16.4 Mood Disorders

Mood refers to a prolonged emotional state that colors many, if not all, aspects of a person’s thought and behavior. It is useful (though oversimplified) to think of a single dimension of mood, running from depression at one end to elation at the other. Because we all have tasted both, we have an idea of what they are like. Depression and elation are normal experiences, but at times either of them can become so intense or prolonged as to promote harmful, even life-threatening, actions. Extreme depression can keep a person from working, lead to withdrawal from friends, or even provoke suicide. Extreme elation, called mania, can lead to outrageous behaviors that turn other people away or to dangerous acts that stem from a false sense of security and bravado.

DSM-5 identifies two main categories of mood disorders: depressive disorders, characterized by prolonged or extreme depression, and bipolar and related disorders, characterized usually by alternating episodes of mania and depression.

Depressive Disorders

Artists and other creative people who suffer from depression may find inspiration in their depressive moods, even if they are more productive during periods when they feel less depressed.

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Depression is characterized primarily by prolonged sadness, self-blame, a sense of worthlessness, and absence of pleasure. Other common symptoms include decreased or increased sleep, decreased or increased appetite, and either retarded or agitated motor symptoms. Retarded motor symptoms include slowed speech and slowed body movements. Agitated symptoms, which are less common than retarded symptoms, include repetitive, aimless movements such as hand wringing and pacing. To warrant a diagnosis of a depressive disorder, the symptoms must be either very severe or very prolonged and not attributable just to a specific life experience, though they may be triggered or exacerbated by such an experience.

Two main classes of depressive disorders are distinguished in DSM-5. Major depression is characterized by very severe symptoms that last essentially without remission for at least 2 weeks. Dysthymia[dǐs-thī-mē-ǝ], also referred to as persistent depressive disorder, is characterized by less-severe symptoms that last for at least 2 years. It is not unusual for bouts of major depression to be superimposed over a more chronic state of dysthymia, in which case the person is said to have double depression. Surveys in North America suggest that as many as 15 percent of people suffer from major depression, and 2 to 3 percent suffer from dysthymia, at some time in their lives (González et al., 2010; Kessler et al., 2005).

Comparisons Between Depression and Generalized Anxiety

Much has been written about the similarities and differences between depression and generalized anxiety disorder. The two disorders are apparently predisposed by the same genes. The identical twins of people suffering from either generalized anxiety disorder or major depression exhibit equally enhanced rates of either disorder (Kendler et al., 2006). Other studies reveal that the two disorders often occur in the same individuals. Approximately 60 percent of people diagnosed with generalized anxiety disorder also suffer from a depressive disorder at some point in their lives (Hettema, 2008; Kessler et al., 2008). Typically, generalized anxiety occurs before onset of major depression (Hunt et al., 2004; Wittchen et al., 2000).

One way to conceive of the difference between generalized anxiety and depression is to think of the former as a frantic, relatively ineffective attempt to cope with life’s real and imagined threats through worry and hypervigilance, and to think of the latter as a kind of giving up, despairing of coping and concluding that life is not worth living. Cognitively, anxious individuals worry about what might happen in the future, while depressed individuals feel that all is already lost (see Table 16.3). Depressed individuals are much more likely than anxious individuals to stop caring for themselves and to stay in bed all day. The sense of giving up is commonly accompanied by strong feelings of self-blame, of not deserving to live. The feelings of worthlessness are captured in the following quotation from Norman Endler (1982), a highly respected psychologist describing his own bout with depression:

Table 16.3: Table 16.3
Comparison of anxious thoughts with depressive thoughts

Negative Thought Pattern as a Cause of Depression

Negative thoughts are characteristic of people who are depressed, and they may also characterize people who are not depressed but are vulnerable to becoming so. Consider two nondepressed college students who have just taken and failed their first test in Introductory Psychology. One responds to the failure by thinking: “I’m stupid. I’m going to fail this course. I’m going to flunk out of college.” The other responds by thinking: “Ouch. That was a tough test. I didn’t study enough, and I was up too late the night before.” The first student illustrates a pattern of thought that is very likely to lead to depression, while the opposite is true of the second.

