assessment
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C H A P T E R 7
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Depressive and Bipolar Disorders
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TOPIC OVERVIEW
Unipolar Depression: The Depressive Disorders How Common Is Unipolar Depression? What Are the Symptoms of Depression? Diagnosing Unipolar Depression Stress and Unipolar Depression The Biological Model of Unipolar Depression The Psychological Models of Unipolar Depression The Sociocultural Model of Unipolar Depression Integrating the Models: The Developmental Psychopathology Perspective
Bipolar Disorders What Are the Symptoms of Mania? Diagnosing Bipolar Disorders What Causes Bipolar Disorders? What Are the Treatments for Bipolar Disorders?
Making Sense of All That Is Known
The first conscious thought that all was not well with me came … when I was twenty-two. I had been
living in Los Angeles for two years, working various temp jobs while trying to establish myself as a
writer and performance artist. Out of nowhere and for no apparent reason — or so it seemed — I started
feeling strong sensations of grief. I don’t remember the step-by-step progression of the illness. What I
can recall is that my life disintegrated; first, into a strange and terrifying space of sadness and then, into
a cobweb of fatigue. I gradually lost my ability to function. It would take me hours to get up out of bed,
get bathed, put clothes on. By the time I was fully dressed, it was well into the a�ernoon….
A�er a while I stopped showing up at my temp job, stopped going out altogether, and locked myself in
my home. It was over three weeks before I felt well enough to leave. During that time, I cut myself off
from everything and everyone. Days would go by before I bathed. I did not have enough energy to clean
up myself or my home. There was a trail of undergarments and other articles of clothing that ran from
the living room to the bedroom to the bathroom of my tiny apartment. Dishes with decaying food
covered every counter and tabletop in the place. Even watching TV or talking on the phone required too
much concentration…. All I could do was take to my pallet of blankets and coats positioned on the
living room floor and wait for whatever I was going through to pass. And it did. Slowly….
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… Deep down, I knew that something had gone wrong with me, in me. But what could I do? Stunned
and defenseless, the only thing I felt I could do was move on. I assured myself that my mind and the
behaviors it provoked were well within my control. In the future I would just have to be extremely
aware. I would make sure that what happened did not happen again. But it did. Again and again, no
matter how aware, responsible, or in control I tried to be….
Each wave of the depression cost me something dear. I lost my job because the temp agencies where I
was registered could no longer tolerate my lengthy absences. Unable to pay rent, I lost my apartment
and ended up having to rent a small room in a boarding house. I lost my friends. Most of them found it
too troublesome to deal with my sudden moodiness and passivity so they stopped calling and coming
around.
(Danquah, 1998)
Most people’s moods come and go. Their feelings of elation or sadness are understandable reactions to daily events and do not affect their lives greatly. However, the moods of certain people last a long time. As in the case of Meri Nana-Ama Danquah, a performance artist and poet who described her disorder above, their moods color all of their interactions with the world and even interfere with normal functioning. Such people struggle in particular with depression, mania, or both. Depression is a low, sad state in which life seems
dark and its challenges overwhelming. Mania, the opposite of depression, is a state of breathless euphoria, or at least frenzied energy, in which people may have an exaggerated belief that the world is theirs for the taking.
Mood problems of these kinds are at the center of two groups of disorders —
depressive disorders and bipolar disorders (APA, 2022). These groups are examined in this chapter. People with depressive disorders suffer only from depression, a pattern called unipolar depression. They have no history of mania and return to a normal or nearly normal mood when their depression lifts. In contrast, those with bipolar disorders have periods of mania that alternate with periods of depression.
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Mood problems have always captured people’s interest, in part because so many famous people have suffered from them. The Bible speaks of the severe depressions of Nebuchadnezzar, Saul, and Moses. Queen Victoria of England and Abraham Lincoln seem to have experienced recurring depressions. Mood
difficulties also have plagued writers Ernest Hemingway and Sylvia Plath, comedian Jim Carrey, and musical performers Bruce Springsteen and Beyoncé. Their problems have been shared by millions.
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Unipolar Depression: The Depressive Disorders
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. All of us experience dejection from time to time,
but only some experience a depressive disorder. Depressive disorders bring severe and long-lasting psychological pain that may intensify as time goes by. Those who suffer from such disorders may lose their will to carry out the simplest of life’s activities; some even lose their will to live.
Almost every day we have ups and downs in mood. How can we distinguish the everyday blues from clinical depression?
How Common Is Unipolar Depression? Around 8 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 (DBSA, 2020; Krishnan, 2019). Around 20 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, France, and many other
countries. Moreover, the rate of depression — mild or severe — is higher among poor people than wealthier people (HP, 2020a; Elflein, 2019).
Women are at least twice as likely as men to have episodes of severe unipolar depression (WHO, 2020b). As many as 26 percent of women have an episode at
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some time in their lives, compared with 12 percent of men. As you will see in Chapter 16, among children the prevalence of unipolar depression is similar for girls and boys.
An episode of severe depression can occur at any point throughout the life span. The average age of onset is 19 years, with the peak age being late adolescence or early adulthood (Elflein, 2019). In any given year, the rate of severe depression is twice as high among adults under 65 years of age as among those 65 years and older (Krishnan, 2019).
Approximately 85 percent of people with unipolar depression, including severe depression, recover within 6 months, some without treatment. More than half of those who recover from severe depression have at least one other episode later in their lives (Simon, 2019a).
What Are the Symptoms of Depression? 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.
of NOTE … World Count
More than 262 million people suffer from depression worldwide (WHO, 2020c).
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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 (Chen et al., 2019). 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:
Nights I could handle. I fell asleep easily, and sleep allowed me to forget. But my mornings were
unmanageable. To wake up each morning was to remember once again that the world by which I
defined myself was no more. Soon a�er opening my eyes, the crying bouts would start and I’d sit alone
for hours, weeping and mourning my losses.
