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C H A P T E R :6
Disorders of Mood
TO P I C OV E RV I E W
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
L E C T U R E O U T L I N E
I. THERE ARE TWO KEY EMOTIONS IN MOOD DISORDERS:
A. Depression—a low, sad state in which life seems dark and its challenges overwhelming
B. Mania—a state of
eathless euphoria or frenzied energy
C. People with depressive disorders suffer only from depression, a pattern called unipola
depression
1. Person has no history of mania
2. Mood returns to normal when depression lifts
D. In contrast, those who display bipolar disorders experience periods of mania that alternate
with periods of depression
E. Mood problems have always captured people’s interest
1. Millions of people have mood disorders
2. Economic costs of mood disorders amount to many billions of dollars each yea
3. The human suffering is beyond calculation
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II. UNIPOLAR DEPRESSION
A. The term “depression” is often used to describe general sadness or unhappiness
1. This loose use of the term confuses a normal mood swing with a clinical syndrome
2. Clinical depression can
ing severe and long-lasting psychological pain that may in-
tensify as time goes by
B. How common is unipolar depression?
1. Around 8 percent of adults in the United States suffer from severe unipolar depres-
sion in any given yea
2. As many as 5 percent suffer from mild forms
3. Around 19 percent of all adults experience unipolar depression at some time in thei
lives
4. The prevalence is similar in Canada, England, France, and many other countries
5. The rate of depression is higher among poor people than wealthy people
6. Women are at least twice as likely as men to experience severe unipolar depression
a. Lifetime prevalence: 26 percent of women vs. 12 percent of men
. Among children, the prevalence is similar among boys and girls
7. Approximately 85 percent of people with unipolar depression recover, some without
treatment
a. Around 40 percent will experience another episode later in their lives
C. What are the symptoms of depression?
1. Symptoms may vary from person to person
2. Five main areas of functioning may be affected:
a. Emotional symptoms—feeling “miserable,” “empty,” “humiliated”; experienc-
ing little pleasure
. Motivational symptoms—lacking drive, initiative, spontaneity
(a) Between 6 percent and 15 percent of those with severe depression die by
suicide
c. Behavioral symptoms—less active, less productive
d. Cognitive symptoms—hold negative views of themselves, blame themselves
for unfortunate events; pessimistic
e. Physical symptoms—headaches, dizzy spells, general pain
D. Diagnosing unipolar depression
1. A major depressive episode is a period of two or more weeks marked by five or more
symptoms of depression
a. In extreme cases, symptoms are psychotic, including hallucinations and delu-
sions
2. DSM-5 lists several types of depressive disorders:
a. Major depressive disorde
(a) People who experience a major depressive episode with no history of
mania
. Dysthymic disorde
(a) Individuals who experience a longer-lasting (at least two years) but less
disabling pattern of depression
c. Premenstrual dysphoric disorde
(a) A diagnosis given to women who repeatedly experience clinically signifi-
cant depressive symptoms during the week before menstruation
d. Disruptive mood regulation disorde
(a) A disorder characterized by a combination of persistent depressive symp-
toms and recu
ent outbursts of severe tempe
E. Stress and unipolar depression
1. Stress may be a trigger for depression
2. People with depression experience a greater number of stressful life events during
the month just before the onset of their symptoms
3. Some clinicians distinguish reactive (exogenous) depression from endogenous de-
pression, which seems to be a response to internal factors
4. Today’s clinicians usually concentrate on recognizing both the situational and the in-
ternal aspects of any given case
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Disorders of Mood 85
F. The Biological model of unipolar depression
1. Evidence from genetic, biochemical, anatomical, and immune system studies sug-
gests that unipolar depression has biological causes
2. Genetic factors
a. Family pedigree, twin, adoption, and molecular biology gene studies suggest
that some people inherit a biological predisposition
. Researchers have found that as many as 20 percent of relatives of those with de-
pression are themselves depressed, compared with fewer than 10 percent of the
general population
c. Twin studies demonstrate a strong genetic component:
(a) Concordance rates for identical (MZ) twins = 46 percent
(b) Concordance rates for fraternal (DZ) twins = 20 percent
d. Using techniques from the field of molecular biology, researchers have found
evidence that unipolar depression may be tied to specific genes
3. Biochemical factors
a. The key neurotransmitters are serotonin and norepinephrine
(a) In the 1950s, medications for high blood pressure were found to cause de-
pression: some lowered serotonin, others lowered norepinephrine
(b) The discovery of truly effective antidepressant medications, which re-
lieved depression by increasing either serotonin or norepinephrine, con-
firmed the NT role
(c) Depression likely involves not just serotonin or norepinephrine; a compli-
cated interaction is at work, and other neurotransmitters may be involved
. Factors related to the endocrine system and hormone release may also be at
work
(a) People with depression have been found to have abnormal levels of cor-
tisol, a hormone released by the adrenal glands during times of stress
(b) People with depression have been found to have abnormal melatonin se-
cretion—sometimes called the “Dracula hormone”
(c) Other researchers are investigating deficiencies of important proteins
within neurons as tied to depression
c. Model has produced much enthusiasm but has certain limitations:
(a) Relies on analogue studies: depression-like symptoms created in lab animals
(i) Do these symptoms co
elate with human emotions?
