Abnormal Psych Ch 8 Mood Disorders & Suicide PDF

CHAPTER 8 Mood Disorders and Suicide LEARNING OBJECTIVES 1. Describe the general characteristics of mood disorders. 2. Explain psychological theories of mood disorders. 3. Explain biological theories of mood disorders. 4. Compare and contrast the components and effectiveness of therapies for mood...

CHAPTER 8 Mood Disorders and Suicide LEARNING OBJECTIVES 1. Describe the general characteristics of mood disorders. 2. Explain psychological theories of mood disorders. 3. Explain biological theories of mood disorders. 4. Compare and contrast the components and effectiveness of therapies for mood disorders. s. Describe various perspectives on suicide, suicide prevention efforts, and related ethical issues. Billy, a Student with Major Depressive Disorder BILLY is a 20-year-old white male".... presenting for counselling Beck, Steer, & Brown, 1996). The BDl-11 consists of 21 sets of state- with depressive symptoms, feelings of being 'overwhelmed' with ments representing symptoms of depression and the respond ent anxiety about school performance and value conflicts pertaining indicates which statements apply to them. Billy received a BDl-11 to his choice of major. Billy is a first-generation college student score of 35, which exceeds the cut-off point for severe depres- who was awarded a teaching fellowship to attend the university in sion, and his counsellor confirmed that he met diagnostic criteria recognition of his achievements as a high school student and his for major depressive disorder. His symptoms included depressed interest in becoming a teacher in the rural community in which he mood, significant weight gain, sleep disturbance, loss of energy, was rea red " (Mobley, 2008, p. 87). inappropriate guilt, and a diminished ability to concentrate. Billy was referred for counselling by his family physician, who We will return to Billy in other segments of this chapter. The diagnosed him provisionally with major depressive disorder. His good news is that as a result of the counsellor using a wide range of main symptoms were depressed mood and low self-esteem but no techniques (cognitive-behavioural therapy, Adlerian lifestyle assess- suicide ideation. Billy completed the most well-known self-report ment, and the Gestalt emptychair technique) across 20 sessions, Billy measure of depression, the Beck Depression Inventory- II (BDl-11; was no longer depressed, as reflected by his final BDl-11 score of 5. t........... - · Chapter 8 examines mood disorders. Billy experienced many problems, such as panic attacks, substance abuse, sexual dys- symptoms of major depressive disorder. We begin with a further function, and personality disorders. The presence of other dis- description of depression followed by bipolar disorder and orders can increase severity and result in poorer prognosis chronic mood disorders. We then present research on biological (Government of Canada, 2006). Throughout history, while they and psychological factors relevant to these disorders and dis- may not have been formally diagnosed, many famous artists, com- cuss their treatment. in the final section we examine suicide. posers, and writers, such as Paul Gauguin (see painting) and Pyotr Tchaikovsky (see photo), probably had a mood disorder. s.1 General Characteristics Depression: Signs and Symptoms of Mood Disorders Depression was illustrated by the case of Billy. Depression is an emotional state marked by great sadness and feelings of worth- Mood disorders involve disabling disturbances in emotion, from lessness and guilt. Additional symptoms may include withdrawal the sadness of depression to the elation and irritability of mania. from others and loss of interest and pleasure in usual activities, Mood disorders are often associated with other psychological including a loss of sexual desire. Sleep and appetite may be 201 202 CHAPTER 8 Mood Disorders and Suicide affected in either direction: some people with depression sleep more than usual, others less. Similarly, appetite may increase or decrease, possibly leading to weight gain or weight loss. Most of us experience occasional sadness, although perhaps not to a degree or with a frequency that warrants the diagnosis of depression. Paying attention is exhausting for depressed people. They cannot take in what they read and what other people say to them. Conversation is also a chore; depressed individuals may speak slowly, after long pauses, using few words and a low, monotonous voice. Many prefer to sit alone and remain silent. Others are agi- tated and cannot sit still. They pace, wring their hands, continu- ally sigh and moan, or complain. When depressed individuals are confronted with a problem, no ideas for its solution occur to them. Every moment has a great heaviness, and their heads fill and reverberate with self-recriminations. Depressed people may neglect personal hygiene and appearance and make numerous complaints of somatic symptoms with no apparent physical basis. Utterly dejected and completely without hope and initiative, they may be apprehensive, anxious, and despondent much of the time. The symptoms and signs of depression vary somewhat across the lifespan. Depression in children often results in somatic complaints, such as headaches or stomachaches. In older adults, depression is often characterized by distractibility and complaints of memory loss. Symptoms of depression exhibit some cross- cultural variation, probably resulting from differences in cultural standards of acceptable behaviour. For example, depression is substantially less prevalent in China than in North America, due Self-portrait by Paul Gauguin. He is but one of the many artists and in part to cultu ral mores that make it less appropriate for Chinese writers who apparently suffered from a mood disorder. Self Portrait in people to display emotional symptoms (Parker, Gladstone, & Caricature by Paul Gauguin/National Gallery of Art. Chee, 2001). Although it is commonly believed that people from non-Western cultures emphasize somatic symptoms of depres- sion, while people from Western cultures emphasize emotional symptoms, studies by Montreal researcher Lawrence Kirmayer suggest that people from various cultures, including