13 Psychological Disorders
Learning Objectives
By the end of this section, you will be able to:
- Understand the problems inherent in defining the concept of psychological disorder
- Describe what is meant by harmful dysfunction
- Identify the formal criteria that thoughts, feelings, and behaviors must meet to be considered abnormal and, thus, symptomatic of a psychological disorder
A psychological disorder is a condition characterized by abnormal thoughts, feelings, and behaviors. Psychopathology is the study of psychological disorders, including their symptoms, etiology (i.e., their causes), and treatment. The term psychopathology can also refer to the manifestation of a psychological disorder. Although consensus can be difficult, it is extremely important for mental health professionals to agree on what kinds of thoughts, feelings, and behaviors are truly abnormal in the sense that they genuinely indicate the presence of psychopathology. Certain patterns of behavior and inner experience can easily be labeled as abnormal and clearly signify some kind of psychological disturbance. The person who washes his hands 40 times per day and the person who claims to hear the voices of demons exhibit behaviors and inner experiences that most would regard as abnormal: beliefs and behaviors that suggest the existence of a psychological disorder. But, consider the nervousness a young man feels when talking to an attractive person or the loneliness and longing for home a first-year student experiences during her first semester of college—these feelings may not be regularly present, but they fall in the range of normal. So, what kinds of thoughts, feelings, and behaviors represent a true psychological disorder? Psychologists work to distinguish psychological disorders from inner experiences and behaviors that are merely situational, idiosyncratic, or unconventional.
Definition of a Psychological Disorder
Perhaps the simplest approach to conceptualizing psychological disorders is to label behaviors, thoughts, and inner experiences that are atypical, distressful, dysfunctional, and sometimes even dangerous, as signs of a disorder. For example, if you ask a classmate for a date and you are rejected, you probably would feel a little dejected. Such feelings would be normal. If you felt extremely depressed—so much so that you lost interest in activities, had difficulty eating or sleeping, felt utterly worthless, and contemplated suicide—your feelings would be atypical, would deviate from the norm, and could signify the presence of a psychological disorder. Just because something is atypical, however, does not necessarily mean it is disordered.
For example, only about 4% of people in the United States have red hair, so red hair is considered an atypical characteristic (Figure 15.2), but it is not considered disordered, it’s just unusual. And it is less unusual in Scotland, where approximately 13% of the population has red hair (“DNA Project Aims,” 2012). As you will learn, some disorders, although not exactly typical, are far from atypical, and the rates in which they appear in the population are surprisingly high.
If we can agree that merely being atypical is an insufficient criterion for having a psychological disorder, is it reasonable to consider behavior or inner experiences that differ from widely expected cultural values or expectations as disordered? Using this criterion, a person who walks around a subway platform wearing a heavy winter coat in July while screaming obscenities at strangers may be considered as exhibiting symptoms of a psychological disorder. Their actions and clothes violate socially accepted rules governing appropriate dress and behavior; these characteristics are atypical.
Cultural Expectations
Violating cultural expectations is not, in and of itself, a satisfactory means of identifying the presence of a psychological disorder. Since behavior varies from one culture to another, what may be expected and considered appropriate in one culture may not be viewed as such in other cultures. For example, returning a stranger’s smile is expected in the United States because a pervasive social norm dictates that we reciprocate friendly gestures. A person who refuses to acknowledge such gestures might be considered socially awkward—perhaps even disordered—for violating this expectation. However, such expectations are not universally shared. Cultural expectations in Japan involve showing reserve, restraint, and a concern for maintaining privacy around strangers. Japanese people are generally unresponsive to smiles from strangers (Patterson et al., 2007). Eye contact provides another example. In the United States and Europe, eye contact with others typically signifies honesty and attention. However, most Latin-American, Asian, and African cultures interpret direct eye contact as rude, confrontational, and aggressive (Pazain, 2010). Thus, someone who makes eye contact with you could be considered appropriate and respectful or brazen and offensive, depending on your culture (Figure 15.3).
Hallucinations (seeing or hearing things that are not physically present) in Western societies is a violation of cultural expectations, and a person who reports such inner experiences is readily labeled as psychologically disordered. In other cultures, visions that, for example, pertain to future events may be regarded as normal experiences that are positively valued (Bourguignon, 1970). Finally, it is important to recognize that cultural norms change over time: what might be considered typical in a society at one time may no longer be viewed this way later, similar to how fashion trends from one era may elicit quizzical looks decades later—imagine how a headband, legwarmers, and the big hair of the 1980s would go over on your campus today.
Harmful Dysfunction
If none of the criteria discussed so far is adequate by itself to define the presence of a psychological disorder, how can a disorder be conceptualized? Many efforts have been made to identify the specific dimensions of psychological disorders, yet none is entirely satisfactory. No universal definition of psychological disorder exists that can apply to all situations in which a disorder is thought to be present (Zachar & Kendler, 2007). However, one of the more influential conceptualizations was proposed by Wakefield (1992), who defined psychological disorder as a harmful dysfunction. Wakefield argued that natural internal mechanisms—that is, psychological processes honed by evolution, such as cognition, perception, and learning—have important functions, such as enabling us to experience the world the way others do and to engage in rational thought, problem-solving, and communication. For example, learning allows us to associate a fear with a potential danger in such a way that the intensity of fear is roughly equal to the degree of actual danger. Dysfunction occurs when an internal mechanism breaks down and can no longer perform its normal function. But, the presence of a dysfunction by itself does not determine a disorder. The dysfunction must be harmful in that it leads to negative consequences for the individual or for others, as judged by the standards of the individual’s culture. The harm may include significant internal anguish (e.g., high levels of anxiety or depression) or problems in day-to-day living (e.g., in one’s social or work life).
The American Psychiatric Association (APA) Definition
Many of the features of the harmful dysfunction model are incorporated into a formal definition of psychological disorder developed by the American Psychiatric Association (APA). According to the APA (2013), a psychological disorder is a condition that is said to consist of the following:
- There are significant disturbances in thoughts, feelings, and behaviors.
- The disturbances reflect some kind of biological, psychological, or developmental dysfunction.
- The disturbances lead to significant distress or disability in one’s life.
- The disturbances do not reflect expected or culturally approved responses to certain events.
Some believe that there is no essential criterion or set of criteria that can definitively distinguish all cases of disorder from nondisorder (Lilienfeld & Marino, 1999). In truth, no single approach to defining a psychological disorder is adequate by itself, nor is there universal agreement on where the boundary is between disordered and not disordered. From time to time we all experience anxiety, unwanted thoughts, and moments of sadness; our behavior at other times may not make much sense to ourselves or to others. These inner experiences and behaviors can vary in their intensity, but are only considered disordered when they are highly disturbing to us and/or others, suggest a dysfunction in normal mental functioning, and are associated with significant distress or disability in social or occupational activities.
Learning Objectives
By the end of this section, you will be able to:
- Explain why classification systems are necessary for the study of psychopathology
- Describe the basic features of the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5)
- Discuss changes in the DSM over time, including criticisms of the current edition
- Identify which disorders are generally the most common
A first step in the study of psychological disorders is carefully and systematically discerning significant signs and symptoms. How do mental health professionals ascertain whether or not a person’s inner states and behaviors truly represent a psychological disorder? Arriving at a proper diagnosis—that is, appropriately identifying and labeling a set of defined symptoms—is absolutely crucial. This process enables professionals to use a common language with others in the field and aids in communication about the disorder with the patient, colleagues, and the public. A proper diagnosis is an essential element to guide proper and successful treatment. For these reasons, classification systems that organize psychological disorders systematically are necessary.
The Diagnostic and Statistical Manual of Mental Disorders (DSM)
Although a number of classification systems have been developed over time, the one that is used by most mental health professionals in the United States is the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), published by the American Psychiatric Association (2013). (Note that the American Psychiatric Association differs from the American Psychological Association; both are abbreviated APA.) The first edition of the DSM, published in 1952, classified psychological disorders according to a format developed by the U.S. Army during World War II (Clegg, 2012). In the years since, the DSM has undergone numerous revisions and editions. The most recent edition, published in 2013, is the DSM-5 (APA, 2013). The DSM-5 includes many categories of disorders (e.g., anxiety disorders, depressive disorders, and dissociative disorders). Each disorder is described in detail, including an overview of the disorder (diagnostic features), specific symptoms required for diagnosis (diagnostic criteria), prevalence information (what percent of the population is thought to be afflicted with the disorder), and risk factors associated with the disorder. Some believe that establishing new diagnoses might over pathologize the human condition by turning common human problems into mental illnesses (The Associated Press, 2013). Indeed, the finding that nearly half of all Americans will meet the criteria for a DSM disorder at some point in their life (Kessler et al., 2005) likely fuels much of this skepticism. The DSM-5 is also criticized on the grounds that its diagnostic criteria have been loosened, thereby threatening to “turn our current diagnostic inflation into diagnostic hyperinflation” (Frances, 2012, para. 22).
The Compassionate View of Psychological Disorders
As these disorders are outlined, please bear two things in mind. First, remember that psychological disorders represent extremes of inner experience and behavior. If, while reading about these disorders, you feel that these descriptions begin to personally characterize you, do not worry—this moment of enlightenment probably means nothing more than you are normal. Each of us experiences episodes of sadness, anxiety, and preoccupation with certain thoughts—times when we do not quite feel ourselves. These episodes should not be considered problematic unless the accompanying thoughts and behaviors become extreme and have a disruptive effect on one’s life. Second, understand that people with psychological disorders are far more than just embodiments of their disorders. We do not use terms such as schizophrenics, depressives, or phobics because they are labels that objectify people who suffer from these conditions, thus promoting biased and disparaging assumptions about them. It is important to remember that a psychological disorder is not what a person is; it is something that a person has—through no fault of his or her own. As is the case with cancer or diabetes, those with psychological disorders suffer debilitating, often painful conditions that are not of their own choosing. These individuals deserve to be viewed and treated with compassion, understanding, and dignity.
