Psychological Bulletin © 2009 American Psychological Association

2009, Vol. 135, No. 5, 679 –706 0033-2909/09/$12.00 DOI: 10.1037/a0016311

Psychosis as a Risk Factor for Violence to Others: A Meta-Analysis

Kevin S. Douglas Laura S. Guy

Simon Fraser University University of Massachusetts Medical School

Stephen D. Hart
Simon Fraser University

The potential association between psychosis and violence to others has long been debated. Past research
findings are mixed and appear to depend on numerous potential moderators. As such, the authors
conducted a quantitative review (meta-analysis) of research on the association between psychosis and
violence. A total of 885 effect sizes (odds ratios) were calculated or estimated from 204 studies on the
basis of 166 independent data sets. The central tendency (median) of the effect sizes indicated that
psychosis was significantly associated with a 49%– 68% increase in the odds of violence. However, there
was substantial dispersion among effect sizes. Moderation analyses indicated that the dispersion was
attributable in part to methodological factors, such as study design (e.g., community vs. institutional
samples), definition and measurement of psychosis (e.g., diagnostic vs. symptom-level measurement,
type of symptom), and comparison group (e.g., psychosis compared with externalizing vs. internalizing
vs. no mental disorder). The authors discuss these findings in light of potential causal models of the
association between psychosis and violence, the role of psychosis in violence risk assessment and
management, and recommendations for future research.

Keywords: psychosis, violence, risk assessment, mental illness, schizophrenia

People have long assumed that there is a link between major
mental illness (MMI) and violence. This belief is prevalent across
cultures and has been quite stable over at least the past five
millennia (Monahan, 1992a). Surveys of community residents
indicate that this idea is still widespread in contemporary Ameri-
can society (Link & Cullen, 1986; Link, Cullen, Frank, &
Wozniak, 1987; Pescosolido, Monahan, Link, Stueve, &
Kikuzawa, 1999; Riskind & Wahl, 1992; Socall & Holtgraves,
1992). Starting in the 1960s and continuing into the mid-1980s,
critics began to question this assumption. The basis for the criti-
cisms was twofold: First, there was a general lack of empirical
evidence supporting the association and, second, the results of
follow-up studies of psychiatric patients released into the commu-
nity were interpreted as evidence against an association (Bonta,
Law, & Hanson, 1998; Monahan, 1981/1995; Rabkin, 1979;
Steadman & Halfon, 1971; Steadman & Keveles, 1972; Teplin,
Kevin S. Douglas and Stephen D. Hart, Department of Psychology,
Simon Fraser University; Laura S. Guy, Department of Psychiatry, Uni-
versity of Massachusetts Medical School.
Kevin S. Douglas gratefully acknowledges the support of the Michael
Smith Foundation for Health Research, Career Scholar Program. During
the study, Kevin S. Douglas served as a Guest Professor of Applied
Criminology at Mid-Sweden University. Laura S. Guy gratefully acknowl-
edges the support of the Social Science and Humanities Research Council
of Canada, Doctoral Fellowship. We thank Ray Koopman for his statistical
consultation, and Sarah Spain for her assistance in conducting the study.
Correspondence concerning this article should be addressed to Kevin S.
Douglas, Department of Psychology, Simon Fraser University, 8888 Uni-
versity Drive, Burnaby, British Columbia, Canada, V5A 1S6. E-mail:
douglask@sfu.ca
1985). Some critics were cautious, concluding that the extant
research was an inadequate basis from which to draw any firm
conclusions (the “absence of proof” position; e.g., Monahan, 1981/
1995). Others held more extreme views, arguing that, despite its
weaknesses, the evidence was sufficient to disprove a link between
mental disorder and violence (the “proof of absence” position; e.g.,
Teplin, 1985).
Whether there is a link between MMI and violence, and, more
importantly, what the nuances of such a link may be, is important
for several reasons. First, persons with MMI are among the most
stigmatized groups in society (Corrigan & O’Shaughnessy, 2007;
Corrigan & Penn, 1999). Moreover, persons who carry a psychi-
atric diagnosis may internalize such stigma and experience dimin-
ished self-esteem and self-efficacy (Watson, Corrigan, Larson, &
Sells, 2007). A perception that persons with MMI are violent un-
doubtedly contributes to this well-documented stigma (Phelan &
Link, 1998). Understanding the relationship between these constructs
could inform efforts to dispel myths (if there is not an association) or,
conversely, could educate the public about the realities of MMI,
including the limits of its association with violence.
Second, various symptoms and syndromes of MMI, such as
delusions and hallucinations, are often used in violence risk as-
sessments to determine whether persons’ constitutionally protected
liberties should be violated in the name of public safety. Perhaps
the clearest example of this is involuntary civil commitment,
where (depending on jurisdiction) laws dictate that a person may
be detained against his or her will if, inter alia, a risk to others is
posed that is connected to a MMI.
Third, research has demonstrated that violence perpetration is
correlated with other adverse outcomes for persons with MMI,
such as victimization and suicide/self-harm (Hillbrand, 2001;

679
680 DOUGLAS, GUY, AND HART
Nicholls, Brink, Desmarais, Webster, & Martin, 2006). Although
causal statements cannot be made about this association, it high-
lights the need to understand the connection between MMI and
violence in that the perpetration of violence could inform under-
standing of risk for the experience of victimization and suicide/
self-harm. Similarly, violence to others ostensibly could disrupt
treatment efforts, as well as lead to psychiatric deterioration and
overall worse mental health and quality of life. In turn, these
outcomes could elevate the risk for self-harm, self-neglect, victim-
ization, and alienation from familial and other supports.
Fourth, violence to others poses a salient public health concern.
To the extent that MMI raises the risk for violence, persons in the
community will be victimized. Often, when persons with MMI are
violent, the victims of violence are family members (Estroff,
Swanson, Lachicotte, Swartz, & Bolduc, 1998), who therefore
may bear a disproportionate risk of victimization and personal
suffering.
Finally, there are enormous potential costs associated with a
potential link between MMI and violence. Financial costs associ-
ated both with MMI/mental health treatment and with violence are
estimated to be in the hundreds of billions, or trillions, of dollars
per year (Anderson, 1999; D. P. Rice, Kelman, & Miller, 1992). To
the extent that violence is associated with MMI, there may be
concomitant economic and personal costs due to increased violent
behavior (costs to members of the public, to the patient) and
society at large (costs of hospitalization, incarceration).
Numerous narrative reviews of the literature on mental disorder
and violence or crime have been written. Popular academic posi-
tion has shifted over the years. Prior to the 1990s, the conventional
view held that there is no association (e.g., Teplin, 1985) or at least
no demonstrable association (Monahan, 1981/1995; Rabkin, 1979)
between mental disorder and violence. Starting in the 1990s,
however, the conventional view evolved to one acknowledging
that the association between mental disorder and violence was
small but statistically robust and practically important (Monahan,
1992b; Mulvey, 1994). This position is aptly summarized by E.
Silver (2006):
The vast body of research conducted . . ., including studies of violence
committed by psychiatric inpatients before, during and after hospital-
ization, studies of rates of mental disorder among inmates incarcerated
for violent offenses, epidemiological and birth cohort studies measur-
ing the onset and prevalence of mental disorder and violence cross-
sectionally and over the life course, and several comprehensive liter-
ature reviews summarizing these studies, suggests that: Although
most people with major mental disorder do not engage in violence, the
likelihood of committing violence is greater for people with a major
mental disorder than for those without. (p. 685)
Similarly, in a review of a cluster of family, twin, adoption, and
epidemiological studies, Tehrani, Brennan, Hodgins, and Mednick
(1998) stated the following:
Violent offending by the mentally ill and the offspring of the mentally
ill tends to be recidivistic. These groups tend to commit a dispropor-
tionately high percentage of the total number of violent crimes com-
mitted by the total cohort. The absolute number of the violent crimes
committed by these individuals has some societal significance.
(p. S85)
Of the various forms of MMI, most reviewers identified psy-
chotic disorders as having the clearest association with violence
(Bjørkly, 2002a, 2002b; Bloom, 1989; Bradford, 1983; De Pauw &
Szulecka; Junginger, 1996; Krakowski, Volavka, & Brizer, 1986;
Monahan, 1992b; Tardiff, 1984; Wessely, 1993). For example, in
a Danish birth cohort of more than 358,000 people, Brennan,
Mednick, and Hodgins (2000) reported that the risk for violent
offending for men with schizophrenia was 4.6 times higher than
that of the general population, even after controlling for the po-
tentially confounding factor of low socioeconomic status (SES).
For women, the risk was 23.2 times higher. Similarly, a recent U.S.
study of 1,410 patients with schizophrenia drawn from 57 mental
health sites across 24 states (Swanson et al., 2006) found that
positive symptoms of schizophrenia were associated with both
minor and serious violence, even after controlling for numerous
possible confounds and covariates.
However, others have rejected the view that violence has any
substantial association with MMI more generally, or with psycho-
sis more specifically. A large, multisite follow-up of patients
discharged from psychiatric emergency units in three states found
that MMI was typically unrelated, and sometimes slightly nega-
tively related, to violence (Appelbaum, Robbins, & Monahan,
2000; Monahan et al., 2001; Steadman et al., 1998). Some very
specific symptoms, such as command hallucinations to perpetrate
violence, predicted violence (Monahan et al., 2001), as did comor-
bid MMI and substance use disorders (Steadman et al., 1998).
However, a fair summary of this study is that MMI, including
psychotic disorders, played a very small role in the violence of
patients.
Elbogen and Johnson (2009) analyzed a two-wave epidemio-
logical data set of 34,653 persons residing in the community in the
United States. The authors reported that MMI, measured at Time
1, did not predict violence, measured between Times 1 and 2.
However, comorbid MMI and substance use disorders did predict
later violence, more so than substance use disorders alone, sug-
gesting an interaction between MMI and substance use disorders.
Although the odds of future violence among those with schizo-
phrenia alone were about double the odds of future violence
among persons without schizophrenia, this association was not
statistically significant, despite the large sample size, perhaps
attributable to extreme skew in cell frequencies.
A lack of association has been reported in studies of mentally
disordered offenders. For example, on the basis of studies of a
large cohort of forensic psychiatric patients, Quinsey, Harris, Rice,
and Cormier (2006) concluded the following:
The presence of schizophrenia and psychotic symptoms exhibited
around the time of the index offense or admission to hospital were
negatively related to risk. Psychosis, psychotic symptoms, and exac-
erbation of those symptoms have little value as indicators of the risk
of violence in offender populations. (p. 113)
The same conclusion was reached in a meta-analysis of variables
associated with recidivism among mentally disordered offenders.
Bonta et al. (1998) found that the average association between
psychosis and violence was small and negative (r ⫽ ⫺.04) across
the 11 studies in their meta-analysis reporting on psychosis.
Why have findings and opinions been so discrepant? One likely
explanation is methodological diversity. Researchers have exam-
ined the association between MMI and violence in many different
samples, using many different research designs, defining and mea-
suring MMI and violence in many different ways. As such, one
 PSYCHOSIS AND VIOLENCE
cannot easily determine from a cursory reading of the literature
why some studies find support for an association and others do not.
One can find studies from all types of settings that report positive
associations, including samples of criminal offenders (Etherington,
1993), forensic patients (Erb, Hodgins, Freese, Müller-Isberner, &
Jöckel, 2001), civil patients (Aarsland, Cummings, Yenner, &
Miller, 1996), and the general population (Brennan et al., 2000).
Similarly, one can locate studies from these same settings that fail
to find a positive association between mental disorder and vio-
lence: criminal offenders (Arboleda-Florez et al., 1995), forensic
patients (Harris, Rice, & Quinsey, 1993), civil patients (Appel-
baum et al., 2000), and the general population (Elbogen & John-
son, 2009; Swartz & Lurigio, 2004). Given such discrepant find-
ings across different populations, it is simply understandable why
different conclusions are reached by different commentators.
Another explanation is confounding factors. Understanding the
link between MMI and violence is complicated by the fact that
mental illness is associated with a host of other variables, many of
which, in turn, increase the odds for violence (Elbogen & Johnson,
2009). Some researchers have raised the sensible possibility that
the association between MMI and violence, should it be observed,
could be attributable to confounding factors, such as young age,
low SES, comorbid substance use, or personality disorder (Walsh,
Buchanan, & Fahy, 2002). Controlling or adjusting for potential
confounding factors may result in a dramatic change in the inter-
pretation of findings. This is a legitimate possibility. Some studies
have reported that, once other putative risk factors are controlled or
adjusted for, the relationship between MMI and violence becomes
nonsignificant (Mojtabai, 2006). Yet, many studies— often of
good quality— have found the converse: MMI remains predictive
of violence in the presence of other risk factors that have been
entered into multivariate analyses (Swanson et al., 2006) or after
adjusting for population parameters, such as age (Brennan et al.,
2000; Eronen, Hakola, & Tiihonen, 1996b), marital status, and
SES (Brennan et al., 2000). Resolving this confounder issue will
require as much theory as data in that some possible covariates
could be consequences, rather than causes, of MMI. For instance,
some research shows that MMI causes low SES, rather than the
converse (e.g., the geographic drift hypothesis; Dembling,
Rovnyak, Mackey, & Blank, 2002; see also Hudson, 2005). Hence,
it is not clear whether such variables should be controlled for in
analyses of the association between mental illness and violence.
Despite these methodological and conceptual complications
within the literature, one theme that has emerged from past nar-
rative reviews and research is that the key to understanding the
relationship between MMI and violence may lie with a more
focused approach on its symptoms. In particular, commentators
have suggested that psychotic disorders (e.g., schizophrenia) and
symptoms (e.g., delusions) might form the basis for the bridge
between MMI and violence (Monahan, 1992b). We turn our at-
tention to this issue.
Possible Conceptual Links Between Psychosis
and Violence
Psychosis is a syndrome found in mental disorders such as
schizophrenia, delusional disorders, bipolar mood disorder, and
some forms of severe depression. The syndrome comprises symp-
toms reflecting profound disturbances in thought, perception, and
681
behavior. The thought disturbances include delusions (false be-
liefs, often bizarre, held with conviction even in the face of
disconfirmatory evidence) and impaired communication (disorga-
nized, illogical, or incoherent speech). Perceptual disturbances
include hallucinations (perception in the absence of an external
stimulus, such as hearing voices or seeing things that are not
there), derealization (a sense that the external world is not real),
and depersonalization (a sense that one is no longer a real, auton-
omous human being). The behavioral disturbances include disrup-
tions in activity level (extreme agitation or lethargy) and disorga-
nized or purposeless behavior (odd gestures, gait, and posturing;
social withdrawal and poor hygiene; and strange habits, such as
eating cigarette butts or playing with feces). People with psychosis
also frequently experience disturbances of mood (flat or blunted
emotions, silliness) and motivation (extreme apathy).
Clearly, psychosis is a heterogeneous syndrome. But it is em-
pirically robust: Certain symptoms co-occur much more frequently
than would be expected by chance and wax or wane together over
time. Moreover, events or circumstances that tend to exacerbate or
alleviate one symptom often influence several others at the same
time. In fact, factor analytic techniques suggest that the broad
syndrome of psychosis appears to subsume at least three distinct
domains of symptomatology: positive, disorganized, and negative
(Ratakonda, Gorman, Yale, & Amador, 1998; see also Baxter,
1997, who provided a conceptual discussion of the three-domain
model as it relates to violence). The positive domain includes
symptoms that are pathological by their presence, such as delu-
sions and hallucinations. The negative domain includes symptoms
that are pathological by their absence, such as flat or blunted
affect, poverty of speech, apathy, and social withdrawal. Finally,
the disorganization domain includes symptoms that reflect impair-
ment in basic cognitive functioning, such as in odd or purposeless
behavior, impaired communication, and inappropriate affect.
Why might psychosis be associated with violence? There are at
least three possible explanations. It is possible that psychosis is a
cause of violence. Psychotic symptoms may provide a clear, if
delusional, motivation for violence or interfere with the ability to
manage interpersonal conflict. An important point here is that
proof of causation requires demonstration that psychotic symp-
toms occur before (certain) acts of violence. Psychosis also may be
a consequence of violence. Perhaps the stress of perpetrating
violence triggers the onset of psychotic symptoms in people who
are so predisposed. Finally, psychosis may be a simple correlate of
violence. The association between the two may be statistical rather
than causal, the result of links with some third variable, such as
stressful life events, lack of social support, personality traits,
substance use, victimization, and so forth. If this explanation were
true, we would expect to find no clear temporal or statistical
association between psychosis and violence, at least after control-
ling for potential confounding factors. At the present time, there
exists no clear, unambiguous evidence to rule out any of these
potential mechanisms.
If psychosis is a cause of violence, there are three major roles it
may play. First, psychosis may play a role in focusing (organizing)
decision and behavior, giving individuals a clear motivation for
violence. Many people with psychosis report clear explanations for
their behavior and commit acts that are complex, organized, and
goal-oriented, even if appearing illogical to outside observers. This
has been described aptly as the “principle of rationality within
682 DOUGLAS, GUY, AND HART
irrationality” (Link & Stueve, 1994, p. 143). If psychotic symp-
toms play a focusing role in violence, they are almost certain to be
symptoms from the positive domain (i.e., delusions or hallucina-
tions).
Second, certain types of psychosis may play a role in destabi-
lizing (disorganizing) decisions and behavior, interfering with the
ability of individuals to manage interpersonal conflicts. Here,
disturbances of thought, behavior, and affect (illogical speech,
agitation, labile mood) may frustrate psychotic individuals or the
people with whom they interact, increasing the likelihood that
someone will become angry or make an impulsive decision to act
violently. Hiday (1995; see also Hiday, 1997) has posited a model
in which violence may occur through “tense situations” elicited by
active psychotic symptoms. Baxter (1997) has hypothesized that
this type of psychosis can lead to “disorganized/impulsive” vio-
lence and crime.
Third, psychosis may play a disinhibiting role in violence.
Whereas positive symptoms motivate or excite behavior and dis-
organization symptoms destabilize behavior, negative symptoms
interfere with goal-directed behavior. Because of their retarding
influence on behavior, negative symptoms probably play a rather
limited role in decisions to act violently. However, negative symp-
toms may increase violence risk in specific circumstances. For
example, if individuals have comorbid substance use or personality
disorders, symptoms or consequences of the comorbid disorder
may give rise to motivations for violence, and negative psychotic
symptoms may result in a lack of inhibitions to act violently by
(further) impairing one’s ability to experience empathy, remorse,
or anxiety. Moreover, negative symptoms that result in depression
or suicidality may increase violence risk, as morbid thoughts of
self-harm may change or expand in focus to include others. These
theoretical routes to violence underscore the need for an analysis at
the level of symptom or at least that of symptom domain.
Methodological Challenges in the Study of Psychosis
and Violence
The interest sparked by the psychosis–violence debate has led to
increased awareness of methodological weaknesses in the research
(see discussions by Junginger & McGuire, 2004; Krakowski et al.,
1986; Monahan, 1981/1995, 1988, 1992b; Monahan & Steadman,
1994; Mulvey, 1994; Mulvey, Blumstein, & Cohen, 1986;Walsh et
al., 2002; Wessely, 1993). At least four major areas of concern
have been identified: study design, conceptualization and measure-
ment of MMI, conceptualization and measurement of violence,
and the role of potential confounding factors.
Study design. In the past, many studies were based on rela-
tively small samples of convenience comprising cohorts of civil or
forensic psychiatric patients who had undergone assessment, were
treated for months or years, and then were followed up some time
after their release into the community. Problems with such a design
include the lack of an appropriate comparison group (e.g., Was the
rate of violence among patients higher or lower than that among
nonpatients?) and an inability to control for interventions (e.g., Did
treatment or community support alter the likelihood of violence?).
Further, studies on the connection between mental illness and
violence have been conducted in a variety of samples, including
civil psychiatric patients (Monahan et al., 2001), forensic psychi-
atric patients or “insanity acquittees” (Rosenfeld & Harmon,
2002), criminal offenders (Porporino & Motiuk, 1995), community
residents (Brennan et al., 2000; Elbogen & Johnson, 2009), or
some mixture of the foregoing (Ryan, Hart, Messick, Aaron, &
Burnette, 2004). Comparisons can be made among persons with
different disorders (Tardiff, Marzuk, Leon, & Portera, 1997) or to
individuals without a diagnosis of mental illness (Beaudoin, Hod-
gins, & Lavoie, 1993). Some studies have used a form of random
sampling, such as consecutive admissions (Klassen & O’Connor,
1988a), whereas others have not (Asnis, Kaplan, van Praag, &
Sanderson, 1994). Some have used matching designs (Hodgins,
1992). Both prospective (Monahan et al., 2001) and postdictive
designs (Modestin & Wuermle, 2005) commonly have been used,
and violence has sometimes counted only if it occurred in a
hospital or prison (Krakowski & Czobor, 2004b) and in other cases
has counted only if it occurred in the community (Swanson,
Borum, Swartz, & Hiday, 1999).
MMI. In past research, mental illness often was considered a
unitary, static construct and was inferred from an individual’s
(former) status as a psychiatric patient. The state of clinical prac-
tice with respect to diagnosis and record keeping often did not
permit comprehensive and reliable assessments of mental disorder.
This made it impossible to determine whether violence was dif-
ferentially associated with various forms of mental disorder (e.g.,
Which is more strongly related to violence: schizophrenia or
substance use disorder?) and whether the severity or course of the
disorder had an impact (e.g., Is remission of symptoms associated
with decreased likelihood of violence?). Monahan (1988; Mona-
han & Steadman, 1994) has described the problem of “impover-
ished” predictor variables in the field of violence risk assessment,
which is closely allied with the issue of the relationship between
psychosis and violence. The problem is rooted in gross categori-
zations of complex phenomena, such as MMI. Finer gradations of
conceptualization, to the symptom level if possible, are likely to
provide more meaningful data on the relationship between psy-
chosis and violence. Very broadband definitions, such as “any
mental disorder,” are apt to blur important distinctions between
specific psychotic syndromes and violence. Junginger (1996) made
a similar point in his narrative review, in which he described the
concept of “psychotic action,” which refers to violence that stems
from and is consistent with the contents and themes of symptoms,
such as delusions and hallucinations.
In addition to the level of conceptualization, studies differ in
terms of how they measure psychosis: Some use only chart-based
diagnoses (e.g., Quinsey et al., 2006), others use well-validated
research-based interview measures (e.g., Crocker et al., 2005), and
yet others simply rely on the diagnoses arrived at by clinicians in
the course of their everyday duties. All such differences can impact
the observed association between violence and mental illness, if
only because of the systematically higher reliability of research-
based, standardized interview procedures relative to unstructured
clinical diagnostic procedures (e.g., First, 2003).
Violence. There is no simple way to define or measure vio-
lence (e.g., Douglas & Ogloff, 2003; Monahan & Steadman, 1994;
Monahan et al., 2001; Mulvey, Shaw, & Lidz, 1994). In the past,
there was a tendency to conceptualize violence in dichotomous
terms—that is, present versus absent— on the basis of reviews of
official criminal or psychiatric records. This practice may be
described as providing an impoverished criterion variable (Mona-
han, 1988; Monahan & Steadman, 1994) and possesses the same
 PSYCHOSIS AND VIOLENCE 683

