Schizophrenia

During their most severe periods, people with schizophrenia live in a private inner world, preoccupied with the strange ideas and images that haunt them. The word itself means “split” (schizo) “mind” (phrenia). It refers not to a multiple-personality split but rather to the mind’s split from reality, as shown in disturbed perceptions, disorganized thinking and speech, and diminished, inappropriate emotions. Schizophrenia is the chief example of a psychotic disorder. This group of disorders is marked by irrationality, distorted perceptions, and lost contact with reality.

As you can imagine, these characteristics profoundly disrupt relationships and work. Given a supportive environment and medication, over 40 percent of people with schizophrenia will have periods of a year or more of normal life experience (Jobe & Harrow, 2010). But only 1 in 7 experience a full and enduring recovery (Jääskeläinen et al., 2013).

Symptoms of Schizophrenia

14-14 What patterns of perceiving, thinking, and feeling characterize schizophrenia?

Schizophrenia comes in varied forms. Schizophrenia patients with positive symptoms—the presence of inappropriate behaviors—may experience hallucinations, talk in disorganized and deluded ways, and exhibit inappropriate laughter, tears, or rage. Those with negative symptoms—the absence of appropriate behaviors—may have toneless voices, expressionless faces, or mute and rigid bodies.

DISTURBED PERCEPTIONS People with schizophrenia sometimes have hallucinations—they see, feel, taste, or smell things that exist only in their minds. Usually, the hallucinations are sounds, often voices making insulting remarks or giving orders. The voices may tell the person that she is bad or that she must burn herself with a cigarette lighter. Imagine your own reaction if a dream broke into your waking consciousness, making it hard to separate your experience from your imagination. When the unreal seems real, the resulting perceptions are at best bizarre, at worst terrifying.

DISORGANIZED THINKING AND SPEECH Hallucinations are false perceptions. People with schizophrenia also have disorganized, fragmented thinking, which is often distorted by false beliefs called delusions. If they have paranoid tendencies, they may believe they are being threatened or pursued.

Maxine, a young woman with schizophrenia, believed she was Mary Poppins. Communicating with Maxine was difficult because her thoughts spilled out in no logical order. Her biographer, Susan Sheehan (1982, p. 25), observed her saying aloud to no one in particular, “This morning, when I was at Hillside [Hospital], I was making a movie. I was surrounded by movie stars…. I’m Mary Poppins. Is this room painted blue to get me upset? My grandmother died four weeks after my eighteenth birthday.”

Jumbled ideas may make no sense even within sentences, forming what is known as word salad. One young man begged for “a little more allegro in the treatment,” and suggested that “liberationary movement with a view to the widening of the horizon” will “ergo extort some wit in lectures.”

One cause of disorganized thinking may be a breakdown in selective attention. Normally, we have a remarkable capacity for giving our undivided attention to one set of sensory stimuli while filtering out others. People with schizophrenia cannot do this. Thus, tiny, irrelevant stimuli, such as the grooves on a brick or the inflections of a voice, may distract their attention from a bigger event or a speaker’s meaning. As one former patient recalled, “What had happened to me … was a breakdown in the filter, and a hodge-podge of unrelated stimuli were distracting me from things which should have had my undivided attention” (MacDonald, 1960, p. 218). This selective-attention difficulty is but one of dozens of cognitive differences associated with schizophrenia (Reichenberg & Harvey, 2007).

DIMINISHED AND INAPPROPRIATE EMOTIONS The expressed emotions of schizophrenia are often utterly inappropriate, split off from reality (Kring & Caponigro, 2010). Maxine laughed after recalling her grandmother’s death. On other occasions, she cried when others laughed, or became angry for no apparent reason. Others with schizophrenia lapse into an emotionless flat affect state of no apparent feeling. Most also have an impaired theory of mind—they have difficulty reading other people’s facial emotions and state of mind (Green & Horan, 2010; Kohler et al., 2010). These emotional deficiencies occur early in the illness and have a genetic basis (Bora & Pantelis, 2013).

Motor behavior may also be inappropriate and disruptive. Those with schizophrenia may experience catatonia, characterized by motor behaviors ranging from a physical stupor—motionless for hours—to senseless, compulsive actions, such as continually rocking or rubbing an arm, to severe and dangerous agitation.