Learning Objectives
By the end of this section, you will be able to:
- Discuss supernatural perspectives on the origin of psychological disorders, in their historical context
- Describe modern biological and psychological perspectives on the origin of psychological disorders
- Identify which disorders generally show the highest degree of heritability
- Describe the diathesis-stress model and its importance to the study of psychopathology
Scientists, mental health professionals, and cultural healers may adopt different perspectives in attempting to understand or explain the underlying mechanisms that contribute to the development of a psychological disorder. The specific perspective used in explaining a psychological disorder is extremely important. Each perspective explains psychological disorders, their causes or etiology, and effective treatments from a different viewpoint. Different perspectives provide alternate ways for how to think about the nature of psychopathology.
Biological Perspectives on Psychological Disorders
The biological perspective views psychological disorders as linked to biological phenomena, such as genetic factors, chemical imbalances, and brain abnormalities; it has gained considerable attention and acceptance in recent decades (Wyatt & Midkiff, 2006). Evidence from many sources indicates that most psychological disorders have a genetic component; in fact, there is little dispute that some disorders are largely due to genetic factors. The graph in Figure 15.8 shows heritability estimates for schizophrenia.
Findings such as these have led many of today’s researchers to search for specific genes and genetic mutations that contribute to mental disorders. Also, sophisticated neural imaging technology in recent decades has revealed how abnormalities in brain structure and function might be directly involved in many disorders, and advances in our understanding of neurotransmitters and hormones have yielded insights into their possible connections. The biological perspective is currently thriving in the study of psychological disorders.
The Diathesis-Stress Model of Psychological Disorders
Despite advances in understanding the biological basis of psychological disorders, the psychosocial perspective is still very important. This perspective emphasizes the importance of learning, stress, faulty and self-defeating thinking patterns, and environmental factors. Perhaps the best way to think about psychological disorders, then, is to view them as originating from a combination of biological and psychological processes. Many develop not from a single cause, but from a delicate fusion between partly biological and partly psychosocial factors.
The diathesis-stress model (Zuckerman, 1999) integrates biological and psychosocial factors to predict the likelihood of a disorder. This diathesis-stress model suggests that people with an underlying predisposition for a disorder (i.e., a diathesis) are more likely than others to develop a disorder when faced with adverse environmental or psychological events (i.e., stress), such as childhood maltreatment, negative life events, trauma, and so on. A diathesis is not always a biological vulnerability to an illness; some diatheses may be psychological (e.g., a tendency to think about life events in a pessimistic, self-defeating way).
The key assumption of the diathesis-stress model is that both factors, diathesis, and stress, are necessary for the development of a disorder. Different models explore the relationship between the two factors: the level of stress needed to produce the disorder is inversely proportional to the level of diathesis.
Learning Objectives
By the end of this section, you will be able to:
- Distinguish normal anxiety from pathological anxiety
- List and describe the major anxiety disorders, including their main features and prevalence
- Describe basic psychological and biological factors that are suspected to be important in the etiology of anxiety disorder
Everybody experiences anxiety from time to time. Although anxiety is closely related to fear, the two states possess important differences. Fear involves an instantaneous reaction to an imminent threat, whereas anxiety involves apprehension, avoidance, and cautiousness regarding a potential threat, danger, or other negative event (Craske, 1999). While anxiety is unpleasant to most people, it is important to our health, safety, and well-being. Anxiety motivates us to take actions—such as preparing for exams, watching our weight, showing up to work on time—that enable us to avert potential future problems. Anxiety also motivates us to avoid certain things—such as running up debts and engaging in illegal activities—that could lead to future trouble. Most individuals’ level and duration of anxiety approximates the magnitude of the potential threat they face. For example, suppose a student who came to the U.S. as a “Dreamer” (someone whose parents didn’t lawfully immigrate) is concerned about the possibility of being unable to continue in the university program or of losing access to academic financial aid, due to changes and litigation around the Deferred Action for Childhood Arrivals (DACA) program. This person likely would experience anxiety of greater intensity and duration than would a 21-year-old junior who entered college as a birthright citizen. Some people experience anxiety that is excessive, persistent, and greatly out of proportion to the actual threat; if one’s anxiety has a disruptive influence on one’s life, this is a strong indicator that the individual is experiencing an anxiety disorder.
Anxiety disorders are characterized by excessive and persistent fear and anxiety, and by related disturbances in behavior (APA, 2013). Although anxiety is universally experienced, anxiety disorders cause considerable distress. As a group, anxiety disorders are common: approximately 25%–30% of the U.S. population meets the criteria for at least one anxiety disorder during their lifetime (Kessler et al., 2005). Also, these disorders appear to be much more common in women than they are in men; within a 12-month period, around 23% of women and 14% of men will experience at least one anxiety disorder (National Comorbidity Survey, 2007). Anxiety disorders are the most frequently occurring class of mental disorders and are often comorbid with each other and with other mental disorders (Kessler, Ruscio, Shear, & Wittchen, 2009).
Specific Phobia
Phobia is a Greek word that means fear. A person diagnosed with a specific phobia (formerly known as simple phobia) experiences excessive, distressing, and persistent fear or anxiety about a specific object or situation (such as animals, enclosed spaces, elevators, or flying) (APA, 2013). Even though people realize their level of fear and anxiety in relation to the phobic stimulus is irrational, some people with a specific phobia may go to great lengths to avoid the phobic stimulus (the object or situation that triggers the fear and anxiety). Typically, the fear and anxiety a phobic stimulus elicits are disruptive to the person’s life. For example, a man with a phobia of flying might refuse to accept a job that requires frequent air travel, thus negatively affecting his career. Clinicians who have worked with people who have specific phobias have encountered many kinds of phobias, some of which are shown in Table 15.1.
| Specific Phobias | |
|---|---|
| Phobia | Feared Object or Situation |
| Acrophobia | heights |
| Aerophobia | flying |
| Arachnophobia | spiders |
| Claustrophobia | enclosed spaces |
| Cynophobia | dogs |
| Hematophobia | blood |
| Ophidiophobia | snakes |
| Taphophobia | being buried alive |
| Trypanophobia | injections |
| Xenophobia | strangers |
Specific phobias are common; in the United States, around 12.5% of the population will meet the criteria for a specific phobia at some point in their lifetime (Kessler et al., 2005). One type of phobia, agoraphobia, is listed in the DSM-5 as a separate anxiety disorder. Agoraphobia, which literally means “fear of the marketplace,” is characterized by intense fear, anxiety, and avoidance of situations in which it might be difficult to escape or receive help if one experiences symptoms of a panic attack (a state of extreme anxiety that we will discuss shortly). These situations include public transportation, open spaces (parking lots), enclosed spaces (stores), crowds, or being outside the home alone (APA, 2013). About 1.4% of Americans experience agoraphobia during their lifetime (Kessler et al., 2005).
Acquisition of Phobias Through Learning
Many theories suggest that phobias develop through learning. Rachman (1977) proposed that phobias can be acquired through three major learning pathways. The first pathway is through classical conditioning. As you may recall, classical conditioning is a form of learning in which a previously neutral stimulus is paired with an unconditioned stimulus (UCS) that reflexively elicits an unconditioned response (UCR), eliciting the same response through its association with the unconditioned stimulus. The response is called a conditioned response (CR). For example, a child who has been bitten by a dog may come to fear dogs because of a past association with pain. In this case, the dog bite is the UCS and the fear it elicits is the UCR. Because a dog was associated with the bite, any dog may come to serve as a conditioned stimulus, thereby eliciting fear; the fear the child experiences around dogs, then, becomes a CR.
The second pathway of phobia acquisition is through vicarious learning, such as modeling. For example, a child who observes his cousin react fearfully to spiders may later express the same fears, even though spiders have never presented any danger to him. This phenomenon has been observed in both humans and nonhuman primates (Olsson & Phelps, 2007). A study of laboratory-reared monkeys readily acquired a fear of snakes after observing wild-reared monkeys react fearfully to snakes (Mineka & Cook, 1993).
The third pathway is through verbal transmission or information. For example, a child whose parents, siblings, friends, and classmates constantly tell her how disgusting and dangerous snakes are may come to acquire a fear of snakes.
Interestingly, people are more likely to develop phobias of things that do not represent much actual danger to themselves, such as animals and heights, and are less likely to develop phobias toward things that present legitimate danger in contemporary society, such as motorcycles and weapons (Öhman & Mineka, 2001). Why might this be so? One theory suggests that the human brain is evolutionarily predisposed to more readily associate certain objects or situations with fear (Seligman, 1971). This theory argues that throughout our evolutionary history, our ancestors associated certain stimuli (e.g., snakes, spiders, heights, and thunder) with potential danger. As time progressed, the mind has become adapted to more readily develop fears of these things than of others. Experimental evidence has consistently demonstrated that conditioned fears develop more readily to fear-relevant stimuli (images of snakes and spiders) than to fear-irrelevant stimuli (images of flowers and berries) (Öhman & Mineka, 2001). Such prepared learning has also been shown to occur in monkeys. In one study (Cook & Mineka, 1989), monkeys watched videotapes of model monkeys reacting fearfully to either fear-relevant stimuli (toy snakes or a toy crocodile) or fear-irrelevant stimuli (flowers or a toy rabbit). The observer monkeys developed fears of the fear-relevant stimuli but not the fear-irrelevant stimuli.
Social Anxiety Disorder
Social anxiety disorder (formerly called social phobia) is characterized by extreme and persistent fear or anxiety and avoidance of social situations in which the person could potentially be evaluated negatively by others (APA, 2013). As with specific phobias, social anxiety disorder is common in the United States; a little over 12% of all Americans experience social anxiety disorder during their lifetime (Kessler et al., 2005).
The heart of the fear and anxiety in social anxiety disorder is the person’s concern that he may act in a humiliating or embarrassing way, such as appearing foolish, showing symptoms of anxiety (blushing), or doing or saying something that might lead to rejection (such as offending others). The kinds of social situations in which individuals with social anxiety disorder usually have problems include public speaking, having a conversation, meeting strangers, eating in restaurants, and, in some cases, using public restrooms. Although many people become anxious in social situations like public speaking, the fear, anxiety, and avoidance experienced in social anxiety disorder are highly distressing and lead to serious impairments in life. Adults with this disorder are more likely to experience lower educational attainment and lower earnings (Katzelnick et al., 2001), perform more poorly at work and are more likely to be unemployed (Moitra, Beard, Weisberg, & Keller, 2011), and report greater dissatisfaction with their family lives, friends, leisure activities, and income (Stein & Kean, 2000).
