Whenever we feel particularly unhappy, we are likely to describe ourselves as “depressed.” In all likelihood, we are merely responding to sad events, fatigue, or unhappy thoughts. This loose use of the term confuses a perfectly normal mood swing with a clinical syndrome (see InfoCentral). All of us experience dejection from time to time, but only some experience a depressive disorder. Such disorders bring severe and long-lasting psychological pain that may intensify as time goes by. Those who suffer from them may lose their will to carry out the simplest of life’s activities; some even lose their will to live.

Around 9 percent of adults in the United States suffer from a severe unipolar pattern of depression in any given year, while as many as 5 percent suffer from mild forms (Kessler et al., 2012, 2010). Around 18 percent of all adults experience an episode of severe unipolar depression at some point in their lives. These prevalence rates are similar in Canada, England, and many other countries. Moreover, the rate of depression—mild or severe—is higher among poor people than wealthier people (Sareen et al., 2011).

Women are at least twice as likely as men to have episodes of severe unipolar depression (WHO, 2014; Astbury, 2010). As many as 26 percent of women have an episode at some time in their lives, compared with 12 percent of men. As you will see in Chapter 14, among children the prevalence of unipolar depression is similar for girls and boys.

Approximately 85 percent of people with unipolar depression recover, some without treatment. At least 40 percent of them have at least one other episode of depression later in their lives (Halverson et al., 2015; Monroe, 2010).

The picture of depression may vary from person to person. Earlier you saw how Meri’s profound sadness, fatigue, and cognitive deterioration brought her job and social life to a standstill. Some depressed people have symptoms that are less severe. They manage to function, although their depression typically robs them of much effectiveness or pleasure.

As the case of Meri indicates, depression has many symptoms other than sadness. The symptoms, which often exacerbate one another, span five areas of functioning: emotional, motivational, behavioral, cognitive, and physical.

Emotional Symptoms Most people who are depressed feel sad and dejected. They describe themselves as feeling “miserable,” “empty,” and “humiliated.” They tend to lose their sense of humor, report getting little pleasure from anything, and in some cases display anhedonia, an inability to experience any pleasure at all. A number also experience anxiety, anger, or agitation. Terrie Williams, author of Black Pain, a book about depression in African Americans, describes the agony she went through each morning as her depression was unfolding:

185

186

Motivational Symptoms Depressed people typically lose the desire to pursue their usual activities. Almost all report a lack of drive, initiative, and spontaneity. They may have to force themselves to go to work, talk with friends, eat meals, or have sex. Terrie describes her social withdrawal during a depressive episode:

Suicide represents the ultimate escape from life’s challenges. As you will see in Chapter 7, many depressed people become uninterested in life or wish to die; others wish they could kill themselves, and some actually do. It has been estimated that between 6 and 15 percent of people who suffer from severe depression commit suicide (MHF, 2014; Alridge, 2012).

Behavioral Symptoms Depressed people are usually less active and less productive. They spend more time alone and may stay in bed for long periods. One man recalls, “I’d awaken early, but I’d just lie there—what was the use of getting up to a miserable day?” (Kraines & Thetford, 1972, p. 21). Depressed people may also move and even speak more slowly (Behrman, 2014).

Cognitive Symptoms Depressed people hold extremely negative views of themselves. They consider themselves inadequate, undesirable, inferior, perhaps evil (Lopez Molina et al., 2014). They also blame themselves for nearly every unfortunate event, even things that have nothing to do with them, and they rarely credit themselves for positive achievements.

Another cognitive symptom of depression is pessimism. Sufferers are usually convinced that nothing will ever improve, and they feel helpless to change any aspect of their lives. Because they expect the worst, they are likely to procrastinate. Their sense of hopelessness and helplessness makes them especially vulnerable to suicidal thinking (Shiratori et al., 2014).

People with depression frequently complain that their intellectual ability is poor. They feel confused, unable to remember things, easily distracted, and unable to solve even the smallest problems. In laboratory studies, depressed people do perform more poorly than nondepressed people on some tasks of memory, attention, and reasoning (Chen et al., 2013). It may be, however, that these difficulties sometimes reflect motivational problems rather than cognitive ones.

187

Physical Symptoms People who are depressed frequently have such physical ailments as headaches, indigestion, constipation, dizzy spells, and general pain (Bai et al., 2014; Goldstein et al., 2011). In fact, many depressions are misdiagnosed as medical problems at first (Parker & Hyett, 2010). Disturbances in appetite and sleep are particularly common (Jackson et al., 2014). Most depressed people eat less, sleep less, and feel more fatigued than they did prior to the disorder. Some, however, eat and sleep excessively.

According to DSM-5, a major depressive episode is a period of two or more weeks marked by at least five symptoms of depression, including sad mood and/or loss of pleasure (see Table 6.1 below). In extreme cases, the episode may include psychotic symptoms, ones marked by a loss of contact with reality, such as delusions—bizarre ideas without foundation—or hallucinations—perceptions of things that are not actually present. A depressed man with psychotic symptoms may imagine that he cannot eat “because my intestines are deteriorating and will soon stop working,” or he may believe that he sees his dead wife.

DSM-5 lists several types of depressive disorders. People who go through a major depressive episode without having any history of mania receive a diagnosis of major depressive disorder (APA, 2013) (see Table 6.1 again). The disorder may be further described as seasonal if it changes with the seasons (for example, if the depression recurs each winter), catatonic if it is marked by either immobility or excessive activity, peripartum if it occurs during pregnancy or within four weeks of giving birth, or melancholic if the person is almost totally unaffected by pleasurable events.

People whose unipolar depression is particularly long-lasting receive a diagnosis of persistent depressive disorder (APA, 2013) (see Table 6.1 again). Some people with this chronic disorder have repeated major depressive episodes, a pattern technically called persistent depressive disorder with major depressive episodes. Others have less severe and less disabling symptoms, a pattern called persistent depressive disorder with dysthymic syndrome.

A third type of depressive disorder is premenstrual dysphoric disorder, a diagnosis given to certain women who repeatedly have clinically significant depressive and related symptoms during the week before menstruation. The inclusion of this pattern in DSM-5 is controversial, as you will see later (see page 209).

Yet another kind of depressive disorder, disruptive mood dysregulation disorder, is characterized by a combination of persistent depressive symptoms and recurrent outbursts of severe temper. This disorder emerges during mid-childhood or adolescence and so is discussed in Chapter 14, “Disorders Common Among Children and Adolescents.”

