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A functional analysis of schizophrenia.

Recently, there has been a renaissance in research on psychosocial risk factors for the development of schizophrenia and related psychotic disorders that has led to a number of "startling" findings (McGrath, 2007, p. 14). Moreover, in part because of these findings, McGrath noted that there is an urgent need to understand the role of the environment in the development of schizophrenia as well as a need to move beyond traditional genetic versus environmental divisions in the field. The purpose of this article is to review recent data on psychosocial risk factors in schizophrenia and related psychotic disorders and to explain, from a Skinnerian functional analytic perspective, how those factors, in conjunction with biological factors, may be associated with the development and maintenance of these difficulties, as well as to show how a functional analysis may aid in advancing the clinical treatment of these complex and disabling psychological disorders.

The Functional Analysis of Behavior

The functional analysis of human behavior examines behavior via its consequences (see, for example, Skinner, 1953). When the consequences are favorable, behaviors are likely to be repeated again in the future. When the consequences are unfavorable, however, behaviors become less likely to recur. Functional consequences operate on an individual as natural selection operates on a species. In both cases, adaptation to the environment is the key end result (Skinner, 1981).

The goals of a functional analysis are different from the goals of other analyses of behavior. Palmer and Donahoe (1992, p. 1345), for example, point out that genetic, biological, and cognitive analyses of behavior tend to be rooted in an essentialist paradigm, defined as "the tendency to view categorical phenomena in nature as reflections of universal, enduring qualities intrinsic to each class or unit." Within this paradigm, the goal of the scientist is to identify these essential properties. Thus, the essential properties of schizophrenia may include genetic factors (such as a defect in the COMT gene), neurological factors (such as the size of the one's hypothalamus), or cognitive factors (such as a defect in episodic memory or executive functioning).

The selectionist paradigm, by contrast, attempts to provide a functional account of behavior by examining how the environment selects for specific behaviors in specific situations. The goal of the scientist within this paradigm is to identify the environmental factors that select for such behaviors dud to show how that behavior is adaptive within that environment. Thus, a selectionist interested in schizophrenia might examine, for example, how natural selection might have led to the development of certain schizophrenia behaviors (e.g., the tendency to hear voices when none are present may be selected for and advantageous when the environment is hostile; Kelleher, Jenner, & Cannon, 2010) or a selectionist might examine how the current environment selects for certain behaviors (e.g., paranoid ideation, thought disorder, or negative symptoms may prevent further social defeat).

Although both essentialist and selectionist paradigms are necessary (we need to understand both the structure of schizophrenia as well as how schizophrenic behavior allows us to adapt to certain environments), the essentialist paradigm has dominated American psychiatry and clinical psychology in recent years. Most vulnerability-stress models of schizophrenia, for example, tend to be essentialist in that they tend to examine how stress (understood generically) changes different biological structures within the individual. While such models are critically important to our understanding of schizophrenia, vulnerability-stress models do not tend to explore the function of specific behaviors within different environments. This article, in contrast, will examine how environmental factors lead to social isolation and defeat in individuals who later develop schizophrenia, how isolation and defeat lead to the development of specific schizophrenia behaviors, and how the effects of specific schizophrenia behaviors on the environment lead to their continued use.

Psychosocial Risk Factors for Schizophrenia and Psychotic Disorders

Three broad risk factors--social adversity, migration, and neighborhood factors--have been associated with the development of schizophrenia and related psychotic disorders (Cantor-Graae, 2007).

Social Adversity

Several studies have found a significant relationship between childhood trauma and the development of schizophrenia. Bendall, Jackson, Hulbert, and McGorry (2008) reviewed 38 studies that examined the prevalence of childhood trauma in individuals with psychotic disorders and found that the prevalence of trauma ranged from 19% to 83%, with a mean rate across studies of 48.9%. Childhood sexual abuse was the most common trauma reported. Bebbington et al. (2004) examined a large national representative survey from the United Kingdom (the British Psychiatric Morbidity Survey; N = 8,580) and found that individuals with psychosis were significantly more likely than those with either another psychiatric disorder or no psychiatric disorder to have been victimized as a child. The biggest difference among psychiatric groups was for sexual abuse.

Other research suggests that parental separation and loss may be related to the development of psychotic disorders. Morgan et al. (2007) found that compared with a population-based control group (N = 391), individuals with a first episode of psychosis (N = 390) were over three times more likely to have experienced a long-term separation (over one year) from one or both parents before the age of 16. Individuals with a first episode of psychosis were also over three times more likely than controls to have a parent die before age 16.

