Schizophrenia Bulletin vol. 44 suppl. no. 2 pp.

S556–S563, 2018
doi:10.1093/schbul/sby012
Advance Access publication February 21, 2018

Models of Schizotypy: The Importance of Conceptual Clarity

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Phillip Grant*,1,2, Melissa J. Green3,4, and Oliver J. Mason5
1
Department of Psychology, Justus-Liebig-University, Giessen, Germany; 2Faculty of Life Science Engineering, Technische Hochschule
Mittelhessen University of Applied Sciences, Giessen, Germany; 3School of Psychiatry, Faculty of Medicine, University of New South
Wales, Sydney, NSW, Australia; 4Neuroscience Research Australia, Sydney, NSW, Australia; 5School of Psychology, University of Surrey,
Stag Hill, Guildford, Surrey, UK
*To whom correspondence should be addressed; Biological Psychology and Individual Differences, Department of Psychology, Justus-
Liebig-University Giessen, Otto-Behaghel-Str. 10F, 35394 Giessen, Germany; tel: +49 641 9926154, fax: +49 641 9926159,
e-mail: [email protected]

The observation of psychosis-like traits that resemble symp- remains a lack of consensus on its core dimensions
toms of schizophrenia and bipolar disorder, both among and the relative import of each. For example, the con-
healthy relatives of psychotic patients and among the ge- sequences for schizophrenia liability of presenting with
neral population, can be traced to the early 20th century.1,2 high values in one but not another schizotypal facet, or
These traits have since been described within various mod- particular combinations of schizotypal traits, remain
els of illness and health (ie, normal/abnormal personality, unclear.
abnormal psychotic continua), each giving rise to concepts The construct of schizotypy is increasingly accepted
such as “schizotypy,” “psychoticism,” and “psychosis-prone- in the clinical sciences as an “influential, comprehen-
ness” that are not necessarily interchangeable, although sive psychological construct in schizophrenia research”7
their subtle distinctions are often overlooked. Historically, (p. S363) and a “useful and unifying construct for un-
there have been 3 major models of schizophrenia-/psycho- derstanding schizophrenia-spectrum psychopathology”8
sis-proneness, one of which is referred to as “taxonic” or (p. S366). Historically, schizotypy has been regarded as a
“quasi-dimensional,”3,4 and 2 models that can be regarded set of personality traits distributed among (at least signif-
as “fully dimensional,”5,6 as distinguished by the relation- icant parts of) the general population, which may repre-
ship that is proposed to exist between psychosis-proneness sent an “endophenotype” on the path to schizophrenia.9,10
and the risk of clinical schizophrenia or other psychotic However, there remains considerable lack of concep-
disorder. In this review, we outline the key assumptions of tual clarity about schizotypy and its relevance in under-
each model and its implications for research of psychosis in standing the causes of psychotic disorder. We believe this
relation to mental illness and health and for the alternative partly reflects failure to acknowledge the historical devel-
models. We integrate historical concept development with opment of the schizotypy construct, particularly, subtle
current findings from various fields of research (eg, person- differences among key theoretical models from which the
ality, neurobiology, and behavioral genetics) and highlight construct emerged. This review highlights the key assump-
the remaining questions each model poses in relation to un- tions of various schizotypy models as they emerged over
derstanding the development of psychotic illness and the dis- time, contributing to current concepts (and potential mis-
tribution of psychotic-like traits in the general population. understandings) about the use of the schizotypy construct.
We review these different models and urge researchers in
Key words:  schizotypy/psychosis proneness/schizotypal this field to consider these distinctions in theoretical foun-
personality/schizophrenia/schizotypy models dations when reporting data concerning “schizotypy.”

Meehlian Model
Introduction
Schizotypy is agreed to comprise a set of inherited traits Historically, the notion of latent schizophrenia-like char-
reflected in personality organization,3,4,6 which present acteristics observable both in patients prior to their first
as qualitatively similar to schizophrenia symptoms and florid episode and in patients’ nonschizophrenic relatives
correlate with schizophrenia liability. There is consensus can be traced at least back to the early 20th century.1,2
that schizotypy is a multifaceted concept—though there Since then, a number of terms have been used to denote

© The Author(s) 2018. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved.