Episodes of unipolar depression often seem to be triggered by stressful events (Fried et al., 2015). In fact, researchers have found that depressed people have a larger number of stressful life events during the month just before the onset of their disorder than do other people during the same period of time. Of course, stressful life events also precede other psychological disorders, but depressed people often report more such events than anybody else.

188

Some clinicians consider it important to distinguish a reactive (exogenous) depression, which follows clear-cut stressful events, from an endogenous depression, which seems to be a response to internal factors. But can one ever know for certain whether a depression is reactive or not? Even if stressful events occurred before the onset of depression, that depression may not be reactive. The events could actually be a coincidence. Thus, today’s clinicians usually concentrate on recognizing both the situational and the internal aspects of any given case of unipolar depression.

Medical researchers have been aware for years that certain diseases and drugs produce mood changes. Could unipolar depression itself have biological causes? Evidence from genetic, biochemical, anatomical, and immune system studies suggests that often it does.

Genetic Factors Four kinds of research—family pedigree, twin, adoption, and molecular biology gene studies—suggest that some people inherit a predisposition to unipolar depression (McGuffin, 2014). Family pedigree studies select people with unipolar depression, examine their relatives, and see whether depression also afflicts other members of the family. If a predisposition to unipolar depression is inherited, the relatives should have a higher rate of depression than the population at large. Researchers have in fact found that as many as 30 percent of those relatives are depressed (see Table 6.2), compared with fewer than 10 percent of the general population (Levinson & Nichols, 2014; Berrettini, 2006).

189

If a predisposition to unipolar depression is inherited, you might also expect to find a particularly large number of cases among the close relatives of a proband. Twin studies have supported this expectation (Levinson & Nichols, 2014). One study looked at nearly 200 pairs of twins. When an identical twin had unipolar depression, there was a 46 percent chance that the other twin would have the same disorder. In contrast, when a fraternal twin had unipolar depression, the other twin had only a 20 percent chance of developing the disorder (McGuffin et al., 1996).

Finally, today’s scientists have at their disposal techniques from the field of molecular biology to help them directly identify genes and determine whether certain gene abnormalities are related to depression. Using such techniques, researchers have found evidence that unipolar depression may be tied to genes on chromosomes 1, 4, 9, 10, 11, 12, 13, 14, 17, 18, 20, 21, 22, and X (Jansen et al., 2015; Preuss et al., 2013). For example, a number of researchers have found that people who are depressed often have an abnormality of their 5-HTT gene, a gene located on chromosome 17 that is responsible for the activity of the neurotransmitter serotonin. As you will read in the next section, low activity of serotonin is closely tied to depression.

Biochemical Factors Low activity of two neurotransmitter chemicals, norepinephrine and serotonin, has been strongly linked to unipolar depression. In the 1950s, several pieces of evidence began to point to this relationship. First, medical researchers discovered that certain medications for high blood pressure often caused depression (Ayd, 1956). As it turned out, some of these medications lowered norepinephrine activity and others lowered serotonin. A second piece of evidence was the discovery of the first truly effective antidepressant drugs. Although these drugs were discovered by accident, researchers soon learned that they relieve depression by increasing either norepinephrine or serotonin activity.

For years it was thought that low activity of either norepinephrine or serotonin was capable of producing depression, but investigators now believe that their relation to depression is more complicated (Ding et al., 2014; Goldstein et al., 2011). Research suggests that interactions between serotonin and norepinephrine activity, or between these and other kinds of neurotransmitters in the brain, rather than the operation of any one neurotransmitter alone, may account for unipolar depression.

190

Biological researchers have also learned that the body’s endocrine system may play a role in unipolar depression (see PsychWatch). As you have seen, endocrine glands throughout the body release hormones, chemicals that in turn spur body organs into action (see Chapter 5). People with unipolar depression have been found to have abnormally high levels of cortisol, one of the hormones released by the adrenal glands during times of stress (Owens et al., 2014; Treadway & Pizzagalli, 2014). This relationship is not all that surprising, given that stressful events often seem to trigger depression. Another hormone that has been tied to depression is melatonin, sometimes called the “Dracula hormone” because it is released only in the dark. People who experience a recurrence of depression each winter (a pattern called seasonal affective disorder) may secrete more melatonin during the winter’s long nights than other individuals do.

191

Still other biological researchers are starting to believe that unipolar depression is tied more closely to what happens within neurons than to the chemicals that carry messages between neurons. They believe that activity by key neurotransmitters or hormones ultimately leads to deficiencies of certain proteins and other chemicals within neurons—deficiencies that may impair the health of the neurons and lead in turn to depression (Duman, 2014).

The biochemical explanations of unipolar depression have produced much enthusiasm, but research in this area has certain limitations. Some of it has relied on analogue studies, which create depression-like symptoms in laboratory animals. Researchers cannot be certain that these symptoms do in fact reflect the human disorder. Similarly, until recent years, technology was limited, and studies of human depression had to measure brain biochemical activity indirectly. As a result, investigators could never be certain of the biochemical events that were taking place in the brain. Current studies using newer technology, such as PET and MRI scans, are helping to eliminate such uncertainties about such brain activity.

Brain Anatomy and Brain Circuits In earlier chapters, you read that many biological researchers now believe that emotional reactions of various kinds are tied to brain circuits—networks of brain structures that work together, triggering each other into action and producing a particular kind of emotional reaction. Although research is far from complete, a brain circuit responsible for unipolar depression has begun to emerge (Treadway & Pizzagalli, 2014; Brockmann et al., 2011). An array of brain-imaging studies point to several brain areas that are likely members of this circuit, including the prefrontal cortex, the hippocampus, the amygdala, and Brodmann Area 25, an area located just under the brain part called the cingulate cortex (see Figure 6.1). Research suggests that, among depressed people, activity and blood flow are low in certain parts of the prefrontal cortex (Vialou et al., 2014), yet high in other parts (Lemogne et al., 2010); the hippocampus is undersized and its production of new neurons is low (Kubera et al., 2011; Campbell et al., 2004); activity and blood flow are elevated in the amygdala (Treadway & Pizzagalli, 2014; Goldstein et al., 2011); and Brodmann Area 25 is relatively small and overactive (Eggers, 2014; Mayberg et al., 2005).

