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What Does It Mean to Have a Psychological Disorder?

Mental health experts define a psychological disorder as “a syndrome characterized by clinically significant disturbance in an individual’s cognition, emotion regulation, or behavior that reflects a dysfunction in the psychological, biological, or development processes underlying mental functioning” (APA, 2013, p. 20).But what does this definition actually mean?

Many behaviors considered abnormal are quite similar to normal behaviors. We all know what it feels like to be depressed, but how is that different from having a major depressive disorder? This chapter will help you understand the distinctions, but because those distinctions can be subtle, we also caution you against “first-year medical student’s disease,” or the sense that you have all the disorders that you are studying.

The study of psychological disorders is called abnormal psychology. It is surprisingly difficult, but necessary, for psychologists to agree on the differences between typical and abnormal behaviors because deciding that an individual’s behaviors and mental processes are abnormal is the first step toward labeling that person with a psychological disorder and providing treatment (see Figure 14.1).

Figure 14.1

A Continuum from Normal to Psychological Disorder.

Psychological disorders can be understood both categorically, which means that each has its own set of distinct characteristics used for diagnosis, and as part of a continuum from normal behavior to severely disordered behavior. The diagnostic criteria discussed in this chapter guide psychologists in their identification of the types and severity of disorders their patients and clients might have.

NORMAL

MILD

MODERATE

PSYCHOLOGICAL DISORDER—LESS SEVERE

PSYCHOLOGICAL DISORDER—MORE SEVERE

Emotions

Good alertness and positive emotional state.

Feeling sad or down temporarily, but not for long.

Feeling sad, but a strong positive experience such as a good grade could lift mood.

Intense sadness most of the day with some trouble concentrating and some loss of appetite.

Extreme sadness all of the time with great trouble concentrating and complete loss of appetite.

Cognitions

“I’m not getting the grades I want this semester, but I’ll keep trying to do my best.”

“I’m struggling at school this semester. I wish I could study better, or I’ll fail.”

“These bad grades really hurt. This may set me back for a while. I’m really worried.”

“I’m so worried about these grades that my stomach hurts. I don’t know what to do.”

“These bad grades just show what a failure I am at everything. There’s no hope; I’m not doing anything today.”

Behaviors

Going to classes and studying for the next round of tests. Talking to professors.

Going to classes with some trouble studying. Less contact with others.

Skipping a few classes and feeling somewhat unmotivated to study. Avoiding contact with professors and classmates.

Skipping most classes and unable to maintain eye contact with other people. Strong lack of motivation.

Unable to get out of bed, eat, or leave the house. Lack of energy and frequent crying.

Enlarge Table

Source: Adapted from C. A. Kearney, & T. J. Trull (2012). Abnormal Psychology and Life: A Dimensional Approach. Belmont, CA: Wadsworth/Cengage Learning.

We can start with the literal meaning of the word abnormal. In Latin, the prefix ab means “away from” and norma means “the rule.” In other words, abnormal behavior is literally behavior that is not typical, usual, or regular. This meaning implies a statistical definition of abnormality. By this definition, behaviors that most people do are normal, whereas behaviors that characterize a minority of people are abnormal.

This statistical approach has the advantage of being clear (see Figure 14.2). For example, intellectual disability is one of the categories in the Diagnostic and Statistical Manual of Mental Disorders, a handbook for diagnosis that we discuss in more detail later in the chapter. The diagnosis of intellectual disability relies heavily on statistics. A score of 70 or below on a standard IQ test is the typical cutoff for identifying an individual with intellectual disability (APA, 2013). Even in this relatively clear situation, however, the statistical approach represents merely a starting point. A diagnosis of intellectual disability also requires an individual to demonstrate difficulties with adaptive skills, which include factors such as communication, self-care, safety, and use of community resources.

Figure 14.2

Statistical Abnormality.

The word abnormal literally means “away from the rule.” Both intellectually gifted individuals, usually defined as having an IQ over 130, and individuals with intellectual disability, usually defined as having an IQ below 70, are equally “abnormal” in this statistical sense of the word. Academy Award–winning producer Quentin Tarantino (Pulp Fiction, Kill Bill, Django Unchained, and The Hateful Eight) has a reported IQ of 160. Although neither he nor his films are “typical,” we are unlikely to refer to Tarantino as “abnormal.” Statistics alone do not capture what we mean by abnormal behavior.

An illustration shows a bar graph that depicts Wechsler IQ scores from 55 to 145. Enlarge Image

MARKA/Alamy Stock Photo

A purely statistical approach has several major drawbacks. First, it implies a cultural specificity that we would like to avoid. Because most members of one culture may behave in ways different from those of people in another, the purely statistical approach to abnormality might result in different definitions of psychological disorder from one culture to the next. Second, a statistical definition fails to capture the distress that often accompanies a psychological disorder, both for the person experiencing the disorder and for those interacting with that person.

Our tolerance for people engaging in acts that are harmful to themselves is variable. For example, most states in the United States have prohibitions against committing suicide (the irony in prosecuting under such laws appears to have been lost on the legislators).

To address these concerns, we might suggest that abnormal behavior deviates from some ideal manner of behaving. This approach succeeds in capturing the general distress that most of us experience when observing or experiencing abnormal behavior. Unfortunately, this approach does nothing to avoid cross-cultural differences in defining disordered behavior. Different cultures are often characterized by diverse ideals. In Western nations, hearing voices that others cannot hear is generally considered abnormal. In other cultures, hearing voices may be viewed more positively, as a sign of religious giftedness (Al-Issa, 1977; Kurihara, Kato, Sakamoto, Reverger, & Kitamura, 2000). More troublesome is the simple fact that it is difficult, if not impossible, to reach consensus regarding what constitutes ideal behavior. People, including experts in psychology, have deeply divided value judgments regarding sexual conduct, recreational drug use, and a host of other activities.

A simple modification of this “deviation from the ideal” approach can help us to achieve some consensus. Behaviors that cause harm to others are viewed as less than ideal. Unless the person is acting defensively, most of us would agree that such behavior is negative and undesirable. We are also sympathetic to those who have conditions that cause harm to themselves.

We don’t know how many people have psychological disorders. A person can be diagnosed with comorbid disorders, which means more than one disorder occurs at the same time, so simply adding up the rates for each type of disorder is not a solution. Statistics can look different for different time frames. The estimate of the number of people who experience a psychological disorder during the previous year is around 26% (Kessler, Chiu, Demler, & Walters, 2005), but estimates of the number of people experiencing a disorder as least once during their lifetime can be much higher. In one longitudinal study of individuals from age 19–20 to age 50, the cumulative probability of experiencing at least one disorder was 73.9% (Angst et al., 2016). These numbers certainly challenge our conceptions of abnormal behavior as unusual.

Defining abnormal behavior as a deviation from what is considered ideal immediately runs into problems of cultural specificity. Behaviors like hearing voices that others cannot hear might be considered less than ideal in Western cultures but a gift in others. The ability to hear voices was considered an advantage for shamans, like the one represented transforming into his jaguar spirit companion in this Costa Rican piece from 1000–1500 CE.

A photo shows an image of a shaman transforming to its jaguar spirit in a Costa Rican piece.

Peter Horree/Alamy Stock Photo

We can combine the best aspects of each of these approaches to construct a formal definition of abnormal behavior: Abnormal behavior is distressing and harmful to self or others.

Although college students have the same rate of psychological disorders as their age peers who are not attending college, as shown in Figure 14.3, the rate of psychological disorders in young adults is higher than in the general population and appear to be increasing (Hunt & Eisenberg, 2010). Nearly half of the young adults under the age of 24 who were surveyed met criteria for at least one psychological disorder in the previous year, including 18% for a personality disorder, 12% for an anxiety disorder, and 11% for either major depressive disorder or bipolar disorder (Blanco et al., 2008). Each of these categories is discussed in more detail in this chapter.

Figure 14.3

Rates of Psychological Disorders in College Students.

Based on face-to-face interviews, college students and their same-age peers who do not attend college have a high rate (nearly 50%) of meeting the criteria for at least one psychological disorder over the past 12 months. College students and age peers not in college did not differ significantly in their rates of psychological disorder, with the exception of alcohol-use disorders, which were higher among those attending college.

A graph shows the percentage of psychological disorders in college students and non-college going teenagers. Data from the graph is as follows. Alcohol disorders are seen in 18% of non-college teens and 21% of college students. Personality disorders are seen in 22% of non-college teens and 18% of college students. Anxiety disorders are seen in 12% of non-college teens and 11% of college students. Mood disorders are seen in 12% of non-college teens and 11% of college students. Enlarge Image

PeopleImages/Getty Images Source: Adapted from “Mental Health of College Students and Their Non-College-Attending Peers: Results from the National Epidemiologic Study on Alcohol and Related Conditions,” by C. Blanco et al., 2008, Archives of General Psychiatry, 65(12), 1429–1437. doi:10.1001/archpsyc.65.12.1429.

How Are Psychological Disorders Diagnosed?

The first official effort in the United States to gather data on psychological disorders was the recording of a single category, “idiocy/insanity,” in the 1840 census (APA, 2000).