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the existence of psychotic-like experiences in nonpsy- rather than taxonic.16,17 Furthermore, a single risk-allele
chotic individuals; the term “schizotypy” (a contraction (or “schizogene”) would need to have effects of an order
of “schizophrenic phenotype” introduced by Rado3) of magnitude that makes it highly unlikely not to have
being the most commonly used. Rado’s “schizotypy” been discovered by now. Importantly, in the genetic con-

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was based on genetic liability and heavily built upon by text, Meehl’s model represents a taxonic one because it
Meehl.4 Both authors proposed the existence of a discrete allows for phenotypic variation along a continuum of se-
class of individuals (schizotypes) characterized by an in- verity within schizotypy, but places the entire continuum
tegrative neural defect believed to be caused by a specific within the realm of illness (associated with genetic predis-
“schizo-gene” with a dominant Mendelian pattern of in- position). That is, all schizotypes are necessarily “schizo-
heritance.4 Although modern genetics has ruled out the taxic,” carrying of at least one copy of one or more risk
idea that schizophrenia is a Mendelian disorder, nor likely alleles defining schizotaxia and, by extension, a schizo-
caused by a single gene, Meehl proposed the importance type. Thus, one either is a schizotype or not, but within
of “polygenic potentiators” (see below) believed to influ- the group of schizotypes, there is proposed gradation
ence a number of genetic factors that may interact with regarding symptom severity. Claridge6 attempted to dis-
the proposed “schizogene” to determine the likelihood tinguish his fully dimension model of schizotypy (which
of transition to clinical schizophrenia.11 One major mis- allowed “schizotypy” to exist in both illness and health)
conception of Meehl’s model has been in understanding by referring to Meehl’s model as “quasi-dimensional.”
the expected transition rates of schizotypes into schizo- Thus, while Meehl’s model allows schizophrenia risk to
phrenia: not all schizotypes were presumed to transition. vary in severity on a dimension within a (clinical) taxon
Instead, according to the prevalence of schizophrenia, [schizotypy], Meehl did not believe that schizotypal per-
Meehl surmized that 10% of the population be regarded sonality extended outside of the taxon throughout the
as schizotypes, but only 10% of these would decompen- general population. Meehl’s model, thus, represents a
sate into schizophrenia, while the other 90% would re- quasi-dimensional account because of the proposed clear
main asymptomatic or show a subclinical expression of demarcation between the healthy and schizotaxic brain:
symptoms. the abnormal brain state (schizotaxia) is taken as a ref-
Furthermore, Meehl did not assume that schizotypy erence point, and dimensions of the spectrum of schiz-
was (fully) inherited, rather that the phenotype emerged otypal behaviors are construed as degrees of expression
from gene-environment interactions. He specifically of “disorder,” with the ultimate end-point being schizo-
proposed that the aforementioned “schizogene” would phrenia.18 The most commonly used schizotypy scales de-
lead to an integrative neural defect (schizotaxia), which veloped within the framework of the Meehlian model are
could result in schizotypal personality organization (this the Wisconsin Schizotypy Scales by the research team of
not being synonymous with schizotypal personality dis- Jean and Loren Chapman.
