A Proposed Explanation for the Paradoxically Consistent

Incidence of Schizophrenia
Chris Howard
Brandeis University
Spring 2010

Among evolutionary psychologists and psychiatric geneticists, the reasonably stable
rate of incidence of schizophrenia over time is almost invariably considered to be a paradox.
How could the genetic precursors of a disorder that seems to significantly inhibit the ability
of affected individuals to successfully reproduce consistently survive processes of natural
selection?
In this paper, I propose a possible explanation of this paradox that draws from a
wide body of psychological and genetic research. Specifically, I propose that processes of
natural selection dont know what to do, so to speak, with some of the genes that are
typically cited as having at least some causal role in the development of the disorder in light
of the potential evolutionary advantages that seem to be plausibly associated, given certain
environmental conditions, with our having these genes.
In section 1, I discuss some recent psychological research that suggests that some of
the personality traits that are predictive of schizophrenia are also associated with artistic
creativity and, rather importantly, that artistically creative individuals who have these
schizotypal personality traits tend to experience increased reproductive success (Nettle &
Clegg 2006). In section 2, I discuss the plausibility of a particular genetic model for
schizophrenia according to which the genetic origins of schizophrenia are not attributable to
basic DNA sequence variation but rather, to heritable change in gene expression (DeLisi et
al., 2002; Costa et al., 2006; Crow, 2007a). Simply, I discuss the plausibility of an epigenetic
account of the genetic origins of schizophrenia. In section 3, I discuss the degree to which
certain environmental conditions seem to precipitate the emergence of schizophrenia in
individuals who are genetically predisposed to the illness and subsequently argue that those
conditions play an especially significant role in determining the way in which genes associated
with schizophrenia and artistic creativity are ultimately expressed. In section 4, I draw from
each of the aforementioned discussions in order to offer, what I take to be, a plausible
explanation of the paradoxically consistent incidence of schizophrenia throughout the global
population over time. In section 5, I anticipate and respond to some potential worries that
might be precipitated by my proposed explanation.
I. Schizotypy and Creativity: An Interesting Correlation
Schizophrenia-proneness tends to manifest in a group of personality traits
collectively known as schizotypy (Mason et al. 1995; Claridge 1997). These personality traits
consist of, and are measured in, the following four separable dimensions: unusual
experiences, cognitive disorganization, impulsive non-conformity, and introvertive
anhedonia. On questionnaires designed to measure the prominence of schizotypal traits,
schizophrenia patients tend to score higher than controls in all of the aforementioned four
dimensions (Kendell & Gourlay 1970; Kendell & Brockington 1980; Crow 1990).
Interestingly, data retrieved from these questionnaires has also shown that artistically
creative individuals tend to have similarly elevated levels of certain schizotypal traits
specifically, those measured in the dimensions of unusual experiences and impulsive non-
conformity (Schuldberg 1988; Schuldberg 2000, Nettle 2006). In other words, the data from
these questionnaires seems to show that there is a significant positive correlation between
certain schizotypal traits and artistic creativity. In light of this, some psychologists have
suggested that the association with artistic creativity is a candidate for the evolutionarily
beneficial effect of schizotypy and thus, that the paradoxically consistent incidence of
schizophrenia over time is explicable in terms of the potential adaptive advantages that
schizotypal traits associated with creativity afford to those who have them (OReilly et al.
2001, quote from Nettle and Clegg 2006).
But why should we assume that there is a positive correlation between artistic
creativity and reproductive success in the first place? It is certainly not obvious, at least
initially, that artistically creative individuals are particularly likely to experience reproductive
success. However, according to Geoffrey Miller, there might be good reasons to think that
they are. He hypothesizes that human artistic production has its origins in costly displays
of quality whose function, like that of the peacocks tail or bower birds bower, is to attract
mates. And, in light of this, that a direct prediction would seem to be that successful
engagement in artistic production should be correlated with achieved number and/or quality
of sexual partners (Miller 2000, 2001; quotes from Nettle & Clegg 2006).
Now, if it is true that (1) artistically creative individuals are more apt to experience
reproductive success and (2) that certain schizotypal personality traits are associated with
artistic creativity, then there might be reason to think that (3) the particular schizotypal
personality traits associated with artistic creativity might be positively related to increased
reproductive success. That is, there might be good reason to think that certain schizotypal
traits could afford significant evolutionary advantages to those who have them.
In a 2006 study entitled, Schizotypy, creativity, and mating success, Daniel Nettle
and Helen Clegg set out to test just this that is, they set out to test whether there is, in fact,
a significant positive correlation between particular schizotypal traits and increased
reproductive success. Their prediction was that increasing those components of schizotypy
that are associated with creativity (unusual experiences, impulsive non-conformity) should
lead to an increase in number of sexual partners (Nettle & Clegg 2006). And, interestingly,
they were right.
