As with many other kinds of disorders, biological, psychological, and sociocultural theorists have each proposed explanations for schizophrenia. So far, the biological explanations have received by far the most research support. This is not to say that psychological and sociocultural factors play no role in the disorder. Rather, a diathesis-stress relationship may be at work: people with a biological predisposition will develop schizophrenia only if certain kinds of events or stressors are also present. Similarly, a diathesis-stress relationship often seems to be operating in the development of other kinds of psychotic disorders (see PsychWatch below).

What is arguably the most enlightening research on schizophrenia during the past several decades has come from genetic and biological investigations. These studies have revealed the key roles of inheritance and brain activity in the development of schizophrenia and have opened the door to important treatment changes.

Genetic FactorsFollowing the principles of the diathesis-stress perspective, genetic researchers believe that some people inherit a biological predisposition to schizophrenia and develop the disorder later when they face extreme stress, usually during late adolescence or early adulthood (Pocklington et al., 2014; Winchester et al., 2014). The genetic view has been supported by studies of (1) relatives of people with schizophrenia, (2) twins with schizophrenia, (3) people with schizophrenia who are adopted, and (4) genetic linkage and molecular biology.

ARE RELATIVES VULNERABLE?Family pedigree studies have found repeatedly that schizophrenia and schizophrenia-like brain abnormalities are more common among relatives of people with the disorder (Scognamiglio et al., 2014; Tamminga et al., 2008). And the more closely related the relatives are to the person with schizophrenia, the more likely they are to develop the disorder (see Figure 14-2).

As you saw earlier, 1 percent of the general population develops schizophrenia. The prevalence rises to 3 percent among second-degree relatives with the disorder—that is, half-siblings, uncles, aunts, nephews, nieces, and grandchildren (Gottesman & Reilly, 2003)—and it reaches an average of 10 percent among first-degree relatives (parents, siblings, and children). Of course, this trend by itself does not establish a genetic basis for the disorder. Neuroscientist Solomon Snyder (1980) has pointed out, “Attendance at Harvard University also runs in families but would hardly be considered a genetic trait.” Close family members are exposed to many of the same environmental influences as the person with schizophrenia, and it may be these influences that lead to the disorder.

IS AN IDENTICAL TWIN MORE VULNERABLE THAN A FRATERNAL TWIN?Twins, who are among the closest of relatives, have in particular been studied by schizophrenia researchers. If both members of a pair of twins have a particular trait, they are said to be concordant for that trait. If genetic factors are at work in schizophrenia, identical twins (who share all their genes) should have a higher concordance rate for schizophrenia than fraternal twins (who share only some genes). This expectation has been supported consistently by research (Higgins & George, 2007; Gottesman, 1991). Studies have found that if one identical twin develops schizophrenia, there is a 48 percent chance that the other twin will do so as well. If the twins are fraternal, on the other hand, the second twin has approximately a 17 percent chance of developing the disorder.

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Once again, however, factors other than genetics may explain these concordance rates. For example, if one twin is exposed to a particular danger during the prenatal period, such as an injury or virus, the other twin is likely to be exposed to it as well. This is especially true for identical twins, whose prenatal environment is especially similar. Thus a predisposition to schizophrenia could be the result of a prenatal problem, and twins, particularly identical twins, would still be expected to have a higher concordance rate.

ARE THE BIOLOGICAL RELATIVES OF AN ADOPTEE VULNERABLE?Adoption studies look at adults with schizophrenia who were adopted as infants and compare them with both their biological and their adoptive relatives. Because they were reared apart from their biological relatives, similar symptoms in those relatives would indicate genetic influences. Conversely, similarities to their adoptive relatives would suggest environmental influences. Researchers have repeatedly found that the biological relatives of adoptees with schizophrenia are more likely than their adoptive relatives to develop schizophrenia or another schizophrenia spectrum disorder (Andreasen & Black, 2006; Kety, 1988, 1968).