order) dependent on individual environmental expo-
sure and a range of genetically determined personality
Eysenckian Model
dimensions (independent of schizotaxia) referred to as
“polygenic potentiators.”11 Thus, only schizotaxia (the In contrast to the Meehlian disease-based model, the
neural integrative defect) was proposed to be inherited.4 “fully dimensional” view emerged from European school
In other words, Meehl proposed that schizotaxia almost of temperament rooted in experimental psychology, par-
invariably leads to schizotypy and sometimes to schizo- ticularly pioneered by Hans Eysenck.5,19 Eysenck’s theory
phrenia—perhaps due to other genes, the learning envi- saw psychotic illness as the extreme end of a continuous
ronment etcetera. Importantly, the Meehlian model does personality dimensions, couched within natural variation
not exclude influences of other genes than the “schizo- in brain functioning. At the time, Eysenck’s proposal of
gene” on idiosyncratic expression of schizotypy, both as an inextricable connection between normal and abnormal
“potentiators” and “depotentiators (ie, influencing idio- personality along with the assumption of biological cau-
syncratic schizotypal organization and altering the risk sation dissected many issues within the debate between
of decompensation, but only “given the presence of the psychiatry and the antipsychiatry movement. Eysenck
schizogene”11; p. 39). proposed that all major dimensions of personality were
Although the single-gene aspect of Meehl’s model is genetically based, interacted with the environment, and
inconsistent with Genome Wide Association Studies expressed themselves phenotypically via biological inter-
(GWAS) of schizophrenia,12–14 suggesting that the proba- mediaries (eg, hormones, neurotransmitters). It is impor-
bility of a monogenetic cause of schizophrenia liability is tant, therefore, to emphasize that—although Eysenck did
highly unlikely, it has been asserted that the model is com- not research individual genetic contributions—his theory
patible with a polygenic basis of schizotaxia.15 Others, (and by extension that of his former student, Claridge)
however, have illustrated that an increasing number of is fully rooted in genetics.20 Additionally, it is often mis-
involved alleles (with individually small effect-sizes) leads construed that Eysenck and his followers used statisti-
to the resulting quantitative trait becoming dimensional cal methods (ie, factor analysis) to reach theories (as is
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the case, eg, regarding the Big Five personality model), and delinquency. This is emphasized by Claridge, whose
while the opposite was true in actuality: Eysenck consist- schizotypy model is built on the older conceptualization
ently maintained that personality research should always of Psychoticism. This older concept—although only ever
start with hypotheses and that experiments and statis- (and very tentatively) published in out-of-print-books5—

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tical methods be used to test these hypotheses, not vice was far more closely related to psychosis than psychopa-
versa.5,20 Thus, while modern personality models (eg, the thy. Furthermore, as the validity of separable functional
Five Factor Model) are mainly data driven, Eysenck’s psychoses is currently being brought into question, it is a
approach was of a truly deductive (ie, theory driven) very germane issue whether “schizotypal” traits are spe-
nature. cific to schizophrenia or more generally relevant to psy-
The Eysenckian model differs from the Meehlian not chosis. A related issue, and in fact a major weakness of
only in the assumption of complete dimensionality of Eysenck’s account, is that it fails to make a clear distinc-
schizophrenia liability but also in the assumption that tion between traits and clinical states or offer any cogent
there cannot be a single “pure dimension of schizotypy.” explanation about how traits lead to illness. We have seen
Eysenck did not see room for its existence,21 because it how Meehl’s account approached this distinction and can
relied on the Kraepelin-Bleuler dichotomy of schizophre- now turn to Claridge’s extension of a fully dimensional
nia and bipolar disorder as qualitatively discrete entities. model of schizotypy.6
In other words, if schizotypy existed, it should be distin-
guishable from another trait one might call “cyclotypy.”
Claridge’s Model
This notion was prima facie proposed by Kretschmer,2
when he formulated his temperaments of schizothymia According to Claridge,26 schizotypy denotes a range of
and cyclothymia. Kretschmer did not view these as dis- enduring personality traits, reflected in cognitive style
crete entities, however, rather as opposing expressions and perceptual experiences, arising from a combination
of the same trait; also assuming a continuum from nor- of polygenetic and environmental determinants, which
mal to psychotic. On this notion, Eysenck convincingly are normally distributed within the general population.
argued that one “cannot have a single dimension with ‘psy- An important distinction between the fully dimensional
chosis’ at both ends”22 (p.  767); instead, proposing the model proposed by Claridge6,26 and Eysenck’s earlier
existence of 3 personality dimensions: (“Psychoticism”, model is that the former proposes a boundary between
“Extraversion”, and “Neuroticism”). According to this health and illness along the schizotypy-schizophrenia
model, psychotic disorders are focal points of quanti- continuum, where signs of discontinuity of function are
tative dimensions (ie, extreme values in Psychoticism used to denote abnormality (ie, disorder). For Claridge,
combined with individual expressions of Extraversion/ schizotypal traits comprise dual properties insofar as
Neuroticism) and equivalent with clinical syndromes, they represent adaptive variation in personality but also
though Eysenck largely eschewed psychiatric concepts. comprise the potential for maladaptive functioning (ie,
Eysenck proposed that all clinical disorders were they are necessary but not sufficient for schizophrenia).