Children who are unwanted may be at increased risk of developing schizophrenia. In a survey of 11,017 pregnant women during their first visit to a prenatal clinic, children who were unwanted were more than twice as likely to develop schizophrenia as adults than those who were desired, even after controlling for perinatal and birth complications, maternal depression, and both mothers' and fathers' socioeconomic status (SES; Myhrman, Rantakallio, Isohanni, Jones, & Parttanen, 1996).

In a population-based study of all children born in Sweden between 1963 and 1983, Wicks, Hjern, Gunnell, Lewis, and Dalman (2005) found that a broad range of social adversity factors--such as receiving social welfare benefits, low SES, living in a single-parent household, parental unemployment, and living in a rented apartment--were associated with the risk of developing schizophrenia, even after controlling for factors such as urbanicity, parental psychosis, and parental alcohol and drug abuse. Moreover, as the number of social adversity risk factors increased, the probability of developing schizophrenia increased as well.

Finally, Varese et al. (2012) conducted a meta-analysis of 41 studies (N = 81,253) and found that patients with psychosis were 2.72 times more likely to have been exposed to childhood trauma (sexual abuse, physical abuse, emotional/psychological abuse, neglect, parental death, and bullying) than controls. The relationship between childhood adversity and psychosis was significant when examining both population-based cross-sectional studies and prospective designs. Significant associations were also observed between each type of childhood trauma and psychosis, and no specific type of adversity was a stronger predictor of psychosis than any other.


Some immigrants and children of immigrants are at increased risk of developing psychotic disorders. In a recent meta-analysis, Bourque, van der Ven, and Malla (2011) found that the mean relative risk for developing schizophrenia among first-generation immigrants was 2.3 (across 61 samples), whereas the mean relative risk for developing schizophrenia among second-generation immigrants was 2.1 (across 28 samples). The greatest effect size was for Black or dark-skinned immigrants moving to developed countries where the dominant population was White or light skinned (relative risk = 4.0 for first-generation immigrants; relative risk = 5.4 for second-generation immigrants). The surprising finding that the risk of developing schizophrenia is at least as high if not higher among second-generation than first-generation immigrants would appear to rule out the hypothesis that the greater risk of developing schizophrenia among immigrants is due to either the selection migration of vulnerable individuals or to genetic factors exclusively.

Neighborhood Risk Factors

Growing up in an urban environment is the most common social factor associated with schizophrenia onset. Van Os, Hanssen, Bijl, and Vollebergh (2001) reported, in a random sample of 7,076 adults in the Netherlands, that as levels of urbanicity increased, the percentage of individuals who had a psychotic disorder and the mean number of psychotic symptoms per individual increased as well. Kirkbride et al. (2006), in a population-based study in the United Kingdom, found that the incidence of initial-onset schizophrenia was significantly greater in Southeast London than in less densely populated areas in the United Kingdom, even after controlling for ethnicity, gender, and age, and Pedersen and Mortensen (2001) found that the longer a child lived in an urban environment during childhood, the greater his or her risk of developing schizophrenia. Household crowding, social class, obstetric complications, and prenatal exposure to influenza could not explain these effects. Moving frequently during childhood across different municipalities was also associated with the development of the disorder.

Other neighborhood characteristics, in addition to urbanicity, have been associated with schizophrenia onset. Boydell et al. (2001) found that the rate of first-incidence schizophrenia in non-White ethnic minorities increased as the proportion of ethnic minorities in one's neighborhood decreased, even after controlling for neighborhood levels of economic deprivation. In a related study, Veling, Susser, and van Os (2008) found that the rate of first-incident psychotic disorder in The Hague, the Netherlands, was elevated most significantly for immigrants who lived in neighborhoods in which there were a relatively small proportion of individuals of their own ethnic group.

Zammit, Lewis, Rasbash, Dalman, Gustafsson, and Allebeck (2010), in a study of all individuals born in Sweden between 1972 and 1977, found that the association between urbanicity and psychosis could be explained by social fragmentation factors. They found that individuals who were most different from others in their local environment were most at risk of developing psychosis. Finally, Kirkbride et al. (2008) examined incidence rates of schizophrenia across 33 wards in Southeast London and reported that 26% of the variance in schizophrenia could be accounted for by neighborhood risk factors, suggesting that "social capital" or the extent to which a neighborhood is cohesive and one in which neighbors care for and trust one another may play a role in preventing the development of schizophrenia.