Onset and Development of Schizophrenia

14-15 How do chronic and acute schizophrenia differ?

Nearly 1 in 100 people (about 60 percent of them men) will experience schizophrenia this year, joining an estimated 24 million people worldwide (Global, 2015). It typically strikes as young people are maturing into adulthood. It knows no national boundaries. Men tend to be struck earlier, more severely, and slightly more often (Aleman et al., 2003; Eranti et al., 2013; Picchioni & Murray, 2007).

When schizophrenia is a slow-developing process, called chronic schizophrenia, recovery is doubtful (WHO, 1979). This was the case with Maxine’s schizophrenia, which took a slow course, emerging from a long history of social inadequacy and poor school performance (MacCabe et al., 2008). Those with chronic schizophrenia often exhibit the persistent and incapacitating negative symptom of social withdrawal (Kirkpatrick et al., 2006). Men, whose schizophrenia develops on average four years earlier than women’s, more often exhibit negative symptoms and chronic schizophrenia (Räsänen et al., 2000).

When previously well-adjusted people develop schizophrenia rapidly following particular life stresses, this is called acute schizophrenia, and recovery is much more likely. People with acute schizophrenia often have positive symptoms that respond to drug therapy (Fenton & McGlashan, 1991, 1994; Fowles, 1992).

Understanding Schizophrenia

Schizophrenia is a dreaded psychological disorder. It is also one of the most heavily researched. Most studies now link it with abnormal brain tissue and genetic predispositions. Schizophrenia is a disease of the brain manifested in symptoms of the mind.

BRAIN ABNORMALITIES

14-16 What brain abnormalities are associated with schizophrenia?

Might chemical imbalances in the brain explain schizophrenia? Scientists have long known that strange behavior can have strange chemical causes. Have you ever heard the saying “mad as a hatter”? That phrase dates back to the behavior of British hatmakers whose brains were slowly poisoned as they used their tongue and lips to moisten the brims of mercury-laden felt hats (Smith, 1983). Could schizophrenia symptoms have a similar biochemical key? Scientists continue to track the mechanisms by which chemicals produce hallucinations and other symptoms.

DOPAMINE OVERACTIVITY One possible answer emerged when researchers examined schizophrenia patients’ brains after death. They found an excess number of dopamine receptors, including a sixfold excess for the dopamine receptor D4 (Seeman et al., 1993; Wong et al., 1986). The resulting hyper-responsive dopamine system could intensify brain signals, creating positive symptoms such as hallucinations and paranoia (Grace, 2010). Drugs that block dopamine receptors often lessen these symptoms. Drugs that increase dopamine levels, such as amphetamines and cocaine, sometimes intensify them (Seeman, 2007; Swerdlow & Koob, 1987).

ABNORMAL BRAIN ACTIVITY AND ANATOMY Abnormal brain activity accompanies schizophrenia. Some people diagnosed with schizophrenia have abnormally low brain activity in the brain’s frontal lobes, which help us reason, plan, and solve problems (Morey et al., 2005; Pettegrew et al., 1993; Resnick, 1992). The brain waves that reflect synchronized neural firing in the frontal lobes decline noticeably (Spencer et al., 2004; Symond et al., 2005).

One study took PET scans of brain activity while people were hallucinating (Silbersweig et al., 1995). When participants heard a voice or saw something, their brain became vigorously active in several core regions. One was the thalamus, the structure that filters incoming sensory signals and transmits them to the brain’s cortex. Another PET scan study of people with paranoia found increased activity in the amygdala, a fear-processing center (Epstein et al., 1998).

Many studies of people with schizophrenia have found enlarged, fluid-filled areas and a corresponding shrinkage and thinning of cerebral tissue (Goldman et al., 2009; Wright et al., 2000). People often inherit these brain differences. If one affected identical twin shows brain abnormalities, the odds are at least 1 in 2 that the other twin will have them (van Haren et al., 2012). Even people who will later develop the disorder may show these symptoms (Karlsgodt et al., 2010). The greater the brain shrinkage, the more severe the thought disorder (Collinson et al., 2003; Nelson et al., 1998; Shenton, 1992).

Two smaller-than-normal areas are the cortex, and the corpus callosum that connects the brain’s two hemispheres (Arnone et al., 2008). Another is the thalamus, which may explain why filtering sensory input and focusing attention can be difficult for people with schizophrenia (Andreasen et al., 1994; Ellison-Wright et al., 2008). The bottom line: Schizophrenia involves not one isolated brain abnormality but problems with several brain regions and their interconnections (Andreasen, 1997, 2001).