When people with social anxiety disorder are unable to avoid situations that provoke anxiety, they typically perform safety behaviors: mental or behavioral acts that reduce anxiety in social situations by reducing the chance of negative social outcomes. Safety behaviors include avoiding eye contact, rehearsing sentences before speaking, talking only briefly, and not talking about oneself (Alden & Bieling, 1998). Other examples of safety behaviors include the following (Marker, 2013):
- assuming roles in social situations that minimize interaction with others (e.g., taking pictures, setting up equipment, or helping prepare food)
- asking people many questions to keep the focus off of oneself
- selecting a position to avoid scrutiny or contact with others (sitting in the back of the room)
- wearing bland, neutral clothes to avoid drawing attention to oneself
- avoiding substances or activities that might cause anxiety symptoms (such as caffeine, warm clothing, and physical exercise)
Although these behaviors are intended to prevent the person with social anxiety disorder from doing something awkward that might draw criticism, these actions usually exacerbate the problem because they do not allow the individual to disconfirm his negative beliefs, often eliciting rejection and other negative reactions from others (Alden & Bieling, 1998).
People with social anxiety disorder may resort to self-medication, such as drinking alcohol, as a means to avert the anxiety symptoms they experience in social situations (Battista & Kocovski, 2010). The use of alcohol, when faced with such situations, may become negatively reinforcing: encouraging individuals with social anxiety disorder to turn to the substance whenever they experience anxiety symptoms. The tendency to use alcohol as a coping mechanism for social anxiety, however, can come with a hefty price tag: a number of large scale studies have reported a high rate of comorbidity between social anxiety disorder and alcohol use disorder (Morris, Stewart, & Ham, 2005).
As with specific phobias, it is highly probable that the fears inherent to social anxiety disorder can develop through conditioning experiences. For example, a child who is subjected to early unpleasant social experiences (e.g., bullying at school) may develop negative social images of herself that become activated later in anxiety-provoking situations (Hackmann, Clark, & McManus, 2000). Indeed, one study reported that 92% of a sample of adults with social anxiety disorder reported a history of severe teasing in childhood, compared to only 35% of a sample of adults with panic disorder (McCabe, Antony, Summerfeldt, Liss, & Swinson, 2003).
One of the most well-established risk factors for developing social anxiety disorder is behavioral inhibition (Clauss & Blackford, 2012). Behavioral inhibition is thought to be an inherited trait, and it is characterized by a consistent tendency to show fear and restraint when presented with unfamiliar people or situations (Kagan, Reznick, & Snidman, 1988). Behavioral inhibition is displayed very early in life; behaviorally inhibited toddlers and children respond with great caution and restraint in unfamiliar situations, and they are often timid, fearful, and shy around unfamiliar people (Fox, Henderson, Marshall, Nichols, & Ghera, 2005). A recent statistical review of studies demonstrated that behavioral inhibition was associated with more than a sevenfold increase in the risk of development of social anxiety disorder, demonstrating that behavioral inhibition is a major risk factor for the disorder (Clauss & Blackford, 2012).
Panic Disorder
Imagine that you are at the mall one day with your friends and—suddenly and inexplicably—you begin sweating and trembling, your heart starts pounding, you have trouble breathing, and you start to feel dizzy and nauseous. This episode lasts for 10 minutes and is terrifying because you start to think that you are going to die. When you visit your doctor the following morning and describe what happened, she tells you that you have experienced a panic attack (Figure 15.9). If you experience another one of these episodes two weeks later and worry for a month or more that similar episodes will occur in the future, it is likely that you have developed panic disorder.
People with panic disorder experience recurrent (more than one) and unexpected panic attacks, along with at least one month of persistent concern about additional panic attacks, worry over the consequences of the attacks, or self-defeating changes in behavior related to the attacks (e.g., avoidance of exercise or unfamiliar situations) (APA, 2013). As is the case with other anxiety disorders, the panic attacks cannot result from the physiological effects of drugs and other substances, a medical condition, or another mental disorder. A panic attack is defined as a period of extreme fear or discomfort that develops abruptly and reaches a peak within 10 minutes. Its symptoms include accelerated heart rate, sweating, trembling, choking sensations, hot flashes or chills, dizziness or lightheadedness, fears of losing control or going crazy, and fears of dying (APA, 2013). Sometimes panic attacks are expected, occurring in response to specific environmental triggers (such as being in a tunnel); other times, these episodes are unexpected and emerge randomly (such as when relaxing). According to the DSM-5, the person must experience unexpected panic attacks to qualify for a diagnosis of panic disorder.
Experiencing a panic attack is often terrifying. Rather than recognizing the symptoms of a panic attack merely as signs of intense anxiety, individuals with panic disorder often misinterpret them as a sign that something is intensely wrong internally (thinking, for example, that the pounding heart represents an impending heart attack). Panic attacks can occasionally precipitate trips to the emergency room because several symptoms of panic attacks are, in fact, similar to those associated with heart problems (e.g., palpitations, racing pulse, and a pounding sensation in the chest) (Root, 2000). Unsurprisingly, those with panic disorder fear future attacks and may become preoccupied with modifying their behavior in an effort to avoid future panic attacks. For this reason, panic disorder is often characterized as a fear of fear (Goldstein & Chambless, 1978).
Panic attacks themselves are not mental disorders. Indeed, around 23% of Americans experience isolated panic attacks in their lives without meeting the criteria for panic disorder (Kessler et al., 2006), indicating that panic attacks are fairly common. Panic disorder is, of course, much less common, afflicting 4.7% of Americans during their lifetime (Kessler et al., 2005). Many people with panic disorder develop agoraphobia, which is marked by fear and avoidance of situations in which escape might be difficult or help might not be available if one were to develop symptoms of a panic attack. People with panic disorder often experience a comorbid disorder, such as other anxiety disorders or major depressive disorder (APA, 2013).
Researchers are not entirely sure what causes panic disorder. Children are at a higher risk of developing panic disorder if their parents have the disorder (Biederman et al., 2001), and family and twin studies indicate that the heritability of panic disorder is around 43% (Hettema, Neale, & Kendler, 2001). The exact genes and gene functions involved in this disorder, however, are not well-understood (APA, 2013). Neurobiological theories of panic disorder suggest that a region of the brain called the locus coeruleus may play a role in this disorder. Located in the brainstem, the locus coeruleus is the brain’s major source of norepinephrine, a neurotransmitter that triggers the body’s fight-or-flight response. Activation of the locus coeruleus is associated with anxiety and fear, and research with nonhuman primates has shown that stimulating the locus coeruleus either electrically or through drugs produces panic-like symptoms (Charney et al., 1990). Such findings have led to the theory that panic disorder may be caused by abnormal norepinephrine activity in the locus coeruleus (Bremner, Krystal, Southwick, & Charney, 1996).
Conditioning theories of panic disorder propose that panic attacks are classical conditioning responses to subtle bodily sensations resembling those normally occurring when one is anxious or frightened (Bouton, Mineka, & Barlow, 2001). For example, consider a child who has asthma. An acute asthma attack produces sensations, such as shortness of breath, coughing, and chest tightness, that typically elicit fear and anxiety. Later, when the child experiences subtle symptoms that resemble the frightening symptoms of earlier asthma attacks (such as shortness of breath after climbing stairs), he may become anxious, fearful, and then experience a panic attack. In this situation, the subtle symptoms would represent a conditioned stimulus, and the panic attack would be a conditioned response. The finding that panic disorder is nearly three times as frequent among people with asthma as it is among people without asthma (Weiser, 2007) supports the possibility that panic disorder has the potential to develop through classical conditioning.
Cognitive factors may play an integral part in panic disorder. Generally, cognitive theories (Clark, 1996) argue that those with panic disorder are prone to interpret ordinary bodily sensations catastrophically, and these fearful interpretations set the stage for panic attacks. For example, a person might detect bodily changes that are routinely triggered by innocuous events such as getting up from a seated position (dizziness), exercising (increased heart rate, shortness of breath), or drinking a large cup of coffee (increased heart rate, trembling). The individual interprets these subtle bodily changes catastrophically (“Maybe I’m having a heart attack!”). Such interpretations create fear and anxiety, which trigger additional physical symptoms; subsequently, the person experiences a panic attack. Support of this contention rests with findings that people with more severe catastrophic thoughts about sensations have more frequent and severe panic attacks, and among those with panic disorder, reducing catastrophic cognitions about their sensations is as effective as medication in reducing panic attacks (Good & Hinton, 2009).
Generalized Anxiety Disorder
Alex suffers from generalized anxiety disorder: a relatively continuous state of excessive, uncontrollable, and pointless worry and apprehension. People with generalized anxiety disorder often worry about routine, everyday things, even though their concerns are unjustified (Figure 15.10). For example, an individual may worry about her health and finances, the health of family members, the safety of her children, or minor matters (e.g., being late for an appointment) without having any legitimate reason for doing so (APA, 2013). A diagnosis of generalized anxiety disorder requires that the diffuse worrying and apprehension characteristic of this disorder—what Sigmund Freud referred to as free-floating anxiety—is not part of another disorder, occurs more days than not for at least six months, and is accompanied by any three of the following symptoms: restlessness, difficulty concentrating, being easily fatigued, muscle tension, irritability, and sleep difficulties.
About 5.7% of the U.S. population will develop symptoms of generalized anxiety disorder during their lifetime (Kessler et al., 2005), and females are 2 times as likely as males to experience the disorder (APA, 2013). Generalized anxiety disorder is highly comorbid with mood disorders and other anxiety disorders (Noyes, 2001), and it tends to be chronic. Also, generalized anxiety disorder appears to increase the risk of heart attacks and strokes, especially in people with preexisting heart conditions (Martens et al., 2010).
Although there have been few investigations aimed at determining the heritability of generalized anxiety disorder, a summary of available family and twin studies suggests that genetic factors play a modest role in the disorder (Hettema et al., 2001). Cognitive theories of generalized anxiety disorder suggest that worry represents a mental strategy to avoid more powerful negative emotions (Aikins & Craske, 2001), perhaps stemming from earlier unpleasant or traumatic experiences. Indeed, one longitudinal study found that childhood maltreatment was strongly related to the development of this disorder during adulthood (Moffitt et al., 2007); worrying might distract people from remembering painful childhood experiences.