Social Isolation as an Integrative Framework for the Development of Schizophrenia

In examining the social environmental factors that have been associated with the onset of schizophrenia, the common denominator appears to be an early environment that is socially isolating and leaves an individual feeling socially defeated (Cantor-Graae & Selten, 2005). The individual may feel like an outsider, as if he or she does not belong. Dark-skinned individuals from developing countries who move to developed countries with a predominately White population; individuals who have been traumatized, who are unwanted, or who grow up without one or both parents; minorities who grow up in environments with few similar individuals; and those who grow up in fragmented communities are all individuals who may grow up feeling alone and isolated.

Other research also suggests that social isolation is critical in the development of schizophrenia. Lencz, Smith, Auther, Correll, and Cornblatt (2004), for example, found that the most common presenting symptoms for individuals at high risk of developing schizophrenia were social withdrawal and isolation, and Kwapil (1998) found that a lack of interest in social activities and social isolation predicted the development of a schizophrenia-spectrum disorder at a 10-year follow-up. A longitudinal study indicated that individuals who later develop schizophrenia show a preference for solitary play at age 3 (Jones, Rodgers, Murray, & Marmot, 1994), and a meta-analysis found poor social functioning during childhood to be a "relatively sensitive and potentially specific predictor of schizophrenia" (Tarbox & Pogue-Geile, 2008, p. 576). Social isolation, therefore, appears central to the onset of schizophrenia.

It should be pointed out, however, that many studies merely show a correlation between broad, unspecified social factors, such as SES, and schizophrenia symptoms. Moreover, social adversity plays a role in the development of other psychiatric disorders as well. Childhood sexual abuse, for example, has been shown to be associated with the development of many psychiatric disorders (Kendler et al., 2000). Yet, the ubiquitous and encompassing nature of the deprivating social experiences associated with schizophrenia and related disorders (e.g., neglect and abuse, parental separation and loss, growing up in a single-parent household with an unemployed parent, moving frequently during childhood, being an immigrant or a member of a minority group with a different-colored skin, growing up in a fragmented social environment) has not been found to be associated with any other psychiatric disorder. In addition, there appears to be a dose-response relationship between adversity and symptomatology in schizophrenia (e.g., Scott, Chant, Andrews, Martin, & McGrath, 2007; Van Os et al., 2001; Wicks et al., 2005), suggesting a causal role for social deprivation in the development of the disorder.

It should also be pointed out, however, that most individuals with extreme social deprivation fail to develop schizophrenia. Genetic factors, therefore, appear critical to the development of the disorder. Furthermore, because social adversity is also associated with other psychiatric disorders, the data suggest that the timing, duration, and accumulation of adverse psychosocial experiences play a critical role in the onset of schizophrenia and that these adversities interact with genetic factors in a complex, multifactorial manner to produce different psychiatric symptoms. As van Os, Kenis, and Rutten (2010, p. 208) recently stated, "gene--environment interaction research is a logical next step but in practice remains very rare, because to date there has been little collaboration between 'environmental' and 'genetic' groups in this area."

Isolation and Defeat and the Development of Hallucinations

Auditory hallucinations are the most common symptom of schizophrenia. The World Health Organization estimates that 74% of patients with schizophrenia have auditory hallucinations (Sartorius, Shapiro, & Jablensky, 1974). Auditory hallucinations are also quite common in the population at large. Of the population studied in the National Comorbidity survey, 8.3% reported auditory hallucinations (Shevlin, Dorahy, Adamson, 2007), and a recent population-based study of 7- to 8-year-old children in the Netherlands (N = 3,870) found that 9% of the children experienced auditory vocal hallucinations in the past year (Bartels-Velthuis, Jenner, van de Willige, van Os, & Wiersma, 2010).

Functionally, social isolation and defeat may lead to the development of hallucinations, as research suggests that hallucinations develop when other, more potent and appropriate reinforcers are unavailable. Grimby (1993), for example, reported that one month after the death of a spouse, 82% of widowers reported hallucinations and/or illusions. Prolonged isolation (Zuckerman & Cohen, 1964) and solitary confinement (Grassian, 1983; Mason & Brady, 2009) have also been shown to produce hallucinations, and Hoffman (2007) found that that most patients with schizophrenia report that their hallucinations began during a period of social isolation. People with schizophrenia also report that being alone increases the severity of their hallucinations (Nayani & David, 1996).

