hw help

PSYC HELP DUE SAT

PSYC 430

Case Study: Depression Answer Sheet

Ellen: Depression and Suicidality

Student Name:

Diagnosing Ellen

1a. Refer to the DSM-IV checklist and list all symptoms that Ellen has that match the criteria for major depressive episode. Which of Ellen’s symptoms meet any of the criteria? (Be sure to match specific symptoms with specific criteria.)

1b. Can Ellen be said to be suffering from a major depressive disorder?

1c. Explain and defend your diagnoses or lack thereof.

2. Where does Ellen fit with Shneidman’s taxonomy of people who intentionally end their lives?

3. What factors are present that may trigger a suicide attempt by Ellen?

Explaining Ellen’s Depression and Suicidality

1. What genetic factors might play a role in Ellen’s depression?

2. What biochemical factors might play a role in Ellen’s depression?

3a.What would a psychodynamic theorist say about the origins of Ellen’s depression?

4. How might Freud’s concept of symbolic or imagined loss help explain Ellen’s depression?

5. What evidence is there that Ellen is engaging in the cognitive triad and automatic thoughts?

6. How might the hormone theory help explain Ellen’s depression?

7. How would the body dissatisfaction explanation lend to understanding Ellen’s depression?

8. With regard to Ellen’s wish to commit suicide, which of Durkheim’s categories does Ellen belong and why?

Treating Ellen

1. Explain how a psychodynamic therapist would treat Ellen for her depression and suicidal tendencies.

2. Explain how a behavioral therapist would treat Ellen for her depression and suicidal tendencies.

3. Explain how a cognitive therapist would treat Ellen for her depression and suicidal tendencies.

4. Explain how an interpersonal therapist would treat Ellen for her depression and suicidal tendencies.

5. Explain what biological treatment might be appropriate for Ellen.

Page 2 of 2

Somatoform and Dissociative Disorders : 1 91
\\\NIPJK r)tili///:
,:
re’
re.
/7:”..•
4.
7:
(?)::
7A:
iz.:
7′
.*::.
7 .,..
1. What are the symptoms of each
of the hysterical somatoform
disorders? How do practitioners
distinguish hysterical disorders
from “genuine” medical problems?
pp. 164-167
2. How does a somatoform disorder
differ from a factitious disorder?
pp. 167- 169
3. List the central features of each of
the preoccupation somatoform
disorders. pp. 169-170
..,,,..
4. What are the leading explanations
and treatments for the somatoform
disorders? How well does research
support them? pp. 170- 176
5. List and describe the different dis-
sociative disorders. pp. 176-184
6. What are four kinds of dissociative
amnesia? pp. 177-780
7. What are the different kinds of rela-
tionships that the subpersonalities
may have in dissociative identity
disorder? pp. 182-183
• #!,,A
8′ 0’1.5, 4, 4, {“,$’47.
8. Describe the psychodynamic,
behavioral, state-dependent learn-
ing, and self-hypnosis explanations
of dissociative disorders. How well
is each supported by research?
pp. 184- 187
9. What approaches have been used
to treat dissociative amnesia and
dissociative fugue? pp. 187- 188
10. What are the key features of
treatment for dissociative identity
disorder? Is treatment successful?
pp. 188-189
Search the Fundamentals of Abnormal Psychology Video Tool Kit
www.worthpublishers.com/apvtk
A Chapter 6 Video Cases
Beyond Perfection: Body Dysmorphic Disorder
Repressed Memories or False Memories?
Three Faces of Eve: The Real Patient
A Video case discussions, study guides, and questions
Log on to the Corner Web Page
www.worthpublishers.com/comer
A Chapter 6 outline, learning objectives, research exercises, study tools,
and practice test questions
A Additional Chapter 6 case studies, Web links, and FAQs
Somatoform and Dissociative Disorders : 1 91
\\\NIPJK r)tili///:
,:
re’
re.
/7:”..•
4.
7:
(?)::
7A:
iz.:
7′
.*::.
7 .,..
1. What are the symptoms of each
of the hysterical somatoform
disorders? How do practitioners
distinguish hysterical disorders
from “genuine” medical problems?
pp. 164-167
2. How does a somatoform disorder
differ from a factitious disorder?
pp. 167- 169
3. List the central features of each of
the preoccupation somatoform
disorders. pp. 169-170
..,,,..
4. What are the leading explanations
and treatments for the somatoform
disorders? How well does research
support them? pp. 170- 176
5. List and describe the different dis-
sociative disorders. pp. 176-184
6. What are four kinds of dissociative
amnesia? pp. 177-780
7. What are the different kinds of rela-
tionships that the subpersonalities
may have in dissociative identity
disorder? pp. 182-183
• #!,,A
8′ 0’1.5, 4, 4, {“,$’47.
8. Describe the psychodynamic,
behavioral, state-dependent learn-
ing, and self-hypnosis explanations
of dissociative disorders. How well
is each supported by research?
pp. 184- 187
9. What approaches have been used
to treat dissociative amnesia and
dissociative fugue? pp. 187- 188
10. What are the key features of
treatment for dissociative identity
disorder? Is treatment successful?
pp. 188-189
Search the Fundamentals of Abnormal Psychology Video Tool Kit
www.worthpublishers.com/apvtk
A Chapter 6 Video Cases
Beyond Perfection: Body Dysmorphic Disorder
Repressed Memories or False Memories?
Three Faces of Eve: The Real Patient
A Video case discussions, study guides, and questions
Log on to the Corner Web Page
www.worthpublishers.com/comer
A Chapter 6 outline, learning objectives, research exercises, study tools,
and practice test questions
A Additional Chapter 6 case studies, Web links, and FAQs

MOOD DISORDERS

or … a six-month period, her irritability bordered on the irrational. She screamed in
anger or sobbed in despair at every dirty dish left on the coffee table or on the bedroom
floor. Each day the need to plan the dinner menu provoked agonizing indecision. How
L: could all the virtues or, more likely, vices of hamburgers be accurately compared to those
of spaghetti? . . . She hod her whole family walking on eggs. She thought they would be better
off if she were dead.
Beatrice could not cope with her job. As a branch manager of a large chain store, she had many
decisions to make. Unable to make them herself, she would ask employees who were much
less competent for advice, but then she could not decide whose advice to take. Each morning
before going to work, she complained of nausea. . . .
Beatrice’s husband loved her, but he did not understand what was wrong. He thought that she
would improve if he made her life easier by taking over more housework, cooking, and child
care. His attempt to help only made Beatrice feel more guilty and worthless. She wanted to
make a contribution to her family. She wanted to do the chores “like normal people” did but
broke down crying at the smallest impediment to a perfect job. . . . Months passed, and Bea-
trice’s problem became more serious. Some days she was too upset to go to work. She stopped
seeing her friends. She spent most of her time at home either yelling or crying. Finally, Beatrice’s
husband called the psychiatrist and insisted that something was seriously wrong.
Lickey & Gordon, 1991, p. 181
Most people’s moods come and go. Their feelings of elation or sadness are under-
standable reactions to daily events and do not affect their lives greatly.The moods
of people with mood disorders, in contrast, tend to last a long time.As in Beatrice’s
case, the mood colors all of their interactions with the world and interferes with
normal functioning.
Depression and mania are the key emotions in mood disorders. 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. Most people with a mood disorder 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. Others experi-
ence periods of mania that alternate with periods of depression, a pattern called
bipolar disorder.
Mood disorders 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 disorders also
have plagued such writers as Ernest Hemingway, Eugene O’Neill,Virginia Woolf,
and Sylvia Plath. Their severe mood problems have been shared by millions.
TOPIC OVERVIEW
Unipolar Depression
How Common Is Unipolar
Depression?
What Are the Symptoms
of Depression?
Diagnosing Unipolar Depression
Stress and Unipolar Depression
The Biological Model
of Unipolar Depression
Psychological Models
of Unipolar Depression
The Sociocultural Model of Unipolar
Depression
Bipolar Disorders
What Are the Symptoms of Mania?
Diagnosing Bipolar Disorders
What Causes Bipolar Disorders?
What Are the Treatments for Bipolar
Disorders?
Putting It Together: Making Sense
of All That Is Known
MOOD DISORDERS

1 94 ://CHAPTER 7
,,Unipogar Depression
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 unipolar depression. Clinical depression brings
severe and long-lasting psychological pain that may intensify as time goes by.
Those who suffer from it may lose their will to carry out the simplest of life’s
activities; some even lose their will to live.
1,1i1-‘-fyfil r,!Iltoi.j.6-t-C-jim,°•HI-‘,'[-“,’-‘-°-4-‘1b!-‘,–°}-
1N,
fir \”4+ ?il
edepressioneA low, sad state marked
by lack of energy, low self-worth, guilt,
or related symptoms.
emaniacA state or episode of euphoria
or frenzied activity in which people may
have an exaggerated belief that the
world is theirs for the taking.
ounipolar depression*Depression
without a history of mania.
ebipolar disorder°A disorder marked
by alternating or intermixed periods of
mania and depression.
How Common Is Unipolar Depression?
Almost 7 percent of adults in the United States suffer from a severe unipolar pat-
tern of depression in any given year, while as many as 5 percent suffer from mild
forms (Kessler & Wang, 2009; Taube-Schiff & Lau, 2008). Around 17 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 (Vasiliadis et al., 2007; WHO, 2004).
In almost all countries, women are at least twice as likely as men to experi-
ence episodes of severe unipolar depression (Taube-Schiff & Lau, 2008). As
many as 26 percent of women may have an episode at some time in their lives,
compared with 12 percent of men. Among children the prevalence is similar
for girls and boys (Avenevoli et al., 2008). All of these rates hold steady across
the various socioeconomic classes and ethnic groups.
Approximately half of the people with unipolar depression recover within
six weeks and 90 percent recover within a year, some without treatment
(Kessler, 2002; Kendler et al., 1997). However, most of them have at least one other
episode of depression later in their lives (Taube-Schiff & Lau, 2008).
What Are the Symptoms of Depression?
The picture of depression may vary from person to person. Earlier you saw how Beatrice’s
indecisiveness, uncontrollable sobbing, and feelings of despair, anger, and worthlessness
brought her job and social life to a standstill. Other depressed people have symptoms
that are less severe. They manage to function, although their depression typically robs
them of much effectiveness or pleasure, as you can see in the case of Derek:
Derek has probably suffered from depression all of his adult life but was unaware of it for
many years. Derek called himself a night person, claiming that he could not think clearly
until after noon even though he was often awake by 4:00 A.M. He tried to schedule his
work as editorial writer for a small town newspaper so that it was compatible with his de-
pressed mood at the beginning of the day. Therefore, he scheduled meetings for the morn-
ings; talking with people got him moving. He saved writing and decision making for later in
the day.
.. Derek’s private thoughts were rarely cheerful and self-confident. He felt that his
marriage was a mere business partnership. He provided the money, and she provided a
home and children. Derek and his wife rarely expressed affection for each other. Occasion-
ally, he had images of his own violent death in a bicycle crash, in a plane crash, or in a
murder by an unidentified assailant.
Derek felt that he was constantly on the edge of job failure. He was disappointed that
his editorials had not attracted the attention of larger papers. He was certain that several
of the younger people on the paper had better ideas and wrote more skillfully than he
did. He scolded himself fora bad editorial that he had written ten years earlier. Although
that particular piece had not been up to his usual standards, everyone else on the paper
1 94 ://CHAPTER 7
,,Unipogar Depression
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 unipolar depression. Clinical depression brings
severe and long-lasting psychological pain that may intensify as time goes by.
Those who suffer from it may lose their will to carry out the simplest of life’s
activities; some even lose their will to live.
1,1i1-‘-fyfil r,!Iltoi.j.6-t-C-jim,°•HI-‘,'[-“,’-‘-°-4-‘1b!-‘,–°}-
1N,
fir \”4+ ?il
edepressioneA low, sad state marked
by lack of energy, low self-worth, guilt,
or related symptoms.
emaniacA state or episode of euphoria
or frenzied activity in which people may
have an exaggerated belief that the
world is theirs for the taking.
ounipolar depression*Depression
without a history of mania.
ebipolar disorder°A disorder marked
by alternating or intermixed periods of
mania and depression.
How Common Is Unipolar Depression?
Almost 7 percent of adults in the United States suffer from a severe unipolar pat-
tern of depression in any given year, while as many as 5 percent suffer from mild
forms (Kessler & Wang, 2009; Taube-Schiff & Lau, 2008). Around 17 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 (Vasiliadis et al., 2007; WHO, 2004).
In almost all countries, women are at least twice as likely as men to experi-
ence episodes of severe unipolar depression (Taube-Schiff & Lau, 2008). As
many as 26 percent of women may have an episode at some time in their lives,
compared with 12 percent of men. Among children the prevalence is similar
for girls and boys (Avenevoli et al., 2008). All of these rates hold steady across
the various socioeconomic classes and ethnic groups.
Approximately half of the people with unipolar depression recover within
six weeks and 90 percent recover within a year, some without treatment
(Kessler, 2002; Kendler et al., 1997). However, most of them have at least one other
episode of depression later in their lives (Taube-Schiff & Lau, 2008).
What Are the Symptoms of Depression?
The picture of depression may vary from person to person. Earlier you saw how Beatrice’s
indecisiveness, uncontrollable sobbing, and feelings of despair, anger, and worthlessness
brought her job and social life to a standstill. Other depressed people have symptoms
that are less severe. They manage to function, although their depression typically robs
them of much effectiveness or pleasure, as you can see in the case of Derek:
Derek has probably suffered from depression all of his adult life but was unaware of it for
many years. Derek called himself a night person, claiming that he could not think clearly
until after noon even though he was often awake by 4:00 A.M. He tried to schedule his
work as editorial writer for a small town newspaper so that it was compatible with his de-
pressed mood at the beginning of the day. Therefore, he scheduled meetings for the morn-
ings; talking with people got him moving. He saved writing and decision making for later in
the day.
.. Derek’s private thoughts were rarely cheerful and self-confident. He felt that his
marriage was a mere business partnership. He provided the money, and she provided a
home and children. Derek and his wife rarely expressed affection for each other. Occasion-
ally, he had images of his own violent death in a bicycle crash, in a plane crash, or in a
murder by an unidentified assailant.
Derek felt that he was constantly on the edge of job failure. He was disappointed that
his editorials had not attracted the attention of larger papers. He was certain that several
of the younger people on the paper had better ideas and wrote more skillfully than he
did. He scolded himself fora bad editorial that he had written ten years earlier. Although
that particular piece had not been up to his usual standards, everyone else on the paper

he Color of Depression
1.’
! .I.;…ili.ii.r.; ,…0.I.I.q.1.!,.1!1:11′ ;.5:…, z III ., “:

“….) I ., ^::, . . -PI; 11:::cIi.:

1..f.1 .. …..ff!I ..I. 1.’il…’..:. IV’ —'”
-6 II !. .•_.1′ …- . I.:.’,?j.1–7.7=.’` J. .’,. .2, .’

, -. ! : ,I ;aiiin r!,:,’.. •
i Ili
LOW SELF-ESTEEM
Mood Disorders :11 195
had forgotten it a week after it appeared. But ten years later, Derek was still ruminating
over that one editorial. . . .
Derek brushed off his morning confusion as a lack of quick intelligence. He had no
way to know that it was a symptom of depression. He never realized that his death
images might be suicidal thinking. People do not talk about such things. For all Derek
knew, everyone had similar thoughts.
(Lithe) , & Gordon, 1991, pp. 183-185)

MP.

As the cases of Beatrice and Derek indicate, depression has many symptoms other
than sadness. The symptoms, which often feed upon one another, span five areas of
functioning: emotional, motivational, behavioral, cognitive, and physical.
Emotion El 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 o I humor, report getting little pleasure from anything, and in some cases dis-
play anlredonia, an inability to experience any pleasure at all. A number also experience
anxiety; ange r, or agitation.This sea of misery may lead to crying spells.
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
Williams, author of Black Pain, a book about depression in African Americans, 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. Then on the morn-
ing of the fourth day there was a knock on my door. Since I hadn’t ordered food I ignored
it. The knocking kept up and I kept ignoring it. 1 heard the sound of keys rattling in my
front door. Slowly the bedroom door opened and in the painful light from the doorway I
saw the figures of two old friends. “Terrie, are you in there?”
(Williams, 2008, p. xxiv)
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 commit suicide (Taube-Schiff & Lau, 2008; Stolberg et al., 2002).
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 ( Joiner, 2002).
COgnitiVe Symptoms Depressed people hold extremely negative views
of themselves.They consider themselves inadequate, undesirable, inferior, per-
haps evil.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.
he Color of Depression
1.’
! .I.;…ili.ii.r.; ,…0.I.I.q.1.!,.1!1:11′ ;.5:…, z III ., “:

“….) I ., ^::, . . -PI; 11:::cIi.:

1..f.1 .. …..ff!I ..I. 1.’il…’..:. IV’ —'”
-6 II !. .•_.1′ …- . I.:.’,?j.1–7.7=.’` J. .’,. .2, .’

MP.

196 :id/CHAPTER 7
51 ‘Riess at he Happiest of Times
omen usually expect the birth of a
child to be a happy experience. But
for 10 to 30 percent of new mothers, the
weeks and months after childbirth bring
clinical depression (Rubertsson et al.,
2005; O’Hara, 2003). Postpartum depres-
sion typically begins within four weeks
after the birth of a child (APA, 2000), and
it is far more severe than simple “baby
blues.” It is also different from other post-
partum syndromes such as postpartum
psychosis, a problem that will be examined
in Chapter 12.
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 experience crying spells, fa-
tigue, anxiety, insomnia, and sadness. These
symptoms usually disappear within days
or weeks (Horowitz et al., 2005, 1995;
Najman et al., 2000).
In postpartum depression, however, de-
pressive symptoms continue and may last
up to a year. The symptoms include extreme
sadness, despair, tearfulness, insomnia,
anxiety, intrusive thoughts, compulsions,
panic attacks, feelings of inability to cope,
and suicidal thoughts (Lindcihl et al., 2005).
The mother-infant relationship and the health
of the child may suffer as a result (Buist
et al., 2006; Monti et al., 2004). Women
who experience postpartum depression have
a 25 to 50 percent chance of developing it
again with a subsequent birth (Stevens
et al., 2002).
Many clinicians believe that the hormonal
changes accompanying childbirth trigger
postpartum depression. All women experi-
ence a kind of hormone “withdrawal” after
delivery, as estrogen and progesterone lev-
els, which rise as much as 50 times above
normal during pregnancy, now drop sharply
to levels for below normal (Horowitz et al.,
2005, 1995). Perhaps some women are
particularly influenced by these dramatic
hormone changes. Still other theorists sug-
gest a genetic predisposition to postpartum
depression. (APA, 2000).
At the same time, psychological and so-
ciocultural factors may play important roles
in the disorder. The birth of a baby brings
enormous psychological and social change
(Nydegger, 2006; Gjerdingen & Center,
2005). 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 in-
crease. Perhaps she feels the added stress of
giving up a career—or of trying to maintain
one. This pileup of stress may heighten the
risk of depression (Horowitz et al., 2005;
Swendsen & Mazure, 2000).
Fortunately, treatment can make a big
difference for most women with postpartum
depression. Self-help support groups have
proved extremely helpful for many women
with the disorder (O’Hara, 2003; Stevens
et al., 2002). In addition, many respond
well to the same approaches that are ap-
plied to other forms of depression—anti-
depressant medications, cognitive therapy,
interpersonal psychotherapy, or a combina-
tion of these approaches (Kleiman, 2009;
O’Hara, 2003; Stuart et al., 2003).
However, a large number of 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 joy-
ous and are concerned about being judged
harshly (WooIhouse et al., 2009; APA,
2000). For them, and for their spouses and
family members, 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. Recogniz-
ing and addressing such feelings are in
everyone’s best interest.
AP
P f
ia t
o /A
!C
Inc
., C
or d
N
ot i
so
n 196 :id/CHAPTER 7
51 ‘Riess at he Happiest of Times
omen usually expect the birth of a
child to be a happy experience. But
for 10 to 30 percent of new mothers, the
weeks and months after childbirth bring
clinical depression (Rubertsson et al.,
2005; O’Hara, 2003). Postpartum depres-
sion typically begins within four weeks
after the birth of a child (APA, 2000), and
it is far more severe than simple “baby
blues.” It is also different from other post-
partum syndromes such as postpartum
psychosis, a problem that will be examined
in Chapter 12.
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 experience crying spells, fa-
tigue, anxiety, insomnia, and sadness. These
symptoms usually disappear within days
or weeks (Horowitz et al., 2005, 1995;
Najman et al., 2000).
In postpartum depression, however, de-
pressive symptoms continue and may last
up to a year. The symptoms include extreme
sadness, despair, tearfulness, insomnia,
anxiety, intrusive thoughts, compulsions,
panic attacks, feelings of inability to cope,
and suicidal thoughts (Lindcihl et al., 2005).
The mother-infant relationship and the health
of the child may suffer as a result (Buist
et al., 2006; Monti et al., 2004). Women
who experience postpartum depression have
a 25 to 50 percent chance of developing it
again with a subsequent birth (Stevens
et al., 2002).
Many clinicians believe that the hormonal
changes accompanying childbirth trigger
postpartum depression. All women experi-
ence a kind of hormone “withdrawal” after
delivery, as estrogen and progesterone lev-
els, which rise as much as 50 times above
normal during pregnancy, now drop sharply
to levels for below normal (Horowitz et al.,
2005, 1995). Perhaps some women are
particularly influenced by these dramatic
hormone changes. Still other theorists sug-
gest a genetic predisposition to postpartum
depression. (APA, 2000).
At the same time, psychological and so-
ciocultural factors may play important roles
in the disorder. The birth of a baby brings
enormous psychological and social change
(Nydegger, 2006; Gjerdingen & Center,
2005). 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 in-
crease. Perhaps she feels the added stress of
giving up a career—or of trying to maintain
one. This pileup of stress may heighten the
risk of depression (Horowitz et al., 2005;
Swendsen & Mazure, 2000).
Fortunately, treatment can make a big
difference for most women with postpartum
depression. Self-help support groups have
proved extremely helpful for many women
with the disorder (O’Hara, 2003; Stevens
et al., 2002). In addition, many respond
well to the same approaches that are ap-
plied to other forms of depression—anti-
depressant medications, cognitive therapy,
interpersonal psychotherapy, or a combina-
tion of these approaches (Kleiman, 2009;
O’Hara, 2003; Stuart et al., 2003).
However, a large number of 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 joy-
ous and are concerned about being judged
harshly (WooIhouse et al., 2009; APA,
2000). For them, and for their spouses and
family members, 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. Recogniz-
ing and addressing such feelings are in
everyone’s best interest.
AP
P f
ia t
o /A
!C
Inc
., C
or d
N
ot i
so
n