PRENATAL ENVIRONMENT AND RISK

14-17 What prenatal events are associated with increased risk of developing schizophrenia?

What causes brain abnormalities in people with schizophrenia? Some scientists point to mishaps during prenatal development or delivery (Fatemi & Folsom, 2009; Walker et al., 2010). Risk factors for schizophrenia include low birth weight, maternal diabetes, older paternal age, and oxygen deprivation during delivery (King et al., 2010). Famine may also increase risks. People conceived during the peak of World War II’s Dutch famine later developed schizophrenia at twice the normal rate. Those conceived during the famine of 1959 to 1961 in eastern China also displayed this doubled rate (St. Clair et al., 2005; Susser et al., 1996).

Let’s consider another possible culprit. Might a midpregnancy viral infection impair fetal brain development (Brown & Patterson, 2011)? To test this fetal-virus idea, scientists have asked these questions:

These converging lines of evidence suggest that fetal-virus infections contribute to the development of schizophrenia. This finding strengthens the U.S. government recommendation that “pregnant women need a flu shot” (CDC, 2014).

Why might a second-trimester maternal flu bout put fetuses at risk? Is the virus itself the culprit? The mother’s immune response to it? Medications taken (Wyatt et al., 2001)? Does the infection weaken the fetal brain’s supportive glial cells, leading to reduced synaptic connections (Moises et al., 2002)? In time, answers may become available.

GENETIC INFLUENCES

14-18 How do genes influence schizophrenia?

Fetal-virus infections may increase the odds that a child will develop schizophrenia. But many women get the flu during their second trimester of pregnancy, and only 2 percent of them bear children who develop schizophrenia. Why does prenatal exposure to the flu virus put some children at risk but not others? Might some people be more vulnerable because of an inherited predisposition? The evidence indicates that, Yes, some may inherit a predisposition to schizophrenia. For most people, the odds of being diagnosed with schizophrenia are only 1 in 100. For those who have a sibling or parent with the disorder, the odds increase to about 1 in 10. And if the affected sibling is an identical twin, the odds increase to nearly 1 in 2 (FIGURE 14.11). Those odds are unchanged even when the twins are reared apart (Plomin et al., 1997). (Only about a dozen such cases are on record.)

Remember, though, that identical twins share more than their genes. They also share a prenatal environment. About two-thirds also share a placenta and the blood it supplies; the other one-third have separate placentas. Shared placentas matter. If the co-twin of an identical twin with schizophrenia shared the placenta, the chances of developing the disorder are 6 in 10. If the identical twins had separate placentas, the co-twin’s chances of developing schizophrenia drop to 1 in 10 (Davis & Phelps, 1995; Davis et al., 1995; Phelps et al., 1997). Twins who share a placenta are more likely to share the same prenatal viruses. So perhaps shared germs as well as shared genes produce identical twin similarities.

Adoption studies help untangle genetic and environmental influences. Children adopted by someone who develops schizophrenia do not “catch” the disorder. Rather, adopted children have a higher risk if a biological parent has schizophrenia (Gottesman, 1991). Genes matter.

The search is on for specific genes that, in some combination, predispose schizophrenia-inducing brain abnormalities (FIGURE 14.12). (It is not our genes but our brains that directly control our behavior.) In the biggest-ever study of the genetics of psychiatric disorder, scientists from 35 countries pooled data from the genomes of 37,000 people with schizophrenia and 113,000 people without (Schizophrenia Working Group, 2014). They found 103 genome locations linked with the disorder. Some of these genes influence the activity of dopamine and other brain neurotransmitters. Others affect the production of myelin, a fatty substance that coats the axons of nerve cells and lets impulses travel at high speed through neural networks.

Although genes matter, the genetic formula is not as straightforward as the inheritance of eye color. The new result confirms other genome studies which show that schizophrenia is a group of disorders that are influenced by many genes, each with very small effects (Arnedo et al., 2015; International Schizophrenia Consortium, 2009).