Research suggests that the loss of social reinforcement may lead people to focus inward. People who hallucinate, for example, are likely to score high on scales of self-focused attention (Morrison & Haddock, 1997). When no external reinforcers are available, hallucinations may serve to mask other aversive experiences, such a silence or inactivity. As Ferster (1973, p. 859) has noted, "irrational" behavior becomes prepotent over no behavior at all: It seems likely ... that any factor which causes a temporary or long-term reduction in positively reinforced ways of acting because of emotional or temporary factors will also produce bizarre or irrational behavior as a byproduct."

Hallucinations may also serve to focus attention away from negative or anxious feelings. In a survey, most psychotic patients reported that their voices occurred in response to sadness, fear, or anger (Nayani & David, 1996). In another study, Delespaul, deVries, and van Os (2002) asked 94 patients with psychosis to record their thoughts, feelings, and experiences when beeped randomly several times a day for one week. Results indicated that reports of anxiety were significantly likely to precede reports of auditory hallucinations.

Hallucinations may also have reinforcing qualities. Benjamin (1989), for example, in a study of 30 individuals with severe mental illness, found that all patients developed "integrated, interpersonally coherent relationships" with their voices, and Nayani and David (1996) found that patients often relied on their voices to guide them when confronted with dilemmas. Birchwood, Meaden, Trower, Gilbert, and Plaistow (2000) and Gilbert et al. (2001) found that the relationship an individual developed with his or her voice mirrored relationships he or she had with others in everyday life. Voices were commonly seen as powerful, dominant, and shaming, which led individuals to see themselves as subordinate, shamed, and inferior (Birchwood et al., 2004). Voices therefore may serve a function similar to self-critical thoughts (Gilbert et al., 2001). They may serve to keep people isolated and alone when prior attempts to achieve social closeness have been punished.


Maher (2001, 2003) has provided a cogent, functional account of how delusions may develop. Delusions seem to develop in the way all beliefs develop, via the need to find an explanation for some phenomenon. The differences in schizophrenia, however, are that. the phenomena that require explanation may be unusual sensory experiences, and individuals with schizophrenia, because of isolation, often lack corrective social feedback to normalize their unusual experiences (Broome et al., 2005). The most common unusual experiences that require explanation are auditory hallucinations. Once an individual begins to hear voices, he or she needs to explain why the hallucination has occurred. Thus, if I hear my dead mother speaking to me, perhaps it is because I have special abilities that others do not have. Similarly, paranoid delusions often begin with unusual sensory experiences that require explanation, such as the sensation of being followed, or the "feeling" that someone has been through one's mail. These sensory experiences, in fact, may be quite common (see Bell, Halligan, & Ellis, 2006), but when individuals are isolated and alone, they are less likely to have someone to help explain why the phenomenon occurred and more likely to see others as responsible for the negative experience.

Several lines of evidence support Maher's theory. First, as with hallucinations, delusions or irrational beliefs are also quite common in the population at large. In a study of 7,075 randomly selected adults in the Netherlands, 11% were judged to a have a psychotic delusion, although most were not bothered by their beliefs (van Os, Hanssen, Bijl, & Ravelli, 2000). Johns et al. (2004) surveyed 8,580 adults in the United Kingdom and found that 21.2% responded yes to the question, "Over the past year, have there been times when you felt that people were against you?" and Ross and Joshi (1992), in a survey of 502 adults in Winnipeg, Canada, reported that 15.6% of the population believed in mental telepathy and 5.2% reported contact with ghosts.

Second, delusional beliefs can be induced in individuals without schizophrenia by having them experience anomalous sensory experiences. In an ingenious experiment, Zimbardo, Andersen, and Kabat (1981) induced, through hypnotic suggestion, normal male college students to become partially deaf. Those participants who were unaware of the induction were more paranoid on standard psychological tests and less likely to work with others on a common task than those participants who were hypnotized to become partially deaf but were aware of the source of their deafness.

Third, in neutral, ambiguous situations, individuals with high levels of perceptual anomalies are most likely to experience delusional beliefs. Freeman, Pugh et al. (2008), for example, asked 200 nonclinical individuals to experience a neutral virtual-reality social environment for four minutes and found that individuals scoring highly on measures of anxiety, worry, cognitive inflexibility, and perceptual anomalies prior to the virtual reality experience were most likely to score high on a social paranoia questionnaire immediately after the experience (see also Freeman, Gittins et al., 2008).