problems as do impoverished predictor variables. Recently, re- Method

searchers have paid more attention to the nature of the violence
committed. Numerous studies on the topic, however, still decline Studies Included in the Meta-Analysis
to define violence (e.g., Alexander, Crouch, Halstead, & Piachaud,
Search procedure. Relevant studies were located in four ways.
2006). Others include within their definitions ostensibly nonvio-
First, we conducted searches of the PsycINFO, MEDLINE, Crim-
lent behavior, such as damaging property (e.g., Cooper, Browne,
inal Justice Abstracts, Google Scholar, National Criminal Justice
McClean, & King, 1983; Grassi, Peron, Marangoni, Zanchi, &
Reference Service (NCJRS), Sociological Abstracts, Humanities
Vanni, 2001) or self-harming behavior (e.g., Barlow, Grenyer, &
and Social Sciences Index Database, and Dissertation Abstracts
Ilkiw-Lavallle, 2000; Barnard, Robbins, Newman, & Carrera,
computerized literature databases. The stems of the following
1984).
identifier and subject words were used in separate and combined
Research has varied greatly in interpretations of exactly what
searches: mental illness/disorder, psychopathology, psychosis,
behaviors constitute violence. Some have limited the definition to
schizophrenia, hallucination, delusion, affective disorders, mood
physical acts that cause demonstrable harm to victims (Monahan et
disorders, violent/aggressive behavior, aggression, homicide, as-
al., 2001); others have studied only homicide (Schanda et al.,
sault, crime, and criminal. Second, we searched the reference lists
2004); and yet others have included less serious forms of behavior,
of major narrative review articles. Third, we examined the tables
such as minor physical acts (i.e., pushing) or verbal behavior (i.e.,
of contents of 65 journals. The journals selected comprised all
threats to harm someone; Troisi, Kustermann, Di Genio, & Sir-
sources in which studies included in the present meta-analysis
acusano, 2003). Moreover, the method of detecting violence has
were published, as well as several additional journals known to
ranged from relatively simple procedures, such as sole reliance on
publish high-quality research. Finally, we searched the reference
official state or federal recidivism records (Kaliski & Zabow,
lists of articles identified in the first three steps. We limited our
1995), to more comprehensive procedures involving official
search to articles published in the scientific literature before or
records, self-report, and reports from collateral informants (Mona-
during August 2006. Unpublished research was limited to disser-
han et al., 2001).
tations.
Confounding factors. As reported above, some studies have
Inclusion and exclusion criteria. Studies were coded for the
reported on the relationship between MMI and violence after
meta-analysis if they met two inclusion criteria. First, they needed
controlling for possible competing risk factors. A related issue
to present data on the association between psychosis and violent
stems from the particular diagnostic mix in a given sample. For
behavior. Any disorder characterized by psychosis was included
instance, as Quinsey et al. (2006) have argued, it could be that,
(e.g., any schizophrenia-spectrum disorder, bipolar disorder, de-
when compared with the risk posed by persons with primary
pression with psychotic features) so long as the assessment was not
diagnoses of personality disorder or substance abuse/dependence,
based solely on a self-report measure of personality or psychopa-
MMI poses an inverse relative risk for violence. Evidence has
thology (e.g., Brief Symptom Inventory, Derogatis & Melisaratos,
accumulated to support both substance use (especially alcohol) and
1983; Minnesota Multiphasic Personality Inventory-2, Butcher,
certain personality disorders (Cluster B; psychopathic personality)
Dahlstrom, Graham, Tellegen, & Kaemmer, 1989; Personality
as robust risk factors for violence (for substance use/alcohol, see
Assessment Inventory, Morey, 1991), as self-reports do not di-
Mulvey et al., 2006; Steadman et al., 1998; Swanson et al., 2002;
rectly assess the presence of psychotic symptoms (e.g., the studies
for psychopathic personality, see Grann, Långström, Tengström, &
of Parker, Morton, Lingefelt, & Johnson, 2005, and Valliant,
Kullgren, 1999; Monahan et al., 2001; Skeem & Mulvey, 2001).
Gristey, Pottier, & Kosmyna, 1999, were deemed not to meet this
Some studies have indeed reported that once such diagnoses are
inclusion criterion because the only assessment of psychosis com-
controlled, or when major mental illness is compared with these
prised MMPI scores). Studies that did not state explicitly that the
other diagnoses, its relative association with violence is decreased
mentally ill participants in their sample had some form of psycho-
(Tengström, Hodgins, Grann, Långström, & Kullgren, 2004). Yet,
sis were deemed not to meet this inclusion criterion (e.g., Lagos,
as with other areas of this literature, one can locate studies that fail
Perlmutter, & Saexinger, 1977, p. 1134, was not coded because
to demonstrate a reduced association (Stueve & Link, 1997).
participants were described only as having a “mental illness”). For
some studies, despite there being a focus on psychosis, we could
Purpose of the Meta-Analysis not parse out psychotic from nonpsychotic participants.
In an effort to strike a balance between our competing interests
Given the divergent findings on the association between of wanting to compare “uncontaminated” groups of people with
psychosis and violence reported within the body of research (sum- and without psychosis and wanting to include as many studies as
marized above), a quantitative synthesis of the literature seems possible for the sake of generalizability, we created the following
necessary to move the field forward. We decided to conduct a rule: Studies were deemed to have met this inclusion criterion if no
meta-analysis of the association between MMI and violence, fo- more than 5% of the persons in the “psychosis group” had or might
cusing more specifically on psychosis. We had two goals for this have had disorders without psychosis and/or if no more than 5% of
meta-analysis: first, to characterize, in general terms, the magni- the persons in the “non–psychosis group” had or might have had
tude of the association between psychosis and violence observed in some form of psychosis. Several high-quality studies (e.g., McNiel
research to date and, second, to identify moderating factors—such & Binder, 1989, 1994) were not included in the meta-analysis on
as study design and issues related to the conceptualization and this basis (i.e., more than 5% of the study’s “psychosis group” did
measurement of psychosis and violence (as discussed above)—that not have psychosis and/or more than 5% of the study’s non–
might moderate this association. psychosis group” had psychosis). The number of studies that were
684 DOUGLAS, GUY, AND HART
included in the meta-analysis according to these criteria was
small.1 Further, in an effort to ensure that persons without psy-
chosis were not included within the “psychosis group,” we did not
code effect sizes on the basis of total scores from clinician- or
researcher-rated measures, such as the Brief Psychiatric Rating
Scale (BPRS; Overall, & Gorham, 1962) or the Positive and
Negative Syndrome Scale (PANSS; Kay, Fiszbein, & Opler,
1987). When psychosis was assessed with these types of measures,
only individual scales and items that assessed psychosis specifi-
cally (e.g., “hallucinatory behavior”) were coded (e.g., scales that
assessed “general psychopathology” were not coded).
Violence was defined as any actual, attempted, or threatened
harm to another person or persons (Webster, Douglas, Eaves, &
Hart, 1997). Thus, studies in which episodes of self-harm or
violence against objects formed part of the definition of violence
were not included in the meta-analysis. As such, many studies that
used the total score on structured measures of violence that record
several types of “violence” (such as the Overt Aggression Scale;
Yudofsky, Silver, Jackson, Endicott, & Williams, 1986) were not
included because harm to property or self is part of the definition
of violence or aggression in these measures. We also followed the
“5% rule” for violence such that only studies in which less than 5%
of the “nonviolent” group was violent and/or less than 5% of the
“violent” group was not violent were included. Very few studies
were included on the basis of this rule.2
The second inclusion criterion was that the data needed to be
presented in a manner that allowed us to calculate odds ratios or to
estimate them from other statistics, such as Pearson’s r or Cohen’s
d. As such, we did not include studies or effect sizes in which the
association between psychosis and violence was described as
being “not significant” or otherwise lacked sufficient information
to compute an effect size (i.e., that psychosis was significant but
only a p value was reported). Although a few studies were deemed
not to meet this inclusion criterion on this basis (e.g., Walsh et al.,
2004), this strategy more typically led to the exclusion of a subset
of effect sizes from a study rather than exclusion of the entire
study. In addition, some studies did not meet this inclusion crite-
rion because, although they reported the percentage of violent
persons who were psychotic or vice versa (i.e., the percentage of
nonviolent individuals who were not psychotic), there was no
comparison group (e.g., Fazel & Grann, 2004) and, hence, esti-
mating an effect size for the effect of psychosis on violence
literally was impossible. A detailed record pertaining to selection
of studies and effect sizes (as well as all transformational proce-
dures used; see below) is available from the authors.
Overlapping studies and data sets. When two or more dissem-
inations examined the same sample and no unique odds ratios for
psychosis and violence could be calculated, the more methodolog-
ically sound dissemination was included (e.g., peer-reviewed pub-
lications were selected rather than the dissertations on which they
were based; studies that provided more descriptive information
about relevant moderator variables were selected). Studies that
clearly presented data on the same sample were coded as being
from the same data set. Studies also were coded as representing the
same data set if, in the opinions of the authors, the majority of the
participants in the samples were judged to overlap. Such judgment
was exercised for two groups of studies.3 In one case, two dis-
seminations (Wallace, Mullen, & Burgess, 2004; Wallace et al.,
1998) were judged to overlap only minimally and were coded as
comprising separate data sets.4
Choice and Calculation of Effect Size
Odds ratios were chosen as the effect size because they are
appropriate for characterizing the association between two natu-
rally dichotomous variables (e.g., psychotic or not; violent or not)
and are easily calculated from data presented in the form of 2 ⫻ 2
contingency tables. Of special relevance to the present investiga-
tion, odds ratios are directly comparable across studies with dif-
ferent experimental designs (i.e., retrospective, cross-sectional,
and prospective), which typifies this literature. As Fleiss (1994)
noted,
The odds ratio is not prone to the artifactual appearance of interaction
across studies due to the influence on other measures of association or
effect of varying marginal frequencies or to constraints on one or the
other sample proportion. On the basis of this and all of its other
positive features, the odds ratio is recommended as the measure of
choice for measuring effect or association when the studies contrib-
uting to the research synthesis are summarized by fourfold tables.
(p. 259, emphasis added)
As the majority of studies presented frequency data reducible to
fourfold tables, we opted for the odds ratio as the effect size of
choice. The use of odds ratios in meta-analyses also has been
discussed and recommended by Haddock, Rindskopf, and Shadish
(1998). Odds ratios are relatively easy to interpret, with the ob-
served values indicating the increased relative risk of one variable
(in this case, violence) associated with the presence of the other
variable (in this case, psychosis). Odds ratios of 1 indicate no
association between the two variables; those greater than 1 indicate
a positive association (i.e., increased risk), and those less than one
1
Two studies were coded in which the “psychotic” group contained
(fewer than 5%) individuals without psychosis (Fido, Razik, Mizra, &
El-Islam, 1992; Fulwiler, Grossman, Forbes, & Ruthazer, 1997), and one
study was coded in which there were (fewer than 5%) persons with
psychosis in the “nonpsychotic” group (Oulis, Lykouras, Dascalopoulou, &
Psarros, 1996).
2
In one study (Nestor, Haycock, Doiron, Kelly, & Kelly, 1995), 2
participants in the nonviolent group had committed acts of violence; in one
study (Raja & Azzoni, 2005), self-harm was included in the definition of
violence; and in one study (Buckley et al., 2004), individuals who com-
mitted minor acts of violence against property might have been included in
the violent group.
3
Three disseminations by researchers at the Penetanguishene mental
health center (Harris et al., 1993; M. E. Rice & Harris, 1992, 1995), and
four disseminations by Krakowski and colleagues (Krakowski, & Czobor,
1997, 2004a, 2004b; Krakowski, Czobor, & Chou, 1999) were judged to
have samples in which the majority of participants overlapped between
studies.
4
Participants in these studies were selected via case linkage from a
crime database and a psychiatric registrar in the Australian state of Vic-
toria. Wallace et al. (1998; N ⫽ 1,044) linked persons convicted between
1993 and 1995 to the psychiatric register, whereas Wallace et al. (2004;
N ⫽ 2,861) studied individuals with criminal records who were diagnosed
with schizophrenia during a first admission to a psychiatric hospital in
1975, 1980, 1985, 1990, and 1995 and compared them with community
residents. Thus, some overlap in the two samples was possible.
 PSYCHOSIS AND VIOLENCE
indicate a negative association (i.e., decreased risk). Epidemiolo-
gists usually consider odds ratios of 2.0 –2.5 and higher to repre-
sent clinically or practically meaningful associations (Fleiss, Wil-
liams, & Dubro, 1986); odds ratios of 3.0 or greater are considered
to be large (Haddock et al., 1998).
Whenever possible, we calculated or estimated multiple odds
ratios from a single study so that we could determine whether
various aspects of study design were related systematically to the
strength of the association between psychosis and violence (see
below). The majority of studies either presented odds ratios or
provided the necessary information to calculate them directly.
When a study presented both adjusted and unadjusted odds ratios,
we coded both but used the unadjusted value in the main analyses.5
We opted for unadjusted effect sizes because the majority of
studies reported only such effects. We report the differences be-
tween adjusted and unadjusted effects in the Results section. When
a study only provided other types of effect size—such as r, d, or
␹2— odds ratios were estimated by converting the effect size
provided with formulas presented in Lipsey and Wilson (2001) and
Rosenthal (1991). We converted rate ratios to odds ratios using the
formula detailed in Zocchetti, Consonni, and Bertazzi (1997).
Unstandardized beta coefficients from logistic regression analyses
were converted to odds ratios with eb and were exponentiated if
necessary. The Appendix presents all transformational formulas
used.
Most odds ratios (k ⫽ 446; 50.4%) were calculated directly from
frequency counts provided in the studies of the number of people
who were violent or not violent, as a function of having or not
having psychosis. The remaining odds ratios were reported in the
study (k ⫽ 158; 17.9%) or estimated from formulas given in the
Appendix (k ⫽ 281; 31.7%). Seven of these latter studies reported
a mean rating or the mean number of violent acts committed by
people with and without psychosis. For those studies, a Cohen’s d
value was calculated and then converted to an odds ratio. Simi-
larly, when a study presented mean scores for violent and nonvi-
olent participants on scales or items of measures of psychosis, a
Cohen’s d value was calculated and then converted to an odds
ratio.
In total, then, 885 effect sizes were calculated or estimated from
204 studies of 166 independent data sets. (Studies included in the
meta-analysis are marked with an asterisk in the Reference sec-
tion.) Coding of the odds ratios and moderator variables (described
below) were based on consensus ratings of the first two authors.
Weighting
Because an effect size estimate obtained from a large sample is
assumed to be a more precise estimate of the population of effect
sizes in comparison with one based on a relatively small sample,
effect sizes typically are weighted such that those supplied by
larger samples make a relatively more substantial contribution.
Optimally, effect sizes should be weighted by their inverse vari-
ances (Lipsey & Wilson, 2001). Because of the number of effect
sizes that needed to be estimated, it was impossible to use the
inverse variance to weight each effect size. Therefore, we
weighted all 885 odds ratios using weights that were proportional
to the inverse of the sum of the variance of the true log odds ratios
in the universe of studies and the sampling variance of the log odds