192

The Immune System As you will see in Chapter 8, the immune system is the body’s network of activities and body cells that fight off bacteria, viruses, and other foreign invaders. When people are under intense stress for a while, their immune systems may become dysregulated, leading to lower functioning of important white blood cells called lymphocytes and to increased production of C-reactive protein (CRP), a protein that spreads throughout the body and causes inflammation and various illnesses. There is a growing belief among some researchers that immune system dysregulation of this kind helps produce depression (Anderson et al., 2014; Yoon et al., 2012).

What Are the Biological Treatments for Unipolar Depression? Usually biological treatment means antidepressant drugs or popular herbal supplements, but for severely depressed people who do not respond to other forms of treatment, it sometimes means electroconvulsive therapy, or a relatively new group of approaches called brain stimulation.

ELECTROCONVULSIVE THERAPY One of the most controversial forms of treatment for depression is electroconvulsive therapy (ECT). In this procedure, two electrodes are attached to the patient’s head, and 65 to 140 volts of electricity are passed through the brain for half a second or less. This results in a brain seizure that lasts from 25 seconds to a few minutes. After 6 to 12 such treatments, spaced over two to four weeks, most patients feel less depressed (Fink, 2014, 2007).

The discovery that electric shock can be therapeutic was made by accident. In the 1930s, clinical researchers mistakenly came to believe that brain seizures, or the convulsions (severe body spasms) that accompany them, could cure schizophrenia and other psychotic disorders, and so they searched for ways to induce seizures as a treatment for patients with psychosis. One early technique was to give patients the drug metrazol. Another was to give them large doses of insulin (insulin coma therapy). These procedures produced the desired brain seizures, but each was quite dangerous and sometimes even caused death. Finally, an Italian psychiatrist named Ugo Cerletti discovered that he could produce seizures more safely by applying electric currents to a patient’s head. ECT soon became popular and was tried out on a wide range of psychological problems, as new techniques so often are. Its effectiveness with severe depression in particular became apparent.

In the early years of ECT, broken bones and dislocations of the jaw or shoulders sometimes resulted from patients’ severe convulsions. Today’s practitioners avoid these problems by giving patients strong muscle relaxants to minimize convulsions. They also use anesthetics to put patients to sleep during the procedure, reducing their terror.

Patients who receive ECT often have difficulty remembering certain events, most often events that took place immediately before and after their treatments (Martin et al., 2015; Merkl et al., 2011). In most cases, this memory loss clears up within a few months, but some patients are left with gaps in more distant memory, and this form of amnesia can be permanent (Hanna et al., 2009; Wang, 2007).

ECT is clearly effective in treating unipolar depression, although it has been difficult to determine why it works so well (Baldinger et al., 2014; Fink et al., 2014). The procedure seems to be particularly effective in cases of depression that include delusions (Rothschild, 2010).

193

ANTIDEPRESSANT DRUGS Two kinds of drugs discovered in the 1950s reduce the symptoms of depression: monoamine oxidase (MAO) inhibitors and tricyclics. These drugs have now been joined by a third group, the so-called second-generation antidepressants (see Table 6.3).

The effectiveness of MAO inhibitors as a treatment for unipolar depression was discovered accidentally. Physicians noted that iproniazid, a drug being tested on patients with tuberculosis, had an interesting effect: it seemed to make the patients happier (Sandler, 1990). It was found to have the same effect on depressed patients (Kline, 1958; Loomer et al., 1957). What this and several related drugs had in common biochemically was that they slowed the body’s production of the enzyme monoamine oxidase (MAO). Thus they were called MAO inhibitors.

Normally, brain supplies of the enzyme MAO break down, or degrade, the neurotransmitter norepinephrine. MAO inhibitors block MAO from carrying out this activity and thereby stop the destruction of norepinephrine. The result is a rise in norepinephrine activity and, in turn, a reduction of depressive symptoms. Approximately half of depressed patients who take MAO inhibitors are helped by them (Ciraulo et al., 2011; Thase et al., 1995). There is, however, a potential danger with regard to these drugs. When people who take MAO inhibitors eat foods containing the chemical tyramine—including such common foods as cheeses, bananas, and certain wines—their blood pressure rises dangerously. Thus people on these drugs must stick to a rigid diet.

The discovery of tricyclics in the 1950s was also accidental. Researchers who were looking for a new drug to combat schizophrenia ran some tests on a drug called imipramine (Kuhn, 1958). They discovered that imipramine was of no help in cases of schizophrenia, but it did relieve unipolar depression in many people. The new drug (trade name Tofranil) and related ones became known as tricyclic antidepressants because they all share a three-ring molecular structure.

In hundreds of studies, depressed patients taking tricyclics have improved much more than similar patients taking placebos, although the drugs must be taken for at least 10 days before such improvements take hold (Advokat et al., 2014). About 65 percent of patients who take tricyclics are helped by them (FDA, 2014). If the patients stop taking tricyclics immediately after obtaining relief, they run a high risk of relapsing within a year. If, however, they continue taking the drugs for five months or more after being free of depressive symptoms—“continuation therapy” or “maintenance therapy”—their chances of relapse decrease considerably (Borges et al., 2014; FDA, 2014).

194

Most researchers have concluded that tricyclics reduce depression by acting on neurotransmitter “reuptake” mechanisms (Ciraulo et al., 2011). Remember from Chapter 2 that messages are carried from the “sending” neuron across the synaptic space to a receiving neuron by a neurotransmitter, a chemical released from the axon ending of the sending neuron. However, there is a complication in this process. While the sending neuron releases the neurotransmitter, a pumplike mechanism in the neuron’s ending immediately starts to reabsorb it in a process called reuptake. The purpose of this reuptake process is to control how long the neurotransmitter remains in the synaptic space and to prevent it from overstimulating the receiving neuron. Unfortunately, the reuptake mechanism may be too successful in some people—cutting off norepinephrine or serotonin activity too soon, preventing messages from reaching the receiving neurons, and producing clinical depression. Tricyclics block this reuptake process, thus increasing their neurotransmitter activity (see Figure 6.2).

A third group of effective antidepressant drugs, structurally different from the MAO inhibitors and tricyclics, has been developed during the past few decades. Most of these second-generation antidepressants are called selective serotonin reuptake inhibitors (SSRIs) because they increase serotonin activity specifically, without affecting norepinephrine or other neurotransmitters. The SSRIs include fluoxetine (trade name Prozac), sertraline (Zoloft), and escitalopram (Lexapro). More recently developed selective norepinephrine reuptake inhibitors, such as atomoxetine (Strattera), which increase norepinephrine activity only, and serotonin-norepinephrine reuptake inhibitors, such as venlafaxine (Effexor), which increase both serotonin and norepinephrine activity, are also now available (Advokat et al., 2014).