As we have seen in so many different contexts, nature and nurture interact. Recall that epigenetic (literally “in addition to genetic”) factors influence whether or not genes will be expressed. Like hot water activating a tea bag, environmental factors such as viral infections, nutritional deprivation, and maternal stress can “turn on” the genes that put some of us at higher risk for this disorder. Identical twins’ differing histories in the womb and beyond explain why they may show differing gene expressions (Dempster et al., 2013; Walker et al., 2010). Our heredity and our life experiences work together. Neither hand claps alone.

Thanks to our expanding understanding of genetic and brain influences on maladies such as schizophrenia, the general public increasingly attributes psychiatric disorders to biological factors (Pescosolido et al., 2010).

* * *

Few of us can relate to the strange thoughts, perceptions, and behaviors of schizophrenia. Sometimes our thoughts jump around, but we rarely talk nonsensically. Occasionally we feel unjustly suspicious of someone, but we do not believe the world is plotting against us. Often our perceptions err, but rarely do we see or hear things that are not there. We feel regret after laughing at someone’s misfortune, but we rarely giggle in response to our own bad news. At times we just want to be alone, but we do not live in social isolation. However, millions of people around the world do talk strangely, suffer delusions, hear nonexistent voices, see things that are not there, laugh or cry at inappropriate times, or withdraw into private imaginary worlds. The quest to solve the cruel puzzle of schizophrenia continues, more vigorously than ever.

Dissociative Disorders

14-19 What are dissociative disorders, and why are they controversial?

Among the most bewildering disorders are the rare dissociative disorders, in which a person’s conscious awareness dissociates (separates) from painful memories, thoughts, and feelings. The result may be a fugue state, a sudden loss of memory or change in identity, often in response to an overwhelmingly stressful situation. Such was the case for one Vietnam veteran who was haunted by his comrades’ deaths, and who had left his World Trade Center office shortly before the 9/11 attack. Later, he disappeared. Six months later, when he was discovered in a Chicago homeless shelter, he reported no memory of his identity or family (Stone, 2006).

Dissociation itself is not so rare. Any one of us may have a fleeting sense of being unreal, of being separated from our body, of watching ourselves as if in a movie. A massive dissociation of self from ordinary consciousness occurs in dissociative identity disorder (DID), in which two or more distinct identities—each with its own voice and mannerisms—seem to control the person’s behavior. Thus, the person may be prim and proper one moment, loud and flirtatious the next. Typically, the original personality denies any awareness of the other(s).

People diagnosed with DID (formerly called multiple personality disorder) are rarely violent. But cases have been reported of dissociations into a “good” and a “bad” (or aggressive) personality—a modest version of the Dr. Jekyll-Mr. Hyde split immortalized in Robert Louis Stevenson’s story. One unusual case involved Kenneth Bianchi, accused in the “Hillside Strangler” rapes and murders of 10 California women. During a hypnosis session, Bianchi’s psychologist “called forth” a hidden personality: “I’ve talked a bit to Ken, but I think that perhaps there might be another part of Ken that … maybe feels somewhat differently from the part that I’ve talked to…. Would you talk with me, Part, by saying, ‘I’m here’?” Bianchi answered “Yes” and then claimed to be “Steve” (Watkins, 1984).

Speaking as Steve, Bianchi stated that he hated Ken because Ken was nice and that he (Steve), aided by a cousin, had murdered women. He also claimed Ken knew nothing about Steve’s existence and was innocent of the murders. Was Bianchi’s second personality a trick, simply a way of disavowing responsibility for his actions? Indeed, Bianchi—a practiced liar who had read about multiple personality in psychology books—was later convicted.

UNDERSTANDING DISSOCIATIVE IDENTITY DISORDER Skeptics have raised serious concerns about DID. First, they find it suspicious that the disorder has such a short and localized history. Between 1930 and 1960, the number of North American DID diagnoses averaged 2 per decade. By the 1980s, when the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders (DSM) contained the first formal code for this disorder, the number exploded to more than 20,000 (McHugh, 1995a). The average number of displayed personalities also mushroomed—from 3 to 12 per patient (Goff & Simms, 1993).

Second, note the skeptics, DID varies by culture. It is much less prevalent outside North America. In Britain, DID—which some have considered “a wacky American fad” (Cohen, 1995)—is rare. In India and Japan, it is essentially nonexistent (or at least unreported). Such findings, skeptics have noted, point to a disorder of suggestible, fantasy-prone people created by therapists in a particular social context (Giesbrecht et al., 2008, 2010; Lynn et al., 2014; Merskey, 1992).