ratio for each study.6 This procedure—a random effects model—is
685
an approximation to the standard weighting practices presented by
Hedges and Vevea’s (1998) Equation 13 or DerSimonian and
Laird’s (1986) Equation 3 but one that avoids using n_i where
possible and gives more weight to studies with larger samples but
down-weights them appropriately to the extent that there is evi-
dence of true between-studies variability (DerSimonian & Laird,
1986; Hedges & Vevea, 1998). We considered down-weighting
extreme sample sizes important in the current analyses because
several studies had population-sized Ns (i.e., 100,000 – 400,000),
and we were concerned about giving them undue influence in
analyses.7
Choice of Statistical Tests and Analyses
Our first goal was to characterize the association between psy-
chosis and violence in overall terms across all studies, so the
primary data analytic strategy was descriptive in nature. Because
odds ratios are not normally distributed, we used nonparametric
measures of central tendency and dispersion—the median (Mdn)
and interquartile range (IQR), respectively—to describe the distri-
5
Forty-seven studies presented only adjusted odds ratios, which there-
fore were used in the main analyses. An adjusted odds ratio takes into
account the influence of potential covariates (e.g., age) specified by the
researcher on the association between the two variables of interest that are
used to form the odds ratio (i.e., psychosis and violence).
6
By using the natural logarithm of the odds ratios, ln(ORs), weights
were applied that were proportional to 1/(U ⫹ Vi), where U ⫽ the variance
of the true ln(ORs) in the universe of studies (i.e., tau squared, which
represents the random effects variance component) and Vi ⫽ the sampling
variance of the ln(ORs) for study i. The lower bound, 16/ni, was substituted
for Vi, which is the smallest value that Vi can have. This lower bound
occurs when the four cells are the same, n/4: v_min ⫽ 1/(n/4) ⫹ 1/(n/4) ⫹
1/(n/4) ⫹ 1/(n/4) ⫽ 16/n. U was estimated as U ⫽ {[⌺(Li – L)2]/(k ⫺ 1)} ⫺
{[16 ⫻ ⌺(1/ni)]/k}, where ni ⫽ the sample size for study i; Li ⫽ the
ln(ORs) for study i; L ⫽ the unweighted average ln(ORs); and k ⫽ the
number of studies. The weight for study i was proportional to wi ⫽ 1/(u ⫹
16/ni) ⫽ ni /[(ni ⫻ (u ⫹ 16)].
7
Because the inverse variance weighting method often is preferred, we
also calculated inverse variance weights for as many effect sizes as pos-
sible so that we could compare weighting methods. We were able to
calculate inverse variance weights for 79.5% of effect sizes. We compared
the mean weighted logged odds ratios for this 79.5% with the mean
weighted logged odds ratios using the method we ultimately used for
analyses, described in the text and Footnote 6. The inverse variance
weighting method produced somewhat larger logged odds ratios (M ⫽
.628, 95% CI ⫽ .468 –.788) compared with the method we adopted (M ⫽
.378, 95% CI ⫽ .294 –.463). The back-transformed raw odds ratios were
1.87 and 1.46, respectively. We also compared the two methods using the
entire sample of 885 effect sizes (though weights for 181 effect sizes
necessarily were computed with our original approach, as the inverse
variance was not calculable). Using the inverse variance weighting method,
we obtained a mean log odds ratio of .637, with a 95% CI of .510 –.765.
Using the method we adopted, we obtained a mean log odds ratio of .441
with a 95% CI of .363–.520. In back-transforming, we obtained odds ratios
of 1.89 and 1.56, respectively. The findings that the inverse variance
weighting method produced larger logged odds ratios than did our pre-
ferred method are consistent with our concern that the inverse weighting
method might give undue influence to extreme sample sizes (e.g.,
100,000⫹), some of which were present amongst studies that also had
large odds ratios (i.e., epidemiological studies; studies of community
residents rather than persons in institutions).
686 DOUGLAS, GUY, AND HART
bution of odds ratios, although we report the mean and the
weighted mean as well. Possible values of odds ratios range from
0 to ⬁, with 1 representing chance levels of association (negative
relationships are indicated by values between 0 and 1, and positive
relationships are represented by values between 1 and ⬁). We
then performed parametric analyses to examine the distribution
of the natural logarithms of the odds ratios (log odds),
ESLOR ⫽ ln共OR兲. Log odds are distributed more normally than
their corresponding raw odds ratios. The theoretical range of log
odds is ⫺⬁ to ⬁, with 0 indicating chance association (negative
relationship ⬍0 and positive relationship ⬎0). Results were then
converted back into odds ratios via the inverse natural log function,
OR ⫽ eESLOR. To ensure that the overall findings were represen-
tative, we repeated the descriptive analyses after controlling for
multiple effect sizes per study and per data set. The latter controls
were accomplished by replacing the multiple effect sizes per study
or data set with a single value, namely, the median of effect sizes
within that study or data set.8,9 For studies in which odds ratios
were coded both for scales on a measure (e.g., BPRS positive
symptoms scale) and for the individual items that comprised the
scale, only the odds ratio for the scale was included among the
values considered in computing the median for the overall odds
ratio estimate (i.e., the “one per study or data set” odds ratio).
We also aggregated weighted effect sizes using a meta-analysis
macro for SPSS written by David B. Wilson (see Lipsey & Wilson,
2001; available online at http://mason.gmu.edu/⬃dwilsonb/
ma.html). The macro calculates upper and lower 95% confidence
intervals (CIs) and performs a homogeneity test with the Q statis-
tic. The Q statistic (Hedges & Olkin, 1985) is used to identify data
sets that produce significant heterogeneity and thus could be
construed as outliers. It is distributed as a chi-square with k ⫺ 1
degrees of freedom, where k is the number of data sets.
Moderators
Our goal in terms of moderators was to identify variables
relating to method, disorder, violence, and demographics that
might moderate the association between psychosis and violence, as
described in the introduction. We examined three categories of
methodological factors: study design, definition and measurement
of psychosis, and definition and measurement of violence.
Study design. Study design comprised eight variables related
to the basic design of the studies. Sample setting was coded
according to whether studies included civil psychiatric patients,
forensic psychiatric patients, correctional offenders, community
residents, or a combination of participants from two or more of the
four settings. The method used to select participants from within a
given setting was coded as sampling procedure. This variable had
four levels, including random sampling, matching, nonrandom
sampling, and unspecified sampling procedure. The distinction
between retrospective or cross-sectional, archival (or pseudo-)
prospective, and true prospective studies was coded as method.
Sample size was coded continuously. The gender of participants in
the sample was coded as men only, women only, or both men and
women. Country of data collection was coded dichotomously as
United States or any other country. The nature of the comparison
group was coded as no mental disorder or other mental disorder.
Finally, for those studies in which the comparison group was
another mental disorder, mental disorder comparison group was
coded for whether the disorder was an internalizing, externalizing,
organic/cognitive, or other disorder.
Definition and measurement of psychosis. We coded four vari-
ables related to the definition and measurement of psychosis. The
nature of the psychotic group was coded as type of psychosis. We
differentiated among studies that examined schizophrenia, affec-
tive psychoses, mixed or unspecified psychotic disorders, and
presence versus absence of psychotic symptoms. We parsed type of
psychotic symptoms into the following categories: positive, nega-
tive, disorganized, and other or unspecified. We also coded
whether positive symptoms comprised hallucinations and delu-
sions versus other positive symptoms, such as grandiosity and
suspiciousness. Symptoms that were of the threat/control-override
type also were coded. A threat/control-override psychotic symp-
tom is one that involves either a threatening component, such as
delusions of persecution in which a person believes that others
wish to harm him or her, or the delusional belief that outside forces
control one’s mind, such as thought insertion or withdrawal (Link
& Stueve, 1994). Purpose of assessment reflected whether diag-
noses were made for clinical, research, or other/unspecified pur-
poses. Although studies typically had not examined whether there
were active symptoms of psychosis at the time of violence perpe-
tration, we were able to code two variables that approximated this
temporal relation. Timing of assessment was coded according to
whether psychosis was assessed before, at the time of, or after the
occurrence of violence; in some studies, psychosis was assessed
before and after the violence, and in other studies the timing was
unspecified.
Definition and measurement of violence. The final four vari-
ables pertained to the manner in which studies defined and mea-
8
Of course, several analytic choices are available in meta-analysis. The
single odds ratio for each data set could have been computed in at least two
ways, both of which take into account the non-normal distribution of odds
ratios. In one approach, the median value of a data set’s raw odds ratios
could be taken and subsequently transformed into a log odds ratio. In the
other approach, each raw odds ratio in a data set first could be transformed
into a log odds ratio, and then the mean of those values could be computed.
Calculations using both approaches were completed in determining the
single independent effect size for each data set. Both approaches yielded
similar findings (r ⫽ .97, p ⬍ .01, across the 166 pairs of effect sizes). For
all analyses reported, we used the first of the two strategies described here.
9
As described in more detail below, one of the moderator variables
coded was whether people with psychosis were compared with individuals
without a mental illness or with individuals with another mental illness. For
studies in which odds ratios could be calculated for both comparison
groups, it typically was the case that more effect sizes could be calculated
for comparisons with other mental illness (e.g., separate effects could be
computed for psychosis versus depression, psychosis versus substance
abuse). To determine whether the computation of the overall association
between psychosis and violence might have been biased in either direction
by not considering this variable, we took an alternative approach to
computing a single effect size for each data set. Specifically, we also
computed the median of effect sizes within a study or data set by taking the
average of two values: (a) the median of effect sizes based on comparisons
between persons with psychosis and with persons without a mental illness
and (b) the median of effect sizes based on comparisons between persons
with psychosis and with another mental illness. Results obtained with
this alternative approach yielded different values for 9 of 166 data sets
(mean difference among the 9 pairs of odds ratios was 1.29).
 PSYCHOSIS AND VIOLENCE
sured violence. Setting of violence was coded according to whether
studies examined violence that occurred in an institution, in the
community, or both. Method of assessing violence had three levels:
official records (including direct observation), self-report (includ-
ing interviews), or multiple methods (i.e., both official records and
self-reports). Severity of violence contrasted studies that examined
severe violence (homicide, attempted homicide, sexual violence,
or assaults resulting in serious physical injury), less severe vio-
lence (assaults not resulting in serious physical injury and threats
of violence), and any or unspecified acts of violence. Finally, we
also coded violence comparison group, which detailed whether
participants who committed violence were compared with partic-
ipants who engaged in criminal/antisocial but nonviolent acts (e.g.,
theft or fraud) or in no detected criminal/aggressive behavior at all.
Using a nonparametric test of the differences between medians
(␹2), we determined whether the magnitude of observed (un-
weighted) odds ratios varied significantly as a function of the
methodological factors described above. We also aggregated
weighted effect sizes using the SPSS macro written by David B.
Wilson, a meta-analytic analogue to the one-way analysis of vari-
ance (ANOVA), to investigate each moderator variable.
Results
Association Between Psychosis and Violence
Central tendency. Table 1 summarizes the central tendency
(mean, median) and distribution (standard deviation, 95% confi-
dence interval, interquartile range, standard error) of unweighted
raw and log odds ratios across (a) all 885 effect sizes, (b) one effect
size per study, and (c) one effect size per data set. The raw and
logged odds ratios for the analyses evaluating one effect size per
study were statistically significant, indicating a very small proba-
bility that we would have observed these effect sizes if the popu-
lation effect sizes had been zero ( p ⬍ .0000001).
The mean raw odds ratios were highly negatively skewed in part
because of the natural distribution of odds ratios. That is, very high
odds ratios can influence the mean more so than can very low odds
ratios. As such, although we present them for descriptive purposes,
we consider the median raw odds and both the mean and median
log odds ratios to be more accurate depictions of central tendency.
Analyses of the (natural) log-transformed odds ratios indicated
that their distribution was quasi-normal, as the stem-and-leaf plot
in Table 2 indicates. Back-transformation of the mean and median
log odds ratio in Table 1 yielded values ranging from 1.49 to 1.68,
which is highly consistent with the reported median raw odds
ratios. The consistency of findings across these analyses indicates
Table 1
Association Between Psychosis and Violence: Distribution of Nonweighted Effect Sizes (Odds Ratios and Natural Log Odds)
Odds ratio
Effect size k M 95% CI SD
All effect sizes 885 3.50 2.53 to 4.46 14.59
One effect size per study 204 2.62 2.20 to 3.03 2.99
One effect size per data set 166 2.17 1.85 to 2.50 2.11
Note. k ⫽ number of effect sizes; Q1 ⫽ first quartile; Q3 ⫽ third quartile.
687
that psychosis was reliably and significantly associated with an
approximately 49% to 68% increase in the odds of violence
relative to the odds of violence in the absence of psychosis. This
may be interpreted as a small, though reliable effect, correspond-
ing to a standardized mean difference score (d) of .24 to .32 (see
Haddock et al., 1998, p. 349).
Dispersion. As Tables 1 and 2 also indicate, there was con-
siderable dispersion of odds ratios around the central tendency.
The IQR for all 885 odds ratios revealed that at least 25% of all of
the effect sizes were negative in magnitude (ⱕ0.73), indicating a
negative association between psychosis and violence. On the other
hand, about 25% of the odds ratios were large in magnitude
(ⱖ3.30), including about 14% that were very large (ⱖ5.00). A
similar pattern emerged when controlling for multiple effects per
study and per data set.
The distribution of log odds closely approximated a normal
curve. We evaluated the heterogeneity of the 166 independent
effect sizes (one effect size per sample) by calculating Q, follow-
ing Shadish and Haddock (1994, p. 266). Q (169.17) was not
significant. Although these findings suggest that the distribution of
effect sizes is homogeneous, the observed variability did, in fact,
exceed expectation but merely not to such a degree as to be
statistically significant at p ⬍ .05. More specifically, because the
expected value of a chi-square is equal to its degrees of freedom,
and the observed Q value of 169.17 is larger than its 166 associated
degrees of freedom, the observed variability exceeds what would
be expected by chance (see Lipsey & Wilson, p. 135). These
analyses indicate that, notwithstanding the nonsignificance of Q,
there was considerable variability with respect to the magnitude of
effect sizes. This supports the search for factors that potentially
moderate the psychosis–violence association. This is also consis-
tent with our observation that 25% of the effect sizes were nega-
tive, indicating an inverse association between psychosis and vi-
olence, and 25% were positive and large (ⱖ3), indicating a strong
association between psychosis and violence.
Potentially Moderating Variables Between Psychosis
and Violence
Publication bias. Meta-analysts have acknowledged that there
may exist a publication bias that favors positive findings. This
means that the effect sizes reported in the published scientific
literature may systematically overestimate the true magnitude of
the effect. This is often referred to as the “file drawer” problem, as
numerous studies with null results— especially studies based on
Natural log odds
Mdn Q1 to Q3 M (⫾SE) 95% CI SD Mdn Q1 to Q3
1.53 0.73 to 3.33 .42 (.04) .34 to .50 1.15 0.43 ⫺0.32 to 1.20
1.69 0.81 to 3.36 .51 (.07) .37 to .64 0.97 0.52 ⫺0.21 to 1.21
1.66 0.79 to 3.09 .40 (.07) .26 to .54 0.91 0.51 ⫺0.24 to 1.13
688 DOUGLAS, GUY, AND HART