When you visit your physician or student health center complaining of a sore throat, your health care provider notes your symptoms, compares them to known categories of illness, swabs your throat for a sample, and then determines your diagnosis: You have strep throat. Based on that diagnosis, you are given a prescription for an antibiotic. Unlike medical illnesses, however, psychological disorders are diagnosed purely on the basis of observable behaviors. There are no blood tests, scans, or other medical diagnostic procedures that can be used to determine whether a person has a psychological disorder.

To promote consistency in the diagnosis of psychological disorders, mental health professionals typically refer to the Diagnostic and Statistical Manual of Mental Disorders (DSM), first published by the American Psychiatric Association (APA) in 1952. The current, fifth edition is known as DSM-5 (APA, 2013). A second classification system in wide use is the International Statistical Classification of Diseases and Related Health Problems, 10th edition (ICD-10), which was published by the World Health Organization (WHO) in 1992. An updated 11th edition is due to be published in 2018 (WHO, 2017). Professionals responsible for the DSM and ICD-10 classification systems have coordinated their efforts to reduce the differences between the two systems (APA, 2013).

The DSM is not without its critics. Beginning with DSM-III in 1980, some normal behaviors seem to have been categorized as abnormal by the system. Allen Frances, a psychiatrist who chaired the task force in charge of writing the DSM-IV (published in 1994), expressed concern that the committee’s well-meaning efforts had led to three “false epidemics”—attention deficit hyperactivity disorder (ADHD), autism, and childhood bipolar disorder—and that the DSM-5 was even worse (Frances, 2010). For example, the DSM-5 lists the following (very normal) behavior as a criterion for ADHD:

often avoids, dislikes, or is reluctant to engage in tasks that require sustained mental effort (e.g. schoolwork or homework; for older adolescents and adults, preparing reports, completing forms, reviewing lengthy papers). (APA, 2013, p. 59)

The Diagnostic and Statistical Manual of Mental Disorders (DSM) has undergone a number of revisions since its first edition in 1952. Over its history, the DSM has become less Freudian and more sensitive to cross-cultural issues. The DSM is published by the American Psychiatric Association.

The Diagnostic and Statistical Manual of Mental Disorders (DSM) has undergone a number of revisions since its first edition in 1952. Over its history, the DSM has become less Freudian and more sensitive to cross-cultural issues. The DSM is published by the American Psychiatric Association.

Studio 101/Alamy Stock Photo Source: Reprinted with permission from the DSM-5.

Despite its flaws, the DSM remains the most frequently used tool in the United States for the diagnosis of psychological disorders. Our discussion of types of psychological disorders, therefore, is grounded in the DSM system.

What Do the Psychological Perspectives Tell Us about Disorders?

We have seen many examples in this textbook of behaviors that are best understood when viewed from multiple perspectives. The study of psychological disorders provides yet another example of how an integration of multiple perspectives can be useful. This is particularly the case when considering the possible causes for abnormal behaviors.

What might an integrated approach to psychological disorder look like? First, we propose that the various perspectives discussed in this textbook (biological, clinical, developmental, cognitive, and social/personality) all have a great deal to say about disorders, but each has more to say about some disorders than about others. By considering the contributions of factors from multiple perspectives, we should have a greater appreciation of the complex interactions that occur among perspectives.

Philippe Pinel (1745–1826) is often called “the father of modern psychiatry.” After observing the more humane treatment of inmates by a former patient turned employee named Jean-Baptiste Pussin at Bicêtre Hospital outside Paris, Pinel followed Pussin’s example by removing the patients’ iron shackles. Instead of the usual “treatments” of the day—bleeding, purging, and blistering—Pinel made a practice of conversing with the patients regularly.

An illustration shows a painting depicting Philippe Pinel, the father of modern psychiatry, removing his patients’ iron shackles.

Philippe Pinel (1745–1826) releasing lunatics from their chains at the Salpetriere asylum in Paris in 1795 (colour litho), Robert-Fleury, Tony (1837–1912) (after)/Bibliotheque des Arts Decoratifs, Paris, France/Archives Charmet/The Bridgeman Art Library

In addition, an integrated perspective helps us understand the reciprocal relationships among factors leading to psychological disorders. Just as a person who is diagnosed with depression might show low levels of serotonin activity in the brain, being in a leadership position boosts a person’s serotonin levels. A simple biological explanation suggesting that chemical imbalances lead to depression, or a simple psychological explanation stating that people who feel powerless are more likely to be depressed, misses the nuances of these reciprocal relationships. The richer understanding of the causal factors leading to a psychological disorder pays off in the development of more effective treatments. Single-perspective thinking usually leads to single-perspective treatments. If you believe that depression is purely the result of chemical imbalances of the brain, then a simple prescription should do the trick. If you believe that hearing voices that others can’t hear is the result of childhood communication patterns, you will miss the opportunity to provide medication that can effectively end these troubling symptoms. Inclusive models describing the entire range of causal factors are more likely to result in effective treatments tailored to the needs of individuals.

Which Disorders Emerge in Childhood?

Many disorders might have roots in childhood but are more typically diagnosed in adolescence and adulthood. The DSM-5 uses the term neurodevelopmental disorders to refer to disorders that instead are diagnosed typically in childhood, yet often continue throughout the life span (APA, 2013). Two of these neurodevelopmental disorders are examined in this section: ASD and ADHD.

Autism Spectrum Disorder (ASD)

The word autism literally means “within oneself.” In 1943, psychiatrist Leo Kanner worked with a group of children who shared problems in social communication and interaction and restricted, repetitive patterns of behavior, interests, or activities. Kanner’s observations form the basis of our current diagnostic criteria for autism spectrum disorder (ASD; APA, 2013), which combines previous categories of autism and Asperger’s syndrome. ASD represents a spectrum because the severity of the observed deficits can vary widely from individual to individual. Adjustment can range from relatively normal, allowing independent living, to intellectual disability, requiring living with parents or in institutional settings.

Rates of ASD have been increasing rapidly over the last two decades (see Figure 14.4). Approximately 1 child out of every 68 has ASD, with rates for boys (1 in 42) significantly higher than rates for girls (1 in 189) (Christensen, 2016). Whether the rates are actually increasing or diagnostic criteria and awareness are changing remains unknown. In the United States, individuals can receive a medical diagnosis using the DSM-5 or be educationally verified by teams of school personnel (Ramsey, Kelly-Vance, Allen, Rosol, & Yoerger, 2016). These different methods of assessment produce different numbers, with higher rates of diagnosis in the educational than in the medical/psychological setting.

Figure 14.4

The Prevalence of ASD Appears to Be Increasing.

Rates of ASD continue to increase, but the reasons for this change remain a source of debate in the scientific community. It is possible that the rates are truly increasing, but greater awareness by parents and health care providers, relaxed applications of the diagnostic criteria, and improved availability of services might also be contributing to the observed change.

A graph shows the occurrence of ASD per 1000 children from 2000 - 2010. Data from the graph is as follows. 7 cases per 1000 children were reported in 2000. 7 cases per 1000 children were reported in 2002. 8 cases per 1000 children were reported in 2004. 9 cases per 1000 children were reported in 2008. 14 cases per 1000 children were reported in 2010.

Source: Centers for Disease Control and Prevention (CDC, 2014). Data and statistics. Retrieved from www.cdc.com/ncbddd/autism/data.html

Diagnosing ASD

Problems with social relatedness are at the core of this disorder, regardless of the individual’s level of intelligence and adjustment. Beginning in infancy, most children with ASD do not make eye contact or take pleasure in reciprocal games like peekaboo. Insight into the thoughts and points of view of others is particularly lacking. As discussed in Chapter 11, children develop a theory of mind by the time they are 3–4 years of age. Many researchers believe that a failure to develop a normal theory of mind is responsible for many of the social deficits observed in ASD (Baron-Cohen, 1991; Senju, Southgate, White, & Frith, 2009). Language skills of individuals with ASD can vary widely, from having no language abilities to delayed acquisition of language to normal skills (Ellis Weismer, Lord, & Esler, 2010). Even when language skills are relatively normal, though, individuals with ASD usually experience difficulty maintaining conversations with others because of their social skills deficits.

Individuals with ASD often object strenuously to changes in their environments and show a high level of repetitive, routine behavior. Rituals may include repetitive movements, such as rocking, hand flapping, head banging, and twirling. Other individuals may engage in extremely limited preoccupations, such as learning all models of cars ever made by Ford. One possible source of this ritualistic behavior is a general dysfunction in sensory networks. Most individuals with ASD show unusually increased or decreased sensitivity to stimuli (Lane, Young, Baker, & Angley, 2010). They may be relatively insensitive to pain or cold but distressed by normal sound levels (see Figure 14.5). Ritualistic behavior may control or override these disparate sensations.

Figure 14.5

Sensory Sensitivity Is Different in ASD.

Children with ASD often show differences from healthy children in their sensitivity to environmental stimuli. This graph shows the percentage of children with ASD whose scores on an instrument measuring sensitivity were the same as those of typical children, mildly different from those of typical children (between one and two standard deviations from the mean), and rare compared to those of typical children (more than two standard deviations from the mean). The domains measured included sensitivity to touch (tactile), sensitivity to taste and smell, sensitivity to movement (e.g., fear of falling), underresponsiveness (e.g., touches people), auditory filtering (e.g., fails to respond to name when called), low energy (e.g., tires easily), and visual or auditory (e.g., responds negatively to loud noises or bright lights).