“observed constellations […] of traits”19 (p.  28); in this Thus, high expressions of schizotypy are necessary for
view, “Psychoticism” was an aspect of general person- psychotic disorders, but it is an independent dimension
ality capturing the underlying dimensional liability for (which Claridge suggestively called “health”6) that marks
all psychotic disorders: keeping with the concept of the risk of transition into illness. As such, Claridge’s fully
Einheitspsychose (unitary psychosis). It is noteworthy dimensional model of schizotypy6,26 takes normal varia-
that he cites Kraepelin himself as having potential doubts tion in personality as the starting point of the schizotypal
about the dichotomy of schizophrenia and bipolar dis- spectrum, and this is also reflected in the scale compo-
order: “it is becoming increasingly clear that we cannot sition of the associated Oxford-Liverpool Inventory of
distinguish satisfactorily between these two illnesses and Feelings and Experiences (O-LIFE27). Claridge’s model
this raises the suspicion that our formulation of the prob- of schizotypy draws parallels between psychiatric illness
lem may be incorrect.”23 (cited in22; p. 758). Regarding the and somatic disorders, using the example of hypertension
Eysenckian view of Psychoticism, however, there is an as a template (ie, sustained high blood pressure brings
ongoing, heated debate (currently, tending to favor “the about irreversible signs of disease evidenced in multiple
old Eysenck over the new”): It is commonly known—and physiological systems, just as high schizotypal character-
often stressed by Lenzenweger15,24—that the current con- istics bring about signs of psychotic illness across multi-
ceptualization of the Eysenck P-scale25 bears little resem- ple physiological and psychological domains). Claridge26
blance to traits understood as “schizotypal.” Rather, argued that both systemic and mental diseases could be
modern Psychoticism captures cold heartedness, tough seen to arise from a breakdown in the otherwise normal
mindedness, low Agreeableness, impulsivity, and similar functioning of a biological system, rather than as an
traits more related to psychopathy than psychosis; thus, affliction imposed on the body. A second shared quality
reflecting the academic perception common to the times reflects the continuity between adaptive and maladap-
of schizophrenics being inherently prone to violence tive functioning of the system, given arbitrary cut-off
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points for determining abnormality. Thirdly, both sys- This notion is substantiated by the finding that genetic
temic and mental diseases may have multiple causes; in risk scores for schizophrenia are inversely related to
the case of hypertension, a number of environmental psychotic-like experiences and psychometric measures
factors (like smoking, diet, and stress) may contribute of positive schizotypy in healthy individuals34,35 and the

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to aberrant, sustained high blood pressure. Similarly, a converse finding36 (and unpublished data from Schultze-
variety of factors including genetic, psychosocial, and Lutter) that while negative but not positive schizotypy is
adverse life experiences may contribute to psychological highly predictive of clinical high risk for schizophrenia, it
illness vs health. In summary, Claridge26 (p. 11) argued: is the newly accrual of positive symptoms that ultimately
“the genetically influenced variations in brain organization leads individuals from clinical high-risk populations to
which underlie temperamental and personality differences seek professional help. In other words, “benign schizo-
[…] can be construed as dispositions to varying forms of typy” and clinical high risk may constitute opposite sides
mental disorder; and that the emergence of such disorder is, of the same coin, namely, high values in one but not an-
in essence, a transformation of these biological dispositions other schizotypy facet.
