14
Theories of cognition, emotion and the social
world: missing links in psychosis
Paul Bebbington, David Fowler, Philippa Garety, Daniel Freeman
and Elizabeth Kuipers
Introduction
Throughout the twentieth century, clinicians and researchers struggled to establish
a convincing account of psychosis and the processes and mechanisms underlying
its manifestations. This effort depended on refinements of classification and case
definition over the whole course of the century. However, despite the huge invest-
ment of intellectual energy and monetary resources, results have been slow in
coming and disappointingly piecemeal. It has become clear that psychosis is a
phenomenon of great complexity. Recent social and cognitive models of psychosis
are attempts to deal with some aspects of this complexity. We will argue for the
appositeness of such models, and place them within the broader research effort in
psychosis. Before doing this, we need to revisit some of the consequences of the
formulation of the concept of schizophrenia, the disorder that represents the core
of psychotic phenomena.
A failed category?
The idea that schizophrenia is a failed category emerges regularly in the psychiatric
and psychological literature, the most prominent current advocate being Bentall
(2003). This is essentially a criticism of approaching schizophrenia as a medical
entity. The medical strategy of investigation involves the identification of syn-
dromes, which, in turn, form the basis of theories. These include those relating to
aetiology, pathology, outcome and treatment (Wing, 1978). Syndromes are essen-
tially theoretical constructs: while they can be regarded as disease entities, they are
never really more than tentative. Nevertheless, there is a tendency in psychiatry to
Society and Psychosis, ed. Craig Morgan, Kwame McKenzie and Paul Fearon. Published by Cambridge
University Press. # Cambridge University Press 2008.
regard psychiatric syndromes as having more virtue than they actually possess.
They do, however, form a useful basis for research. If theories about syndromes are

cognitive accounts represent understanding at a different level from biological
explanations. The resulting biological hegemony held sway in psychiatry until the
last decades of the twentieth century, and is only now being replaced by a more
flexible and comprehensive approach to the problems besetting scientific research
in schizophrenia.
Jaspers himself never regarded schizophrenia as a no-go area for social and
psychological research. He was quite happy with the idea that psychosis could be
meaningfully connected to circumstances, although reluctant to see the process
220 P. Bebbington, D. Fowler, P. Garety et al.
as wholly understandable. He did acknowledge that it was difficult to identify the
point at which paranoia became delusional, and there is now considerable evi-
dence confirming his view.
Psychosis as a continuum with normal experience
Modern cognitive models of psychosis actually start by postulating continuities
between psychosis and normal experience. The emergence of psychotic phenom-
ena thus reflects an abnormal concatenation of largely normal mechanisms. What
is weakness in the medical category, in this theoretical formulation becomes
strength. In the past, the urge to make a categorical distinction between psychosis
and normality almost certainly led to a Procrustean tendency to discount unusual
beliefs and experiences in people we would be reluctant to see as undergoing a
psychosis. However, it became apparent by the late 1980s that paranoid ideation
and anomalous experiences, such as hearing voices, were not confined to clinical
groups. It is clear that the frequency of auditory hallucinosis greatly exceeds the
accepted prevalence of psychosis (e.g., Wiles et al., 2006). The distinguishing
feature of those in contact with services is the level of distress occasioned by their
unusual experiences (Hanssen et al., 2003; van Os et al., 1999).
The distribution of unusual beliefs in the populace is also extensive. Many
people are convinced of the truth of ideas that are not supported by available
and accessible evidence. These include beliefs in astrology, alien beings, telepathy
or ghosts. Political beliefs are held with strong conviction even though they may be