Table 2
Association Between Psychosis and Violence: Stem-and-Leaf
Plot of Distribution of Effect Sizes (Natural Log Odds)

Frequency Stem Leaf

5 Extremes ⬍⫺2.8
9 ⫺2.0 4&
28 ⫺1.0 556789
54 ⫺1.0 000112223334
87 ⫺0.0 555556666777778888899
130 ⫺0.0 000000111111222222223333334444
151 0.0 0000001111111122222222223333334444444
150 0.0 5555555566666666677777777788888999999
126 1.0 0000111111112222222333333344444
80 1.0 5555666667788889999
38 2.0 001112234
12 2.0 57&
11 3.0 03& Figure 1. Trim-and-fill funnel plot. s.e. ⫽ standard error.
4 Extremes ⬎3.7

Note. N ⫽ 885 effect sizes; stem width ⫽ 1.00; each leaf ⫽ 4 cases;
& ⫽ fractional leaf.
represents the odds ratio. This is not meaningfully different than
the unadjusted ln(OR) of .43. On the basis of these results, we do
not believe that publication bias was operative in the current study.
small samples—may go unpublished and be relegated to the file
drawer. Moderating Effects: Study Design
Logically, bias in favor of positive findings is unlikely to plague
this area of research as much as it might affect other areas of For all moderator analyses, we tested the difference among
research because many, if not most, studies have investigated levels of moderators using weighted log odds and the Q statistic,
numerous possible predictors of violence. Hence, if psychosis was which provides an ANOVA analog. However, the odds ratios
not significant, but other predictors were, the paper, in theory, presented in Tables 3–17 are raw odds (as opposed to log odds), to
would not be more likely to be rejected for publication than studies facilitate interpretation. We note that nonparametric significance
finding a positive effect for psychosis. In addition, on the basis of tests (median tests) of the raw odds ratios produced the same
our narrative review at the outset of this article, we were much less findings, in terms of which moderators were significant.
interested in the overall effect size than we were in moderated Setting. As Table 3 indicates, most studies were of civil psy-
effect sizes, which promise to be much more meaningful. chiatric patients. The difference among the effect sizes across the
To help minimize any potential publication bias, we searched four settings was statistically significant, with the highest odds
and included unpublished research in the form of dissertations. We ratios obtained in community (i.e., general population) samples.
located only six dissertations that were not subsequently published Odds ratios were significantly greater than chance among civil
as journal articles. The mean log odds for effect sizes estimated psychiatric, correctional, and community samples, indicating that
from unpublished dissertations was 0.90, as compared with 1.68 persons with psychosis in those samples were more likely to be
for published articles. Although the odds ratio for dissertations was violent than persons without psychosis in those samples.
smaller, the difference was not statistically significant, ␹2(1,
166) ⫽ 0.69, p ⫽ .41.
We also investigated possible publication bias by conducting Table 3
trim-and-fill analyses (Duval & Tweedie, 2000). This procedure is Moderating Effect of Setting
a quantitative form of the more traditional funnel graph, a scatter- Median odds
plot of the association between sample size and effect size. The Setting k ratio IQR (Q1 to Q3)
“filled” trim-and-fill funnel graph is presented in Figure 1. The
figure includes a reference line for the overall mean log odds effect Civil psychiatricⴱⴱ 86 1.69b 0.88 to 2.80
Forensic psychiatric 38 0.91c 0.43 to 3.07
size as well as 95% confidence intervals. Visual inspection does Correctionalⴱ 21 1.27b,c 0.89 to 2.87
not reveal evidence of publication bias. Communityⴱⴱ 15 3.46a 2.21 to 5.50
We used the metatrim procedure in Stata 10 (StataCorp LP, Mixed 9 1.30b,c 0.58 to 2.30
2007) with the linear estimator (the most stable estimator). This
procedure indicated that there were 0 effect sizes to trim and that Note. k ⫽ number of effect sizes; IQR ⫽ interquartile range; Q1 ⫽ first
quartile (25th percentile); Q3 ⫽ third quartile (75th percentile). Overall
the adjusted effect size was identical to the raw effect size. Using QB(4) ⫽ 16.70, p ⫽ .0022. Median odds ratios that do not share subscripts
the run estimator, we obtained a “number to trim” result of 2, differ significantly from one another at p ⱕ .05. Moderators in the left-
meaning that there may be two missing studies with large, negative hand column marked with designated symbols have weighted mean log
effect sizes (see funnel plot, which shows the imputed effects odds ratios that differed significantly from chance, as indicated by a z-test.
Tau squared∧ for each level is as follows: u ⫽ .41 for civil psychiatric; u ⫽
surrounded by large squares). The adjusted effect size obtained 1.01 for forensic psychiatric; u ⫽ .46 for correctional; u ⫽ .67 for
with a random effects model and the run estimator was ln(OR) ⫽ community; and u ⫽ 1.12 for mixed.
0.427, z ⫽ 10.35, p ⬍ .001, 95% CI ⫽ 0.347– 0.508, where OR ⴱ
p ⬍ .05. ⴱⴱ p ⬍ .001.
 PSYCHOSIS AND VIOLENCE 689

Sampling procedure. Most studies used some form of random Table 5

sampling (see Table 4), although a fair number did not specify Moderating Effect of Study Design
their sampling procedure. Odds ratios differed significantly as a
function of sampling procedure, ranging from a low of 1.49 for Median odds
Design k ratio IQR (Q1 to Q3)
simple random sampling to a high of 5.50 for matching (mostly
epidemiological studies), a procedure designed to control for pos- ⴱⴱⴱ
Retrospective 123 1.88a 0.81 to 3.10
sible confounding factors. Odds ratios were significant at each Archival (pseudo-)prospective 18 1.55a 0.62 to 3.89
level of the moderator except for nonrandom sampling, although True prospectiveⴱⴱ 37 1.49a 0.83 to 2.96
this effect was based on only seven studies.
Note. k ⫽ number of effect sizes; IQR ⫽ interquartile range; Q1 ⫽ first
Design. Design was not a statistically significant moderating quartile (25th percentile); Q3 ⫽ third quartile (75th percentile). Overall
factor, and odds ratios were homogeneous across types of design QB(2) ⫽ 1.06, ns. Median odds ratios that do not share subscripts differ
(see Table 5). Odds ratios were significant only for retrospective significantly from one another at p ⱕ .05. Moderators in the left-hand
and true prospective designs, although the number of pseudopro- column marked with designated symbols have weighted mean log odds
ratios that differed significantly from chance, as indicated by a z-test.
spective studies (k ⫽ 18) was small and, hence, power was limited Tau-square∧ for each level is as follows: u ⫽ .71 for retrospective; u ⫽
within this level of the variable. 1.36 for archival (pseudo-)prospective; and u ⫽ .54 for true prospective.
ⴱⴱ
Sample size. We tested whether sample size influenced ob- p ⬍ .01. ⴱⴱⴱ p ⬍ .001.
served effect sizes by treating it as a continuous variable in a
meta-analytic analog to regression analysis (MetaReg macro in
with internalizing disorders (nonpsychotic mood disorders, anxiety
SPSS; Lipsey & Wilson, 2001). The model was not significant
disorders) than when compared with externalizing disorders (Clus-
(Q ⫽ 0.88, ns). The unstandardized beta for sample size was 0.00.
ter B personality disorders, substance-related disorders). In fact,
Thus, sample size appears not to have influenced effect size, a
the effect size for psychosis was not significantly different from
finding that is consistent with our trim-and-fill analyses reported
chance when the comparison group comprised externalizing dis-
above.
orders.
Gender. Gender did not moderate effect size. Studies that used
We also tested the relationship between psychosis and violence
only men, only women, or both men and women as participants did
when the comparison group was limited to personality disorder
not produce effect sizes that differed significantly from one an-
(k ⫽ 34). For approximately half of the 34 data sets for which we
other. Effect sizes were significantly different from chance at each
could parse out this subgroup, the nature of the personality disor-
level of this moderator (see Table 6).
der was not specified; for those in which it was specified, the group
Country of data collection. Effect sizes did not differ between
consisted of antisocial or borderline personality disorders or psy-
U.S. and non-U.S. samples and were significantly different from
chopathic personality disorder. The median odds ratio for this
chance at both levels of this moderator (see Table 7).
subset of analyses was 0.59, and the mean log odds was ⫺0.38
Comparison group. Effect size varied significantly as a func-
(SD ⫽ 1.00), which was a statistically significant inverse effect
tion of the nature of the comparison group (see Table 8). As might
(Z ⫽ ⫺2.06, p ⬍ .05). That is, psychosis was associated with
be expected, odds ratios were higher when individuals with psy-
significantly lower odds for violence than were these personality
chosis were compared with persons without mental disorder
disorders.
(Mdn ⫽ 3.68) than when compared with individuals with other
In addition, we tested the impact of substance-related disorders
mental disorders (Mdn ⫽ 1.51). However, odds ratios were sig-
on the psychosis–violence association. The cleanest comparisons
nificantly greater than chance at both levels of the moderator.
we could make were from studies that divided their samples into
We further broke down the nature of the comparison group, as
participants with psychosis who either did or did not have a
shown in Table 9. Psychosis had a stronger effect when compared
comorbid substance-related disorder. We located 12 independent
data sets that permitted this comparison. The mean log odds for
Table 4
Moderating Effect of Sampling Procedure
Table 6
Median odds Moderating Effect of Gender
Sampling procedure k ratio IQR (Q1 to Q3)
Median odds
ⴱⴱ
Random 125 1.49b 0.65 to 2.64 Gender group k ratio IQR (Q1 to Q3)
Nonrandom 7 1.84b 1.40 to 3.10
Matched to populationⴱⴱ 17 5.50a 3.33 to 7.85 Menⴱⴱ 56 1.37a 0.76 to 3.22
Not specifiedⴱⴱ 20 1.69b 0.91 to 2.94 Womenⴱⴱ 21 1.73a 0.92 to 4.98
Men and womenⴱⴱⴱ 109 1.76a 0.79 to 2.83
Note. k ⫽ number of effect sizes; IQR ⫽ interquartile range; Q1 ⫽ first
quartile (25th percentile); Q3 ⫽ third quartile (75th percentile). Overall Note. k ⫽ number of effect sizes; IQR ⫽ interquartile range; Q1 ⫽ first
QB(3) ⫽ 64.99, p ⫽ .0001. Median odds ratios that do not share super- quartile (25th percentile); Q3 ⫽ third quartile (75th percentile). Overall
scripts differ significantly from one another at p ⱕ .05. Moderators in the QB(2) ⫽ 2.00, ns. Median odds ratios that do not share superscripts differ
left-hand column marked with the designated symbol have weighted mean significantly from one another at p ⱕ .05. Moderators in the left-hand
log odds ratios that differed significantly from chance, as indicated by a column marked with designated symbols have weighted mean log odds
z-test. Tau squared∧ for each level is as follows: u ⫽ .62 for random; u ⫽ ratios that differed significantly from chance, as indicated by a z-test.
.71 for nonrandom; u ⫽ .40 for matched to population; and u ⫽ .14 for not Tau-square∧ for each level is as follows: u ⫽ .87 for men; u ⫽ 1.43 for
specified. women; and u ⫽ .71 for men and women.
ⴱⴱ ⴱⴱ
p ⬍ .001. p ⬍ .01. ⴱⴱⴱ p ⬍ .001.
690 DOUGLAS, GUY, AND HART

Table 7 Table 9
Moderating Effect of Country of Data Collection Moderating Effect of Type of Mental Disorder Comparison
Group
Median odds
Country k ratio IQR (Q1 to Q3) Comparison Median odds
ⴱⴱⴱ
group k ratio IQR (Q1 to Q3)
United States 82 1.72a 0.81 to 2.75
Not United Statesⴱⴱⴱ 83 1.56a 0.73 to 3.47 Internalizingⴱ
27 2.15a 0.76 to 4.17
Externalizing 47 0.85b 0.41 to 2.00
Note. k ⫽ number of effect sizes; IQR ⫽ interquartile range; Q1 ⫽ first Organic 16 1.41a,b 0.96 to 2.62
quartile (25th percentile); Q3 ⫽ third quartile (75th percentile). Overall Otherⴱⴱⴱ 123 1.69a 0.96 to 2.80
QB(1) ⫽ 0.35, ns. Median odds ratios that do not share subscripts differ
significantly from one another at p ⱕ .05. Moderators in the left-hand Note. k ⫽ number of effect sizes; IQR ⫽ interquartile range; Q1 ⫽ first
column marked with the designated symbol have weighted mean log odds quartile (25th percentile); Q3 ⫽ third quartile (75th percentile). Overall
ratios that differed significantly from chance, as indicated by a z-test. QB (3) ⫽ 14.90, p ⫽ .0019. Median odds ratios that do not share super-
Tau-square∧ for each level is as follows: u ⫽ .57 for United States, and u ⫽ scripts differ significantly from one another at p ⱕ .05. Moderators in the
.76 for not United States. left column marked with designated symbols have weighted mean log odds
ⴱⴱⴱ
p ⬍ .001. ratios that differed significantly from chance, as indicated by a z-test:
Tau-square∧ for each level is as follows: u ⫽ 1.29 for internalizing; u ⫽ .79
for externalizing; u ⫽ .46 for organic; and u ⫽ .47 for other.
noncomorbid psychosis was 1.54 (SD ⫽ 0.55), and that for co- ⴱ
p ⬍ .05. ⴱⴱⴱ p ⬍ .001.
morbid psychosis was 2.37 (SD ⫽ 1.16). The difference between
these effect sizes was large (Cohen’s d ⫽ 0.97). The raw odds
ratios associated with the log odds are 4.67 and 10.70, indicating violence association (see Table 10). That is, studies that coded at
that these 12 studies had odds ratios that were larger than the the level of the symptom had significantly higher effect sizes than
average odds across all studies. those that either failed to specify how they defined psychosis or
Finally, we tested the difference between adjusted and unad- combined different types of psychotic disorders into one category.
justed effect sizes reported in studies, with the rationale that The effect sizes for both the symptom and the schizophrenia level
adjusted effect sizes control for various other potential risk factors of analysis were significantly greater than chance.
for violence. We did so with some caution, as it is not clear which We looked in more detail at the potential impact of type of
variables, in fact, should be controlled statistically (Dembling et symptom on the strength of the association between psychosis and
al., 2002; Hudson, 2005), in that some covariates, such as SES, violence. As shown in Table 11, the overall moderating effect of
might actually themselves be consequences of mental illness rather type of symptom (positive, negative, disorganized, other/
than truly competing causes of violence. Further, different studies unspecified) showed a trend toward significance. Pairwise com-
controlled for different factors. Nonetheless, we located 59 pairs of parisons revealed that positive symptoms were associated with a
adjusted and unadjusted odds ratios. The mean (SD) unadjusted larger odds ratio (2.32) than were negative symptoms (1.32).
odds ratio was 5.11 (4.95), and the mean adjusted odds ratio was However, effect sizes at all levels of this moderator were signifi-
3.22 (3.06), which represented a significant difference, t(58) ⫽ cantly greater than chance.
3.98, p ⬍ .001. Median odds were 3.50 and 2.21, respectively. The We evaluated whether more specific categories of positive
standardized difference between means was moderate (d ⫽ 0.47). symptoms were associated with violence. Of the data sets, 37
permitted a test of whether hallucinations and/or delusions were
Moderating Effects: Definition and Measurement associated with violence, 25 permitted a test of other positive
of Psychosis symptoms (e.g., bizarre behavior, excitement, suspiciousness, non-

Type of psychosis. The manner in which psychosis was con-

ceptualized in studies significantly moderated the psychosis– Table 10
Moderating Effect of Type of Psychosis
Table 8 Median odds
Moderating Effect of Type of Comparison Group Type of psychosis k ratio IQR (Q1 to Q3)
ⴱⴱⴱ
Median odds Schizophrenia 68 1.71a,b 0.61 to 3.83
Comparison group k ratio IQR (Q1 to Q3) Affective psychoses 22 1.36a,b 0.66 to 3.27
Mixed/unspecified psychoses 62 1.25a 0.62 to 2.85
Other mental disorderⴱⴱⴱ 149 1.51a 0.73 to 2.59 Psychotic symptomsⴱⴱⴱ 77 2.07b 1.29 to 3.17
No mental disorderⴱⴱⴱ 29 3.68b 0.98 to 6.20
Note. k ⫽ number of effect sizes; IQR ⫽ interquartile range; Q1 ⫽ first
Note. k ⫽ number of effect sizes; IQR ⫽ interquartile range; Q1 ⫽ first quartile (25th percentile); Q3 ⫽ third quartile (75th percentile). Overall
quartile (25th percentile); Q3 ⫽ third quartile (75th percentile). Overall QB(3) ⫽ 9.28, p ⫽ .026. Median odds ratios that do not share subscripts
QB(1) ⫽ 13.24, p ⫽ .0003. Median odds ratios that do not share subscripts differ significantly from one another at p ⱕ .05. Moderators in the left-
differ significantly from one another at p ⱕ .05. Moderators in the left- hand column marked with the designated symbol have weighted mean log
hand column marked with the designated symbol have weighted mean log odds ratios that differed significantly from chance, as indicated by a z-test.
odds ratios that differed significantly from chance, as indicated by a z-test. Tau-square∧ for each level is as follows: u ⫽ 1.10 for schizophrenia; u ⫽
Tau-square∧ for each level is as follows: u ⫽ .55 for other mental disorder, .64 for affective psychoses; u ⫽ .98 for mixed/unspecified psychoses; and
and u ⫽ 1.13 for no mental disorder. u ⫽ .26 for psychotic symptoms.
ⴱⴱⴱ ⴱⴱⴱ
p ⬍ .001. p ⬍ .001.
 PSYCHOSIS AND VIOLENCE 691