Canadians, tend to emphasize somatic symptoms rather than the emo- tional symptoms, especially when being evaluated in a medical setting (see Kirmayer, 2001). Overall, only 15% of depressed primary care patients in Canada are what Kirmayer refers to as psychologizers (people who emphasize the psychological aspects of depression). Fortunately, most depression, although recurrent, tends to dissipate with time. But an average untreated episode may stretch for months or longer. In cases where depression becomes chronic, the person does not completely "snap back" to an earlier level of functioning between bouts. Mania: Signs and Symptoms Mania is an emotional state or mood of intense but unfounded elation accompanied by irritability, hyperactivity, talkativeness, flight of ideas, distractibility, and impractical, grandiose plans. Some people who experience episodic periods of depression may at times suddenly become manic. Although there are Mood disorders are common among artists and writers. Van Gogh, clinical reports of individuals who experience mania but not Tchaikovsky (shown here), and Whitman were all affected. depression, this condition is quite rare.  8.1 General Characteristics of Mood Disorders 203 r Mania at the Post Office: A Case Excerpt MR. W., a 32·year-old postal worker, had been married for eight The following bit of conversation from the period after years. In retrospect, there appeared to be no warning of what was Mr. W. entered treatment indicates his incorrigible optimism and to happen. One morning, Mr. W. told his wife that he was bursting provocativeness: with energy and ideas, that his job as a mail carrier was unfulfill- Therapist. Well, you seem pretty happy today. ing, and that he was just wasting his talent. That night he slept lit- Client. Happy! Happy! You certainly are a master of under- tle, spending most of the time at a desk, writing furiously. The next statement, you rogue! [Shouting, literally jumping out of his seat.] morning, he left for work at the usual time but returned home at Why I'm ecstatic. I'm leaving for the West Coast today, on my 11:00 a.m., his car filled to overflowing with aquariums and other daughter's bicycle. Only 3,100 miles. That's nothing, you know. equipment for tropical fish. He had quit his job, then withdrawn all I could probably walk, but I want to get there by next week. And the money from the family's savings account and spent it on tropi- along the way I plan to contact a lot of people about investing in cal fish equipment. Mr. W. reported that the previous night he had my fish equipment. I'll get to know more people that way-you worked out a way to modify existing equipment so that fish " won't die anymore. We'll be millionaires." After unloading the parapher- know, Doc, "know" in the biblical sense [leering at the therapist nalia, Mr. W. set off to canvass the neighbourhood for possible buy- seductively.] Oh, God, how good it feels. It's almost like a non- ers, going door-to-door and talking to anyone who would listen. stop orgasm. The person in the throes of a manic episode, which may Diagnosis of Depression The formal DSM-5 diagno- last from several days to several months, is readily recognized sis of a major depressive disorder (MDD) requires the pres- by his or her loud and incessant stream of remarks, sometimes ence of five of the following symptoms for at least two weeks. full of puns, jokes, rhyming, and interjections about objects Either depressed mood or loss of interest and pleasure must be and happenings that have attracted the speaker's attention. one of the five symptoms: This speech is difficult to interrupt and reveals the manic per- sad, depressed mood, most of the day, nearly every day son's flight of ideas. Although small bits of talk are coherent, the individual shifts rapidly from topic to topic. The need for loss of interest and pleasure in all, or almost all, activities activity may cause him or her to be annoyingly sociable and difficulties in sleeping (insomnia); not falling asleep initially, intrusive, constantly and sometimes purposelessly busy, and, not returning to sleep after awakening in the middle of the unfortunately, oblivious to the obvious pitfalls of his or her night, and early morning awakenings; or, in some individuals, endeavours. Any attempt to curb this momentum can bring a desire to sleep a great deal of the time quick anger and even rage. Mania usually comes on suddenly shift in activity level, becoming either lethargic (psychomotor over a period of a day or two. The following description of a retardation) or agitated. This is known as psychomotor agi- case of mania is from our files. The irritability that is often part tation or retardation of this state was not evident in this person. poor appetite and weight loss, or increased appetite and weight gain Formal Diagnostic Listings of Mood loss of energy, great fatigue nearly every day negative self-concept, self-reproach and self-blame, feelings Disorders of worthlessness, and guilt Two major mood disorders are listed in DSM-5: major depressive complaints or evidence of difficulty in concentrating, such as disorder, referred to earlier as unipolar depression, and bipolar slowed thinking and indecisiveness disorder. As mentioned in Chapter 3, other depressive disorders recurrent thoughts of death or suicide added to the DSM-5 include disruptive mood dysregulation dis- order and premenstrual dysphoric disorder. Here will we focus While the presence or absence of MOD still involves a categor- on major depressive disorder and bipolar disorder. The dropping ical decision, DSM-5 incorporates dimensional ratings of the of the bereavement exclusion in depression was also discussed severity, frequency, and duration of the symptoms. This infor- in Chapter 3. Another change in OSM-5 is that the manual now mation is believed to be useful for both clinical and research has separate chapters for depressive disorders and bipolar and purposes (for a discussion, see Dhingra et al., 2011). related disorders. It is mentioned specifically in the DSM-5 that There is no question that these are the major symptoms the chapter on bipolar and related disorders is located between of depression. What is controversial, though, is