Learning Objectives
By the end of this section, you will be able to:
- Describe the main features and prevalence of obsessive-compulsive disorder, body dysmorphic disorder, and hoarding disorder
- Understand some of the factors in the development of obsessive-compulsive disorder
Obsessive-compulsive and related disorders are a group of overlapping disorders that generally involve intrusive, unpleasant thoughts, and repetitive behaviors. Many of us experience unwanted thoughts from time to time (e.g., craving double cheeseburgers when dieting), and many of us engage in repetitive behaviors on occasion (e.g., pacing when nervous). However, obsessive-compulsive and related disorders elevate the unwanted thoughts and repetitive behaviors to a status so intense that these cognitions and activities disrupt daily life. Included in this category are obsessive-compulsive disorder (OCD), body dysmorphic disorder, and hoarding disorder.
Obsessive-Compulsive Disorder
People with obsessive-compulsive disorder (OCD) experience thoughts and urges that are intrusive and unwanted (obsessions) and/or the need to engage in repetitive behaviors or mental acts (compulsions). A person with this disorder might, for example, spend hours each day washing his hands or constantly checking and rechecking to make sure that a stove, faucet, or light has been turned off.
Obsessions are more than just unwanted thoughts that seem to randomly jump into our heads from time to time, such as recalling an insensitive remark a coworker made recently, and they are more significant than day-to-day worries we might have, such as justifiable concerns about being laid off from a job. Rather, obsessions are characterized as persistent, unintentional, and unwanted thoughts and urges that are highly intrusive, unpleasant, and distressing (APA, 2013). Common obsessions include concerns about germs and contamination, doubts (“Did I turn the water off?”), order and symmetry (“I need all the spoons in the tray to be arranged a certain way”), and urges that are aggressive or lustful. Usually, the person knows that such thoughts and urges are irrational and thus tries to suppress or ignore them, but has an extremely difficult time doing so. These obsessive symptoms sometimes overlap, such that someone might have both contamination and aggressive obsessions (Abramowitz & Siqueland, 2013).
Compulsions are repetitive and ritualistic acts that are typically carried out primarily as a means to minimize the distress that obsessions trigger or to reduce the likelihood of a feared event (APA, 2013). Compulsions often include such behaviors as repeated and extensive hand washing, cleaning, checking (e.g., that a door is locked), and ordering (e.g., lining up all the pencils in a particular way), and they also include such mental acts as counting, praying, or reciting something to oneself (Figure 15.11). Compulsions characteristic of OCD are not performed out of pleasure, nor are they connected in a realistic way to the source of the distress or feared event. Approximately 2.3% of the U.S. population will experience OCD in their lifetime (Ruscio, Stein, Chiu, & Kessler, 2010) and, if left untreated, OCD tends to be a chronic condition creating lifelong interpersonal and psychological problems (Norberg, Calamari, Cohen, & Riemann, 2008).
Body Dysmorphic Disorder
An individual with body dysmorphic disorder is preoccupied with a perceived flaw in physical appearance that is either nonexistent or barely noticeable to other people (APA, 2013). These perceived physical defects cause people to think they are unattractive, ugly, hideous, or deformed. These preoccupations can focus on any bodily area, but they typically involve the skin, face, or hair. The preoccupation with imagined physical flaws drives the person to engage in repetitive and ritualistic behavioral and mental acts, such as constantly looking in the mirror, trying to hide the offending body part, comparisons with others, and, in some extreme cases, cosmetic surgery (Phillips, 2005). An estimated 2.4% of the adults in the United States meet the criteria for body dysmorphic disorder, with slightly higher rates in women than in men (APA, 2013).
Hoarding Disorder
Although hoarding was traditionally considered to be a symptom of OCD, considerable evidence suggests that hoarding represents an entirely different disorder (Mataix-Cols et al., 2010). People with hoarding disorder cannot bear to part with personal possessions, regardless of how valueless or useless, these possessions are. As a result, these individuals accumulate excessive amounts of usually worthless items that clutter their living areas (Figure 15.12). Often, the quantity of cluttered items is so excessive that the person is unable to use his kitchen, or sleep in his bed. People who suffer from this disorder have great difficulty parting with items because they believe the items might be of some later use, or because they form a sentimental attachment to the items (APA, 2013). Importantly, a diagnosis of hoarding disorder is made only if the hoarding is not caused by another medical condition and if the hoarding is not a symptom of another disorder (e.g., schizophrenia) (APA, 2013).
Causes of OCD
The results of family and twin studies suggest that OCD has a moderate genetic component. The disorder is five times more frequent in the first-degree relatives of people with OCD than in people without the disorder (Nestadt et al., 2000). Additionally, the concordance rate of OCD among identical twins is around 57%; however, the concordance rate for fraternal twins is 22% (Bolton, Rijsdijk, O’Connor, Perrin, & Eley, 2007). Studies have implicated about two dozen potential genes that may be involved in OCD; these genes regulate the function of three neurotransmitters: serotonin, dopamine, and glutamate (Pauls, 2010). Many of these studies included small sample sizes and have yet to be replicated. Thus, additional research needs to be done in this area.
A brain region that is believed to play a critical role in OCD is the orbitofrontal cortex (Kopell & Greenberg, 2008), an area of the frontal lobe involved in learning and decision-making (Rushworth, Noonan, Boorman, Walton, & Behrens, 2011) (Figure 15.13). In people with OCD, the orbitofrontal cortex becomes especially hyperactive when they are provoked with tasks in which, for example, they are asked to look at a photo of a toilet or of pictures hanging crookedly on a wall (Simon, Kaufmann, Müsch, Kischkel, & Kathmann, 2010). The orbitofrontal cortex is part of a series of brain regions that, collectively, is called the OCD circuit; this circuit consists of several interconnected regions that influence the perceived emotional value of stimuli and the selection of both behavioral and cognitive responses (Graybiel & Rauch, 2000). As with the orbitofrontal cortex, other regions of the OCD circuit show heightened activity during symptom provocation (Rotge et al., 2008), which suggests that abnormalities in these regions may produce the symptoms of OCD (Saxena, Bota, & Brody, 2001). Consistent with this explanation, people with OCD show a substantially higher degree of connectivity of the orbitofrontal cortex and other regions of the OCD circuit than do those without OCD (Beucke et al., 2013).
The findings discussed above were based on imaging studies, and they highlight the potential importance of brain dysfunction in OCD. However, one important limitation of these findings is the inability to explain differences in obsessions and compulsions. Another limitation is that the correlational relationship between neurological abnormalities and OCD symptoms cannot imply causation (Abramowitz & Siqueland, 2013).
Learning Objectives
By the end of this section, you will be able to:
- Describe the nature and symptoms of posttraumatic stress disorder
- Identify the risk factors associated with this disorder
- Understand the role of learning and cognitive factors in its development
Extremely stressful or traumatic events, such as combat, natural disasters, and terrorist attacks, place the people who experience them at an increased risk for developing psychological disorders such as posttraumatic stress disorder (PTSD). Throughout much of the 20th century, this disorder was called shell shock and combat neurosis because its symptoms were observed in soldiers who had engaged in wartime combat. The term posttraumatic stress disorder was developed given that these symptoms could happen to anyone who experienced psychological trauma.
A Broader Definition of PTSD
PTSD was listed among the anxiety disorders in previous DSM editions. In DSM-5, it is now listed among a group called Trauma-and-Stressor-Related Disorders. For a person to be diagnosed with PTSD, she must be exposed to, witness, or experience the details of a traumatic experience (e.g., a first responder), one that involves “actual or threatened death, serious injury, or sexual violence” (APA, 2013, p. 271). These experiences can include such events as combat, threatened or actual physical attack, sexual assault, natural disasters, terrorist attacks, and automobile accidents. This criterion makes PTSD the only disorder listed in the DSM in which a cause (extreme trauma) is explicitly specified.
Symptoms of PTSD include intrusive and distressing memories of the event, flashbacks (states that can last from a few seconds to several days, during which the individual relives the event and behaves as if the event were occurring at that moment [APA, 2013]), avoidance of stimuli connected to the event, persistently negative emotional states (e.g., fear, anger, guilt, and shame), feelings of detachment from others, irritability, proneness toward outbursts, and an exaggerated startle response (jumpiness). For PTSD to be diagnosed, these symptoms must occur for at least one month.
Roughly 7% of adults in the United States, including 9.7% of women and 3.6% of men, experience PTSD in their lifetime (National Comorbidity Survey, 2007), with higher rates among people exposed to mass trauma and people whose jobs involve duty-related trauma exposure (e.g., police officers, firefighters, and emergency medical personnel) (APA, 2013).
Risk Factors For PTSD
Of course, not everyone who experiences a traumatic event will go on to develop PTSD; several factors strongly predict the development of PTSD: trauma experience, greater trauma severity, lack of immediate social support, and more subsequent life stress (Brewin, Andrews, & Valentine, 2000). Traumatic events that involve harm by others (e.g., combat, rape, and sexual molestation) carry greater risk than do other traumas (e.g., natural disasters) (Kessler, Sonnega, Bromet, Hughes, & Nelson, 1995). Women are more likely to have been traumatized because of sexual trauma, childhood neglect, and childhood physical abuse. Men are more likely to have been traumatized by natural disaster, life-threatening accident, and physical violence, either witnessed or directed at them. Adolescent boys are more likely to experience accident, physical assault, and witness death/injury; adolescent girls are more likely to experience rape/sexual assault, intimate partner violence, or unexpected death or injury of a loved one. Assaultive violence and witnessing trauma to others is more prevalent among non-whites when compared to whites. African American males are more likely to be exposed to and victims of violence than males of other races (Kilpatrick, Badour, & Resnick, 2017). A 2012 study found that 27% of corrections officers reported experiencing symptoms of PTSD in the past 30 days. Rates were higher for males (31%) than females (22%) (Spinaris, Denhof, & Kellaway, 2012). A study conducted by Jaegers et al (2019) found that 53.4% of jail correctional officers screened positively for PTSD. PTSD is more prevalent in prison populations than in the general public, with prevalence estimates of 6% in male prisoners and 21% in female prisoners (Facer-Irwin et al, 2019). Factors that increase the risk of PTSD include female gender, low socioeconomic status, low intelligence, personal history of mental disorders, history of childhood adversity (abuse or other trauma during childhood), and family history of mental disorders (Brewin et al., 2000). Personality characteristics such as neuroticism and somatization (the tendency to experience physical symptoms when one encounters stress) have been shown to elevate the risk of PTSD (Bramsen, Dirkzwager, & van der Ploeg, 2000). People who experience childhood adversity and/or traumatic experiences during adulthood are at significantly higher risk of developing PTSD if they possess one or two short versions of a gene that regulates the neurotransmitter serotonin (Xie et al., 2009). This suggests a possible diathesis-stress interpretation of PTSD: its development is influenced by the interaction of psychosocial and biological factors.