A graph shows the percentage of children suffering from ASD with varying sensory domains. Enlarge Image

Source: Adapted from “Sensory Processing Subtypes in Autism: Association with Adaptive Behavior,” by A. Lane, R. Young, A. Baker, and M. Angley, 2010, Journal of Autism and Developmental Disorders, 40(1), 112–122. doi:10.1007/s10803-009-0840-2.

Causes of ASD

Although the causes of ASD remain somewhat mysterious and probably show variable patterns from case to case, scientists are making progress in their understanding. Family and twin studies provide strong evidence that ASD is influenced by genetics (Frazier et al., 2014). The concordance rate for ASD between identical twins may be 76% to 88%, and possibly more (Ronald & Hoekstra, 2011), which means that if one twin has ASD, the other twin has between a 76% and an 88% chance of also having ASD. Hundreds of genes are probably involved, and research attention is focusing on the expression of these genes during brain development (Sakai et al., 2011; Vorstman et al., 2017). Autopsies of the brains of people with ASD and people with no history of psychological disorder show dramatic differences (Voineagu et al., 2011). In the typical control brains, 174 genes were expressed differently in the frontal lobes than in the temporal lobes, but in the brains of people with ASD, no gene showed evidence of being expressed differently in these two areas.

Abnormalities in cortical development might lead to unusual minicolumns, vertical arrays of neurons perpendicular to the surface of the cerebral cortex that represent the smallest processing units of the brain. Individuals with ASD have narrower minicolumns containing normal numbers of cells, but spaced farther apart than those found in healthy individuals. These structural differences are consistent with a pattern of connectivity that favors detailed focus, which could produce the unusual interests and hobbies of people with ASD, over more global processing, like understanding the social environment (Opris & Casanova, 2014).

Narrow minicolumns similar to those found in the brains of people with ASD were observed in the brains of three distinguished scientists, none of whom had ASD symptoms, who donated their brains for scientific study. These similarities suggest that the minicolumn structure might account for the extreme focus of interests typical in ASD (Casanova, Switala, Trippe, & Fitzgerald, 2007). Outstanding scientists, like people with autism, have been known to study minute details for long periods of time.

Additional structural abnormalities in cases of ASD have been observed in the amygdala, hippocampus, and cerebellum (Barnea-Goraly et al., 2014; Stoodley, 2014). Researchers continue to debate a possible role in ASD for the mirror system, which has been implicated in empathy, imitation, and language (see Chapter 8).

Environmental factors probably interact with genetic factors associated with ASD during sensitive periods of brain development (Engel & Daniels, 2011). Parental age is also a risk factor, with older parents more likely than younger parents to give birth to a child with ASD (Grether, Anderson, Croen, Smith, & Windham, 2009; Shelton, Tancredi, & Hertz-Picciotto, 2010), although the effect is rather small. Prenatal exposure to infection and nutritional factors increase the risk for ASD (Hamlyn, Duhig, McGrath, & Scott, 2013). Use of common antidepressants known as selective serotonin reuptake inhibitors (SSRIs) during pregnancy is associated with a higher risk for producing a child with ASD (Boukhris, Sheehy, Mottron, & Bérard, 2016; Harrington, Lee, Crum, Zimmerman, & Hertz-Picciotto, 2014).

One of the unfortunate consequences of the uncertainty surrounding the causes of ASD has been the vulnerability of concerned parents seeking answers. In a paper later retracted by the British medical journal Lancet, unsubstantiated claims that the routine measles, mumps, and rubella vaccination caused ASD were published. Similar controversies ensued in the United States about thimerosal, a mercury-containing preservative used in some vaccines.

Minicolumns in the cerebral cortex function like the microprocessors in modern computers by serving as the basic unit that receives input, processes it, and responds. Individuals with ASD (lower image) have smaller minicolumns than do healthy controls (top image). What does this difference mean for information processing? Smaller minicolumns favor the process of discrimination, described in Chapter 8 as distinguishing among stimuli, while larger minicolumns favor generalization, or applying a response to similar stimuli. Behavioral domains that are difficult for people with ASD, such as language, face recognition, and following another person’s gaze, require more generalization than discrimination.

Two images show close-up photos of mini columns in the cerebral cortex of (a) healthy individuals and (b) individuals with autism.

Manuel F. Casanova, M.D., Department of Psychiatry and Behavioral Sciences, University of Louisville

In a meta-analysis involving over 1 million children, no relationship was found between ASD and vaccination in general, vaccination with the measles-mumps-rubella combination, or thimerosal (Taylor, Swerdfeger, & Eslick, 2014; see Figure 14.6). Despite the clear data and reassurances from medical experts, however, worried parents have withheld vaccinations from their children, leading to increasing numbers of cases of life-threatening, preventable diseases that had previously been believed to be under control. For example, in the first half of 2008, measles cases in the United States doubled compared to the rates observed between 2000 and 2007, and all cases involved unvaccinated school children (CDC, 2008).

Figure 14.6

Scientific Evidence Does Not Support a Role for Vaccinations in the Development of ASD.

Cumulative exposure to thimerosal, a mercury-containing preservative that has been used in vaccines, was the same for children diagnosed with ASD and healthy controls. Despite clear scientific evidence contradicting the link between vaccines and autism, many people have been influenced by celebrities such as model Jenny McCarthy and have withheld vaccinations from their children. As a result, communities are facing epidemics of clearly avoidable and disabling diseases, such as measles.

Attention Deficit Hyperactivity Disorder (ADHD)

Attention deficit hyperactivity disorder (ADHD) is perhaps one of the most contentious categories described in the DSM-5. The criteria for the disorder are difficult to distinguish from the behaviors of many typical young children. Because many children diagnosed with ADHD are treated with medication, the stakes for accurately diagnosing the condition are high indeed.

Diagnosing ADHD

One of the DSM-5 criteria for ADHD is “often fidgets with hands or feet or squirms in seat.” If you have visited an elementary school classroom lately, you might have noticed that most children are active. At what point does squirming become a psychological disorder requiring medication?

ADHD involves inattention and hyperactivity. Some individuals show both inattention and hyperactivity, but others show inattention without hyperactivity or vice versa (APA, 2013). The core feature of inattention is the inability to maintain sustained attention or on-task behavior for an age-appropriate length of time. This problem is evidenced in the diagnostic criteria for inattention, such as difficulties in following instructions, in organizing and completing work, and in avoiding careless mistakes. Children with hyperactivity express a high level of motor activity and find engaging in structured activities, such as waiting in line or sitting quietly in class, challenging. These children are noisy, active, and boisterous, and they often appear to take action without thinking it through. Even as adults, individuals who were diagnosed with ADHD as children have more traffic accidents than do people without the disorder (Barkley & Cox, 2007).

Many of these behaviors are also seen in children who do not have psychological disorders. Although the DSM-5 provides guidelines for distinguishing between normal and abnormal inattentiveness and hyperactivity, fewer than 40% of surveyed pediatricians reported using those criteria to evaluate cases of ADHD (Wasserman et al., 1999). More than half the children in a large sample who were receiving medication for ADHD did not meet even the relaxed diagnostic criteria for the disorder, let alone the carefully constructed criteria spelled out in the DSM-5 (Angold, Erkanli, Egger, & Costello, 2000).

In 2011, 11% of children between the ages of 4 and 17 years had been diagnosed with ADHD in the United States, representing an increase of 42% over rates of ADHD as recently as 2003 (Visser et al., 2014; see Figure 14.7). ADHD is diagnosed at least twice as frequently in males as in females, and females are more likely than males to be diagnosed with inattentiveness without hyperactivity (APA, 2013).

Figure 14.7

Diagnoses of ADHD in the United States.

The number of children diagnosed with ADHD in a 2007 report from the Centers for Disease Control and Prevention (CDC) varies dramatically by region in the United States, from a low of 5.6%–7.9% in the Southwest to 11%–15.9% in parts of the Midwest and Southeast. Reasons for these regional discrepancies are not clear, although low socioeconomic status is considered a risk factor for ADHD. The differences also might represent variations in how the diagnostic criteria are applied by local health care providers.

An illustration of the map of the U.S.A shows the percentage of children diagnosed with ADHD in each region. Data from the illustration is as follows. 14 - 15.9% of children were diagnosed in Louisiana, Alabama, and North Carolina. 11 - 13.9% of children were diagnosed in Oklahoma, Arkansas, Tennessee, Kentucky, Indiana, Ohio, West Virginia, Maryland, South Carolina, and Florida. 9.6 - 10.9% of children were diagnosed in Mississippi, Kansas, Missouri, Iowa, North Dakota, Wisconsin, Michigan, Pennsylvania, Maine, Vermont, Massachusetts, and Virginia. 8 - 9.5% of children were diagnosed in Georgia, New York, New Hampshire, Washington, Oregon, Idaho, Montana, Wyoming, South Dakota, and Nebraska. 5.6 - 7.9% of children were diagnosed in California, Arizona, Nevada, Utah, New Mexico, Colorado, Texas, Minnesota, and Illinois.