whether a per- the chapter on schizophrenia spectrum disorders and the depres- son with five symptoms and a two-week duration is distinctly sive disorders chapter to connote the bipolar disorder's "place as different from one who has only three symptoms for 10 days. In a bridge between the two diagnostic classes in terms of symp- an evaluation of this issue with a sample of twins, the number tomatology, family history, and genetics" (APA, 2013, p. 123). of symptoms and the duration of depression were used to 204 CHAPTER 8 Mood Disorde rs and Su icide as defined by DSM-IV criteria, the lifetime prevalence of major depression exceeds 20% and may be as high as 50%. Noting the broad spectrum of severity, he concluded that, "In commu- nity populations, fulfillment of DSM-IV criteria for MD is prob- ably not an effective proxy for treatment need" (Patten, 2008, p. 411). In other words, not all of these individuals necessarily require intensive treatment! Patten et al. (2015) examined the CCHS 2012 data and found that 3.9% met criteria for MDD in the past year. Of those with past-year MDD, close to two-thirds had sought some form of treatment, and about one-third were tak- ing antidepressant medication. Prevalence was higher in women and in younger age groups. The high prevalence of depression in the general population carries through to celebrities, some of whom have gone public with their illness, such as Canadian singers Serena Ryder (see photo) and Nelly Furtado (see photo). MDD is about two times more common in women than in men (e.g., Kessler et al., 2005; Offord et al., 1996), a gender dif- ference found in numerous countries and in a majority of ethnic groups (Seedat et al., 2009). Clues to the etiology of depression may come from understanding the cause and timing of this Canadian singer and Juno Award winner Serena Ryder described gender difference. Focus on Discovery 8.1 explores some pos- her bouts of depression in a 2012 Chatelaine article. Ryder had sible reasons for this gender difference. to terminate her tour when depression was combined with panic DSM-5 also includes a diagnostic category of persistent attacks. She describes eventually hitting "rock bottom" in terms depressive disorder (combining chronic depression and the of the severity of her depression. Ryder attributes much of her condition formerly known as dysthymia) and there is a sub- depression to an identity crisis and credits her recovery to combined stantial research literature on people with chronic depression. therapy (drug treatment and psychotherapy) as well as meeting the A large Australian study by Murphy and Byrne (2012) found that love of her life. She also refers to music as a form of medicine. In 2016, Ryder became a spokesperson for Bell Canada's Let's Talk campaign the lifetime prevalence of chronic depression lasting at least two to end the stigma surrounding mental health. years was 4.6% (about 1 in 20 people). Predictors of a chronic depressive disorder included comorbid diagnoses, a younger age of onset, and not surprisingly, a history of more frequent predict the likelihood of future episodes and the probability episodes of depression. Walker and Druss (2015) examined pre- that a co-twin would also be diagnosed as depressed. Even dictors of persistent depressive disorder using American data. with fewer than five symptoms and a duration of less than two They found the following predictors: being female, never mar- weeks, co-twins were also likely to be diagnosed with depression ried, two or more medical conditions, limits on activity, and and were likely to have recurrences (Kendler & Gardner, 1998). reduced contact with family. They advocated for comprehensive Other research suggests that depression exists on a con- approaches to treatment, which include physical health, social tinuum of severity (Flett, Vredenburg, & Krames, 1997). The DSM support, and mental health. Kohler et al. (2015) compared treat- diagnostic criteria identify people at a relatively severe end of ment response among in-patients with chronic depression and the continuum. Whether depression is best seen as being on those with episodic depression. Although they found similar a continuum or as a discrete diagnostic category is far from rates of symptom reduction in both groups, those with chronic resolved. One study with children and adolescents concluded depression had higher symptom rates, reduced remission rates, unequivocally that depression is continuous (Hankin, Fraley, and a longer duration of treatment. Again, there appears to be Lakey, & Waldman, 2005), while another conducted with adults a different level of need for this subgroup of patients. Future found some evidence that depression reflects a taxononic, cate- research is recommended to identify this particular subgroup at gorical structure (Solomon, Ruscio, Seeley, & Lewinsohn, 2006). the outset (Gunn et al., 2013). MDD is very prevalent. Lifetime prevalence rates ranged The World Health Organization (WHO, 2004) identified from 5.2% to 17.1% in three large-scale American studies major depression as one of the leading causes of "disability- (Kessler et al., 1994; Kessler et al., 2005; Weissman et al., 1996). adjusted life years." MDD is currently the second-leading cause This large discrepancy possibly reflects differences between of disability worldwide and it is expected to rank first in disease studies in diagnostic criteria used, in the amount of training of burden in high-income countries by the year 2030 (see Cuijpers the interviewers, and in the use of interviews for collecting et al., 2008). Kessler et al. (2006) assessed the effects of mood symptom information. The 12-month prevalence of MDD in disorders on work performance. Although MDD was associated the National Comorbidity Survey-Replication (NCS-R) study with 27.2 lost workdays per ill worker per year, bipolar disorder (Kessler et al., 2005) was 6.7%. In Canada, usingCCHS 2012 data, was associated with 65.5 lost workdays. They attributed the the lifetime prevalence of MDD was 11.3%. In a 2008 review, Scott difference to more severe and persistent depressive episodes Patten, a preeminent Canadian epidemiologist, concluded that in workers with bipolar disorder.  