A prominent modern theory of depression is the hopelessness theory, developed by Lyn Abramson and her colleagues (1989). According to this theory, depression results from a pattern of thinking about negative events that has the following three characteristics:

• The person assumes that the negative event will have disastrous consequences. (The failed test will lead to flunking out of college.)
• The person assumes that the negative event reflects something negative about him- or herself. (The failure is proof of stupidity or some such personal inadequacy.)
• The person attributes the cause of the negative event to something that is stable (will not change) and global (capable of affecting many future events). (Stupidity is an unchangeable characteristic that will affect all realms of endeavor.)

A major controversy concerning the hopelessness theory is whether the hopeless thought pattern merely reflects depression or is also a cause of depression (Joormann, 2009). Certainly, depressed people manifest this negative manner of thinking. By DSM-5 criteria or any other criteria, negative thinking is part of the definition of depression. But Abramson and her colleagues have shown that the hopeless manner of thinking about negative events can also occur, to varying degrees, in people who by other measures are not depressed, and in those people it is predictive of future depression.

In one study, first-year, nondepressed college students with no prior history of clinical depression filled out a questionnaire designed to measure the hopeless style of thinking about negative events and another questionnaire designed to assess their current level of mood. Then they were assessed at various times for depression over a 2.5-year follow-up period (Alloy et al., 2006). The result was that those who had scored high on the measure of negative thinking were over six times as likely to manifest an episode of major depression at some point during the follow-up period than were those who had scored low on that measure. This was true even when just those who were equivalent in mood level at the beginning of the study were compared.

Other evidence that negative thinking is a cause of depression comes from research on cognitive therapy (discussed in Chapter 17). This therapeutic approach, which is aimed at helping people change their habitual patterns of thinking, can help people overcome depression and can reduce the likelihood of its recurrence. Moreover, several studies have shown that children and adolescents who have never been depressed can be at least partially inoculated against future depression by training in which they learn to interpret negative events in hope-promoting ways (Munoz et al., 2009).

Stressful Experiences Plus Genetic Predisposition as Cause of Depression

Many studies have shown that people who have recently suffered a severely stressful experience are much more likely to become depressed than are those who have not (Monroe et al., 2009; Kessler, 1997). The kinds of stressful events that are most strongly associated with depression are losses that alter the nature of one’s life—loss of a spouse or other close daily companion, loss of a job that one has held for a long time, loss in social status, sharp loss in income, or permanent loss in health. Such events interrupt one’s life routines and render ineffective well-established ways of satisfying one’s needs and desires. They can promote the kind of hopeless thinking that corresponds with and predicts depression.

Yet, research has also shown very clearly that not everyone becomes depressed in response to such occurrences. Some people are resilient, even in the face of severe losses. They experience sadness, but not major depression, and they put their efforts effectively into restructuring their lives. The difference appears to reside largely in genes.

In a research study dramatically supporting this conclusion, Kenneth Kendler and his colleagues identified over 1,000 women who had twin sisters (Kendler, 1998; Kendler et al., 1995). They studied each to identify (a) whether or not she had recently experienced a highly stressful life event (defined as assault, serious marital problems, divorce or breakup of a marriage or other romantic relationship, or death of a close relative), (b) whether or not a period of major depression began within a month after that stressful event (or within a comparable time period for those who had not experienced a serious stressor), and (c) her level of genetic predisposition for depression. The level of genetic predisposition was judged on the basis of whether or not the woman’s twin sister (co-twin) did or did not have a history of major depression and whether she was an identical twin or a nonidentical twin.

