, University of New Mexico, Albuquerque, New Mexico, USA


Ronald A. Yeo, Department of Psychology, University of New Mexico, Albuquerque, New Mexico, USA

Abstract: Fluctuating asymmetries (FA) and minor physical anomalies (MPAs) are
markers of developmental instability (DI), an index of the degree to which an organism was
subject to genomic or environmental stress during development. Measures of DI are
characteristic of schizophrenia and are thought to reflect an underlying genetic liability for
schizophrenia spectrum disorders. Whereas MPAs reflect developmental stress relatively
early in the first trimester in utero, skeletal FAs reflect developmental stress throughout the
lifespan. Both measures were collected to provide some indication of the associated
developmental time course. In addition to DI measures, several psychometric measures of
schizotypy were administered in a sample of university students (n = 81). It was
hypothesized that increased DI may relate to schizotypal symptoms in a group of healthy
undergraduate students. Schizotypy scores were positively correlated with FA, but not
MPAs. This finding suggests that DI, as indexed by FA, is important for normal range
variation in schizotypal characteristics, just as it is important for normal range variation in
intelligence. Second, considered in the context of studies demonstrating that schizophrenia
is associated with elevated MPAs, these results suggest that developmental stress likely
occurs earlier in development for schizophrenia than schizotypy.

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Developmental instability and schizotypy

Keywords: schizotypy, developmental instability, fluctuating asymmetry, minor physical
anomalies.
________________________________________________________________________________________

Introduction
Yeo, Gangestad, and Thoma (2007) recently proposed a two-factor theory of the
etiology of schizophrenia spectrum disorders based upon an evolution-based model of
developmental instability. The authors proposed that a possible mediator and moderator of
genetic and environmental influences on schizophrenia spectrum disorders is
developmental instability (DI). DI concerns the accuracy with which genotypes are
translated into phenotypes (Møller and Swaddle, 1997). It has been defined as propensity to
experience “developmental noise” (Adams and Niswander, 1967; Waddington, 1957), or
the effects of genetic or environmental stresses (e.g., mutations, pathogens, toxins) during
development to which an organism is not fully adapted. This results in the imprecise
expression of developmental design (Lerner, 1954; Ludwig, 1932; Parsons, 1990). Two
commonly measured markers of DI in humans include fluctuating asymmetry (FA), defined
as deviation from bilateral symmetry on traits that are typically symmetric at a population
level (Van Valen, 1962), and phenodeviant physical traits, or minor physical anomalies
(MPAs).
In the Yeo et al. (2007) model, developmental instability represents a general
vulnerability factor that is shared across developmental disorders. Each disorder also has a
set of unique genetic (and perhaps environmental) causes. For example, multiple studies
have shown increased MPAs in patients with schizophrenia when compared to normal
control subjects (for a review, see Murphy and Owen, 1996). In addition, dermatoglyphic
fluctuating FA appears to be increased in twins with schizophrenia compared to the
unaffected co-twin (e.g., Markow and Gottesman, 1989), suggesting that early events in
gestational development interact with other genetic and environmental sources of influence
to predispose the disorder. Other studies have linked the presence of schizophrenia to
prenatal exposure to influenza virus and cold temperatures (Brown et al., 2004; Venables,
1996), suggesting a neurodevelopmental role for a specific physiological stressor in the
development of schizophrenia.
“Schizotypy” is a term commonly used to describe a continuum of correlated
personality traits that include a tendency to report unusual sensory experiences, hold odd or
sometimes paranoid beliefs, and show less interest in and enjoyment from social
interactions. Mild cognitive difficulties are often reported in schizoptyic individuals,
representing in mild form some of the attention deficits encountered in schizophrenia.
Meehl’s influential formulation (1990) specifically drew attention to the relationship
between schizotypy and schizophrenia. He suggested that schizotypy or “schizoid taxon”
denote individuals who carry the predisposing gene pattern for schizophrenia, but this
genotype is not fully expressed as schizophrenia. This genetic predisposition is
phenotypically expressed as specific personality traits, cognitive slippage, soft neurological
signs, and “soft psychometric signs” (Meehl, 1990).
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Developmental instability and schizotypy
The aim of the current study was to investigate associations between normal
variation in DI and expression of these soft psychometric signs.
Several recent studies have investigated the role of markers of DI in the etiology of
schizotypy. One recent study, using a single dermatoglyphic FA measure, found it to be
positively correlated with scores on the Social Anhedonia Scale in males, but not in
females (Rosa et al., 2000). Other recent studies demonstrated that groups of college
students identified as schizotypic exhibit more dermatoglyphic anomalies than control
groups (Chok, Kwapil, and Scheuermann, 2005; Chok and Kwapil, 2005). As no previous
studies have comprehensively investigated a relationship between measures of skeletal
fluctuating asymmetry and schizotypy, we chose to investigate the role of developmental
instability in the etiology of schizotypy via a comprehensive measurement of DI indicators.
In an unselected sample of university students, we investigated whether individuals scoring
relatively higher on schizotypy scales would have increased FA and MPAs. We predicted
positive correlations between markers of DI and schizotypy.
Materials and Methods
Participants
Sixteen males and forty-four females ranging in age from 17 to 49 years were
recruited from the University of New Mexico (UNM) Psychology Department subject pool
and were given credits toward psychology classes for participation in the experiment.
Twenty-one males, ranging in age from 19 to 28, were recruited by posters on the
University of Utah (U of U) campus (total n = 81). University of Utah participants were
paid $16 per hour for their participation in several lab projects, including the current
project. All potential participants were screened for history of neurological disorder or
disease, serious medical illness or disease, learning disability, or head injury. Using a
subset of questions derived from the SCID-I for DSM-III, potential participants were also
screened for history of significant mood disorders, psychotic disorders and anxiety
disorder. Before all testing procedures, participants were informed of potential risks related
to participation and signed a consent form describing procedures and advising them of their
right to leave the study at any time.