8.1 General ChMacteristics of Mood Disorders 205 Focus on Discovery.1 Depression in Females vs. Males: Why is there important relationships (akin to "suffering in silence"). A defini- tive longitudinal test of the hypot hesis remains to be conducted. a Gender Difference? Another explanation is objectification theory (McKinley & Hyde, "She sat by the window, looking inward rather than 1996), based on the premise that the tendency to be viewed as an looking out. Her thoughts were consumed with her object, scrutinized and appraised by others, including appraisals sadness. She viewed her life as a broken one, and yet of physical appearance, has a greater negative influence on the she cou ld not place her finger on the exact moment it self-esteem of girls than boys. Indeed, adolescent girls, relative to fell apart. 'How did I get to feel this way?' she repeatedly boys, have higher reported levels of objectification, shame, and asked herself. By asking, she hoped to transcend her depression (Grabe, Hyde, & Lindberg, 2007). depressed state; through understanding, she hoped Janet Stoppard from the University of New Brunswick (2000) to repa ir it. Instead her questions led her deeper and argues that depression must be interpreted within the broad deeper inside herself-further away from the path that socio-cultural context and the societal conditions that influence would lead to her recovery." the everyday lives of women, including stressors more germane to women and feelings of disempowerment. A Toronto study found -Reported by Treynor, Gonzalez, ond Nolen·Hoeksema, that 52% of women receiving in-patient treatment for depression 2003, p.247 had been sexually victim ized in childhood and adulthood (Sa hay, Piran, & Maddocks, 2000). Other evidence for the link between A European study confirmed that the gender difference in depres- childhood sexual abuse and various forms of psychopathology, sion was found in all 23 countries that were assessed (Van de Velde, including depression, was reviewed in Chapter 4. Bracke, & Levecque, 2010). The authors concluded that "One of Another possibility advanced by Hammen (1991) is that girls the most consistent findings in the social epidemiology of men· and women are more likely than boys and men to take a more active tal health is the gender gap in depression (p. 305). But why does role in generating stress for themselves. The link between stress major depression generally occur about twice as often in women as generation and depression is considered in Focus on Discovery 8.2. in men? Nolen·Hoeksema and Girgus (1994) traced the sex differ- However, in terms of general life stressors, a comprehensive study ence back to adolescence and concluded that girls are more likely failed to find a gender difference and found that the number of than boys to have certain risk factors for depression even before stressful events predicted first onsets of depression for males and adolescence, but it is only when these risk factors interact with the females (Slopen, Williams, Fitzmaurice, & Gilman, 2011). challenges of adolescence that the gender differences in depres- Finally, what about the possible role of biological differences sion emerge. between women and men? Evidence in support of the theory that Several explanations have been offered. The one referred to women's vulnerability to depression is related to their hormones, above is the notion that females are more llkelythan males to engage in ruminative coping, while males are more likely to engage in specifically estrogen and progesterone, is mixed (Nolen-Hoeksema, distracting activities such as watching a hockey game (Nolen- 2002). Nonetheless, it is probable that gender differences in depression are due to multiple, interacting factors and can best be understood Hoeksema, Larson, & Grayson, 1999). Ruminators focus their atten- from a complex biopsychosocial perspective. tion on their depressive symptoms (e.g., saying things to themselves such as "Why do I feel this way?"). Subsequently, Treynor et al. (2003) refined this theory by differentiating between a more adaptive form of reflective pondering vs. a maladaptive rumination component referred to as brooding (or moody pondering). They concluded that the relationship between gender and depression cou ld be due to the brooding component (e.g., "What am I doing to deserve this?"). Also, an interpersonal form of rumination called co-rumination, in which friends, typically female friends, discuss and brood over each other's problems as part of their friendship, has been linked with depression in adolescent girls but, on a positive note, it also fosters stronger friendships (Starr & Davila, 2009). More recent longitudinal research shows that co-rumination predicts the developmental onset, sever- ity, and duration of depression, even after controlling for ruminative brooding (Stone, Hankin, Gibb, &Abela, 2011). Feminist scholar Dana Jack (1999) suggested that fema les are more likely than males to engage in silencing the self- a passive Canadian singer Nelly Furtado has acknowledged dealing with style of keeping upsets and concerns to oneself in order to maintain depression following her rap id rise to fame. Diagnosis of Bipolar Disorder DSM-5 defines bipolar A formal diagnosis of a manic episode requires the presence l disorder as involving episodes of mania or mixed episodes that of elevated or irritable mood and abnormally and persistently include symptoms of both mania and depression. Most people increased goal-directed activity or energy plus three additional with bipolar I disorder also experience episodes of depression. symptoms (four if the mood is irritable). The inclusion of the 206 CHAPTER 8 Mood Disorders ar'ld Suici de increased activity criterion is new to DSM-5. Some clinicians do not regard euphoria as a core symptom and report that irri- table mood and even depressive features are more common (Goodwin & Jamison, 1990). The symptoms must be sufficiently severe to impair social and occupational functioning: increase in goal-directed activity more talkative than usual or pressure to keep talking flight of ideas or subjective impression that thoughts are racing less than the usual amount of sleep needed inflated self-esteem; belief