(Williams, 2008, p. 9)
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:
I woke up one morning with a knot of fear in my stomach so crippling that I couldn’t face light, much
less day, and so intense that I stayed in bed for three days with the shades drawn and the lights out.
Three days. Three days not answering the phone. Three days not checking my e-mail. I was
disconnected completely from the outside world, and I didn’t care.
(Williams, 2008, p. xxiv)
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Suicide represents the ultimate escape from life’s challenges. As you will see in Chapter 8, 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 die by suicide; 20 percent of severely depressed people who do not
receive treatment die in this manner (Halverson, 2019; 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, “My eyes would open at the crack of dawn, but getting out of bed was impossible. I just stayed there, and stayed there, and stayed there some more, virtually paralyzed, knowing that a day filled with misery awaited me.” Depressed people may also
move, and even speak, more slowly (Liu et al., 2020).
Cognitive Symptoms
Depressed people hold extremely negative views of themselves. They consider themselves inadequate, undesirable, inferior, perhaps even evil (Scheffers et al., 2019). 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.
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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 (Schreiber & Culpepper, 2019).
People with depression frequently complain that their intellectual ability is very poor (Lyness, 2019). They feel confused, unable to remember things, easily distracted, and unable to solve even the smallest problems. In laboratory studies, depressed people do perform somewhat, but not extremely, more poorly than nondepressed people on tasks of memory, attention, and reasoning (Lyness, 2019). It may be, however, that these difficulties sometimes reflect motivational problems rather than cognitive ones.
Physical Symptoms
People who are depressed frequently have such physical ailments as headaches, indigestion, constipation, dizzy spells, and general pain (Dunlop et al., 2020). In fact, many depressions are misdiagnosed as medical problems at first. Disturbances in appetite and sleep are particularly common (Lyness, 2019). Most depressed people eat less, sleep less, and feel more fatigued than they did prior to the disorder. Some, however, eat and sleep excessively.
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Diagnosing Unipolar Depression According to DSM-5-TR, 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 7-1). 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.
TABLE: 7-1
Checklist
Major Depressive Episode
1. For a 2-week period, person displays an increase in depressed mood for the majority of each day and/or a decrease in enjoyment or interest across most activities for the majority of each day.
2. For the same 2 weeks, person also experiences at least 3 or 4 of the following symptoms: Considerable weight change or appetite change Daily insomnia or hypersomnia Daily agitation or decrease in motor activity Daily fatigue or lethargy Daily feelings of worthlessness or excessive guilt Daily reduction in concentration or decisiveness Repeated focus on death or suicide, a suicide plan, or a suicide attempt.
3. Significant distress or impairment.
Major Depressive Disorder
1. Presence of a major depressive episode.
2. No pattern of mania or hypomania.
Persistent Depressive Disorder
1. Person experiences the symptoms of major or mild depression for at least 2 years.
2. During the 2-year period, symptoms not absent for more than 2 months at a time.
3. No history of mania or hypomania.
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4. Significant distress or impairment.
Information from: APA, 2022.
DSM-5-TR 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, 2022) (see Table 7-1 again). The disorder may be additionally 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 4 weeks of giving birth (see PsychWatch), or melancholic if the person is almost totally unaffected by pleasurable events.
PSYCHWATCH Sadness at the Happiest of Times
Women usually expect the birth of a child to be a happy experience. But for at least 9 percent
of new mothers, the weeks and months a�er childbirth bring clinical depression (Johansen et al.,
2020). Peripartum depression, popularly called postpartum depression, typically begins within 4
weeks a�er the birth of a child; many cases actually begin during pregnancy (APA, 2022). This
disorder is far more severe than simple “baby blues.” It is also different from other postpartum
syndromes such as postpartum psychosis, a problem that is examined in Chapter 13.
The “baby blues” are so common — as many as 80 percent of women experience them — that most
researchers consider them normal. As new mothers try to cope with the wakeful nights, rattled
emotions, and other stresses that accompany the arrival of a new baby, they may have crying spells,
fatigue, anxiety, insomnia, and sadness (Viguera, 2019a). These symptoms usually disappear within
days or weeks.
In postpartum depression, however, depressive symptoms continue and may last up to a year or
more. The symptoms include extreme sadness, despair, tearfulness, insomnia, anxiety, intrusive
thoughts, compulsions, panic attacks, feelings of inability to cope, and suicidal thoughts (Hutchens
& Kearney, 2020). The mother–infant relationship and the psychological and physical health of the
child may suffer as a result (Jacques et al., 2019). Women who have an episode of postpartum
depression have a 25 to 50 percent chance of developing it again with a subsequent birth (Viguera,
2019b, 2018).
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Many clinicians believe that the hormonal changes accompanying childbirth trigger postpartum
depression. All women go through a kind of hormone “withdrawal” a�er delivery, as estrogen and
progesterone levels, which rise as much as 50 times above normal during pregnancy, now drop
sharply to levels far below normal. Perhaps some women are particularly influenced by these
dramatic hormone changes (Viguera, 2019b, 2018). Other theorists suggest that some women may
have a genetic predisposition to postpartum depression (McEvoy et al., 2017). Women who suffered
from depression previously in their lives are at particular risk for this kind of depression, but a
woman with a family history of mood disorders also appears to have an elevated risk, even if she
herself has not previously had a mood disorder (Johansen et al., 2020).
Fending off postpartum depression This woman participates in COMPASS (Collaborative Care Model for Perinatal Depression Support Services) at Northwestern Medicine in Chicago, Illinois. In this program, a team
of clinicians and physicians provide support, therapy, and medications to new mothers at risk for postpartum depression.