The results of the study are depicted in Figure 16.5. Among women who had not recently experienced a highly stressful life event, the incidence of depression was very low regardless of level of genetic predisposition. However, among those who had recently experienced such an event, the incidence of depression was strongly related to the level of genetic predisposition. The results are quite consistent with the idea that major depression generally requires both a genetic predisposition for depression and some severely stressful event to bring it on.

Figure 16.5: Roles of genetic predisposition and stressful experiences in the incidence of depression Women who had recently experienced a severely stressful event were far more likely to experience the onset of major depression than were those who had not. This effect of stress was greater for those who were judged to be more genetically predisposed for depression (based on the status of their twin sisters, as shown in the key) than for those who were judged to be less genetically predisposed.

(Based on data from Kendler et al., 1995.)

Figure 16.6: Adolescent depression and maternal rejection Adolescents who possessed one combination of alleles (TT) experienced significantly greater levels of clinical depression as a result of high level of maternal rejection than adolescents with alternate combinations of alleles (CC or CT), demonstrating an interaction between genes and environment.

(Based on data from Haeffel et al., 2008.)

More recently, research has focused on specific gene alleles that may be conducive to, or protective against, depression. The most consistent findings to date concern a gene (5-HTT) that alters the effects of the neurotransmitter serotonin in the brain. Recall from Chapter 12 that this gene comes in two alleles—a short form and the long form. In Chapter 12, we describe research indicating that infants who have two copies of the long allele are protected from at least some of the negative effects of insensitive parenting. Several research studies suggest that this allele also tends to protect adults from becoming depressed in response to severe stressful events, but only under certain rearing environments. For example, in research by Avshalom Caspi and his colleagues (2003), people who had the short version of the 5-HTT gene were more likely to experience depression than people with the long version, but only if they experienced multiple stressful events in childhood. Although this finding has been replicated (Kendler et al., 2005), not all researchers who have looked for this relationship have found it (Risch et al., 2009), making the finding controversial. In other research looking at different alleles of a gene (called DAT1) involved in the transportation of the neurotransmitter dopamine, adolescents were more apt to be classified as clinically depressed if they had experienced high levels of maternal rejection as children than nonrejected adolescents, but only if they had one combination of alleles (TT versus CC or CT; see Figure 16.6) (Haeffel et al., 2008). Thus, rather than the 5-HTT or DAT1 genes being “for” depression, the research suggests an interaction between genetic disposition and childhood experience in depression.

Possible Brain Mechanisms of Depression

Depression, like every other psychological state, is a product of the brain. Thus, one route to understanding depression is to try to identify changes in the brain that might cause bouts of depression to appear and disappear.

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All the drugs that are used regularly to treat depression have the effect of increasing the amount or activity of one or both of two neurotransmitters in the brain: norepinephrine and serotonin. For that reason, an early theory of depression posited that the disorder results from a brain deficiency in one or both of these transmitters (Schildkraut, 1965). Today, however, that simple theory is much doubted (Krishnan & Nestler, 2008). One problem is that it does not explain the delayed effectiveness of drug treatments. Antidepressant drugs begin to enhance the activity of norepinephrine or serotonin (or both) in the brain immediately, yet they typically do not begin to relieve depression until at least 2 weeks of continuous treatment have elapsed. Moreover, by various measures, most depressed people do not appear to have unusually low levels of these neurotransmitters (Cowen, 2005).

At present, many neuroscientists interested in depression are focusing on the ways that the brain changes during periods of psychological distress. Stress and worry are often associated with an increased release of cortisol, a hormone produced by the adrenal glands. Research with animals shows that cortisol can act on the brain to shut off certain growth-promoting processes. Over periods of weeks or months, a high level of cortisol can result in a small but measurable shrinkage in some portions of the brain, including portions of the prefrontal cortex and the hippocampus (Jacobs, 2004). These brain changes are reversible. During periods of reduced stress, the shrunken brain areas may regain their former size. Moreover, increases in norepinephrine and serotonin over periods of weeks can stimulate growth in these brain areas, and this observation may explain the delayed effects of drug treatments in relieving depression.