Table 11 Timing of assessment. Overall, timing of assessment ap-

Moderating Effect of Type of Psychotic Symptom proached significance as a moderating factor (Table 13). The only
significant pairwise difference occurred between assessments of
Type of psychotic Median odds psychosis made before the measurement of violence and studies
symptom k ratio IQR (Q1 to Q3)
that did not specify the relative timing of assessment. It is notable
ⴱⴱⴱ that the largest effect size was that for studies in which the
Positive 62 2.32a 1.23 to 3.46
Negativeⴱ 22 1.32b 0.87 to 2.05 assessment of psychosis occurred at approximately the same time
Disorganizedⴱ 20 1.85a,b 1.20 to 3.06 as the violent incident. It likely did not differ from the other
Other/unspecifiedⴱⴱ 22 1.78a,b 1.23 to 3.42
categories because there were few studies (k ⫽ 10) that fell into
Note. k ⫽ number of effect sizes; IQR ⫽ interquartile range; Q1 ⫽ first this category. When all effect sizes were used, this odds ratio was
quartile (25th percentile); Q3 ⫽ third quartile (75th percentile). Overall significantly greater than those in the “before” or “after” catego-
QB(3) ⫽ 6.88, p ⫽ .076. Median odds ratios that do not share subscripts ries.
differ significantly from one another at p ⱕ .05. Moderators in the left
column marked with designated symbols have weighted mean log odds
ratios that differed significantly from chance, as indicated by a z-test. Moderating Effects: Definition and Measurement
Tau-square∧ for each level is as follows: u ⫽ .43 for positive psychotic of Violence
symptoms; u ⫽ .25 for negative psychotic symptoms; u ⫽ .46 for disor-
ganized psychotic symptoms; and u ⫽ .51 for other/unspecified psychotic Setting of violence. Setting was not a significant moderator.
symptoms. As Table 14 indicates, the strength of association between psy-
ⴱ
p ⬍ .05. ⴱⴱ p ⬍ .01. ⴱⴱⴱ p ⬍ .001.
chosis and violence did not differ as a function of whether violence
was measured within an institution (i.e., psychiatric hospital) or in
the community, and effect sizes were significantly greater than
delusional or nonhallucinatory paranoia) in relation to violence, 16
chance at both levels of this moderator.
allowed us to assess the relationship between some type of para-
Method of violence detection. The method of violence detec-
noid symptom and violence, and 18 enabled us to examine threat/
tion did not significantly moderate effect sizes (see Table 15), and
control-override symptoms in relation to violence.
there were no pairwise differences between levels. Effects were
The median odds ratio for hallucinations/delusions was 2.31,
significant when either official records or self-report was used to
with a mean log odds of .66 (SD ⫽ .91), which was significantly
measure violence, but not when a combination of these methods
different from chance (Z ⫽ 4.32, p ⬍ .0001). For other positive
was used.
symptoms, the median was 2.37, and the mean log odds was 0.87
Severity of violence. Severity of violence was not a significant
(SD ⫽ .61), Z ⫽ 6.75, p ⬍ .0001. These types of symptoms did not
moderator (Table 16). Psychosis was related to violence whether it
differ from one another. Paranoid symptoms showed a trend to-
was severe, moderate, or not specified.
ward significance: median odds ⫽ 1.11; mean log odds ⫽ 0.30
Violence comparison group. As shown in Table 17, the
(SD ⫽ 0.73), Z ⫽ 1.81, p ⫽ .07. Threat/control-override symptoms
psychosis–violence relationship was stronger when the compari-
were significantly different than chance: median odds ⫽ 1.92;
son of violent individuals was made to individuals without anti-
mean log odds ⫽ 0.68 (SD ⫽ 0.98), Z ⫽ 3.09, p ⫽ .002.
social behaviors, as opposed to nonviolent but still antisocial/
Method of assessment. As shown in Table 12, whether eval-
criminal incidents. When the comparison was to nonviolent,
uations of psychosis occurred in the context of clinical practice,
though antisocial conduct, the odds ratio was not different from
took place in the context of research, or were unspecified did not
chance.
moderate the association between psychosis and violence. In the
vast majority of studies, either the purpose of evaluations was
specified or it could be inferred. Odds ratios were significant for
Table 13
both of these types of evaluation.
Moderating Effect of Timing of Assessment

Median odds
Table 12 Timing of diagnosis k ratio IQR (Q1 to Q3)
Moderating Effect of Purpose of Assessment
Assessment made before
Diagnostic Median odds violence 51 1.30a 0.62 to 2.40
method k ratio IQR (Q1 to Q3) Assessment made at violenceⴱ 10 2.51a,b 0.78 to 4.43
Assessment made after
Clinicalⴱⴱ 79 1.51a 0.62 to 3.09 violenceⴱⴱⴱ 84 1.57a,b 0.76 to 2.30
Researchⴱⴱⴱ 87 1.88a 0.94 to 3.15 Unspecifiedⴱⴱⴱ 36 2.22b 1.01 to 3.91
Unspecified/other 6 1.27a 0.91 to 2.27
Note. k ⫽ number of effect sizes; IQR ⫽ interquartile range; Q1 ⫽ first
Note. k ⫽ number of effect sizes; IQR ⫽ interquartile range; Q1 ⫽ first quartile (25th percentile); Q3 ⫽ third quartile (75th percentile). Overall
quartile (25th percentile); Q3 ⫽ third quartile (75th percentile). Overall QB(3) ⫽ 6.89, p ⫽ .076. Median odds ratios that do not share subscripts
QB(2) ⫽ 1.87, ns. Median odds ratios that do not share subscripts differ differ significantly from one another at p ⱕ .05. Moderators in the left
significantly from one another at p ⱕ .05. Moderators in the left-hand column marked with designated symbols have weighted mean log odds
column marked with designated symbols have weighted mean log odds ratios that differed significantly from chance, as indicated by a z-test.
ratios that differed significantly from chance, as indicated by a z-test. Tau-square∧ for each level is as follows: u ⫽ .72 for assessment made
Tau-square∧ for each level is as follows: u ⫽ 1.08 for clinical; u ⫽ .43 for before violence; u ⫽ .64 for assessment made at violence; u ⫽ .59 for
research; and u ⫽ .36 for unspecified/other. assessment made after violence; and u ⫽ .77 for unspecified.
ⴱⴱ
p ⬍ .01. ⴱⴱⴱ p ⬍ .001. ⴱ
p ⬍ .05. ⴱⴱⴱ p ⬍ .001.
692 DOUGLAS, GUY, AND HART

Table 14 Table 16
Moderating Effect of Setting in Which Violence Occurred Moderating Effect of Severity of Violence

Setting in which violence Median odds Median odds

occurred k ratio IQR (Q1 to Q3) Severity of violence k ratio IQR (Q1 to Q3)
ⴱⴱⴱ ⴱⴱⴱ
Institutional 47 1.84a 1.00 to 3.09 Severe 52 1.79a 0.64 to 3.54
Communityⴱⴱⴱ 117 1.59a 0.73 to 3.08 Moderateⴱⴱⴱ 72 1.86a 0.88 to 2.97
Unspecified/otherⴱⴱⴱ 67 1.45a 0.73 to 2.83
Note. k ⫽ number of effect sizes; IQR ⫽ interquartile range; Q1 ⫽ first
quartile (25th percentile); Q3 ⫽ third quartile (75th percentile). Overall Note. k ⫽ number of effect sizes in analysis; IQR ⫽ interquartile range;
QB(1) ⫽ 0.36, ns. Median odds ratios that do not share subscripts differ Q1 ⫽ first quartile (25th percentile); Q3 ⫽ third quartile (75th percentile).
significantly from one another at p ⱕ .05. Moderators in the left-hand Overall QB(2) ⫽ 0.79, ns. Median odds ratios that do not share subscripts
column marked with the designated symbol have weighted mean log odds differ significantly from one another at p ⱕ .05. Moderators in the left-
ratios that differed significantly from chance, as indicated by a z-test. hand column marked with the designated symbol have weighted mean log
Tau-square∧ for each level is as follows: u ⫽ .57 for institutional, and u ⫽ odds ratios that differed significantly from chance, as indicated by a z-test.
.69 for community. Tau-square∧ for each level is as follows: u ⫽ .96 for severe; u ⫽ .54 for
ⴱⴱⴱ
p ⬍ .001. moderate; and u ⫽ .79 for unspecified/other.
ⴱⴱⴱ
p ⬍ .001.

To gain a better sense of how the strength of association be-

tween psychosis and violence varied as a function of the number of
significant moderators present, we plotted the mean log odds ratios
as a function of the number of moderators present in a given study.
The result is shown in Figure 2 and illustrates that with no
moderators present, log odds ratios were below chance levels.
With one moderator present, log odds ratios were small and lower
than the sample mean. With two to four moderators present, the
log odds ratios were larger than the sample mean. Translating from
the log odds shown in the data labels in Figure 2, we obtained raw
odds ratios corresponding to the number of moderators as follows:
no moderators, OR ⫽ 0.81; one moderator, OR ⫽ 1.09; two
moderators, OR ⫽ 1.83; three moderators, OR ⫽ 3.66; four mod-
erators, OR ⫽ 4.56. These data illustrate quite clearly why such
divergent conclusions have been drawn about the association be-
tween psychosis and violence.
Discussion
The findings of our meta-analysis provided strong support for
the view that psychosis and violence are associated with one
another, albeit with a small overall effect size that varies consid-
erably and in important ways across study features and aspects of
Table 15
Moderating Effect of Method of Detecting Violence
psychosis and violence themselves. Across 885 effect sizes from
204 studies of 166 independent data sets, psychosis was reliably
associated with a 49%– 68% increased likelihood of violence. We
observed substantial variability as a function of the moderators we
tested. In fact, perhaps of more importance than the overall effect
size estimates were the moderator analyses, which shed light on
the discrepant findings and professional opinions discussed in the
introduction. That is, depending on the number of moderators
present in a given study, odds ratios ranged from a meaningful
inverse association to a large positive association. Given this range
in effect sizes, the range in conclusions about psychosis and
violence makes complete sense.
The Status of Psychosis as a Risk Factor for Violence
Putting aside the issue of moderation for the moment, one might
ask: How does psychosis compare with other risk factors for
violence in terms of strength of association? It is difficult to
interpret the effect size for the psychosis–violence association in
relation to other risk factors because of a lack of appropriate
comparison data. Only some of the studies included in our meta-
analysis permitted us to examine systematically the effect size
associated with other diagnoses of mental disorder, demographic
characteristics, or criminal history variables. Furthermore, there
are no other meta-analyses of which we are aware that have