At the same time, psychological and sociocultural factors may play important roles in the disorder
(Hutchens & Kearney, 2020). The birth of a baby brings enormous psychological and social change. A
woman typically faces changes in her marital relationship, daily routines, and social roles. Sleep and
relaxation are likely to decrease, and financial pressures may increase. Perhaps she feels the added
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stress of giving up a career or of trying to maintain one. This pileup of stress may heighten the risk of
depression. Mothers whose infants are sick or temperamentally “difficult” may be under yet
additional pressure.
Fortunately, treatment can make a big difference for most women with postpartum depression. Self-
help support groups have proved extremely helpful. In addition, many individuals respond well to
the same approaches that are applied to other forms of depression — antidepressant medications,
cognitive-behavioral therapy, interpersonal psychotherapy, or a combination of these approaches
(Dennis et al., 2020; Viguera, 2019b). Moreover, in 2019 the U.S. Food and Drug Administration
approved brexanolone (brand name Zulresso), the first drug specifically approved for postpartum
depression. Currently, this drug is very expensive and can be administered only by intravenous
infusion in a medical facility, but studies suggest that it can be of great help in many cases.
However, many women who would benefit from treatment do not seek help because they feel
ashamed about being sad at a time that is supposed to be joyous, and they are concerned about
being judged harshly (Helfenbaum, 2020). For them, and for the spouses and family members close
to them, a large dose of education is in order. Even positive events, such as the birth of a child, can
be stressful if they also bring major change to one’s life. Recognizing and addressing such feelings
are in everyone’s best interest.
People whose unipolar depression is chronic receive a diagnosis of persistent depressive disorder (see Table 7-1 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 technically 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-TR is controversial. Many clinicians believe that the category is sexist and “pathologizes” severe cases of premenstrual syndrome (PMS), premenstrual discomforts that are common and normal among women.
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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 16.
“Idk what peace feels like” A few months a�er this 2016 concert in New Orleans, rap artist and actor Kid Cudi revealed on his Facebook page that he had
entered an inpatient program to receive treatment for depression and suicidal urges. He wrote to his fans,
“My anxiety and depression have ruled my life for as long as I can remember … Idk what peace feels like.”
He returned to performing a month later.
Stress and Unipolar Depression Episodes of unipolar depression often seem to be triggered by stressful events in an individual’s life (Krishnan, 2019). In fact, researchers have found that 80
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percent of all severe episodes occur within a month or two of a significant negative event (Hammen, 2018, 2016). Stressful life events also precede other psychological disorders, but depressed people report more such events than anybody else.
Why might stressful life events trigger depressed feelings and other negative emotions?
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.
The Biological Model 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? Studies of genetic factors, biochemical factors, brain circuits, and the immune system suggest that often it does.
Genetic Factors
Three kinds of research — family pedigree, twin, and gene studies — suggest
that some people inherit a predisposition to unipolar depression. 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
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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 7- 2), compared with fewer than 10 percent of the general population (Krishnan, 2019).
TABLE: 7-2
Comparing Depressive and Bipolar Disorders
One-Year Prevalence
(%)
Female-to- Male Ratio
Typical Age at Onset (Years)
Prevalence Among First-
Degree Relatives
Receiving Treatment
Currently (%)
Major depressive disorder
8.0 2:1 18−29 Elevated 52
Persistent depressive disorder (with
dysthymic syndrome)
1.5−5.0 Between 3:2 and 2:1
10−25 Elevated 62
Bipolar I disorder 1.7 1:1 15−44 Elevated 49
Bipolar II disorder 1.1 1:1 15−44 Elevated 49
Cyclothymic disorder 0.4 1:1 15−25 Elevated Unknown
Information from: NIMH, 2020i, 2017g; Stovall, 2020; WHO, 2020b; Krishnan, 2019; Bressart, 2018; Weissman et al., 2016; Kessler et al., 2012, 2010; Wang et al., 2005.
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 depressed persons. Twin studies have supported this expectation. When an identical twin has unipolar depression, there is a 38 percent chance that the other twin has already had or will eventually have the same disorder. In contrast, when a fraternal twin has unipolar depression, the other twin has only a 20 percent
chance of having the disorder (Krishnan, 2019).
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
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on at least two-thirds of the body’s 23 chromosomes (Wang et al., 2020; Davies et al., 2019).
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 initial antidepressant drugs were discovered by accident,
researchers soon learned that while the drugs were relieving depression, they also were bringing about increases in norepinephrine and/or serotonin activity.
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Lighting up depression On one of the darkest days of the year, these Londoners try to beat the winter blues
by soaking up the illumination from “The Light Station,” a Seasonal Affective Disorder lighting
installation available in a tunnel under Southwark Bridge.
For years it was thought that low activity of either norepinephrine or serotonin directly produces depression, but theorists now believe that their relationship to depression is more complicated (Krishnan, 2019). Research indicates that depression is probably linked to interactions between serotonin and
norepinephrine activity, or between them and additional key neurotransmitters, particularly glutamate, a neurotransmitter responsible for stimulating neurons and promoting connectivity and communication among neurons (Krystal et al., 2019). In addition, as you will read shortly, a number of studies suggest that the activity of these neurotransmitters may either reflect or help produce dysfunction of a depression-related circuit in the brain, dysfunction that may be the key to the development of depression.
Biological researchers have also learned that another group of chemicals — the body’s hormones — are linked to depression. As you read in Chapter 6, whenever we confront stressors in life, our brain triggers into action two stress- related routes throughout the brain and body. One of those routes, the hypothalamic-pituitary-adrenal (HPA) axis, ultimately brings about the release of
hormones at various locations throughout the body, and those hormones spur assorted body organs into action, causing us to temporarily experience a heightened state of arousal (see page 154). You may recall that the HPA axis of people with posttraumatic stress disorder (PTSD) and certain anxiety disorders consistently overreacts when those individuals confront stressors. Research indicates that the HPA axis of people with depression is also overly reactive in the face of stress, causing excessive releases of cortisol and related hormones at times of stress (Iob, Kirschbaum, & Steptoe, 2019). This relationship is not all
that surprising, given that stressful events so often seem to trigger depression. Once again, it is possible that the HPA axis overreactivity and heightened
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hormone activity found in depressed people either reflect or help produce dysfunction in a depression-related circuit in the brain, the biological focus that we turn to next.