DSM Checklist
API` %Oar)
Mood Disorders :// 1 97
Another cognitive symptom. of depression is pessimism. Sufferers are usually con-
vinced 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
(Taube-Schiff & Lau, 2008).
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 individuals do perform more
poorly than nondepressed persons on some tasks of memory, attention, and reasoning
(Bremner et al., 2004). It may be, however, that these difficulties sometimes reflect mo-
tivational problems rather than cognitive ones.
PhySiCal Symptoms People who are depressed often have such physical ailments
as headaches, indigestion, constipation, dizzy spells, and general pain (Fishbain, 2000).
In fact, many depressions are misdiagnosed as medical problems at first. Disturbances
in appetite and sleep are particularly common (Neckelmann et al., 2007; Genchi et al.,
2004). Most depressed people eat less, sleep less, and feel more fatigued than they did
prior to the disorder. Some, however, eat and sleep excessively.Terrie Williams describes
the changes in the pattern of her sleep:
•
At first I didn’t notice the change. Then things got worse. I always hated waking up, but
slowly it was turning into something deeper; it was less like I didn’t want to wake up, and
more like couldn’t. l didn’t feel tired, but I had no energy. I didn’t feel sleepy, but I would
have welcomed sleep with open arms. I had the sensation of a huge weight, invisible but
gigantic, pressing down on me, almost crushing me into the bed and pinning me there.
(Williams, 2008, p. xxii)
omajor depressive disorder0A severe
pattern of depression that is disabling
and is not caused by such factors as
drugs or a general medical condition.
odysthymic disorderoA mood disorder
that is similar to but longer-lasting and
less disabling than a major depressive
disorder.
Diagnosing Unipolar Depression
According to DSM-IV-TR, a major depressive episode is a period marked by
at least five symptoms of depression and lasting for two weeks or more (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 can’t eat “because my intestines are deteriorating and will soon stop
working,” or he may believe that he sees his dead wife.
People who experience a major depressive episode without having
any history of mania receive a diagnosis of major depressive disorder.
Individuals who display a longer-lasting but less disabling pattern of uni-
polar depression may receive a diagnosis of dysthymic disorder. When
dysthymic disorder leads to major depressive disorder, the sequence is called
double depression (Taube-Schiff & Lau, 2008).
Stress and Unipolar Depression
Episodes of unipolar depression often seem to be triggered by stressful events
(Hammen et al., 2009; Henn &Vollmayr, 2005; Paykel, 2003). In fact, research-
ers have found that depressed people experience a greater number of stress-
ful life events during the month just before the onset of their disorder than
do other people during the same period of time (Monroe & Hadjiyannakis,
2002). Of course, stressful life events also precede other psychological disor-
ders, but depressed people report more such events than anybody else.
DSM Checklist
API` %Oar)
Mood Disorders :// 1 97
Another cognitive symptom. of depression is pessimism. Sufferers are usually con-
vinced 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
(Taube-Schiff & Lau, 2008).
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 individuals do perform more
poorly than nondepressed persons on some tasks of memory, attention, and reasoning
(Bremner et al., 2004). It may be, however, that these difficulties sometimes reflect mo-
tivational problems rather than cognitive ones.
PhySiCal Symptoms People who are depressed often have such physical ailments
as headaches, indigestion, constipation, dizzy spells, and general pain (Fishbain, 2000).
In fact, many depressions are misdiagnosed as medical problems at first. Disturbances
in appetite and sleep are particularly common (Neckelmann et al., 2007; Genchi et al.,
2004). Most depressed people eat less, sleep less, and feel more fatigued than they did
prior to the disorder. Some, however, eat and sleep excessively.Terrie Williams describes
the changes in the pattern of her sleep:
•
At first I didn’t notice the change. Then things got worse. I always hated waking up, but
slowly it was turning into something deeper; it was less like I didn’t want to wake up, and
more like couldn’t. l didn’t feel tired, but I had no energy. I didn’t feel sleepy, but I would
have welcomed sleep with open arms. I had the sensation of a huge weight, invisible but
gigantic, pressing down on me, almost crushing me into the bed and pinning me there.
(Williams, 2008, p. xxii)
omajor depressive disorder0A severe
pattern of depression that is disabling
and is not caused by such factors as
drugs or a general medical condition.
odysthymic disorderoA mood disorder
that is similar to but longer-lasting and
less disabling than a major depressive
disorder.
Diagnosing Unipolar Depression
According to DSM-IV-TR, a major depressive episode is a period marked by
at least five symptoms of depression and lasting for two weeks or more (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 can’t eat “because my intestines are deteriorating and will soon stop
working,” or he may believe that he sees his dead wife.
People who experience a major depressive episode without having
any history of mania receive a diagnosis of major depressive disorder.
Individuals who display a longer-lasting but less disabling pattern of uni-
polar depression may receive a diagnosis of dysthymic disorder. When
dysthymic disorder leads to major depressive disorder, the sequence is called
double depression (Taube-Schiff & Lau, 2008).
Stress and Unipolar Depression
Episodes of unipolar depression often seem to be triggered by stressful events
(Hammen et al., 2009; Henn &Vollmayr, 2005; Paykel, 2003). In fact, research-
ers have found that depressed people experience a greater number of stress-
ful life events during the month just before the onset of their disorder than
do other people during the same period of time (Monroe & Hadjiyannakis,
2002). Of course, stressful life events also precede other psychological disor-
ders, but depressed people report more such events than anybody else.

198 : 1/CHAPTER 7
r_)r •
–
It Iritlp”1i 4
,
■3 ,
Some clinicians consider it important to distinguish a reactive (exo-
genous) depression, which follows clear-cut stressful events, from an endo-
genous depression, which seems to be a response to internal factors (Kessing,
2004). 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 co-
incidence. 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? Evidence from genetic, biochemical, and anatomical
studies suggests that often it does.
Genetic Factors Three kinds of research—family pedigree, twin,
and molecular biology 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 depres-
sion also afflicts other members of the family. If a predisposition to unipo-
lar 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 20 percent of those
relatives are depressed (see Table 7-2), compared with fewer than 10 percent of the gen-
eral population (Taub e-Schiff & Lau, 2008; B erre ttini, 2006).
If a predisposition to unipolar depression is inherited, you might also expect to find
a particularly large number of cases among the closer relatives of depressed persons. Twin
studies have supported this expectation (Richard & Lyness, 2006). 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 abnor-
malities 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 (Carlson, 2008). For example, a number of researchers have
Mood Disorders Profile
Prevalence Percentage
One-year
Prevalence
Female
to Male
Typical Age
at Onset
among
First-Degree
Currently
Receiving
(Percent) Ratio (Years) Relatives Treatment
Major depressive disorder 7.0% 2:1 24-29 Elevated 32.9%
Dysthymic disorder 1.5-5.0% Between 3:2
and 2:1
10-25 Elevated 36.8%
Bipolar I disorder 1.6% 1:6 15-44 Elevated 33.8%
Bipolar II disorder 1 .0% 1:1 15-44 Elevated 33.8%
Cyclothymic disorder 0.4% 1:1 15-25 Elevated Unknown
Source; Taube-Schiff ar Lau, 2003; Kessler et al., 2005, 1994; APA, 2000, 1994; Regier et al., 1993; Weissman et al., 1991.
198 : 1/CHAPTER 7
r_)r •
–
It Iritlp”1i 4
,
■3 ,
Some clinicians consider it important to distinguish a reactive (exo-
genous) depression, which follows clear-cut stressful events, from an endo-
genous depression, which seems to be a response to internal factors (Kessing,
2004). 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 co-
incidence. 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? Evidence from genetic, biochemical, and anatomical
studies suggests that often it does.
Genetic Factors Three kinds of research—family pedigree, twin,
and molecular biology 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 depres-
sion also afflicts other members of the family. If a predisposition to unipo-
lar 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 20 percent of those
relatives are depressed (see Table 7-2), compared with fewer than 10 percent of the gen-
eral population (Taub e-Schiff & Lau, 2008; B erre ttini, 2006).
If a predisposition to unipolar depression is inherited, you might also expect to find
a particularly large number of cases among the closer relatives of depressed persons. Twin
studies have supported this expectation (Richard & Lyness, 2006). 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 abnor-
malities 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 (Carlson, 2008). For example, a number of researchers have
Mood Disorders Profile
Prevalence Percentage
One-year
Prevalence
Female
to Male
Typical Age
at Onset
among
First-Degree
Currently
Receiving
(Percent) Ratio (Years) Relatives Treatment
Major depressive disorder 7.0% 2:1 24-29 Elevated 32.9%
Dysthymic disorder 1.5-5.0% Between 3:2
and 2:1
10-25 Elevated 36.8%
Bipolar I disorder 1.6% 1:6 15-44 Elevated 33.8%
Bipolar II disorder 1 .0% 1:1 15-44 Elevated 33.8%
Cyclothymic disorder 0.4% 1:1 15-25 Elevated Unknown
Source; Taube-Schiff ar Lau, 2003; Kessler et al., 2005, 1994; APA, 2000, 1994; Regier et al., 1993; Weissman et al., 1991.

1
Popular. Search ::.
• •
Mood Disorders :1/ 1 99
found that individuals who are depressed often have an abnormality of their 5-HTT gene,
a gene located on chromosome 17 that is responsible for activity of the neurotransmitter
serotonin (Hecimovic & Gilliam, 2006). As you will read in the next section, low activity
of serotonin is closely tied to depression.
Biocilemicai 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 (Carlson, 2008). First, medical research-.
ers 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 (Carlson, 2008; Drevets & Todd, 2005). Research
suggests that interactions between serotonin and norepinephrine activity, or between
these neurotransmitters and other kinds of neurotransmitters in the brain, rather than
the operation of any one neurotransmitter alone, may account for unipolar depression
(Thase et al., 2002).
Biological researchers have also learned that the body’s endocrine system may play a
role in unipolar depression. 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
(Neumeister et al., 2005). This relationship is not all that surprising, given that stress-
ful 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 pat-
tern called seasonal affective disorder) may secrete more melotonin during the winter’s long
nights than other individuals do (Kasof, 2009; Neto & Araujo, 2004).
Still other biological researchers are starting to believe that unipolar depres-
sion is tied more closely to what happens within neurons than to the chemicals
that carry messages from neuron to neuron ( Julien, 2008). They believe that
activity by key neurotransmitters or hormones ultimately leads to deficiencies of
important proteins and other chemicals within neurons—deficiencies that may
impair the health of the neurons and lead, in turn, to depression.
The biochemical explanations of unipolar depression have produced much
enthusiasm, but research in this area has certain limitations. Some of it has re-
lied 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 indi-
rectly.As a result, investigators could never be certain of the biochemical events
that were occurring 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 Chapter ____apter 4, 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, trig-
gering 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 also begun to emerge (Insel, 2007). An array of brain-
imaging studies point to several brain areas that are likely members of this circuit,
—‘
L -1
1171 [.k 1=; ■ MWt1F 1•Mi’
1
Popular. Search ::.
• •
Mood Disorders :1/ 1 99
found that individuals who are depressed often have an abnormality of their 5-HTT gene,
a gene located on chromosome 17 that is responsible for activity of the neurotransmitter
serotonin (Hecimovic & Gilliam, 2006). As you will read in the next section, low activity
of serotonin is closely tied to depression.
Biocilemicai 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 (Carlson, 2008). First, medical research-.
ers 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 (Carlson, 2008; Drevets & Todd, 2005). Research
suggests that interactions between serotonin and norepinephrine activity, or between
these neurotransmitters and other kinds of neurotransmitters in the brain, rather than
the operation of any one neurotransmitter alone, may account for unipolar depression
(Thase et al., 2002).
Biological researchers have also learned that the body’s endocrine system may play a
role in unipolar depression. 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
(Neumeister et al., 2005). This relationship is not all that surprising, given that stress-
ful 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 pat-
tern called seasonal affective disorder) may secrete more melotonin during the winter’s long
nights than other individuals do (Kasof, 2009; Neto & Araujo, 2004).
Still other biological researchers are starting to believe that unipolar depres-
sion is tied more closely to what happens within neurons than to the chemicals
that carry messages from neuron to neuron ( Julien, 2008). They believe that
activity by key neurotransmitters or hormones ultimately leads to deficiencies of
important proteins and other chemicals within neurons—deficiencies that may
impair the health of the neurons and lead, in turn, to depression.
The biochemical explanations of unipolar depression have produced much
enthusiasm, but research in this area has certain limitations. Some of it has re-
lied 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 indi-
rectly.As a result, investigators could never be certain of the biochemical events
that were occurring 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 Chapter ____apter 4, 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, trig-
gering 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 also begun to emerge (Insel, 2007). An array of brain-
imaging studies point to several brain areas that are likely members of this circuit,
—‘
L -1
1171 [.k 1=; ■ MWt1F 1•Mi’

200 ://CHAPTER 7
° e I ectr o co nvu Is ive therapy (ECT)°A
treatment for depression in which elec-
trodes attached to a patient’s head send
an electrical current through the brain,
causing a convulsion.
9MAO inhibitoroAn antidepressant
drug that prevents the action of the
enzyme monoamine oxidase.
particularly the prefrontal cortex, the hippocampus, the amygdala, and Brod-
mann Area 25, an area located just under the brain part called the cingulate
cortex (see Figure 7-1).
The prefrontal cortex is located within the frontal cortex of the brain.
Several imaging studies have found lower activity and blood flow in
the prefrontal cortex of depressed research participants than in the pre-
frontal cortex of nondepressed individuals (Lambert & Kinsley, 2005;
Rajkowska, 2000). However, other studies, focusing on select areas of
the prefrontal cortex, have found increases in activity during depres-
sion (Carlson, 2008; Drevets, 2001, 2000). Given these varied findings,
researchers currently believe that the prefrontal cortex plays a critical
role in depression but that the specific nature of this role has yet to be
clarified (Higgins & George, 2007).
The prefrontal cortex has strong neural connections with another
part of the depression brain circuit, the hippoccunpus. Indeed, messages are
both sent and received between the two brain areas. The hippocarnpus
is one of the few brain areas to produce new neurons throughout adult-
hood, an activity known as neurogenesis (Carlson, 2008). Several stud-
ies indicate that such hippocampal neurogenesis decreases dramatically
when individuals become depressed (Airan et al., 2007; Sapolsky, 2004,
2000). Moreover, some imaging studies have detected a reduction in
the size of the hippocampus among depressed persons (Campbell et al.,
2004; Frodl et al., 2004).
You may also recall from Chapters 5 and 6 that the amygdala is a brain area that
repeatedly seems to be involved in the expression of negative emotions and memories.
PET and IMRI scans indicate that activity and blood flow in the amygdala is 50 percent
greater among depressed persons than nondepressed persons (Drevets, 2001). In fact, one
study suggests that as a patient’s depression increases, the activity in his or her amygdala
increases proportionately (Abercrombie et al., 1998).
The fourth part of the depression brain circuit, Brodmann Area 25, has received
enormous attention in recent years (Lozano et al., 2008; Insel, 2007; Mayberg, 2006,
2003). This area, located just under the brain area called the cingulate cortex, tends to
be smaller in depressed people than nondepressed people. Moreover, like the amygdala,
it is significantly more active among depressed people than among nondepressed people.
In fact, brain scans reveal that when a person’s depression subsides, the activity in his or
her Area 25 decreases significantly.
What Are the Biological Treatments for Unipolar Depression? Usually
biological treatment means antidepressant drugs or popular herbal supplements, but for
severely depressed individuals who do not respond to other forms of treatment, it some-
times means electroconvulsive therapy or a relatively new group of approaches called brain
stimulation.
ELECTROCONVULSIVE THERAPY One of the most controversial forms of treatment for de-
pression is electroconvulsive therapy, or 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 a half 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 (Medda et al., 2009; Fink, 2007, 2001).
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 convul-
sions (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 the patients the drug tnetrazol.
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
200 ://CHAPTER 7
° e I ectr o co nvu Is ive therapy (ECT)°A
treatment for depression in which elec-
trodes attached to a patient’s head send
an electrical current through the brain,
causing a convulsion.
9MAO inhibitoroAn antidepressant
drug that prevents the action of the
enzyme monoamine oxidase.
particularly the prefrontal cortex, the hippocampus, the amygdala, and Brod-
mann Area 25, an area located just under the brain part called the cingulate
cortex (see Figure 7-1).
The prefrontal cortex is located within the frontal cortex of the brain.
Several imaging studies have found lower activity and blood flow in
the prefrontal cortex of depressed research participants than in the pre-
frontal cortex of nondepressed individuals (Lambert & Kinsley, 2005;
Rajkowska, 2000). However, other studies, focusing on select areas of
the prefrontal cortex, have found increases in activity during depres-
sion (Carlson, 2008; Drevets, 2001, 2000). Given these varied findings,
researchers currently believe that the prefrontal cortex plays a critical
role in depression but that the specific nature of this role has yet to be
clarified (Higgins & George, 2007).
The prefrontal cortex has strong neural connections with another
part of the depression brain circuit, the hippoccunpus. Indeed, messages are
both sent and received between the two brain areas. The hippocarnpus
is one of the few brain areas to produce new neurons throughout adult-
hood, an activity known as neurogenesis (Carlson, 2008). Several stud-
ies indicate that such hippocampal neurogenesis decreases dramatically
when individuals become depressed (Airan et al., 2007; Sapolsky, 2004,
2000). Moreover, some imaging studies have detected a reduction in
the size of the hippocampus among depressed persons (Campbell et al.,
2004; Frodl et al., 2004).
You may also recall from Chapters 5 and 6 that the amygdala is a brain area that
repeatedly seems to be involved in the expression of negative emotions and memories.
PET and IMRI scans indicate that activity and blood flow in the amygdala is 50 percent
greater among depressed persons than nondepressed persons (Drevets, 2001). In fact, one
study suggests that as a patient’s depression increases, the activity in his or her amygdala
increases proportionately (Abercrombie et al., 1998).
The fourth part of the depression brain circuit, Brodmann Area 25, has received
enormous attention in recent years (Lozano et al., 2008; Insel, 2007; Mayberg, 2006,
2003). This area, located just under the brain area called the cingulate cortex, tends to
be smaller in depressed people than nondepressed people. Moreover, like the amygdala,
it is significantly more active among depressed people than among nondepressed people.
In fact, brain scans reveal that when a person’s depression subsides, the activity in his or
her Area 25 decreases significantly.
What Are the Biological Treatments for Unipolar Depression? Usually
biological treatment means antidepressant drugs or popular herbal supplements, but for
severely depressed individuals who do not respond to other forms of treatment, it some-
times means electroconvulsive therapy or a relatively new group of approaches called brain
stimulation.
ELECTROCONVULSIVE THERAPY One of the most controversial forms of treatment for de-
pression is electroconvulsive therapy, or 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 a half 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 (Medda et al., 2009; Fink, 2007, 2001).
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 convul-
sions (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 the patients the drug tnetrazol.
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

Mood Disorders :11 201
the trectIthe I 14 1
patients-are
,
I li ill
-slee MSC r
table:
Drugs That Reduce Unipolar Depression
Class/Generic Name Trade Name
Monoamine oxidase inhibitors
caused death. Finally, an Italian psychiatrist named Ugo Cerletti discovered
that he could produce seizures more safely by applying electric currents to pa-
tients’ heads (Cerletti & Bini, 1938). 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 shoul-
ders sometimes resulted from patients’ severe convulsions. Today’s practitioners
avoid this problem by giving the individuals strong muscle relaxants to minimize
convulsions.’They also use anesthetics (barbiturates) to put patients to sleep during
the procedure, reducing their terror.
Patients who receive ECT typically have difficulty remembering the events
immediately before and after their treatments. In most cases, this memory loss
clears up within a few months (Calev et al., 1995,1991; Squire & Slater, 1983).
Some patients, however, experience gaps in more distant memory, and this
form of amnesia can be permanent (Wang, 2007; Squire, 1977).
ECT is clearly effective in treating unipolar depression, although it has
been difficult to determine why it works so well (Garrett, 2008). Studies find
that between 60 and 80 percent of ECT patients improve (Richard & Lyness,
2006). The procedure seems to be particularly effective in severe cases of de-
pression that include delusions. At least 50,000 patients per year are believed
to receive ECT each year (Cauchon, 1999).
ANTIDEPRESSANT DRUGS Two kinds of drugs discovered in the 1950s reduce
the symptoms of depression: monoamine oxidase (MAO) inhibitors and tricyclics.
These drugs have been joined in recent years by a third group, the so -called
second generation antidepressants (see Table 7 -3).
The effectiveness of MAO inhibitors as a treatment for unipolar de-
pression 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, Saunders, & Kline, 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 carry-
ing 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
Isocarboxazid
Phenelzine
Tranylcypromine
Selegiline
Tricyclics
Imipramine
Amitriptyline
Doxepin
Trim ipramine
Desipramine
Nortripiyline
Protriptyline
Second-generation
Maprotiline
Amoxopine
Trozodone
Clomipramine
Fluoxetine
Sertraline
Paroxetine
Venlafaxine
Fluvoxamine
Nefazodone
Bupropion
Mirtazapine
Citalopram
Escitaropram
Duloxetine
Reboxetine
Atomoxetine
antidepressants
Ludiomil
Asendin
Desyrel
Anafranil
Prozac
Zoloft
Paxil
Effexor
Generic only
Generic only
Wellbutrin
Remeron
Celexo
Lexapro
Cymbalta
Edronax
Strattera
Tofranil
Elavil
Adapin; Sinequan
Surmontil
Norpramin; Pertofrane
Aventil; Pamelor
Vivactil
Marplan
Nardil
Parnate
Eldepril
( Julien, 2008)
Mood Disorders :11 201
the trectIthe I 14 1
patients-are
,
I li ill
-slee MSC r
table:
Drugs That Reduce Unipolar Depression
Class/Generic Name Trade Name
Monoamine oxidase inhibitors
caused death. Finally, an Italian psychiatrist named Ugo Cerletti discovered
that he could produce seizures more safely by applying electric currents to pa-
tients’ heads (Cerletti & Bini, 1938). 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 shoul-
ders sometimes resulted from patients’ severe convulsions. Today’s practitioners
avoid this problem by giving the individuals strong muscle relaxants to minimize
convulsions.’They also use anesthetics (barbiturates) to put patients to sleep during
the procedure, reducing their terror.
Patients who receive ECT typically have difficulty remembering the events
immediately before and after their treatments. In most cases, this memory loss
clears up within a few months (Calev et al., 1995,1991; Squire & Slater, 1983).
Some patients, however, experience gaps in more distant memory, and this
form of amnesia can be permanent (Wang, 2007; Squire, 1977).
ECT is clearly effective in treating unipolar depression, although it has
been difficult to determine why it works so well (Garrett, 2008). Studies find
that between 60 and 80 percent of ECT patients improve (Richard & Lyness,
2006). The procedure seems to be particularly effective in severe cases of de-
pression that include delusions. At least 50,000 patients per year are believed
to receive ECT each year (Cauchon, 1999).
ANTIDEPRESSANT DRUGS Two kinds of drugs discovered in the 1950s reduce
the symptoms of depression: monoamine oxidase (MAO) inhibitors and tricyclics.
These drugs have been joined in recent years by a third group, the so -called
second generation antidepressants (see Table 7 -3).
The effectiveness of MAO inhibitors as a treatment for unipolar de-
pression 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, Saunders, & Kline, 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 carry-
ing 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
Isocarboxazid
Phenelzine
Tranylcypromine
Selegiline
Tricyclics
Imipramine
Amitriptyline
Doxepin
Trim ipramine
Desipramine
Nortripiyline
Protriptyline
Second-generation
Maprotiline
Amoxopine
Trozodone
Clomipramine
Fluoxetine
Sertraline
Paroxetine
Venlafaxine
Fluvoxamine
Nefazodone
Bupropion
Mirtazapine
Citalopram
Escitaropram
Duloxetine
Reboxetine
Atomoxetine
antidepressants
Ludiomil
Asendin
Desyrel
Anafranil
Prozac
Zoloft
Paxil
Effexor
Generic only
Generic only
Wellbutrin
Remeron
Celexo
Lexapro
Cymbalta
Edronax
Strattera
Tofranil
Elavil
Adapin; Sinequan
Surmontil
Norpramin; Pertofrane
Aventil; Pamelor
Vivactil
Marplan
Nardil
Parnate
Eldepril
( Julien, 2008)