Causes of ADHD

The National Institute of Mental Health (NIMH, 2009, p. 3) concluded that “scientists are not sure what causes ADHD.” However, twin and adoption studies support a significant role for genetics in the development of ADHD. Heritability may be 70% or more (Faraone & Mick, 2010). Environmental factors might interact with genetic risk. Known environmental risks for ADHD are lead contamination, low birth weight, and prenatal exposure to tobacco, alcohol, and other drugs (Banerjee, Middleton, & Faraone, 2007).

All children can be active and noisy, but most usually learn quickly to restrict those behaviors to the right times and places. Children with ADHD often have trouble sitting quietly in class or waiting in line.

All children can be active and noisy, but most usually learn quickly to restrict those behaviors to the right times and places. Children with ADHD often have trouble sitting quietly in class or waiting in line.

Suzanne Tucker/ Shutterstock.com

ADHD is correlated with a number of structural and functional differences in the brain. The frontal lobes may be underactive in cases of ADHD (Barkley, 1997). Because the frontal lobes inhibit unwanted behavior, lower activity in this part of the brain may lead to hyperactivity and impulsivity. In addition, smaller volume in the amygdala, basal ganglia, and hippocampus, and the brain as a whole was observed in ADHD (Hoogman et al., 2017). Disruption in the corpus callosum, a major white-matter pathway connecting the two cerebral hemispheres, was correlated with the severity of symptoms in ADHD (Ameis et al., 2016).

The frontal lobes, and the prefrontal areas in particular, appear to mature more slowly in children with ADHD than in healthy controls (Shaw et al., 2007). Peak cortical thickness, a measure of brain maturity, occurred in healthy controls around the age of 7.5 years, but not until the age of 10.5 years in children with ADHD. Patterns of cortical thinning during adolescence predicted which individuals would continue to experience ADHD symptoms in adulthood and which would “outgrow” their symptoms (Shaw et al., 2013). White-matter circuits connecting the basal ganglia and the frontal lobes matured differently in people with and without ADHD (Helpern et al., 2011). A study of 1,713 individuals between the ages of 4 and 63 years with ADHD supported the idea that ADHD involves delays in maturation (Hoogman et al., 2017).

The parts of the brain implicated in ADHD, such as the prefrontal cortex and the basal ganglia, feature large amounts of dopamine activity. As will be shown in Chapter 15, most of the medications used to treat ADHD, such as methylphenidate (Ritalin), dextroamphetamine (Dexedrine or Dextrostat), or amphetamine salts (Adderall), act by boosting the activity of dopamine, suggesting that dopamine activity might be lower than usual in cases of ADHD (Volkow et al., 2009).

Among the many differences observed in the brains of children with ADHD compared to those of healthy controls is the rate of brain maturity, as measured by cortical thickening. These images demonstrate areas of the brain that developed later in children with ADHD than in healthy controls. Peak cortical thickness occurred around the age of 7.5 years in healthy children but was not seen in children with ADHD until an average age of 10.5 years. This finding implies that children with ADHD can be expected to lag their age peers in some tasks, but will eventually experience improvement.

An illustration shows three different images of brains of children with ADHD. Parts of the images are shaded to indicate delayed a growth of 0- 2 years and a darker shade to indicate a growth delay of over 2 years.

Source: From “Attention-Deficit/Hyperactivity Disorder Is Characterized by a Delay in Cortical Maturation,” by P. Shaw et al., 2007, Proceedings of the National Academy of Sciences, 104(49), 19649–19654. Copyright 2007 National Academy of Sciences. U.S.A.

As in ASD, myths about the causes of ADHD are common. Sugar is often blamed for hyperactive behavior, but evidence from carefully controlled studies does not support this belief (Milich, 1986; Wolraich, 1996). However, as discussed in Chapter 2, a well-controlled study suggested that combinations of common food additives made normal children demonstrate more hyperactivity (McCann et al., 2007). It is unlikely that “poor parenting” is responsible for these symptoms (Schroeder & Kelley, 2009). Parents, however, can learn new behavioral management techniques that greatly improve their child’s behavior.

What Is Schizophrenia?

Schizophrenia is not the most common type of disorder, affecting approximately 1% of the human population worldwide (Kessler et al., 2007), but it is one of the most dramatic. This condition influences and distorts a range of behaviors, including perception, cognition, movement, and emotion.

Symptoms of Schizophrenia

The DSM-5 places schizophrenia within a group of disorders called schizophrenia spectrum and other psychotic disorders (APA, 2013). Among the symptoms of schizophrenia are delusions, hallucinations, disorganized speech, and disorders of movement, which together indicate a state of psychosis. Schizophrenia also features negative symptoms (APA, 2013). Negative symptoms are behaviors that are seen in healthy people but not in patients. These symptoms include “diminished emotional expression and avolition” (APA, 2013, p. 88). A person with diminished emotional expression does not show typical outward signs of emotion, such as facial expressions and tone of voice, when an emotional response is expected. Avolition (the a means “lack of”) refers to a patient’s lack of “volition,” or goal-oriented behavior.

Delusions are defined as unrealistic beliefs. These may take a number of forms, including delusions of persecution by others (paranoia), feelings of unrealistic power or importance (grandiosity), or beliefs that others are directing one’s behavior (control).

Despite having been diagnosed with schizophrenia, John Nash shared the 1994 Nobel Prize in Economic Sciences. Nash was the subject of the 2001 film A Beautiful Mind, starring Russell Crowe. Sadly, both Nash and his wife were killed in a traffic accident in 2015.

Despite having been diagnosed with schizophrenia, John Nash shared the 1994 Nobel Prize in Economic Sciences. Nash was the subject of the 2001 film A Beautiful Mind, starring Russell Crowe. Sadly, both Nash and his wife were killed in a traffic accident in 2015.

Reuters/Corbis Wire/Corbis

Hallucinations are false perceptions. Although hallucinations may occur in several sensory modalities, most hallucinations in schizophrenia are auditory (Tien, 1991). Patients often report hearing voices, which can be accusatory or otherwise unpleasant, contributing to the distress associated with the disorder. Auditory hallucinations are not imaginary; they are real sensations correlated with increased activity in the primary auditory cortex of the temporal lobe (Dierks et al., 1999). Simply asking patients to remember or imagine sounds did not produce the type of activity in the auditory cortex seen during an auditory hallucination, indicating that the hallucination experience is different from simple memory or imagination.

A further symptom of schizophrenia involves disorganized patterns of speech. The patient jumps inexplicably from one topic to the next. People with schizophrenia appear to have difficulty inhibiting secondary meanings for some words (Titone, Levy, & Holzman, 2000). For example, the word jam can refer to either a fruit spread for toast or an impromptu musical session. Most people would use context (a conversation about food or music) to decide which meaning was appropriate. Patients with schizophrenia might not experience this filtering, leading their thoughts to jump from food to jazz and then on to other atypical connections.

This loosening of associations among ideas might occur because of the reduced latent inhibition in patients with schizophrenia, as discussed in Chapter 8. According to this argument, latent inhibition typically results in fewer associations being made to familiar stimuli. If you have had a lot of experience connecting jam and food, you are unlikely to consider other uses of the word jam. The person with schizophrenia, however, would be less inhibited in making connections among ideas, leading to trains of thought that seem bizarre to the rest of us.

Schizophrenia also features “grossly disorganized or abnormal motor behavior” (APA, 2013, p. 88). Some people may be unusually active, while others may barely move throughout an entire day. Unusual behaviors can occur, including grimaces and gestures. The maintenance of awkward or unusual body positions for hours at a time is called catatonia. People experiencing catatonia appear aware of their surroundings, but they don’t move. Most of us would find it difficult to sit for a few minutes, let alone hours, without shifting position.

Causes of Schizophrenia

Like many other types of psychological disorders, it is likely that schizophrenia has multiple sources of causality. No one factor is likely to be sufficient to produce the disorder.

Some people with schizophrenia experience catatonia, which means that they maintain awkward or unusual body positions for hours at a time.

A photo shows a rear view of a wheelchair with a man sitting in it presumably maintain an awkward body position.

Grunnitus Studio/Science Source

Biological Factors in Schizophrenia

Significant evidence points to a genetic vulnerability for schizophrenia. People with close family members who have been diagnosed with schizophrenia are more likely to develop the disorder themselves (Gottesman, 1991). If one identical twin is diagnosed with the disorder, the other twin has nearly a 50% lifetime risk of developing the disorder (see Figure 14.8). Comparisons of adopted children with their biological and adoptive parents also support a role for genetics (Kety, Rosenthal, Wender, & Schulsinger, 1968). A large number of genes have been implicated in the development of schizophrenia and overlap with those involved with bipolar disorder (Cross-Disorder Group of the Psychiatric Genomics Consortium, 2013; Owen, Craddock, & Jablensky, 2007). In one case of identical triplets, two of the triplets were diagnosed with schizophrenia and the third was diagnosed with bipolar disorder (McGuffin, Reveley, & Holland, 1982).

Figure 14.8

Genetics and Schizophrenia.

A person’s lifetime risk of developing schizophrenia increases when closely related family members have been diagnosed with the disorder, suggesting that genes play a significant role. Having a spouse with schizophrenia doubles the risk (from 1% to 2%), which probably reflects the tendency for people to marry others with whom they share similarities.