Brain Circuits
As you have read in previous chapters, biological researchers have determined 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 or behavioral reaction. A brain circuit whose dysfunction contributes to unipolar depression has begun to emerge (Liu et al., 2020; Schmitgen et al., 2019). An array of brain-imaging studies point to several brain structures that are likely members of this depression-related brain
circuit, including the prefrontal cortex, hippocampus, amygdala, and subgenual cingulate (also called Brodmann Area 25), among other structures (see Figure 7- 1). You may notice that several of the structures in this circuit are also members of the brain circuits that contribute to certain anxiety disorders and PTSD. However, the subgenual cingulate is distinctly part of the depression-related circuit.
FIGURE 7-1
The Biology of Depression
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Researchers believe that the brain circuit involved in unipolar depression includes structures such as the prefrontal cortex, hippocampus, amygdala, and subgenual cingulate (le�). The illustration on the right highlights
how the structures of this circuit work together and trigger each other into action, an interconnectivity that is flawed in people with depression. The long axons of the neurons from each structure form fiber-like pathways that
extend to the other structures in the circuit.
Unlike some of the other brain circuits we have discussed, dysfunctions of this depression-related brain circuit cannot be characterized in general terms, as, for example, a “hyperactive” or “underactive” circuit. But there are many indications that the circuit does operate abnormally in persons with depression. Research suggests, for example, that among depressed people, activity and blood flow are unusually low in certain parts and unusually high in other parts of the prefrontal
cortex; the hippocampus is undersized and its production of new neurons is low; activity and blood flow are high in the amygdala; the subgenual cingulate is particularly small and active; and the communication, or interconnectivity, between these various structures is often problematic (Krishnan, 2019; Newman et al., 2017).
Studies indicate that under usual circumstances the neurotransmitters serotonin and norepinephrine are both plentiful and active in this brain circuit. It appears, however, that among depressed people, the activity of serotonin and norepinephrine in this circuit is distinctly lower than among other people (Lee & Han, 2019; Zhou et al., 2019; Avraham et al., 2017). This is not surprising, considering all the research we observed earlier linking depression to low activity by these neurotransmitters. The abnormal activity of these
neurotransmitters in this brain circuit might be the result of dysfunction within or between the circuit’s various structures, or, alternatively, the cause of such circuit dysfunction. At this point researchers do not know which is the case.
The Immune System
As you will see in Chapter 9, 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
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dysregulated, leading to slower functioning of important white blood cells called lymphocytes and to increased production of pro-inflammatory cytokines, proteins that spread throughout the body and cause inflammation and various illnesses (see page 279). There is a growing belief among some researchers that immune
system dysregulation of this kind helps produce depression (Perrin & Pariante, 2020; Faugere et al., 2018).
What Are the Biological Treatments for Unipolar Depression?
Usually biological treatment means antidepressant drugs or popular alternatives such as herbal supplements (see InfoCentral), but for people whose depression does not respond to these medications or to psychotherapy, it sometimes means brain stimulation.
INFOCENTRAL EXERCISE AND DIETARY SUPPLEMENTS
“Complementary and Alternative Medicine (CAM)” is the popular term for interventions that fall
outside of conventional Western treatments. Two of the most common CAM interventions are
physical exercise and dietary supplements (also known as nutraceuticals). Depression is the
psychological problem for which these approaches are used most o�en, and research indicates that
each can indeed help improve the moods of modestly or moderately depressed people, particularly
when integrated with psychotherapy or medication, rather than applied alone (Miller et al., 2020;
Stibich, 2020; Jabr, 2017).
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Flower power Hypericum perforatum, known as Saint-
John’s-wort, is a low, wild-growing shrub, not an antidepressant drug. It is currently among the hottest-
selling products in health stores, with studies indicating that it can be quite helpful in cases of mild
or moderate depression.
ANTIDEPRESSANT DRUGS
There are four kinds of drugs available to reduce the symptoms of depression: monoamine oxidase (MAO) inhibitors, tricyclics, the second-generation antidepressants, and ketamine-based drugs (see Table 7-3).
TABLE: 7-3
Some Drugs That Reduce Unipolar Depression
Monoamine Oxidase Inhibitors
Tricyclics Second-Generation Antidepressants
Ketamine-Based Drugs
Generic Name Trade Name
Generic Name
Trade Name
Generic Name Trade Name
Generic Name
Trade Name
Iscarboxazid Marplan Imipramine Tofranil Trazodone Desyrel Ketamine Ketalar
Phenelzine Nardil Amitriptyline Elavil Fluoxetine Prozac Esketamine Spravato
Tranylcypromine Parnate Doxepin Sinequan; Sertraline Zolo�
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Silenor
Selegiline Eldepryl Trimipramine Surmontil Paroxetine Paxil
Desipramine Norpramin Venlafaxine Effexor
Nortriptyline Aventil; Pamelor
Bupropion Wellbutrin
Protriptyline Vivactil Citalopram Celexa
Clomipramine Anafranil Escitalopram Lexapro
Amoxapine Asendin Duloxetine Cymbalta
Mirtazapine Remeron Desvenlafaxine Pristiq
Atomoxetine Strattera
The effectiveness of MAO inhibitors as a treatment for unipolar depression was discovered accidentally back in 1952. Physicians noted that iproniazid, a drug being tested on patients with tuberculosis, had an interesting effect: it seemed to make the patients happier (Bloom, 2020). It was found to have the same effect on depressed patients (Kline, 1958). 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. By
inhibiting (that is, blocking) the production of MAO, these drugs ultimately increased the activity level of the neurotransmitters serotonin and norepinephrine throughout the brain.