that one has special talents, powers, and abilities distractibility; attention easily diverted excessive involvement in pleasurable activities that are likely to have undesirable consequences, such as reckless spending Bipolar disorder occurs less often than MDD, with a life- time prevalence rate for both bipolar I and II of about 4.4% of the population in the NCS-R (Kessler et al., 2005). The average age of onset is in the 20s, and it occurs equally often in men and women. Among women, episodes of depression are more common and episodes of mania less common than among men (Leibenluft, 1996). More than 50% of bipolar disorder Academy Award-winning actress Catherine Zeta-Jones publicly cases experience a recurrence within 12 months (Yatham et acknowledged having bipolar disorder Type II {i.e., with slightly al., 2009). The severity of the disorder is indicated by the fact milder symptoms) in 2011 after her husband, Michael Douglas, that at 12 months after release from hospital, 76% of clients are inadvertently revealed his wife's depression during an interview rated as impaired and 52% are sufficiently symptomatic that with Oprah Winfrey. t he original d iagnosis is still applicable (Keck et al., 1998). Vio- lent behaviours (e.g., child or spousal abuse) can occur during severe manic episodes (Government of Canada, 2006). People hallucinations. The presence of delusions appears to be a use- with bipolar disorder often lose insight into their condition ful distinction among people with major depression (Johnson, and this can result in treatment resistance, financial and legal Horvath, & Weissman, 1991); depressed people with delusions difficulties, substance abuse, and marital and occupational do not generally respond well to the usual drug therapies for failure (Government of Canada, 2006). Anxiety comorbidity is depression, but they do respond favourably to these drugs prevalent among bipolar individuals and has a great impact on when they are combined with the drugs commonly used to treat quality of life (Kauer-Sant' Anna et al., 2007). Comorbidity with other psychotic disorders, such as schizophrenia. Furthermore, personality disorders also predicts a poor outcome (Bieling, depression with psychoticfeatures is more severe than depres- Green, & Macqueen, 2007). sion without delusions and involves more social impairment and less time between episodes (Coryell et al., 1996). Heterogeneity within the Categories Some people with depression may have melancholic fea- tures. The term "melancholic" refers to a specific pattern of A problem in the classification of mood disorders is their great depressive symptoms. People with melancholic features find heterogeneity; i.e., people with the same diagnosis can vary no pleasure in any activity (anhedonia) and are unable to feel greatly from one another. Some people with bipolar disorder, better even temporarily when something good happens. Their for example, almost every day experience the full range of depressed mood is worse in the morning. They awaken about symptoms of both mania and depression, termed a mixedepi- two hours too early; lose appetite and weight, and are either sode. Others have symptoms of only mania or only depression lethargic or extremely agitated. during a clinical episode. Bipolar II disorder individuals have Both manic and depressive episodes may also occur dur- episodes of major depression accompanied by hypomania ing pregnancy or within four weeks of childbirth; in this case, (hypo comes from the Greek for "under»), a change in behaviour they are noted to have a peripartum onset, more commonly and mood that is less extreme than full-blown mania. This is known as postpartum depression, but the term"peripartum the kind of bipolar disorder experienced by actress Catherine depression" reflects the reality that about half of depressive Zeta-Jones (see photo). episodes actually start in pregnancy, rather than after child- Some people with depression may be diagnosed as hav- birth. Postpartum, perinatal, and prenatal depression research ing psychotic features if they are subject to delusions and in Canada is summarized in Canadian Perspectives 8.1.  8.1 Gcncrnl Char Depression helplessness --..,, I events 2. Attributional Reformulation Aversive events Attribution to 1 global and Sense of helpless- I ness; no response Depression I -.r stable factors - - / available to alter the situation --,/ L 3. Learned Hopelessness Aversive Attribution tol fSense ofhopeless-1 events global and I no response l'- stable factors; available to alter or other - - / the situation and an 1/ cognitive expectation that factor desirable outcomes will not occur m:mam The three helplessness theories of depression. could be avoided, these dogs did not acquire the avoidance depressed people hold themselves responsible fortheir failures. response as efficiently and effectively as did control animals If they see themselves as helpless, how can they blame them- that had not experienced the inescapable shocks. Rather, most selves? This characteristic of feeling helpless yet blaming oneself of them lay down in a corner and whined. Seligman (1975) is referred to as the depressive paradox. proposed that animals acquire a sense of helplessness when The essence of the revised theory is the concept of attri- confronted with uncontrollable aversive stimulation. Later, this bution-the explanation a person has for his or her behaviour sense of helplessness impairs their performance in stressful (Weiner et al., 1971). When a person has experienced failure, he situations that can be controlled. They appear to lose the ability or she will try to attribute the failure to some cause. Table 8.1 and motivation to learn to respond in an effective way to painful applies the Abramson, Seligman, and Teasdale formulation to stimuli. various ways in which a university student might attribute a low Seligman concluded that learned helplessness in ani- score on the mathematics portion of the Graduate Record Exam- mals could provide a model for at least certain forms of ination (GRE}. The formulation is based on answers to three human depression. Like many depressed people, the animals questions: appeared passive in the face of stress, failing to initiate actions that might allow them to cope. They had difficulty eating or 1. Are the reasons for failure believed to be internal (personal) retaining what they ate, and they lost weight. Further, one of or external (environmentally caused}? the neurotransmitter chemicals implicated in depression, nor- 2. Is the problem believed to be stable or unstable? epinephrine, was depleted in Seligman's animals. 