You are probably in a mood right now. Maybe you are happy that it is almost time to get a snack or saddened by something you heard from a friend—or you may feel good or bad without having a clue why. As you learned in the Emotion and Motivation chapter, moods are relatively long-lasting, nonspecific emotional states—and nonspecific means we often may have no idea what has caused a mood. Changing moods lend variety to our experiences, like different-coloured lights shining on the stage as we play out our lives. However, for people like Virginia Woolf and others with mood disorders, moods can become so intense that they are pulled or pushed into life-threatening actions. Mood disorders are mental disorders that have mood disturbance as their predominant feature and take two main forms: depression (also called unipolar depression) and bipolar disorder (so named because people go from one end of the emotional pole [extreme depression] to the other [extreme mania]).

Everyone feels sad, pessimistic, and unmotivated from time to time. But for most people these periods are relatively short-lived and mild. Depression is much more than typical sadness. The experience of Mark, a 34-year-old man who visited his primary care physician complaining of chronic fatigue, is fairly typical. During the visit, he mentioned difficulties falling asleep and staying asleep that left him chronically tired, so much so that he feared maybe he had some kind of medical problem. He complained that over the past 6 months, he no longer had the energy to exercise and had gained 4.5 kg. He also lost all interest in going out with his friends or even talking to other people. Nothing he normally enjoyed, even sexual activity, gave him pleasure anymore; he had trouble concentrating and was forgetful, irritable, impatient, and frustrated. Mark’s change in mood and behaviour, and the sense of hopelessness and weariness he felt goes far beyond normal sadness. Instead, depressive disorders are dysfunctional, chronic, and fall outside the range of socially or culturally expected responses.

Major depressive disorder (or unipolar depression), which we refer to here simply as “depression,” is characterized by a severely depressed mood and/or inability to experience pleasure that lasts 2 or more weeks and is accompanied by feelings of worthlessness, lethargy, and sleep and appetite disturbance. In a related condition called dysthymia, the same cognitive and bodily problems as in depression are present, but they are less severe and last longer, persisting for at least 2 years. When both types co-occur, the resulting condition is called double depression, defined as a moderately depressed mood that persists for at least 2 years and is punctuated by periods of major depression.

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Some people experience recurrent depressive episodes in a seasonal pattern, commonly known as seasonal affective disorder (SAD). In most cases, the episodes begin in fall or winter and remit in spring, and this pattern is due to reduced levels of light over the colder seasons (Westrin & Lam, 2007). Nevertheless, recurrent summer depressive episodes have been reported. A winter-related pattern of depression appears to be more prevalent in higher latitudes.

Approximately 1 in 12 Canadians will experience major depression at some point in their lives (Kessler et al., 2012; Public Health Agency of Canada, 2002a). On average, major depression lasts about 12 weeks (Eaton et al., 2008). However, without treatment, approximately 80 percent of individuals will experience at least one recurrence of the disorder (Judd, 1997; Mueller et al., 1999). Compared with people who have a single episode, individuals with recurrent depression have more severe symptoms, higher rates of depression in their families, more suicide attempts, and higher rates of divorce (Merikangas, Wicki, & Angst, 1994).

Similar to anxiety disorders, the rate of depression is much higher in women (22 percent) than in men (14 percent) (Kessler et al., 2012). Socioeconomic standing has been invoked as an explanation for women’s heightened risk: Their incomes are lower than those of men, and poverty could cause depression. Sex differences in hormones are another possibility: Estrogen, androgen, and progesterone influence depression; some women experience postpartum depression (depression following childbirth) due to changing hormone balances. It is also possible that the higher rate of depression in women reflects greater willingness by women to face their depression and seek out help, leading to higher rates of diagnosis (Nolen-Hoeksema, 2008). Women have a tendency to accept, disclose, and ruminate on their negative emotions, whereas men are more likely to deny negative emotions and engage in self-distraction such as work and drinking alcohol.