Approximately half of depressed patients who take MAO inhibitors are helped
by them (Hirsch & Birnbaum, 2019a). 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
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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 significantly more than similar patients taking placebos, although the drugs must be taken for at least 10 days before such improvements take hold (Hirsch & Birnbaum, 2019b). Around 50 to 60 percent of patients who take tricyclics are helped by them (Simon, 2019a). To avoid the risk of relapse, most clinicians keep
patients on these drugs for at least 5 months after they are free of depressive symptoms, an extension called “continuation therapy” or “maintenance therapy” (DeRubeis et al., 2020; Jarrett & Vittengl, 2019).
of NOTE … Medical Bonding
27–50% Stroke victims who experience clinical depression
25–30% Cancer patients who experience depression
20–33% Heart attack victims who become depressed
18–33% People with diabetes who are depressed
(DBSA, 2020; Caruso et al., 2017)
Many researchers have concluded that one of the ways in which tricyclics are able to reduce depression is by acting on the neurotransmitter “reuptake” mechanisms of key neurons (Hirsch & Birnbaum, 2019b). Remember from Chapter 3 that brain messages are carried from a “sending” neuron across the synaptic space to a receiving neuron by a neurotransmitter, the chemical released from the end of the sending neuron (see page 49). However, there is a
complication in this process. While the sending neuron releases the neurotransmitter, a pumplike mechanism in the neuron’s ending immediately
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starts to reabsorb it in a process called reuptake. The purpose of this reuptake process is to limit how long the neurotransmitter remains in the synaptic space and to prevent it from overstimulating the receiving neuron. However, reuptake does not always progress properly. The reuptake mechanisms for depressed
people are too vigorous in neurons that use either serotonin or norepinephrine — cutting off the activity of those neurotransmitters in their synaptic spaces too soon, preventing messages from reaching the receiving neurons, and helping to produce the symptoms of their disorder. Tricyclics inhibit this overly vigorous reuptake process, allowing serotonin and norepinephrine to remain in their synapses longer, thus increasing their stimulation of receiving neurons (see Figure 7-2).
FIGURE 7-2
Reuptake and Antidepressants
(Le�) Soon a�er a neuron releases neurotransmitters such as norepinephrine or serotonin into its synaptic space, it activates a pumplike reuptake mechanism to reabsorb excess neurotransmitters. In depression, however, this
reuptake process is too active, removing too many neurotransmitters before they can bind to a receiving neuron. (Right) Tricyclic and most second-generation antidepressant drugs block the reuptake process, enabling
norepinephrine or serotonin to remain in the synapse longer and bind to the receiving neuron.
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Recent studies suggest that, for many depressed people, once these reuptake processes are corrected, serotonin and norepinephrine activity becomes smoother and more appropriate throughout their depression-related brain circuit (Rolls, 2017). Correspondingly, the interconnections between the
structures in that circuit become more orderly and functional (James et al., 2017). With such biological corrections in place, depression subsides for many patients.
The antidepressant revolution This worker at a pharmaceutical company operates
sterile equipment during the manufacture of the antidepressant drug Prozac. Global sales of antidepressants now total over $15 billion each year.
Second-generation antidepressants, the third group of effective drugs for
depression, are structurally different from the MAO inhibitors and tricyclics. Developed over the past three decades, most of these drugs 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). Other second-generation antidepressants are selective norepinephrine reuptake inhibitors (such as atomoxetine, or Strattera), which increase norepinephrine activity only, and serotonin–norepinephrine reuptake inhibitors
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(such as venlafaxine, or Effexor), which increase both serotonin and norepinephrine activity (Nelson, 2020).
In effectiveness and speed of action, the second-generation antidepressant drugs are on a par with the tricyclics, yet their sales have skyrocketed (Hirsch & Birnbaum, 2020; Simon, 2019a, 2019b). They do not produce as many undesired effects as MAO inhibitors or tricyclics, although they can produce significant side effects of their own, including weight gain and reduced sex drive.
The fourth group of antidepressants are ketamine-based drugs. In recent years, researchers have learned that the drug ketamine brings significant relief to many people with depression (Zhou et al., 2020). This drug has actually been available as a short-acting anesthetic since 1970, often used in surgery or to reduce pain in injured persons, and it has also gained notoriety as a party drug that can be abused (nicknamed “Special K” on the streets). However, its
antidepressant effect has now caught the attention of the clinical field. It has been hailed as a “breakthrough” by the U.S. Food and Drug Administration (FDA) and as the “first truly new medication for depression” since the approval of the second-generation antidepressant Prozac in 1987 (J. Chen, 2019).
The virtues of ketamine are that it often alleviates depression very quickly, helps people who are unresponsive to other kinds of treatments and those who are suicidal, and combines effectively with other antidepressant drugs and psychotherapies (Zhou et al., 2020; Krystal et al., 2019). Early tests of ketamine, which were administered intravenously, produced extraordinary results — as many as 70 percent of persons with treatment-resistant depression showed immediate improvement and their symptoms decreased within hours, in contrast to the weeks or months needed for other drugs to work. In 2019, the
FDA approved esketamine (trade name Spravato), a more accessible version of ketamine that is taken by nasal spray rather than intravenously (Kim et al., 2019). During a treatment session, the depressed individual receives several rounds of esketamine sprays into the nostrils (while under medical supervision) and is then monitored for a couple of hours. Like intravenous ketamine, the nasal
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spray drug brings very rapid relief for many depression sufferers (Canuso et al., 2018; Daly et al., 2019).