Finally, delusions develop in a wide range of other disorders in which individuals also experience anomalous sensory experiences. Delusions appear to be quite common, for example, among individuals with dementia, Parkinson's disease, multiple sclerosis, and temporal lobe epilepsy (see White, Krengel, & Thompson, 2009, for a review). In a review of 55 studies of 9,749 patients with Alzheimer's disease, Ropacki and Jeste (2005) reported that that 36.9% of patients developed at least one psychotic delusion. Delusions are also common among the hearing impaired (van der Werf et al., 2007) and among individuals who ingest hallucinogenic drugs (Kleinman, Gillin, & Wyatt, 1977). In all these instances, the data suggest that delusions may develop when there is a need to find an explanation for one's altered sensory experiences.

Delusions may also be adaptive. Paranoid ideation, for example, may, at times, protect against low self-esteem. A study found, using a structured diary technique, that paranoid individuals tend to be more inconsistent in their view of themselves than do nonparanoid individuals, and decreases in self-esteem among paranoid participants were associated with a subsequent increase in paranoid ideation (Thewissen, Bentall, Lecomte, van Os, & Myin-Germeys, 2008).

Paranoia may also, at times, help people avoid self-blame. Using an attributional style questionnaire, Fornells-Ambrojo and Garety (2009) found nonpsychiatric controls were likely to blame themselves, and not others, for the occurrence of negative events. Paranoid psychotic individuals, however, were significantly more likely to blame others, and not themselves, for those same negative events.

Delusions may also provide people with a sense of power and grandiosity. People must believe that they are extremely important if they are being followed by the CIA or FBI. Delusions may also compensate for feelings of worthlessness and self-deprecation. Rector (2007) presented the case of a woman whose boyfriend responded with rage and verbal abuse and by breaking off their relationship after she confessed to a prior period of promiscuity. Soon afterward, the woman developed grandiose delusions of saving the world.

Thought Disorder

Others often find that the speech of individuals with schizophrenia lacks clarity and is difficult to understand. Functionally, when speech is disorganized, it has failed to come under the control of the listener. As Maher (2003, p. 9) cogently noted, this deficit "places the locus of the pathology in the realm of the patient's interpersonal interactions." Individuals with schizophrenia, with a history of social isolation and defeat, may never have learned the social cues that indicate, in the moment, that the listener is paying attention or has understood what has just been said. Research suggests, for example, that subtle signs of thought disorder are present in individuals prone to developing schizophrenia (Coleman, Levy, Lenzenweger, & Holzman, 1996; Kerns & Becker, 2008).

Instead of coming under the control of other people, the verbal behavior of individuals with schizophrenia may be under the control of internal stimuli. Maher, Manschreck, Linnet, and Candela (2005), for example, asked people with and without schizophrenia to describe what they saw in an artistic picture. Individuals with schizophrenia were significantly more likely than those without schizophrenia to verbalize words that were related to each other semantically (e.g., sleep and bed), even when the words were separated by several paragraphs.

People with schizophrenia also respond quicker than people without schizophrenia to related words (see Pomarol-Clotet, Oh, Laws, & McKenna, 2008, for a review). In one thoughtful experiment, Spitzer, Braun, Maier, Hermle, and Maher (1993) found that not only could individuals with schizophrenia make associations between related words (e.g., hen and egg) quicker than individuals without schizophrenia, but people with schizophrenia could also see indirect or mediated associations between words when those relationships were indiscernible to those without schizophrenia. People with schizophrenia, for example, were able to quickly determine that the words lemon and sweet are related (both are mediated by the word sour) when both words were presented simultaneously. Individuals without schizophrenia, however, were unable to see the connection between indirectly associated words (i.e., they did not respond more quickly to indirectly associated words than unrelated words) when word pairs were presented simultaneously. Thus, it is possible that because speech is not under the control of interpersonal cues, it becomes more likely to come under the control of internal stimuli. Moreover, speech under the control of internal stimuli rather than under the control of interpersonal cues may further protect individuals with schizophrenia by making it less likely that they will be prone to social adversity.

Negative Symptoms

Negative symptoms are characterized by their absence, specifically the absence of goal-directed behavior (avolition), speech (alogia), and emotional expressiveness (blunted or flat affect; American Psychiatric Association, 2000). Functionally, it is not surprising that those who have been socially defeated lack behaviors that have the potential to increase social interactions. As Gilbert (2006) noted, it is evolutionarily adaptive for organisms to avoid goal pursuits and "keep a low and vigilant profile" (p. 291) when they have been socially rejected.