Procedures

Measurement of FA and MPAs
We measured the right and left sides of seven bilateral traits: ear length, ear width,
elbow width, hand width, wrist width, ankle width, and foot width. FA for a given structure
was calculated by taking the absolute value of the difference between the left and right
sides, divided by one-half the sum of left plus right sides (individual FA = |R – L| / [.5 x (R
+ L)]; Yeo, Gangestad, Thoma, Shaw, and Repa, 1997; Yeo, Gangestad, Edgar, and
Thoma, 1999). These traits generally show very little directional asymmetry (Furlow,
Armijo-Prewitt, Gangestad, and Thornhill, 1997). In our sample, only hand width deviated
from symmetry. Directional asymmetry (DA) exists when a trait is consistently larger on
one side of the body than another across a population. The most straightforward means of
accounting for DA is simply to subtract mean DA from individual asymmetry values
(Palmer and Stroebeck, 1986). Correction for directional bias was implemented by first
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calculating deviation from the population average hand asymmetry for each individual and
then subtracting that average from each individual’s directional asymmetry (Palmer, 1994).
FA measures for the seven individual traits were summed into a total composite measure,
which we simply refer to as FA.
To assess MPAs, we used the procedures outlined in the 1989 revision of the
Waldrop scale (Waldrop, Halverson, and Shetterly, 1989; see also Waldrop, Pedersen, and
Bell, 1968). The measures consisted of observed head circumference, fine electric hair, hair
whorls, inter-ocular distance, height of ears, structure of the ear lobes, steepled palate,
tongue furrows, curvature of the fifth finger, and abnormalities of the toes. A score for
MPAs was then derived from a point system based upon the presence and degree of each of
these body features.