3. How global or specific is the inability to succeed perceived In his classic book Helplessness, Seligman (1975) further to be? elaborated on the implications of helplessness for humans. He also documented cases in which profound states of helplessness The attributional revision of the helplessness theory postulates actually resulted in deaths as if the person had lost the will to live. that the way in which a person cognitively explains failure will determine its subsequent effects: Attribution and learned helplessness Aftertheoriginal Global attributions ("I never do anything right"} increase the research with animals, investigators conducted similar studies generality of the effects of failure. with humans. By 1978, several inadequacies of the theory and unexplained aspects of depression had become apparent, and a Attributions to stable factors ("I never test well"} make them revised learned helplessness model was proposed by Abramson, longterm. Seligman, and Teasdale (1978). Some studies with humans, for Attributions to internal characteristics ("I am stupid"} are example, had indicated th at helplessness inductions sometimes more likely to diminish self-esteem, particularly if the per- led to subsequent improvement of performance. Also, many sonal fault is also global and persistent.  8.2 ?sychological Theories of Mood Disorders 215 TABLE 8.1 Attributional Schema of Depression: Why I Failed My GRE Math Exam Internal (Personal) External (Environmental) Degree Stable Unstable Stable Unstable Global I am stupid. I am exhausted. These tests are all unfair. It's an unlucky day, Friday the 13th. Specific I lack mathematical ability. I am fed up with math. The math tests are unfair. My math test was numbered "13." The theory suggests that people become depressed when in feelings of hopelessness. A similar study conducted with they attribute negative life events to stable and global causes. children in the sixth and seventh grades yielded almost identi- Whether self-esteem also collapses depends on whether they cal results (Robinson, Garber, & Hillsman, 1995). Lewinsohn and blame the bad outcome on their own inadequacies. The indi- his colleagues (1994) also found that depressive attributional vidual prone to depression is thought to show a depressive style and low self-esteem predicted the onset of depression in attributional style-a tendency to attribute bad outcomes to adolescents. Alloy and Abramson and their colleagues (lacov- personal, global, and stable faults of character. When people iello et al., 2006) conducted a prospective study to examine the with this style (a diathesis) have unhappy, adverse experiences course of depression in people at high and low cognitive risk for (stressors), they become depressed (Peterson & Seligman, depression. They found that those high in negative cognitive 1984). styles experienced more episodes of depression, more severe Where does the depressive attributional style come from? episodes, and more chronic courses. In Chapter 2, we noted that the failure to answer such a central One advantage of the hopelessness theory is that it can question is a problem with most cognitive theories of psychopa- deal directly with the comorbidity of depression and anxiety thology. In general terms, the answer is thought to lie in childhood disorders. Alloy and her colleagues (2006) proposed that an experiences (a common theme in many psychological theo- expectation of helplessness creates anxiety. When the expec- ries), but few data have been collected to support this view. A tation of helplessness becomes certain, a syndrome with promising start is the findingthat depressive attributional style elements of anxiety and depression emerges. Finally, if the per- is related to sexual abuse in childhood, parental overprotec- ceived probability of the future occurrence of negative events tiveness, and harsh discipline (Rose et al., 1994). becomes certain (a phenomenon known as depressive predic- tive certainty), hopelessness depression develops. In a review Hooele...,.. · theory The next version of this theory paper, Liu, Kleiman, Nestor, and Cheek (2015) highlighted the (Abramson, Metalsky, & Alloy, 1989) moved even farther away need for greater conceptual clarity between the hopelessness from the original formulation. Some forms of depression (hope- theory and the earlier revised learned helplessness model. lessness depressions) are now regarded as caused by a state of hopelessness, an expectation that desirable outcomes will not occur or that undesirable ones will occur and that the person Interpersonal Theory of Depression has no responses available to change this situation. (The latter part of the definition of hopelessness, of course, refers to help- ln this section, we discuss behavioural aspects of depression lessness, the central concept of earlier versions of the theory.) that generally involve relationships between the depressed As in the attributional reformulation, negative life events inter- person and others. act with diatheses to yield a state of hopelessness. One diathe- Depressed individuals tend to have sparse social networks sis is the attributional pattern already described-attributing and to regard them as providing little support. Reduced social negative events to stable and global factors. However, the the- support may lessen an individual's ability to handle negative ory now considers two other diatheses: low self-esteem and a life events and increase vulnerability to depression (Billings, tendency to infer that negative life events will have severe neg- Cronkite, & Moos, 1983). Depressed people also elicit negative ative consequences. reactions from others, including rejection (Coyne, 1976). For Metalsky and his colleagues (1993) conducted the first test example, the roommates of depressed students rated social of the