Learning Objectives
By the end of this section, you will be able to:
- Distinguish normal states of sadness and euphoria from states of depression and mania
- Describe the symptoms of major depressive disorder and bipolar disorder
- Understand the differences between major depressive disorder and persistent depressive disorder, and identify two subtypes of depression
- Define the criteria for a manic episode
- Understand genetic, biological, and psychological explanations of major depressive disorder
- Discuss the relationship between mood disorders and suicidal ideation, as well as factors associated with suicide
Mood disorders (Figure 15.15) are characterized by severe disturbances in mood and emotions—most often depression, but also mania and elation (Rothschild, 1999). All of us experience fluctuations in our moods and emotional states, and often these fluctuations are caused by events in our lives. We become elated if our favorite team wins the World Series and dejected if a romantic relationship ends or if we lose our job. At times, we feel fantastic or miserable for no clear reason. People with mood disorders also experience mood fluctuations, but their fluctuations are extreme, distort their outlook on life, and impair their ability to function.
The DSM-5 lists two general categories of mood disorders. Depressive disorders are a group of disorders in which depression is the main feature. Depression is a vague term that, in everyday language, refers to an intense and persistent sadness. Depression is a heterogeneous mood state—it consists of a broad spectrum of symptoms that range in severity. Depressed people feel sad, discouraged, and hopeless. These individuals lose interest in activities once enjoyed, often experience a decrease in drives such as hunger and sex, and frequently doubt personal worth. Depressive disorders vary by degree, but this chapter highlights the most well-known: major depressive disorder (sometimes called unipolar depression).
Bipolar and related disorders are a group of disorders in which mania is the defining feature. Mania is a state of extreme elation and agitation. When people experience mania, they may become extremely talkative, behave recklessly, or attempt to take on many tasks simultaneously. The most recognized of these disorders is bipolar disorder.
Major Depressive Disorder
According to the DSM-5, the defining symptoms of major depressive disorder include “depressed mood most of the day, nearly every day” (feeling sad, empty, hopeless, or appearing tearful to others), and loss of interest and pleasure in usual activities (APA, 2013). In addition to feeling overwhelmingly sad most of each day, people with depression will no longer show interest or enjoyment in activities that previously were gratifying, such as hobbies, sports, sex, social events, time spent with family, and so on. Friends and family members may notice that the person has completely abandoned previously enjoyed hobbies; for example, an avid tennis player who develops major depressive disorder no longer plays tennis (Rothschild, 1999).
To receive a diagnosis of major depressive disorder, one must experience a total of five symptoms for at least a two-week period; these symptoms must cause significant distress or impair normal functioning, and they must not be caused by substances or a medical condition. At least one of the two symptoms mentioned above must be present, plus any combination of the following symptoms (APA, 2013):
- significant weight loss (when not dieting) or weight gain and/or significant decrease or increase in appetite;
- difficulty falling asleep or sleeping too much;
- psychomotor agitation (the person is noticeably fidgety and jittery, demonstrated by behaviors like the inability to sit, pacing, hand-wringing, pulling or rubbing of the skin, clothing, or other objects) or psychomotor retardation (the person talks and moves slowly, for example, talking softly, very little, or in a monotone);
- fatigue or loss of energy;
- feelings of worthlessness or guilt;
- difficulty concentrating and indecisiveness; and
- suicidal ideation: thoughts of death (not just fear of dying), thinking about or planning suicide, or making an actual suicide attempt.
Major depressive disorder is considered episodic: its symptoms are typically present at their full magnitude for a certain period of time and then gradually abate. Approximately 50%–60% of people who experience an episode of major depressive disorder will have a second episode at some point in the future; those who have had two episodes have a 70% chance of having a third episode, and those who have had three episodes have a 90% chance of having a fourth episode (Rothschild, 1999). Although the episodes can last for months, a majority of people diagnosed with this condition (around 70%) recover within a year. However, a substantial number do not recover; around 12% show serious signs of impairment associated with major depressive disorder after 5 years (Boland & Keller, 2009). In the long-term, many who do recover will still show minor symptoms that fluctuate in their severity (Judd, 2012).
Results of Major Depressive Disorder
Major depressive disorder is a serious and incapacitating condition that can have a devastating effect on the quality of one’s life. The person suffering from this disorder lives a profoundly miserable existence that often results in unavailability for work or education, abandonment of promising careers, and lost wages; occasionally, the condition requires hospitalization. The majority of those with major depressive disorder report having faced some kind of discrimination and many report that having received such treatment has stopped them from initiating close relationships, applying for jobs for which they are qualified, and applying for education or training (Lasalvia et al., 2013). Major depressive disorder also takes a toll on health. Depression is a risk factor for the development of heart disease in healthy patients, as well as adverse cardiovascular outcomes in patients with preexisting heart disease (Whooley, 2006).
Risk Factors for Major Depressive Disorder
Major depressive disorder is often referred to as the common cold of psychiatric disorders. Around 6.6% of the U.S. population experiences major depressive disorder each year; 16.9% will experience the disorder during their lifetime (Kessler & Wang, 2009). It is more common among women than among men, affecting approximately 20% of women and 13% of men at some point in their life (National Comorbidity Survey, 2007). The greater risk among women is not accounted for by a tendency to report symptoms or to seek help more readily, suggesting that gender differences in the rates of major depressive disorder may reflect biological and gender-related environmental experiences (Kessler, 2003).
Lifetime rates of major depressive disorder tend to be highest in North and South America, Europe, and Australia; they are considerably lower in Asian countries (Hasin, Fenton, & Weissman, 2011). The rates of major depressive disorder are higher among younger age cohorts than among older cohorts, perhaps because people in younger age cohorts are more willing to admit depression (Kessler & Wang, 2009).
A number of risk factors are associated with major depressive disorder: unemployment (including homemakers); earning less than $20,000 per year; living in urban areas; or being separated, divorced, or widowed (Hasin et al., 2011). Comorbid disorders include anxiety disorders and substance abuse disorders (Kessler & Wang, 2009).
Bipolar Disorder
A person with bipolar disorder (commonly known as manic depression) often experiences mood states that vacillate between depression and mania; that is, the person’s mood is said to alternate from one emotional extreme to the other (in contrast to unipolar, which indicates a persistently sad mood).
To be diagnosed with bipolar disorder, a person must have experienced a manic episode at least once in his life; although major depressive episodes are common in bipolar disorder, they are not required for a diagnosis (APA, 2013). According to the DSM-5, a manic episode is characterized as a “distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased activity or energy lasting at least one week,” that lasts most of the time each day (APA, 2013, p. 124). During a manic episode, some experience a mood that is almost euphoric and become excessively talkative, sometimes spontaneously starting conversations with strangers; others become excessively irritable and complain or make hostile comments. The person may talk loudly and rapidly, exhibiting a flight of ideas, abruptly switching from one topic to another. These individuals are easily distracted, which can make a conversation very difficult. They may exhibit grandiosity, in which they experience inflated but unjustified self-esteem and self-confidence. For example, they might quit a job in order to “strike it rich” in the stock market, despite lacking the knowledge, experience, and capital for such an endeavor. They may take on several tasks at the same time (e.g., several time-consuming projects at work) and yet show little, if any, need for sleep; some may go for days without sleep. Patients may also recklessly engage in pleasurable activities that could have harmful consequences, including spending sprees, reckless driving, making foolish investments, excessive gambling, or engaging in sexual encounters with strangers (APA, 2013).
During a manic episode, individuals usually feel as though they are not ill and do not need treatment. However, the reckless behaviors that often accompany these episodes—which can be antisocial, illegal, or physically threatening to others—may require involuntary hospitalization (APA, 2013). Some patients with bipolar disorder will experience a rapid-cycling subtype, which is characterized by at least four manic episodes (or some combination of at least four manic and major depressive episodes) within one year.
Risk Factors for Bipolar Disorder
Bipolar disorder is considerably less frequent than major depressive disorder. In the United States, 1 out of every 167 people meets the criteria for bipolar disorder each year, and 1 out of 100 meet the criteria within their lifetime (Merikangas et al., 2011). The rates are higher in men than in women, and about half of those with this disorder report onset before the age of 25 (Merikangas et al., 2011). Around 90% of those with bipolar disorder have a comorbid disorder, most often an anxiety disorder or a substance abuse problem. Unfortunately, close to half of the people suffering from bipolar disorder do not receive treatment (Merikangas & Tohen, 2011). Suicide rates are extremely high among those with bipolar disorder: around 36% of individuals with this disorder attempt suicide at least once in their lifetime (Novick, Swartz, & Frank, 2010), and between 15%–19% complete suicide (Newman, 2004).
The Biological Basis of Mood Disorders
Mood disorders have been shown to have a strong genetic and biological basis. Relatives of those with major depressive disorder have double the risk of developing major depressive disorder, whereas relatives of patients with bipolar disorder have over nine times the risk (Merikangas et al., 2011). The rate of concordance for major depressive disorder is higher among identical twins than fraternal twins (50% vs. 38%, respectively), as is that of bipolar disorder (67% vs. 16%, respectively), suggesting that genetic factors play a stronger role in bipolar disorder than in major depressive disorder (Merikangas et al. 2011).