Heritability estimates for major depression typically range from 33 to 45 percent (Plomin et al., 1997; Wallace, Schnieder, & McGuffin, 2002). However, like most types of mental disorders, heritability rates vary as a function of severity. For example, a relatively large study of twins found that the concordance rates for severe major depression (defined as three or more episodes) were quite high, with a rate of 59 percent for identical twins and 30 percent for fraternal twins (Bertelsen, Harvald, & Hauge, 1977). In contrast, concordance rates for less severe major depression (defined as fewer than three episodes) fell to 33 percent for identical twins and 14 percent for fraternal twins. Heritability rates for dysthymia are low and inconsistent (Plomin et al., 1997). This makes depression about as heritable as complex medical conditions, like type 2 diabetes and asthma.

Beginning in the 1950s, researchers noticed that drugs that increased levels of the neurotransmitters norepinephrine and serotonin could sometimes reduce depression. This observation suggested that depression might be caused by an absolute or relative depletion of these neurotransmitters and sparked a revolution in the pharmacological treatment of depression (Schildkraut, 1965), leading to the development and widespread use of such popular prescription drugs as Prozac and Zoloft, which increase the availability of serotonin in the brain. Further research has shown, however, that reduced levels of these neurotransmitters cannot be the whole story regarding the causes of depression. For example, some studies have found increases in norepinephrine activity among depressed individuals (Thase & Howland, 1995). Moreover, even though the antidepressant medications change neurochemical transmission in less than a day, they typically take at least 2 weeks to relieve depressive symptoms and are not effective in decreasing depressive symptoms in many cases. A biochemical model of depression has yet to be developed that accounts for all the evidence.

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Newer biological models of depression have tried to understand depression using a diathesis–stress framework. For instance, Avshalom Caspi and his colleagues (2003) found that stressful life events are much more likely to lead to depression among those with a certain genetic trait (vulnerability) related to the activity of the neurotransmitter serotonin: a finding showing that nature and nurture interact to influence brain structure, function, and chemistry in depression (see FIGURE 15.2).

Recent research also has begun to tell us what parts of the brain show abnormalities in depression. For instance, some important findings came out of a recent meta-analysis (which is a quantitative synthesis of the results of many individual studies) of 24 brain imaging studies. Results showed that when viewing negative stimuli (words or images), people suffering from depression showed both increased activity in regions of the brain associated with processing emotional information and decreased activity in areas associated with cognitive control (see FIGURE 15.3) (Hamilton et al., 2012). Of course, this is not the whole picture and these findings do not explain all of the symptoms seen in depression, why and when depression comes and goes, or how treatment works. Given that depression does not arise due to a single gene or brain region, but likely from the interactions of different biological systems that each give rise to the different psychological traits seen in depression, it will likely be many years before we fully understand the biological causes of this disorder (Krishnan & Nestler, 2008).

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If optimists see the world through rose-coloured glasses, people who suffer with depression tend to view the world through dark grey lenses. Their negative cognitive style is remarkably consistent and, some argue, begins in childhood with experiences that create a pattern of negative self thoughts (Blatt & Homann, 1992; Gibb, Alloy, & Tierney, 2001). One of the first theorists to emphasize the role of thought in depression, Aaron T. Beck (1967), noted that his depressed patients distorted perceptions of their experiences and embraced dysfunctional attitudes that promoted and maintained negative mood states. His observations led him to develop a cognitive model of depression, which states that biases in how information is attended to, processed, and remembered lead to and maintain depression.

Elaborating on this initial idea, researchers proposed a theory of depression that emphasizes the role of people’s negative inferences about the causes of their experiences (Abramson, Seligman, & Teasdale, 1978). Helplessness theory, which is a part of the cognitive model of depression, maintains that individuals who are prone to depression automatically attribute negative experiences to causes that are internal (i.e., their own fault), stable (i.e., unlikely to change), and global (i.e., widespread). For example, a student at risk for depression might view a bad grade on a mathematics test as a sign of low intelligence (internal) that will never change (stable) and that will lead to failure in all his or her future endeavours (global). In contrast, a student without this tendency might have the opposite response, attributing the grade to something external (poor teaching), unstable (a missed study session), and/or specific (boring subject).