hopelessness theory in a prospective study that exam- contacts with them as low in enjoyment and reported high ined how students differing in attributional style responded to levels of aggression toward them; mildly depressed students success vs. failure on a class test. Two new features were the were likely to be rejected by their roommates (Joiner, Alfano, & direct measurement of hopelessness and one of the newly Metalsky, 1992). Bieling and Alden (2001) discovered that one proposed diatheses, low self-esteem. As in the earlier study, reason why depressed people may elicit negative reactions attributing poor grades to global and stable factors led to from others is that they tend to reject their partners and dis- more persistent depressed mood. This pattern supported the play relatively few positive social behaviours. This tendency hopelessness theory, for it was found only among students was especially evident among people high in autonomy, as whose self-esteem was low and was mediated by an increase described by Beck. It seems that depressed individuals with 216 CHAPTER 8 Mood Disorders and Suicide an autonomous orientation are oriented toward themselves Studies have also demonstrated that depressed people rather than toward other people. When oriented toward others, are low in social skills across a variety of measures: inter- they can act in a negative, rejecting manner. Therefore it seems personal problem-solving speech patterns (speaking very that there are other factors at play, not just depressed mood slowly, with silences and hesitations, and more negative that is leading to interpersonal problems. A recent study of ado- self-disclosures), and maintenance of eye contact (e.g., Gotlib lescents found that not all adolescents with depression were & Robinson, 1982). rejected by peers; only those who engaged in conversational Another specific idea examined by researchers is that self-focus, a tendency to redirect conversations to the self constant reassurance seeking is a critical variable in depres- (Schwartz-Mette & Rose, 2016). Those who were depressed but sion (Joiner & Schmidt, 1998). In a longitudinal study, Stewart did not engage in conversational self-focus were not rejected and Harkness (2015) found that excessive reassurance seeking by their friends. was related to partner rejection. Perhaps as a result of being Given the interpersonal problems of depressed people, reared in a cold and rejecting environment (Carnelley, Pietro- it is not surprising that depression and marital discord fre- monaco, & Jaffe, 1994), depressed people seek reassurance quently co-occur and thatthe interactions of depressed people that others truly care, but even when reassured, they are only and their spouses involve mutual hostility (Kowalik & Gotlib, temporarily satisfied. Their negative self-concept causes them 1987). Critical comments by spouses are a significant predic- to doubt the truth of the feedback they have received, and tor of recurrence of depression (Hooley & Teasdale, 1989). In a their constant efforts to be reassured come to irritate others. longitudinal study, marital adjustment and perceived criticism Later, they actually seek out negative feedback, which, in a were assessed during the first year of marriage among 132 sense, validates their negative self-concept. Rejection ulti- married couples (Peterson-Post, Rhoades, Stanley, & Mark- mately occurs because of the depressed person's inconsistent man, 2014). Lower marital adjustment and higher perceived behaviour. Focus on Discovery 8.2 explores the possibility that criticism were both associated with depressive symptoms people become depressed because they generate stress for 10 years later. themselves. Focus on Discovery.2 __ J Stress Generation and Depression adolescent girls but not in boys (Ru dolph et al., 2009). In addition, generation of stress among already depressed girls predicted sub- Constance Hammen (1991) advanced the theory that some people sequent bouts of depression. are more prone to depression because they take an active role in Stress generation may interact with other vulnerability fac- creating or generating the stress for themselves that contributes tors. Research by Harkness and associates at Queen's University to distress and despair. This is a radical notion because it portrays found evidence that higher rates of interpersonal stress generation people as active agents in their own stress. Implicit in this work is predicted depression in a sample of adolescent girls with a history the notion that females are more interpersonally sensitive and may of childhood maltreatment (Harkness, Lumley, & Truss, 2008). This engage in more stress generation. effect was not found among the subset of girls without a history of The concept of stress generation is highly relevant to inter- maltreatment. These data underscore the need to examine stress personal theories because one of the major ways to create stress is generation within the context of other individual difference factors to act in a way that creates interpersona l conflict. Another avenue associated with vulnerability to d epression. is to gravitate toward peers or partners who are volatile or non- Harkness and colleagues (Harkness, Bagby, et al., 201S) have supportive, perhaps even abusive. Stress generation can also result also investigated the role of genetic factors (e.g., serotonin trans- from being so high in the need for reassurance that the constant porter gene polymorphisms) and childhood maltreatment on reassurance seeking alienates other people. stress generation. They found an interaction between history of The measurement of stress generation involves making the maltreatment (maternal emotional maltreatment or sexual mal- distinction between independent events (i.e., not due to oneself) treatment) and genetic factors (specifically having the risks-allele), and dependent events (i.e., stemming from personal choices or leading to higher rates of dependent life events. These same factors actions dependent on the self). Dependent vs. independent events were not predictive of independent life events. Further, these same are assessed via a rigorous contextual interview of life experiences. genetic factors interacted