Schizotypy test battery
Several measures of schizotypy were combined into a single questionnaire. The
Schizoid Taxon Scale (STS, Golden and Meehl, 1979) is a 7-item measure whose items
were selected using a taxometric procedure. The items concern a variety of schizotypic
symptoms, including cognitive slippage, social anhedonia, and ambivalence. The Magical
Ideation Scale (MIS, Eckblad and Chapman, 1983) is a measure of “a belief...of the
possibility that events which, according to the causal concepts of this culture, cannot have a
causal relation with each other” (p. 217). Examples of item content include belief that
others can read one’s mind, belief that certain numbers have special powers, and sensing an
evil presence. The Social Anhedonia Scale (SAS; Mishlove and Chapman, 1985) is a
measure of shut-in, schizoid, and avoidant behavior and of lack of pleasure derived from
social relationships. Both the MIS and SAS have been shown to predict later onset of
schizophrenia (Chapman, Chapman, Kwapil, and Eckblad, 1994).

Analysis
A principal components analysis was conducted to construct a measure associated
with variance shared by all three measures. The first principal component accounted for
51% of the total variance in the individual measures. Individual variables had loadings of
.86 (STS), .71 (MIS), and .53 (SAS). A first principal component of schizotypy has been
proposed as a general schizotypy measure (Williams and Irwin, 1991). In our analyses, we
refer to this measure as Schizotypy. Sex and height were partialled out of all correlations,
since body size may be associated with measured FA (Palmer, 1994).
Results
There were no significant correlations between MPAs and measures of Schizotypy.
However, FA correlated significantly and positively with Schizotypy (r = .23, p = .03), the
Magical Ideation Scale (r = .26, p = .02), and with Golden and Meehl’s STS (r = .19, p =
.05). No significant relationship was found for the Social Anhedonia Scale (r = .08, p = .26;
see Table 1). There were no significant interactions between sex or height and DI in
predicting measures of Schizotypy.




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Table 1. Partial Correlations between Schizotypy and DI Measures*
_________________________________________________________
Variables



FA

MPAs
_________________________________________________________
Schizotypy



.23

-.03

p=.03
p=.42
Golden and Meehl Schizoid
.19

.05

Taxon Scale


p=.05
p=.35
Magical Ideation Scale

.24

-.08

p=.02
p=.24
Social Anhedonia Scale

.10

-.04

p=.20
p=.39
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*Controlling for the effect of sex and height.
Note: FA = Fluctuating Asymmetry and MPA = Minor Physical Anomalies.

It should be noted that although the obtained correlations represent relatively small
effect sizes, but they may substantially underestimate the magnitude of the relationship
between schizotypy and the underlying trait of FA. Gangestad and Thornhill (1999) have
estimated that the FA composite used in the current study correlates about .5 with
underlying DI and, hence, correlations with FA underestimate correlations with DI by a
factor of about two. Table 2 shows a summary of inter-scale correlations.

Table 2. Correlations between the Schizotypy Measures
_________________________________________________________________________
Variables



STS MIS SAS
_________________________________________________________________________
Schizotypy (1st PC)

.86
.71
.53


Schizoid Taxon Scale (STS)

.44
.53

Magical Ideation Scale (MIS)


.30
Soc Anhedonia Scale (SAS)
_________________________________________________________________________
Note. n = 81. For all correlations, p < .01 with the exception of MIS and SAS correlation for which p < .05.
STS = Schizoid Taxon Scale, MIS = Magical Ideation Scale, and SAS = Social Anhedonia Scale.