People with mood disorders often have imbalances in certain neurotransmitters, particularly norepinephrine and serotonin (Thase, 2009). These neurotransmitters are important regulators of the bodily functions that are disrupted in mood disorders, including appetite, sex drive, sleep, arousal, and mood. Medications that are used to treat major depressive disorder typically boost serotonin and norepinephrine activity, whereas lithium—used in the treatment of bipolar disorder—blocks norepinephrine activity at the synapses (Figure 15.16).
Depression is linked to abnormal activity in several regions of the brain (Fitzgerald, Laird, Maller, & Daskalakis, 2008) including those important in assessing the emotional significance of stimuli and experiencing emotions (amygdala), and in regulating and controlling emotions (like the prefrontal cortex, or PFC) (LeMoult, Castonguay, Joormann, & McAleavey, 2013). Depressed individuals show elevated amygdala activity (Drevets, Bogers, & Raichle, 2002), especially when presented with negative emotional stimuli, such as photos of sad faces (Figure 15.17) (Surguladze et al., 2005). Interestingly, heightened amygdala activation to negative emotional stimuli among depressed persons occurs even when stimuli are presented outside of conscious awareness (Victor, Furey, Fromm, Öhman, & Drevets, 2010), and it persists even after the negative emotional stimuli are no longer present (Siegle, Thompson, Carter, Steinhauer, & Thase, 2007). Additionally, depressed individuals exhibit less activation in the prefrontal, particularly on the left side (Davidson, Pizzagalli, & Nitschke, 2009). Because the PFC can dampen amygdala activation, thereby enabling one to suppress negative emotions (Phan et al., 2005), decreased activation in certain regions of the PFC may inhibit its ability to override negative emotions that might then lead to more negative mood states (Davidson et al., 2009). These findings suggest that depressed persons are more prone to react to emotionally negative stimuli, yet have greater difficulty controlling these reactions.
Since the 1950s, researchers have noted that depressed individuals have abnormal levels of cortisol, a stress hormone released into the blood by the neuroendocrine system during times of stress (Mackin & Young, 2004). When cortisol is released, the body initiates a fight-or-flight response in reaction to a threat or danger. Many people with depression show elevated cortisol levels (Holsboer & Ising, 2010), especially those reporting a history of early life trauma such as the loss of a parent or abuse during childhood (Baes, Tofoli, Martins, & Juruena, 2012). Such findings raise the question of whether high cortisol levels are a cause or a consequence of depression. High levels of cortisol are a risk factor for future depression (Halligan, Herbert, Goodyer, & Murray, 2007), and cortisol activates activity in the amygdala while deactivating activity in the PFC (McEwen, 2005)—both brain disturbances are connected to depression. Thus, high cortisol levels may have a causal effect on depression, as well as on its brain function abnormalities (van Praag, 2005). Also, because stress results in increased cortisol release (Michaud, Matheson, Kelly, Anisman, 2008), it is equally reasonable to assume that stress may precipitate depression.
A Diathesis-Stress Model and Major Depressive Disorders
Indeed, it has long been believed that stressful life events can trigger depression, and research has consistently supported this conclusion (Mazure, 1998). Stressful life events include significant losses, such as the death of a loved one, divorce or separation, and serious health and money problems; life events such as these often precede the onset of depressive episodes (Brown & Harris, 1989). In particular, exit events—instances in which an important person departs (e.g., a death, divorce or separation, or a family member leaving home)—often occur prior to an episode (Paykel, 2003). Exit events are especially likely to trigger depression if these happenings occur in a way that humiliates or devalues the individual. For example, people who experience the breakup of a relationship initiated by the other person develop major depressive disorder at a rate more than 2 times that of people who experience the death of a loved one (Kendler, Hettema, Butera, Gardner, & Prescott, 2003).
Likewise, individuals who are exposed to traumatic stress during childhood—such as separation from a parent, family turmoil, and maltreatment (physical or sexual abuse)—are at a heightened risk of developing depression at any point in their lives (Kessler, 1997). A recent review of 16 studies involving over 23,000 subjects concluded that those who experience childhood maltreatment are more than 2 times as likely to develop recurring and persistent depression (Nanni, Uher, & Danese, 2012).
Of course, not everyone who experiences stressful life events or childhood adversities succumbs to depression—indeed, most do not. Clearly, a diathesis-stress interpretation of major depressive disorder, in which certain predispositions or vulnerability factors influence one’s reaction to stress, would seem logical.
Cognitive Theories of Depression
Cognitive theories of depression take the view that depression is triggered by negative thoughts, interpretations, self-evaluations, and expectations (Joormann, 2009). These diathesis-stress models propose that depression is triggered by a “cognitive vulnerability” (negative and maladaptive thinking) and by precipitating stressful life events (Gotlib & Joormann, 2010). Perhaps the most well-known cognitive theory of depression was developed in the 1960s by psychiatrist Aaron Beck, based on clinical observations and supported by research (Beck, 2008). Beck theorized that depression-prone people possess depressive schemas or mental predispositions to think about most things in a negative way (Beck, 1976). Depressive schemas contain themes of loss, failure, rejection, worthlessness, and inadequacy, and may develop early in childhood in response to adverse experiences, then remain dormant until they are activated by stressful or negative life events. Depressive schemas prompt dysfunctional and pessimistic thoughts about the self, the world, and the future. Beck believed that this dysfunctional style of thinking is maintained by cognitive biases, or errors in how we process information about ourselves, which lead us to focus on negative aspects of experiences, interpret things negatively and block positive memories (Beck, 2008). A person whose depressive schema consists of a theme of rejection might be overly attentive to social cues of rejection (more likely to notice another’s frown), and he might interpret this cue as a sign of rejection and automatically remember past incidents of rejection. Longitudinal studies have supported Beck’s theory, in showing that a preexisting tendency to engage in this negative, self-defeating style of thinking—when combined with life stress—over time predicts the onset of depression (Dozois & Beck, 2008). Cognitive therapies for depression, aimed at changing a depressed person’s negative thinking, were developed as an expansion of this theory (Beck, 1976).
Another cognitive theory of depression, hopelessness theory, postulates that a particular style of negative thinking leads to a sense of hopelessness, which then leads to depression (Abramson, Metalsky, & Alloy, 1989). According to this theory, hopelessness is an expectation that unpleasant outcomes will occur or that desired outcomes will not occur, and there is nothing one can do to prevent such outcomes. A key assumption of this theory is that hopelessness stems from a tendency to perceive negative life events as having stable (“It’s never going to change”) and global (“It’s going to affect my whole life”) causes, in contrast to unstable (“It’s fixable”) and specific (“It applies only to this particular situation”) causes, especially if these negative life events occur in important life realms, such as relationships, academic achievement, and the like. Suppose a student who wishes to go to law school does poorly on an admissions test. If the student infers negative life events as having stable and global causes, she may believe that her poor performance has a stable and global cause (“I lack intelligence, and it’s going to prevent me from ever finding a meaningful career”), as opposed to an unstable and specific cause (“I was sick the day of the exam, so my low score was a fluke”). Hopelessness theory predicts that people who exhibit this cognitive style in response to undesirable life events will view such events as having negative implications for their future and self-worth, thereby increasing the likelihood of hopelessness—the primary cause of depression (Abramson et al., 1989). One study testing hopelessness theory measured the tendency to make negative inferences for bad life effects in participants who were experiencing uncontrollable stressors. Over the ensuing six months, those with scores reflecting high cognitive vulnerability were 7 times more likely to develop depression compared to those with lower scores (Kleim, Gonzalo, & Ehlers, 2011).
A third cognitive theory of depression focuses on how people’s thoughts about their distressed moods—depressed symptoms in particular—can increase the risk and duration of depression. This theory, which focuses on rumination in the development of depression, was first described in the late 1980s to explain the higher rates of depression in women than in men (Nolen-Hoeksema, 1987). Rumination is the repetitive and passive focus on the fact that one is depressed and dwelling on depressed symptoms, rather than distracting one’s self from the symptoms or attempting to address them in an active, problem-solving manner (Nolen-Hoeksema, 1991). When people ruminate, they have thoughts such as “Why am I so unmotivated? I just can’t get going. I’m never going to get my work done feeling this way” (Nolen-Hoeksema & Hilt, 2009, p. 393). Women are more likely than men to ruminate when they are sad or depressed (Butler & Nolen-Hoeksema, 1994), and the tendency to ruminate is associated with increases in depression symptoms (Nolen-Hoeksema, Larson, & Grayson, 1999), heightened risk of major depressive episodes (Abela & Hankin, 2011), and chronicity of such episodes (Robinson & Alloy, 2003)
Learning Objectives
By the end of this section, you will be able to:
- Describe the essential nature of dissociative disorders
- Identify and differentiate the symptoms of dissociative amnesia, depersonalization/ derealization disorder, and dissociative identity disorder
- Discuss the potential role of both social and psychological factors in dissociative identity disorder
Dissociative disorders are characterized by an individual becoming split off, or dissociated, from her core sense of self. Memory and identity become disturbed; these disturbances have a psychological rather than physical cause. Dissociative disorders listed in the DSM-5 include dissociative amnesia, depersonalization/derealization disorder, and dissociative identity disorder.
Dissociative Amnesia
Amnesia refers to the partial or total forgetting of some experience or event. An individual with dissociative amnesia is unable to recall important personal information, usually following an extremely stressful or traumatic experience such as combat, natural disasters, or being the victim of violence. The memory impairments are not caused by ordinary forgetting. Some individuals with dissociative amnesia will also experience dissociative fugue (from the word “to flee” in French), whereby they suddenly wander away from their home, experience confusion about their identity, and sometimes even adopt a new identity (Cardeña & Gleaves, 2006). Most fugue episodes last only a few hours or days, but some can last longer. One study of residents in communities in upstate New York reported that about 1.8% experienced dissociative amnesia in the previous year (Johnson, Cohen, Kasen, & Brook, 2006).