(b) Measuring
ain activity has been difficult and indirect
(i) Cu
ent studies using newer technology are attempting to address
this issue
4. Brain anatomy and
ain circuits
a. Biological researchers have determined that emotional reactions of various
kinds are tied to
ain circuits
. These are networks of
ain structures that work together, triggering each othe
into action and producing a particular kind of emotional reaction
c. Although research is far from complete, a circuit responsible for unipolar de-
pression has begun to emerge
(a) Likely
ain areas in the circuit include the prefrontal cortex, hippocam-
pus, amygdala, and Brodmann Area 25
5. Immune system
a. This system is the body’s network of activities and cells that fight off bacteria
and other foreign invaders
. When stressed, the immune system may become dysregulated, which some be-
lieve may help produce depression
6. What are the biological treatments for unipolar depression?
a. Usually, biological treatment means antidepressant drugs, but for severely de-
pressed individuals who do not respond to other forms of treatment, it some-
times includes electroconvulsive therapy or
ain stimulation
. Electroconvulsive therapy (ECT)
(a) This is one of the most controversial forms of treatment
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(b) The procedure consists of targeted electrical stimulation to cause a
ain
seizure
(c) The usual course of treatment is 6 to 12 sessions spaced over 2 to 4 weeks
(d) The discovery of the effectiveness of ECT was accidental
(e) The procedure has been modified in recent years to reduce some of the
negative effects
(i) For example, patients are given muscle relaxants and anesthetics be-
fore and during the procedure
(f) Patients generally report some memory loss
(g) ECT is clearly effective in treating unipolar depression, but it has been dif-
ficult to determine why ECT works so well
(h) Studies find improvement in 60 to 80 percent of patients
(i) The procedure seems particularly effective in cases of severe depression
with delusions
c. Antidepressant drugs
(a) In the 1950s, two kinds of drugs were found to reduce the symptoms of
depression: monoamine oxidase inhibitors (MAO inhibitors) and tri-
cyclics; these drugs have been joined in recent years by a third group, the
second-generation antidepressants
(b) Antidepressant drugs: MAO inhibitors
(i) Originally used to treat TB, doctors noticed that the medication
seemed to make patients happie
(ii) The drug works biochemically by slowing down the body’s produc-
tion of MAO, which
eaks down norepinephrine
(iii) MAO inhibitors stop this
eakdown from occu
ing
(iv) This leads to a rise in norepinephrine activity and a reduction in de-
pressive symptoms
(v) Approximately half of patients who take these drugs are helped by
them
(vi) MAO inhibitors pose a potential danger: people who take MAOIs
experience a dangerous rise in blood pressure if they eat foods con-
taining tyramine (cheese, bananas, wine)
(c) Antidepressant drugs: tricyclics
(i) In searching for medications for schizophrenia, researchers discov-
ered that imipramine relieved depressive symptoms
(ii) Imipramine and related drugs are known as tricyclics because they
share a three-ring molecular structure
(iii) Hundreds of studies have found that depressed patients taking tri-
cyclics have improved much more than similar patients taking
placebos
(iv) Drugs must be taken for at least 10 days before such improvement is
seen
(v) About 60–65 percent of patients find symptom improvement
(vi) Most patients who immediately stop taking tricyclics upon relief of
symptoms relapse within one yea
(vii) Patients who take tricyclics for five additional months (“mainte-
nance therapy”) have a significantly decreased risk of relapse
(viii) Tricyclics are believed to reduce depression by affecting neurotrans-
mitter (NT) reuptake mechanisms
(1) To prevent an NT from remaining in the synapse too long, a
pumplike mechanism recaptures the NT and draws it back into
the presynaptic neuron
(2) The reuptake process appears to be too efficient in some peo-
ple, drawing in too much of the NT from the synapse
(3) This reduction in NT activity in the synapse is thought to result
in clinical depression
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Disorders of Mood 87
(4) Tricyclics block the reuptake process, thus increasing NT activ-
ity in the synapse
(d) Second-generation antidepressants
(i) A third group of effective antidepressant drugs is structurally differ-
ent from the MAO inhibitors and tricyclics
(ii) Most of the drugs in this group are labeled selective serotonin reup-
take inhibitors (SSRIs)
(iii) These drugs increase serotonin activity specifically (no other NTs are
affected)
(iv) This class includes fluoxetine (Prozac), sertraline (Zoloft), and esci-
talopram (Lexapro)
(v) Selective norepinephrine reuptake inhibitors and serotonin-norepi-
nephrine reuptake inhibitors are also now available
(vi) The effectiveness and speed of action of these drugs are on a pa
with the tricyclics, yet their sales have skyrocketed
(1) Clinicians often prefer these drugs because it is harder to over-
dose on them than on other kinds of antidepressants
(2) There are no dietary restrictions like there are with MAO