In effectiveness and speed of action, the second-generation antidepressant drugs are about on a par with the tricyclics, yet they are prescribed more often and their sales have skyrocketed. They do not pose the dietary problems of the MAO inhibitors or produce some of the unpleasant effects of the tricyclics, such as dry mouth and constipation. At the same time, the new antidepressants can produce undesirable side effects of their own. Some people gain weight or have a reduced sex drive, for example (Stahl, 2014).

195

As popular as the antidepressants are, it is important to recognize that they do not work for everyone. In fact, as you have read, even the most successful of them fails to help at least 35 percent of clients with depression. In fact, some recent reviews have raised the possibility that the failure rate is higher still (Hegerl et al., 2012; Isacsson & Alder, 2012). How are clients who do not respond to antidepressant drugs treated currently? Researchers have noted that, all too often, their psychiatrists or family physicians simply prescribe alternative antidepressants or antidepressant mixtures—one after another—without directing the clients to psychotherapy or counseling of some kind. Melissa, a depressed woman for whom psychotropic drug treatment has failed to work over many years, reflects on this issue:

BRAIN STIMULATION In recent years, three additional biological approaches have been developed for the treatment of depressive disorders—vagus nerve stimulation, transcranial magnetic stimulation, and deep brain stimulation.

The vagus nerve, the longest nerve in the human body, runs from the brain stem through the neck down the chest and on to the abdomen. A number of years ago, a group of depression researchers surmised that they might be able to stimulate the brain by electrically stimulating the vagus nerve with ECT. Their efforts gave birth to a new treatment for depression—vagus nerve stimulation.

In this procedure, a surgeon implants a small device called a pulse generator under the skin of the chest. The surgeon then guides a wire, which extends from the pulse generator, up to the neck and attaches it to the vagus nerve (see Figure 6.3). Electrical signals travel from the pulse generator through the wire to the vagus nerve. The stimulated vagus nerve then delivers electrical signals to the brain. In 2005, the U.S. Food and Drug Administration (FDA) approved this procedure.

Ever since vagus nerve stimulation was first tried on depressed human beings, research has found that it brings significant relief to many depressed people. In fact, in studies of severely depressed people who have not responded to any other form of treatment, as many as 40 percent improve significantly when treated with this procedure (Howland, 2014; Berry et al., 2013).

Transcranial magnetic stimulation (TMS) is another technique that is used to try to stimulate the brain without subjecting depressed patients to the undesired effects or trauma of ECT. In this procedure, the clinician places an electromagnetic coil on or above the patient’s head. The coil sends a current into the prefrontal cortex. As you’ll remember, some parts of the prefrontal cortex of depressed people are underactive; TMS appears to increase neuron activity in those regions. A number of studies have found that TMS reduces depression for many patients when it is administered daily for two to four weeks (Dunner et al., 2014; Fox et al., 2012).

196

As you read earlier, researchers have recently linked depression to high activity in Brodmann Area 25. This finding led neurologist Helen Mayberg and her colleagues (2005) to administer an experimental treatment called deep brain stimulation (DBS) to six severely depressed patients who had previously been unresponsive to all other forms of treatment. The Mayberg team drilled two tiny holes into the patient’s skull and implanted electrodes in Area 25. The electrodes were connected to a battery, or “pacemaker,” that was implanted in the patient’s chest (for men) or stomach (for women). The pacemaker powered the electrodes, sending a steady stream of low-voltage electricity to Area 25. Mayberg’s expectation was that this repeated stimulation would reduce Area 25 activity to a normal level and “recalibrate” and regulate the depression brain circuit.

In the initial study of DBS, four of the six severely depressed patients became almost depression-free within a matter of months (Mayberg et al., 2005). Subsequent research with other severely depressed individuals has also yielded promising findings (Berlim et al., 2014; Taghva, Malone, & Rezai, 2013). Understandably, this work has produced considerable enthusiasm in the clinical field, but it is important to recognize that research on DBS is in its early stages.

The psychological models that have been most widely applied to unipolar depression are the psychodynamic, behavioral, and cognitive models. The psychodynamic model has not been strongly supported by research, and the behavioral model has received moderate support. In contrast, the cognitive model has received considerable research support and gained a large following.

The Psychodynamic Model Sigmund Freud (1917) and his student Karl Abraham (1916, 1911) developed the first psychodynamic explanation and treatment for depression. Their emphasis on dependence and loss continues to influence today’s psychodynamic clinicians.

PSYCHODYNAMIC EXPLANATIONS Freud and Abraham began by noting the similarity between clinical depression and grief in people who lose loved ones: constant weeping, loss of appetite, difficulty sleeping, loss of pleasure in life, and social withdrawal. According to the theorists, a series of unconscious processes is set in motion when a loved one dies. Unable to accept the loss, mourners at first regress to the oral stage of development, the period of total dependency when infants cannot distinguish themselves from their parents. By regressing to this stage, the mourners merge their own identity with that of the person they have lost, and so symbolically regain the lost person. They direct all their feelings for the loved one, including sadness and anger, toward themselves. For most mourners, this reaction is temporary. For some, however, grief worsens over time, and they, in fact, become depressed.

Of course, many people become depressed without losing a loved one. To explain why, Freud proposed the concept of symbolic loss, or imagined loss, in which a person equates other kinds of events with the loss of a loved one. A college student may, for example, experience failure in a calculus course as the loss of her parents, believing that they love her only when she excels academically.

Although many psychodynamic theorists have parted company with Freud and Abraham’s theory of depression, it continues to influence current psychodynamic thinking (Desmet, 2013; Zuckerman, 2011). For example, object relations theorists (the psychodynamic theorists who emphasize relationships) propose that depression results when people’s relationships leave them feeling unsafe and insecure (Schattner & Sharar, 2011; Blatt, 2004). People whose parents pushed them toward either excessive dependence or excessive self-reliance are more likely to become depressed when they later lose important relationships.