WHAT DO GENETIC LINKAGE AND MOLECULAR BIOLOGY STUDIES SUGGEST?As with bipolar disorders (see Chapter 7), researchers have run studies of genetic linkage and molecular biology to pinpoint the possible genetic factors in schizophrenia (Singh et al., 2014; Winchester et al., 2014). In one approach, they select large families in which schizophrenia is very common, take blood and DNA samples from all members of the families, and then compare gene fragments from members with and without schizophrenia. Applying this procedure to families from around the world, various studies have identified possible gene defects on chromosomes 1, 2, 6, 8, 10, 13, 15, 18, 20, and 22 and on the X chromosome, each of which may help predispose a person to develop schizophrenia (Huang et al., 2014; Muller, 2014).

These varied findings may indicate that some of the suspected gene sites are cases of mistaken identity and do not actually contribute to schizophrenia. Alternatively, it may be that different kinds of schizophrenia are linked to different genes. It is most likely, however, that schizophrenia, like a number of other disorders, is a polygenic disorder, caused by a combination of gene defects (Goudriaan et al., 2014; Purcell et al., 2014).

How might genetic factors lead to the development of schizophrenia? Research has pointed to two kinds of biological abnormalities that could conceivably be inherited—biochemical abnormalities and abnormal brain structure.

Biochemical AbnormalitiesAs you have read, the brain is made up of neurons whose electrical impulses (or “messages”) are transmitted from one to another by neurotransmitters. After an impulse arrives at a receiving neuron, it travels down the axon of that neuron until it reaches the nerve ending. The nerve ending then releases neurotransmitters that travel across the synaptic space and bind to receptors on yet another neuron, thus relaying the message to the next “station.” This neuron activity is known as “firing.”

Over the past four decades, researchers have developed a dopamine hypothesis to explain their findings on schizophrenia: certain neurons that use the neurotransmitter dopamine (particularly neurons in the striatum region of the brain) fire too often and transmit too many messages, thus producing the symptoms of schizophrenia (Brisch et al., 2014; During et al., 2014; Laruelle, 2014). This hypothesis has undergone challenges and adjustments in recent years, but it is still the foundation for current biochemical explanations of schizophrenia (Rao & Remington, 2014). The chain of events leading to this hypothesis began with the accidental discovery of antipsychotic drugs, medications that help remove the symptoms of schizophrenia. As you will see in Chapter 15, the first group of antipsychotic medications, the phenothiazines, were discovered in the 1950s by researchers who were looking for better antihistamine drugs to combat allergies. Although phenothiazines failed as antihistamines, it soon became obvious that they were effective in reducing schizophrenic symptoms, and clinicians began to prescribe them widely (Adams et al., 2014).

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Researchers later learned that these early antipsychotic drugs often produce troublesome muscular tremors, symptoms that are identical to the central symptom of Parkinson’s disease, a disabling neurological illness. This undesired reaction to antipsychotic drugs offered the first important clue to the biology of schizophrenia. Scientists already knew that people who suffer from Parkinson’s disease have abnormally low levels of the neurotransmitter dopamine in some areas of the brain and that lack of dopamine is the reason for their uncontrollable shaking. If antipsychotic drugs produce Parkinsonian symptoms in people with schizophrenia while removing their psychotic symptoms, perhaps the drugs reduce dopamine activity. And, scientists reasoned further, if lowering dopamine activity helps remove the symptoms of schizophrenia, perhaps schizophrenia is related to excessive dopamine activity in the first place.

HOW STRONG IS THE DOPAMINE-SCHIZOPHRENIA LINK?Since the 1960s, research has supported and helped clarify the dopamine hypothesis. It has been found, for example, that some people with Parkinson’s disease develop schizophrenia-like symptoms if they take too much L-dopa, a medication that raises Parkinson’s patients’ dopamine levels (Grilly, 2002). The L-dopa apparently raises the dopamine activity so much that it produces psychosis.