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Thus, one current theory, which is far from proven, is that depression in humans results at least partly from a stress-induced loss of neurons or neural connections in certain parts of the brain and that recovery from depression results from regrowth in those brain areas (Jacobs, 2004; Martinowich et al., 2007; Perera et al., 2008). This theory is consistent with the evidence that depression often follows a rather prolonged period of anxiety. Anxiety stimulates production of the hormones that interfere with brain growth. The theory is also consistent with the idea that altered ways of thinking can change one’s predisposition for depression. Hopefulness reduces psychological distress, which reduces the production of the growth-inhibiting hormones and thereby protects the brain from the changes that lead to depression. It will be interesting to see how well this theory holds up to the tests of future research.

Possible Evolutionary Bases for Depression

Psychologists viewing depression from an evolutionary perspective have suggested that it may be an exaggerated form of a response to loss that in less extreme form is adaptive (Allen & Badcock, 2006; Nesse, 2000). Only a minority of people develop clinically severe depression, but most of us, at some periods in our lives, experience a low mood or moderate depression. A depressed mood slows us down, makes us think realistically rather than optimistically, leads us to turn away from goals that we can no longer hope to achieve, and signals to others that we are no threat to them and need their help. The signals of helplessness by depressed persons resemble the appeasement displays used by other animals to signal submissiveness and need for care (Price et al., 2004). A depressed mood can also lead to a kind of soul-searching, the end result of which may be the establishment of new, more realistic goals and a new approach to life (Welling, 2003).

Matthew Keller and Randolph Nesse (2005, 2006) have suggested that depressed moods may come in a variety of different forms, each adapted for different survival purposes. Most people who live in northern latitudes experience some degree of depressed mood during the winter (Dam et al., 1998). When it occurs in extreme form, such winter-limited depression is diagnosed as seasonal affective disorder, or SAD. This form of depression is accompanied by increased appetite, increased sleepiness, and lethargy—all responses that, in less extreme form, may have been useful to our evolutionary ancestors for building layers of fat and conserving energy to survive the harsh winter. That form of depression is generally not accompanied by the degrees of sadness, crying, and self-reproach that occur in other forms of depression.

In their own research, Keller and Nesse (2006) found that depressed mood following the death of a loved one or the loss of a romantic partner is especially characterized by crying and other expressions of sadness, which may signal the need for help from others. In contrast, they found that depressed mood following repeated failure is especially characterized by self-blame and pessimism, which may motivate the person to withdraw from futile activities and begin a period of realistic reappraisal of life goals. It remains for future research to test further the idea that depressed moods come in different forms that serve different adaptive purposes.

Bipolar Disorders

Major depression and dysthymia are sometimes called unipolar disorders because they are characterized by mood changes in only one direction—downward from normal. In contrast, bipolar disorders (formerly called manic-depression) are characterized by mood swings in both directions: downward in depressive episodes and upward in manic episodes. Such episodes may last anywhere from a few days to several months, often separated by months or years of relatively normal mood.

DSM-5 identifies two main varieties of bipolar disorders. Bipolar I disorder is the classic type, characterized by at least one manic episode and at least one depressive episode. Bipolar II disorder is similar to bipolar I disorder except that its high phase is less extreme and is referred to as hypomania rather than mania. Bipolar I disorder occurs, at some time in life, in about 1 percent of people in the population, and bipolar II disorder occurs in about 2 to 3 percent of people the population (Merikangas et al., 2011; Kessler et al., 2005). In some cases, episodes of mania may occur without intervening episodes of depression (Belmaker, 2004).

Research with twins and adoptees has shown that the predisposition for bipolar disorder is strongly heritable, more so than is unipolar depression or most other mental disorders (Johnson et al., 2009). Stressful life events may help bring on manic and depressive episodes in people who are predisposed (Ambelas, 1987; Hlastala et al., 2000), but the evidence for such effects is not as strong as it is for unipolar depression. Bipolar disorder, unlike unipolar depression, can usually be controlled with regular doses of the element lithium, used as a drug, but how lithium works is as yet unknown (Pilcher, 2003).