Individuals with high levels of negative symptoms may have adapted a risk-averse strategy to social interactions (Allen & Badcock, 2003); they avoid social contexts in which they have been excluded in the past. Research suggests, for example, that individuals with high levels of negative symptoms tend to have defeatist attitudes toward task performance (e.g., "If I fail partly, it is as bad as being a complete failure"), even when controlling for depressive symptoms (Beck, Grant, Huh, Perivoliotis, & Chang, 2013; Rector, 2004). Thus, negative symptoms may emerge when efforts at goal pursuits have led to defeat. These past failures may have also led to the internalization of defeatist attitudes to help prevent future attempts at task initiation. Individuals with high levels of negative symptoms are also less likely than other patients with schizophrenia to be fearful of negative evaluation and more likely to show high self-esteem (Beck et al., 2012). As Beck et al. (2012, p. 7) noted, because of past marginalization experiences, these individuals may have learned to devalue the importance of social judgment by others. This devaluation may also lead to greater self-acceptance and self-esteem.

At times, negative symptoms may emerge as a way of coping with positive symptoms. In recent-onset patients, for example, negative symptom exacerbations were found to coincide with positive symptom exacerbations (Ventura et al., 2004) and Rector, Beck, and Stolar (2005) presented a case analysis of a patient who was alogic and showed withdrawal and anergia symptoms because of his delusional beliefs. The patient, they reported, did not speak to people and avoided activities because he was fearful of becoming sexually aroused and having an erection, of which he was deeply ashamed.

Research also suggests that although individuals with schizophrenia may appear to have blunted or flat affect, subjectively, they may be experiencing emotions as intensely as other people (see Kring & Moran, 2008, for a review). In one seminal study (Kring, Kerr, Smith, & Neale, 1993), results indicated that although individuals with schizophrenia were significantly less emotionally expressive than individuals without schizophrenia while watching happy and sad movies, individuals with schizophrenia experienced the movies as being as emotionally evocative as those without schizophrenia. It may be that individuals with schizophrenia who show blunted or flat affect have learned over time to diminish their emotional reactions to avoid censure or criticism. Possibly, individuals with schizophrenia have intact subjective experiences, compared to those without schizophrenia, because subjective experiences are not observable to others and thus may not be subject to their negative scrutiny.

Integration With Biological Factors

A functional analysis does not preclude the importance of biological factors in the etiology of schizophrenia. It seems clear that there is an interaction between biological or genetic factors and environmental causes in the development of schizophrenia (van Os et al., 2010). Research suggests, for example, that a stressful family environment may be associated with the development of a schizophrenia-spectrum disorder only when there is also a high genetic risk of developing the disorder (e.g., Tienari et al., 2004).

Two factors may explain how a genetic predisposition may be associated with the development of schizophrenia. First, a genetic predisposition may lead some individuals to be more likely than others to encounter environments that are socially isolating and defeating. Childhood neuromotor abnormalities (Erlenmeyer-Kimling et al., 2000; Walker, Savoie, & Davis, 1994) and intellectual deficits (Cannon et al., 2000), for example, have both been shown to be important predictors of the development of schizophrenia. Children with these deficits often lack the ability to discern the subtle social cues that are necessary for effective social relationships and thus may be more likely than others to be rejected by their peers. These children may also be less likely than others to be reinforced by interpersonal engagement, which may add further to their social isolation.

Second, some people may be more likely than others to react to socially isolating environments with schizophrenia symptoms. A genetic predisposition may lead some people to react to some stressors with schizophrenia symptoms, whereas others, with a different genetic predisposition, may react to similar stressors with other behavior. At present, we know little about how genetic factors interact with specific psychosocial stressors in the development of specific psychiatric symptoms (van Os et al., 2010).

Despite the importance of genetic factors in schizophrenia, research in animals suggests that social factors may lead to some of the biological deficits often seen in individuals with schizophrenia. Rats, for example, that have been socially defeated show both increased dopaminergic activity in the prefrontal cortex (Tidey & Miczek, 1996) and increased NMDA receptor stimulation (Covington et al., 2008) while subordinate macaques (Kaplan, Manuck, Fontenot, & Mann, 2002; Morgan et al., 2002) and neonatal rats deprived of maternal care (Hall, Wilkinson, Humby, & Robbins, 1999) also show increased dopaminergic activity in the brain. It is impossible to separate the effects of genetic versus environmental influences on the development of schizophrenia; all symptoms are clearly the result of both.