Support for the dopamine hypothesis has also come from research on amphetamines, drugs that, as you saw in Chapter 12, stimulate the central nervous system. Investigators first noticed during the 1970s that people who take high doses of amphetamines may develop amphetamine psychosis—a syndrome very similar to schizophrenia (Hawken & Beninger, 2014; Li et al., 2014). They also found that antipsychotic drugs can reduce the symptoms of amphetamine psychosis, just as they reduce the symptoms of schizophrenia. Eventually researchers learned that amphetamines and similar stimulant drugs increase dopamine activity in the brain, thus producing schizophrenia-like symptoms (Peng, Chiang, & Liang, 2014).

Investigators have located areas of the brain that are rich in dopamine receptors and have found that phenothiazines and other antipsychotic drugs bind to many of these receptors (Yoshida et al., 2014). Apparently the drugs are dopamine antagonists—drugs that bind to dopamine receptors, prevent dopamine from binding there, and so prevent the neurons from firing. Researchers have identified five kinds of dopamine receptors in the brain—called the D-1, D-2, D-3, D-4, and D-5 receptors—and have found that phenothiazines bind most strongly to the D-2 receptors (Chun et al., 2014; Seeman, 2011).

WHAT IS DOPAMINE’S PRECISE ROLE?These and related findings suggest that in schizophrenia, messages traveling from dopamine-sending neurons to dopamine receptors on other neurons, particularly to the D-2 receptors, may be transmitted too easily or too often. This theory is appealing because certain dopamine neurons are known to play a key role in guiding attention (Brisch et al., 2014). People whose attention is severely disturbed by excessive dopamine activity might well be expected to suffer from the problems of attention, perception, and thought found in schizophrenia (see MindTech below).

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Why might dopamine be overactive in people with schizophrenia? It may be that people with schizophrenia have a larger-than-usual number of dopamine receptors, particularly D-2 receptors, or their dopamine receptors may be too sensitive or operate abnormally in some other way (During et al., 2014; Seeman & Seeman, 2014). Remember that when dopamine carries a message to a receiving neuron, it must bind to a receptor on the neuron. A larger number of receptors or abnormal operation by the receptors could result in more dopamine binding and thus more neuron firing. Autopsies have in fact found an unusually large number of dopamine receptors in people with schizophrenia (Owen et al., 1987, 1978; Lee & Seeman, 1980), and imaging studies have revealed particularly high occupancy levels of dopamine at D-2 receptors in patients with schizophrenia (Kim et al., 2014; Abi-Dargham & Grace, 2011).

Though enlightening, the dopamine hypothesis has certain problems. The biggest challenge to it has come with the recent discovery of a new group of antipsychotic drugs, initially referred to as atypical antipsychotic drugs and now called second-generation antipsychotic drugs, which are often more effective than the traditional ones. The new drugs bind not only to D-2 dopamine receptors, like the traditional, or conventional, antipsychotic drugs, but also to many D-1 receptors and to receptors for other neurotransmitters such as serotonin (Waddington, O’Tuathaigh, & Remington, 2011; Goldman-Rakic et al., 2004). Thus, it may be that schizophrenia is related to abnormal activity or interactions of both dopamine and serotonin and perhaps other neurotransmitters (for example, glutamate and GABA) as well, rather than to abnormal dopamine activity alone (Hashimoto, 2014; Juckel, 2014; Pocklington et al., 2014).

In yet another challenge to the dopamine hypothesis, some theorists claim that excessive dopamine activity contributes primarily to the positive symptoms of schizophrenia such as delusions and hallucinations. In support of that notion, it turns out that positive symptoms respond well to the conventional antipsychotic drugs, which bind so strongly to D-2 receptors, whereas some of the negative symptoms (such as restricted affect and loss of volition) respond best to the second-generation antipsychotic drugs, which bind less strongly to D-2 receptors (Advokat et al., 2014; Millan et al., 2014). Still other studies suggest that negative symptoms may be related primarily to abnormal brain structure, rather than to dopamine overactivity.