Nettle and Clegg found, via a multiple regression analysis, that there indeed was a
significant positive correlation between the prevalence of schizotypal traits in the dimension
of unusual experiences and number of partners and also, between the prevalence of
schizotypal traits in the dimension of impulsive non-conformity and number of partners. In
light of their results, Nettle and Clegg suggest not only that Millers hypothesis is right that
is, that creativity positively correlates with increased reproductive success but also, that the
schizotypal traits associated with both creativity and schizophrenia have plausibly been
preserved by processes of natural selection as a result of their obvious potential, in some
cases, to promote reproductive success. They write, these results are consistent with the
view that schizotypal traits are maintained in the human population at significant levels
because the negative effects in terms of psychosis and other psychopathology are offset by
enhanced mating success (Nettle & Clegg 2006).
What, then, differentiates the schizophrenic from the creative artist? In other words,
how is it that the same schizotypal traits can manifest in either adaptively advantageous ways, as
in the case of the artist, or adaptively disadvantageous ways, as in the case of the
schizophrenic? Nettle and Clegg suggest that the consequences of having schizotypic traits in
the dimension of unusual experiences and/or those in the dimension of impulsive non-
conformity are determined, in large part, by environmental conditions. That is, they suggest
that whether these schizotypic traits manifest as either schizophrenic illness or artistic
creativity is dependent, to a significant degree, on the environmental conditions to which an
individual with these schizotypic traits is exposed. They write,
It may be that the consequences of traits like unusual experiences and impulsive non-
conformity are condition-dependent. Individuals in good conditions can channel
them into creative output and adaptive behaviors, while those in poor overall
condition succumb to their disorganizing effects, and develop psychiatric disorders
(Nettle & Clegg 2006).
While it is reasonably uncontroversial that environmental conditions have at least
some causal role in the precipitation of schizophrenia in predisposed individuals, it is a bit
more controversial whether they have as significant a role as Nettle and Clegg seem to suggest,
especially given the widely held view that schizophrenia, in light of its obvious heritability, is
predominantly a genetic disorder. In order to motivate this view, then, it will be necessary to
provide further evidence for its plausibility specifically, evidence that is compatible with
contemporary accounts of the genetic origins of schizophrenia.
Thus, in the following section, I discuss a recently proposed account of the genetic
origins of schizophrenia that (1) potentially corroborates the view suggested by Nettle and
Clegg and (2) fills out an important part of my proposed explanation of the evolutionary
paradox at issue.
II. A Discussion of the Genetic Basis of Schizophrenia
It is widely held that schizophrenia has a genetic basis in light of the fact that the
illness tends to aggregate in families. Experimental results have consistently shown that
having a family member who is affected by the disorder significantly increases ones risk of
developing it. In fact, in a 1993 study conducted by Kendler et al., it was shown that the risk
for schizophrenia increases as the degree of genetic affinity with the affected family
member increases (R. Tandon et al., 2008). Additionally, a number of twin studies,
conducted with the aim of estimating the heritability of the disorder, showed that genetic
factors, coupled with certain environmental factors, contribute about 80% of the liability for
schizophrenia (Cannon et al., 1998; Cardno et al., 1999; Sullivan et al., 2003).
While psychiatric geneticists have not yet been able to identify the exact genes
associated with an increased risk for the development of the disorder, they have been able to
identify particular chromosomal regions in which the schziophrenia genes likely reside.
Specifically, the chromosomal regions 8p21-22 and 22q11-12 have been identified as
potentially harboring the genes associated with the development of the disorder (Badner and
Gershon, 2002; Lewis et al., 2003). However, these results, though significant, do not
provide us with any real insight into which genes, specifically, contribute to the risk for
developing schizophrenia as, the total number of genes in chromosomal regions linked to
schizophrenia approximates 4000 genes (about one quarter of all known genes)(R. Tandon et
al., 2008).
Failure to pinpoint exactly which genes are associated with the development of the
disorder, despite numerous genome-wide scans, has prompted some researchers to suggest
that our genetic conceptualization of schizophrenia is wrong (R. Tandon et al., 2008). One
of the more promising alternative conceptualizations has been offered by T.J. Crow, who
hypothesizes that the inability of genome-wide scans to yield any definitive conclusions as to
which genes are primarily responsible for the development of schizophrenia is attributable to
the possibility that the genetic origins of the illness cannot be explained in terms of DNA
sequence variation. Instead, he proposes that the genetic origins of schizophrenia might be
best explained by heritable changes in gene expression caused by epigenetic factors
factors [that] exert their effect on genomic functions principally through DNA methylation
and histone remodeling of chromatin structure (Crow, 2007a; quote from R. Tandon et al.,
2008).