It is also important to point out that there are limits to genetic, biological, and cognitive analyses of schizophrenia. As discussed previously, such analyses tend to be rooted in an essentialist paradigm. The most important limitation to essentialism is that the causes of the essential property may never be examined (Palmer & Donahoe, 1992). So, in schizophrenia, we may never examine, functionally, why some people have a smaller hypothalamus than others or why some people have a deficit in executive functioning. Essentialist paradigms may also lead to explanations that are prone to reification or circular reasoning. Essentialist explanations, for example, may explain a phenomenon by "inventing a property of the organism responsible for the phenomenon" (Palmer & Donahue, 1992, p. 1349). Metaphors may be created to explain behavior, and these metaphors may then be seen as actual physical structures within the organism. In schizophrenia research, for example, terms such working memory or attention are often used metaphorically and may fail to refer to specific behavioral deficits.

Finally, essentialist arguments may lack parsimony, as they may lead to separate explanations of separate behaviors. The legacy of a functional account lies in its simplicity. Not only did Darwin's theory of natural selection unify disparate finding under a single cogent umbrella, but similar processes can account for the selection of organisms and the selection of behaviors within an organism. In schizophrenia, researchers may explain different schizophrenic behaviors by appealing to different brain or cognitive structures. Thus, positive symptoms may be explained by one defect, negative symptoms by another, and thought disorder by a third structural abnormality. Yet, all three defects may have emerged from a similar mechanism, the consequences of an isolating and defeating social environment on oneself and on one's ancestors.

From a selectionist perspective, there is continuity between the effects of contingencies of survival in one's ancestors (as reflected in one's genetic endowment) and contingencies of reinforcement in an individual (as reflected in the development of specific behaviors in specific situations). Research suggests, for example, that individuals who have experienced the death of a parent early in life (Morgan et al., 2007) or individuals whose mothers experienced the death or serious illness of a close relatives while their mothers were in utero (Khashan et al., 2008) are at increased risk of developing schizophrenia. Through epigenetic processes, these individuals may be more likely to have children who develop schizophrenia if they are also traumatized as children or in utero (see Rutten & Mill, 2009. for a review of epigenetic processes in schizophrenia). Functionally, just as children whose biological ancestors are obese are more prone to be reinforced by high-caloric foods than children whose biological ancestors are not obese, children whose biological ancestors have had a history of trauma and have adapted to those environments with schizophrenia behaviors are themselvec more prone to react with schizophrenia behaviors when faced with traumatic environments. Thus, there is an important continuity among the effects of trauma on one's ancestors (as reflected in one's genetic predisposition to develop schizophrenia), the effects of trauma in utero or during childhood, and the effects of trauma on one's progeny.

Clinical Implications of a Functional Analysis

Ferster (1973) likened bizarre or irrational symptomatology to the erratic patterns on a television screen when the television is not working. The patterns tells us the TV is not working but do not inform us of what to change to fix the problem. In the same way, the symptoms of schizophrenia emerge when an individual has not been sufficiently reinforced for appropriate social behaviors. The symptoms merely tell us what is missing; they do not tell us how to create and build appropriate social repertoires.

Two current behavior analytic treatment programs attempt to build positive social repertoires but do so in different ways. Acceptance and commitment therapy (ACT; Hayes, Strosahl, & Wilson, 1999) teaches clients to accept symptoms nonjudgmentally, and instead of focusing on changing symptoms, the treatment teaches clients to concentrate on pursuing their valued goals (e.g., to live independently). In a randomized controlled trial, Bach and Hayes (2002) assigned 80 in-patients with positive psychotic symptoms to receive either four sessions of ACT or treatment as usual (TAU). Results indicated that patients who received TAU were twice as likely as patients who received ACT to be rehospitalized during a four-month follow-up period (40% vs. 20%), despite the fact that almost twice as many ACT participants endorsed positive psychotic symptoms at the follow-up assessment (60% vs. 31%). ACT thus appears to have helped patients by teaching them to be more accepting and less focused on changing their symptoms and more focused on making positive behavioral changes in their lives.