Abnormal Brain StructureDuring the past decade, researchers have also linked schizophrenia, particularly cases dominated by negative symptoms, to abnormalities in brain structure (Millan et al., 2014; Shinto et al., 2014). Using brain scans, they have found, for example, that many people with schizophrenia have enlarged ventricles—the brain cavities that contain cerebro-spinal fluid (Hartberg et al., 2011; Cahn et al., 2002; Lieberman et al., 2001). In addition to displaying more negative symptoms and fewer positive ones, patients who have enlarged ventricles tend to be more poorly adjusted socially before the onset of schizophrenia, to have more cognitive disturbances, and to respond less well to conventional antipsychotic drugs (Bornstein et al., 1992).

It may be that enlarged ventricles are actually a sign that nearby parts of the brain have not developed properly or have been damaged, and perhaps these problems are the ones that help produce schizophrenia. In fact, studies suggest that some patients with schizophrenia also have smaller temporal and frontal lobes than other people, smaller amounts of cortical white and gray matter and, perhaps most important, abnormal blood flow—either reduced or heightened—in certain areas of the brain (Kochunov & Hong, 2014; Lener et al., 2014). Still other studies have linked schizophrenia to abnormalities of the hippocampus, amygdala, and thalamus, among other brain structures (Arnold et al., 2014; Chun et al, 2014; Markota et al., 2014) (see Figure 14-3).

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Viral ProblemsWhat might cause the biochemical and structural abnormalities found in many cases of schizophrenia? Various studies have pointed to genetic factors, poor nutrition, fetal development, birth complications, immune reactions, and toxins (Brown, 2012; Clarke et al., 2012; Borrajo et al., 2011). In addition, some investigators suggest that the brain abnormalities may result from exposure to viruses before birth. Perhaps the viruses enter the fetus’ brain and interrupt proper brain development, or perhaps the viruses remain quiet until puberty or young adulthood, when, activated by changes in hormones or by another viral infection, they help to bring about schizophrenic symptoms (Fox, 2010; Torrey, 2001, 1991).

Some of the evidence for the viral theory comes from animal model investigations, and other evidence is circumstantial, such as the finding that an unusually large number of people with schizophrenia are born during the winter (Patterson, 2012; Fox, 2010). The winter birth rate among people with schizophrenia is 5 to 8 percent higher than among other people (Harper & Brown, 2012; Tamminga et al., 2008). This could be because of an increase in fetal or infant exposure to viruses at that time of year. The viral theory has also received support from investigations of fingerprints. Normally, identical twins have almost identical numbers of fingerprint ridges. People with schizophrenia, however, often have significantly more or fewer ridges than their nonschizophrenic identical twins (van Os et al., 1997; Torrey et al., 1994). Fingerprints form in the fetus during the second trimester of pregnancy, just when the fetus is most vulnerable to certain viruses. Thus the fingerprint irregularities of some people with schizophrenia could reflect a viral infection contracted during the prenatal period, an infection that also predisposed the individuals to schizophrenia.

More direct evidence for the viral theory of schizophrenia comes from studies showing that mothers of people with schizophrenia were more likely to have been exposed to the influenza virus during pregnancy than were mothers of people without schizophrenia (Canetta et al., 2014; Brown & Patterson, 2011; Fox, 2010). Other studies have found antibodies to certain viruses, including viruses usually found in animals, in the blood of 40 percent of research participants with schizophrenia (Leweke et al., 2004; Torrey et al., 1994). The presence of such antibodies suggests that these people had at some time been exposed to those particular viruses.

Together, the biochemical, brain structure, and viral findings are shedding much light on the mysteries of schizophrenia. At the same time, it is important to recognize that many people who have these biological abnormalities never develop schizophrenia. Why not? Possibly, as you read earlier, because biological factors merely set the stage for schizophrenia, while key psychological and sociocultural factors must be present for the disorder to appear.