Some have questioned the validity of dissociative amnesia (Pope, Hudson, Bodkin, & Oliva, 1998); it has even been characterized as a “piece of psychiatric folklore devoid of convincing empirical support” (McNally, 2003, p. 275). Notably, scientific publications regarding dissociative amnesia rose during the 1980s and reached a peak in the mid-1990s, followed by an equally sharp decline by 2003; in fact, only 13 cases of individuals with dissociative amnesia worldwide could be found in the literature that same year (Pope, Barry, Bodkin, & Hudson, 2006). Further, no description of individuals showing dissociative amnesia following a trauma exists in any fictional or nonfictional work prior to 1800 (Pope, Poliakoff, Parker, Boynes, & Hudson, 2006). However, a study of 82 individuals who enrolled for treatment at a psychiatric outpatient hospital found that nearly 10% met the criteria for dissociative amnesia, perhaps suggesting that the condition is underdiagnosed, especially in psychiatric populations (Foote, Smolin, Kaplan, Legatt, & Lipschitz, 2006).
Depersonalization/Derealization Disorder
Depersonalization/derealization disorder is characterized by recurring episodes of depersonalization, derealization, or both. Depersonalization is defined as feelings of “unreality or detachment from, or unfamiliarity with, one’s whole self or from aspects of the self” (APA, 2013, p. 302). Individuals who experience depersonalization might believe their thoughts and feelings are not their own; they may feel robotic as though they lack control over their movements and speech; they may experience a distorted sense of time and, in extreme cases, they may sense an “out-of-body” experience in which they see themselves from the vantage point of another person. Derealization is conceptualized as a sense of “unreality or detachment from, or unfamiliarity with, the world, be it individuals, inanimate objects, or all surroundings” (APA, 2013, p. 303). A person who experiences derealization might feel as though he is in a fog or a dream, or that the surrounding world is somehow artificial and unreal. Individuals with depersonalization/derealization disorder often have difficulty describing their symptoms and may think they are going crazy (APA, 2013).
Dissociative Identity Disorder
By far, the most well-known dissociative disorder is dissociative identity disorder (formerly called multiple personality disorder). People with dissociative identity disorder exhibit two or more separate personalities or identities, each well-defined and distinct from one another. They also experience memory gaps for the time during which another identity is in charge (e.g., one might find unfamiliar items in her shopping bags or among her possessions), and in some cases may report hearing voices, such as a child’s voice or the sound of somebody crying (APA, 2013). The study of upstate New York residents mentioned above (Johnson et al., 2006) reported that 1.5% of their sample experienced symptoms consistent with dissociative identity disorder in the previous year.
Dissociative identity disorder (DID) is highly controversial. Some believe that people fake symptoms to avoid the consequences of illegal actions (e.g., “I am not responsible for shoplifting because it was my other personality”). In fact, it has been demonstrated that people are generally skilled at adopting the role of a person with different personalities when they believe it might be advantageous to do so. As an example, Kenneth Bianchi was an infamous serial killer who, along with his cousin, murdered over a dozen females around Los Angeles in the late 1970s. Eventually, he and his cousin were apprehended. At Bianchi’s trial, he pled not guilty by reason of insanity, presenting himself as though he had DID and claiming that a different personality (“Steve Walker”) committed the murders. When these claims were scrutinized, he admitted faking the symptoms and was found guilty (Schwartz, 1981).
A second reason DID is controversial is that rates of the disorder suddenly skyrocketed in the 1980s. More cases of DID were identified during the five years prior to 1986 than in the preceding two centuries (Putnam, Guroff, Silberman, Barban, & Post, 1986). Although this increase may be due to the development of more sophisticated diagnostic techniques, it is also possible that the popularization of DID—helped in part by Sybil, a popular 1970s book (and later film) about a woman with 16 different personalities—may have prompted clinicians to overdiagnose the disorder (Piper & Merskey, 2004). Casting further scrutiny on the existence of multiple personalities or identities is the recent suggestion that the story of Sybil was largely fabricated, and the idea for the book might have been exaggerated (Nathan, 2011).
Despite its controversial nature, DID is clearly a legitimate and serious disorder, and although some people may fake symptoms, others suffer their entire lives with it. People with this disorder tend to report a history of childhood trauma, some cases having been corroborated through medical or legal records (Cardeña & Gleaves, 2006). Research by Ross et al. (1990) suggests that in one study about 95% of people with DID were physically and/or sexually abused as children. Of course, not all reports of childhood abuse can be expected to be valid or accurate. However, there is strong evidence that traumatic experiences can cause people to experience states of dissociation, suggesting that dissociative states—including the adoption of multiple personalities—may serve as a psychologically important coping mechanism for threat and danger (Dalenberg et al., 2012).
Learning Objectives
By the end of this section, you will be able to:
- Describe the nature and symptoms of attention deficit/hyperactivity disorder and autism spectrum disorder
- Discuss the prevalence and factors that contribute to the development of these disorders
Most of the disorders we have discussed so far are typically diagnosed in adulthood, although they can and sometimes do occur during childhood. However, there are a group of conditions that, when present, are diagnosed early in childhood, often before the time a child enters school. These conditions are listed in the DSM-5 as neurodevelopmental disorders, and they involve developmental problems in personal, social, academic, and intellectual functioning (APA, 2013). In this section, we will discuss two such disorders: attention deficit/ hyperactivity disorder and autism.
Attention Deficit/Hyperactivity Disorder
Diego is always active, from the time he wakes up in the morning until the time he goes to bed at night. His mother reports that he came out of the womb kicking and screaming, and he has not stopped moving since. He has a sweet disposition but always seems to be in trouble with his teachers, parents, and after-school program counselors. He seems to accidentally break things; he lost his jacket three times last winter, and he never seems to sit still. His teachers believe he is a smart child, but he never finishes anything he starts and is so impulsive that he does not seem to learn much in school.
Diego likely has attention deficit/hyperactivity disorder (ADHD). The symptoms of this disorder were first described by Hans Hoffman in the 1920s. While taking care of his son while his wife was in the hospital giving birth to a second child, Hoffman noticed that the boy had trouble concentrating on his homework, had a short attention span, and had to repeatedly go over easy homework to learn the material (Jellinek & Herzog, 1999). Later, it was discovered that many hyperactive children—those who are fidgety, restless, socially disruptive, and have trouble with impulse control—also display short attention spans, problems with concentration, and distractibility. By the 1970s, it had become clear that many children who display attention problems often also exhibit signs of hyperactivity. In recognition of such findings, the DSM-III (published in 1980) included a new disorder: attention deficit disorder with and without hyperactivity, now known as attention deficit/hyperactivity disorder (ADHD).
A child with ADHD shows a constant pattern of inattention and/or hyperactive and impulsive behavior that interferes with normal functioning (APA, 2013). Some of the signs of inattention include great difficulty with and avoidance of tasks that require sustained attention (such as conversations or reading), failure to follow instructions (often resulting in failure to complete schoolwork and other duties), disorganization (difficulty keeping things in order, poor time management, sloppy and messy work), lack of attention to detail, becoming easily distracted, and forgetfulness. Hyperactivity is characterized by excessive movement, and includes fidgeting or squirming, leaving one’s seat in situations when remaining seated is expected, having trouble sitting still (e.g., in a restaurant), running about and climbing on things, blurting out responses before another person’s question or statement has been completed, difficulty waiting for one’s turn for something, and interrupting and intruding on others. Frequently, the hyperactive child comes across as noisy and boisterous. The child’s behavior is hasty, impulsive, and seems to occur without much forethought; these characteristics may explain why adolescents and young adults diagnosed with ADHD receive more traffic tickets and have more automobile accidents than do others (Thompson, Molina, Pelham, & Gnagy, 2007).
ADHD occurs in about 5% of children (APA, 2013). On average, boys are three times more likely to have ADHD than are girls; however, such findings might reflect the greater propensity of boys to engage in aggressive and antisocial behavior and thus incur a greater likelihood of being referred to psychological clinics (Barkley, 2006). Children with ADHD face severe academic and social challenges. Compared to their non-ADHD counterparts, children with ADHD have lower grades and standardized test scores and higher rates of expulsion, grade retention, and dropping out (Loe & Feldman, 2007). they also are less well-liked and more often rejected by their peers (Hoza et al., 2005).
Previously, ADHD was thought to fade away by adolescence. However, longitudinal studies have suggested that ADHD is a chronic problem, one that can persist into adolescence and adulthood (Barkley, Fischer, Smallish, & Fletcher, 2002). A recent study found that 29.3% of adults who had been diagnosed with ADHD decades earlier still showed symptoms (Barbaresi et al., 2013). Somewhat troubling, this study also reported that nearly 81% of those whose ADHD persisted into adulthood had experienced at least one other comorbid disorder, compared to 47% of those whose ADHD did not persist.
Causes of ADHD
Family and twin studies indicate that genetics play a significant role in the development of ADHD. Burt (2009), in a review of 26 studies, reported that the median rate of concordance for identical twins was .66 (one study reported a rate of .90), whereas the median concordance rate for fraternal twins was .20. This study also found that the median concordance rate for unrelated (adoptive) siblings was .09; although this number is small, it is greater than 0, thus suggesting that the environment may have at least some influence. Another review of studies concluded that the heritability of inattention and hyperactivity were 71% and 73%, respectively (Nikolas & Burt, 2010).
The specific genes involved in ADHD are thought to include at least two that are important in the regulation of the neurotransmitter dopamine (Gizer, Ficks, & Waldman, 2009), suggesting that dopamine may be important in ADHD. Indeed, medications used in the treatment of ADHD, such as methylphenidate (Ritalin) and amphetamine with dextroamphetamine (Adderall), have stimulant qualities and elevate dopamine activity. People with ADHD show less dopamine activity in key regions of the brain, especially those associated with motivation and reward (Volkow et al., 2009), which provides support to the theory that dopamine deficits may be a vital factor in the development of this disorder (Swanson et al., 2007).
Brain imaging studies have shown that children with ADHD exhibit abnormalities in their frontal lobes, an area in which dopamine is in abundance. Compared to children without ADHD, those with ADHD appear to have smaller frontal lobe volume, and they show less frontal lobe activation when performing mental tasks. Recall that one of the functions of the frontal lobes is to inhibit our behavior. Thus, abnormalities in this region may go a long way toward explaining the hyperactive, uncontrolled behavior of ADHD.