A new drug arrives In 2019 the FDA approved esketamine (brand name Spravato) for people with
treatment-resistant depression. This ketamine-based nasal spray can only be administered in a medical
facility under medical supervision.
The nasal spray has become the ketamine treatment of choice. Typically, it is
combined with other kinds of antidepressant drugs, because esketamine alone has only a short-term effect and because such combinations seem to be more effective than any one of those treatments alone (J. Chen, 2019; Thase & Connolly, 2019). Although ketamine-based treatments are obviously very promising, the drugs have some major limitations, including the fact that they have only a short-term impact for each administration, are addictive over time, are expensive, and can, in some people, produce dizziness, confusion, memory
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problems, feelings of depersonalization and derealization, and/or high blood pressure (Basso et al., 2020; Acevedo-Diaz et al., 2019; Thase & Connolly, 2019).
The ketamine-based treatments appear to alleviate the symptoms of depression by increasing the activity of the neurotransmitter glutamate in the brain, in contrast to the increases in serotonin and norepinephrine produced by the other antidepressant drugs (Krystal et al., 2019). Thus many clinical theorists now suspect that low glutamate activity may be equally or even more important than low serotonin or norepinephrine activity in depression, or that low activity of all of these transmitters collectively helps produce the disorder. It is
noteworthy that there are many more glutamate receptors than serotonin or norepinephrine receptors in the brain’s depression-related circuit. Thus it may be that by increasing glutamate activity throughout the circuit, ketamine improves connectivity between the structures in the circuit more directly or completely than the other antidepressant drugs do, accounting for its more immediate and powerful impact on depressed individuals (Thase & Connolly, 2019). There is also evidence that ketamine may help trigger the development of some new neural pathways in the circuit (Krystal et al., 2019; Meisner, 2019).
If antidepressant drugs are effective, why do many people seek out herbal supplements, such as Saint-John’s-wort or melatonin, for depression?
As popular as the different kinds of antidepressants are, it is important to recognize that they do not work for everyone. As you have read, even the most successful of them fails to help at least 30 percent of clients with depression. In fact, a number of recent reviews have raised the strong possibility that the failure rate is higher still (see Trending). When antidepressants fail, psychiatrists
or family physicians often augment treatment by adding certain antipsychotic medications (Fornaro et al., 2019; Gerhard et al., 2018). Some researchers have lamented the fact that, all too often, prescribers deal with a patient’s unresponsiveness to antidepressant drugs by prescribing new drugs or drug mixtures — one after another — without directing the individual toward
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psychotherapy or counseling of some kind (Rush, 2019). Melissa, a depressed woman for whom psychotropic drug treatment has failed to work over many years, reflects on this issue:
[S]he spoke, in a wistful manner, of how she wished her treatment could have been different. “I do
wonder what might have happened if [at age 16] I could have just talked to someone, and they could
have helped me learn about what I could do on my own to be a healthy person…. Instead, it was you
have this problem with your neurotransmitters, and so here, take this pill Zolo�, and when that didn’t
work, it was take this pill Prozac, and when that didn’t work, it was take this pill Effexor, and then when I
started having trouble sleeping, it was take this sleeping pill,” she says, her voice sounding more wistful
than ever. “I am so tired of the pills.”
(Whitaker, 2010)
…TRENDING How Effective Are Antidepressant Drugs, Really?
One of the most talked-about issues in the clinical field today is the possibility that many
antidepressant drugs may not be as effective as previously thought. For years, clinical researchers
believed that tricyclic and second-generation antidepressants help around 65 percent of people
suffering from depression, an effectiveness rate much higher than the 35 percent of depressed
people who seem to improve in response to placebo drugs. It turns out that this rate of 65 percent is
correct with regard to published studies. But, apparently, the story is different when unpublished
studies are considered.
This issue had its beginnings a decade ago when two separate teams of researchers decided to
examine the possible impact of publication bias on the reported effectiveness rates of
antidepressant drugs (Turner et al., 2020, 2008; Kirsch, 2019, 2014). Publication bias refers to the
tendency of professional journals to accept for publication mainly those studies that have positive
findings. For example, they may primarily publish antidepressant drug studies that find
antidepressants to be significantly more effective than placebo drugs.
One of the research teams, headed by investigator Erick Turner, reviewed 74 antidepressant drug
studies — some of them published and, very importantly, some that had not been published (Turner
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et al., 2020, 2008). The researchers found that only 38 of the 74 studies yielded positive findings (that
is, the drug was clearly effective), and all but one of these studies were published. In contrast, the
other 36 studies yielded findings that were negative or questionable (the drug was not particularly
effective), and 22 of them were not published. When the reviewers combined the findings from all
the studies — both published and unpublished — the percentage of people helped by antidepressant
drugs turned out to be lower than the percentage yielded in published studies alone. That is,
antidepressants helped improve the symptoms of approximately 50 percent of depressed people,
not 65 percent. In short, antidepressant drugs may not be as superior to placebo drugs as previously
believed.
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In recent years, other reviews have also examined the performance of antidepressant drugs, again
combining findings from published and unpublished studies, and they have uncovered the same
story (Turner et al., 2020; de Vries et al., 2019; Kirsch, 2019).
This is a very serious matter to be sure. When making decisions about treatment, clinicians must
know how likely it is that depressed clients will be helped by the various available interventions. In
light of these multiple reviews, it may be most prudent to conclude that today’s antidepressant
drugs are indeed helpful, but, for many depressed people, perhaps not as helpful nor as superior (to
placebo treatments) as once believed.