When schizophrenia investigators began to identify genetic and biological factors during the 1950s and 1960s, many clinicians abandoned the psychological theories of the disorder. During the past few decades, however, the tables have been turned and psychological factors are once again being considered as important pieces of the schizophrenia puzzle (Green et al., 2014). The leading psychological theories come from the psychodynamic, behavioral, and cognitive perspectives.

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The Psychodynamic ExplanationFreud (1924, 1915, 1914) believed that schizophrenia develops from two psychological processes: (1) regression to a pre-ego stage and (2) efforts to reestablish ego control. He proposed that when their world has been extremely harsh or withholding—for example, when their parents have been cold or unnurturing or when they have experienced severe traumas—some people regress to the earliest point in their development, to the pre-ego state of primary narcissism, in which they recognize and meet only their own needs. This sets the stage for schizophrenia. Their near-total regression leads to self-centered symptoms such as neologisms, loose associations, and delusions of grandeur. Once people regress to such an infantile state, Freud continued, they then try to reestablish ego control and contact with reality. Their efforts give rise to yet other psychotic symptoms. Auditory hallucinations, for example, may be a person’s attempt to substitute for a lost sense of reality.

In support of Freud’s theory, some studies show that people with schizophrenia have great difficulty forming an integrated sense of self (Lysaker et al., 2014). In addition, studies have often found that people with schizophrenia went through severe stress or traumas early in their lives (Bebbington & Kuipers, 2011). Beyond these findings, however, Freud’s explanation for the disorder has received little research support.

Years later, noted psychodynamic clinician Frieda Fromm-Reichmann (1948) elaborated on Freud’s notion that cold or unnurturing parents may set schizophrenia in motion. She described the mothers of people who develop the disorder as cold, domineering, and uninterested in their children’s needs. According to Fromm-Reichmann, these mothers may appear to be self-sacrificing but are actually using their children to meet their own needs. At once overprotective and rejecting, they confuse their children and set the stage for schizophrenic functioning. She called them schizophrenogenic (schizophrenia-causing) mothers.

Fromm-Reichmann’s theory, like Freud’s, has received little research support (Willick, 2001). The majority of people with schizophrenia do not appear to have mothers who fit the schizophrenogenic description. Most of today’s psychodynamic theorists have rejected the views of Freud and Fromm-Reichmann. Typically, they believe that biological abnormalities leave certain people particularly prone to extreme regression or other unconscious acts that may contribute to schizophrenia (Berzoff, Flanagan, & Hertz, 2008; Willick, Milrod, & Karush, 1998). For example, self theorists, who believe that schizophrenia reflects a struggling fragmented self, suggest that biological deficiencies explain the failure of people with schizophrenia to develop an integrated self (Lysaker & Hermans, 2007).

The Behavioral ViewBehaviorists usually cite operant conditioning and principles of reinforcement as the cause of schizophrenia. They propose that most people become quite proficient at reading and responding to social cues—that is, other people’s smiles, frowns, and comments. People who respond to such cues in a socially acceptable way are better able to satisfy their own emotional needs and reach their goals. Some people, however, are not reinforced for their attention to social cues, either because of unusual circumstances or because important figures in their lives are socially inadequate. As a result, they stop attending to such cues and focus instead on irrelevant cues—the brightness of light in a room, a bird flying above, or the sound of a word rather than its meaning. As they attend more and more to irrelevant cues, their responses become increasingly bizarre (Pinkham, 2014). Because the bizarre responses are rewarded with attention or other types of reinforcement, they are likely to be repeated again and again.