A graph depicts the risks of contracting schizophrenia through genetics. Data from the graph is as follows. Having both parents who are schizophrenic increases your chances by 46%. Having a schizophrenic identical twin increases your chances by 48%. Having one parent who is schizophrenic increases your chances by 5%. Having a schizophrenic fraternal twin increases your chances by 18%. Having a schizophrenic sibling increases your chances by 9%. Having a schizophrenic child increases your chances by 12%. Having a schizophrenic half sibling increases your chances by 5%. Having a schizophrenic grandchild increases your chances by 4%. Having a schizophrenic nephew or niece increases your chances by 3%. Having a schizophrenic uncle/aunt increases your chances by 2%. Having a schizophrenic first cousin increases your chances by 2%. Having a schizophrenic spouse increases your chances by 2%.

A number of structural and biochemical features accompany schizophrenia. One reliable correlate of schizophrenia is the presence of enlarged ventricles (Yotsutsuji et al., 2003). As discussed in Chapter 4, the ventricles are fluid-filled spaces in the brain that are not responsible for any particular behavior. The ventricles enlarge in response to any condition resulting in a loss of neural tissue in adjacent areas, so we can assume that schizophrenia is associated with neural degeneration.

Patients with schizophrenia demonstrate differences in brain activity compared with healthy people. For example, patients with schizophrenia often show a lower level of frontal lobe activity than that of healthy controls, both at rest and during effortful cognitive tasks (Berman, Torrey, Daniel, & Weinberger, 1992). The importance of the frontal lobes to higher cognitive processes and attention suggests that this difference would have significant influences on behavior, and lower levels of activity might account for the emotional disturbances and social withdrawal seen in these patients (Andreasen et al., 1992). Pathways in the brain that manage olfaction, or the sense of smell, travel through the frontal lobe. Lower overall frontal lobe activity might account for some difficulties that patients with schizophrenia experience with their sense of smell. In addition, distortions in the brain’s default mode network (see Chapter 6) predict the severity of patients’ psychotic symptoms (Garrity et al., 2007; Pomarol-Clotet et al., 2008).

Magnetic resonance images of the brains of a pair of identical twins show the differences in the size of the lateral ventricles (arrows) found in healthy people (left) and in people with schizophrenia (right). The ventricles are fluid-filled spaces and enlarge whenever significant numbers of nearby neurons have died.

Two images show the MRI scans of a pair of identical twins out of which one is healthy and the other is schizophrenic.

Courtesy D. R. Weinberger, NIMH, St. Elizabeth’s Hospital

Schizophrenia might involve abnormal brain development during adolescence. Teens typically experience a burst of cortical gray matter growth at puberty, followed by a wave of thinning of the gray matter extending into their early 20s. Healthy teens experience little loss of gray matter, whereas teens diagnosed with schizophrenia experience a loss that has been likened to a forest fire (Thompson et al., 2001).

Abnormalities in dopamine activity might be the major biochemical culprit in schizophrenia. Drugs that boost dopamine activity, such as amphetamine and the Parkinson’s disease treatment l-dopa, can produce hallucinations and paranoid delusions (Goetz, Leurgans, Pappert, Raman, & Stemer, 2001). Medications that block dopamine activity are usually quite effective in reducing these same symptoms.

However, this dopamine hypothesis of schizophrenia is not perfect. About one fourth of patients with schizophrenia do not respond favorably to drugs that reduce dopamine activity. In particular, the negative symptoms, such as diminished emotional expression, are not improved by these drugs (Goff & Evins, 1998; Kane & Freeman, 1994). In addition, medications that influence neurotransmitters other than dopamine are often effective (Syvalahti, 1994). Finally, phencyclidine (PCP, or angel dust) produces a syndrome that is quite similar to schizophrenia, although PCP acts on synapses using glutamate, not dopamine (Mössner et al., 2008). Because glutamate and dopamine are often important to the same brain circuits, it is possible that disturbances in one, the other, or both could lead to similar behavioral outcomes. Disturbances in the balance between brain excitation and inhibition, not related to any one neurochemical system, might also contribute to symptoms of schizophrenia (Jardri et al., 2016).

Environmental Factors in Schizophrenia

The nearly 50% concordance rate for schizophrenia in identical twins indicates a role for genetics in the development of the disorder. However, 50% is not 100%, and we need to account for the remaining factors.

When the brain activity of these identical twins is observed through brain imaging, the frontal lobes (arrows) appear to be more active in the healthy twin (left) than in the twin with schizophrenia (right). Red and yellow areas indicate greater activity, while green and dark areas are relatively inactive.

Two MRI scans show the brain activity of a pair of identical twins out of which one is healthy and the other is schizophrenic.

Photo courtesy of Daniel R. Weinberger, M.D. E. Fuller Torrey, M.D. (formerly of NIMH) and Karen Berman, M.D. NIMH Clinical Brain Disorders Branch Division of Intramural Research Programs, NIMH 1990.

Extreme stress contributes to the appearance and severity of schizophrenia among genetically vulnerable people. Schizophrenia appears nearly five times more frequently in members of lower than in those of higher socioeconomic groups (Keith, Regier, & Rae, 1991). The stress of living in poverty may trigger schizophrenia in vulnerable individuals. However, others argue that people who are susceptible to schizophrenia drift into lower-paying jobs. In other words, the disorder reduces the patients’ socioeconomic status, accounting for the higher rates of the disorder among the poor. Other stresses might accompany a person’s minority status in a community (Boydell, 2003). African immigrants living in London neighborhoods with the lowest proportions of African immigrants were twice as likely to be diagnosed with schizophrenia as African immigrants living in neighborhoods with the highest proportion of minorities (see Figure 14.9). The stress of social isolation because of minority status may have contributed to higher rates of schizophrenia.

Figure 14.9

Stress and Schizophrenia.

African immigrants living in South London were more likely to be diagnosed with schizophrenia if they lived in a predominantly White neighborhood than if they lived in a primarily non-White neighborhood; that is, if you divide neighborhoods into thirds based on the percentage of non-Whites (high, medium, and low), schizophrenia was more common in the middle and lower groups. An explanation based on self-selection (people choosing to live in each type of neighborhood) is unlikely in this case because nearly all the study participants were assigned to public housing units rather than choosing where to live. These findings suggest that the stress of minority status might contribute to higher risk for schizophrenia.

A graph shows the occurrence of schizophrenia per 100,000 in non-white ethnic minorities in neighborhoods. Enlarge Image

Janine Wiedel Photolibrary/Alamy Stock Photo Source: Adapted from “Incidence of Schizophrenia in Ethnic Minorities in London: Ecological Study into Interactions with Environment,” by J. Boydell et al., 2001, British Medical Journal, 323(7325), 1336–1338.

When we talk about environmental influences, factors such as stress come to mind (see Chapter 16). However, environmental influences also include biological variables such as the prenatal environment, including the pregnant woman’s exposure to viral illness. Another environmental variable that might trigger schizophrenia in genetically vulnerable individuals is marijuana use (Kelley et al., 2016; Marconi, Di Forti, Lewis, Murray, & Vassos, 2016). A 25-year longitudinal study concluded that cannabis use nearly doubled the risk of schizophrenia (Fergusson, Horwood, & Ridder, 2005). As mentioned in Chapter 11, adolescence is a time of brain growth, and heavy marijuana use during this period produces a reduction in white matter volume in the frontal lobes that might interact with a person’s genetic vulnerabilities for schizophrenia (Ho et al., 2011).

Teens typically experience a burst of gray matter growth at puberty, followed by a wave of gray matter thinning that extends into their early 20s. Compared with their healthy peers, teens diagnosed with schizophrenia experience much greater gray matter loss. Purple and red areas indicate the greatest amount of loss, followed by yellow and green areas.

An illustration depicts the rate of gray matter loss in normal teens and schizophrenic patients.

Source: From “Mapping Adolescent Brain Changes Reveals Dynamic Wave of Accelerated Gray Matter Loss in Very Early-Onset Schizophrenia,” by P. M. Thompson et. al., 2001, Proceedings of the National Academy of Sciences, 98(20), 11650–11655. Photo Courtesy of Paul Thompson/USC Institute for Neuroimaging and Informatics.

What Is Bipolar Disorder?

Bipolar disorder serves as a bridge between psychotic disorders, such as schizophrenia, and depressive disorders with respect to symptoms, family histories, and genetics (APA, 2013, p. 123). Bipolar disorder features a period of mania, which may or may not be followed by a period of depression. The symptoms of depression that can accompany bipolar disorder are identical to those used to diagnose major depressive disorder, which is described in What Is Major Depressive Disorder (MDD)? of this chapter.

A manic phase consists of “a distinct period of abnormally and persistently elevated, expansive, or irritable mood, abnormally and persistently increased goal-directed activity or energy” (APA, 2013, p. 124). Patients may demonstrate grandiosity, in which they feel unrealistically special or important. The person’s behavior, characterized by little need for sleep, rapid speech, difficulty concentrating, and rapidly shifting ideas, seems to be running at an abnormally high speed. Unlike many other disorders, however, mania increases productive, goal-directed behavior. However, because of the person’s tendency to meet the DSM-5 criterion for “excessive involvement in activities that have a high potential for painful consequences,” hospitalization is often necessary for the patient’s protection (APA, 2013, p. 124). Many variations occur in the timing and severity of the mania and depression observed in bipolar disorder.