Since the Chapman scales (i.e., Magical Ideation and Social Anhedonia Scales)
were designed as taxon scales, a further analysis was done to investigate how many of the
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subjects in this sample may have met the suggested criteria for inclusion in the “schizotypy
taxon.” Three of the 81 subjects reached criteria for schizotypy as assessed with the
Magical Ideation Scale, and four reached criteria for schizotypy using the Social
Anhedonia Scale. There were no significant differences between these subjects and the rest
of the sample on DI measures or on any demographic variables.
To investigate the possibility that motivational differences may exist between samples
drawn from UNM (compensated with class credits) and U of U (compensated at $16 per
hour), group differences on Schizotypy scale scores were investigated. Of the three
Schizotypy taxon scales, there was a group difference on one; the U of U group had lower
scores on the Magical Ideation Scale (p = .002). No other comparisons approached the level
of significance. It seems unlikely that this difference was secondary to motivational issues
because it is doubtful that motivation would affect one schizotypy taxon scale and not
others. To test whether the DI-schizotypy relationships generalized across samples, group
differences in Pearson correlations were investigated (Cohen, 1988). None of the group
comparisons between correlations approached the level significance, indicating no
correlational differences between the UNM and U of U groups.
Discussion
Fluctuating asymmetry (FA) correlated positively with test scores on instruments
assessing schizophrenia proneness in a sample of normal, undergraduate university
students. There are two important implications of this association between schizotypy
scores and FA. The first is that DI, as indexed by FA, is important for normal range
variation in schizotypy, just as it is important for normal range variation in intelligence
(Furlow et al., 1997; Prokosch, Yeo, and Miller, 2005; Thoma, Yeo, Gangestad, Halgren,
Sanchez and Lewine, 2005). Hence, the genetic factors linked with DI, including mutation
load and epistatic interactions among genes (Leamy and Klingenberg, 2005; Yeo et al.,
1999), might be relevant for normal variation in schizotypy scores. Second, the current
results are relevant for our understanding of the role of DI in schizophrenia, suggesting that
increased MPAs and FA in schizophrenia do not result from some feature of the disorder
per se (e.g., lifestyle influences or medication effects) and likely index a broad underlying
vulnerability to schizophreniform disorders.
In contrast, MPAs, another marker of DI, were not related to schizotypy in the
current study, although MPAs have long been associated with schizophrenia. Whereas
MPAs reflect slowed or disrupted development in the first or second trimester, skeletal FA
reflects less of a “time-locked” developmental abnormality and actually increases during
adulthood (Gangestad and Thornhill, 1999). The current data suggest that schizotypy is
associated with developmental perturbations later in development and not necessarily early
prenatal perturbations. Some studies have found increased MPAs in schizotypal
adolescents (Weinstein, Diforio, Schiffman, Walker, and Bonsall, 1999) and in unaffected
relatives of schizophrenics (Ismail, Cantor-Graae, and McNeil, 2000) suggesting that
further research is needed to investigate the temporal specificity of each category of DI
measure and possibly to delineate the timing of DI associated events in each disorder. Of
possible relevance, a recent study did not show a schizophrenia group to have increased
skeletal FA (Edgar et al., 2006). Hence, though both schizophrenia and schizotypy are
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Developmental instability and schizotypy
disorders characterized by increased DI, the current findings suggest that the impact of DI
on the developing brain occurs somewhat later in those with schizotypal characteristics.
These findings thus suggest a novel interpretation of the distinction between
schizophrenia and schizotypy. The timing, rather than the nature of neurodevelopmental
stresses, may determine whether an individual’s genotype is expressed as schizophrenia or
schizotypy. Both schizophrenia and schizotypy appear to be characterized by an increased
vulnerability factor, indexed by DI, as well as an increased dose of unknown specific and
unique etiologic factors for schizophreniform disorders. Theoretically, schizophrenia might
entail a greater loading of the disorder-specific factor, the general vulnerability factor, or
both. Direct comparison in a single study of FA levels in schizotypal personality disorder
versus schizophrenia would be especially informative, but we are aware of no such studies.

Acknowledgements: We thank Jeffrey D. Lewine and Eric Halgren, who helped in the
subject recruitment and data collection phase of this project, and Gregory A. Miller, whose
advice and encouragement to Thoma during the preparation of this manuscript was
invaluable. Preparation of this manuscript was made possible by funding derived from a
NARSAD Young Investigator Award and a NIAAA Grant (1 K23 AA016544-01) to
Thoma.

Received 31 July 2008; Revision submitted 25 September 2008; Accepted 7 October
2008
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