Third, skeptics have asked, could DID be an extension of our normal capacity for personality shifts? Nicholas Spanos (1986, 1994, 1996) asked college students to pretend they were accused murderers being examined by a psychiatrist. Given the same hypnotic treatment Bianchi received, most spontaneously expressed a second personality. This discovery made Spanos wonder: Are dissociative identities simply a more extreme version of the varied “selves” we normally present—as when we display a goofy, loud self while hanging out with friends, and a subdued, respectful self around grandparents? If so, say the critics, clinicians who discover multiple personalities may merely have triggered role playing by fantasy-prone people. After all, clients do not enter therapy saying “Allow me to introduce myselves.” Rather, charge the critics, some therapists go fishing for multiple personalities: “Have you ever felt like another part of you does things you can’t control? Does this part of you have a name? Can I talk to the angry part of you?” Once patients permit a therapist to talk, by name, “to the part of you that says those angry things,” they begin acting out the fantasy. Like actors who lose themselves in their roles, vulnerable patients may “become” the parts they are acting out. The result may be the experience of another self.

Other researchers and clinicians believe DID is a real disorder. They find support for this view in the distinct body and brain states associated with differing personalities (Putnam, 1991). People with DID exhibit heightened activity in brain areas linked with the control and inhibition of traumatic memories (Elzinga et al., 2007). Abnormal brain anatomy can also accompany DID. Brain scans show shrinkage in areas that aid memory and detection of threat (Vermetten et al., 2006).

Both the psychodynamic and learning perspectives have interpreted DID symptoms as ways of coping with anxiety. Some psychodynamic theorists see them as defenses against the anxiety caused by unacceptable impulses. In this view, a second personality could allow the discharge of forbidden impulses. Learning theorists see dissociative disorders as behaviors reinforced by anxiety reduction.

Some clinicians include dissociative disorders under the umbrella of posttraumatic stress disorder. In this view, DID is a natural, protective response to traumatic experiences during childhood (Putnam, 1995; Spiegel, 2008). Many DID patients recall being physically, sexually, or emotionally abused as children (Gleaves, 1996; Lilienfeld et al., 1999). In one study of 12 murderers diagnosed with DID, 11 had suffered severe abuse, even torture, in childhood (Lewis et al., 1997). One had been set afire by his parents. Another had been used in child pornography and was scarred from being made to sit on a stove burner. Some critics wonder, however, whether vivid imagination or therapist suggestion contributed to such recollections (Kihlstrom, 2005).

So the debate continues. On one side are those who believe multiple personalities are the desperate efforts of people trying to detach from a horrific existence. On the other are skeptics who think DID is constructed out of the therapist-patient interaction and acted out by fantasy-prone, emotionally vulnerable people. If the skeptics’ view wins, predicted psychiatrist Paul McHugh (1995b), “this epidemic will end in the way that the witch craze ended in Salem. The [multiple personality phenomenon] will be seen as manufactured.”

Personality Disorders

14-20 What are the three clusters of personality disorders? What behaviors and brain activity characterize the antisocial personality?

The disruptive, inflexible, and enduring behavior patterns of personality disorders interfere with social functioning. These disorders tend to form three clusters, characterized by

ANTISOCIAL PERSONALITY DISORDER A person with antisocial personality disorder is typically a male whose lack of conscience becomes plain before age 15, as he begins to lie, steal, fight, or display unrestrained sexual behavior (Cale & Lilienfeld, 2002). About half of such children become antisocial adults—unable to keep a job, irresponsible as a spouse and parent, and violent or otherwise criminal (Farrington, 1991). (These people are sometimes called sociopaths or psychopaths.) They may show lower emotional intelligence—the ability to understand, manage, and perceive emotions (Ermer et al., 2012). Despite their remorseless and sometimes criminal behavior, criminality is not an essential component of antisocial behavior (Skeem & Cooke, 2010). Moreover, many criminals do not fit the description of antisocial personality disorder. Why? Because they show responsible concern for their friends and family members.