Median Table 17
odds IQR Moderating Effect of Violence Comparison Group
Method of detecting violence k ratio (Q1 to Q3)
Median odds
ⴱⴱⴱⴱ
Official records (including observation) 114 1.66a 0.79 to 3.09 Comparison group k ratio IQR (Q1 to Q3)
Self-reports (including interview)ⴱⴱⴱⴱ 38 2.02a 1.25 to 3.02
Mixed/not specified 18 0.80a 0.60 to 1.78 Nonviolent antisocial incident 42 1.07a 0.64 to 1.88
No incidentⴱⴱⴱ 119 1.92b 0.80 to 3.15
Note. k ⫽ number of effect sizes; IQR ⫽ interquartile range; Q1 ⫽ first
quartile (25th percentile); Q3 ⫽ third quartile (75th percentile). Overall Note. k ⫽ number of effect sizes; IQR ⫽ interquartile range; Q1 ⫽ first
QB(2) ⫽ 4.18, ns. Median odds ratios that do not share subscripts differ quartile (25th percentile); Q3 ⫽ third quartile (75th percentile). Overall
significantly from one another at p ⱕ .05. Moderators in the left-hand QB(1) ⫽ 8.13, p ⫽ .0043. Median odds ratios that do not share subscripts
column marked with the designated symbol have weighted mean log odds differ significantly from one another at p ⱕ .05. Moderators in the left-
ratios that differed significantly from chance, as indicated by a z-test. hand column marked with the designated symbol have weighted mean log
Tau-square∧ for each level is as follows: u ⫽ .66 for official records odds ratios that differed significantly from chance, as indicated by a z-test.
(including observation); u ⫽ .72 for self-reports (including interview); and Tau-square∧ for each level is as follows: u ⫽ .55 for nonviolent antisocial
u ⫽ .50 for mixed/not specified. incident, and u ⫽ .72 for no incident.
ⴱⴱⴱⴱ ⴱⴱⴱ
p ⬍ .0001. p ⬍ .001.
 PSYCHOSIS AND VIOLENCE
Figure 2. Effect of number of significant moderators on size of log odds ratio.
summarized the effect size of a violence risk factor across multiple
settings. Some meta-analyses have examined a range of risk fac-
tors in a specific setting (e.g., mentally disordered offenders, as per
Bonta et al., 1998) or a specific risk factor in a few settings (e.g.,
psychopathy in correctional and forensic psychiatric settings, as
per Guy, Edens, Anthony, & Douglas, 2005; Hemphill, Hare, &
Wong, 1998; Salekin, Rogers, & Sewell, 1996).
With this caveat in mind, it appears that the average effect size
for psychosis in the present meta-analysis (r ⫽ .12–.16, as derived
from transformation from OR to r) is comparable to numerous
individual risk factors studied in the Bonta et al. (1998) meta-
analysis (most of which were estimated from fewer than 10 stud-
ies). For example, Bonta et al. obtained mean effect sizes (Zr) for
the following predictors: history of violence (.16), marital status
(.13), weapon use (.12), nonviolent criminal history (.13), institu-
tional adjustment (.14), and hospital admissions (.17). Antisocial
personality (.18) and juvenile delinquency (.20) were only slightly
more strongly associated with violence in Bonta et al. than was
psychosis in the current study. Several risk factors had smaller
effect sizes in Bonta et al. than psychosis had in the present study:
substance use (.08), offense seriousness (.06), mood disorder (.01),
violent index offense (⫺.04), race (.09), intelligence (⫺.02), and
education (⫺.02).
The effect size for psychosis appears meaningfully smaller than
that for psychopathy according to several meta-analyses that re-
ported mean correlations typically in the .25⫺.30 range (Hemphill
et al., 1998; Salekin et al., 1996; Walters, 2003). Some meta-
analyses (Guy et al., 2005) have reported smaller effect sizes (rs ⫽
.11–.16) between psychopathy and violence in particular settings,
such as within prisons.
In general, then, psychosis appears to be intermediate in com-
parison with other putative risk factors. It is comparable to, or
693
larger than, numerous other risk factors, though tends to be smaller
than externalizing disorders, such as antisocial personality or psy-
chopathy, or early-onset criminal behavior. Our finding that psy-
chosis is associated with violence is consistent with that of previ-
ous narrative reviews (e.g., Bradford, 1983; De Pauw & Szulecka,
1988; Junginger, 1996; McNiel, 1994; Monahan, 1992b; Mulvey,
1994; Taylor, 1995; Taylor et al., 1994; Wessely, 1993). However,
some readers may be surprised by our finding in light of the
meta-analysis of factors associated with recidivism among men-
tally disordered offenders described above (Bonta et al., 1998).
Bonta et al. reported that the association between psychosis and
violence was heterogeneous across studies, with the overall asso-
ciation being small and negative in direction (Zr ⫽ ⫺.04). How-
ever, it is important to recognize that Bonta et al.’s review was
limited to a small number of effect sizes dealing with psychosis
and violence (k ⫽ 11) from a specific type of study (longitudinal
studies of mentally disordered offenders released from correctional
institutions).
The Importance of Moderators
Perhaps the most important finding to emerge from the present
meta-analysis is the extent to which the strength of association
between psychosis and violence differed as a function of moder-
ator variables. Indeed, if one generalized from a certain group of
studies, the conclusion would be that psychosis is inversely related
to violence. With another set of studies, the conclusion would be
that psychosis is a very strong correlate of violence. To some
extent, this systematic variation in strength of association, depicted
clearly in Figure 2, should provide guidance for researchers in
terms of framing hypotheses about the anticipated relationship
between psychosis and violence in any given study, depending on
694 DOUGLAS, GUY, AND HART
the characteristics of the study (i.e., nature of comparison groups,
level of measurement).
First, several potential moderators were not significant. As such,
a reasonable inference is that the psychosis–violence relationship
is relatively robust across levels of these moderators, including
gender, country, and severity of violence.
Design-related moderators. Of the study design or sampling
variables, both sample type and sampling procedure moderated the
psychosis–violence relationship. In particular, studies with com-
munity samples and studies using epidemiological designs pro-
duced larger effect sizes than did studies conducted in other
settings and those using other designs. However, psychosis was
still a significant predictor of violence within correctional and civil
psychiatric settings and in studies where random sampling was
used. Study design was not a significant moderator, with both
retrospective and prospective designs producing significant and
comparable effects.
Another one of the stronger moderators came from the study
design category of potential moderators: the nature of the compar-
ison group. That is, to whom are people with psychosis being
compared? If the comparison was to individuals with other—
nonpsychotic—mental illnesses, the odds of violence were slightly
higher for persons with psychosis (OR ⫽ 1.51). However, when
the comparison group consisted of individuals who had not been
identified as having mental disorders, the odds ratio was substan-
tially higher, and large (OR ⫽ 3.68). Splitting up “other mental
illness” further, we found that comparing psychosis with internal-
izing disorders produced a meaningful effect size (OR ⫽ 2.15),
whereas comparing it with externalizing disorders did not (OR ⫽
0.85).
Although we were not able to conduct exactly the same type of
analyses with substance use disorders as we could for externalizing
disorders more broadly, our findings indicated that comorbid psy-
chosis and substance-related diagnoses produced substantially
larger effect sizes than did psychosis alone (d ⫽ .97). This obser-
vation is consistent with leading studies (Elbogen & Johnson,
2009; Monahan et al., 2001) pointing to the crucial role of sub-
stance use problems in understanding risk for violence.
There are three important points to consider with respect to the
comparison group issue. First, these analyses shed some light on
the relative ranking of categories of mental illness vis-à-vis their
relationship to violence. Notably, externalizing disorders are likely
more strongly related to violence than are psychotic disorders. This
assertion is consistent with several meta-analyses showing mean
correlational effect sizes between psychopathy and violence in the
.25 to .30 range (i.e., Hemphill et al., 1998; Salekin et al., 1996;
Walters, 2003), although there are exceptions in which smaller
effect sizes have been reported (Guy et al., 2005).
Second, the findings suggest that, compared with persons with-
out mental illness (or, presumably, any externalizing disorders),
psychosis is, in fact, a strong risk factor for violence, increasing the
odds of violence three- to fourfold. This issue of comparison group
has important implications for the role that psychosis might play in
violence risk assessment. It is tempting to interpret these findings
such that psychosis should be considered a noncorrelate in samples
consisting of many highly externalizing people. This is true, how-
ever, only under two conditions: (a) that only group-level behavior
is of interest and (b) that there is no possibility that another
reference group would be of relevance for decisions.
Concerning the first point, we note that at an individual assess-
ment level, decisions must be made about a specific person, not
about groups of people. The presence of some comparison group
is of only peripheral relevance to a given individual’s risk. The
evidence from this meta-analysis suggests that psychosis be con-
sidered a possible risk factor at an individual level whenever it is
present. For instance, upon release from a correctional institution,
mutually exclusive groups of persons with psychosis may be at
lower risk than groups of persons with primary externalizing
diagnoses. However, when released to the general population
(largely comprising people without any externalizing disorders),
individuals with psychosis may be considered to be at higher risk
relative to the majority of people in the population. Viewed in this
way, individuals with either psychosis or externalizing disorders
would be at elevated risk compared with their nondisordered
community counterparts. Those with externalizing disorders
would just be at higher risk than those with psychotic disorders.
Second, if analysis is at the level of the sample or the popula-
tion, then the composition of the reference group clearly matters in
terms of hypothesis generation. Researchers should expect effect
sizes that range from negative (comparison with personality dis-
order) to small (comparison with nonpsychotic mental disorder
broadly) to large (comparison with internalizing disorders or no
disorder at all), depending on the nature of the comparison group.
This could be an important issue in the context of a particular
study. For instance, if a researcher were interested in predicting
violence within a prison therapeutic community setting in which
most participants had antisocial personality disorder, it would be
reasonable to predict that psychosis would have a minimal predic-
tive effect. If, however, a researcher were predicting violence
within a community residential setting consisting of numerous
individuals with internalizing disorders, then psychosis might be
expected to play a more important predictive role.
Psychosis-related moderators. Turning to the measurement of
psychosis as a potential moderator, we observe several noteworthy
findings. The psychosis–violence association was significant when
psychosis was measured as a diagnosis of schizophrenia or mea-
sured at the level of the symptom. It was not significant for
affective psychoses or when researchers either failed to specify
how they measured it or aggregated across all types of psychosis.
These findings argue against the practice in research of lumping
individuals with psychoses into a single, gross category, a point
that has been made cogently in the past (e.g., Monahan & Stead-
man, 1994). At the level of the symptom, positive symptoms were
significantly more strongly related to violence than were negative
symptoms, providing some support for causal models that empha-
size these types of symptoms (i.e., “psychotic action”; Junginger,
1996). However, we also note that symptoms of disorganization
(and other/unspecified) symptoms predicted violence. It is impos-
sible to comment on the other/unspecified category in that it is
possible that it included positive symptoms. The positive finding
for symptoms of disorganization would suggest that researchers
should investigate whether such symptoms might play a role in
violence, perhaps by disrupting executive functioning, by compro-
mising the ability to remain composed, or by leading to tense or
stressful interpersonal encounters (see Hiday, 1997, 2006). We
also note that most studies did not report the effects of different
types of symptoms while controlling for the others, which would
be an important step in future research.
 PSYCHOSIS AND VIOLENCE
Much has been made in the psychosis–violence literature about
the role of different types of positive symptoms: hallucinations,
delusions, paranoid symptoms, threat/control-override symptoms,
and so forth. Our findings revealed few differences among these in
terms of their relation to violence: Hallucinations and delusions,
threat/control-override symptoms, and other positive symptoms
were all associated with violence, and symptoms with some sort of
paranoid element approached significance. Whereas some past
studies (e.g., Link, Andrews, & Cullen, 1992; Link & Stueve,
1994) have reported that threat/control-override symptoms predict
violence more strongly than other symptoms, other studies have
failed to replicate this. For example, Appelbaum et al. (2000)
provided a detailed analysis of the association between threat/
control-override symptoms and violence and reported that the
association did not hold up when patients’ reports of putatively
delusional experiences were confirmed for true delusional status,
although subthreshold (non-delusional) perceptions similar in na-
ture to threat/control-override delusions were associated with past
violence. Few studies in this meta-analysis provided such a de-
tailed level of analysis. As such, our findings cannot address such
fine, though important, distinctions. However, we argue that it is
unlikely that a median odds ratio of 2.32 for positive symptoms is
generally artifactual across five dozen samples. The precise con-
tours and boundaries of the symptom–violence association will
need to be addressed in further primary studies, drawing on inves-
tigations such as Appelbaum et al. (2000) and models of
psychosis–violence such as those proposed by Hiday (1997); Jung-
inger (1996), or Taylor and colleagues (Taylor, 1998, 2006; Taylor
& Hodgins, 1994).
Finally, with respect to the timing of the psychosis determina-
tion vis-à-vis the occurrence of violence, the largest effect was for
the small number of studies (k ⫽ 10) where diagnosis and violence
occurred at approximately the same time. This potential moderator
is muddied by the fact that 36 studies failed to specify the timing
of diagnosis vis-à-vis violence. In theory, if psychosis is a causal
risk factor, then its presence must precede the outcome of violence.
However, when psychosis was assessed prior to the measurement
of violence, it produced a small and nonsignificant odds ratio of
1.30. Before concluding that this means that psychosis cannot,
therefore, be considered a causal risk factor for violence, we point
out two very important limits to this general timing variable.
First, in addition to information about whether the diagnosis of
psychosis occurred before or after violence, it is important to know
how close in time the two occurred, particularly if it is active
symptoms that are most crucial in the psychosis–violence associ-
ation. Although for most studies we were able to code whether
diagnosis preceded or followed the occurrence of violence, we
were not able to systematically determine how far apart diagnosis
and violence were. That is, an assessment of psychosis in, say,
1990, may have little relevance for a person’s behavior in 1997,
being separated by 7 years. This idea is consistent with calls in the
literature to focus on the dynamic, changing nature of risk factors
and on the consideration that certain risk factors that are prone to
change, such as psychotic symptoms, may only be of relevance to
violence when they are in some active or elevated state (see
Douglas & Skeem, 2005; Skeem & Mulvey, 2002). As such, the
increased odds ratio associated with assessments of psychosis and
violence that occurred close in time is meaningful. However, we
695
encourage researchers to always report the time between diagnosis
and violence.
Second, it is artificial to presume that studies capture, in any
systematic way, all of the violence that a person has perpetrated
and either the first break of psychosis or the complex waxing and
waning of psychotic symptoms across time. As such, most studies
represent some snapshot of the timing of psychosis and violence
vis-à-vis one another, a view that could change if the snapshot
were taken at a different point in a person’s life or included a larger
time frame. As such, one cannot presume that if psychosis were
diagnosed after violence had occurred (say, for instance, that