The relationship between one’s perceptions and depression has been further developed and supported over the past several decades. The update to Beck’s cognitive model suggests that due to a combination of a genetic vulnerability and negative early life events, people with depression have developed a negative schema (described in the Development chapter). This negative schema is characterized by biases in

For example, a student at risk for depression who got a bad grade on a test might interpret a well-intentioned comment from the teacher (“Good job on the test”) negatively (“She’s being sarcastic!”); have trouble forgetting about both the test score and the perceived negative comment; and have better memory about this test in the future (“Sure, I did well on my English exam, but don’t forget about that bad math test last month”). The presence of these biases may help to explain the internal, stable, and global attributions seen in depression. In addition, recent research suggests that some of the differences in brain structure and function seen in those with depression can help to explain some of these cognitive biases. For instance, people with depression show abnormalities in parts of the brain involved in attention and memory, especially when presented with negative information (Disner et al., 2011). Although we do not fully understand the causes of depression, pieces of the puzzle are being discovered and put together as you read this.

If depression is distressing and painful, would the opposite extreme be better? Not for Virginia Woolf or for Julie, a 20-year-old second-year American university student. When first seen by a clinician, Julie had gone 5 days without sleep and, like Woolf, was extremely active and expressing bizarre thoughts and ideas. She proclaimed to friends that she did not menstruate because she was “of a third sex, a gender above the two human sexes.” She claimed to be a “superwoman,” capable of avoiding human sexuality and yet still able to give birth. Preoccupied with the politics of global disarmament, she felt that she had switched souls with a Congressman from her state, had tapped into his thoughts and memories, and could save the world from nuclear destruction. She began to campaign for an elected position in the United States government (even though no elections were scheduled at that time). Worried that she would forget some of her thoughts, she had been leaving hundreds of notes about her ideas and activities everywhere, including on the walls and furniture of her dormitory room (Vitkus, 1999).

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In addition to her manic episodes, Julie (like Woolf) had a history of depression. The diagnostic label for this constellation of symptoms is bipolar disorder, a condition characterized by cycles of abnormal, persistent high mood (mania) and low mood (depression). In about two thirds of people with bipolar disorder, manic episodes immediately precede or immediately follow depressive episodes (Whybrow, 1997). The depressive phase of bipolar disorder is often clinically indistinguishable from major depression (Johnson, Cuellar, & Miller, 2009). In the manic phase, which must last at least 1 week to meet DSM requirements, mood can be elevated, expansive, or irritable. Other prominent symptoms include grandiosity, decreased need for sleep, talkativeness, racing thoughts, distractibility, and reckless behaviour (such as compulsive gambling, sexual indiscretions, and unrestrained spending sprees). Psychotic features such as hallucinations (erroneous perceptions) and delusions (erroneous beliefs) may be present, so the disorder can be misdiagnosed as schizophrenia (described in a later section).

Here’s how Kay Redfield Jamison (1995, p. 67) described her own experience with bipolar disorder in An Unquiet Mind: A Memoir of Moods and Madness.

There is a particular kind of pain, elation, loneliness, and terror involved in this kind of madness. When you are high it is tremendous. The ideas and feelings are fast and frequent like shooting stars, and you follow them until you find better and brighter ones.…But, somewhere, this changes. The fast ideas are far too fast, and there are far too many; overwhelming confusion replaces clarity. Memory goes. Humour and absorption on friends’ faces are replaced by fear and concern. Everything previously moving with the grain is now against—you are irritable, angry, frightened, uncontrollable, and enmeshed totally in the blackest caves of the mind. You never knew those caves were there. It will never end, for madness carves its own reality.