Antisocial personalities behave impulsively, and then feel and fear little (Fowles & Dindo, 2009). Their impulsivity can have violent, horrifying consequences (Camp et al., 2013). Consider the case of Henry Lee Lucas. He killed his first victim when he was 13. He felt little regret then or later. He confessed that, during his 32 years of crime, he had brutally beaten, suffocated, stabbed, shot, or mutilated some 360 women, men, and children. For the last six years of his reign of terror, Lucas teamed with Ottis Elwood Toole, who reportedly slaughtered about 50 people he “didn’t think was worth living anyhow” (Darrach & Norris, 1984).

UNDERSTANDING ANTISOCIAL PERSONALITY DISORDER Antisocial personality disorder is woven of both biological and psychological strands. Twin and adoption studies reveal that biological relatives of people with antisocial and unemotional tendencies are at increased risk for antisocial behavior (Frisell et al., 2012; Tuvblad et al., 2011). No single gene codes for a complex behavior such as crime. Molecular geneticists have, however, identified some specific genes that are more common in those with antisocial personality disorder (Gunter et al., 2010). There may be a genetic predisposition toward a fearless and uninhibited life. The genes that put people at risk for antisocial behavior also increase the risk for substance use disorder, which helps explain why these disorders often appear in combination (Dick, 2007).

Genetic influences, often in combination with negative environmental factors such as childhood abuse, family instability, or poverty, help wire the brain (Dodge, 2009). In people with antisocial criminal tendencies, the emotion-controlling amygdala is smaller (Pardini et al., 2014). The genetic vulnerability of people with antisocial and unemotional tendencies appears as low arousal. Awaiting events that most people would find unnerving, such as electric shocks or loud noises, they show little autonomic nervous system arousal (Hare, 1975; van Goozen et al., 2007). Long-term studies show that their stress hormone levels are lower than average in their early teens, before they have committed any crime (FIGURE 14.13). And children who are slow to develop conditioned fears at age 3 are in later years more likely to commit a crime (Gao et al., 2010). Other studies have found that preschool boys who later became aggressive or antisocial adolescents tended to be impulsive, uninhibited, unconcerned with social rewards, and low in anxiety (Caspi et al., 1996; Tremblay et al., 1994).

Traits such as fearlessness and dominance can be adaptive. If channeled in more productive directions, fearlessness may lead to athletic stardom, adventurism, or courageous heroism (Poulton & Milne, 2002; Smith et al., 2013). One analysis of 42 American presidents showed that they scored higher than the general population on such traits as fearlessness and dominance (Lilienfeld et al., 2012). Lacking a sense of social responsibility, the same disposition may produce a cool con artist or killer (Lykken, 1995).

With antisocial behavior, as with so much else, nature and nurture interact and the biopsychosocial perspective helps us understand the whole story. To explore the neural basis of antisocial personality disorder, scientists are trying to identify brain activity differences in antisocial criminals. Shown emotionally evocative photographs, such as a man holding a knife to a woman’s throat, criminals with antisocial personality disorder display blunted heart rate and perspiration responses, and less activity in brain areas that typically respond to emotional stimuli (Harenski et al., 2010; Kiehl & Buckholtz, 2010). They also have a larger and hyper-reactive dopamine reward system, which predisposes their impulsive drive to do something rewarding despite the consequences (Buckholtz et al., 2010; Glenn et al., 2010). One study compared PET scans of 41 murderers’ brains with those from people of similar age and sex. The murderers’ frontal lobes, an area that helps control impulses, displayed reduced activity (Raine, 1999, 2005; FIGURE 14.14). The reduced activation was especially apparent in those who murdered impulsively. In a follow-up study, researchers found that violent repeat offenders had 11 percent less frontal lobe tissue than normal (Raine et al., 2000). This helps explain another finding: People with antisocial personality disorder fall far below normal in aspects of thinking such as planning, organization, and inhibition, which are all frontal lobe functions (Morgan & Lilienfeld, 2000). Such data remind us: Everything psychological is also biological.

Eating Disorders

14-21 What are the three main eating disorders, and how do biological, psychological, and social-cultural influences make people more vulnerable to them?

Our bodies are naturally disposed to maintain a steady weight, including stored energy reserves for times when food becomes unavailable. But sometimes psychological influences overwhelm biological wisdom. This becomes painfully clear in three eating disorders:

A U.S. National Institute of Mental Health-funded study reported that, at some point during their lifetime, 0.6 percent of Americans met the criteria for anorexia, 1 percent for bulimia, and 2.8 percent for binge-eating disorder (Hudson et al., 2007). So, how can we explain these disorders?