202 .//CHAPTER 7
etricyclicoAn antidepressant drug such
as imiprarnine that has three rings in its
molecular structure.
°selective serotonin reuptake
inhibitors (SSRIs)oA group of second-
generation antidepressant drugs that
increase serotonin activity specifically,
without affecting other neurotransmitters.
symptoms. Approximately half of depressed patients who take MAO inhibitors are
helped by them (Thase et al., 1995).There is, however, a potential danger with regard to
these drugs. People who take them experience a dangerous rise in blood pressure if they
eat foods containing the chemical tyramine, including such common foods as cheeses,
bananas, and certain wines. Thus people on MAO inhibitors 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 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 ( Julien, 2008; APA, 1993). About 60 to
65 percent of patients who take tricyclics are helped by them (Gitlin, 2002; Hirschfeld,
1999). If the patients stop taking these drugs immediately after obtaining relief, they
run a high risk of relapsing within a year. Thus, clinicians typically keep patients on
these drugs for five months or more after being free of depressive symptoms—a practice
called maintenance therapy (Williams et al., 2009; Mauri et al., 2005).
Most researchers have concluded that tricyclics reduce depression by acting on neu-
rotransmitter “reuptake” mechanisms ( Julien, 2008). Remember from Chapter 2 that
messages are carried from the “sending” neuron across the synaptic space to a receiv-
ing neuron by a neurotransmitter, a chemical released from the ending of the sending
neuron. However, there is a complication in this process. While the sending neuron
First Dibs on Antidepressant Drugs?
n our society, the likelihood of being
treated for depression and the types
of treatment received by clients often differ
greatly from ethnic group to ethnic group.
In revealing studies, researchers have
examined the antidepressant prescriptions
written for depressed individuals, particu-
larly Medicaid recipients with depres-
sion (Melfi et al., 2000; Stagnitti, 2005;
Strothers et al., 20051. The following pat-
terns have emerged:
Almost 40 percent of depressed Med-
icaid recipients are seen by a mental
health provider, irrespective of gender,
race, or ethnic group.
African Americans, Hispanic Ameri-
cans, and Native Americans are half
as likely as white Americans to be
prescribed antidepressant medications
on their initial therapy visits.
Although African Americans are
less likely to receive antidepressant
drugs, some (but not all) clinical trials
suggest that they may be more likely
than white Americans to respond to
proper antidepressant medications
(Lesser et al., 2007; Lawson, 1996,
1986).
African Americans also receive fewer
prescriptions than white Americans for
most nonpsychiatric disorders (HiK,
2008; Khandker & Simoni-Wastila,
1998).
Among those individuals prescribed
antidepressant drugs, African Ameri-
cans are significantly more likely than
white Americans to receive tricyclic
and older second-generation antide-
pressant drugs, while white Americans
are more likely than African Americans
to receive newer second-generation
antidepressant drugs. The older drugs
tend to be less expensive for insurance
providers.
5 Although African Americans are more
likely to be prescribed tricyclic anti-
depressants, clinical trials suggest that
they may be more susceptible than
white Americans to the undesired ef-
fects of those kinds of drugs (Sramek
& Pi, 1996; Strickland et al., 1991).
202 .//CHAPTER 7
etricyclicoAn antidepressant drug such
as imiprarnine that has three rings in its
molecular structure.
°selective serotonin reuptake
inhibitors (SSRIs)oA group of second-
generation antidepressant drugs that
increase serotonin activity specifically,
without affecting other neurotransmitters.
symptoms. Approximately half of depressed patients who take MAO inhibitors are
helped by them (Thase et al., 1995).There is, however, a potential danger with regard to
these drugs. People who take them experience a dangerous rise in blood pressure if they
eat foods containing the chemical tyramine, including such common foods as cheeses,
bananas, and certain wines. Thus people on MAO inhibitors 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 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 ( Julien, 2008; APA, 1993). About 60 to
65 percent of patients who take tricyclics are helped by them (Gitlin, 2002; Hirschfeld,
1999). If the patients stop taking these drugs immediately after obtaining relief, they
run a high risk of relapsing within a year. Thus, clinicians typically keep patients on
these drugs for five months or more after being free of depressive symptoms—a practice
called maintenance therapy (Williams et al., 2009; Mauri et al., 2005).
Most researchers have concluded that tricyclics reduce depression by acting on neu-
rotransmitter “reuptake” mechanisms ( Julien, 2008). Remember from Chapter 2 that
messages are carried from the “sending” neuron across the synaptic space to a receiv-
ing neuron by a neurotransmitter, a chemical released from the ending of the sending
neuron. However, there is a complication in this process. While the sending neuron
First Dibs on Antidepressant Drugs?
n our society, the likelihood of being
treated for depression and the types
of treatment received by clients often differ
greatly from ethnic group to ethnic group.
In revealing studies, researchers have
examined the antidepressant prescriptions
written for depressed individuals, particu-
larly Medicaid recipients with depres-
sion (Melfi et al., 2000; Stagnitti, 2005;
Strothers et al., 20051. The following pat-
terns have emerged:
Almost 40 percent of depressed Med-
icaid recipients are seen by a mental
health provider, irrespective of gender,
race, or ethnic group.
African Americans, Hispanic Ameri-
cans, and Native Americans are half
as likely as white Americans to be
prescribed antidepressant medications
on their initial therapy visits.
Although African Americans are
less likely to receive antidepressant
drugs, some (but not all) clinical trials
suggest that they may be more likely
than white Americans to respond to
proper antidepressant medications
(Lesser et al., 2007; Lawson, 1996,
1986).
African Americans also receive fewer
prescriptions than white Americans for
most nonpsychiatric disorders (HiK,
2008; Khandker & Simoni-Wastila,
1998).
Among those individuals prescribed
antidepressant drugs, African Ameri-
cans are significantly more likely than
white Americans to receive tricyclic
and older second-generation antide-
pressant drugs, while white Americans
are more likely than African Americans
to receive newer second-generation
antidepressant drugs. The older drugs
tend to be less expensive for insurance
providers.
5 Although African Americans are more
likely to be prescribed tricyclic anti-
depressants, clinical trials suggest that
they may be more susceptible than
white Americans to the undesired ef-
fects of those kinds of drugs (Sramek
& Pi, 1996; Strickland et al., 1991).

Serotonin or
–inorepinephrine
Serotonin or
norepinephrine
reuptake
Serotonin or
norepinephrine
release
Tricyclic
or second-
generation
1–

antidepressants
block reuptake
Mood Disorders :1/ 203
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. It may be that the
reuptake mechanism is too successful in some people—
reducing norepinephrine or serotonin activity too soon,
preventing messages from reaching the receiving neu-
rons, and producing clinical depression. Tricyclics block
this reuptake process, thus increasing neurotransmitter
activity (see Figure 7-2).
A third group of effective antidepressant drugs, struc-
turally different from the MAO inhibitors and tricyclics,
has been developed during the past few decades. Most
of these second-generation antidepressants are labeled
selective serotonin reuptake inhibitors (SSR1s) be-
cause they increase serotonin activity specifically, without
affecting norepinephrine or other neurotransmitters.The
SSRIs include fluoxetine (trade name Prozac), sertraline
(Zoloft), and esdtaloprarn (Lexapro). Newly developed
selective norepinephrine reuptake inhibitors, such as atomoxetine (Strattera), which increase
norepinephrine activity only, and serotonin-norepinephrine reuptake inhibitors, such as venla-
faxine (Effexor), which increase both serotonin and norepinephrine activity, are also now
available.
In effectiveness and speed of action the second-generation antidepressant drugs are
about on par with the tricyclics ( Julien, 2008), yet their sales have skyrocketed. Clini-
cians often prefer the new antidepressants because it is harder to overdose on them than
on the other kinds of antidepressants. In addition, they do not pose the dietary problems
of the MAO inhibitors or produce some of the unpleasant side 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 experience a reduction in
their sex drive, for example ( Julien, 2008).
sending
neuron neuron
3
.2
i_1 ‘
n
inn
-nr
n..ri ni ■. [, [ 1. -.=[, =[ [ [ [•11 1 ,,,,,
T, 71 Li, i , : ‘ 1
111
1: [ ..11i1″ 1 ,

r inlIn linlic in _n`o;n12iirc I ,
Eii , oiuiii]Hri `, -= r[[..17[[1=1 1, -= [
, !I 11. , clic.o.171’!-.0ill: H
C., -1.1 ■- 1.1 o , I :UtiLol-.1.: crro .._
1 _ ‘ , i.:1’, ,, : 1 101 ° Ilu , rl’ol rnr i ‘ 1 . 2n 20 1 , Y.ii ,
n I ‘1212 .rn, ir Ir’n1r[1112 1 J1’ririci
ll
i clic c’ i1 .1 , 2

‘
,,,,iil.:r,
c 2 riirli:=_
112
rvrirni2 n o r ,
fn ?In
nr
Of course your daddy loves you.
He’s on Prozac—he loves everybody”
Serotonin or
–inorepinephrine
Serotonin or
norepinephrine
reuptake
Serotonin or
norepinephrine
release
Tricyclic
or second-
generation
1–

‘
,,,,iil.:r,
c 2 riirli:=_
112
rvrirni2 n o r ,
fn ?In
nr
Of course your daddy loves you.
He’s on Prozac—he loves everybody”

ulation
helmet
I Iliat
al
nscr
oman sr
sins an
urrents
Left vagus nerve
Electrodes
Pulse generator
–liiTILI 1 (;:1 – 11
c c
[11 !’ , 1101 , I r
IL all I I

H , I
1110k1+11.-,’01.:H 1:1;!II- CII I I
, ‘7,1 1■1 1L II 0 ‘ .
204 ://CHAPTER 7
BRAIN STIMULATION A careful look at treatment studies reveals that one-third of people
with unipolar depression are not helped by interventions of any kind. Thus, in recent
years, three more promising biological approaches have been developed—vagus nerve
stimulation, transcranial magnetic stimulation, and deep brain stimulation.
We each have two vagus nerves, one on each side of our body. 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 research-
ers surmised that they might be able to stimulate the brain by electrically stimulating
the vagus nerve.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 gen-
erator, up to the neck and attaches it to the left vagus nerve (see Figure 7-3). Electrical
signals periodically travel from the pulse generator through the wire to the vagus nerve.
In turn, the stimulated vagus nerve delivers electrical signals to the brain. 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 vagus nerve stimulation
(Graham, 2007; Nahas et al., 2005).
Transcranial magnetic stimulation (TMS) is another technique that seeks to stimulate
the brain without subjecting depressed individuals to the undesired effects or trauma of
electroconvulsive therapy. In this procedure, first developed in 1985, 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, at least some parts of the prefrontal cortex of de-
pressed people are underactive;TMS appears to increase neuron activity in those areas.A
number of studies have found that TMS reduces depression when it is administered daily
for two to four weeks (Garrett, 2008; Triggs et al., 1999). The procedure has, however,
not yet been approved by the FDA, partly because it can cause significant discomfort to
the patient’s scalp and can, in some cases, produce seizures (Carlson, 2008).
ulation
helmet
I Iliat
al
nscr
oman sr
sins an
urrents
Left vagus nerve
Electrodes
Pulse generator
–liiTILI 1 (;:1 – 11
c c
[11 !’ , 1101 , I r
IL all I I

Mood Disorders :lir 205
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, including electroconvulsive therapy. 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”
the entire depression brain circuit.
In the initial study of DBS, four of the six severely depressed patients became al-
most depression-free within a matter of months (Mayberg et al., 2005). Subsequent
research with other severely depressed individuals has also yielded promising findings
(Burkholder, 2008). Understandably, this has produced considerable enthusiasm in the
clinical field (Dobbs, 2006), but it is important to recognize that research on DBS is in
its earliest stages.
Psychological Models of Unipolar Depression
The psychological models that have been most widely applied to unipolar depression
are the psychodynamic, behavioral, and cognitive models.The psychodynamic explana-
tion has not been strongly supported by research, and the behavioral view has received
modest support. In contrast, cognitive explanations have received considerable research
support and have gained a large following.
The Psychodynarnic Model Sigmund Freud (1917) and his student Karl Abraham
(1916, 1911) developed the first psychodynamic explanation and treatment for depres-
sion. Their emphasis on dependence and loss continues to influence today’s psychody-
namic clinicians.
PSYCHODYNAMIC EXPLANATIONS Freud and Abraham began by noting the similarity be-
tween clinical depression and grief in people who lose loved ones: constant weeping,
loss of appetite, difficulty sleeping, loss of pleasure in life, and general withdrawal. Ac-
cording to the two 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, or imagined,
loss, in which persons equate other kinds of events with 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 (Busch et al., 2004). 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 (Allen et al., 2004; 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.
°symbolic loss0According to Freudian
theory, the loss of a valued object (for
example, a loss of employment) that is
unconsciously interpreted as the loss of a
loved one. Also called imagined loss.
Ik)
•
1-(7tiii 6
I (-;
1.1.%4,1 ‘;,:’,.711-ititTal IT] TZ: -1) 1.,;-,D1,• •
– –
Mood Disorders :lir 205
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, including electroconvulsive therapy. 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”
the entire depression brain circuit.
In the initial study of DBS, four of the six severely depressed patients became al-
most depression-free within a matter of months (Mayberg et al., 2005). Subsequent
research with other severely depressed individuals has also yielded promising findings
(Burkholder, 2008). Understandably, this has produced considerable enthusiasm in the
clinical field (Dobbs, 2006), but it is important to recognize that research on DBS is in
its earliest stages.
Psychological Models of Unipolar Depression
The psychological models that have been most widely applied to unipolar depression
are the psychodynamic, behavioral, and cognitive models.The psychodynamic explana-
tion has not been strongly supported by research, and the behavioral view has received
modest support. In contrast, cognitive explanations have received considerable research
support and have gained a large following.
The Psychodynarnic Model Sigmund Freud (1917) and his student Karl Abraham
(1916, 1911) developed the first psychodynamic explanation and treatment for depres-
sion. Their emphasis on dependence and loss continues to influence today’s psychody-
namic clinicians.
PSYCHODYNAMIC EXPLANATIONS Freud and Abraham began by noting the similarity be-
tween clinical depression and grief in people who lose loved ones: constant weeping,
loss of appetite, difficulty sleeping, loss of pleasure in life, and general withdrawal. Ac-
cording to the two 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, or imagined,
loss, in which persons equate other kinds of events with 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 (Busch et al., 2004). 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 (Allen et al., 2004; 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.
°symbolic loss0According to Freudian
theory, the loss of a valued object (for
example, a loss of employment) that is
unconsciously interpreted as the loss of a
loved one. Also called imagined loss.
Ik)
•
1-(7tiii 6
I (-;
1.1.%4,1 ‘;,:’,.711-ititTal IT] TZ: -1) 1.,;-,D1,• •
– –

206 ://CHAPTER 7
kl`,14.t.1
1)tr%:,ci_1; . ff-
▪
41
•
A ji
1-0 A (3) pi • =
v.`141311`;` -‘;,lit.k
a^Jii
The following therapist description of a depressed middle-aged woman illustrates
the psychodynamic concepts of dependence, loss of a loved one, and symbolic loss:
Marie Carls . had always felt very attached to her mother. As a matter of fact, they
used to call her “Stamp” because she stuck to her mother as a stamp to a letter. She
always tried to placate her volcanic mother, to please her in every possible way . . .
After marriage [to Julius], she continued her pattern of submission and compliance.
Before her marriage she had difficulty in complying with a volcanic mother, and after her
marriage she almost automatically assumed a submissive role. . . .
[W]hen she was thirty years old … [Marie] and her husband invited Ignatius, who was
single, to come and live with them. Ignatius and the patient 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 ter-
ribly alone and despondent…
Her suffering had become more acute as she realized that old age was ap-
proaching 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. . . . She felt that everything she had built in her fife was
false or based on a false premise.
(Arieti & Bemporad, 1978, pp. 275-284)
Studies have offered general support for the psychodynamic idea that depression
may be triggered by a major loss.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 always is at the core of
depression. In fact, it is estimated that less than 10 percent of all people who experi-
ence major losses in life actually become depressed (Bonanno, 2004; Paykel & Cooper,
1992). Moreover, research into the loss-depression link has provided inconsistent find-
ings. Though some studies find evidence of a relationship between childhood loss and
later depression, others do not (Parker, 1992).
WHAT ARE THE PSYCHODYNAMIC TREATMENTS FOR UNIPOLAR DEPRESSION? Psychodynamic
therapists use the same basic procedures with depressed clients as they use with others:
They encourage the 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:
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 left 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 left him with the doctor. He recalled how he
had kicked and screamed, raging at her for leaving him.
(Lorand, 1968, pp. 325-326)
206 ://CHAPTER 7
kl`,14.t.1
1)tr%:,ci_1; . ff-
▪
41
•
A ji
1-0 A (3) pi • =
v.`141311`;` -‘;,lit.k
a^Jii
The following therapist description of a depressed middle-aged woman illustrates
the psychodynamic concepts of dependence, loss of a loved one, and symbolic loss:
Marie Carls . had always felt very attached to her mother. As a matter of fact, they
used to call her “Stamp” because she stuck to her mother as a stamp to a letter. She
always tried to placate her volcanic mother, to please her in every possible way . . .
After marriage [to Julius], she continued her pattern of submission and compliance.
Before her marriage she had difficulty in complying with a volcanic mother, and after her
marriage she almost automatically assumed a submissive role. . . .
[W]hen she was thirty years old … [Marie] and her husband invited Ignatius, who was
single, to come and live with them. Ignatius and the patient 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 ter-
ribly alone and despondent…
Her suffering had become more acute as she realized that old age was ap-
proaching 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. . . . She felt that everything she had built in her fife was
false or based on a false premise.
(Arieti & Bemporad, 1978, pp. 275-284)
Studies have offered general support for the psychodynamic idea that depression
may be triggered by a major loss.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 always is at the core of
depression. In fact, it is estimated that less than 10 percent of all people who experi-
ence major losses in life actually become depressed (Bonanno, 2004; Paykel & Cooper,
1992). Moreover, research into the loss-depression link has provided inconsistent find-
ings. Though some studies find evidence of a relationship between childhood loss and
later depression, others do not (Parker, 1992).
WHAT ARE THE PSYCHODYNAMIC TREATMENTS FOR UNIPOLAR DEPRESSION? Psychodynamic
therapists use the same basic procedures with depressed clients as they use with others:
They encourage the 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:
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 left 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 left him with the doctor. He recalled how he
had kicked and screamed, raging at her for leaving him.
(Lorand, 1968, pp. 325-326)

Mood Disorders :1/ 207
• MT4iiia6:2 – • – HOME • SEND EXPLORE ——– • ‘ ° ” ” – ”
How Well Do Colleges Treat Depression?
BY DANIEL MCGINN AND RON DEPASQUALE, NEWSWEEK, AUGUST 23, 2004
n the long list of worries that Mom and Dad have when a
child goes to college—grades, homesickness, partying—
there’s a new issue gaining prominence: the apparent rise in
mental illness on campus. More than 1,100 college students com-
mit suicide each year, according to estimates by mental-health
groups. And even when students aren’t in acute distress, they’re
suffering in surprisingly large numbers. In a 2003 survey by the
American College Health Association, more than 40 percent of
students reported feeling “so depressed it was difficult to func-
tion” at least once during the year. Thirty percent identified them-
selves as suffering from an anxiety disorder or depression. . . .
Given that kind of assessment, it’s inevitable that mental-health
issues are starting to filter into admissions conversations. One
counselor at an East Coast private high school says that dur-
ing the 2003-04 admissions cycle, officials from two colleges
confided they were particularly focused on admitting a class that
was “rock solid” emotionally, both to help prevent suicides and
to reduce the toll on overbooked school therapists. . .
Since the admissions process requires students to appear
flawless, many families avoid disclosing a child’s history of
emotional problems, especially before they get an acceptance
letter. However, parents are starting to ask tough questions
about just which kind of mental-health services they can expect
from schools
. . . While nearly every school has a counseling office,
almost half lack a full-fledged staff psychiatrist, according to
Robert Gallagher, a University of Pittsburgh professor who con-
ducts an annual survey of college counseling offices. That means
it may be difficult for a student to receive prescription drugs
to treat depression or anxiety, and that students with serious
problems may be referred off campus for treatment. “Not only
are the [on-campus] services more accessible, but the people
providing the services are more familiar with college pressures,”
says Gallagher. And while some schools offer unlimited therapy
for students, others restrict them to eight or 10 appointments a
year. That may be fine for the average student, who often sees
a counselor just once or twice to discuss homesickness, a bad
grade or a relationship breakup. For those with more serious
problems, such limits may mean rushed care.
Experts cite a mix of reasons that campus therapists’ offices
are so crowded. . . . [According to one explanation,] the quest
to get into a top college has grown so cutthroat for many that
more students are emerging from it emotionally damaged. “Kids
are burning out sooner and sooner,” says Leigh Martin Lowe,
director of college counseling at Roland Park Country School
in Baltimore. “They’re not being allowed to enjoy their teenage
years, and many of them end up in college and they don’t have
the energy or stamina to really turn it on.” .. .
For students with [emotional problems], college counselors
and therapists say that fact should play some role in their col-
lege search. . . . There may also be benefits in choosing smaller
schools. . . . According to the University of Pittsburgh study, at
colleges with 2,500 or fewer students, health centers had one
counselor for every 818 students. At colleges with more than
15,000 students, the counselor-to-student ratio jumped to 1 to
2,426.
The trickiest task faces parents whose children seem 100 per-
cent healthy when they leave for college. Donna Satow . and
her husband run the Jed Foundation, which helps colleges de-
velop strategies for dealing with student depression. . . . Satow
advises parents of every student to become informed about
mental-health services at their child’s school. . [I]n a world
where families agonize over finding the cushiest dorm room and
the perfect meal plan, it’s a question that deserves to be asked.
Copyright C 2004. Reprinted by permission of
PARS International Corp. on behalf of Newsweek.
• • • • • T • .
Despite successful case reports such as this, researchers have found that long-term
psychodynainic therapy is only occasionally helpful in cases of unipolar depression
(Prochaska & Norcross, 2007). Two features of the approach may help limit its ef-
fectiveness. First, depressed clients may be too passive and feel too weary to join fully
Mood Disorders :1/ 207
• MT4iiia6:2 – • – HOME • SEND EXPLORE ——– • ‘ ° ” ” – ”
How Well Do Colleges Treat Depression?
BY DANIEL MCGINN AND RON DEPASQUALE, NEWSWEEK, AUGUST 23, 2004
n the long list of worries that Mom and Dad have when a
child goes to college—grades, homesickness, partying—
there’s a new issue gaining prominence: the apparent rise in
mental illness on campus. More than 1,100 college students com-
mit suicide each year, according to estimates by mental-health
groups. And even when students aren’t in acute distress, they’re
suffering in surprisingly large numbers. In a 2003 survey by the
American College Health Association, more than 40 percent of
students reported feeling “so depressed it was difficult to func-
tion” at least once during the year. Thirty percent identified them-
selves as suffering from an anxiety disorder or depression. . . .
Given that kind of assessment, it’s inevitable that mental-health
issues are starting to filter into admissions conversations. One
counselor at an East Coast private high school says that dur-
ing the 2003-04 admissions cycle, officials from two colleges
confided they were particularly focused on admitting a class that
was “rock solid” emotionally, both to help prevent suicides and
to reduce the toll on overbooked school therapists. . .
Since the admissions process requires students to appear
flawless, many families avoid disclosing a child’s history of
emotional problems, especially before they get an acceptance
letter. However, parents are starting to ask tough questions
about just which kind of mental-health services they can expect
from schools
. . . While nearly every school has a counseling office,
almost half lack a full-fledged staff psychiatrist, according to
Robert Gallagher, a University of Pittsburgh professor who con-
ducts an annual survey of college counseling offices. That means
it may be difficult for a student to receive prescription drugs
to treat depression or anxiety, and that students with serious
problems may be referred off campus for treatment. “Not only
are the [on-campus] services more accessible, but the people
providing the services are more familiar with college pressures,”
says Gallagher. And while some schools offer unlimited therapy
for students, others restrict them to eight or 10 appointments a
year. That may be fine for the average student, who often sees
a counselor just once or twice to discuss homesickness, a bad
grade or a relationship breakup. For those with more serious
problems, such limits may mean rushed care.
Experts cite a mix of reasons that campus therapists’ offices
are so crowded. . . . [According to one explanation,] the quest
to get into a top college has grown so cutthroat for many that
more students are emerging from it emotionally damaged. “Kids
are burning out sooner and sooner,” says Leigh Martin Lowe,
director of college counseling at Roland Park Country School
in Baltimore. “They’re not being allowed to enjoy their teenage
years, and many of them end up in college and they don’t have
the energy or stamina to really turn it on.” .. .
For students with [emotional problems], college counselors
and therapists say that fact should play some role in their col-
lege search. . . . There may also be benefits in choosing smaller
schools. . . . According to the University of Pittsburgh study, at
colleges with 2,500 or fewer students, health centers had one
counselor for every 818 students. At colleges with more than
15,000 students, the counselor-to-student ratio jumped to 1 to
2,426.
The trickiest task faces parents whose children seem 100 per-
cent healthy when they leave for college. Donna Satow . and
her husband run the Jed Foundation, which helps colleges de-
velop strategies for dealing with student depression. . . . Satow
advises parents of every student to become informed about
mental-health services at their child’s school. . [I]n a world
where families agonize over finding the cushiest dorm room and
the perfect meal plan, it’s a question that deserves to be asked.
Copyright C 2004. Reprinted by permission of
PARS International Corp. on behalf of Newsweek.
• • • • • T • .
Despite successful case reports such as this, researchers have found that long-term
psychodynainic therapy is only occasionally helpful in cases of unipolar depression
(Prochaska & Norcross, 2007). Two features of the approach may help limit its ef-
fectiveness. First, depressed clients may be too passive and feel too weary to join fully