By the 1970s, many had become aware of the connection between nutritional factors and childhood behavior. At the time, much of the public believed that hyperactivity was caused by sugar and food additives, such as artificial coloring and flavoring. Undoubtedly, part of the appeal of this hypothesis was that it provided a simple explanation of (and treatment for) behavioral problems in children. A statistical review of 16 studies, however, concluded that sugar consumption has no effect at all on the behavioral and cognitive performance of children (Wolraich, Wilson, & White, 1995). Additionally, although food additives have been shown to increase hyperactivity in non-ADHD children, the effect is rather small (McCann et al., 2007). Numerous studies, however, have shown a significant relationship between exposure to nicotine in cigarette smoke during the prenatal period and ADHD (Linnet et al., 2003). Maternal smoking during pregnancy is associated with the development of more severe symptoms of the disorder (Thakur et al., 2013).
Is ADHD caused by poor parenting? Not likely. Remember, the genetics studies discussed above suggested that the family environment does not seem to play much of a role in the development of this disorder; if it did, we would expect the concordance rates to be higher for fraternal twins and adoptive siblings than has been demonstrated. All things considered, the evidence seems to point to the conclusion that ADHD is triggered more by genetic and neurological factors and less by social or environmental ones.
Autism Spectrum Disorder
A seminal paper published in 1943 by psychiatrist Leo Kanner described an unusual neurodevelopmental condition he observed in a group of children. He called this condition early infantile autism, and it was characterized mainly by an inability to form close emotional ties with others, speech and language abnormalities, repetitive behaviors, and an intolerance of minor changes in the environment and in normal routines (Bregman, 2005). What the DSM-5 refers to as autism spectrum disorder today, is a direct extension of Kanner’s work.
Autism spectrum disorder is probably the most misunderstood and puzzling of the neurodevelopmental disorders. Children with this disorder show signs of significant disturbances in three main areas: (a) deficits in social interaction, (b) deficits in communication, and (c) repetitive patterns of behavior or interests. These disturbances appear early in life and cause serious impairments in functioning (APA, 2013). The child with autism spectrum disorder might exhibit deficits in social interaction by not initiating conversations with other children or turning their head away when spoken to. Typically, these children do not make eye contact with others and seem to prefer playing alone rather than with others. In a certain sense, it is almost as though these individuals live in a personal and isolated social world others are simply not privy to or able to penetrate. Communication deficits can range from a complete lack of speech to one-word responses (e.g., saying “Yes” or “No” when replying to questions or statements that require additional elaboration), to echoed speech (e.g., parroting what another person says, either immediately or several hours or even days later), to difficulty maintaining a conversation because of an inability to reciprocate others’ comments. These deficits can also include problems in using and understanding nonverbal cues (e.g., facial expressions, gestures, and postures) that facilitate normal communication.
Repetitive patterns of behavior or interests can be exhibited in a number of ways. The child might engage in stereotyped, repetitive movements (rocking, head-banging, or repeatedly dropping an object and then picking it up), or she might show great distress at small changes in routine or the environment. For example, the child might throw a temper tantrum if an object is not in its proper place or if a regularly-scheduled activity is rescheduled. In some cases, the person with autism spectrum disorder might show highly restricted and fixated interests that appear to be abnormal in their intensity. For instance, the person might learn and memorize every detail about something even though doing so serves no apparent purpose. Importantly, autism spectrum disorder is not the same thing as intellectual disability, although these two conditions are often comorbid. The DSM-5 specifies that the symptoms of autism spectrum disorder are not caused or explained by intellectual disability.
Life Problems From Autism Spectrum Disorder
Autism spectrum disorder is referred to in everyday language as autism; in fact, the disorder was termed “autistic disorder” in earlier editions of the DSM, and its diagnostic criteria were much narrower than those of autism spectrum disorder. The qualifier “spectrum” in autism spectrum disorder is used to indicate that individuals with the disorder can show a range, or spectrum, of symptoms that vary in their magnitude and severity: some severe, others less severe. The previous edition of the DSM included a diagnosis of Asperger’s disorder, generally recognized as a less severe form of autistic disorder; individuals diagnosed with Asperger’s disorder were described as having average or high intelligence and a strong vocabulary, but exhibiting impairments in social interaction and social communication, such as talking only about their special interests (Wing, Gould, & Gillberg, 2011). However, because research has failed to demonstrate that Asperger’s disorder differs qualitatively from autistic disorder, the DSM-5 does not include it, which is prompting concerns among some parents that their children may no longer be eligible for special services (“Asperger’s Syndrome Dropped,” 2012). Some individuals with autism spectrum disorder, particularly those with better language and intellectual skills, can live and work independently as adults. However, most do not because the symptoms remain sufficient to cause serious impairment in many realms of life (APA, 2013).
Current estimates from the Center for Disease Control and Prevention’s Autism and Developmental Disabilities Monitoring Network indicate that 1 in 59 children in the United States has autism spectrum disorder; the disorder is 4 times more common among boys (1 in 38) than in girls (1 in 152) (Baio et al., 2018). Rates of autistic spectrum disorder have increased dramatically since the 1980s. For example, California saw an increase of 273% in reported cases from 1987 through 1998 (Byrd, 2002); between 2000 and 2008, the rate of autism diagnoses in the United States increased 78% (CDC, 2012). Although it is difficult to interpret this increase, it is possible that the rise in prevalence is the result of the broadening of the diagnosis, increased efforts to identify cases in the community, and greater awareness and acceptance of the diagnosis. In addition, mental health professionals are now more knowledgeable about autism spectrum disorder and are better equipped to make the diagnosis, even in subtle cases (Novella, 2008).
Causes of Autism Spectrum Disorder
Early theories of autism placed the blame squarely on the shoulders of the child’s parents, particularly the mother. Bruno Bettelheim (an Austrian-born American child psychologist who was heavily influenced by Sigmund Freud’s ideas) suggested that a mother’s ambivalent attitudes and her frozen and rigid emotions toward her child were the main causal factors in childhood autism. In what must certainly stand as one of the more controversial assertions in psychology over the last 50 years, he wrote, “I state my belief that the precipitating factor in infantile autism is the parent’s wish that his child should not exist” (Bettelheim, 1967, p. 125). As you might imagine, Bettelheim did not endear himself to a lot of people with this position; incidentally, no scientific evidence exists supporting his claims.
The exact causes of autism spectrum disorder remain unknown despite massive research efforts over the last two decades (Meek, Lemery-Chalfant, Jahromi, & Valiente, 2013). Autism appears to be strongly influenced by genetics, as identical twins show concordance rates of 60%–90%, whereas concordance rates for fraternal twins and siblings are 5%–10% (Autism Genome Project Consortium, 2007). Many different genes and gene mutations have been implicated in autism (Meek et al., 2013). Among the genes involved are those important in the formation of synaptic circuits that facilitate communication between different areas of the brain (Gauthier et al., 2011). A number of environmental factors are also thought to be associated with increased risk for autism spectrum disorder, at least in part, because they contribute to new mutations. These factors include exposure to pollutants, such as plant emissions and mercury, urban versus rural residence, and vitamin D deficiency (Kinney, Barch, Chayka, Napoleon, & Munir, 2009).
In the late 1990s, a prestigious medical journal published an article purportedly showing that autism is triggered by the MMR (measles, mumps, and rubella) vaccine. These findings were very controversial and drew a great deal of attention, sparking an international forum on whether children should be vaccinated. In a shocking turn of events, some years later the article was retracted by the journal that had published it after accusations of fraud on the part of the lead researcher. Despite the retraction, the reporting in popular media led to concerns about a possible link between vaccines and autism persisting. A recent survey of parents, for example, found that roughly a third of respondents expressed such a concern (Kennedy, LaVail, Nowak, Basket, & Landry, 2011); and perhaps fearing that their children would develop autism, more than 10% of parents of young children refuse or delay vaccinations (Dempsey et al., 2011).
Why does concern over vaccines and autism spectrum disorder persist? The notion that autism spectrum disorder is caused by vaccinations is appealing to some because it provides a simple explanation for this condition. Like all disorders, however, there are no simple explanations for autism spectrum disorder. Although the research discussed above has shed some light on its causes, science is still a long way from a complete understanding of the disorder.
Additional Supplemental Resources
Websites
- NIH Mental Health Information
- The National Institute of Mental Health (NIMH) offers expert-reviewed information on mental disorders, a range of related topics, and the latest mental health research.
- SAMSHA Substance Abusive and Mental Health Alliance
- Find treatment facilities and programs in the United States or U.S. Territories for mental and substance use disorders
- NAMI National Alliance on Mental Illness
- NAMI provides advocacy, education, support and public awareness so that all individuals and families affected by mental illness can build better lives.
Videos
- Ted-Ed: What is depression?
- How is having depression different from feeling depressed? Watch this Ted-Ed video to learn more about the causes, symptoms, and treatment of depression. A variety of discussion and assessment questions are included with the video (free registration is required to access the questions). Closed captioning available.
- Crash Course Video #28 – Psychological Disorders
- This video on psychological disorders includes information on topics such as mental health reform, definitions of psychological disorders, and the advantages and disadvantages of the DSM. Closed captioning available.
- Crash Course Video #29 – OCD and Anxiety Disorders
- This video on Obsessive-Compulsive Disorder (OCD) and Anxiety Disorder includes information on topics such as stigma, anxiety disorders, and OCD. Closed captioning available.
- Crash Course Video #30 – Depressive and Bipolar Disorders
- This video includes information on topics such as Bipolar Disorder, causes of Mood Disorders, and Major Depression. Closed captioning available.
- Crash Course Video #31 – Trauma and Addiction
- This video on trauma and addiction includes information on topics such as causes of Post-Traumatic Stress Disorder, substance abuse, and the dual diagnosis model of treatment. Closed captioning available.
- Crash Course Video #32 – Schizophrenia and Dissociative Disorders
- This video on Schizophrenia and Dissociative Disorders includes information on topics such as delusions, hallucinations, positive vs. negative symptoms, and dissociative disorders. Closed captioning available.
- Crash Course Video #34 – Personality Disorders
- This video on personality disorders includes information on topics such as borderline personality disorder, antisocial personality disorder, and treatment. Closed captioning available.