The Manic Condition

Manic episodes are typically characterized by expansive, euphoric feelings; elevated self-esteem; increased talkativeness; decreased need for sleep; and enhanced energy and enthusiasm, which may be focused on one or more grandiose projects or schemes (American Psychiatric Association, 2013). The inordinate feelings of power, confidence, and energy are illustrated by the following quotation from a woman describing her own disorder:

During hypomania and the early stages of a manic episode, the high energy and confidence may lead to an increase in productive work, but, as a manic episode progresses, judgment becomes increasingly poor and behavior increasingly maladaptive. Full-blown mania may be accompanied by bizarre thoughts and dangerous behaviors, such as jumping off a building in the false belief that one can fly; and even hypomania may be accompanied by spending sprees, absence from work, or sexual escapades that the affected person later regrets (Akiskal, 2002). Moreover, not all people with bipolar disorders experience the manic state as euphoric: Some experience it as a time of extraordinary irritability, suspicious-ness, or destructive rage (Carroll, 1991).

Possible Relation of Hypomania to Enhanced Creativity

Ups and downs of a composer Like many highly creative people, composer Robert Schumann suffered from a mood disorder. He attempted suicide twice during bouts of severe depression and eventually died, in 1856, from self-starvation in an asylum. His depression waxed and waned over long cycles, and during two prolonged periods, in 1840 and 1849, he was hypomanic (exhibited moderate mania) (Jamison, 1995). Those were his most productive years by far: He composed 24 musical works in 1840 and 27 in 1849.

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Analyses of biographies and historical documents concerning eminently creative writers, artists, and musicians suggest that a disproportionate percentage of them suffered from a bipolar disorder (Andreasen, 1987; Jamison, 1995). The same studies suggest that those people were most productive during hypomanic phases of their illness—when their mood was elevated, but not to such an extreme as to prevent coherent thought and action. As one example, the composer Robert Schumann—who often suffered from severe depression—produced an extraordinary number of his valued musical works during two episodes of apparent hypomania, one in 1840 and the other in 1849 (Jamison, 1995). As another example, the poet Emily Dickinson wrote much of her best poetry during episodes of apparent hypomania that followed bouts of winter depression (Ramey & Weisberg, 2004).

Such analyses have been criticized on the grounds that the diagnoses of mood disorders and the judgments concerning hypomania were generally made after the fact, on the basis of written material that may not have been fully accurate (Rothenberg, 2001). It is also possible that hypomania in highly creative people is more a result of high creativity than a cause: People who become strongly absorbed in and excited by their work may, as a result, exhibit manic-like behaviors (Ramey & Weisberg, 2004). Still another possibility is that people who suffer from extremes of mood may not, on average, be naturally more creative than others, but may be more drawn to creative activities. Such activities may provide a means for them to deal with or express the unusual feelings and thoughts that accompany their low and high moods.

Further evidence for a correlation between creativity and hypomania—regard-less of causal direction—comes from studies of creativity in people who are not famous for their creative accomplishments. In one study, people who manifested moderate mood swings—states of hypomania alternating with moderate levels of depression—were judged to be more creative in their regular work and home life than were those who exhibited greater stability in their moods (Richards et al., 1988). Another study, of 16-year-olds with no diagnosable mood disorders, revealed positive correlations between tendencies to experience hypomania and high scores on tests of creativity and of openness to experience, a personality trait that itself correlates positively with creativity (Furnham et al., 2008). People with bipolar disorder have also been found, on average, to score higher than others on tests of creativity and openness to experience (Nowakowska et al., 2005; Santosa et al., 2007). All in all, the weight of the evidence seems to favor the idea of a link between hypomanic mood states and heightened creativity, but the causal nature of that link has yet to be determined.