197

The following description by the therapist of a depressed middle-aged woman illustrates the psychodynamic concepts of dependence, loss of a loved one, and symbolic loss:

Studies have offered general support for the psychodynamic idea that major losses, especially ones suffered early in life, may set the stage for later depression (Gilman, 2013; Gutman & Nemeroff, 2011). When, for example, a depression scale was administered to 1,250 medical patients during visits to their family physicians, the patients whose fathers had died during their childhood scored higher on depression (Barnes & Prosen, 1985). At the same time, research does not indicate that loss is always at the core of depression. In fact, it is estimated that less than 10 percent of all people who have major losses in life actually become depressed (Bonanno, 2004; Paykel & Cooper, 1992). Moreover, research into the loss–depression link has yielded inconsistent findings. Though some studies find evidence of a relationship between childhood loss and later depression, others do not.

WHAT ARE THE PSYCHODYNAMIC TREATMENTS FOR UNIPOLAR DEPRESSION? Believing that unipolar depression results from unconscious grief over real or imagined losses, compounded by excessive dependence on other people, psychodynamic therapists seek to help clients bring these underlying issues to consciousness and work through them. They encourage the depressed client to associate freely during therapy; suggest interpretations of the client’s associations, dreams, and displays of resistance and transference; and help the person review past events and feelings (Busch et al., 2004). Free association, for example, helped one man recall the early experiences of loss that, according to his therapist, had set the stage for his depression:

198

Despite successful case reports such as this, researchers have found that long-term psychodynamic therapy is only occasionally helpful in cases of unipolar depression (Prochaska & Norcross, 2013). Two features of the approach may help limit its effectiveness. First, depressed clients may be too passive and feel too weary to join fully into the subtle therapy discussions. And second, they may become discouraged and end treatment too early when this long-term approach is unable to provide the quick relief that they desperately seek. Short-term psychodynamic therapies have performed better than traditional, longer-term approaches (Midgley et al., 2013; Lemma et al., 2011).

The Behavioral Model Behaviorists believe that unipolar depression results from significant changes in the number of rewards and punishments people receive in their lives, and they treat depressed people by helping them build more desirable patterns of reinforcement (Dygdon & Dienes, 2013). Clinical researcher Peter Lewinsohn was one of the first clinical theorists to develop a behavioral explanation (Lewinsohn et al., 1990, 1984).

THE BEHAVIORAL EXPLANATION Lewinsohn suggested that the positive rewards in life dwindle for some people, leading them to perform fewer and fewer constructive behaviors. The rewards of campus life, for example, disappear when a young woman graduates from college and takes a job; and an aging baseball player loses the rewards of high salary and adulation when his skills deteriorate. Although many people manage to fill their lives with other forms of gratification, some become particularly disheartened. The positive features of their lives decrease even more, and the decline in rewards leads them to perform still fewer constructive behaviors. In this manner, they spiral toward depression.

In a number of studies, behaviorists have found that the number of rewards people receive in life is indeed related to the presence or absence of depression. Not only do depressed participants typically report fewer positive rewards than nondepressed participants, but when their rewards begin to increase, their mood improved as well (Bylsma et al., 2011; Lewinsohn et al., 1979). Similarly, other investigations have found a strong relationship between positive life events and feelings of life satisfaction and happiness (Carvalho & Hopko, 2011).

Lewinsohn and other behaviorists have further proposed that social rewards are particularly important in the downward spiral of depression (Martell et al., 2010). This claim has been supported by research showing that depressed persons receive fewer social rewards than nondepressed persons and that as their mood improves, their social rewards increase. Although depressed people are sometimes the victims of social circumstances (see MediaSpeak below), it may also be that their dark mood and flat behaviors help produce a decline in social rewards (Constantino et al., 2012; Coyne, 2001).

199

200

WHAT ARE THE BEHAVIORAL TREATMENTS FOR UNIPOLAR DEPRESSION? Behavioral therapists use a variety of strategies to help increase the number of rewards experienced by their depressed clients (Dimidjian et al., 2014; Martell et al., 2010): (1) First the therapist selects activities that the client considers pleasurable, such as going shopping or taking photos, and encourages the person to set up a weekly schedule for engaging in them. Studies have shown that adding positive activities to a person’s life—sometimes called behavioral activation—can indeed lead to a better mood. (2) Second, while reintroducing pleasurable events into a client’s life, the therapist makes sure that the person’s various behaviors are reinforced correctly. Behaviorists argue that when people become depressed, their negative behaviors—crying, ruminating, complaining, or self-criticism—keep others at a distance, reducing chances for rewarding interactions. To change this pattern, therapists guide clients to monitor their negative behaviors and to try new, more positive ones. In addition, the therapist may try to systematically ignore a client’s depressive behaviors while praising or otherwise rewarding constructive statements and behavior, such as going to work. (3) Finally, behavioral therapists may train clients in effective social skills. In group therapy programs, for example, members may work together to improve eye contact, facial expression, posture, and other behaviors that send social messages.

These behavioral techniques seem to be of only limited help when just one of them is applied. However, when two or more such techniques are combined, behavioral treatment does appear to reduce depressive symptoms, particularly if the depression is mild. It is worth noting that Lewinsohn himself has combined behavioral techniques with cognitive strategies in recent years in an approach similar to the cognitive-behavioral treatments discussed in the next section.

The Cognitive Model Cognitive theorists believe that people with unipolar depression persistently view events in negative ways and that such perceptions lead to their disorder. The two most influential cognitive explanations are the theory of learned helplessness and the theory of negative thinking.

LEARNED HELPLESSNESS Feelings of helplessness fill this account of a young woman’s depression:

201

Mary feels that she is “losing control of her life.” According to psychologist Martin Seligman (1975), such feelings of helplessness are at the center of her depression. Since the mid-1960s Seligman has been developing the learned helplessness theory of depression. It holds that people become depressed when they think (1) that they no longer have control over the reinforcements (the rewards and punishments) in their lives and (2) that they themselves are responsible for this helpless state.

Seligman’s theory first began to take shape when he was working with laboratory dogs. In one procedure, he strapped dogs into an apparatus called a hammock, in which they received shocks periodically no matter what they did. The next day each dog was placed in a shuttle box, a box divided in half by a barrier over which the animal could jump to reach the other side (see Figure 6.4). Seligman applied shocks to the dogs in the box, expecting that they, like other dogs in this situation, would soon learn to escape by jumping over the barrier. However, most of these dogs failed to learn anything in the shuttle box. After a flurry of activity, they simply “lay down and quietly whined” and accepted the shock.