Bipolar disorder affects approximately 2.6% of American adults each year (Kessler et al., 2005). Women are more likely to be diagnosed with bipolar disorder than men, by a ratio of approximately 3:2 (CDC, 2013). The average age of onset for bipolar disorder is 25 years. Children and youth under the age of 18 years with symptoms of bipolar disorder are diagnosed instead with disruptive mood dysregulation disorder (APA, 2013).

Actors, actresses, poets, painters, and musicians seem to have a disproportionate risk for bipolar disorder compared to people in other occupations. The late Carrie Fisher, of Star Wars fame, was outspoken regarding her challenges with bipolar disorder. We do not know whether having bipolar disorder allows these creative people to express emotion more effectively in their art, the arts are simply more welcoming than the corporate boardroom to those who have psychological disorders, or some combination of the two.

Actors, actresses, poets, painters, and musicians seem to have a disproportionate risk for bipolar disorder compared to people in other occupations. The late Carrie Fisher, of Star Wars fame, was outspoken regarding her challenges with bipolar disorder. We do not know whether having bipolar disorder allows these creative people to express emotion more effectively in their art, the arts are simply more welcoming than the corporate boardroom to those who have psychological disorders, or some combination of the two.

Cpuk/Alamy Stock Photo

Genetic predispositions play a significant role in bipolar disorder. Concordance rates between identical twins for bipolar disorder are commonly reported to be as high as 70% (Craddock & Sklar, 2013). Adoption studies also support a powerful role for genetics (Taylor, Faraone, & Tsuang, 2002). As mentioned previously, there is considerable overlap between the genes believed to play a role in bipolar disorder and those implicated in schizophrenia. Not surprisingly because of their genetic overlap, bipolar disorder shares some of the same abnormalities in brain structure and function as observed in schizophrenia (De Peri et al., 2012; Van Haren et al., 2012).

Among the many possible environmental factors that could interact with genes associated with bipolar disorder is diet. Omega-3 fatty acids, generally found in fish, may provide some protection from bipolar disorder (Noaghiul & Hibbeln, 2003). As shown in Figure 14.10, prevalence rates for bipolar disorder are highest in countries where fish is rarely consumed (such as Germany) and lowest in countries where fish is an important diet staple (such as Iceland). However, attempts to improve symptoms in patients with bipolar disorder by administering omega-3 supplements have produced weak results (Murphy et al., 2012; Stahl, Begg, Weisinger, & Sinclair, 2008). The impact of omega-3 fatty acids on a person’s vulnerability for bipolar disorder might be more important during prenatal development than later in life.

Figure 14.10

Bipolar Rates Are Lower in Nations with High Seafood Consumption.

Rates of bipolar disorder are negatively correlated with a nation’s consumption of seafood, suggesting that the omega-3 fatty acids contained in seafood might help prevent bipolar disorder.

A graph shows the percentage of bipolar cases in people high on seafood consumption. Bipolar cases are highest in areas that are lowest in seafood consumption such as Germany and lowest in areas that are highest in seafood consumption such as Iceland.

Source: Adapted from S. Noaghiul, & R. Hibbeln (2003). “Cross-National Comparisons of Seafood Consumption and Rates of Bipolar Disorders,” by S. Noaghiul and J. R. Hibbeln, 2003, American Journal of Psychiatry, 160(12), 2222–2227. doi:10.1176/appi.ajp.160.12.2222.

Many unanswered questions regarding the development of this condition remain. Bipolar disorder may be overrepresented in groups of people with artistic and creative talent (Jamison, 1993, 1995). Based on biographical accounts, the poet William Blake, the composers George Frideric Handel and Gustav Mahler, and visual artists Vincent van Gogh and Michelangelo might have had bipolar disorder. Many noted actors and actresses, including Carrie Fisher (Star Wars) and Vivien Leigh (Gone with the Wind), have been diagnosed with bipolar disorder. Comparisons between people with bipolar disorder and major depressive disorder and healthy people in creative and noncreative professions support this hypothesis. The patients with bipolar disorder scored similarly on tests of creativity to healthy people in creative occupations and higher than people with major depression and healthy people in noncreative occupations (Santosa et al., 2007). The parts of the brain that are affected in bipolar disorder are similar to those seen in cases of frontotemporal dementia. In both conditions, lower activity in these areas may reduce inhibition, which in turn leads to more creativity in some individuals (Seeley et al., 2008).

What Is Major Depressive Disorder (MDD)?

Although most of us experience the occasional “blues,” these feelings are not as severe or chronic as the depressed feelings that characterize major depressive disorder. According to the DSM-5, major depressive disorder (MDD) is characterized by depressed mood most of the day, nearly every day, for a period of at least 2 weeks (APA, 2013). Patients with MDD complain about feeling sad and empty, and periods of tearfulness are common. The DSM-5 also notes that MDD can produce anhedonia, or loss of pleasure. You are probably already familiar with the term hedonist, which refers to a person who is a pleasure seeker. Anhedonia refers to a person’s disinterest in activities that previously provided pleasure, such as sex, eating, or social activities.

To be diagnosed with MDD, a person must show at least five symptoms, one of which must be either depressed mood or anhedonia. The remaining symptoms can be divided into physical and cognitive groups. The physical symptoms of MDD are related to disturbances in autonomic function typically found in the presence of high levels of stress, described in Chapter 16. Appetite and sleep may be disturbed. Some patients experience a loss of appetite, whereas others begin to eat too much. As observed in Chapter 6, many patients with depression experience frequent wakefulness, whereas others experience oversleeping (more than 9 hours per night). Fatigue or restlessness may occur. Among the cognitive symptoms of depression are difficulty concentrating, feelings of hopelessness and worthlessness, and in some cases, thoughts of suicide (APA, 2013).

Prevalence of MDD

MDD is one of the most frequently diagnosed psychological disorders, affecting approximately 7% of the adult population each year (APA, 2013). MDD decreases with age, and people between the ages of 18 and 29 years have rates that are three times as high as those for people over the age of 60 years.

Women experience MDD more frequently than men do (Nolen-Hoeksema, 1987; Nolen-Hoeksema, Larson, & Grayson, 1999). This discrepancy between rates of MDD in men and those in women has been observed to be independent of race, ethnicity, social class, and country of residence (Strickland, 1992; Üstün, Ayuso-Mateos, Chatterji, Mathers, & Murray, 2004; see Figure 14.11). It is possible that female hormones participate in mood through some unknown mechanism. Mood disturbances can be associated with hormonal changes in women, including postpartum depression and mood changes accompanying menopause (Rapkin, Mikacich, Moatakef-Imani, & Rasgon, 2002). However, it is also possible that women are more likely than men to admit feeling depressed to others and to seek help with depression. Men may mask or cover their depressed mood by engaging in activities such as drinking alcohol.

Causes of MDD

Theories attempting to explain MDD range from the learning, social, and cognitive to the strictly biological. It is likely that some combination of these approaches provides the greatest understanding of the sources of depression.

Learning Explanations for MDD

According to learning theories, MDD occurs when a person experiences a reduction in positive reinforcement or an increase in negative outcomes. The loss of an important relationship can lead to depression because it reduces the amount of positive reinforcement that a person experiences.

A variation of the learning approach suggests that MDD results from learned helplessness, which is an application of operant conditioning. Instead of experiencing consequences that are clearly linked to your previous behavior (I studied hard and earned an A on my test), learned helplessness occurs when consequences of behavior appear to be random or uncontrolled (the amount of studying that I do doesn’t seem to make a difference in my test grades). If you get low grades whether you study hard or not, you might begin to believe that grades are outcomes that cannot be controlled. You may begin to feel helpless in preparing for your exams, and this belief in your own helplessness can lead to depression.

Cognitive Explanations for MDD

Cognitive theories frame depression as the result of a combination of negative thoughts about the self, the world, and the future (Beck, 1975). For example, students failing an exam might respond by doubting their academic abilities (self), assuming that they will fail the course (future), and deciding that they hate the class (world). The resulting dysfunctional beliefs would lead to depression. Beck’s view of the development of depression led directly to the use of cognitive therapies for depression, which are discussed in Chapter 15.

Rates of both depression and rumination drop in middle adulthood. Young adults often find it frustrating when they are trying to ruminate about problems with their parents, only to have their parents immediately shift into problem-solving mode. The young adult might not feel “ready” to fix the problem yet.

Another cognitive process that contributes to the development and maintenance of depressed mood is rumination (Nolen-Hoeksema, 2003). Susan Nolen-Hoeksema describes rumination in depression as “repetitively focusing on the fact that one is depressed; on one’s symptoms of depression; and on the causes, meanings, and consequences of symptoms of depression” (Nolen-Hoeksema, 1991, p. 569). Rumination can arise from attempts to gain insight into one’s problems, but too much rumination interferes with problem solving (Watkins & Brown, 2002). When rumination is encouraged by asking study participants to focus on their mood, they find it difficult to solve several types of problems (see Figure 14.12). When the participants are distracted from this inward focus by thinking about neutral topics (such as “think about the Statue of Liberty”), their problem-solving abilities improve immediately. Typically, rumination is correlated with negative outcomes, including delaying recovery from MDD during treatment (Siegle, Sagratti, & Crawford, 1999), predicting MDD following the death of a loved one (Nolen-Hoeksema & Girgus, 1994) and increasing a person’s likelihood to abuse alcohol (Nolen-Hoeksema, 2003). Responding to problems by either ruminating or distracting oneself might help explain some gender differences in depression rates. Women are more likely to ruminate than men, whose coping strategies are more likely to consist of finding distractions (Nolen-Hoeksema, 1987; Nolen-Hoeksema, Larson, & Grayson, 1999).