psychosis were diagnosed in an individual in a psychiatric hospital
and that it was clear from arrest records or the person’s self-report
that she or he had been violent in the past), psychosis did not exist
prior to the violence. Rather, the only conclusions that could be
made under such circumstances would be either that (a) psychosis
was not diagnosed or measured at that time or (b) studies failed to
report or measure age of first onset of psychosis. Similarly, if
psychosis were diagnosed today and a person was not detected as
having been violent in a 6-month follow-up period, it would not
mean that psychosis and violence had not co-occurred for that
individual at some point or that these variables would not co-occur
at some point in the future. In such a case, it could only be said that
violence was not observed to occur in the 6 months after psychosis
was measured.
Studies on mental illness and violence rarely document either
onset or course of illness (waxing and waning of symptoms) or
violence across a person’s life, or whether these are systematically
related to one another. Such a design is exactly what is needed,
however, to make firm conclusions about exactly how psychosis
and violence may or may not be related. On the basis of the
preceding issues, we argue that because (a) symptom-level mea-
surement produced the largest odds and (b) close timing between
assessment of psychosis and measurement of violence produced
the largest odds, there is some support for the view that risk for
violence is particularly elevated when the course of psychosis is
active.
It is also important to note that the correlation between psycho-
sis and violence could, in part, stem from other forms of possible
relationships between them. That is, a person may become psy-
chotic in the stressful context of being violent or in a transaction
that involves both violence and victimization. In such a scenario,
it would not be appropriate to describe psychosis as a cause of that
particular violent act. A complicating factor to such a scenario,
however, is that it is unlikely that psychosis would develop in
response to violence-related stress without there being an under-
lying psychotic disorder present, such as schizophrenia. In such a
case, then, a psychotic disorder precedes the violence, which in
turn leads to decompensation involving onset of florid symptoms.
Moreover, it is unlikely that acting violently would cause a disor-
der itself, such as schizophrenia, but more likely that it could
exacerbate some of the symptoms of the disorder. We were not
able to meta-analyze the literature at such a fine level, although we
again call for researchers to clearly indicate specific details about
the timing and onset not only of active symptoms but also of the
course of the disorder more generally, as well as how these
variables relate to the occurrence of violent behavior. It is certainly
possible that for some individuals, or for the same person at
different times, violence may cause psychotic decompensation. At
696 DOUGLAS, GUY, AND HART
other times or for other people, psychosis may cause violence. The
two possibilities are not mutually exclusive.
Violence-related moderators. In terms of violence-related
moderators, strongest support was found for the outcome compar-
ison group. That is, psychosis was not predictive of violence when
the outcome comparison was other antisocial (though nonviolent)
behavior, as opposed to no known antisocial behavior. Given the
relatively high correlation between violent and nonviolent antiso-
cial behavior, however, we expect that this effect would be ob-
served for other risk factors as well. Results also indicated that the
psychosis–violence relationship was not moderated by the severity
of violence, with severe and moderate violence producing compa-
rable odds ratios. This finding should indicate that, to the extent
that psychosis is a risk factor for violence, it is not limited to trivial
acts of violence.
The method for assessing violence (i.e., reliance on single vs.
multiple methods) was not a significant moderator. Studies that
relied on official records, observation, or self/other reports pro-
duced significant effects. Studies that incorporated multiple meth-
ods, or failed to specify the measurement approach for violence,
did not. There were relatively few (k ⫽ 18) of the latter type of
study. This finding was not expected, given that multiple methods
of measurement typically capture a greater amount of violence
(Steadman et al., 1998). However, it may be the case that the
official records and observation methods in the current studies
were confounded by other variables (such as retrospective design)
or were based on cases with known outcomes (i.e., all violent
offenders in a prison sample were “detected” to be violent accord-
ing to official records). As such, the value of multiple methods of
measurement is likely greater in prospective studies in which
participants are tracked in the community after release from an
institution, and there is a very real risk of failing to detect violence
by sole reliance on single measurement procedures, such as formal
recidivism records.
Implications for Future Research
Posing the question, “Are individuals with psychosis more
likely to be violent than individuals without psychosis?” is sort of
like asking whether 10-year olds are tall. Compared with toddlers,
they certainly are. Compared with adults, they are decidedly short.
And so it is with psychosis: Compared with individuals with no
mental disorders, people with psychosis seem to be at a substan-
tially elevated risk for violence. Compared with individuals with
externalizing psychopathology, psychosis does not appear to fur-
ther elevate the risk for violence. Whereas we did find a statisti-
cally significant, though small, overall relationship between psy-
chosis and violence, we argue that the general question should be
abandoned in favor of the more complex and sophisticated ques-
tion, “What particular symptoms of psychosis, under which situ-
ational circumstances, and in combination with which personal or
situational factors, are associated with increased or decreased risk
of various kinds of violence?”
With respect to psychosis, future research should focus on
specific diagnostic groups (formed according to standardized di-
agnostic criteria) and on specific clusters of psychotic symptoms
(assessed with standardized measures). It would be helpful if, in
the future, researchers provided more detail concerning their as-
sessments of psychosis, including analyses of the prevalence and
interrater reliability of, as well as the risk associated with, indi-
vidual symptoms of psychosis. In addition, future research should
control for the effects of comorbid mental disorders within both
psychotic and nonpsychotic samples statistically, by selection, or
by matching. Such control would enhance the precision of the
estimate of risk for violence associated with psychosis and also
may identify important cofactors, such as substance use or person-
ality disorder. Finally, future research should examine which psy-
chotic disorders or symptoms are active versus in remission at the
time of violence, and, if possible, track both the onset and course
of psychosis and violence. It may be that the association between
psychosis and violence is strongest when the symptoms are active
(Krakowski et al., 1986; Monahan, 1988, 1992b; Monahan &
Steadman, 1994), a view partially supported by the present anal-
ysis. The general point here is that better measurement of psycho-
sis should allow strong tests of competing causal models of its
association with violence.
Researchers also need to pay more attention to the measurement,
conceptualization, and context of violence. Although relying
solely on records or self-reports is sometimes necessary, it often
precludes measurement of other features of violence, such as
motivation, targets, or location. It is probable that some types of
violence (predatory, instrumental violence against strangers) are
not frequently committed by persons with psychosis but that other
types may be (reactive violence against family members or cohab-
itants following stressful or tense encounters). Indeed, research has
identified that family members are commonly at risk of acts of
violence by persons with psychosis (Estroff et al., 1998).
Longitudinal research would be well-suited to identifying the
possible transactions between elements of psychosis and violence
across time, an area that little research has been able to address. It
would be particularly interesting to track the first onset of psycho-
sis and violence. In addition, additional studies of the possible
mediating role of third variables are necessary. Psychosis might be
associated with violence because it is related to other risk factors
(Elbogen & Johnson, 2009), such as unemployment or housing
problems. From one perspective, this would reduce psychosis to a
nuisance variable if these other variables were considered caus-
ative of both psychosis and violence. However, if mental illness
itself plays a causal role in housing problems or unemployment
(Dembling et al., 2002; Hudson, 2005), then it is not clear, theo-
retically, that these variables should be controlled for. Rather, it
could be the case that violence is but one of a host of adverse
outcomes associated with mental illness, many of which are asso-
ciated with basic problems in living (employment, housing, rela-
tionships, education, health). We expect that many of these vari-
ables could influence onset of illness as well as transact with
course of illness and violence over time. A simple A3 B concep-
tualization of the issue is unlikely to capture it adequately.
Implications for Clinical Practice: Evaluating Risk
of Violence
The findings reported herein have a number of implications for
violence risk assessment. First, psychosis should be evaluated in
all violence risk assessments. At first, this seems inconsistent with
findings that psychosis was not associated with violence under
certain conditions (e.g., comparison with externalizing psychopa-
thology, within forensic psychiatric samples). However, we base
 PSYCHOSIS AND VIOLENCE
this argument on two premises: (a) There was an overall associa-
tion between psychosis and violence, and this was particularly
strong when the comparison group consisted of individuals with-
out mental disorder, and (b) as we outlined above, all of our
findings, and those of the original studies, are based on groups.
Further, some studies (Elbogen & Johnson, 2009) have reported
that close to half of persons with MMI have a co-occurring
substance-related disorder, and comorbidity elevates the risk of
violence substantially (see also Monahan et al., 2001). As such, it
is important to know whether a person with either an MMI or a
substance-related disorder has a co-occurring disorder.
Clinical assessment of risk for violence inherently is about
making individual decisions. In our view, the evidence from the
current meta-analysis is sufficient to conclude that psychosis may
elevate a person’s risk compared with the case in which psychosis
is absent in that individual. At the very least, the current meta-
analysis supports treating the violence relevance of psychosis in an
individual as a hypothesis to be disconfirmed through an assess-
ment of its relevance to a person’s history of violence and likeli-
hood for future violence. In essence, evaluators should be asking
themselves what potential role psychosis might play vis-à-vis
violence for the given individual whom they are evaluating.
Further, the issue of “compared with what or whom?” can be
factored into an individual risk assessment. That is, an evaluator
might conclude that risk is lower for his or her patient with
psychosis compared with persons with externalizing disorders but
that it is still higher than it would be if psychosis were absent. The
evaluator might also conclude, depending on the context in which
the patient might be residing in the future, that the patient likely is
at lower risk for violence than is his or her externalizing counter-
parts but that he or she is at higher risk than individuals without
any mental disorders. Note that this does not mean that clinicians
need to perform exhaustive evaluations of psychosis in every case;
rather, a brief screen for psychosis could be conducted, with a
more comprehensive assessment limited to cases in which the
results of the screen are positive.
The second implication is that the presence of psychosis should
be considered neither necessary nor sufficient for a determination
of high risk. This conclusion is based on the finding that the overall
magnitude of the psychosis–violence association was found to be
small; most violent individuals are not psychotic, and most psy-
chotic individuals are not violent. This means that clinicians con-
ducting a risk assessment should consider the role that psychosis
may have played in past violence (according to the individual’s
history) and could play in future violence (e.g., as an organizing or
a disorganizing factor). Only in cases in which the psychosis seems
logically linked to the occurrence of future violence should clini-
cians consider it an important risk factor. Of course, other cofac-
tors may also be present that increase (e.g., substance abuse,
psychopathy) or decrease (e.g., social support, stable housing) the
individual’s risk for violence. As such, psychosis should never be
the sole factor that is considered in determining a person’s risk– or
lack thereof—for violence.
Limitations
First, although we were able to evaluate some interesting and
important issues, such as the composition of the comparison group,
types of symptoms, and the impact of comorbidity, many questions
697
were out of reach. For example, it was not possible to test partic-
ular theories about why psychosis might elevate the odds for
violence. Such theories come in various forms and are crucial for
moving the field forward. Relatively focused theoretical models
were developed specifically to explain the relationship between
psychosis (or MMI) and violence. Hiday (1997, 2006), for exam-
ple, posited that the features of major mental illness (odd behavior,
difficulty handling stimulation) can lead to tense interpersonal
situations in which the probability of violence is increased. Jung-
inger (1996) developed a theoretical framework to explain when
psychosis might lead to violence. In particular, violence in the
form of “psychotic action” is more likely when the themes and
content of the delusions and hallucinations are aggressively laden
and, hence, consistent with acting violently.
Other theoretical explanations of the link between psychosis and
violence draw from classic psychological theories, such as psy-
chodynamic theory (Mizen, 2003). For instance, some scholars
have tested the role that defense mechanisms such as projection
might play in violence (Porcerelli, Cogan, Kamoo, & Leitman,
2003). Such theoretical approaches—narrow or broad— have great
potential merit in furthering understanding of any link between
psychosis and violence. For example, in principle, it should be
possible to measure whether a particular psychotic symptom, such
as paranoid delusions, was acting as a defense mechanism for an
individual. However, the existing empirical literature on psychosis
and violence did not permit testing such theoretical models in this
meta-analysis, because most studies do not actually measure
whether such psychotic symptoms are indeed manifestations of
these (or other) theoretical postulates. Similarly, very few of the
included studies measured the themes of symptoms and whether
such themes were consistent or inconsistent with violence. Had
they done so, we could have tested Junginger’s (1996) model of
psychotic action. There are simply too few empirical studies that
incorporate measurement of psychosis and violence that also in-
clude tests of these theories. Again, we encourage such steps in
future research.
Moreover, it was not possible to determine the appropriate role
of covariates, such as SES or employment (i.e., are such variables
causes or correlates of mental illness?), or to evaluate the impor-
tance of timing between psychosis and violence across the life
span. These specific and complicated aspects of the psychosis–
violence association are best suited for future in-depth, individual
studies.
Finally, any meta-analysis is limited by the nature and quality of
the research on which it is based. In our view, the research
literature on psychosis and violence is sufficiently large to permit
general conclusions about the overall association, as well as about
some of the specific aspects of the association. However, we also
note— echoing the comments of others (e.g., Krakowski et al.,
1986)—that researchers need to include more detail in their pub-
lished findings that would facilitate reviews, whether narrative or
quantitative. That is, for some moderators, there were a large
number of studies in which important methodological features
were not specified. Despite this, we were able to code enough
studies in sufficient detail to permit a meaningful evaluation of the
overall psychosis–violence relationship and the impact of putative
moderators.
698 DOUGLAS, GUY, AND HART
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706 DOUGLAS, GUY, AND HART