BRAIN STIMULATION: ELECTROCONVULSIVE THERAPY
As you read in Chapter 3, a different form of biological treatment, brain stimulation, refers to interventions that directly or indirectly stimulate certain
areas of the brain. The oldest — and most controversial — such approach is electroconvulsive therapy (ECT). In recent years, three additional kinds of brain stimulation have been developed for the treatment of depressive disorders — vagus nerve stimulation, transcranial magnetic stimulation, and deep brain stimulation.
Clinicians and patients alike vary greatly in their opinions of electroconvulsive therapy (ECT). Some consider it a safe biological approach with minimal risks; others believe it to be an extreme measure that can cause troublesome memory loss and even neurological damage. Despite this controversy, ECT is used frequently, largely because it can be a very effective and relatively fast-acting intervention for unipolar depression.
In an ECT 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 15 to 70 seconds (Li et al., 2020; Kellner, 2018). After 6 to 12 such treatments, spaced over 2 to 4 weeks, most patients feel less depressed (Hauser, 2020).
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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. Thus to provide treatment for
people with such disorders, an Italian psychiatrist named Ugo Cerletti developed a procedure in which electric currents were applied 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, not schizophrenia, became apparent.
ECT today Administering ECT has changed significantly since the treatment’s early
days. Today, patients are given drugs to help them sleep, muscle relaxants to prevent severe jerks of the body and broken bones, and oxygen to guard against brain damage.
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 (barbiturates) to put patients to sleep during the procedure, reducing their terror (Chawla, 2020).
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Patients who receive ECT typically have difficulty remembering some events, most often events that took place immediately before and after their treatments (Li et al., 2020). In most cases, this memory loss clears up within a few months (Anderson et al., 2020), but some patients are left with gaps in more distant
memory, and this form of amnesia can be permanent (Hauser, 2020).
ECT is clearly effective in treating unipolar depression, although it has been difficult to determine why it works so well (Li et al., 2020). Studies find that between 50 and 80 percent of ECT patients improve (APA, 2020c; Kellner, 2018). The approach is particularly effective when patients follow up the initial cluster
of sessions with continuation, or maintenance, therapy — either ongoing antidepressant medications or periodic ECT sessions (Hauser, 2020). ECT also seems to be quite effective in severe cases of depression that include delusions.
OTHER FORMS OF BRAIN STIMULATION
Over the past 15 years, three additional kinds of brain stimulation 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 suspected that they might be able to stimulate the brain by electrically stimulating the vagus nerve. They were hoping
to mimic the positive effects of ECT without producing the undesired effects or trauma associated with ECT. Their efforts gave birth to a new treatment for depression — vagus nerve stimulation.
As you read in Chapter 3, 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 7-3). Electrical signals travel from the pulse generator through the wire to the vagus nerve. The stimulated vagus nerve then
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delivers electrical signals to the brain. The pulse generator is typically programmed to provide 30 seconds of stimulation to the vagus nerve (and, in turn, the brain) every 5 minutes.
FIGURE 7-3
Vagus Nerve Stimulation
In the procedure called vagus nerve stimulation, an
implanted pulse generator sends electrical signals to the vagus nerve, which then delivers electrical signals
to the brain. This stimulation of the brain helps reduce depression in many patients.
Research has found that vagus nerve stimulation can bring significant relief (Holtzheimer, 2019a). In fact, studies find that a substantial number of severely depressed people who have not responded to any other form of treatment may improve significantly when treated with this procedure (Zhang et al., 2020).
Transcranial magnetic stimulation (TMS) is another technique that is being 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
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that structure, and, in turn, may improve functioning throughout the rest of the brain’s depression-related circuit (Eshel et al., 2020; Holtzheimer, 2019b). A number of studies have found that the procedure reduces depression when it is administered daily for 4 to 6 weeks (Kaster et al., 2020; Iimori et al., 2019).
Stimulating the brain In this version of transcranial magnetic stimulation (TMS), a
woman wears headgear that contains an electromagnetic coil. The coil sends currents into and stimulates her brain.
Yet another brain stimulation procedure is called deep brain stimulation (DBS). As you have read, around 15 years ago researchers linked depression to high activity in the subgenual cingulate, a key member of the depression-related brain circuit. This finding led neurologist Helen Mayberg and her colleagues (2005) to administer a then-experimental treatment, 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 the subgenual cingulate. The electrodes were connected to a battery, or “pacemaker,” that was implanted in the patient’s chest (for men)
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or stomach (for women). The pacemaker powered the electrodes, sending a steady stream of low-voltage electricity to the brain structure. Mayberg’s expectation was that this repeated stimulation would reduce activity in the structure to a normal level and help “recalibrate” the depression-related brain
circuit.
In the initial study of DBS, four of the six severely depressed patients became almost depression-free within a matter of months. Subsequent research with other severely depressed individuals has also yielded promising findings (Ramasubbu et al., 2020; Holtzheimer, 2019a). This work has produced
considerable enthusiasm in the clinical field, particularly regarding depressed individuals who are treatment-resistant, but the research on DBS is still in its early stages.
The Psychological Models of Unipolar Depression The psychological models that have been most widely applied to unipolar
depression are the psychodynamic and cognitive-behavioral models. The psychodynamic model has not been strongly supported by research, but the cognitive-behavioral model has received considerable support and has 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,
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difficulty sleeping, loss of pleasure in life, and general 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, called introjection, is temporary. However, for some — particularly those whose various dependency needs were improperly met during infancy and early childhood — grief worsens over time, and they develop clinical depression (Boeker & Kraehenmann, 2018; Bemporad, 1992).
of NOTE … Controversial Change
In past editions of the DSM, people who lose a loved one were excluded from receiving a diagnosis of major depressive disorder during the first 2 months of their bereavement. However, according to
DSM-5-TR, newly bereaved people can qualify for this diagnosis if their depressive symptoms are
severe enough. Critics fear that many people undergoing a normal grief reaction now receive an
incorrect diagnosis of major depressive disorder.