Seligman decided that while receiving inescapable shocks in the hammock the day before, the dogs had learned that they had no control over unpleasant events (shocks) in their lives. That is, they had learned that they were helpless to do anything to change negative situations. Thus, when later they were placed in a new situation (the shuttle box) where they could in fact control their fate, they continued to believe that they were generally helpless. Seligman noted that the effects of learned helplessness greatly resemble the symptoms of human depression, and he proposed that people in fact become depressed after developing a general belief that they have no control over reinforcements in their lives.

In numerous human and animal studies, participants who undergo helplessness training have displayed reactions similar to depressive symptoms (Dygdon & Dienes, 2013). When, for example, human participants are exposed to uncontrollable negative events, they later score higher than other individuals on a depressive mood survey (Miller & Seligman, 1975). Similarly, helplessness-trained animal subjects lose interest in sexual and social activities—a common symptom of human depression (Lindner, 1968).

The learned helplessness explanation of depression has been revised somewhat over the past several decades. According to a newer version of the theory, the attribution-helplessness theory, when people view events as beyond their control, they ask themselves why this is so (Abramson et al., 2002, 1989, 1978). If they attribute their present lack of control to some internal cause that is both global and stable (“I am inadequate at everything and I always will be”), they may well feel helpless to prevent future negative outcomes and they may experience depression. If they make other kinds of attributions, they are unlikely to have this reaction.

202

Consider a college student whose girlfriend breaks up with him. If he attributes this loss of control to an internal cause that is both global and stable—“It’s my fault [internal], I ruin everything I touch [global], and I always will [stable]”—he then has reason to expect similar losses of control in the future and may generally experience a sense of helplessness. According to the learned helplessness view, he is a prime candidate for depression. If the student had instead attributed the breakup to causes that were more specific (“The way I’ve behaved the past couple of weeks blew this relationship”), unstable (“I don’t usually act like that”), or external (“She never did know what she wanted”), he might not expect to lose control again and would probably not experience helplessness and depression. Hundreds of studies have supported the relationship between styles of attribution, helplessness, and depression (Rotenberg et al., 2012).

Some theorists have refined the helplessness model yet again in recent years. They suggest that attributions are likely to cause depression only when they further produce a sense of hopelessness in a person (Wain et al., 2011). By taking this factor into consideration, clinicians are often able to predict depression with still greater precision (Wang et al., 2013).

Although the learned helplessness theory of unipolar depression has been very influential, it too has imperfections. First, much of the learned helplessness research relies on animal subjects. It is impossible to know whether the animals’ symptoms do in fact reflect the clinical depression found in humans. Second, the attributional feature of the theory raises difficult questions. What about the dogs and rats who learn helplessness? Can animals make attributions, even implicitly?

NEGATIVE THINKING Like Seligman, Aaron Beck believes that negative thinking lies at the heart of depression (Beck & Weishaar, 2014; Beck, 2002, 1991, 1967). According to Beck, maladaptive attitudes, a cognitive triad, errors in thinking, and automatic thoughts combine to produce the clinical syndrome.

Beck believes that some people develop maladaptive attitudes as children, such as “My general worth is tied to every task I perform” or “If I fail, others will feel repelled by me.” The attitudes result from their early interactions and experiences (see Figure 6.5). Many failures are inevitable in a full, active life, so such attitudes are inaccurate and set the stage for all kinds of negative thoughts and reactions. Beck suggests that later in these people’s lives, upsetting situations may trigger an extended round of negative thinking. That thinking typically takes three forms, which he calls the cognitive triad: the individuals repeatedly interpret (1) their experiences, (2) themselves, and (3) their futures in negative ways that lead them to feel depressed. The cognitive triad is at work in the thinking of this depressed person:

203

According to Beck, depressed people also make errors in their thinking. In one common error of logic, they draw arbitrary inferences—negative conclusions based on little evidence. A man walking through the park, for example, passes a woman who is looking at nearby flowers and concludes, “She’s avoiding looking at me.” Similarly, depressed people often minimize the significance of positive experiences or magnify that of negative ones. A college student receives an A on a difficult English exam, for example, but concludes that the grade reflects the professor’s generosity rather than her own ability (minimization). Later in the week the same student must miss an English class and is convinced that she will be unable to keep up the rest of the semester (magnification).

Finally, depressed people have automatic thoughts, a steady train of unpleasant thoughts that keep suggesting to them that they are inadequate and that their situation is hopeless. Beck labels these thoughts “automatic” because they seem to just happen, as if by reflex. In the course of only a few hours, depressed people may be visited by hundreds of such thoughts: “I’m worthless…. I’ll never amount to anything …. let everyone down…. Everyone hates me…. My responsibilities are overwhelming…. I’ve failed as a parent…. I’m stupid…. Everything is difficult for me…. Things will never change.”

Many studies have produced evidence in support of Beck’s explanation (Pössel & Black, 2014). Several of them confirm that depressed people hold maladaptive attitudes and that the more of these maladaptive attitudes they hold, the more depressed they tend to be (Thomas & Altareb, 2012). Still other research has found the cognitive triad at work in depressed people (Lai et al., 2014). And still other studies have supported Beck’s claims about errors in logic (Alcalar et al., 2012). In one study, female participants—some depressed, some not—were asked to read and interpret paragraphs about women in difficult situations. Depressed participants made more errors in logic (such as arbitrary inference) in their interpretations than nondepressed women did (Hammen & Krantz, 1976).

Finally, research has supported Beck’s claim that automatic thoughts are tied to depression (Alcalar et al., 2012). In several classic studies, nondepressed participants who are tricked into reading negative automatic-thought-like statements about themselves become increasingly depressed (Bates et al., 1999; Strickland et al., 1975). In a related line of research, it has been found that people who generally make ruminative responses during their depressed moods—that is, repeatedly dwell mentally on their mood without acting to change it—feel dejection longer and are more likely to develop clinical depression later in life than people who avoid such ruminations (Johnson et al., 2014; Watkins & Nolen-Hoeksema, 2014).

204

WHAT ARE THE COGNITIVE TREATMENTS FOR UNIPOLAR DEPRESSION? To help clients overcome this negative thinking, Beck has developed a treatment approach that he calls cognitive therapy (Beck & Weishaar, 2014). However, as you will see, the approach also includes a number of behavioral techniques, particularly as therapists try to get clients moving again and encourage them to try out new behaviors. Thus, many theorists consider this approach a cognitive-behavioral therapy rather than the purely cognitive intervention implied by its name. The approach follows four phases and usually requires fewer than 20 sessions.