into signs of illness. […] It is only at the extremes that the Additionally, we find it helpful to point out that
disease ‘entities’ of psychiatry become clearly definable.” Claridge’s model also relies heavily on a different under-
Claridge’s fully dimensional model of schizotypy, thus, standing of the term “psychosis.” It is commonplace to
spans a multidimensional set of personality traits (which consider “psychosis” as inherently of clinical relevance,
can be loosely mapped to the symptoms of positive, neg- whereby Claridge is often criticized for his view, that
ative and cognitive/disorganized features of psychotic ill- there may exist a state of “healthy psychosis.” It is note-
ness) and is relevant to the spectrum of clinical conditions worthy, however, that both historically (eg, Aristotle and
associated with psychotic features (eg, schizophrenia, Plato37) and etymologically (q.v., OED.com) the concepts
schizoaffective disorders, affective psychotic disorders) of madness and psychosis are not necessarily linked to
in championing the view of Einheitspsychose.27 As such, illness. Claridge’s understanding of the term psychosis is,
the traits underlying the schizotypy construct are pro- therefore, surely uncommon within clinical sciences, but
posed to vary along continuous dimensions in the general also not untenable (figure 1).
population and are not necessarily linked to psychopa-
thology; transition to illness is influenced by a wide range
The Importance of Conceptual Clarity
of biological and psychological factors (not restricted to
genetic influences), and the range of psychopathology With increasing interest in neurodevelopmental models
encompasses functional psychoses and disorders of per- of psychotic disorders, it is important that researchers
sonality. Claridge’s fully dimensional model can, there- heed the distinctions between these models in order to
fore, be viewed upon as an extension of the Eysenckian clarify the meaning of terms like schizotypy or psychosis-
model, considering schizotypy or psychosis-proneness to proneness—even psychosis itself—when using them to
be continuously distributed in the population and a nec- denote risk for disorder, or otherwise. That is, it should
essary but not sufficient condition for the development be clearly articulated which framework the research is
of psychotic illness. As such, it incorporates aspects of being conducted within since the concepts of “schizo-
the quasi-dimensional model within the high-schizotypy typy” or “psychosis-proneness” are not identical among
spectrum, but suggests the issue of clinical relevance to these model. For example, in studies of the general pop-
be a factor of a second dimension (health), rather than ulation where subgroups are operationally defined by
inherent of schizotypy/Psychoticism (as were the views their range of scores on measures of “schizotypy,” it
of Meehl and Eysenck). Thus, within Claridge’s model may be uncritically accepted that a “schizotypy” group
there lies the potential for the existence of “happy schizo- is synonymous with what Meehl defined as schizotypal
types”28 or “benign schizotypy”29, ie, persons who score (or they may be referred to as “psychosis-prone” when
extremely high on measures of positive schizotypy, but there is very low likelihood that they may ever transition
are below the population-average in negative and cogni- to clinical psychosis; these are but some interpretations
tive/disorganized schizotypy30 and, therefore, experience that could arise). At first glance, it may not be obvious
their psychotic-like experiences as rewarding and enhanc- as to the importance of clarifying these finer points of
ing regarding their life satisfaction. Conversely, healthy distinction, but with multiple measures now available
offspring of schizophrenic patients have been shown to to psychometrically assess schizotypy, the different the-
have above-average values in negative and cognitive/dis- oretical backgrounds from which these scales arose are
organized schizotypy, but below-average positive schiz- highly relevant to their interpretation in modern studies.
otypal traits.31 It appears, therefore, that “benign/happy However, this by no means implies that scales derived to
schizotypy”28,29 only refers to a combination of high posi- measure “Meehl’s schizotypy” cannot be used to measure
tive and simultaneously low negative and cognitive/disor- “Claridge’s schizotypy”, or vice versa; it is for this precise
ganized traits, while the co-occurrence of high values in all reason that researchers should be aware of the theoret-
schizotypy facets is highly predictive of schizophrenia.32,33 ical distinctions behind their construction, and what it
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Fig. 1.  Schematic of Meehl’s, Eysenck’s, and Claridge’s continuum models of risk for psychosis spectrum disorders, mapped on 2
axes representing separate dimensions of illness-health and the psychosis-mood spectrum. Within Meehl’s schizotypy model (solid
line), the discrete taxon of schizotypy exists as 10% of the general population and is underpinned by an inherited, integrative neural
defect (schizotaxia). Within Eysenck’s model (dotted-and-dashed line), risk for schizophrenia is seen as a monotonic function of the
personality dimension of Psychoticism; extreme values in Psychoticism represent psychotic disorder, and individual variation in an
independent dimension of cyclothymia/schizothymia is said to explain differences within the group of psychotic disorders. Within
Claridge’s fully dimensional model (dashed line), schizotypy is seen as a set of behaviors and characteristics distributed normally in
the general population, with the potential for illness arbitrarily distinguished at the extreme end of the health-illness spectrum. Like
Eysenck, Claridge proposes that variance within the psychotic disorders (ie, within the psychosis spectrum) would be explained by other
dimensions of personality (not shown here).