Of course, many people become depressed without losing a loved one. To explain why, Freud proposed the concept of symbolic, 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 (Gabbard & DeJean, 2020). For example, object relations theorists (the psychodynamic theorists who emphasize relationships) propose
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that depression results when people’s relationships — especially their early relationships — leave them feeling unsafe, insecure, and dependent on others (Mucci, 2019).
The following description by the therapist of a depressed middle-aged woman illustrates the psychodynamic concepts of dependence, loss of a loved one, symbolic loss, and introjection:
Marie Carls … had always felt very attached to her mother…. She always tried to placate her volcanic
[emotions], to please her in every possible way….
A�er marriage [to Julius], she continued her pattern of submission and compliance…. [W]hen she was
thirty years old … [Marie] and her husband invited Ignatius, who was single, to come and live with
them. Ignatius and [Marie] soon discovered that they had an attraction for each other. They both tried
to fight that feeling; but when Julius had to go to another city for a few days, the so-called infatuation
became much more than that. There were a few physical contacts…. There was an intense spiritual
affinity…. A few months later everybody had to leave the city…. Nothing was done to maintain contact.
Two years later … Marie heard that Ignatius had married. She felt terribly alone and despondent….
Her suffering had become more acute as she [came to believe] that old age was approaching and she
had lost all her chances. Ignatius remained as the memory of lost opportunities…. Her life of
compliance and obedience had not permitted her to reach her goal…. When she became aware of
these ideas, she felt even more depressed.
(Arieti & Bemporad, 1978, pp. 275–284)
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 (Akhtar, 2019; Krishnan, 2019). When, for example, a diagnostic survey was administered to thousands of adults in one study, the individuals whose fathers had died during their childhood scored higher on depression (Jacobs & Bovasso, 2009). Related research supports the psychodynamic idea that people whose childhood needs were poorly met are particularly likely to become depressed after experiencing loss (Conradi et al., 2018). At the same
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time, research does not indicate that loss or problematic early relationships are always at the core of depression. Only a fraction of all people who have major losses in life actually become depressed (Akhtar, 2019; Hammen, 2018, 2016).
of NOTE … Their Words
“Don’t cry because it’s over, smile because it happened.”
Dr. Seuss
WHAT ARE THE PSYCHODYNAMIC TREATMENTS FOR UNIPOLAR DEPRESSION?
Because they believe 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 them through (Gabbard & DeJean, 2020; Busch et al., 2004). Using the arsenal of basic psychodynamic procedures, 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. 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:
Among his earliest memories, possibly the earliest of all, was the recollection of being wheeled in his
baby cart under the elevated train structure and le� there alone. Another memory that recurred vividly
during the analysis was of an operation around the age of five. He was anesthetized and his mother le�
him with the doctor. He recalled how he had kicked and screamed, raging at her for leaving him.
(Lorand, 1968, pp. 325–326)
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Despite case reports of such successes as this, researchers have found that long-term psychodynamic therapy is only occasionally helpful in cases of unipolar depression (Prochaska & Norcross, 2018). Two features of the approach may help limit its effectiveness. First, depressed clients may be too passive and
feel too weary to join fully in 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 the longer-term approaches, especially when they are combined with psychotropic medications (Gabbard & DeJean, 2020).
Early loss A young daughter stands by the casket of her father, a firefighter who died helping to bring a large
wildfire under control. Research has found that people who lose their parents as children have an increased
risk of experiencing depression as adults.
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The Cognitive-Behavioral Model
As with other kinds of psychological disorders, cognitive-behavioral theories contend that unipolar depression results from a combination of problematic behaviors and dysfunctional ways of thinking. These theories fall into three groups: explanations that focus mostly on the behavioral realm, those that give primary attention to negative thinking, and ones that feature a complex interplay between cognitive and behavioral factors.
THE BEHAVIORAL DIMENSION
Clinical researcher Peter Lewinsohn was one of the first theorists to link depression to significant changes in the number of rewards and punishments people receive in their lives (Lewinsohn et al., 1990, 1984). He 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, researchers 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 improves as well (Stein et al., 2020; Santos et al., 2019). Similarly, other investigations have found a strong relationship between positive life events and feelings of life satisfaction and happiness (Diener, 2020; He et al., 2019).
Lewinsohn and other theorists have further proposed that social rewards are particularly important in the downward spiral of depression (Tan, Shallis, &
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Barkus, 2020; Werner-Seidler et al., 2017). 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, it may also be that their dark mood and flat behaviors help produce a decline in social rewards (Tan et al., 2020; Hammen, 2018, 2016).
Eventually the applause stops At his final professional basketball game in 2019, NBA
great Dwyane Wade bathed in the cheers of his adoring fans one more time. The reduction in rewards brought about by retirement may place athletes and other high
achievers at risk for depression unless they find new sources of gratification. Small wonder that shortly before his retirement, Wade said he would be seeking therapy to
help deal with the coming void in his life.
NEGATIVE THINKING
Aaron Beck believes that negative thinking lies at the heart of depression (Beck
& Weishaar, 2019; Beck, 2016, 2002, 1967). According to Beck, maladaptive attitudes, a cognitive triad, errors in thinking, and automatic thoughts combine to produce unipolar depression.
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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 own experiences and the judgments of the people around them. 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:
I can’t bear it. I can’t stand the humiliating fact that I’m the only woman in the world who can’t take
care of her family, take her place as a real wife and mother, and be respected in her community. When I
speak to my young son Billy, I know I can’t let him down, but I feel so ill-equipped to take care of him;
that’s what frightens me. I don’t know what to do or where to turn; the whole thing is too
overwhelming…. I must be a laughing stock. It’s more than I can do to go out and meet people and
have the fact pointed out to me so clearly.
(Fieve, 1975)
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
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