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Support for the behavioral position has been circumstantial. As you’ll see in Chapter 15, researchers have found that patients with schizophrenia are capable of learning at least some appropriate verbal and social behaviors if hospital personnel consistently ignore their bizarre responses and reinforce normal responses with cigarettes, food, attention, or other rewards (Kopelowicz, Liberman, & Zarate, 2007). If bizarre verbal and social responses can be eliminated by appropriate reinforcements, perhaps they were acquired through improper learning in the first place. Of course, an effective treatment does not necessarily indicate the cause of a disorder. Today the behavioral view is usually considered at best a partial explanation for schizophrenia. Although it may help explain why a given person displays more psychotic behavior in some situations than in others, it is too limited, in the opinion of many, to account for schizophrenia’s origins and its many symptoms.

The Cognitive ViewA leading cognitive explanation of schizophrenia is congruent with the biological view that during hallucinations and related perceptual difficulties the brains of people with schizophrenia are actually producing strange and unreal sensations—sensations triggered by biological factors. According to the cognitive explanation, however, when people attempt to understand their unusual experiences, more features of their disoder emerge (Howes & Murray, 2014; Tarrier, 2008). When first confronted by voices or other troubling sensations, these people turn to friends and relatives. Naturally, the friends and relatives deny the reality of the sensations, and eventually the sufferers conclude that the others are trying to hide the truth. They begin to reject all feedback, and some develop beliefs (delusions) that they are being persecuted (Howes & Murray, 2014; Bach, 2007). In short, according to this theory, people with schizophrenia take a “rational path to madness” (Zimbardo, 1976). This process of drawing incorrect and bizarre conclusions (delusions) may be helped along by a cognitive bias that many people with schizophrenia have—a tendency to jump to conclusions (Andreou et al., 2014; Sarin & Wallin, 2014).

Researchers have established that people with schizophrenia do indeed experience sensory and perceptual problems. As you saw earlier, many have hallucinations and most have trouble keeping their attention focused. But researchers have yet to provide clear, direct support for the cognitive notion that misinterpretations of such sensory problems actually produce a syndrome of schizophrenia.

Sociocultural theorists, recognizing that people with mental disorders are subject to a wide range of social and cultural forces, believe that multicultural factors, social labeling, and family dysfunctioning all contribute to schizophrenia. Research has yet to clarify what the precise causal relationships might be.

Multicultural FactorsRates of schizophrenia appear to differ between racial and ethnic groups (Singh & Kunar, 2010), particularly between African Americans and white Americans. As many as 2.1 percent of African Americans receive a diagnosis of schizophrenia, compared with 1.4 percent of white Americans (Lawson, 2008; Folsom et al., 2006). Studies also find that African American patients are more likely than white American patients to be assessed as having symptoms of hallucinations, paranoia, and suspiciousness (Mark et al., 2003; Trierweiler et al., 2000). And still other studies suggest that African Americans with schizophrenia are overrepresented in state hospitals (Lawson, 2008; Barnes, 2004). For example, in Tennessee’s state hospitals, 48 percent of those with a diagnosis of schizophrenia are African American, although only 16 percent of the state population is African American (Lawson, 2008; Barnes, 2004).

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It is not clear why African Americans are more likely than white Americans to receive this diagnosis. One possibility is that African Americans are more prone to develop schizophrenia. Another is that clinicians from majority groups are unintentionally biased in their diagnoses of African Americans or misread cultural differences as symptoms of schizophrenia (Lawson, 2008; Barnes, 2004).

Yet another explanation for the difference between African Americans and white Americans may lie in the economic sphere. On average, African Americans are more likely than white Americans to be poor; when economic differences are controlled for, the prevalence rates of schizophrenia become closer for the two racial groups. Consistent with the economic explanation is the finding that Hispanic Americans, who also tend to be economically disadvantaged, appear to be much more likely to be diagnosed with schizophrenia than white Americans, although their diagnostic rate is not as high as that of African Americans (Blow et al., 2004).