may mean for certain members of the general population interpreted accordingly: The WSS were modeled in light
to score highly on them, their scope (in terms of subdo- of the Meehlian model and include items “transparently
mains assessed) and potential to yield certain results in, concerned with psychopathology”51 (p.  181), while the
eg, factor or latent class analyses. authors of the more recently developed O-LIFE gener-
For example, the content and style of psychometric ally attempted to avoid items of extremely high or low
measures of schizotypy have varied according to the difficulty.49 Thus, while these measures reflect differ-
investigators’ aims and theoretical standing. The earli- ent conceptualizations regarding the dimensionality of
est scales (Wisconsin Schizotypy Scales; WSS) focused schizotypy, the relative likelihood of endorsing partic-
on measurement of vulnerability for specific symptoms ular items on these instruments may affect the interpre-
of schizophrenia, including perceptual aberration,38 tation of scores in clinical or general populations and is
magical ideation,39 as well as physical and social anhe- likely to influence the results of taxometric analyses. The
donia.40 Other psychometric scales tap into hypomanic SPQ46 was originally developed as a self-report screen-
personality traits,41 predisposition to hallucination,42 ing tool for schizotypal personality disorder (which is
delusions,43 paranoia,44 and schizotypal cognitions.45 Yet undoubtedly not identical to schizotypy15). The factor
other scales have been formulated on the basis DSM structure of both WSS and SPQ was, therefore, origi-
conceptualizations of “schizotypal personality” (the nally not aimed at capturing truly disorganized aspects
Schizotypal Personality Questionnaire, SPQ)46 and/or of schizotypy: The WSS were developed at a time when
“borderline personality” disorders,47 or by assuming Meehl placed greater emphasis on anhedonia rather than
the existence of fundamental components like the aso- cognitive slippage as the core feature of schizotypy,4,11
cial element of “Psychoticism.”25 In contrast, recent de- and the SPQ scales “odd behavior” and “odd speech”
velopment of psychometric scales tapping the general are conceptually more related to eccentricity than cogni-
schizotypy construct has been based on the empirically tive disorganization. The O-LIFE,27 on the other hand,
observed factor structure of schizotypal traits.27,48–50 The was developed in accordance with Claridge’s model and
origin of these scales bears relevance to their utility for includes a disorganization scale (CogDis) and an impul-
particular research questions. While all pertinent meas- sive nonconformity scale.
ures are designed to capture “schizotypy,” each was de- It becomes apparent that not only do the different con-
veloped under the assumption of a different model and ceptualizations of schizotypy differ regarding their core
with different aims, such that their results should be assumptions of the nature of the link between personality
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and schizophrenia, but that the finer points regarding polygenic risk scores for schizophrenia are inversely
what should be understood as “core” schizotypy dimen- associated with positive dimensions of schizotypy in
sions may vary according to the theoretical model from healthy individuals.34,35
which a scale has been constructed. Additionally, com- The most prominent issue to be resolved concerns

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paring the commonly used schizotypy inventories (WSS, whether the multidimensional construct of schizotypy
SPQ, and O-LIFE) shows that—while all of these encom- should be regarded as expressions of normal variation in
pass a positive, negative, and disorganized dimension— functioning (ie, normally distributed among the general
they differ slightly regarding their specific content: The population) in a manner that precludes the distinction of
“disorganized” dimension of the SPQ,46,52,53 eg, is more a discrete taxon of individuals at highest risk for schizo-
closely related to “eccentricity” (scales: odd behavior phrenia (or other psychotic disorders) or whether these
and odd speech), while the respective scale “Cognitive concepts (continua and taxon) are actually compatible
Disorganisation” of the O-LIFE is more related to cog- such that both may be true of the construct of schizotypy.