208 //CHAPTER 7
t+1 re a
of haskeiloall’s –
the 1 980s and –
Found new
leaving the
ll e
.7L4i 1
«.1111.1.1F)11 – 1,
‘
r;’)..,1 r0. i.:”1″..!
into the subtle therapy discussions (Widloecher, 2001). 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 traditional approaches (Dreissen et al., 2009; Prochaska
& Norcross, 2007; Leichsenring, 2001).
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 favorable patterns of
reinforcement (Farmer & Chapman, 2008). Clinical researcher Peter Lewinsohn has
developed one of the leading behavioral explanations and treatments (Lewinsohn et al.,
1990,1984).
THE BEHAVIORAL EXPLANATION Lewinsohn suggests that the positive rewards in life dwindle
for some persons, 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; similarly, an aging baseball player loses the rewards of high salary
and praise 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, the individuals spiral toward
depression.
In a series of studies, Lewinsohn and his colleagues have found that the number of
rewards people receive in life is indeed related to the presence or absence of depression.
In some of their early studies, not only did depressed participants report fewer positive
rewards than nondepressed participants, but when their rewards began to increase, their
mood improved as well (Lewinsohn et al., 1979). Similarly, more recent investigations
have found a strong relationship between positive life events and feelings of life satisfac-
tion and happiness (Lu, 1999).
Lewinsohn and other behaviorists have further proposed that social rewards are par-
ticularly important in the downward spiral of depression (Farmer & Chapman, 2008;
Lewinsohn et al., 1984). This claim has been supported by research showing that de-
pressed persons experience fewer social rewards than nondepressed persons and that as
their mood improves, their social rewards increase. Although depressed people are some-
times the victims of social circumstances, it may also be that their dark mood and flat
behaviors help produce a decline in social rewards (Joiner, 2002; Coyne, 2001).
WHAT ARE THE BEHAVIORAL TREATMENTS FOR UNIPOLAR DEPRESSION?
In Lewinsohn’s treatment for unipolar depression, therapists use
a variety of strategies to help increase the positive behaviors of
their clients (Farmer & Chapman, 2008; Lewinsohn et al., 1990,
1982). First, the therapist selects activities that the client considers
pleasurable, such as going shopping or taking photos, and encour-
ages the person to set up a weekly schedule for engaging in them.
Studies have shown that adding positive activities to a person’s life
can indeed lead to a better mood (Farmer & Chapman, 2008).
Second, while reintroducing pleasurable events into a client’s life,
the therapist makes sure that the person’s various behaviors are
rewarded correctly. Behaviorists argue that when people become
depressed, their negative behaviors—crying, ruminating, com-
plaining, or self-criticism—keep others at a distance, reducing
chances for rewarding experiences and interactions. To change
this pattern, therapists may try to systematically ignore a client’s
depressive behaviors while praising or otherwise rewarding con-
structive statements and behavior, such as going to work. Finally,
behavioral therapists may train clients in effective social skills
(Segrin, 2000; Hersen et al., 1984). In group therapy programs,
208 //CHAPTER 7
t+1 re a
of haskeiloall’s –
the 1 980s and –
Found new
leaving the
ll e
.7L4i 1
«.1111.1.1F)11 – 1,
‘
r;’)..,1 r0. i.:”1″..!
into the subtle therapy discussions (Widloecher, 2001). 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 traditional approaches (Dreissen et al., 2009; Prochaska
& Norcross, 2007; Leichsenring, 2001).
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 favorable patterns of
reinforcement (Farmer & Chapman, 2008). Clinical researcher Peter Lewinsohn has
developed one of the leading behavioral explanations and treatments (Lewinsohn et al.,
1990,1984).
THE BEHAVIORAL EXPLANATION Lewinsohn suggests that the positive rewards in life dwindle
for some persons, 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; similarly, an aging baseball player loses the rewards of high salary
and praise 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, the individuals spiral toward
depression.
In a series of studies, Lewinsohn and his colleagues have found that the number of
rewards people receive in life is indeed related to the presence or absence of depression.
In some of their early studies, not only did depressed participants report fewer positive
rewards than nondepressed participants, but when their rewards began to increase, their
mood improved as well (Lewinsohn et al., 1979). Similarly, more recent investigations
have found a strong relationship between positive life events and feelings of life satisfac-
tion and happiness (Lu, 1999).
Lewinsohn and other behaviorists have further proposed that social rewards are par-
ticularly important in the downward spiral of depression (Farmer & Chapman, 2008;
Lewinsohn et al., 1984). This claim has been supported by research showing that de-
pressed persons experience fewer social rewards than nondepressed persons and that as
their mood improves, their social rewards increase. Although depressed people are some-
times the victims of social circumstances, it may also be that their dark mood and flat
behaviors help produce a decline in social rewards (Joiner, 2002; Coyne, 2001).
WHAT ARE THE BEHAVIORAL TREATMENTS FOR UNIPOLAR DEPRESSION?
In Lewinsohn’s treatment for unipolar depression, therapists use
a variety of strategies to help increase the positive behaviors of
their clients (Farmer & Chapman, 2008; Lewinsohn et al., 1990,
1982). First, the therapist selects activities that the client considers
pleasurable, such as going shopping or taking photos, and encour-
ages the person to set up a weekly schedule for engaging in them.
Studies have shown that adding positive activities to a person’s life
can indeed lead to a better mood (Farmer & Chapman, 2008).
Second, while reintroducing pleasurable events into a client’s life,
the therapist makes sure that the person’s various behaviors are
rewarded correctly. Behaviorists argue that when people become
depressed, their negative behaviors—crying, ruminating, com-
plaining, or self-criticism—keep others at a distance, reducing
chances for rewarding experiences and interactions. To change
this pattern, therapists may try to systematically ignore a client’s
depressive behaviors while praising or otherwise rewarding con-
structive statements and behavior, such as going to work. Finally,
behavioral therapists may train clients in effective social skills
(Segrin, 2000; Hersen et al., 1984). In group therapy programs,

Mood Disorders 209
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 behavioral techniques are combined, behavioral
treatment does appear to reduce depressive symptoms, particularly if the depression
is mild (Farmer & Chapman, 2008; Teri & Lewinsohn, 1986). 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 depres-
sion persistently view events in negative ways and that such perceptions lead to their dis-
order.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:
Mary was 25 years old and had just begun her senior year in college. . . . Asked to re-
count how her life had been going recently, Mary began to weep. Sobbing, she said that
for the last year or so she felt she was losing control of her life and that recent stresses
(starting school again, friction with her boyfriend) had left her feeling worthless and fright-
ened. Because of a gradual deterioration in her vision, she was now forced to wear glasses
all day. “The glasses make me look terrible,” she said, and “I don’t look people in the
eye much any more.” Also, to her dismay, Mary had gained 20 pounds in the past year.
She viewed herself as overweight and unattractive. At times she was convinced that with
enough money to buy contact lenses and enough time to exercise she could cast off her
depression; at other times she believed nothing would help. . . Mary saw her life deterio-
rating in other spheres, as well. She felt overwhelmed by schoolwork and, for the first time
in her life, was on academic probation. . In addition to her dissatisfaction with her ap-
pearance and her fears about her academic future, Mary complained of a lack of friends.
Her social network consisted solely of her boyfriend, with whom she was living. Although
there were times she experienced this relationship as almost unbearably frustrating, she
felt helpless to change it and was pessimistic about its permanence.
(Spitzer et al., 1983, pp. 122-123)
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 developed 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 would do. 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 7-4). 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.
olearned helplessnessoThe perception,
based on past experiences, that one has
no control over one’s reinforcements.
Mood Disorders 209
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 behavioral techniques are combined, behavioral
treatment does appear to reduce depressive symptoms, particularly if the depression
is mild (Farmer & Chapman, 2008; Teri & Lewinsohn, 1986). 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 depres-
sion persistently view events in negative ways and that such perceptions lead to their dis-
order.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:
Mary was 25 years old and had just begun her senior year in college. . . . Asked to re-
count how her life had been going recently, Mary began to weep. Sobbing, she said that
for the last year or so she felt she was losing control of her life and that recent stresses
(starting school again, friction with her boyfriend) had left her feeling worthless and fright-
ened. Because of a gradual deterioration in her vision, she was now forced to wear glasses
all day. “The glasses make me look terrible,” she said, and “I don’t look people in the
eye much any more.” Also, to her dismay, Mary had gained 20 pounds in the past year.
She viewed herself as overweight and unattractive. At times she was convinced that with
enough money to buy contact lenses and enough time to exercise she could cast off her
depression; at other times she believed nothing would help. . . Mary saw her life deterio-
rating in other spheres, as well. She felt overwhelmed by schoolwork and, for the first time
in her life, was on academic probation. . In addition to her dissatisfaction with her ap-
pearance and her fears about her academic future, Mary complained of a lack of friends.
Her social network consisted solely of her boyfriend, with whom she was living. Although
there were times she experienced this relationship as almost unbearably frustrating, she
felt helpless to change it and was pessimistic about its permanence.
(Spitzer et al., 1983, pp. 122-123)
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 developed 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 would do. 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 7-4). 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.
olearned helplessnessoThe perception,
based on past experiences, that one has
no control over one’s reinforcements.

VV .:: C:.Eirlcls a879 1 : 6
210 ://CHAPTER 7
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 re-
inforcements in their lives.
In numerous human and animal studies, participants who undergo helplessness
training have displayed reactions similar to depressive symptoms. 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 com-
mon symptom of human depression (Lindner, 1968).
The learned helplessness explanation of depression has been revised somewhat over
the past two decades.According to a new version of the theory, the attribution-helplessness
theory, when people view events as beyond their control, they ask themselves why this
is so (Taube-Schiff & Lau, 2008; 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 may experience depression. If they make other kinds of
attributions, this reaction is unlikely.
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 know what got into me—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 depres-
sion (Taube-Schiff & Lau, 2008;Yu & Seligman, 2002).
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 an indi-
vidual (Abela et al., 2004; Abramson et al., 2002, 1989). By
taking this factor into consideration, clinicians are often able
to predict depression with still greater precision (Robinson
& Alloy, 2003).
Although the learned helplessness theory of unipolar
depression has been very influential, it too has imperfec-
tions. First, much of the learned helplessness research relies
on animal subjects (Henn &Vollmayr, 2005). It is impossible
to know whether the animals’ symptoms do in fact reflect
the clinical depression found in humans. Second, the attri-
butional 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, 2008; Beck, 2002, 1991, 1967).According to Beck,
maladaptive attitudes, a cognitive triad, errors in thinking, and au-
tomatic thoughts combine to produce the clinical disorder.
VV .:: C:.Eirlcls a879 1 : 6
210 ://CHAPTER 7
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 re-
inforcements in their lives.
In numerous human and animal studies, participants who undergo helplessness
training have displayed reactions similar to depressive symptoms. 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 com-
mon symptom of human depression (Lindner, 1968).
The learned helplessness explanation of depression has been revised somewhat over
the past two decades.According to a new version of the theory, the attribution-helplessness
theory, when people view events as beyond their control, they ask themselves why this
is so (Taube-Schiff & Lau, 2008; 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 may experience depression. If they make other kinds of
attributions, this reaction is unlikely.
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 know what got into me—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 depres-
sion (Taube-Schiff & Lau, 2008;Yu & Seligman, 2002).
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 an indi-
vidual (Abela et al., 2004; Abramson et al., 2002, 1989). By
taking this factor into consideration, clinicians are often able
to predict depression with still greater precision (Robinson
& Alloy, 2003).
Although the learned helplessness theory of unipolar
depression has been very influential, it too has imperfec-
tions. First, much of the learned helplessness research relies
on animal subjects (Henn &Vollmayr, 2005). It is impossible
to know whether the animals’ symptoms do in fact reflect
the clinical depression found in humans. Second, the attri-
butional 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, 2008; Beck, 2002, 1991, 1967).According to Beck,
maladaptive attitudes, a cognitive triad, errors in thinking, and au-
tomatic thoughts combine to produce the clinical disorder.

Mood Disorders :1/ 211
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. 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 repeat-
edly interpret (1) their experiences, (2) themselves, and (3) their figures 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 or 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 l can do to go out and meet people and have the fact
pointed up to me so clearly.
(Fieve, 1975)
According to Beck, depressed people also make errors in their thinking. In one com-
mon error of logic, they draw arbitrary bfferences—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 nega-
tive 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 experience automatic thoughts, a steady train of un-
pleasant 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 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. Several
of them co nfirm that depressed people hold maladaptive attitudes and that the more
of these maladaptive attitudes they hold, the more depressed they tend to
be (Evans et al., 2005; Whisman & McGarvey, 1995). Other research has
found the cognitive triad at work in depressed people (Ridout et al., 2003).
And, still other studies have supported Beck’s claims about errors in logic
(Cole & Turner, 1993). In one study, for example, 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. In several 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,
°cognitive triad0The three forms of
negative thinking that Aaron Beck theo-
rizes lead people to feel depressed. The
triad consists of a negative view of one’s
experiences, oneself, and the future.
°automatic thoughtsoNumerous
unpleasant thoughts that help to cause
or maintain depression, anxiety, or other
forms of psychological dysfunction.
‘1 t’i, tA ■rc’..,D i16:411:6
[ — – t…_. ,- .._ „ . 4-,- -,L-
101 – .:11,t,r.”11,11 ,-,7 ,LE \”’A_=.1,,Yf..?_,rij I
-1;:o.11,7357ril!,1’LV..’iillii0F.C1[1 ‘-.-“:-JILv1,1 ‘,=11’
I ‘ t ‘Zfl:, • hil,t,-, r,•`,LiTOti.-,,’,:)i’,,.rt:c.– –
Mood Disorders :1/ 211
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. 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 repeat-
edly interpret (1) their experiences, (2) themselves, and (3) their figures 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 or 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 l can do to go out and meet people and have the fact
pointed up to me so clearly.
(Fieve, 1975)
According to Beck, depressed people also make errors in their thinking. In one com-
mon error of logic, they draw arbitrary bfferences—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 nega-
tive 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 experience automatic thoughts, a steady train of un-
pleasant 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 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. Several
of them co nfirm that depressed people hold maladaptive attitudes and that the more
of these maladaptive attitudes they hold, the more depressed they tend to
be (Evans et al., 2005; Whisman & McGarvey, 1995). Other research has
found the cognitive triad at work in depressed people (Ridout et al., 2003).
And, still other studies have supported Beck’s claims about errors in logic
(Cole & Turner, 1993). In one study, for example, 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. In several 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,
°cognitive triad0The three forms of
negative thinking that Aaron Beck theo-
rizes lead people to feel depressed. The
triad consists of a negative view of one’s
experiences, oneself, and the future.
°automatic thoughtsoNumerous
unpleasant thoughts that help to cause
or maintain depression, anxiety, or other
forms of psychological dysfunction.
‘1 t’i, tA ■rc’..,D i16:411:6
[ — – t…_. ,- .._ „ . 4-,- -,L-
101 – .:11,t,r.”11,11 ,-,7 ,LE \”’A_=.1,,Yf..?_,rij I
-1;:o.11,7357ril!,1’LV..’iillii0F.C1[1 ‘-.-“:-JILv1,1 ‘,=11’
I ‘ t ‘Zfl:, • hil,t,-, r,•`,LiTOti.-,,’,:)i’,,.rt:c.– –

2CnL6246-7
“You’re sad about the wrong things, Albert.”
C
…:12A:4;4(f…u. 14113,11
Self-Help Giles Awry ‘;’
21 2 ://CHAPTER 7
COGNITIVE TREATMENT FOR UNIPOLAR DEPRESSION To help clients
overcome their negative thinking, Beck has developed a treat-
ment approach that he calls cognitive therapy. 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 (Farmer
& Chapman, 2008). The approach follows four phases and usu-
ally 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 individuals 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:
repeatedly dwell mentally on their mood without acting to
change it—experience dejection longer and are more likely
to develop clinical depression later in life than people who
avoid such ruminations (Levens et al., 2009; Nolen•Hoeksema,
2002).
Therapist: On what do you base this belief that you can’t be happy without a man?
Patient 1 wos really depressed for a year and a half when I didn’t have a man.
Therapist: Is there another reason why you were depressed?
Patient As we discussed, I was looking at everything in a distorted way. But f still don’t
know if I could be happy if no one was interested in me.
Therapist: I don’t know either. Is there a way we could find out?
Patient Well, as an experiment, I could not go out on dates for a while and see how
feel.
Therapist: I think that’s a good idea. Although it has its flaws, the experimental method
is still the best way currently available to discover the facts. You’re fortunate in
being able to run this type of experiment. Now, for the first time in your adult life
you aren’t attached to a man. if you find you can be happy without a man, this
will greatly strengthen you and also make your future relationships all the better.
(Beck et al., 1979, pp. 253-254)
2CnL6246-7
“You’re sad about the wrong things, Albert.”
C
…:12A:4;4(f…u. 14113,11
Self-Help Giles Awry ‘;’
21 2 ://CHAPTER 7
COGNITIVE TREATMENT FOR UNIPOLAR DEPRESSION To help clients
overcome their negative thinking, Beck has developed a treat-
ment approach that he calls cognitive therapy. 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 (Farmer
& Chapman, 2008). The approach follows four phases and usu-
ally 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 individuals 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:
repeatedly dwell mentally on their mood without acting to
change it—experience dejection longer and are more likely
to develop clinical depression later in life than people who
avoid such ruminations (Levens et al., 2009; Nolen•Hoeksema,
2002).
Therapist: On what do you base this belief that you can’t be happy without a man?
Patient 1 wos really depressed for a year and a half when I didn’t have a man.
Therapist: Is there another reason why you were depressed?
Patient As we discussed, I was looking at everything in a distorted way. But f still don’t
know if I could be happy if no one was interested in me.
Therapist: I don’t know either. Is there a way we could find out?
Patient Well, as an experiment, I could not go out on dates for a while and see how
feel.
Therapist: I think that’s a good idea. Although it has its flaws, the experimental method
is still the best way currently available to discover the facts. You’re fortunate in
being able to run this type of experiment. Now, for the first time in your adult life
you aren’t attached to a man. if you find you can be happy without a man, this
will greatly strengthen you and also make your future relationships all the better.
(Beck et al., 1979, pp. 253-254)

63%
Pray/meditate
Help othe rs in need
Take a bath or shower
Play with a pet
Exercise /work out
Go out with friends
Eat
Take a drive in a car
Have sex
38%
25%
0 women
Men
1 11 1 -j or: 4110 = ,
.1n1;1 ‘
C.01 : 1, H4,1′
07, -111,1=1 , 1 ■ 1/Lwi- Ilc,
1
I AI
; ,,J1 ■ ! ,-, Ir:r
Mood Disorders :1/ 21 3
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 thera-
pies improve much more than those who receive placebos or no treat-
ment at all (Arnow & Post, 2010; Taube-Schiff & Lau, 2008; DeRubeis
et al., 2005). 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 individu-
als must fully discard their negative cognitions in order to overcome
depression. These therapists, the new wave cognitive-behavioral thera-
pists 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 (StrosahI & Robinson, 2008; Zettle, 2007; Hayes et al., 2006).
The Sociocultural Model of Unipolar Depression
Sociocultural theorists propose that unipolar depression is greatly influenced by the
social context that surrounds people (see Figure 7-5). Their belief is supported by
the finding, discussed earlier, that this disorder is often triggered by outside stressors.
Once again, there are two kinds of sociocultural views—the family -social perspective and
the on perspective.
The FomiGy-Social Perspective Earlier you read that some behaviorists believe
that a decline in social rewards is particularly important in the development of depres-
sion. Although presented as part of their behavioral explanation, this view is consistent
with the family-social perspective. Indeed, depression has been tied repeatedly to the
_ ,,….„ f’;iStlii; :r_ • t , 0 t,7:D. • = …,,t4 ,,_„
-C”• -,:iiijrJf-,Gtik’D .i:7′.4;11 .1: 131;! –4j1 ■:4T3
tib). -, — ,,,,71,,,,’ ik’T-4i1.”&J-: (=.:’,’7.1.f0.1th4-Li „..,
tit. :Ti Lip 7,,-4igitil4t4) ,t’ll 7, .lOa_.- :11-‘:
..u.1.1.;,- 16/;IN41 -4.7. =i-_,.. 1 k-•,-,,T,j_…,,W,It.t,- , ,.7:-.,,ye.,2)..1.1i4.113
• 111..;•’=”41 !` r;: t’ `)It —i’ ‘ i 1
T . ” 01,I. 1.1 4)
if 11 V3 fi.1 1TiFS:ATillii•-‘413’
t7fz74.!(=A1.4 iiit2140ii:k=1. k!,7),Ii.I.,
63%
Pray/meditate
Help othe rs in need
Take a bath or shower
Play with a pet
Exercise /work out
Go out with friends
Eat
Take a drive in a car
Have sex
38%
25%
0 women
Men
1 11 1 -j or: 4110 = ,
.1n1;1 ‘
C.01 : 1, H4,1′
07, -111,1=1 , 1 ■ 1/Lwi- Ilc,
1
I AI
; ,,J1 ■ ! ,-, Ir:r
Mood Disorders :1/ 21 3
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 thera-
pies improve much more than those who receive placebos or no treat-
ment at all (Arnow & Post, 2010; Taube-Schiff & Lau, 2008; DeRubeis
et al., 2005). 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 individu-
als must fully discard their negative cognitions in order to overcome
depression. These therapists, the new wave cognitive-behavioral thera-
pists 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 (StrosahI & Robinson, 2008; Zettle, 2007; Hayes et al., 2006).
The Sociocultural Model of Unipolar Depression
Sociocultural theorists propose that unipolar depression is greatly influenced by the
social context that surrounds people (see Figure 7-5). Their belief is supported by
the finding, discussed earlier, that this disorder is often triggered by outside stressors.
Once again, there are two kinds of sociocultural views—the family -social perspective and
the on perspective.
The FomiGy-Social Perspective Earlier you read that some behaviorists believe
that a decline in social rewards is particularly important in the development of depres-
sion. Although presented as part of their behavioral explanation, this view is consistent
with the family-social perspective. Indeed, depression has been tied repeatedly to the
_ ,,….„ f’;iStlii; :r_ • t , 0 t,7:D. • = …,,t4 ,,_„
-C”• -,:iiijrJf-,Gtik’D .i:7′.4;11 .1: 131;! –4j1 ■:4T3
tib). -, — ,,,,71,,,,’ ik’T-4i1.”&J-: (=.:’,’7.1.f0.1th4-Li „..,
tit. :Ti Lip 7,,-4igitil4t4) ,t’ll 7, .lOa_.- :11-‘:
..u.1.1.;,- 16/;IN41 -4.7. =i-_,.. 1 k-•,-,,T,j_…,,W,It.t,- , ,.7:-.,,ye.,2)..1.1i4.113
• 111..;•’=”41 !` r;: t’ `)It —i’ ‘ i 1
T . ” 01,I. 1.1 4)
if 11 V3 fi.1 1TiFS:ATillii•-‘413′
t7fz74.!(=A1.4 iiit2140ii:k=1. k!,7),Ii.I.,