Figure 14.12

Rumination and Problem Solving.

Rumination and distraction were induced in depressed and nondepressed study participants, who then completed a problem-solving task. To induce rumination, participants were instructed to think about “what your feelings mean.” To induce distraction, participants were asked to think about “the shape of a large black umbrella.” Subsequently, all participants were asked to complete a problem-solving task. More errors occurred in the depressed ruminating group than in the other groups. These results suggest that rumination competes with other cognitive processes, possibly contributing to the problems with concentration experienced by people with depression.

A graph shows the occurrence of rumination and distraction in depressed and non depressed groups.

Source: Adapted from “Rumination and Executive Function in Depression: An Experimental Study,” by E. Watkins and R. G. Brown, 2002, Journal of Neurology, Neurosurgery, and Psychiatry, 72, 400–402.

MDD might be influenced by the types of attributions that a person makes (Abramson, Seligman, & Teasdale, 1978). As mentioned in Chapter 13, an attribution is a belief about causality. Attributions can vary along several dimensions (internal–external, stable–unstable, or global–specific), and making some types of attributions might predispose a person to depression. The internal–external dimension, which is similar to the locus of control discussed in Chapter 12, represents beliefs that outcomes occur because of personal effort or because of luck or chance. The stable–unstable dimension captures beliefs about whether circumstances can change. People make global attributions (I’m stupid) or more specific attributions (I’m not great in algebra, but I’m good at geometry). Overall, people who make internal, stable, and global attributions (what happens to me is my fault, circumstances never change, and I’m always this way) are more prone to depression. People with this attributional style earn lower grades in college, perform more poorly as sales representatives, and experience worse health (Seligman, 1987).

Social Explanations for MDD

Depression reflects feeling generally sad, whereas loneliness is a more social process that reflects feeling badly about the state of one’s relationships with others. The two states are related, yet they can occur independently. In older adults, loneliness increased depressive symptoms, but depression did not increase loneliness (Cacioppo, Hawkley, & Thisted, 2010). Social and evolutionary theories of depression and loneliness suggest that these states might promote an individual’s survival by promoting better relationships with others (Allen & Badcock, 2003; Cacioppo, Cacioppo, & Boomsma, 2014; Cacioppo, Hughes, Waite, Hawkley, & Thisted, 2006). Expressions of depression, such as sad facial expressions and crying, can serve as a safe call to others for connection and comforting responses in what the person may feel is a threatening social context. The response of others to these signals may foster the repair of frayed or broken social connections. Even when others do not respond, the symptoms of MDD may protect people from additional negative interactions by reducing their social activities.

Biological Explanations for MDD

The biological perspective identifies a number of factors contributing to depression. Twin studies suggest that the heritability of MDD is about 40% (Shi et al., 2011). A number of genes have been implicated in depression, including genes affecting serotonin function (Wurtman, 2005). A large body of research points to a role for serotonin in the regulation of mood. Serotonin’s role in brain systems responsible for mood, appetite, and sleep corresponds closely to the symptoms of MDD outlined in the DSM-5. Most effective medications for the treatment of depression boost the activity of serotonin at the synapse.

The anterior cingulate cortex plays an important role in regulating emotion through its connections with the amygdala. In many cases of MDD, the cingulate cortex appears to be overactive. Reductions in activity in the anterior cingulate cortex are correlated with improved mood following several different types of treatments.

MDD might be part of a larger disturbance in daily, or circadian, rhythms (Soria et al., 2010). Among the genes suspected of being related to MDD are those involved with circadian rhythms (see Chapter 6; also see McClung, 2007). The DSM-5 criteria for MDD include sleeping either less than or more than a normal number of hours per night (7–9 hours) (APA, 2013). People who are depressed spend too much time in rapid eye movement (REM) sleep, and most medications that are used to treat MDD reduce REM sleep (Rijnbeek, de Visser, Franson, Cohen, & van Gerven, 2003) (see Figure 14.14).

Figure 14.14

Major Depressive Disorder Disrupts Sleep.

These sleep records show the normal progression of non-REM and REM sleep (upper row) and the disrupted sleep of a person with major depressive disorder (bottom row). Note the lack of Stage 3 and 4 non-REM sleep and the frequent waking experienced by the person with depression (see Chapter 6 for more information).

Two graph chart shows the sleep patterns of a regular person and a patient with major depressive disorder. Data from the graph shows that normal progression of non-REM and REM sleep and the disrupted sleep of a patient. The various stages of sleep are Awake, REM sleep, NREM stage 1, NREM stage 2, NREM stage 3, and NREM stag 4. In typical people, stages progress from NREM stages 1 to 2, 2 to 3,3 to 4, then back to 2, then to REM sleep, then stage 2 to 3 to 4, and then stages 2 to 3 to 2 to REM sleep and then varying between stages 2 and REM sleep and finally being awake. While in patients with major depressive disorder, between each stage, there are periods of wakefulness and they do not progress from NREM stage 2 to stages 3 or 4. Enlarge Image

Source: Adapted from Gillin and Borbely (1985).

Connecting to Research

Recognition of Facial Expression by People with Depression

How does the world look to a person who is depressed? Does the experience of depression affect a person’s attention to negative stimuli? As mentioned in Chapter 7, positive and negative emotions often serve as guides to approach and avoidance behaviors (Davidson & Irwin, 1999). Because it is usually more important to survival that we avoid predators and other dangers than that we miss approaching something positive, such as a tasty food, we have a bias toward noticing the negative. If we’re experiencing an ongoing negative mood, does that have an effect on our sensitivities to positive and negative stimuli?

Among the important types of positive and negative stimuli that we need to process are facial expressions, because these are our clues to navigating the social environment successfully. Few of us would miss dramatic facial expressions, but the subtle ones require more attention (Gollan, McCloskey, Hoxha, & Coccaro, 2010).

The Question: How do people with depression compare to control participants in their ability to detect subtle facial expressions of emotion?

Methods

In one study, 88 participants, half of whom had been diagnosed with major depressive disorder but were not treated with medication, observed photographs of facial expressions on a computer screen. The photographs depicted four basic emotions: happiness, surprise, sadness, and harsh (a category that combined photos showing disgust, fear, and anger). The photos were morphed to present intensities ranging from mostly neutral to very intense (see Figure 14.13). A total of 200 photos were presented for only 0.5 second each. The participants pushed one of six keys to identify the emotion being expressed.

Figure 14.13

Heightened Sensitivity to Sad Expressions in Depression.

Study participants see one photo for only 0.5 second and must determine which of six emotions (happiness, surprise, sadness, disgust, fear, or anger) is being displayed. Morphed images are made by combining neutral (0%) and high-intensity (100%) images. Each emotion is easier to identify as its intensity increases. Participants with depression needed to see the same amount of intensity as healthy control participants before correctly identifying happy, surprised, or “harsh” facial expressions but needed to see less intensity than control participants before correctly identifying sad faces. This heightened sensitivity to the sad moods of others might reinforce the negative feelings of the person with depression.

A series of images and a graph shows us the intensity of sad expression and whether it can be called depressed or controlled.

Source: Reprinted from E. F. Coccaroemail, M. S. McCloskey, D. A. Fitzgerald, & K. L. Phan (2007). “Amygdala and Orbitofrontal Reactivity to Social Threat in Individuals with Impulsive Aggression,” by E. F. Coccaroemail, M. S. McCloskey, D. A. Fitzgerald, and K. L. Phan, 2007, Biological Psychiatry, 62(2), 168–178, with permission from Elsevier.

Ethics

It is unlikely that this procedure would produce distress in any of the participants. Because some of the participants are identified as having a psychological disorder, great care should be taken to protect their confidentiality.

Results

The participants with depression were more sensitive to sad faces than the control participants were. Specifically, all participants identified strong expressions of sadness, but participants with depression were more accurate in the identification of sadness when the emotion was expressed at a lower intensity. The groups were equally accurate in identifying the positive emotions (happiness and surprise) and the harsh emotions (fear, anger, and disgust). The severity of the participants’ depression was positively correlated with their accuracy in recognizing sad faces, but not with their accuracy in recognizing other emotional expressions.

Conclusions

The participants with depression were more sensitive to subtle expressions of sadness than the healthy control participants, and they were more likely to misidentify other emotional facial expressions as sad. In contrast, they were just as likely as control participants to misidentify happy, surprised, or harsh facial expressions. These findings indicate that people with depression not only are more likely to attend to sadder stimuli, but also might misinterpret neutral facial stimuli as sad. These tendencies might reinforce a person’s depressive feelings.