UNDERSTANDING EATING DISORDERS Eating disorders are not (as some have speculated) a telltale sign of childhood sexual abuse (Smolak & Murnen, 2002; Stice, 2002). The family environment may influence eating disorders in other ways, however. For example, anorexia patients’ families tend to be competitive, high achieving, and protective (Berg et al., 2014; Pate et al., 1992; Yates, 1989, 1990). Those with eating disorders often have low self-evaluations, set perfectionist standards, fret about falling short of expectations, and are intensely concerned with how others perceive them (Brauhardt et al., 2014; Pieters et al., 2007; Yiend et al., 2014). Some of these factors also predict teen boys’ pursuit of unrealistic muscularity (Ricciardelli & McCabe, 2004).

Heredity also matters. Identical twins share these disorders more often than fraternal twins do (Culbert et al., 2009; Klump et al., 2009; Root et al., 2010). Scientists are now searching for culprit genes, which may influence the body’s available serotonin and estrogen (Klump & Culbert, 2007). Data from 15 studies indicate that having a gene that reduces available serotonin adds 30 percent to a person’s risk of anorexia or bulimia (Calati et al., 2011).

But eating disorders also have cultural and gender components. Ideal shapes vary across culture and time. In impoverished countries—where plumpness means prosperity and thinness can signal poverty or illness—bigger often seems better (Knickmeyer, 2001; Swami et al., 2010). Bigger does not seem better in Western cultures, where, according to 222 studies of 141,000 people, the rise in eating disorders in the last half of the twentieth century coincided with a dramatic increase in women having a poor body image (Feingold & Mazzella, 1998).

Those most vulnerable to eating disorders are also those (usually women or gay men) who most idealize thinness and have the greatest body dissatisfaction (Feldman & Meyer, 2010; Kane, 2010; Stice et al., 2010). Should it surprise us, then, that when women view real and doctored images of unnaturally thin models and celebrities, they often feel ashamed, depressed, and dissatisfied with their own bodies—the very attitudes that predispose eating disorders (Grabe et al., 2008; Myers & Crowther, 2009; Tiggeman & Miller, 2010)? Eric Stice and his colleagues (2001) tested this modeling idea by giving some adolescent girls (but not others) a 15-month subscription to an American teen-fashion magazine. Compared with those who had not received the magazine, vulnerable girls—defined as those who were already dissatisfied, idealizing thinness, and lacking social support—exhibited increased body dissatisfaction and eating disorder tendencies. Even ultra-thin models do not reflect the impossible standard of the classic Barbie doll, who had, when adjusted to a height of 5 feet 7 inches, a 32–16–29 figure (in centimeters, 82–41–73) (Norton et al., 1996).

There is, however, more to body dissatisfaction and anorexia than media effects (Ferguson et al., 2011). Peer influences, such as teasing, also matter. Nevertheless, the sickness of today’s eating disorders stems in part from today’s weight-obsessed culture—a culture that says “Fat is bad” in countless ways, that motivates millions of women to diet constantly, and that invites eating binges by pressuring women to live in a constant state of semistarvation. One former model recalled walking into a meeting with her agent, starving and with her organs failing as a result of anorexia (Caroll, 2013). Her agent’s greeting: “Whatever you are doing, keep doing it.”

If cultural learning contributes to eating behavior, then might prevention programs increase acceptance of one’s body? Reviews of prevention studies answer Yes. They seem especially effective if the programs are interactive and focused on girls over age 15 (Beintner et al., 2012; Stice et al., 2007; Vocks et al., 2010).

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The bewilderment, fear, and sorrow caused by psychological disorders are real. But as our next topic—therapy—shows, hope, too, is real.

Learning Objectives

Test Yourself by taking a moment to answer each of these Learning Objective Questions (repeated here from within the chapter). Research suggests that trying to answer these questions on your own will improve your long-term memory of the concepts (McDaniel et al., 2009).

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Terms and Concepts to Remember

Test yourself on these terms.

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Experience the Testing Effect

Test yourself repeatedly throughout your studies. This will not only help you figure out what you know and don’t know; the testing itself will help you learn and remember the information more effectively thanks to the testing effect.

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Use to create your personalized study plan, which will direct you to the resources that will help you most in .