1p
a –
ce
de ssi n. n e
companciOnship nand warmth of dogs and
other pets have been found to prevenl
loneliness and isolation and, in tu.
offset depressed feelings.
214 ://CHAPTER 7
*interpersonal psychotherapy (IPT)0
A treatment for unipolar depression that
is based on the belief that clarifying and
changing one’s interpersonal problems
will help lead to recovery.
°couple therapyeA therapy format in
which the therapist works with Iwo peo-
ple who share a long-term relationship.
unavailability of social support (Doss et al., 2008; Kendler et al., 2005). Across the United
States, people who are separated or divorced display three times the depression rate of
married or widowed persons and double the rate of people who have never been mar-
ried (Weissman et al., 1991). In some cases, the spouse’s depression may contribute to
marital problems, a separation, or divorce, but often the interpersonal conflicts and low
social support found in troubled relationships seem to lead to depression (Highet et al.,
2005;Whisman, 2001).
People whose lives are isolated and without intimacy seem particularly likely to
become depressed at times of stress (Kendler et al., 2005; Nezlek et al., 2000). Some
highly publicized studies conducted in England a couple of 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
experiencing stressful events (Brown et al., 1995; 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 (Moos & Cronkite, 1999).
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.
INTERPERSONAL PSYCHOTHERAPY Developed by clinical researchers Gerald Klerman
and Myrna Weissman, interpersonal psychotherapy (IPT) holds that any of four
interpersonal problem areas may lead to depression and must be addressed: interpersonal
loss, interpersonal role dispute, interpersonal role transition, and interpersonal deficits
(Stuart, 2009; [German & Weissman, 1992). Over the course of around 16 sessions, IPT
therapists address these areas.
First, depressed persons may, as psychodynamic theorists suggest, be experiencing a
grief reaction over an important interpersonal loss, the loss of a loved one. In such cases,
IPT therapists encourage clients to explore 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 seek 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 rela-
tionship 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 experiencing 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. IPT thera-
pists may help such individuals recognize 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:
Client: (After a long pause with eyes downcast, a sad facial expression, and slumped
posture) People always make fun of me. I guess I’m just the type of guy who
really was meant to be a loner, damn it. (Deep sigh)
Therapist: Could you do that again for me?
Client What?
Therapist: The sigh, only a bit deeper.
Client: Why? (Pause) Okay, but 1 don’t see what . . . okay. (Client sighs again and
smiles.)
1p
a –
ce
de ssi n. n e
companciOnship nand warmth of dogs and
other pets have been found to prevenl
loneliness and isolation and, in tu.
offset depressed feelings.
214 ://CHAPTER 7
*interpersonal psychotherapy (IPT)0
A treatment for unipolar depression that
is based on the belief that clarifying and
changing one’s interpersonal problems
will help lead to recovery.
°couple therapyeA therapy format in
which the therapist works with Iwo peo-
ple who share a long-term relationship.
unavailability of social support (Doss et al., 2008; Kendler et al., 2005). Across the United
States, people who are separated or divorced display three times the depression rate of
married or widowed persons and double the rate of people who have never been mar-
ried (Weissman et al., 1991). In some cases, the spouse’s depression may contribute to
marital problems, a separation, or divorce, but often the interpersonal conflicts and low
social support found in troubled relationships seem to lead to depression (Highet et al.,
2005;Whisman, 2001).
People whose lives are isolated and without intimacy seem particularly likely to
become depressed at times of stress (Kendler et al., 2005; Nezlek et al., 2000). Some
highly publicized studies conducted in England a couple of 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
experiencing stressful events (Brown et al., 1995; 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 (Moos & Cronkite, 1999).
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.
INTERPERSONAL PSYCHOTHERAPY Developed by clinical researchers Gerald Klerman
and Myrna Weissman, interpersonal psychotherapy (IPT) holds that any of four
interpersonal problem areas may lead to depression and must be addressed: interpersonal
loss, interpersonal role dispute, interpersonal role transition, and interpersonal deficits
(Stuart, 2009; [German & Weissman, 1992). Over the course of around 16 sessions, IPT
therapists address these areas.
First, depressed persons may, as psychodynamic theorists suggest, be experiencing a
grief reaction over an important interpersonal loss, the loss of a loved one. In such cases,
IPT therapists encourage clients to explore 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 seek 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 rela-
tionship 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 experiencing 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. IPT thera-
pists may help such individuals recognize 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:
Client: (After a long pause with eyes downcast, a sad facial expression, and slumped
posture) People always make fun of me. I guess I’m just the type of guy who
really was meant to be a loner, damn it. (Deep sigh)
Therapist: Could you do that again for me?
Client What?
Therapist: The sigh, only a bit deeper.
Client: Why? (Pause) Okay, but 1 don’t see what . . . okay. (Client sighs again and
smiles.)

Mood Disorders 215
Therapist: Weil, that time you smiled, but mostly when you sigh and look so
sad I get the feeling that I better leave you alone in your misery,
that I should walk on eggshells and not get too chummy or l might
hurt you even more.
Client (A bit of anger in his voice) Well, excuse me! 1 was only trying to
tell you how I felt.
Therapist: I know you felt miserable, but I also got the message that you
wonted to keep me at a distance, that I had no way to reach you.
Client: (Slowly) I feel like a loner, I feel that even you don’t care about
rne—making fun of me.
Therapist / wonder if other folks need to pass this test, too?
(Beier & Young, 1984, 9. 270)
Studies suggest that IPT and related interpersonal treatments for
depression have a success rate similar to that of cognitive and cognitive-
behavioral therapies (Markowitz, 2006; Weissman & Markowitz, 2002).
That is, symptoms largely 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 under-
going changes in their careers or social roles (Weissman & Markowitz,
2002).
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 (Beach et al., 2008). In fact,
as many as half of all depressed clients may be in a dysfunctional rela-
tionship. 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.
Therapists who offer behavioral marital therapy help spouses change
harmful marital behavior by teaching them specific communication
and problem-solving skills (see Chapter 2). When a depressed person’s
marriage is filled with conflict, this approach and similar couple thera-
pies may be as effective as individual cognitive therapy, interpersonal
psychotherapy, or drug therapy in helping to reduce depression (Barbato & D’Avanzo,
2008; Snyder & Castellani, 2006).
The Muitlicuitured Perspective Two issues have captured the interest of multi-
cultural depression theorists: (1) links between gender and depression and (2) ties between
cultural and ethnic background and depression.
GENDER AND DEPRESSION As you have read, a strong link exists between gender and
depression. Women in most countries are at least twice as likely as men to receive a
diagnosis of unipolar depression (Lara, 2008; Whiffen & Demidenko, 2006). A variety
of explanations for this gender difference have been offered (Russo & Tartaro, 2008;
Nolen-Hoeksema, 2002, 1995, 1990).
The art fact theory holds that women and men are equally prone to depression but
that clinicians often fail to detect depression in men (Brommelhoff et al., 2004). 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 (McSweeney, 2004).
The hormone explanation holds that hormone changes trigger depression in many
women (Parker & Brotchie, 2004). A woman’s biological life from her early teens to
middle age is marked by frequent changes in hormone levels. Gender differences in
. _
lifliiirii .i• rii,t -fl-iTi. 44`,,,!)!.10(3 -.F.iii
fi-147-’41:00,_’Wf-t) 0ri°1-1;itqiit tk.’
Mood Disorders 215
Therapist: Weil, that time you smiled, but mostly when you sigh and look so
sad I get the feeling that I better leave you alone in your misery,
that I should walk on eggshells and not get too chummy or l might
hurt you even more.
Client (A bit of anger in his voice) Well, excuse me! 1 was only trying to
tell you how I felt.
Therapist: I know you felt miserable, but I also got the message that you
wonted to keep me at a distance, that I had no way to reach you.
Client: (Slowly) I feel like a loner, I feel that even you don’t care about
rne—making fun of me.
Therapist / wonder if other folks need to pass this test, too?
(Beier & Young, 1984, 9. 270)
Studies suggest that IPT and related interpersonal treatments for
depression have a success rate similar to that of cognitive and cognitive-
behavioral therapies (Markowitz, 2006; Weissman & Markowitz, 2002).
That is, symptoms largely 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 under-
going changes in their careers or social roles (Weissman & Markowitz,
2002).
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 (Beach et al., 2008). In fact,
as many as half of all depressed clients may be in a dysfunctional rela-
tionship. 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.
Therapists who offer behavioral marital therapy help spouses change
harmful marital behavior by teaching them specific communication
and problem-solving skills (see Chapter 2). When a depressed person’s
marriage is filled with conflict, this approach and similar couple thera-
pies may be as effective as individual cognitive therapy, interpersonal
psychotherapy, or drug therapy in helping to reduce depression (Barbato & D’Avanzo,
2008; Snyder & Castellani, 2006).
The Muitlicuitured Perspective Two issues have captured the interest of multi-
cultural depression theorists: (1) links between gender and depression and (2) ties between
cultural and ethnic background and depression.
GENDER AND DEPRESSION As you have read, a strong link exists between gender and
depression. Women in most countries are at least twice as likely as men to receive a
diagnosis of unipolar depression (Lara, 2008; Whiffen & Demidenko, 2006). A variety
of explanations for this gender difference have been offered (Russo & Tartaro, 2008;
Nolen-Hoeksema, 2002, 1995, 1990).
The art fact theory holds that women and men are equally prone to depression but
that clinicians often fail to detect depression in men (Brommelhoff et al., 2004). 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 (McSweeney, 2004).
The hormone explanation holds that hormone changes trigger depression in many
women (Parker & Brotchie, 2004). A woman’s biological life from her early teens to
middle age is marked by frequent changes in hormone levels. Gender differences in
. _
lifliiirii .i• rii,t -fl-iTi. 44`,,,!)!.10(3 -.F.iii
fi-147-’41:00,_’Wf-t) 0ri°1-1;itqiit tk.’

216 :IICHAPTER 7
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 (Kessler et al., 2006; Whiffen & Demidenko, 2006). Important social
and life events that occur at puberty, pregnancy, and menopause could likewise
have an effect.
The life stress theory suggests that women in our society experience more
stress than men (Kessler et al., 2006; Keyes & Goodman, 2006). On average they
face more poverty, more menial jobs, less adequate housing, and more discrimi-
nation 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 ap-
proach adolescence, peer pressure may produce greater and greater dissatisfaction
with their weight and body, increasing the likelihood of depression. Consistent
with this theory, gender differences in depression do indeed first appear during
adolescence (Avenevoli et al., 2008), and persons with eating disorders often
experience high levels of depression (Stewart & Williamson, 2008). However, it
is not clear that eating and weight concerns actually cause depression; they may
instead be the result of depression.
The lack -of-control theory picks up on the learned helplessness research and
argues 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 (Whiffen & Demidenko,
2006; Nolen-Hoeksema, 2002).
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 depres-
sion (“Why am I so down? . . . I 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
moods darken, perhaps making them more vulnerable to the onset of clinical depression
(Nolen-Hoeksema & Corte, 2004; 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 inter-
esting and just enough evidence to the contrary to raise questions about its usefulness
(Russo & Tartaro, 2008). 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 Research suggests that depression is a worldwide
phenomenon, and certain symptoms of this disorder seem to be constant across all coun-
tries.A landmark study of four countries—Canada, Switzerland, Iran, and Japan—found
that the great majority of depressed people in those very different countries reported
symptoms of sadness, joylessness, anxiety, tension, lack of energy, loss of interest, loss
of ability to concentrate, ideas of insufficiency, and thoughts of suicide (Matsumoto &
Juang, 2008;WHO, 1983). Beyond these core symptoms, however, the picture of depres-
sion varies from country to country (Matsumoto & Juang, 2008; Kleinman, 2004; Tsai
& Chentsova-Dutton, 2002). Depressed people in non-Western countries—China and
Nigeria, for example—are more likely to be troubled by physical symptoms such as fa-
tigue, 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.
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
differences in the overall rates of depression between such minority groups. Investigators
.stern dela ton
ressed people – in non-Western
ntries tend to have fewer cognitiv
ptbrns such as self-lolcirne and ,1
,sical sye-iptoms, such-as Fatig
e es a = I t a
216 :IICHAPTER 7
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 (Kessler et al., 2006; Whiffen & Demidenko, 2006). Important social
and life events that occur at puberty, pregnancy, and menopause could likewise
have an effect.
The life stress theory suggests that women in our society experience more
stress than men (Kessler et al., 2006; Keyes & Goodman, 2006). On average they
face more poverty, more menial jobs, less adequate housing, and more discrimi-
nation 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 ap-
proach adolescence, peer pressure may produce greater and greater dissatisfaction
with their weight and body, increasing the likelihood of depression. Consistent
with this theory, gender differences in depression do indeed first appear during
adolescence (Avenevoli et al., 2008), and persons with eating disorders often
experience high levels of depression (Stewart & Williamson, 2008). However, it
is not clear that eating and weight concerns actually cause depression; they may
instead be the result of depression.
The lack -of-control theory picks up on the learned helplessness research and
argues 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 (Whiffen & Demidenko,
2006; Nolen-Hoeksema, 2002).
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 depres-
sion (“Why am I so down? . . . I 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
moods darken, perhaps making them more vulnerable to the onset of clinical depression
(Nolen-Hoeksema & Corte, 2004; 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 inter-
esting and just enough evidence to the contrary to raise questions about its usefulness
(Russo & Tartaro, 2008). 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 Research suggests that depression is a worldwide
phenomenon, and certain symptoms of this disorder seem to be constant across all coun-
tries.A landmark study of four countries—Canada, Switzerland, Iran, and Japan—found
that the great majority of depressed people in those very different countries reported
symptoms of sadness, joylessness, anxiety, tension, lack of energy, loss of interest, loss
of ability to concentrate, ideas of insufficiency, and thoughts of suicide (Matsumoto &
Juang, 2008;WHO, 1983). Beyond these core symptoms, however, the picture of depres-
sion varies from country to country (Matsumoto & Juang, 2008; Kleinman, 2004; Tsai
& Chentsova-Dutton, 2002). Depressed people in non-Western countries—China and
Nigeria, for example—are more likely to be troubled by physical symptoms such as fa-
tigue, 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.
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
differences in the overall rates of depression between such minority groups. Investigators
.stern dela ton
ressed people – in non-Western
ntries tend to have fewer cognitiv
ptbrns such as self-lolcirne and ,1
,sical sye-iptoms, such-as Fatig
e es a = I t a

Unica! Bios
‘.1)
S
•
s nu .s cu PArtVi3 IA@ ° • •
Mood Disorders :1/ 21 7
do, however, sometimes find striking differences when they look at specific ethnic popu-
lations living under special circumstances (Matsumoto & Juang, 2008; Ayalon &Young,
2003). A study of one Native American conununity in the United States, for example,
showed that the lifetime risk of developing depression was 37 percent among women,
19 percent among men, and 28 percent overall, much higher than the risk in the general
United States population (Kinzie et al., 1992). High prevalence rates of this kind may
be linked to the terrible social and economic pressures faced by the people who live on
Native American reservations. Similarly, in a survey of Hispanic and African Americans
residing in public housing, almost half of the respondents reported that they were suf-
fering from depression (Bazargan et al., 2005). Within these minority populations, the
likelihood o f being depressed rose along with the individual’s degree of poverty, family
size, and number of health problems.
Multicuiturai Treatments In Chapter 2, you read that culture-sensitive therapies seek
to address the unique issues faced by members of cultural minority groups (Carten,
2006). Such approaches typically include special cultural training of the therapists;
heightened awareness by therapists of their clients’ cultural values and the culture-related
stressors, prejudices, and stereotypes faced by the clients; and efforts by therapists to help
clients recognize the impact of their own culture and the dominant culture on their self-
views and behaviors (Prochaska & Norcross, 2007).
In the treatment of unipolar depression, culture-sensitive approaches increasingly
are being co mbined with traditional forms of psychotherapy to help improve the likeli-
hood of minority clients overcoming their disorders. 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 is-
sues (Stacciarini et al., 2007; Satterfield, 2002). A range of studies indicate that Hispanic
American, African American, Native American, 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 (Dwight Johnson&
Lagomasino, 2007; Ward, 2007).
Unipolcw Depression
People with unipolar depression, the most common pattern of mood disorder, suf-
fer from depression only. The symptoms span five areas of functioning: emotional,
motivational, behavioral, cognitive, and physical. Women are at least twice as likely
as men to experience severe unipolar depression.
According to the biological view, low activity of two neurotransmitters, norepi-
nephrine and serotonin, helps cause depression. Hormonal factors may also be at
work. So too may deficiencies of key proteins and other chemicals within certain
neurons. Brain-imaging research has also tied depression to abnormalities in a cir-
cuit of brain areas, including the prefrontal cortex, hippocampus, amygdala, and
Brodmann Area 25. All such biological problems may be linked to genetic factors.
Most biological treatments consist of antidepressant drugs, but electroconvulsant
therapy is still used to treat some severe cases of depression, and several brain
stimulation techniques recently have been developed to treat severely depressed
patients who are unresponsive to other forms of treatment.
According to the psychodynamic view, certain people who experience real
or imagined losses may regress to an earlier stage of development, fuse with the
person they have lost, and eventually become depressed. Psychodynamic therapists
try to help persons with unipolar depression recognize and work through their losses
and excessive dependence on others.
The behavioral view says that when people experience a large reduction in
their positive rewards in life, they are more and more likely to become depressed.
Unica! Bios
‘.1)
S
•
s nu .s cu PArtVi3 IA@ ° • •
Mood Disorders :1/ 21 7
do, however, sometimes find striking differences when they look at specific ethnic popu-
lations living under special circumstances (Matsumoto & Juang, 2008; Ayalon &Young,
2003). A study of one Native American conununity in the United States, for example,
showed that the lifetime risk of developing depression was 37 percent among women,
19 percent among men, and 28 percent overall, much higher than the risk in the general
United States population (Kinzie et al., 1992). High prevalence rates of this kind may
be linked to the terrible social and economic pressures faced by the people who live on
Native American reservations. Similarly, in a survey of Hispanic and African Americans
residing in public housing, almost half of the respondents reported that they were suf-
fering from depression (Bazargan et al., 2005). Within these minority populations, the
likelihood o f being depressed rose along with the individual’s degree of poverty, family
size, and number of health problems.
Multicuiturai Treatments In Chapter 2, you read that culture-sensitive therapies seek
to address the unique issues faced by members of cultural minority groups (Carten,
2006). Such approaches typically include special cultural training of the therapists;
heightened awareness by therapists of their clients’ cultural values and the culture-related
stressors, prejudices, and stereotypes faced by the clients; and efforts by therapists to help
clients recognize the impact of their own culture and the dominant culture on their self-
views and behaviors (Prochaska & Norcross, 2007).
In the treatment of unipolar depression, culture-sensitive approaches increasingly
are being co mbined with traditional forms of psychotherapy to help improve the likeli-
hood of minority clients overcoming their disorders. 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 is-
sues (Stacciarini et al., 2007; Satterfield, 2002). A range of studies indicate that Hispanic
American, African American, Native American, 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 (Dwight Johnson&
Lagomasino, 2007; Ward, 2007).
Unipolcw Depression
People with unipolar depression, the most common pattern of mood disorder, suf-
fer from depression only. The symptoms span five areas of functioning: emotional,
motivational, behavioral, cognitive, and physical. Women are at least twice as likely
as men to experience severe unipolar depression.
According to the biological view, low activity of two neurotransmitters, norepi-
nephrine and serotonin, helps cause depression. Hormonal factors may also be at
work. So too may deficiencies of key proteins and other chemicals within certain
neurons. Brain-imaging research has also tied depression to abnormalities in a cir-
cuit of brain areas, including the prefrontal cortex, hippocampus, amygdala, and
Brodmann Area 25. All such biological problems may be linked to genetic factors.
Most biological treatments consist of antidepressant drugs, but electroconvulsant
therapy is still used to treat some severe cases of depression, and several brain
stimulation techniques recently have been developed to treat severely depressed
patients who are unresponsive to other forms of treatment.
According to the psychodynamic view, certain people who experience real
or imagined losses may regress to an earlier stage of development, fuse with the
person they have lost, and eventually become depressed. Psychodynamic therapists
try to help persons with unipolar depression recognize and work through their losses
and excessive dependence on others.
The behavioral view says that when people experience a large reduction in
their positive rewards in life, they are more and more likely to become depressed.