PHASE 1: Increasing activities and elevating mood Using behavioral techniques to set the stage for cognitive treatment, therapists first encourage clients to become more active and confident. Clients spend time during each session preparing a detailed schedule of hourly activities for the coming week. As they become more active from week to week, their mood is expected to improve.

PHASE 2: Challenging automatic thoughts Once people are more active and feeling some emotional relief, cognitive therapists begin to educate them about their negative automatic thoughts. The individuals are instructed to recognize and record automatic thoughts as they occur and to bring their lists to each session. Therapist and client then test the reality behind the thoughts, often concluding that they are groundless.

PHASE 3: Identifying negative thinking and biases As people begin to recognize the flaws in their automatic thoughts, cognitive therapists show them how illogical thinking processes are contributing to these thoughts. The therapists also guide clients to recognize that almost all their interpretations of events have a negative bias and to change that style of interpretation.

PHASE 4: Changing primary attitudes Therapists help clients change the maladaptive attitudes that set the stage for their depression in the first place. As part of the process, therapists often encourage clients to test their attitudes, as in the following therapy discussion:

205

Over the past several decades, hundreds of studies have shown that Beck’s therapy and similar cognitive and cognitive-behavioral approaches help with unipolar depression. Depressed adults who receive these therapies improve much more than those who receive placebos or no treatment at all (Young et al., 2014; Hollon & Cuijpers, 2013). Around 50 to 60 percent show a near-total elimination of their symptoms.

It is worth noting that a growing number of today’s cognitive-behavioral therapists do not agree with Beck’s proposition that individuals must fully discard their negative cognitions in order to overcome depression. These therapists, the new-wave cognitive-behavioral therapists about whom you read in Chapters 2 and 4, including those who practice acceptance and commitment therapy (ACT), guide depressed clients to recognize and accept their negative cognitions simply as streams of thinking that flow through their minds, rather than as valuable guides for behavior and decisions. As clients increasingly accept their negative thoughts for what they are, they can better work around the thoughts as they navigate their way through life (Levin et al., 2014; Hayes et al., 2006).

Sociocultural theorists propose that unipolar depression is strongly influenced by the social context that surrounds people. Their belief is supported by the finding, discussed earlier, that depression is often triggered by outside stressors. Once again, there are two kinds of sociocultural views—the family-social perspective and the multicultural perspective.

The Family-Social Perspective Earlier you read that some behaviorists believe that a decline in social rewards is particularly important in the development of depression. Although presented as part of their behavioral explanation, this view is consistent with the family-social perspective. Depression has been tied repeatedly to the unavailability of social support such as that found in a happy marriage (Ito & Sagara, 2014). People who are separated or divorced display at least three times the depression rate of married or widowed people and double the rate of those who have never been married (Schultz, 2007; Weissman et al., 1991). In some cases, the spouse’s depression may contribute to marital discord, a separation, or divorce, but often the interpersonal conflicts and low social support found in troubled relationships seem to lead to depression (Najman et al., 2014).

Researchers have also found that people whose lives are isolated and without intimacy are particularly likely to become depressed at times of stress (Hölzel et al., 2011; Nezlek et al., 2000). Some highly publicized studies conducted in England several decades ago showed that women who had three or more young children, lacked a close confidante, and had no outside employment were more likely than other women to become depressed after going through stressful events (Brown, 2002; Brown & Harris, 1978). Studies have also found that depressed people who lack social support remain depressed longer than those who have a supportive spouse or warm friendships.

Family-Social Treatments Therapists who use family and social approaches to treat depression help clients change how they deal with the close relationships in their lives. The most effective family-social approaches are interpersonal psychotherapy and couple therapy.

206

INTERPERSONAL PSYCHOTHERAPY Developed by clinical researchers Gerald Klerman and Myrna Weissman, interpersonal psychotherapy (IPT) holds that various interpersonal situations may lead to depression and must be addressed. Particularly problematic are interpersonal loss, interpersonal role dispute, interpersonal role transition, and interpersonal deficits (Bleiberg & Markowitz, 2014; Verdeli, 2014). Over the course of around 16 sessions, IPT therapists address these areas.

First, depressed people may, as psychodynamic theorists suggest, be having a grief reaction over an important interpersonal loss, the loss of a loved one. In such cases, IPT therapists encourage clients to look closely at their relationship with the lost person and express any feelings of anger they may discover. Eventually clients develop new ways of remembering the lost person and also look for new relationships.

Second, depressed people may find themselves in the midst of an interpersonal role dispute. Role disputes occur when two people have different expectations of their relationship and of the role each should play. IPT therapists help clients examine whatever role disputes they may be involved in and then develop ways of resolving them.

Depressed people may also be going through an interpersonal role transition, brought about by major life changes such as divorce or the birth of a child. They may feel overwhelmed by the role changes that accompany the life change. In such cases, IPT therapists help them develop the social supports and skills the new roles require.

Finally, some depressed people display interpersonal deficits, such as extreme shyness or social awkwardness, that prevent them from having intimate relationships (see MindTech below). IPT therapists may help such clients identify their deficits and teach them social skills and assertiveness in order to improve their social effectiveness. In the following discussion, the therapist encourages a depressed man to recognize the effect his behavior has on others:

Studies suggest that IPT and related interpersonal treatments for depression have a success rate similar to that of cognitive and cognitive-behavioral therapies (Bleiberg & Markowitz, 2014). That is, symptoms almost totally disappear in 50 to 60 percent of clients who receive treatment. Not surprisingly, IPT is considered especially useful for depressed people who are struggling with social conflicts or undergoing changes in their careers or social roles (Ravitz et al., 2013).

207

208

COUPLE THERAPY As you have read, depression can result from marital discord, and recovery from depression is often slower for people who do not receive support from their spouse (Park & Unützer, 2014). In fact, as many as half of all depressed clients may be in a dysfunctional relationship. Thus many cases of depression have been treated by couple therapy, the approach in which a therapist works with two people who share a long-term relationship (Cohen et al., 2014).

Therapists who offer integrative behavioral couples therapy teach specific communication and problem-solving skills to couples and further guide them to be more accepting of each other (see Chapter 2). When a depressed person’s relationship is filled with conflict, couple treatments such as this may be as effective as individual cognitive therapy, interpersonal psychotherapy, or drug therapy in helping to reduce depression (Lebow et al., 2012, 2010).

The Multicultural Perspective Two issues have captured the interest of multicultural theorists: (1) links between gender and depression and (2) ties between cultural and ethnic background and depression.