Major depressive disorder might result from more global problems with circadian or daily biorhythms. Among the candidate genes producing vulnerability for major depressive disorder are those that contribute to individual circadian rhythms.

Major depressive disorder might result from more global problems with circadian or daily biorhythms. Among the candidate genes producing vulnerability for major depressive disorder are those that contribute to individual circadian rhythms.

Saviour Mifsud/Alamy Stock Photo

Thinking Scientifically

What Should We Do when We Think that Somebody Might Commit Suicide?

People who are depressed sometimes think about suicide or even make suicide attempts (see Figure 14.15). Because of the greater prevalence of major depressive disorder in younger people, they are also at greater risk of suicide. Approximately 1,100 college students in the United States die in suicides each year, making suicide the second-leading cause of death in this population (Wilcox et al., 2010).

Figure 14.15

Depression Carries a High Risk of Suicidal Thinking and Suicide Attempts.

Among individuals experiencing at least one depressive episode in the past year, thinking seriously about suicide and making a suicide attempt happened frequently.

Two graphs show the tendencies for suicides in patients with major depressive disorder. Data from the first graph is as follows. In the age group of 18-20, 22.3% of people with major depressive disorder thought about committing suicide. In the age group of 21-24, 18% of people with major depressive disorder thought about committing suicide. In the age group of 25-34, 17.4% of people with major depressive disorder thought about committing suicide. In the age group of 35-54, 13.5% of people with major depressive disorder thought about committing suicide. In the age group of 55 and older, 7.3% of people with major depressive disorder thought about committing suicide. Data from the second graph is as follows. In the age group of 18-20, 19.5% of people with major depressive disorder attempted suicide. In the age group of 21-24, 14.7% of people with major depressive disorder attempted suicide. In the age group of 25-34, 10.9% of people with major depressive disorder attempted suicide. In the age group of 35-54, 9.8% of people with major depressive disorder attempted suicide. In the age group of 55 and older, 3.9% of people with major depressive disorder attempted suicide.

These statistics raise the possibility that as a college student, you may become aware of another person’s risk for suicide. According to the American Foundation of Suicide Prevention (AFSP), we can make ourselves aware of risk factors and take actions that might save a life (AFSP, 2014). Among these risk factors are evidence of a psychological disorder (particularly depression), alcohol and other substance use, a history of suicide attempts, being male (males have a three to five times higher suicide completion rate than females), and impulsivity. More immediately, the occurrence of a traumatic event (job loss or ending of an important relationship) might increase a person’s risk.

Approximately 75% of individuals who attempt suicide show prior evidence of their intent (AFSP, 2014). People might say things like “My family would be better off without me” or speak in ways that indicate they are saying good-bye. Purchasing a gun or putting one’s affairs in order (e.g., giving away prized possessions like a computer) is a sign of risk. Hopelessness, rage, or increased use of drugs and alcohol is also a common response to feeling suicidal (AFSP, 2014).

If you suspect someone of being suicidal, experts advise you to take the situation seriously. Yes, it may be true that some people “cry wolf,” but with a life at stake, who wants to take that chance? Be a good listener, and reassure the person that depression can be treated, that he or she is not alone, and that you care. If possible, take your friend to a place where professional help is available, whether that is your campus health center or a local emergency room. Do not leave the person alone, and remove possible means of self-harm (drugs, weapons, etc.). If such steps are not possible, call the National Suicide Prevention Lifeline (800-273-TALK) or 911.

Understanding that the combination of depression, impulsivity, alcohol or substance use, a history of suicide attempts, and a recent breakup or other traumatic event may increase the risk of suicide can help us offer support to a person who exhibits these characteristics.

Understanding that the combination of depression, impulsivity, alcohol or substance use, a history of suicide attempts, and a recent breakup or other traumatic event may increase the risk of suicide can help us offer support to a person who exhibits these characteristics.

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Stress and MDD

The experience of severe stress, whether arising from the death of a loved one, illness, or frustration of major life goals, frequently occurs immediately before the onset of a depressive episode (Brown & Harris, 1989; Mazure, 1998). The physical and cognitive responses to high levels of stress, such as difficulty sleeping or concentrating, are quite similar to the symptoms of MDD. However, most people exposed to such stressors do not respond by becoming depressed, reinforcing the complexity of the development of this disorder. MDD provides an example of a diathesis–stress model, which suggests that biological vulnerabilities for a disorder interact with a person’s experience with stress (Zubin & Spring, 1977).

Integrating the Perspectives

The picture emerging from this discussion of causal factors in MDD is complex. It is likely that underlying biological predispositions interact with cognitive patterns and life events to produce the disorder. For example, the serotonin transporter gene, which has been discussed previously in this book in the contexts of personality and responses to bullying, does little by itself to help predict a person’s risk for MDD. However, among people experiencing significant stress, those with one or two copies of the short version of the gene were more likely than those with two copies of the long version to develop MDD (Caspi et al., 2003).

A biological bridge is formed across the experience of stress, circadian rhythms, and the development of depression by the release of hormones (e.g., cortisol) when the stressor is perceived. Cortisol levels follow circadian patterns, with the greatest cortisol release in the early morning followed by a gradual drop throughout the day and evening. However, cortisol is also released at times of stress and helps prepare the body for fight or flight. Feedback loops involving the hippocampus usually prevent too great a release of cortisol. It is possible that in cases of MDD, this feedback loop is not working correctly, and cortisol levels remain high (Stokes, 1995). The body simply cannot maintain high levels of arousal indefinitely, and MDD may result.

What Is an Anxiety Disorder?

Anxiety disorders take many forms, but all share the core characteristic of unrealistic and counterproductive levels of anxiety. Anxiety has two major components:

(1)strong negative emotions and

(2)physical tension because of the anticipation of danger (Barlow, 1988).

It is the anticipation of danger that separates anxiety from the closely related emotion of fear. When we are afraid, usually something is happening in the present to produce that feeling, whereas anxiety occurs when we are worried about the future. Anxiety disorders represent an exaggeration of what is normally a useful response. Normal levels of anxiety protect us from engaging in risky activities, such as running up debts, driving recklessly, or failing to prepare for work or school, but excessive anxiety can cause a person to withdraw from positive life experiences and interpersonal relationships.

Nearly 30% of all Americans experience one or more anxiety disorders during their lifetime, although not all seek treatment (Kessler et al., 2005). People have genetic vulnerabilities for anxiety disorders in general, but not for specific types of anxiety disorders (DiLalla, Kagan, & Reznick, 1994). Families with members who are diagnosed with anxiety disorders are also likely to have members diagnosed with depression because these types of problems appear to share an underlying genetic basis (Weissman, Warner, Wickramaratne, Moreau, & Olfson, 1997). Anxiety disorders differ across gender and ethnicity for reasons that are not well understood. Women are more likely to be diagnosed with anxiety disorders than are men, and African Americans and Hispanics living in the United States are less likely to be diagnosed with anxiety disorders than are White Americans (Kessler et al., 2005).

Anxiety is the anticipation of danger. Normal levels of anxiety remind us about the risks of engaging in dangerous activities, but disordered anxiety can prevent people from engaging in everyday activities.

A photo shows a girl holding her hands tightly over mouth to cover it while a dentist tries to examine her.

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Evidence of a predisposition to anxiety appears early in life (Biederman et al., 1990; Schwartz, Snidman, & Kagan, 1999). As observed in Chapters 11 and 12, children’s initial temperament and reactivity can predispose them to anxiety. In one study, young infants showed consistent levels of response to novel stimuli, such as the smell of cotton swabs dipped in alcohol (Kagan, 1997), and 20% of the infants were classified as “high reactives” to these stimuli because of their increased activity and distress when novel stimuli were presented. When the high-reactive children were placed in a novel laboratory environment at the ages of 4–5 years, they still showed heightened levels of anxiety compared to their peers.

Diverse Voices in Psychology

Race, Ethnicity, and Prevalence of Psychological Disorders

For reasons that are currently poorly understood, a number of psychological disorders appear to be more prevalent in some racial and ethnic groups than others. Possible reasons for these discrepancies include true differences in risk, access to diagnosis and treatment, poverty, and willingness to discuss symptoms. As shown in Figure 14.16, differences appear between non-Hispanic Whites, Caribbean Blacks, and African Americans in prevalence for major depressive disorder (MDD) and general anxiety disorder (GAD) (Watkins, Assari, & Johnson-Lawrence, 2015). These data were collected from about 6,000 participants as part of the National Survey of American Life (NSAL).

Figure 14.16

Race, Ethnicity, and Prevalence of Depression and Anxiety.

Data from over 6,000 participants in a national sample showed that non-Hispanic Whites, Caribbean Blacks, and African Americans differ in their rates of major depressive disorder (MDD) and GAD. The exact reasons for these differences remain unknown but might include true differences in risk, access to diagnosis and treatment, poverty, and willingness to discuss symptoms.

Unlike most other types of psychological disorders, anxiety disorders do not impair a person’s ability to think realistically. In most cases, adults with anxiety disorders recognize that their circumstances do not warrant their extremely anxious responses, but they feel unable to control them. A person looking out the window of a skyscraper is well aware that the likelihood of falling is quite low, but feelings of fear and anxiety persist. Young children with anxiety disorders are usually less aware than adults that their feelings are unrealistic.