T.1111;,’:17
218 ://CHAPTER 7
Paternai Postpartum Depression
Behavioral therapists try to reintroduce clients to activities that they once found plea-
surable, reward nondepressive behaviors, and teach effective social skills.
According to Seligman’s learned helplessness theory, people become depressed
when they believe that they have lost control over the reinforcements in their lives
and when they attribute this loss to causes that are internal, global, and stable.
According to Beck’s theory of negative thinking, maladaptive attitudes, the cogni-
tive triad, errors in thinking, and automatic thoughts help produce unipolar depres-
sion. Beck’s cognitive therapy for depression helps clients increase their activities,
challenge their automatic thoughts, identify negative thinking, and change their
maladaptive attitudes.
Sociocultural theories propose that unipolar depression is influenced by social
and cultural factors. Family-social theorists point out that a low level of social sup-
port is often linked to unipolar depression. Correspondingly, interpersonal psycho-
therapy and couple therapy are often helpful in cases of depression. Multicultural
theories have noted that the character and prevalence of depression often varies
by gender and sometimes by culture, an issue that culture-sensitive therapies for
depression seek to address.
*Bipolar Disorders
People with a bipolar disorder experience both the lows of depression and the highs of
mania. Many describe their life as an emotional roller coaster, as they shift back and forth
between extreme moods.A number of sufferers eventually become suicidal. Their roller-
coaster ride and its impact on relatives and friends are seen in the following case study:
In his early school years he had been a remarkable student and had shown a gift for
watercolor and oils. Later he had studied art in Paris and married an English girl he had
met there. Eventually they had settled in London.
Ten years later, when he was thirty-four years old, he had persuaded his wife and only
son to accompany him to Honolulu, where, he assured them, he would be considered
famous. He felt he would be able to sell his paintings at many times the prices he could
get in London. According to his wife, he had been in an accelerated state, but at that time
the family had left, unsuspecting, believing with the patient in their imminent good fortune.
When they arrived they found almost no one in the art world that he was supposed to
know. There were no connections for sales and deals in Hawaii that he had anticipated.
Settling down, the patient began to behave more peculiarly than ever. After enduring
several months of the patient’s exhilaration, overactivity, weight loss, constant talking,
and unbelievably little sleep, the young wife and child began to fear for his sanity. None
of his plans materialized. After five months in the Pacific, with finances growing thin, the
patient’s overactivity subsided and he fell into a depression.
During that period he refused to move, paint, or leave the house. He lost twenty
pounds, became utterly dependent on his wife, and insisted on seeing none of the friends
he had accumulated in his manic state. His despondency became so severe that several
doctors came to the house and advised psychiatric hospitalization. He quickly agreed and
received twelve electroshock treatments, which relieved his depressed state. Soon after-
ward he began to paint again and to sell his work modestly. Recognition began to come
from galleries and critics in the Far East. Several reviews acclaimed his work as exception-
ally brilliant.
This was the beginning of the lifelong career of his moodswing. While still in Honolulu,
he once again became severely depressed. . Four years later he returned to London in
T.1111;,’:17
218 ://CHAPTER 7
Paternai Postpartum Depression
Behavioral therapists try to reintroduce clients to activities that they once found plea-
surable, reward nondepressive behaviors, and teach effective social skills.
According to Seligman’s learned helplessness theory, people become depressed
when they believe that they have lost control over the reinforcements in their lives
and when they attribute this loss to causes that are internal, global, and stable.
According to Beck’s theory of negative thinking, maladaptive attitudes, the cogni-
tive triad, errors in thinking, and automatic thoughts help produce unipolar depres-
sion. Beck’s cognitive therapy for depression helps clients increase their activities,
challenge their automatic thoughts, identify negative thinking, and change their
maladaptive attitudes.
Sociocultural theories propose that unipolar depression is influenced by social
and cultural factors. Family-social theorists point out that a low level of social sup-
port is often linked to unipolar depression. Correspondingly, interpersonal psycho-
therapy and couple therapy are often helpful in cases of depression. Multicultural
theories have noted that the character and prevalence of depression often varies
by gender and sometimes by culture, an issue that culture-sensitive therapies for
depression seek to address.
*Bipolar Disorders
People with a bipolar disorder experience both the lows of depression and the highs of
mania. Many describe their life as an emotional roller coaster, as they shift back and forth
between extreme moods.A number of sufferers eventually become suicidal. Their roller-
coaster ride and its impact on relatives and friends are seen in the following case study:
In his early school years he had been a remarkable student and had shown a gift for
watercolor and oils. Later he had studied art in Paris and married an English girl he had
met there. Eventually they had settled in London.
Ten years later, when he was thirty-four years old, he had persuaded his wife and only
son to accompany him to Honolulu, where, he assured them, he would be considered
famous. He felt he would be able to sell his paintings at many times the prices he could
get in London. According to his wife, he had been in an accelerated state, but at that time
the family had left, unsuspecting, believing with the patient in their imminent good fortune.
When they arrived they found almost no one in the art world that he was supposed to
know. There were no connections for sales and deals in Hawaii that he had anticipated.
Settling down, the patient began to behave more peculiarly than ever. After enduring
several months of the patient’s exhilaration, overactivity, weight loss, constant talking,
and unbelievably little sleep, the young wife and child began to fear for his sanity. None
of his plans materialized. After five months in the Pacific, with finances growing thin, the
patient’s overactivity subsided and he fell into a depression.
During that period he refused to move, paint, or leave the house. He lost twenty
pounds, became utterly dependent on his wife, and insisted on seeing none of the friends
he had accumulated in his manic state. His despondency became so severe that several
doctors came to the house and advised psychiatric hospitalization. He quickly agreed and
received twelve electroshock treatments, which relieved his depressed state. Soon after-
ward he began to paint again and to sell his work modestly. Recognition began to come
from galleries and critics in the Far East. Several reviews acclaimed his work as exception-
ally brilliant.
This was the beginning of the lifelong career of his moodswing. While still in Honolulu,
he once again became severely depressed. . Four years later he returned to London in

Cl
, _ .1,1
r
11rj!-4(4.1;
Mood Disorders :11 21 9
a high. . . When this manic period subsided and he surveyed the wreckage of his life,
an eight-month interval of normal mood followed, after which he again switched into a
profound depression.
(Fieve, 1975, pp. 64-65)
•
What Are the Symptoms of Mania?
Unlike people sunk in the gloom of depression, those in a state of mania typically ex-
perience dramatic and inappropriate rises in mood. The symptoms of mania span the
same areas of functioning—emotional, motivational, behavioral, cognitive, and physical—as
those of depression, but mania affects those areas in an opposite way.
A person in the throes of mania has active, powerful emotions in search of an outlet.
The mood of euphoric joy and well-being is out of all proportion to the actual happen-
ings in the person’s life. Not every person with mania is a picture of happiness, however.
Some instead become very irritable and angry, especially when others get in the way
of their exaggerated ambitions.
In the motivational realm, people with mania seem to want constant excitement,
involvement, and companionship. They enthusiastically seek out new friends and old,
new interests and old, and have little awareness that their social style is overwhelming,
domineering, and excessive.
The behavior of people with mania is usually very active. They move quickly, as
though there were not enough time to do everything they want to do. They may talk
rapidly and loudly, their conversations filled with jokes and efforts to be clever or, con-
versely, with complaints and verbal outbursts. Flamboyance is not uncommon: dressing
in flashy clothes, giving large sums of money to strangers, or even getting involved in
dangerous activities.
In the cognitive realm, people with mania usually show poor judgment and plan-
ning, as if they feel too good or move too fast to consider possible pitfalls. Filled with
optimism, they rarely listen when others try to slow them down.They may also hold an
inflated opinion of themselves, and sometimes their self-esteem approaches grandiosity.
During severe episodes of mania, some have trouble remaining coherent or in touch
with reality.
Finally, in the physical realm, people with mania feel remarkably energetic. They
typically get little sleep yet feel and act wide awake. Even if they miss a night or two of
sleep, their energy level may remain high.
Diagnosing Bipolar Disorders
People are considered to be in a full manic episode when for at least one week they display
an abnormally high or irritable mood, along with at least three other symptoms of mania
(see Table 7-4 on the next page).The episode may even include psychotic features such
as delusions or hallucinations.When the symptoms of mania are less severe (causing little
impairment), the person is said to be experiencing a lzypomanic episode (APA, 2000).
DSM-IV-TR distinguishes two kinds of bipolar disorders—bipolar I and bipolar
II. People with bipolar I disorder have full manic and major depressive episodes.
Most of them experience an alternation of the episodes; for example, weeks of mania
followed by a period of wellness, followed, in turn, by an episode of depression. Some
people, however, have mixed episodes, in which they swing from manic to depressive
symptoms and back again on the same day. In bipolar II disorder, hypomanic—that
is, mildly manic—episodes alternate with major depressive episodes over the course of
time. Without treatment, the mood episodes tend to recur for people with either type
of bipolar disorder ( Julien, 2008). In most cases, the individual’s depressive episodes
outnumber his or her manic episodes ( Julien, 2008).
Surveys from around the world indicate that between l and 2.6 percent of all adults
suffer from a bipolar disorder at any given time (Merikangas et al., 2007; Kessler et al.,
°bipolar I disordereA type of bipolar
disorder marked by full manic and major
depressive episodes.
°bipolar II disordereA type of bipolar
disorder marked by mildly manic (hypo-
manic) episodes and major depressive
episodes.
Cl
, _ .1,1
r
11rj!-4(4.1;
Mood Disorders :11 21 9
a high. . . When this manic period subsided and he surveyed the wreckage of his life,
an eight-month interval of normal mood followed, after which he again switched into a
profound depression.
(Fieve, 1975, pp. 64-65)
•
What Are the Symptoms of Mania?
Unlike people sunk in the gloom of depression, those in a state of mania typically ex-
perience dramatic and inappropriate rises in mood. The symptoms of mania span the
same areas of functioning—emotional, motivational, behavioral, cognitive, and physical—as
those of depression, but mania affects those areas in an opposite way.
A person in the throes of mania has active, powerful emotions in search of an outlet.
The mood of euphoric joy and well-being is out of all proportion to the actual happen-
ings in the person’s life. Not every person with mania is a picture of happiness, however.
Some instead become very irritable and angry, especially when others get in the way
of their exaggerated ambitions.
In the motivational realm, people with mania seem to want constant excitement,
involvement, and companionship. They enthusiastically seek out new friends and old,
new interests and old, and have little awareness that their social style is overwhelming,
domineering, and excessive.
The behavior of people with mania is usually very active. They move quickly, as
though there were not enough time to do everything they want to do. They may talk
rapidly and loudly, their conversations filled with jokes and efforts to be clever or, con-
versely, with complaints and verbal outbursts. Flamboyance is not uncommon: dressing
in flashy clothes, giving large sums of money to strangers, or even getting involved in
dangerous activities.
In the cognitive realm, people with mania usually show poor judgment and plan-
ning, as if they feel too good or move too fast to consider possible pitfalls. Filled with
optimism, they rarely listen when others try to slow them down.They may also hold an
inflated opinion of themselves, and sometimes their self-esteem approaches grandiosity.
During severe episodes of mania, some have trouble remaining coherent or in touch
with reality.
Finally, in the physical realm, people with mania feel remarkably energetic. They
typically get little sleep yet feel and act wide awake. Even if they miss a night or two of
sleep, their energy level may remain high.
Diagnosing Bipolar Disorders
People are considered to be in a full manic episode when for at least one week they display
an abnormally high or irritable mood, along with at least three other symptoms of mania
(see Table 7-4 on the next page).The episode may even include psychotic features such
as delusions or hallucinations.When the symptoms of mania are less severe (causing little
impairment), the person is said to be experiencing a lzypomanic episode (APA, 2000).
DSM-IV-TR distinguishes two kinds of bipolar disorders—bipolar I and bipolar
II. People with bipolar I disorder have full manic and major depressive episodes.
Most of them experience an alternation of the episodes; for example, weeks of mania
followed by a period of wellness, followed, in turn, by an episode of depression. Some
people, however, have mixed episodes, in which they swing from manic to depressive
symptoms and back again on the same day. In bipolar II disorder, hypomanic—that
is, mildly manic—episodes alternate with major depressive episodes over the course of
time. Without treatment, the mood episodes tend to recur for people with either type
of bipolar disorder ( Julien, 2008). In most cases, the individual’s depressive episodes
outnumber his or her manic episodes ( Julien, 2008).
Surveys from around the world indicate that between l and 2.6 percent of all adults
suffer from a bipolar disorder at any given time (Merikangas et al., 2007; Kessler et al.,
°bipolar I disordereA type of bipolar
disorder marked by full manic and major
depressive episodes.
°bipolar II disordereA type of bipolar
disorder marked by mildly manic (hypo-
manic) episodes and major depressive
episodes.

220 .1/CHAPTER 7
table:
DSM Checklist
0 1 q11.•0;..::
I -pail i 1 ..’.;161;..-0,’.1
.i.1.. ..E!, ..= I .. RIO- 1:I.! 9 i ”
. 1 i ■ ;1 1 1.;”
:. 1 F 19 ,.:1 !7 ,?! ….f:iliiO.
3 11.1i-lEi 1.:1
•
, 1(0 i. I -r…..,……..!….,
..0 . ., Iii I r I I q , , iii.:rafPolei
‘..: .._. ….-:._…..,……
11…..00.. . ri;).1!1. 0 (.0 I. °
,.:
la .. al i,l’?::IT:l; lii1::l I a al.. I.: 2
012,’,.
1 (1
.1(*

, 0) 1 I
or. 0 Cc: 01.
ci
41:91 -J1;.Ji;-:, /
■ ::1
p ,11•1 5i1.41 , 2
1 . 1
• r.h.’ 1? …p.15’1 14 1 .0:1 •.1 1 :0 11:• 0 fr.. 01
r 1 1 .:11’1 1
— 1.
▪
,11,:r1r`?.11. 1i111
(11
41! lla .ala. 1
B6:sed
•
Frenzied Mpsfeipibee:
C
2005).The disorders appear to be equally common in women and men and among all
socioeconomic classes and ethnic groups (Shastry, 2005). Onset usually occurs between
the ages of 15 and 44 years. In most untreated cases of bipolar disorder, the manic and
depressive episodes eventually subside, only to recur at a later time (APA, 2000).
When a person experiences numerous periods of hypomanic symptoms and mild
depressive symptoms, DSM-IV-TR assigns a diagnosis of cyclothymic disorder The symp-
toms of this milder form of bipolar disorder continue for two or more years, inter-
rupted occasionally by normal moods that may last for only days or weeks. At least 0.4
percent of the population develops cyclothymic disorder (APA, 2000). In some cases,
the milder symptoms eventually blossom into a bipolar I or II disorder.
What Causes Bipolar Disorders?
Throughout the first half of the twentieth century, the search for the cause of bipolar
disorders made little progress. More recently, biological research has produced some
promising clues. The biological insights have come from research into neurotransmitter
activity, ion activity, brain structirre, and genetic factors.
Neurotransmitiers Could overactivity of norepinephrine be related to mania? This
was the expectation of clinicians back in the 1960s after investigators first found a relation-
ship between low norepinephrine activity and unipolar depression (Schildkraut, 1965).
Several studies did indeed find the norepinephrine activity of persons with mania to be
higher than that of depressed or control research participants (Post et al., 1980, 1978).
Because serotonin activity often parallels norepinephrine activity in unipolar de-
pression, theorists at first expected that mania would also be related to high serotonin
activity, but no such relationship has been found. Instead, research suggests that mania,
like depression, may be linked to low serotonin activity (Shastry, 2005; Sobczak et al.,
220 .1/CHAPTER 7
table:
DSM Checklist
0 1 q11.•0;..::
I -pail i 1 ..’.;161;..-0,’.1
.i.1.. ..E!, ..= I .. RIO- 1:I.! 9 i ”
. 1 i ■ ;1 1 1.;”
:. 1 F 19 ,.:1 !7 ,?! ….f:iliiO.
3 11.1i-lEi 1.:1
•
, 1(0 i. I -r…..,……..!….,
..0 . ., Iii I r I I q , , iii.:rafPolei
‘..: .._. ….-:._…..,……
11…..00.. . ri;).1!1. 0 (.0 I. °
,.:
la .. al i,l’?::IT:l; lii1::l I a al.. I.: 2
012,’,.
1 (1
.1(*

Mood Disorders :1/ 221
2002). Perhaps low activity of serotonin opens the door to a mood disorder and permits
the activity of norepinephrine (or perhaps other neurotransmitters) to define the par-
ticular form the disorder will take. That is, low serotonin activity accompanied by low
norepinephrine activity may lead to depression; low serotonin activity accompanied by
high norepinephrine activity may lead to mania.
on Activity Electrically charged ions help transmit messages down each neuron’s
axon to its nerve endings. Positively charged sodium ions (Na+) sit on both sides of a
neuron’s cell membrane. When the neuron is at rest, more sodium ions sit outside the
membrane.When the neuron receives an incoming message at its receptor sites, however,
pores in the ‘cell membrane open, allowing the sodium ions to flow to the inside of the
membrane, thus increasing the positive charge inside the neuron. This starts a wave of
electrical activity that travels down the length of the neuron and results in its “firing.”
After the neuron “fires,”potassium ions (K+) flow from the inside of the neuron across the
cell membrane to the outside, helping to return the neuron to its original resting state.
If messages are to be relayed effectively down the axon, the ions must be able to
travel easily between the outside and the inside of the neural membrane. Sonic theorists
believe that irregularities in the transport of these ions may cause neurons to fire too
easily (resulting in mania) or to stubbornly resist firing (resulting in depression) (Li &
El-Mallakh, 2004; El-Mallakh & Huff, 2001). Not surprisingly, investigators have found
membrane defects in the neurons of people suffering from bipolar disorder and have
observed abnormal functioning in the proteins that help transport ions across a neuron’s
membrane (Sassi & Soares, 2002).
Brain Structure Brain imaging and postmortem studies have identified a number of
abnormal brain structures in people with bipolar disorders (Lambert & Linsley, 2005;
Shastry, 2005). For example, the basal ganglia and cerebellum of these individuals tend to
be smaller than those of other people. It is not clear what role these and other structural
abnormalities play in bipolar disorders.
Genetic Factors Many theorists believe that people inherit a biological predisposi-
tion to develop bipolar disorders. Family pedigree studies support this idea (Maier et al.,
2005). Identical twins of persons with a bipolar disorder have a 40 percent likelihood of
developing the same disorder, and fraternal twins, siblings, and other close relatives of
such persons have a 5 to 10 percent likelihood, compared to the 1 to 2.6 percent preva-
lence rate in the general population.
.[Ot kOtU
liu1-(:) glint,A![Fil 4. qz:Ii11,,S;i1 , ,;11f. ,..71
!:.if 7,3 f A .• • ASY, ‘IA_ I _
4.e11 C-j•ATA=:.ar.
° – 0•10,-8:5,t,;741 -K°2■/j,
; A
4 4”; -P,’4 1
Tii411-!rbt,7Th Q2.!:1E1 1,L=5-1;

“Those? Oh, just a few souvenirs from my bipolar-disorder days.”
Mood Disorders :1/ 221
2002). Perhaps low activity of serotonin opens the door to a mood disorder and permits
the activity of norepinephrine (or perhaps other neurotransmitters) to define the par-
ticular form the disorder will take. That is, low serotonin activity accompanied by low
norepinephrine activity may lead to depression; low serotonin activity accompanied by
high norepinephrine activity may lead to mania.
on Activity Electrically charged ions help transmit messages down each neuron’s
axon to its nerve endings. Positively charged sodium ions (Na+) sit on both sides of a
neuron’s cell membrane. When the neuron is at rest, more sodium ions sit outside the
membrane.When the neuron receives an incoming message at its receptor sites, however,
pores in the ‘cell membrane open, allowing the sodium ions to flow to the inside of the
membrane, thus increasing the positive charge inside the neuron. This starts a wave of
electrical activity that travels down the length of the neuron and results in its “firing.”
After the neuron “fires,”potassium ions (K+) flow from the inside of the neuron across the
cell membrane to the outside, helping to return the neuron to its original resting state.
If messages are to be relayed effectively down the axon, the ions must be able to
travel easily between the outside and the inside of the neural membrane. Sonic theorists
believe that irregularities in the transport of these ions may cause neurons to fire too
easily (resulting in mania) or to stubbornly resist firing (resulting in depression) (Li &
El-Mallakh, 2004; El-Mallakh & Huff, 2001). Not surprisingly, investigators have found
membrane defects in the neurons of people suffering from bipolar disorder and have
observed abnormal functioning in the proteins that help transport ions across a neuron’s
membrane (Sassi & Soares, 2002).
Brain Structure Brain imaging and postmortem studies have identified a number of
abnormal brain structures in people with bipolar disorders (Lambert & Linsley, 2005;
Shastry, 2005). For example, the basal ganglia and cerebellum of these individuals tend to
be smaller than those of other people. It is not clear what role these and other structural
abnormalities play in bipolar disorders.
Genetic Factors Many theorists believe that people inherit a biological predisposi-
tion to develop bipolar disorders. Family pedigree studies support this idea (Maier et al.,
2005). Identical twins of persons with a bipolar disorder have a 40 percent likelihood of
developing the same disorder, and fraternal twins, siblings, and other close relatives of
such persons have a 5 to 10 percent likelihood, compared to the 1 to 2.6 percent preva-
lence rate in the general population.
.[Ot kOtU
liu1-(:) glint,A![Fil 4. qz:Ii11,,S;i1 , ,;11f. ,..71
!:.if 7,3 f A .• • ASY, ‘IA_ I _
4.e11 C-j•ATA=:.ar.
° – 0•10,-8:5,t,;741 -K°2■/j,
; A
4 4”; -P,’4 1
Tii411-!rbt,7Th Q2.!:1E1 1,L=5-1;

“Those? Oh, just a few souvenirs from my bipolar-disorder days.”