nitive slippage or formal thought disorder. Pertaining to The latter notion suggests that, rather than a true taxon,
schizotypal traits, the adjective “cognitive,” on the other qualitative entities (eg, schizophrenia, but also “clinical
hand, is also found in the positive (aka cognitive/percep- high risk” or “benign schizotypy”) may be focal points
tual) facets of the SPQ and the WSS, but here the ad- or observed constellations of several traits (ie, taxon-like
jective “cognitive” more closely resembles delusional clusters). This would be in line with original interpreta-
thinking (rather than formal though disorder as in the tions of “types” and “syndromes” by Kretschmer and
O-LIFE). Eysenck19 and has also been suggested by other authors
Researchers should therefore be clear about whether (eg, Gale et  al,57 Grant,9,58 Mason59). Similarly, a com-
their measurement of schizotypy is to be understood as prehensive review of the dimensionality of schizophre-
an index liability for schizophrenia only, liability for all nia symptoms60 concludes that although (at first glance)
psychotic disorders, or liability for “psychosis in schiz- the majority of taxometric research calls into question
ophrenia”54 and/or psychosis in other non-neurological the dimensional distribution of schizophrenia symp-
disorders or even the otherwise healthy (eg, as a func- toms in the general population, serious methodological
tion of psychotomimetic substances55,56). Moreover, flaws often challenge the validity of these findings, and
researchers should be clear on whether they are testing that the dimensionality of schizotypy remains to be ade-
a model in which there are circumstances given which quately tested. When introducing variables commonly
proneness for psychosis in the general population may associated with schizophrenia additionally to schizotypy
become pathological (ie, consistent with Claridge) or data (eg, schizophrenia-related genetic polymorphisms,
whether all forms of schizotypy are regarded as abnor- cannabis use, obstetric complications, familial risk);
mal personality traits (ie, consistent with Meehl). This however, a clear taxonic pattern emerges.61 We, thus, sug-
potential distinction between the existence of “normal” gest that—while relevant facets of personality (gathered
and “abnormal” personality features has yet to be fully under the wide rubric of “schizotypy”) may be individ-
resolved. ually dimensional in nature—risk-for-schizophrenia is
not, but rather likely to be represented in the co-occur-
Summary and Conclusions rence of several highly “schizotypal” traits, forming a
taxon-like cluster.
Although there is widespread consensus that a per- It is not the major aim of this review, however, to argue
sonality framework exists that is related to psychotic for an inherently correct, single solution. Primarily, we
disorders and psychotic/psychotic-like experiences in aim to illustrate the importance of conceptual clarity
other illnesses or even the otherwise healthy, a number and to encourage researchers not only to keep in mind
of aspects of the liability models remain to be agreed the model that they are working within but also to—
upon. A  great amount of disagreement can be traced perhaps most importantly—place their research find-
back to subtle but crucial differences in conceptuali- ings within the scope of the contending models and
zation of health and disease, with implications for the discuss the implications regarding the models’ verisimil-
concept of “schizotypy” as liability for schizophrenia or itude. We believe that only with such increased clarity
rather as proneness to unusual experiences and beliefs and acknowledgment of these issues will there be sub-
that are commonly experienced in the general popula- stantial progress in determining the status of “schizo-
tion. Despite these major point of disagreement, there typy” on the path to clinical psychotic states and related
is arguably some consensus insofar as risk for schiz- psychopathology.
ophrenia is likely caused by a complex interaction of
genetic and environmental influences and is primarily
Acknowledgment
represented through cognitive disorganization and neg-
ative facets of schizotypy (rather than positive schizo- The authors have declared that there are no conflicts in
typy). This notion is consistent with recent findings that relation to the subject of this study.

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