These findings have considerable relevance to the aetiology of psychosis. They
imply that in some people movement along a continuum (indeed probably more
than one continuum) results in the emergence of psychosis. Thus the role of
aetiology is to explain exactly why particular people make this journey at particular
times in their lives. In the genetic arena, this suggests a focus on quantitative
analyses (Linney et al., 2003), along with the identification of quantitative trait loci
(Plomin et al., 1994). In the psychological domain, it implies the concatenation of
different psychological attributes, some cognitive, some emotional (Hanssen et al.,
30
25
20
15
10
5
0
05
Total number of
paranoia ideas
10 15 20
Proportion of population (%)
y = 24.474e
–0.2569x
R
2
= 0.9286
Figure 14.1 Distribution of paranoia scores in a student population (taken with permission from Freeman
et al., 2005b)
222 P. Bebbington, D. Fowler, P. Garety et al.
2005; Krabbendam and van Os, 2005; Krabbendam et al., 2005). There are also
implications for treatment, in particular psychological treatments, such as cogni-

psychosis, a reductionist position placing genetic explanations at the beginning of
the aetiological process. Virtually all genetic research in schizophrenia has been
based on the assumption that genetic abnormalities lead to abnormalities in
protein function, with consequent distortions of enzymatic activity, and that
223 Cognition, emotion and the social world
these in turn lead to corresponding deficits in neuronal function. These deficits
then result in cognitive dysfunctions that form the substrate for the schizophrenic
experiences that permit the diagnosis of the disorder. This is obviously a very
useful working paradigm, but it must be treated with caution.
The high heritability of schizophrenia is easy to demonstrate from twin studies
(Craddock et al., 2005). However, recent research has served to emphasise that not
only is schizophrenia a complex disorder to the clinical observer, it is also complex
in genetic terms. Such disorders have relatively high population prevalence, are
non-Mendelian and are imprecisely distinguished from the normal range. The
search for genes linked to schizophrenia has been long, arduous and expensive
(Norton et al., 2006; Owen et al., 2005). Candidates have been unearthed, but their
association with schizophrenia remains tentative. The genes encoding dysbindin
(DTNBP1) and neuroregulin (NRG1) are the strongest contenders, with evidence
for other genes (disrupted in schizophrenia (DISC1), D-aminoacid oxidase activator
(DAOA), regulator of G-protein signalling 4 (RGS4) and V-AKT murine thymoma
viral oncogene homolog 1 (AKT1)) being at least suggestive (Norton et al., 2006).
Some have been associated with abnormalities of brain structure and enzyme
function, which, albeit plausible, would seem to have a tenuous connection to
the schizophrenic phenotype (Callicott et al., 2005; Harrison and Weinberger,
2005; Meyer-Lindenberg et al., 2005). Given the modern synthesis of evolutionary
theory, genetics and developmental biology, focusing solely on encoding for
enzymes is likely to prove simplistic, even though links with schizophrenia may
be found. After all, only two percent or so of the DNA in human cells produce
proteins that act as enzymes, while much more is involved in complex regulatory
systems that switch the functions of protein-encoding genes on and off, something

physical, rather than the other way around. Furthermore, our knowledge about
putative aetiological factors is based on induction. Thus, because some people with
schizophrenia have, for example, a family history of the same condition, an
inductive leap is made to the conclusion that all schizophrenia has a genetic
basis. The frailty of the logic underpinning this inference is apparent. As the same
caveat applies to social theories, aetiological modesty is imperative on all sides.
The final problem relates to the nature of schizophrenic symptoms themselves.
Most of the experiences that form the basis of the identified symptoms of schizo-
phrenia are about something: they carry within them representations of the social
world (paranoid ideation is an obvious example of this). This is the characteristic
of intentionality identified by Brentano (1874). Defining a medical condition in
terms of experiences that have intentionality means that explanations in purely
physical terms will always be incomplete.
This is the context in which models of psychosis involving social, emotional and
cognitive elements have been developed. They do not deny an important role for the
physical matrix of disorder, but they do add to the complexity and probably to the
potential of explanation. They form one part of the overall model. There are several
variants, and all are better described as social-cognitive-emotional models. They
focus on the sorts of explanation that can be developed for considering the person
with psychosis as an agent in a social and societal context. They also seek to explain
psychosis by trying to explain single symptoms or coherent groups of symptoms.
Analysing single symptoms
The study of single psychotic symptoms, or single types of symptom, is assisted by
a clear account of the symptoms themselves. Thus cognitive models encourage a
225 Cognition, emotion and the social world