Functional analytic psychotherapy (FAP; Kohlenberg & Tsai, 1991) uses the therapeutic relationship to shape new behavior repertoires. FAP therapists attempt to respond "naturally" (i.e., by providing feedback consistent with the therapist's genuine private emotional reactions) to clinically relevant behaviors (known as CRBs in FAP) that emerge during the course of treatment. The assumption is that new behaviors shaped within the context of a genuine interpersonal relationship will be maintained in the client's natural environment. Baruch, Kanter, Busch, and Juskiewicz (2009) demonstrated how FAP could be used successfully to treat a 21-year-old college student who presented with depression and psychotic symptoms. Treatment focused, in part, on reinforcing both the open discussion of the client's paranoid thoughts and fears regarding the therapist and the open expression of the client's emotional experiences. In this case, reinforcement consisted of having the therapist respond contingently to these client behaviors by openly sharing his own thoughts and feelings about what the client had just said.

Much research indicates that the behavior of individuals with schizophrenia is responsive to environmental contingencies. Paul and Lentz (1977), in a seminal study, developed a comprehensive social learning program (SLP) based on a token economy, which included reinforcement for socially appropriate behaviors and the removal of tokens for inappropriate behaviors. Residents at a state hospital who had been hospitalized an average of 16.9 years were randomly assigned to either the SLP treatment, a milieu treatment based on a therapeutic community model, or traditional custodial care. Results indicated that despite the chronicity of the participants, 97.5% of those who participated in the SLP treatment were successfully discharged into the community for a period of at least 90 consecutive days, compared with 71% of milieu patients and 44.8% of the controls. In addition, by the end of the study, 10.7% of the SLP group were self-supporting and living independently, compared to 0% of the control patients, and 89.3% of SLP participants were no longer on any psychotropic medication, while 100% of the control participants continued to take psychotropic medication. Every resident who participated in the SLP program showed a significant improvement in their psychosocial functioning,

More recently, Silverstein et al. (2006) developed an inpatient behavioral rehabilitation program for "treatment-refractory" patients with schizophrenia who had been at a state hospital in New York a minimum of three years. As in the Paul and Lentz (1977) study, treatment focused on the development of community living skills through reinforcement of socially appropriate behaviors. One hundred ninety patients participated in the program, and despite the chronicity of the population (participants had been hospitalized an average of 7.4 years), 78% were able to be discharged into the community, and at the end of the four-year study, 67% of patients were continuing to live in the community.

Two problems plague efforts to change the behavior of individuals with schizophrenia. First, once the contingencies supporting the behavior are withdrawn, the new behaviors often fail to maintain or generalize to new environmental settings. This is not surprising, and, currently, much effort is being made to promote the generalization of new behaviors learned in a supported therapeutic environment. Glynn et al. (2002), for example, added an in vivo amplified skills training component to a traditional behaviorally oriented social skills protocol to help individuals with schizophrenia improve their social functioning. The in vivo component included training sessions held in settings conducive to learning the skills that were being taught (e.g., in a coffee shop to learn communication skills). Results indicated that patients who were given the amplified in-vivo sessions developed closer family relationships and had a better overall social adjustment and quality of life at the end of treatment than those not given the amplified treatment.

A second problem with psychosocial treatments for schizophrenia is that the ways new behaviors are learned within the treatments are very different from the way the same behaviors are learned naturally. Social skills are learned over the course of one's life through subtle interactions among individuals. The dynamic interplay and subtle nuances that characterize the learning of social behaviors cannot be replicated in a short time in either a clinical laboratory or therapist's office. Despite these hurdles, however, as Silverstein et al. (2006, p. 167) pointed out, enough is now known about how to help people with schizophrenia that failure "no longer need be an option."


It would be foolhardy to believe that one theory or model could explain all facets of schizophrenia. Yet, our field has been dominated by biological, structural, and reductionistic ways of looking at this complex disorder. Recent evidence suggests, though, that environmental factors play a central role in the development of specific schizophrenic behaviors and that social isolation and defeat appear integral to our comprehensive understanding of these difficulties. Future research into the functional aspects of schizophrenia and psychosis will aid our theoretical understanding of how these symptoms develop and spur further empirical work into psychosocial factors that contribute to the etiology and treatment of this disorder.


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The author would like to thank Sharon Foster, Nancy Docherty, Milton Brown, and Robert Kohlenberg for their helpful comments on the manuscript.

Correspondence concerning this article should be addressed to Irwin S. Rosenfarb, California School of Professional Psychology, Alliant International University, 10455 Pomerado Road, San Diego, CA 92131. E-mail:


Irwin S. Rosenfarb

California School of Professional Psychology, Alliant International University, San Diego
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