It also appears that schizophrenia differs from country to country in key ways (Johnson et al., 2014; McLean et al., 2014). Although the overall prevalence of this disorder is stable—around 1 percent—in countries across the world, the course and outcome of the disorder may vary considerably. According to a 10-country study conducted by the World Health Organization (WHO), the 25 million schizophrenic patients who live in developing countries have better recovery rates than schizophrenic patients in Western and other developed countries (Vahia & Vahia, 2008; Jablensky, 2000). The WHO study followed the progress of 467 patients from developing countries (Colombia, India, and Nigeria) over a two-year period and compared it with that of 603 patients from developed countries (the Czech Republic, Denmark, Ireland, Japan, Russia, the United Kingdom, and the United States). As you can see in Figure 14-4, during the course of the two-year study, the schizophrenic patients from the developing countries were more likely than those in the developed countries to recover from their disorder and less likely to have continuous or episodic symptoms, to have impaired social functioning, or to require heavy antipsychotic drugs or hospitalization.

Some clinical theorists believe that these differences partly reflect genetic differences from population to population. However, others argue that the psychosocial environments of developing countries tend to be more supportive and therapeutic than those of developed countries, leading to more favorable outcomes for people with schizophrenia (Vahia & Vahia, 2008; Jablensky, 2000). In developing countries, for example, there may be more family and social support for people with schizophrenia; more relatives and friends available to help care for such people; and less judgmental, critical, and hostile attitudes toward people with schizophrenia. The Nigerian culture, for example, is generally more tolerant of the presence of voices than are Western cultures (Matsumoto & Juang, 2008).

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Social LabelingMany sociocultural theorists believe that the features of schizophrenia are influenced by the diagnosis itself. In their opinion, society assigns the label “schizophrenic” to people who fail to conform to certain norms of behavior. Once the label is assigned, justified or not, it becomes a self-fulfilling prophecy that promotes the development of many schizophrenic symptoms. Certainly sufferers of schizophrenia have attested to the power that labeling has had on their lives:

Like this man, people who are labeled schizophrenic may be viewed and treated as “crazy” (Farrelly et al., 2014). Perhaps the expectations of other people subtly encourage the individuals to display psychotic behaviors (Omori, Mori, & White, 2014) and they come to accept their assigned role and learn to play it convincingly.

We have already seen the very real dangers of diagnostic labeling. In the famous Rosenhan (1973) study, discussed in Chapter 3, eight normal people presented themselves at various mental hospitals, complaining that they had been hearing voices utter the words “empty,” “hollow,” and “thud.” They were quickly diagnosed as schizophrenic, and all eight were hospitalized. Although the pseudopatients then dropped all symptoms and behaved normally, they had great difficulty getting rid of the label and gaining release from the hospital.

The pseudopatients reported that staff members were authoritarian in their behavior toward patients, spent limited time interacting with them, and responded curtly and uncaringly to questions. They generally treated patients as though they were invisible. “A nurse unbuttoned her uniform to adjust her brassiere in the presence of an entire ward of viewing men. One did not have the sense that she was being seductive. Rather, she didn’t notice us.” In addition, the pseudopatients described feeling powerless, bored, tired, and uninterested. The deceptive design and possible implications of this study have aroused the emotions of clinicians and researchers, pro and con. The investigation does demonstrate, however, that the label “schizophrenic” can itself have a negative effect not just on how people are viewed but also on how they themselves feel and behave.

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Family DysfunctioningTheorists have suggested for years that certain patterns of family interactions can promote—or at least sustain—schizophrenic symptoms. One leading theory has focused on double-bind communications.

DO DOUBLE-BIND COMMUNICATIONS CAUSE SCHIZOPHRENIA?One of the best-known family theories of schizophrenia is the double-bind hypothesis (Visser, 2003; Bateson et al., 1956). It says that some parents repeatedly communicate pairs of mutually contradictory messages that place children in so-called double-bind situations: the children cannot avoid displeasing their parents because nothing they do is right. In theory, the symptoms of schizophrenia represent the child’s attempt to deal with the double binds.