GENDER AND DEPRESSION As you have read, there is a strong link between gender and depression. Women in places as far apart as France, Sweden, Lebanon, New Zealand, and the United States are at least twice as likely as men to receive a diagnosis of unipolar depression (Schuch et al., 2014). Why the huge difference between the sexes? A variety of theories have been offered.

The artifact theory holds that women and men are equally prone to depression but that clinicians often fail to detect depression in men (Emmons, 2010). Perhaps depressed women display more emotional symptoms, such as sadness and crying, which are easily diagnosed, while depressed men mask their depression behind traditionally “masculine” symptoms such as anger. Although a popular explanation, this view has failed to receive consistent research support. It turns out that women are actually no more willing or able than men to identify their depressive symptoms and to seek treatment (McSweeney, 2004; Nolen-Hoeksema, 1990).

The hormone explanation holds that hormone changes trigger depression in many women (Kurita et al., 2013). A woman’s biological life from her early teens to middle age is marked by frequent changes in hormone levels. Gender differences in rates of depression also span these same years. Research suggests, however, that hormone changes alone are not responsible for the high levels of depression in women (Whiffen & Demidenko, 2006). Important social and life events that occur at puberty, pregnancy, and menopause could likewise have an effect. Hormone explanations have also been criticized as sexist, since they imply that a woman’s normal biology is flawed (see PsychWatch below).

The life stress theory suggests that women in our society are subject to more stress than men (Astbury, 2010). On average they face more poverty, more menial jobs, less adequate housing, and more discrimination than men—all factors that have been linked to depression. And in many homes, women bear a disproportionate share of responsibility for child care and housework.

The body dissatisfaction explanation states that females in Western society are taught, almost from birth, to seek a low body weight and slender body shape—goals that are unreasonable, unhealthy, and often unattainable. As you will observe in Chapter 9, the cultural standard for males is much more lenient. As girls approach adolescence, peer pressure may result in them becoming more and more dissatisfied with their weight and body, increasing the likelihood of depression. Consistent with this theory, gender differences in depression do indeed first appear during adolescence (Naninck et al., 2011), and people with eating disorders often have high levels of depression (Calugi et al., 2014). However, it is not clear that eating and weight concerns actually cause depression; they may instead be the result of depression.

209

The lack-of-control theory draws on the learned helplessness research and proposes that women may be more prone to depression because they feel less control than men over their lives. It has been found that victimization of any kind, from burglary to rape, often produces a general sense of helplessness and increases the symptoms of depression. Women in our society are more likely than men to be victims, particularly of sexual assault and child abuse (Astbury, 2010).

A final explanation for the gender differences found in depression is the rumination theory. As you read earlier, rumination is the tendency to keep focusing on one’s feelings when depressed and to consider repeatedly the causes and consequences of that depression (“Why am I so down? …. won’t be able to finish my work if I keep going like this….”). It turns out that women are more likely than men to ruminate when their mood darkens, perhaps making them more vulnerable to the onset of clinical depression (Johnson & Whisman, 2013; Nolen-Hoeksema, 2002, 2000).

Each of these explanations for the gender difference in unipolar depression offers food for thought. Each has gathered just enough supporting evidence to make it interesting and just enough evidence to the contrary to raise questions about its usefulness. Thus, at present, the gender difference in depression remains one of the most talked-about but least understood phenomena in the clinical field.

CULTURAL BACKGROUND AND DEPRESSION Depression is a worldwide phenomenon, and certain symptoms of this disorder seem to be constant across all countries. A landmark study of four countries—Canada, Switzerland, Iran, and Japan—found that the great majority of depressed people in these very different countries reported symptoms of sadness, joylessness, tension, lack of energy, loss of interest, loss of ability to concentrate, ideas of insufficiency, and thoughts of suicide (Matsumoto & Juang, 2008). Beyond such core symptoms, however, research suggests that the precise picture of depression varies from country to country (Kok et al., 2012; Kleinman, 2004). Depressed people in non-Western countries—China and Nigeria, for example—are more likely to be troubled by physical symptoms such as fatigue, weakness, sleep disturbances, and weight loss. Depression in those countries is less often marked by cognitive symptoms such as self-blame, low self-esteem, and guilt.

210

Within the United States, researchers have found few differences in the symptoms of depression among members of different ethnic or racial groups. Nor have they found significant differences in the overall rates of depression between such minority groups. On the other hand, recent research has revealed that there are often striking differences between ethnic/racial groups in the recurrence of depression. Hispanic Americans and African Americans are 50 percent more likely than white Americans to have recurrent episodes of depression (González et al., 2010). Why this difference? Around 54 percent of depressed white Americans receive treatment for their disorders (medication and/or psychotherapy), compared with 34 percent of depressed Hispanic Americans and 40 percent of depressed African Americans (González et al., 2010). It may be that minority groups in the United States are more vulnerable to repeated experiences of depression partly because many of their members have more limited treatment opportunities when they are depressed.

Research has also revealed that depression is distributed unevenly within some minority groups. This is not totally surprising, given that each minority group itself consists of people of varied backgrounds and cultural values. For example, depression is more common among Hispanic and African Americans born in the United States than among Hispanic and African American immigrants (González et al., 2010; Miranda et al., 2005). Moreover, within the Hispanic American population, Puerto Ricans have a higher rate of depression than do Mexican Americans or Cuban Americans.

Multicultural Treatments In Chapter 2, you read that culture-sensitive therapies seek to address the unique issues faced by members of cultural minority groups (Comas-Díaz, 2014). For such approaches, therapists typically have special cultural training and a heightened awareness of their clients’ cultural values and the culture-related stressors, prejudices, and stereotypes that their clients face. They make an effort to help clients develop a comfortable (for them) bicultural balance and to recognize the impact of their own culture and the dominant culture on their views of themselves and on their behaviors (Prochaska & Norcross, 2013).

In the treatment of unipolar depression, culture-sensitive approaches increasingly are being combined with traditional forms of psychotherapy to help minority clients overcome their disorders (Aguilera et al., 2010; Stacciarini et al., 2007). A number of today’s therapists, for example, offer cognitive-behavioral therapy for depressed minority clients while also focusing on the clients’ economic pressures, minority identity, and related cultural issues. A range of studies indicate that Hispanic American, African American, American Indian, and Asian American clients are more likely to overcome their depressive disorders when a culture-sensitive focus is added to the form of psychotherapy that they are otherwise receiving (Comas-Díaz, 2014).

211