222 //CHAPTER 7
V
N
to
/R
ich
ar
d
Da
vi
[;-
I ;:f • /
Z r.:=7-q7/ 11.! ‘L•711 • °
.1`iff:k*Ir iLikoiti)
– –
ofithiumeA metallic element that occurs
in nature as a mineral salt and is an
effective treatment for bipolar disorders.
Researchers have also conducted genetic linkage studies to identify possible patterns
in the inheritance of bipolar disorders. They select large families that have had high
rates of a disorder over several generations, observe the pattern of distribution of the
disorder among family members, and determine whether it closely follows a predict-
able pattern of inheritance. Still other researchers have used techniques from molecular
biology to examine genetic factors. These various undertakings have linked bipolar
disorders to genes on chromosomes 1, 4, 6, 10, 11, 12, 13, 15, 18, 21, and 22 (Schulze
& McMahon, 2009; Maier et al., 2005; Baron, 2002). Such wide-ranging findings
suggest that a number of genetic abnormalities probably combine to help bring about
bipolar disorders.
What Are the Treatments for Bipolar Disorders?
Until the latter part of the twentieth century, people with bipolar disorders were des-
tined to spend their lives on an emotional roller coaster. Psychotherapists reported
almost no success, and antidepressant drugs were of limited help (Prien et al., 1974). In
fact, the drugs sometimes triggered a manic episode (Post, 2005; Suppes et al., 2005).
Lithium and Other Mood Stabilizers This gloomy picture changed dramati-
cally in 1970 when the FDA approved the use of lithium, a silvery-white element found
in various simple mineral salts throughout the natural world, as a treatment for bipolar
disorder. Other kinds of mood stabilizing, or antibipolar, drugs have since been developed,
and several of them, including the antiseizure drugs carbamazepine (Tegretol) or valproate
(Depakote), are now used widely, either because they produce fewer undesired effects
than lithium or because they are even more effective than lithium. Some people respond
best to a combination of these various mood stabilizers, and still others do well with a
combination of mood stabilizers and atypical antipsychotic drugs, medications that you will
read about in Chapter 12 (Donner, 2005). Nevertheless, it was lithium that first brought
hope to those suffering from bipolar disorder.
All manner of research has attested to the effectiveness of lithium and other mood
stabilizers in treating manic episodes (Grof, 2005). More than 60 percent of patients with
mania improve on these medications. In addition, most such individuals experience fewer
new episodes as long as they continue taking the medications (Carney & Goodwin,
2005). One study found that the risk of relapse is 28 times greater if patients stop taking
a mood stabilizer (Suppes et al., 1991). Thus today’s clinicians usually continue patients
on some level of a mood stabilizing drug even after their manic episodes subside ( Julien,
2008; Swann, 2005).
The mood stabilizers also help those with bipolar disorder overcome their depressive
episodes, though to a lesser degree than they help with their manic episodes (El-Mallakh,
2006). Given the drugs’ less powerful impact on depressive episodes, many clinicians use
222 //CHAPTER 7
V
N
to
/R
ich
ar
d
Da
vi
[;-
I ;:f • /
Z r.:=7-q7/ 11.! ‘L•711 • °
.1`iff:k*Ir iLikoiti)
– –
ofithiumeA metallic element that occurs
in nature as a mineral salt and is an
effective treatment for bipolar disorders.
Researchers have also conducted genetic linkage studies to identify possible patterns
in the inheritance of bipolar disorders. They select large families that have had high
rates of a disorder over several generations, observe the pattern of distribution of the
disorder among family members, and determine whether it closely follows a predict-
able pattern of inheritance. Still other researchers have used techniques from molecular
biology to examine genetic factors. These various undertakings have linked bipolar
disorders to genes on chromosomes 1, 4, 6, 10, 11, 12, 13, 15, 18, 21, and 22 (Schulze
& McMahon, 2009; Maier et al., 2005; Baron, 2002). Such wide-ranging findings
suggest that a number of genetic abnormalities probably combine to help bring about
bipolar disorders.
What Are the Treatments for Bipolar Disorders?
Until the latter part of the twentieth century, people with bipolar disorders were des-
tined to spend their lives on an emotional roller coaster. Psychotherapists reported
almost no success, and antidepressant drugs were of limited help (Prien et al., 1974). In
fact, the drugs sometimes triggered a manic episode (Post, 2005; Suppes et al., 2005).
Lithium and Other Mood Stabilizers This gloomy picture changed dramati-
cally in 1970 when the FDA approved the use of lithium, a silvery-white element found
in various simple mineral salts throughout the natural world, as a treatment for bipolar
disorder. Other kinds of mood stabilizing, or antibipolar, drugs have since been developed,
and several of them, including the antiseizure drugs carbamazepine (Tegretol) or valproate
(Depakote), are now used widely, either because they produce fewer undesired effects
than lithium or because they are even more effective than lithium. Some people respond
best to a combination of these various mood stabilizers, and still others do well with a
combination of mood stabilizers and atypical antipsychotic drugs, medications that you will
read about in Chapter 12 (Donner, 2005). Nevertheless, it was lithium that first brought
hope to those suffering from bipolar disorder.
All manner of research has attested to the effectiveness of lithium and other mood
stabilizers in treating manic episodes (Grof, 2005). More than 60 percent of patients with
mania improve on these medications. In addition, most such individuals experience fewer
new episodes as long as they continue taking the medications (Carney & Goodwin,
2005). One study found that the risk of relapse is 28 times greater if patients stop taking
a mood stabilizer (Suppes et al., 1991). Thus today’s clinicians usually continue patients
on some level of a mood stabilizing drug even after their manic episodes subside ( Julien,
2008; Swann, 2005).
The mood stabilizers also help those with bipolar disorder overcome their depressive
episodes, though to a lesser degree than they help with their manic episodes (El-Mallakh,
2006). Given the drugs’ less powerful impact on depressive episodes, many clinicians use

Mood Disorders :1,1 223

Abnormality and the Arts •

bnorrnality and Creativity: A Delicate Balance
li
I –

;mania, anxiety, and even confusion
, p to a point, states of depression,
mania
can be useful. This may be particularly true
in the arts. The ancient Greeks believed
that various forms of “divine madness”
inspired creative acts, from poetry to
performance (Ludwig, 1995). Even today
many people expect “creative geniuses”
to be psychologically disturbed. A popu-
lar image of the artist includes a glass of
liquor, a cigarette, and a tormented expres-
sion. Classic examples include poet Sylvia
Plath, who experienced depression most of
her life and eventually committed suicide,
and dancer Vaslav Nilinsky, who suffered
from schizophrenia and spent many years
in institutions. In fact, a number of stud-
ies indicate that artists and writers are
somewhat more likely than others to suffer
from mental disorders, particularly mood
disorders (Sample, 2005; lauronen et al.,
2004; Jamison, 1995).
Why might creative people be prone
to psychological disorders? Some may be
predisposed to such disorders long before
they begin their artistic careers; the careers
may simply bring attention to their emo-
tional struggles (Ludwig, 1995). Indeed,
creative people often have a family history
of psychological problems. A number also
have experienced intense psychological
trauma during childhood. English novelist
and essayist Virginia Woolf, for example,
endured sexual abuse as a child.
Another reason for the creativity link
may be that creative endeavors create emo-
tional turmoil that is overwhelming. Truman
Capote said that writing his famous book
In Cold Blood “killed” him psychologically.
Before writing this account of the brutal
murders of a family, he considered himself
“a stable person…. Afterward something
happened to me” (Ludwig, 1995).
Yet a third explanation for the link
between creativity and psychological
disorders is that the creative professions
offer a welcome climate for those with
psychological disturbances. In the worlds
of poetry, painting, and acting, for exam-
ple, emotional expression and personal
turmoil are valued as sources of inspira-
tion and success (Sample, 2005; Ludwig,
1995).
Much remains to be learned about the
relationship between emotional turmoil
and creativity, but work in this area has
already clarified two important points.
First, psychological disturbance is hardly
a requirement for creativity. Many “cre-
ative geniuses” are, in fact, psychologi-
cally stable and happy throughout their
entire lives (Schlesinger & Ismail, 2004).
Second, mild psychological disturbances
relate to creative achievement much more
strongly than severe disturbances do. For
example, nineteenth-century composer
Robert Schumann produced 27 works
during one mildly hypomanic year but
next to nothing during years when he was
severely depressed and suicidal (Jamison,
1995).
Some artists worry that their creativity
would disappear if their psychological
suffering were to stop. In fact, however,
research suggests that successful treat-
ment for severe psychological disorders
more often than not improves the creative
process (Jamison, 1995; Ludwig, 1995).
Romantic notions aside, severe mental dys-
functioning has little redeeming value, in
the arts or anywhere else.
OOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOOO •,,,,•11.711.11101..fy■ .•••••••■ •••.116.•

Mood Disorders :1,1 223

Abnormality and the Arts •

bnorrnality and Creativity: A Delicate Balance
li
I –

F\VAVA ’71 K.
.. ace : and Noticonipliarice.
osecond messengersoChemicai
changes within a neuron just after the
neuron receives a neurotransmitter mes-
sage and just before it responds.
a combination of mood stabilizers and antidepressant drugs to treat bipolar depression
(Grunze, 2005; Swann, 2005). In addition, continued doses of mood stabilizers (or mood
stabilizers combined with antidepressant drugs) apparently reduce the risk of future de-
pressive episodes, just as they seem to prevent the return of manic episodes (Carney &
Goodwin, 2005).
Researchers do not fully understand how mood stabilizing drugs operate (Lambert
Kinsley, 2005).They suspect that the drugs change synaptic activity in neurons, but in
a way different from that of antidepressant drugs.The firing of a neuron actually consists
of several phases that ensue at lightning speed. When the neurotransmitter binds to a
receptor on the receiving neuron, a series of changes occur within the receiving neuron
to set the stage for firing. The substances in the neuron that carry out those changes
are often called second messengers because they relay the original message from
the receptor site to the firing mechanism of the neuron. (The neurotransmitter itself
is considered the first messenger) Whereas antidepressant drugs affect a neuron’s initial
reception of neurotransmitters, mood stabilizers appear to affect a neuron’s second mes-
sengers ( Julien, 2008).
It has been found that lithium and other mood stabilizing drugs also increase the
production of neuroprotective proteins—key proteins within certain neurons whose job is
to prevent cell death. In so doing, the drugs may increase the health and functioning of
those cells and, in turn, reduce bipolar symptoms (Gray et al., 2003; Ren et al., 2003).
Adiunctive Psychotherapy Psychotherapy alone is rarely helpful for persons with
bipolar disorder. At the same time, clinicians have learned that mood stabilizing drugs
alone are not always sufficient either.Thirty percent or more of patients with these dis-
orders may not respond to lithium or a related drug, may not receive the proper dose, or
may relapse while taking it. In addition, a number of patients stop taking mood stabilizers
on their own ( Julien, 2008; Lewis, 2005).
In view of these problems, many clinicians now use individual, group, or family
therapy as an adjunct to mood stabilizing drugs (Leahy, 2005;Vieta, 2005). Most often,
therapists use these formats to emphasize the importance of continuing to take medi-
cations and to help patients solve the special family, social, school, and occupational
problems caused by their disorder. Few controlled studies have tested the effectiveness
of such adjunctive therapy, but those that have been done, along with numerous clini-
cal reports, suggest that it helps reduce hospitalization, improves social functioning, and
increases patients’ ability to obtain and hold a job (Scott & Colom, 2005;Vieta, 2005).
Bipolcir Disorders
In bipolar disorders, episodes of mania alternate or intermix with episodes of de-
pression. These disorders are much less common than unipolar depression. They
may take the form of bipolar I, bipolar II, or cyclothymic disorder.
Mania may be related to high norepinephrine activity along with a low level of
serotonin activity. Some researchers have also linked bipolar disorders to improper
transport of ions back and forth between the outside and the inside of a neuron’s
membrane, others have focused on deficiencies of key proteins and other chemicals
within certain neurons, and still others have uncovered abnormalities in key brain
structures. Genetic studies suggest that people may inherit a predisposition to these
biological abnormalities.
Lithium and other mood stabilizing drugs have proved to be very effective in
reducing and preventing both the manic and the depressive episodes of bipolar dis-
orders. These drugs may reduce bipolar symptoms by affecting the activity of second
messengers or key proteins or other chemicals within certain neurons throughout the
brain. Patients tend to fare better when antibipolar drugs and/or other psychotropic
drugs are combined with adjunctive psychotherapy.
224 .//CHAPTER 7
F\VAVA ’71 K.
.. ace : and Noticonipliarice.
osecond messengersoChemicai
changes within a neuron just after the
neuron receives a neurotransmitter mes-
sage and just before it responds.
a combination of mood stabilizers and antidepressant drugs to treat bipolar depression
(Grunze, 2005; Swann, 2005). In addition, continued doses of mood stabilizers (or mood
stabilizers combined with antidepressant drugs) apparently reduce the risk of future de-
pressive episodes, just as they seem to prevent the return of manic episodes (Carney &
Goodwin, 2005).
Researchers do not fully understand how mood stabilizing drugs operate (Lambert
Kinsley, 2005).They suspect that the drugs change synaptic activity in neurons, but in
a way different from that of antidepressant drugs.The firing of a neuron actually consists
of several phases that ensue at lightning speed. When the neurotransmitter binds to a
receptor on the receiving neuron, a series of changes occur within the receiving neuron
to set the stage for firing. The substances in the neuron that carry out those changes
are often called second messengers because they relay the original message from
the receptor site to the firing mechanism of the neuron. (The neurotransmitter itself
is considered the first messenger) Whereas antidepressant drugs affect a neuron’s initial
reception of neurotransmitters, mood stabilizers appear to affect a neuron’s second mes-
sengers ( Julien, 2008).
It has been found that lithium and other mood stabilizing drugs also increase the
production of neuroprotective proteins—key proteins within certain neurons whose job is
to prevent cell death. In so doing, the drugs may increase the health and functioning of
those cells and, in turn, reduce bipolar symptoms (Gray et al., 2003; Ren et al., 2003).
Adiunctive Psychotherapy Psychotherapy alone is rarely helpful for persons with
bipolar disorder. At the same time, clinicians have learned that mood stabilizing drugs
alone are not always sufficient either.Thirty percent or more of patients with these dis-
orders may not respond to lithium or a related drug, may not receive the proper dose, or
may relapse while taking it. In addition, a number of patients stop taking mood stabilizers
on their own ( Julien, 2008; Lewis, 2005).
In view of these problems, many clinicians now use individual, group, or family
therapy as an adjunct to mood stabilizing drugs (Leahy, 2005;Vieta, 2005). Most often,
therapists use these formats to emphasize the importance of continuing to take medi-
cations and to help patients solve the special family, social, school, and occupational
problems caused by their disorder. Few controlled studies have tested the effectiveness
of such adjunctive therapy, but those that have been done, along with numerous clini-
cal reports, suggest that it helps reduce hospitalization, improves social functioning, and
increases patients’ ability to obtain and hold a job (Scott & Colom, 2005;Vieta, 2005).
Bipolcir Disorders
In bipolar disorders, episodes of mania alternate or intermix with episodes of de-
pression. These disorders are much less common than unipolar depression. They
may take the form of bipolar I, bipolar II, or cyclothymic disorder.
Mania may be related to high norepinephrine activity along with a low level of
serotonin activity. Some researchers have also linked bipolar disorders to improper
transport of ions back and forth between the outside and the inside of a neuron’s
membrane, others have focused on deficiencies of key proteins and other chemicals
within certain neurons, and still others have uncovered abnormalities in key brain
structures. Genetic studies suggest that people may inherit a predisposition to these
biological abnormalities.
Lithium and other mood stabilizing drugs have proved to be very effective in
reducing and preventing both the manic and the depressive episodes of bipolar dis-
orders. These drugs may reduce bipolar symptoms by affecting the activity of second
messengers or key proteins or other chemicals within certain neurons throughout the
brain. Patients tend to fare better when antibipolar drugs and/or other psychotropic
drugs are combined with adjunctive psychotherapy.
224 .//CHAPTER 7

.1-Iti-iiiOlt Li.’,”..+)0i.F11:14.11:11.Ritl:fiLi::il.rfroil’tilli17-ii‘””
• ;72_ 6 • i • ..iiiii. ,] lk,lc- fil ‘i-.7.-; 1 `piF6tf.), ciwi4 F
-V, 1, 0,1 ‘ .f1.1D kV Eli:1y iiiit I pr4: tib; !161/’ ■ “&_,iM
1ft- .1 ‘ 4 ILID3IFF.51 .: ..
Yil:*11.–314′;” I t ’71-
Mood Disorders :// 225
PUTTING IT… together
Making Sense of Al] That Is Known
During the past 40 years, researchers and clinicians have made tremendous gains in
the understanding and treatment of mood disorders. Unipolar depression, for example,
has become one of the most treatable of all psychological disorders. Cognitive therapy,
interpersonal psychotherapy, and antidepressant drugs are all helpful in cases of any
severity; couple therapy is helpful in select cases; ECT is useful in severe cases; some
new biological treatments seem promising; and combinations of various approaches are
sometimes more helpful than one approach alone.
During the same period of time, several factors have been tied closely to unipolar
depression, including biological abnormalities, life stress, a reduction in positive rein-
forcements, negative ways of thinking, a perception of helplessness, and sociocultural
influences. Precisely how all of these factors relate to unipolar depression, however, is
unclear. Several relationships are possible:
1. One or the factors may be the key cause of unipolar depression. If so, cognitive
or biological factors seem to be leading candidates.
2. Different factors may be capable of initiating unipolar depression in different
persons. Some people may, for example, begin with low serotonin activity,
which predisposes them to react helplessly in stressful situations, interpret
events negatively, and enjoy fewer pleasures in life. Others may first suffer a
severe loss, which triggers helplessness reactions, low serotonin activity, and
reductions in positive rewards.
3. An interaction between two or more specific factors may be necessary to produce
unipolar depression (Klocek et al., 1997). Perhaps people will become de-
pressed only if they have low levels of serotonin activity, feel helpless, and
repeatedly blame themselves for negative events.
4. The various factors may play different roles in unipolar depression. Some may
cause the disorder, some may result from it, and some may keep it going.
As with unipolar depression, clinicians and researchers have learned much about
bipolar disorders during the past 40 years. But bipolar disorders appear to be best
explained by a focus largely on one kind of variable—biological factors. The evidence
suggests that biological abnormalities, perhaps inherited and perhaps triggered by life
stress, cause bipolar disorders. In addition, the key focus of treatment for these disorders
.1-Iti-iiiOlt Li.’,”..+)0i.F11:14.11:11.Ritl:fiLi::il.rfroil’tilli17-ii‘””
• ;72_ 6 • i • ..iiiii. ,] lk,lc- fil ‘i-.7.-; 1 `piF6tf.), ciwi4 F
-V, 1, 0,1 ‘ .f1.1D kV Eli:1y iiiit I pr4: tib; !161/’ ■ “&_,iM
1ft- .1 ‘ 4 ILID3IFF.51 .: ..
Yil:*11.–314’;” I t ’71-
Mood Disorders :// 225
PUTTING IT… together
Making Sense of Al] That Is Known
During the past 40 years, researchers and clinicians have made tremendous gains in
the understanding and treatment of mood disorders. Unipolar depression, for example,
has become one of the most treatable of all psychological disorders. Cognitive therapy,
interpersonal psychotherapy, and antidepressant drugs are all helpful in cases of any
severity; couple therapy is helpful in select cases; ECT is useful in severe cases; some
new biological treatments seem promising; and combinations of various approaches are
sometimes more helpful than one approach alone.
During the same period of time, several factors have been tied closely to unipolar
depression, including biological abnormalities, life stress, a reduction in positive rein-
forcements, negative ways of thinking, a perception of helplessness, and sociocultural
influences. Precisely how all of these factors relate to unipolar depression, however, is
unclear. Several relationships are possible:
1. One or the factors may be the key cause of unipolar depression. If so, cognitive
or biological factors seem to be leading candidates.
2. Different factors may be capable of initiating unipolar depression in different
persons. Some people may, for example, begin with low serotonin activity,
which predisposes them to react helplessly in stressful situations, interpret
events negatively, and enjoy fewer pleasures in life. Others may first suffer a
severe loss, which triggers helplessness reactions, low serotonin activity, and
reductions in positive rewards.
3. An interaction between two or more specific factors may be necessary to produce
unipolar depression (Klocek et al., 1997). Perhaps people will become de-
pressed only if they have low levels of serotonin activity, feel helpless, and
repeatedly blame themselves for negative events.
4. The various factors may play different roles in unipolar depression. Some may
cause the disorder, some may result from it, and some may keep it going.
As with unipolar depression, clinicians and researchers have learned much about
bipolar disorders during the past 40 years. But bipolar disorders appear to be best
explained by a focus largely on one kind of variable—biological factors. The evidence
suggests that biological abnormalities, perhaps inherited and perhaps triggered by life
stress, cause bipolar disorders. In addition, the key focus of treatment for these disorders

226 ://CHAPTER 7
is narrow and simple—lithium and/or other mood stabilizers, perhaps combined with
other psychotropic drugs. Adjunctive psychotherapy may also be of significant help in
cases of bipolar disorder.
There is no question that investigations into mood disorders have been fruitful, and
valuable insights should continue to unfold in the years ahead. On the other hand, the
sobering fact remains that one-third of people with a mood disorder do not improve
under treatment and must suffer depression or manic episodes until they run their
course. Now that clinical researchers have gathered so many important pieces of the
puzzle, they must put the pieces together into a still more meaningful picture that will
suggest even better ways to predict, prevent, and treat these disorders.
2,.•••••••,•-••••••••,•••
•̀ ‘,:z.•/-P.V./VaC.;#•. ,
•
\\\ THOUqHTS ///
0. 1. Almost every day we experience ups
and downs in mood. Flow can we
distinguish the everyday blues from
clinical depression? pp. 193- 198
2. In one study, students who listened to
a sad song became more depressed
than those who listened to a happy
song (Stratton & Zalanowski, 1999,
1994). Yet the sad-song students
reported “enjoying” their musical
experience more than the happy-song
students. What might be going on
here? pp. 193-198
3. Many comedians report that they
have grappled with depression.

— • -6 • •
A/4, 6. 6,
• \\\ KEY TEPAPS///
#77: depression, p. 193
mania, p. 193
unipolar depression, p. 193
0: bipolar disorder, p. 193 molar depressive disorder, p. 197
dysthmic disorder, p. 197
reactive depression, p. 198
405:7: endogenous depression, p. 198
norepinephrine, p. 199
serotonin, p. 199
melatonin, p. 199
,for. seasonal affective disorder, p. 199
prefrontal cortex, p. 200
hippocampus, p. 200
Is there something about perform-
ing that might improve their mood?
Is there something about being
depressed that might make them
more skilled at thinking or acting
funny? pp. 193-222, 223
4. Some people argue that antide-
pressant drugs serve to curb useful
behavior, destroy individuality, and
blunt people’s concerns about soci-
etal ills. Are such concerns justified?
pp. 201 -203
5. Several different kinds of theories
keep pointing to the social sphere
as a key factor in depression—for
amygdala, p. 200
Brodmann Area 25, p. 200
electroconvulsive therapy (ECT), p. 200
MAO inhibitors, p. 201
tyramine, p. 202
tricyclics, p. 202
selective serotonin reuptake inhibitors
(SSR1s), p. 203
vagus nerve stimulation, p. 204
transcranial magnetic stimulation,
p. 204
deep brain stimulation (DBS), p. 205
symbolic loss, p. 205
learned helplessness, p. 209
example, social loss, social ties,
social rewards, and social attitudes.
Why might problems in the social
arena be particularly tied to
depression? pp. 205-206,
208-210, 213-215
6. Friends and family members try,
with limited success, to convince
depressed people that their gloom-
and-doom view of things is wrong.
How does the successful cognitive
approach to unipolar depression
differ from such efforts at friendly
persuasion? pp. 212-213
• •
attribution, p. 210
cognitive triad, p. 211
automatic thoughts, p. 211
rumination, pp. 211, 216
cognitive therapy, p. 212
interpersonal psychotherapy (IPT),
p.214
couple therapy, p. 215
hypomanic episode, p. 219
bipolar 1 disorder, p. 219
biopolar 11 disorder, p. 219
cyclothymic disorder, p. 220
lithium, p. 222
second messengers, p. 224
226 ://CHAPTER 7
is narrow and simple—lithium and/or other mood stabilizers, perhaps combined with
other psychotropic drugs. Adjunctive psychotherapy may also be of significant help in
cases of bipolar disorder.
There is no question that investigations into mood disorders have been fruitful, and
valuable insights should continue to unfold in the years ahead. On the other hand, the
sobering fact remains that one-third of people with a mood disorder do not improve
under treatment and must suffer depression or manic episodes until they run their
course. Now that clinical researchers have gathered so many important pieces of the
puzzle, they must put the pieces together into a still more meaningful picture that will
suggest even better ways to predict, prevent, and treat these disorders.
2,.•••••••,•-••••••••,•••
•̀ ‘,:z.•/-P.V./VaC.;#•. ,
•
\\\ THOUqHTS ///
0. 1. Almost every day we experience ups
and downs in mood. Flow can we
distinguish the everyday blues from
clinical depression? pp. 193- 198
2. In one study, students who listened to
a sad song became more depressed
than those who listened to a happy
song (Stratton & Zalanowski, 1999,
1994). Yet the sad-song students
reported “enjoying” their musical
experience more than the happy-song
students. What might be going on
here? pp. 193-198
3. Many comedians report that they
have grappled with depression.