Appendix

Transformational Formulas

Estimating an Odds Ratio From Frequencies Provided in 3. r, which subsequently was converted to d, was estimated from
an Article (Hasselblad & Hedges, 1995) a chi-square value (␹ 2 ) with df ⫽ 1 and total sample size (N)
(Lipsey & Wilson, 2001, p. 201), as follows:
Status Psychosis No psychosis
|r| ⫽ 冑␹ 2/N
Violent a b 4. d was estimated from an independent t test (t) and total
Not violent c d
sample size (N) (Lipsey & Wilson, 2001, p. 198), as follows:
Note. OR ⫽ ad/bc. When a twofold table contained one or more empty
cells, 0.5 was added to each cell of the table to allow the calculation of an
d⫽ 冑2t/N 共assumes n1 ⫽ n2)
OR (Fleiss, 1994). 5. d was estimated from an independent t test (t) and the sample
size for each group (n) (Lipsey & Wilson, 2001, p. 198), as
Estimating an Odds Ratio From a Standardized Mean follows:
Difference (d) Effect Size (Hasselblad & Hedges, 1995;
d⫽ 冑t 共n1 ⫹ n2兲/共n1n2兲
see also Lipsey & Wilson, 2001, p. 198)
6. d was estimated with an F ratio (F) from a one-way analysis
␲d/冑 3
OR ⫽ e of variance and total sample size (N) as follows (Lipsey & Wilson,
2001, p. 199):
1. If d needed to be estimated, formulas presented in Table B10
by Lipsey and Wilson (2001, pp. 198 –200) were used depending
|d| ⫽ 冑z F/N 共assumes n 1 ⫽ n 2兲
on the information presented in the article. Most commonly, stan-
Estimating an Odds Ratio From a Rate Ratio (Zocchetti,
dardized mean difference effect sizes were estimated with each of
the two means (X), the standard deviation (s), and the sample size
Consonni, & Bertazzi, 1997)
(n) for each group (Lipsey & Wilson, 2001, p. 198), as follows: POR ⫽ PRR关共1 – PrE ⫹ 共PRR ⫻ PrE 兲 – Pr D 兲/共1 ⫺ PrE 兲
d ⫽ 共X1 ⫺ X2 兲/冑spooled ⫹ 共PRR ⫻ PrE 兲 – 共PRR ⫻ PrD 兲兴,
where PrD ⫽ prevalence of psychosis, PrE ⫽ prevalence of the
spooled ⫽ 冑共n1 ⫺ 1兲s21 ⫹ 共n2 ⫺ 1兲s22/关共n1 ⫹ n2兲 ⫺ 2兴 exposure, POR ⫽ prevalence odds ratio, and PRR ⫽ prevalence
2. d was estimated from r (Lipsey & Wilson, 2001, p. 199), as rate ratio.
follows:
Received February 25, 2008

d ⫽ 2r/ 冉冑 冊1 ⫺ r2
Revision received April 9, 2009
Accepted April 20, 2009 䡲