The lifetime risk for bipolar disorder is about 1 in 40 and does not differ between men and women (Kessler et al., 2012). Bipolar disorder is typically a recurrent condition, with approximately 90 percent of afflicted people suffering from several episodes over a lifetime (Coryell et al., 1995). About 10 percent of people with bipolar disorder have rapid cycling bipolar disorder, characterized by at least four mood episodes (either manic or depressive) every year, and this form of the disorder is particularly difficult to treat (Post et al., 2008). Rapid cycling is more common in women than in men and is sometimes precipitated by taking certain kinds of antidepressant drugs (Liebenluft, 1996; Whybrow, 1997). Unfortunately, bipolar disorder tends to be persistent. In one study, 24 percent of the participants had relapsed within 6 months of recovery from an episode, and 77 percent had at least one new episode within 4 years of recovery (Coryell et al., 1995).

Some have suggested that people with psychotic and mood (especially bipolar) disorders have higher creativity and intellectual ability (Andreasen, 2011). In bipolar disorder, the suggestion goes, before the mania becomes too pronounced, the energy, grandiosity, and ambition that it supplies may help people achieve great things. In addition to Virginia Woolf, notable individuals thought to have had the disorder include Isaac Newton, Vincent van Gogh, Abraham Lincoln, Ernest Hemingway, Winston Churchill, and Theodore Roosevelt.

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Among the various mental disorders, bipolar disorder has one of the highest rates of heritability, with concordance from 40 to 70 percent for identical twins and 10 percent for fraternal twins (Craddock & Jones, 1999). Like most other disorders, it is likely that bipolar disorder is polygenic, arising from the interaction of multiple genes that combine to create the symptoms observed in those with this disorder; however, these have been difficult to identify. Adding to the complexity, there also is evidence of pleiotropic effects, in which one gene influences one’s susceptibility to multiple disorders. For instance, one recent study revealed a shared genetic vulnerability for bipolar disorder and schizophrenia. The genes linked to both disorders are associated with compromised abilities both in filtering unnecessary information and recognition memory, as well as problems with dopamine and serotonin transmission—factors present in both types of disorders (Huang et al., 2010). A follow-up study examining more than 60 000 people revealed that common genetic risk factors are associated with bipolar disorder and schizophrenia, as well as major depression, autism spectrum disorder, and attention-deficit/hyperactivity disorder. These disorders share overlapping symptoms such as problems with mood regulation, cognitive impairments, and social withdrawal (Cross-Disorder Group of the Psychiatric Genomics Consortium, 2013). Findings like these are exciting because they help us begin to understand why we see similar symptoms in people with what we previously thought were unrelated disorders. Although some genetic links have been made, we currently lack an understanding of how different biological factors work together to create the symptoms observed in bipolar and other disorders.

There is growing evidence that the epigenetic changes you learned about in the Neuroscience and Behaviour chapter can help to explain how it is that genetic risk factors influence the development of bipolar and related disorders. Remember how rat pups whose moms spent less time licking and grooming them experienced epigenetic changes (decreased DNA methylation) that led to a poorer stress response? As you might expect, these same kinds of epigenetic effects seem to help explain who develops symptoms of mental disorders and who does not. For instance, studies examining monozygotic twin pairs (identical twins who share 100 percent of their DNA) in which one develops bipolar disorder or schizophrenia and one does not, reveal significant epigenetic differences between the two, with decreased methylation at genetic locations known to be important in brain development and the occurrence of bipolar disorders and schizophrenia (Dempster et al., 2011; Labrie, Pai, & Petronis, 2012).

Stressful life experiences often precede manic and depressive episodes (Johnson, Cuellar, et al., 2008). One study found that severely stressed individuals took an average of 3 times longer to recover from an episode than did individuals not affected by stress (Johnson & Miller, 1997). The stress–disorder relationship is not simple, however: High levels of stress have less impact on people with extraverted personalities than on those with more introverted personalities (Swednsen et al., 1995). Personality characteristics such as neuroticism and conscientiousness have also been found to predict increases in bipolar symptoms over time (Lozano & Johnson, 2001). Finally, people living with family members high on expressed emotion, which in this context is a measure of how much hostility, criticism, and emotional overinvolvement are used when speaking about a family member with a mental disorder, are more likely to relapse than people with supportive families (Miklowitz & Johnson, 2006). This is true not just of those with bipolar disorder: Expressed emotion is associated with higher rates of relapse across a wide range of mental disorders (Hooley, 2007).

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