Mood Disorders :11. 227
\\\ rili I i3K r)U 12 &/
7
6
6
6
6
14
1. What are the key symptoms of
depression and mania? pp. 194-
198, 219-220
2. What is the difference between
unipolar depression and bipolar
disorder? p. 194
3. Describe the role of norepinephrine
and serotonin in unipolar
depression. p. 199
4. Describe Freud and Abraham’s
psychodynamic theory of
depression and the evidence that
supports it. pp. 205-206
5. How do behaviorists describe
the role of rewards in depression?
pp. 208-209
6. How might learned helplessness
be related to human depression?
pp. 209-210
7. What kinds of negative thinking
may lead to mood problems?
pp. 210-212
8. How do sociocultural theorists
account for unipolar depression?
pp. 213-214, 215-217
9. What roles do biological and
genetic factors seem to play in
bipolar disorders? pp. 220-222
10. Discuss the leading treatments for
unipolar depression and bipolar
disorders. How effective are these
various approaches? pp. 200-205,
206-208, 208-209, 212-213,
214-215, 217, 222-224
■

,J11.
’40
Search the Fundamentals ofAbnormal Psychology Video Tool Kit
www.worthpublishers.com/apvtk
A Chapter 7 Video Cases
Depression: A Pervasive Disorder
‘Wire Mothers” and Attachment: Harlow’s Monkeys
Seeking Happiness: To Each His Own
Cognitive Therapy in Action
ECT: Effective and Frightening
Light Therapy: Treating Seasonal Affective Disorder
A Video case discussions, study guides, and questions
Log on to the Corner Web Page
www.worthpublishers.com/comer
A Chapter 7 outline, learning objectives, research exercises, study tools,
and practice test questions
A Additional Chapter 7 case studies, Web links, and FAQs
Mood Disorders :11. 227
\\\ rili I i3K r)U 12 &/
7
6
6
6
6
14
1. What are the key symptoms of
depression and mania? pp. 194-
198, 219-220
2. What is the difference between
unipolar depression and bipolar
disorder? p. 194
3. Describe the role of norepinephrine
and serotonin in unipolar
depression. p. 199
4. Describe Freud and Abraham’s
psychodynamic theory of
depression and the evidence that
supports it. pp. 205-206
5. How do behaviorists describe
the role of rewards in depression?
pp. 208-209
6. How might learned helplessness
be related to human depression?
pp. 209-210
7. What kinds of negative thinking
may lead to mood problems?
pp. 210-212
8. How do sociocultural theorists
account for unipolar depression?
pp. 213-214, 215-217
9. What roles do biological and
genetic factors seem to play in
bipolar disorders? pp. 220-222
10. Discuss the leading treatments for
unipolar depression and bipolar
disorders. How effective are these
various approaches? pp. 200-205,
206-208, 208-209, 212-213,
214-215, 217, 222-224
■

SUICIDE CHAPTER

he war in Iraq never ended for Jonathan Michael Boucher. Not when he flew home from
Baghdad, not when he moved to Saratoga Springs for a fresh start and, especially, not
when nighttime arrived.
– Tortured by what he saw as on 18-year-old Army private during the 2003 invasion and
occupation, Boucher was diagnosed with post-traumatic stress disorder (PTSD) and honorably
discharged from the military less than two years later.
On May 15 three days before his 24th birthday, the young veteran committed suicide in his
apartment’s bathroom, stunning friends and family . . There was no note. . .
Johnny Boucher joined the Army right after graduating from East Lyme High School in Connecti-
cut in 2002 because he was emotionally moved by the Sept. 11, 2001, terrorist attacks. “He
felt it was his duty to do what he could for America,” his father, Steven Boucher, 50, said.
Shortly after enlisting, the 6-foot-2-inch soldier deployed with the “Wolf Pack”— 1 st Battalion,
41st Field Artillery—and fought his way north in Iraq. He landed with his unit at Baghdad In-
ternational Airport and was responsible for helping guard it. The battalion earned a Presidential
Unit Citation for “exceptional bravery and heroism in the liberation of Baghdad.”
But it was during those early months of the war that Johnny Boucher had the evils of combat
etched into his mind. The soldier was devastated by seeing a young Iraqi boy holding his dead
father, who had been shot in the head. Later, near the airport, the soldier saw four good friends
in his artillery battery killed in a vehicle accident minutes after one of them relieved him from
duty, his father said.
Boucher tried to rescue the soldiers. Their deaths and other things his son saw deeply impacted
his soul after he returned because he was sensitive about family and very patriotic, Steven
Boucher said. . . .
But when the sun set, memories of combat and lost friends rose to the top, causing the for-
mer artilleryman severe nightmares. Sometimes he would curl up in a ball and weep, causing
his parents to try to comfort him. . . . ‘At nighttime, he was just haunted,” Steven Boucher
said. . . “Haunted, 1 think, by war” Bitterness about the war had crept in, and the troubled
former soldier started drinking to calm himself .
Supported by a huge family he adored … Johnny Boucher recently got his own apartment on
Franklin Street and appeared to be getting back on track. He seemed to be calm and enjoying
life. But it was difficult to tell, and he was still fearful of sleep, his father said. They had plans
for a hike, a birthday party and attending his brother Jeffrey’s graduation. . . . Then, without
warning, Johnny Boucher was gone. He hanged himself next to a Bible, his Army uniform and
a garden statue of an angel, said his mother, who discovered him after he failed to show up
to work for two days. . . .
Yiisko, 2008
Salmon spawn and then die, after an exhausting upstream swim to their breeding
ground. Lemmings rush to the sea and drown. But only humans knowingly take
their own lives.The actions of salmon and lemmings are instinctual responses that
may even help their species survive in the long run. Only in the human act of
suicide do beings act for the specific purpose of putting an end to their lives.
TOPIC OVERVIEW
What Is Suicide?
How Is Suicide Studied?
Patterns and Statistics
What Triggers a Suicide?
Stressful Events and Situations
Mood and Thought Changes
Alcohol and Other Drug Use
Mental Disorders
Modeling: The Contagion of Suicide
What Are the Underlying Causes
of Suicide?
The Psychodynamic View
Durkheim’s Sociocultural View
The Biological View
Is Suicide Linked to Age?
Children
Adolescents
The Elderly
Treatment and Suicide
What Treatments Are Used after
Suicide Attempts?
What Is Suicide Prevention?
Do Suicide Prevention Programs
Work?
Putting It Together: Psychological
and Biological Insights Lag Behind
SUICIDE CHAPTER

oparasuicidecA suicide attempt that
does not result in death.
esuicide0A self-inflicted death in which
the person acts intentionally, directly, and
consciously.
Suicide has been recorded throughout history. The Old Testament described King
Saul’s suicide:”There Saul took a sword and fell on it.”The ancient Chinese, Greeks, and
Romans also provided examples. In more recent times, twentieth-century suicides by
such celebrated individuals as writer Ernest Hemingway, actress Marilyn Monroe, and
rock star Kurt Cobain both shocked and fascinated the public. Even more disturbing
are mass suicides such as those of the Heaven’s Gate cult in 1997.
Before you finish reading this page, someone in the United States will try to
kill himself. At least 60 Americans will have taken their own lives by this time
tomorrow…. Many of those who attempted will try again, a number with lethal
success.
(Shneidwan & Mandelkorn, 1983)
Today suicide is one of the leading causes of death in the world. It has been esti-
mated that 700,000 or more people may die by it each year, more than 31,000 in the
United States alone (Ohayon, 2009; Stolberg et al., 2002) (see Table 8-1). Millions of
other people throughout the world-600,000 in the United States—make unsuccessful
attempts to kill themselves; such attempts are called parasuicides. Actually, it is difficult
to obtain accurate figures on suicide, and many investigators believe that estimates are
often low. For one thing, suicide can be difficult to distinguish from unintentional drug
overdoses, automobile crashes, drownings, and other accidents (Wertheimer, 2001; Lester,
2000). Many apparent “accidents” were probably intentional. For another, since suicide
is frowned on in our society, relatives and friends often refuse to acknowledge that loved
ones have taken their own lives.
Suicide is not classified as a mental disorder by DSM-IV-TR, but clinicians are aware
of the high frequency with which psychological dysfunctioning—a breakdown of coping
skills, emotional turmoil, a distorted view of life—plays a role in this act. Although suicide
is frequently linked to depression, around half of all suicides result from other mental
disorders, such as schizophrenia or alcohol dependence, or involve no clear psychological
disorder at all (Maris, 2001). Jonathan Boucher, the young combat veteran about whom
you read at the beginning of this chapter, had intense feelings of depression and devel-
oped a severe drinking problem, but these symptoms and his act of suicide seemed to
derive from the posttraumatic stress disorder that engulfed his life and functioning.
able:
Most Common Causes of Death in the United States
Rank Cause
Deaths
Per Year
Percentage of
Total Deaths
1 Heart disease 696,947 28.5
2 Cancer 557,271 22.8
3 Stroke 162,672 6.7
4 Chronic respiratory diseases 124,816 5.1
5 Accidents 106,742 4.4
6 Diabetes 73,249 3.0
7 Pneumonia and influenza 65,681 2.7
8 Alzheimer’s 58,866 2.4
9 Kidney disease 40,974 1.7
10 Septicemia 33,965 1.4
11 Suicide 31,655 1.3
Source: National Center for Health Statistics, National Vital Health Statistics Report (2005).
230 ://CHAPTER 8
oparasuicidecA suicide attempt that
does not result in death.
esuicide0A self-inflicted death in which
the person acts intentionally, directly, and
consciously.
Suicide has been recorded throughout history. The Old Testament described King
Saul’s suicide:”There Saul took a sword and fell on it.”The ancient Chinese, Greeks, and
Romans also provided examples. In more recent times, twentieth-century suicides by
such celebrated individuals as writer Ernest Hemingway, actress Marilyn Monroe, and
rock star Kurt Cobain both shocked and fascinated the public. Even more disturbing
are mass suicides such as those of the Heaven’s Gate cult in 1997.
Before you finish reading this page, someone in the United States will try to
kill himself. At least 60 Americans will have taken their own lives by this time
tomorrow…. Many of those who attempted will try again, a number with lethal
success.
(Shneidwan & Mandelkorn, 1983)
Today suicide is one of the leading causes of death in the world. It has been esti-
mated that 700,000 or more people may die by it each year, more than 31,000 in the
United States alone (Ohayon, 2009; Stolberg et al., 2002) (see Table 8-1). Millions of
other people throughout the world-600,000 in the United States—make unsuccessful
attempts to kill themselves; such attempts are called parasuicides. Actually, it is difficult
to obtain accurate figures on suicide, and many investigators believe that estimates are
often low. For one thing, suicide can be difficult to distinguish from unintentional drug
overdoses, automobile crashes, drownings, and other accidents (Wertheimer, 2001; Lester,
2000). Many apparent “accidents” were probably intentional. For another, since suicide
is frowned on in our society, relatives and friends often refuse to acknowledge that loved
ones have taken their own lives.
Suicide is not classified as a mental disorder by DSM-IV-TR, but clinicians are aware
of the high frequency with which psychological dysfunctioning—a breakdown of coping
skills, emotional turmoil, a distorted view of life—plays a role in this act. Although suicide
is frequently linked to depression, around half of all suicides result from other mental
disorders, such as schizophrenia or alcohol dependence, or involve no clear psychological
disorder at all (Maris, 2001). Jonathan Boucher, the young combat veteran about whom
you read at the beginning of this chapter, had intense feelings of depression and devel-
oped a severe drinking problem, but these symptoms and his act of suicide seemed to
derive from the posttraumatic stress disorder that engulfed his life and functioning.
able:
Most Common Causes of Death in the United States
Rank Cause
Deaths
Per Year
Percentage of
Total Deaths
1 Heart disease 696,947 28.5
2 Cancer 557,271 22.8
3 Stroke 162,672 6.7
4 Chronic respiratory diseases 124,816 5.1
5 Accidents 106,742 4.4
6 Diabetes 73,249 3.0
7 Pneumonia and influenza 65,681 2.7
8 Alzheimer’s 58,866 2.4
9 Kidney disease 40,974 1.7
10 Septicemia 33,965 1.4
11 Suicide 31,655 1.3
Source: National Center for Health Statistics, National Vital Health Statistics Report (2005).
230 ://CHAPTER 8

eft Behind
• • i • • .
PI
I I
1
Suicide :11 231
41What Is Suicide?
Not every self-inflicted death is a suicide. A man who crashes his car into a tree
after falling asleep at the steering wheel is not trying to kill himself. Thus Edwin
Shneidman (2005,1993, 1963), one of the most influential writers on this topic,
defines suicide as an intentioned death—a self-inflicted death in which one
makes an intentional, direct, and conscious effort to end one’s life.
Intentioned deaths may take various forms. Consider the following ex-
amples. All three of these people intended to die, but their motives, concerns,
and actions differed greatly.
Dave was a successful man. By the age of 50 he had risen to the vice presidency
of a small but profitable investment firm. He had a caring wife and two teenage
sons who respected him. They lived in an upper-middle-class neighborhood, had a
spacious house, and enjoyed a life of comfort.
In August of his fiftieth year, everything changed. Dave was fired. just like that.
The economy had gone bad once again, the firm’s profits were down and the firm’s
president wanted to try new, fresher investment strategies and marketing approaches. He
wanted to try a younger person in Dave’s position.
The experience of failure, loss, and emptiness was overwhelming for Dave. He looked
for another position, but found only low-paying jobs for which he was overqualified. Each
day as he looked for work Dave became more depressed, anxious, and desperate. He
thought of trying to start his own investment company or to be a consultant of some
kind, but, in the cold of night, he believed he was just fooling himself with such notions.
He kept sinking, withdrew from others, and felt increasingly hopeless.
Six months after losing his job, Dave began to consider ending his life. The pain was too
great, the humiliation unending. He hated the present and dreaded the future. Throughout
February he went back and forth. On some days he was sure he wanted to die. On other
days, an enjoyable evening or uplifting conversation might change his mind temporarily.
On a Monday late in February he heard about a job possibility, and the anticipation of the
next day’s interview seemed to lift his spirits. But Tuesday’s interview did not go well. It
was clear to him that he would not be offered the job. He went home, took a recently pur-
chased gun from his locked desk drawer, and shot himself
Demaine never truly recovered from his mother’s death. He was only 7 years old and
unprepared for such a loss. His father sent him to live with his grandparents for a time, to
a new school with new kids and a new way of life. In Demaine’s mind, all these changes
were for the worse. He missed the joy and laughter of the past. He missed his home, his
father, and his friends. Most of all he missed his mother.
He did not really understand her death. His father said that she was in heaven now,
at peace, happy. Demaine’s unhappiness and loneliness continued day after day and he
began to put things together in his own way. He believed he would be happy again if he
could join his mother. He felt she was waiting for him, waiting for him to come to her.
These thoughts seemed so right to him; they brought him comfort and hope. One evening,
shortly after saying good night to his grandparents, Demaine climbed out of bed, went up
the stairs to the roof of their apartment house, and jumped to his death. In his mind he
was joining his mother in heaven.
Tya and Noah had been going together for a year. It was Tya’s first serious relationship; it
was her whole life. Thus when Noah told her that he no longer loved her and was leaving
her for someone else, she was shocked and shaken.
As the weeks went by, Tya was filled with two competing feelings—depression and
anger. Several times she called Noah, begged him to reconsider, and pleaded for a chance
to win him back. At the same time, she hated him for putting her through such misery.
_ AO 41 – ° 11. • •
f
eft Behind
• • i • • .
PI
I I
1
Suicide :11 231
41What Is Suicide?
Not every self-inflicted death is a suicide. A man who crashes his car into a tree
after falling asleep at the steering wheel is not trying to kill himself. Thus Edwin
Shneidman (2005,1993, 1963), one of the most influential writers on this topic,
defines suicide as an intentioned death—a self-inflicted death in which one
makes an intentional, direct, and conscious effort to end one’s life.
Intentioned deaths may take various forms. Consider the following ex-
amples. All three of these people intended to die, but their motives, concerns,
and actions differed greatly.
Dave was a successful man. By the age of 50 he had risen to the vice presidency
of a small but profitable investment firm. He had a caring wife and two teenage
sons who respected him. They lived in an upper-middle-class neighborhood, had a
spacious house, and enjoyed a life of comfort.
In August of his fiftieth year, everything changed. Dave was fired. just like that.
The economy had gone bad once again, the firm’s profits were down and the firm’s
president wanted to try new, fresher investment strategies and marketing approaches. He
wanted to try a younger person in Dave’s position.
The experience of failure, loss, and emptiness was overwhelming for Dave. He looked
for another position, but found only low-paying jobs for which he was overqualified. Each
day as he looked for work Dave became more depressed, anxious, and desperate. He
thought of trying to start his own investment company or to be a consultant of some
kind, but, in the cold of night, he believed he was just fooling himself with such notions.
He kept sinking, withdrew from others, and felt increasingly hopeless.
Six months after losing his job, Dave began to consider ending his life. The pain was too
great, the humiliation unending. He hated the present and dreaded the future. Throughout
February he went back and forth. On some days he was sure he wanted to die. On other
days, an enjoyable evening or uplifting conversation might change his mind temporarily.
On a Monday late in February he heard about a job possibility, and the anticipation of the
next day’s interview seemed to lift his spirits. But Tuesday’s interview did not go well. It
was clear to him that he would not be offered the job. He went home, took a recently pur-
chased gun from his locked desk drawer, and shot himself
Demaine never truly recovered from his mother’s death. He was only 7 years old and
unprepared for such a loss. His father sent him to live with his grandparents for a time, to
a new school with new kids and a new way of life. In Demaine’s mind, all these changes
were for the worse. He missed the joy and laughter of the past. He missed his home, his
father, and his friends. Most of all he missed his mother.
He did not really understand her death. His father said that she was in heaven now,
at peace, happy. Demaine’s unhappiness and loneliness continued day after day and he
began to put things together in his own way. He believed he would be happy again if he
could join his mother. He felt she was waiting for him, waiting for him to come to her.
These thoughts seemed so right to him; they brought him comfort and hope. One evening,
shortly after saying good night to his grandparents, Demaine climbed out of bed, went up
the stairs to the roof of their apartment house, and jumped to his death. In his mind he
was joining his mother in heaven.
Tya and Noah had been going together for a year. It was Tya’s first serious relationship; it
was her whole life. Thus when Noah told her that he no longer loved her and was leaving
her for someone else, she was shocked and shaken.
As the weeks went by, Tya was filled with two competing feelings—depression and
anger. Several times she called Noah, begged him to reconsider, and pleaded for a chance
to win him back. At the same time, she hated him for putting her through such misery.
_ AO 41 – ° 11. • •
f

4`r.r,Db’
rj;-01714 Ce!„Eti
nA)Lri’6 w
:The Ilitipidt:of interpmen
“.;ct. •
Murphy, 2005). Relatives, friends, therapists, or physicians may remember past
statements, conversations, and behaviors that shed light on a suicide. Retrospec-
tive information may also be provided by the suicide notes that some victims
leave behind (Wong et al., 2009). However, such sources of information are not
always available or reliable (Sudak et al., 2008). Around half of all suicide victims
have never been in psychotherapy (Stolberg et al., 2002), and less than one-third
leave notes (Maris, 2001).
Because of these limitations, many researchers also use a second strategy—
studying people who survive their suicide attempts. It is estimated that there are 8 to 20
nonfatal suicide attempts for every fatal suicide (Maris, 2001). However, it may
be that people who survive suicide differ in important ways from those who do
not (Cutler et al., 2001). Many of them may not really have wanted to die, for
example. Nevertheless, suicide researchers have found it useful to study survivors
of suicide, and this chapter shall consider those who attempt suicide and those
who commit suicide as more or less alike.
234 ://CHAPTER 8

kl The Private
Dreams and
1.’Despair of a
111,otk Legend

Patterns and Statistics
Suicide happens within a larger social setting, and researchers have gathered
many statistics regarding the social contexts in which such deaths take place.
They have found, for example, that suicide rates vary from country to country
(Sadock & Sadock, 2007). Russia, Hungary, Germany, Austria, Finland, Den-
mark, China, and Japan have very high rates, more than 20 suicides annually per
100,000 persons; conversely, Egypt, Mexico, Greece, and Spain have relatively
low rates, fewer than 5 per 100,000. The United States and Canada fall in be-
tween, each with a suicide rate of around 12 per 100,000 persons; England has a rate
of 9 per 100,000.
Religious affiliation and beliefs may help account for these national differences
(Sadock & Sadock, 2007). For example, countries that are largely Catholic, Jewish, or
Muslim tend to have low suicide rates. Perhaps in these countries, strict prohibitions
against suicide or a strong religious tradition discourage many people from committing
suicide (Stack & Kposowa, 2008).Yet there are exceptions to this rule. Austria, a largely
Roman Catholic country, has one of the highest suicide rates in the world.
Research is beginning to suggest that religious affiliation may not help prevent sui-
cide as much as the degree of an individual’s devoutness. Regardless of their particular
persuasion, very religious people seem less likely to commit suicide (Stack & Kposowa,
2008). Similarly, it seems that people who hold a greater reverence for life are less prone
to consider or attempt self-destruction (Lee, 1985).
The suicide rates of men and women also differ (see Figure 8-1). Three times as
many women attempt suicide as men, yet men succeed at more than three times the
rate of women (Humphrey, 2006). Around the world 19 of every 100,000 men kill
themselves each year; the suicide rate for women is 4 per 100,000 (Levi et al., 2003).
One reason for these differing rates appears to be the different methods used by men
and women (Stack & Wasserman, 2009). Men tend to use more violent methods, such
as shooting, stabbing, or hanging themselves, whereas women use less violent methods,
such as drug overdose. Guns are used in nearly two-thirds of the male suicides in the
United States, compared to 40 percent of the female suicides (Maris, 2001).
Suicide is also related to social support and marital status (Cutright et al., 2007). In
one study, around half of the individuals who had committed suicide were found to
have no close friends (Maris, 2001). Fewer still had close relationships with parents and
other family members. In a related vein, research has revealed that divorced persons have
a higher suicide rate than married or cohabitating individuals (Stolberg et al., 2002).
Finally, in the United States at least, suicide rates seem to vary according to race.The
overall suicide rate of white Americans, 12 per 100,000 persons, is almost twice as high
as that of African Americans, Hispanic Americans, and Asian Americans (Walker et al.,
2008; Oquendo et al., 2005).A major exception to this pattern is the very high suicide
4`r.r,Db’
rj;-01714 Ce!„Eti
nA)Lri’6 w
:The Ilitipidt:of interpmen
“.;ct. •
Murphy, 2005). Relatives, friends, therapists, or physicians may remember past
statements, conversations, and behaviors that shed light on a suicide. Retrospec-
tive information may also be provided by the suicide notes that some victims
leave behind (Wong et al., 2009). However, such sources of information are not
always available or reliable (Sudak et al., 2008). Around half of all suicide victims
have never been in psychotherapy (Stolberg et al., 2002), and less than one-third
leave notes (Maris, 2001).
Because of these limitations, many researchers also use a second strategy—
studying people who survive their suicide attempts. It is estimated that there are 8 to 20
nonfatal suicide attempts for every fatal suicide (Maris, 2001). However, it may
be that people who survive suicide differ in important ways from those who do
not (Cutler et al., 2001). Many of them may not really have wanted to die, for
example. Nevertheless, suicide researchers have found it useful to study survivors
of suicide, and this chapter shall consider those who attempt suicide and those
who commit suicide as more or less alike.
234 ://CHAPTER 8

kl The Private
Dreams and
1.’Despair of a
111,otk Legend

(a) Age
35 70
(b) Age and Gender
0,
43`
4-,
0
4)7 hry 4,2

a. a. a a

a 4-, .0 n

44 a. 4-i . ) .0
Age Group
^-■ (le
4 4 4
•
<4 44''' 4 Age Group (d) Age, Gender, and Race 50 (c) Age and Race 20 0 ti <,?" a, <02 hx Age Group Age Group lr Suicide :11 235 1 , 11.1011 H rate of Native Americans, which overall is one and a half times the national average (Hill, 2009). Altho ugh the extreme poverty of many Native Americans may partly explain this trend, studies show that factors such as alcohol use, modeling, and the availability of guns may also play a role (Goldston et al., 2008). Studies of Native Americans in Canada yield similar results (Matsumoto & _Nang, 2008). Some of these statistics on suicide have been questioned (Leach & Leong, 2008). One analysis suggests that the actual rate of suicide may be 15 percent higher for African Americans and 6 percent higher for women than usually reported (Phillips & Ruth, 1993). People in these groups are more likely than others to use methods of suicide that can be mistaken for causes of accidental death, such as poisoning, drug overdose, single-car crashes, and pedestrian accidents. S u ic id es p er i o o ,0 0 0 P o p u la t i on 20 30 25 15 10 S u ic id es p er l o o ,0 0 0 P o p u l a ti on cr- ILir---.1 Ar T-', hx (r) African American females 0 5v 7) 7'

Turn in your highest-quality paper
Get a qualified writer to help you with

“ hw help ”

Get high-quality paper

Guarantee! All work is written by expert writers!

Still stressed from student homework?

Get quality assistance from academic writers!

Order now