Double-bind messages typically consist of a verbal communication (the primary communication) and an accompanying—and contradictory—nonverbal communication (the metacommunication). If one person says to another, “I’m glad to see you,” yet frowns and avoids eye contact, the two messages are incongruent. According to this theory, a child who is repeatedly exposed to double-bind communications will adopt a special life strategy for coping with them. One strategy, for example, is always to ignore primary communications and respond only to metacommunications: be suspicious of what anyone is saying, wonder about its true meaning, and focus on clues only in gestures or tones. People who increasingly respond to messages in this way may progress toward paranoid schizophrenia.

The double-bind hypothesis is closely related to the psychodynamic notion of a schizophrenogenic mother. When Fromm-Reichmann described schizophrenogenic mothers as overprotective and rejecting at the same time, she was describing someone who is likely to send double-bind messages. Like the schizophrenogenic mother theory, the double-bind hypothesis has been popular in the clinical field over the years, but systematic investigations have not supported it (Chaika, 1990). In one study, clinicians analyzed letters written by parents to their children in the hospital (Ringuette & Kennedy, 1966). One group of parents had children with schizophrenia; the other had children with other disorders. On average, the letters of both groups of parents contained similar degrees of double-bind communication.

THE ROLE OF FAMILY STRESSAlthough the double-bind explanation and certain other family theories of schizophrenia have not received much research support, studies do suggest that schizophrenia, like a number of other mental disorders, is often linked to family stress (Cullen et al., 2014; Quah, 2014; Schiffman et al., 2002, 2001). Parents of people with schizophrenia often (1) display more conflict, (2) have more difficulty communicating with one another, and (3) are more critical of and overinvolved with their children than other parents.

Family theorists have long recognized that some families are high in expressed emotion—that is, members frequently express criticism, disapproval, and hostility toward each other and intrude on one another’s privacy. People who are trying to recover from schizophrenia are almost four times more likely to relapse if they live with such a family than if they live with one low in expressed emotion (Okpokoro, Adams, & Sampson, 2014). Do such findings mean that family dysfunctioning helps cause and maintain schizophrenia? Not necessarily. It is also the case that people with schizophrenia greatly disrupt family life (Friedrich et al., 2014). In so doing, they themselves may help produce the family problems that clinicians and researchers continue to observe (Hsiao et al., 2014; McFarlane, 2011).

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R. D. Laing’s ViewOne final sociocultural explanation of schizophrenia continues to have legions of supporters in the public at large despite the fact that it is controversial and largely untested by research. Famous clinical theorist R. D. Laing (1967, 1964, 1959) combined sociocultural principles with existential philosophy, arguing that schizophrenia is actually a constructive process in which people try to cure themselves of the confusion and unhappiness caused by their social environment. Laing believed that, left alone to complete this process, people with schizophrenia would indeed achieve a healthy outcome.

According to Laing’s existential principles, human beings must be in touch with their true selves in order to give meaning to their lives. Unfortunately, said Laing, this is difficult to do in present-day society. Other people’s expectations, demands, and standards require us to develop a false self rather than a true one. Moreover, Laing believed, some people—those who develop schizophrenia—have especially difficult obstacles to deal with. They experience a lifetime of confusing communications and demands from their families and community. Out of desperation they eventually undertake an inner search for strength and purpose. They withdraw from others and attend increasingly to their own inner cues in order to recover their wholeness as human beings. Laing argued that these people would emerge stronger and less confused if they were allowed to continue this inner search. Instead, as he saw it, society and its clinicians tell these people that they are sick, manipulate them into the role of patient, and subject them to treatments that actually produce further psychotic symptoms. In attempting to cure these people, he said, society dooms them to suspension in an inner world.

Most of today’s theorists reject Laing’s controversial notion that schizophrenia is constructive. For the most part, research simply has not addressed the issue. Laing’s ideas do not lend themselves to empirical research, and the existentialists who embrace his view typically have little confidence in traditional research approaches (Burston, 2000). It is also worth noting that many people with schizophrenia have themselves rejected the theory.

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