with childhood maltreatment in predict- Thus far, strong empirical findings, often in longitudinal ing symptoms of depression (Harkness, Strauss et al., 2015). research, have supported the role of stress generation in depres- Finally, longitudinal research led by Amanda Uliaszek from sion among adolescents and adu lts. It has been suggested that the University of Toronto has examined whether stress generation stress generation accounts for the gender differences in depression simply keeps stress going (i.e., stress continuation) or creates new that emerge during adolescence. Shih, Eberhart, Hammen, and stress (i.e., stress causation). This work, conducted in collaboration Brennan (2006) found that interpersonal episodic stress that was with Susan Mineka and Constance Hammen and others, found sub- self-generated predicts depression in girls; for boys, chronic stress stantial evidence in favour of stress causation but also found that in general contributed to depression. Another longitudinal inves- stress generation among adolescents is implicated in anxiety as tigation confirmed that stress generation predicted depression in well as in depression (Uliaszek et al., 2012).  8.3 Biological Theories of Mood Disorders 217 Do any interpersonal characteristics of depressed people precede the onset of depression, suggesting a causal relation- s.3 Biological Theories ship? Some research using the high-risk method suggests the answer is yes. For example, low social competence predicted the onset of depression among children (Cole, Martin, Powers, of Mood Disorders & Truglio, 1990) and poor interpersonal problem-solving skills Since biological processes are known to have considerable predicted increases in depression among adolescents (Davila effects on moods, it is not surprising that investigators have et al., 1995). Thus, social skills deficits may be a cause and con- sought biological causes for depression and mania. Further- sequence of depression. Interpersonal behaviour clearly plays more, disturbed biological processes must be part of the causal a major role in depression. chain if a predisposition for a mood disorder can be genetically transmitted, and evidence that a predisposition for a mood dis- order is heritable would provide some support for the view that Psychological Theories of Bipolar the disorder has a biological basis. In the treatment of mood Disorder disorders, the effectiveness of drug therapies that increase the levels of certain neurotransmitters suggests that biological fac- While bipolar disorder has been relatively neglected by psy- tors are important. In this century, there have been tremendous chological theorists and researchers, there is now an increas- advances by researchers in behaviour genetics and cognitive ing focus on psychological aspects of bipolar disorder. As with neuroscience, in part, due to technological changes, such as major depression, life stress seems important in precipitating functional neuroimaging, that have facilitated breakthroughs episodes (e.g., Malkoff-Schwartz et al., 1998). in our understanding of relations among biological, cognitive, Cognitive factors may also play a role. Scott et al. (2000) and experiential factors in the development of depression. We showed that people with bipolar depression have elevated will look at some of the research in the areas of genetics, neu- levels of the dysfunctional attitudes described by Beck, as rochemistry, and the neuroendocrine system. There is also a well as problems in autobiographical memory and the ability growing literature on structural abnormalities of the brains of to generate solutions in a problem-solving task. The manic people with mood disorders. These abnormalities are similar phase of the disorder is seen as a defence against a debHitat- to those found in schizophrenia (see Chapter 11). As noted by ing psychological state. The specific negative state that is being Beck (2008), new research has provided "a preliminary basis for avoided varies from theory to theory; however, many theo- formulating the neurobiological correlates of such psycholog- rists have concluded that the manic state serves a protective ical constructs as cognitive vulnerability, cognitive reactivity, function. Clinical experience with people with manic episodes and cognitive biases" (p. 972). The genetic and neurobiologi- and studies of their personalities when they are in remission cal discoveries also suggest some probable causal pathways to indicate that they appear relatively well-adjusted bet ween depression. episodes. But if mania is a defence, it must be a defence against something, suggesting that the apparently good adjustment between manic episodes may not be an accurate reflection of Genetic Vulnerability their true state. Individuals who experience mania, even when between episodes, have very low self-esteem (Lyon, Startup, & Research on genetic factors in bipolar disorder and MOD has Bentall, 1999). used twin, family, and adoption methods. Bipolar disorder is one One promising theory is the behavioural activation system of the most heritable of disorders. Overall, the concordance rate dysregulation theory (Alloy & Abramson, 2010). This model is for bipolar disorder is as high as 85% (McGuffin et al., 2003). That based on findings such as the association that mania has with is, genes account for possibly 85% of the variance in whether a excessive goal striving and greater cognitive reactivity to success person becomes manic. These data plus the results of adoption experiences (Johnson, 2005). The essence of this model is that at studies (e.g., Wender et al., 1986) support the notion that bipolar the root of mania and bipolar disorder is a hyperresponsiveness disorder has a strong heritable component. However, genetic to reward cues that can be traced back to high behavioural activa- factors do not determine when manic symptoms will occur. tion system (BAS) activation (Alloy & Abramson, 2010). The BAS The risk for mania is apparently also related to a higher risk for is a reward-sensitive system postulated by Gray (1990, 1991) depression (McGuffin et al., 2003). The information available on that mediates goal-directed behaviour (Gray & McNaughton, MOD indicates that genetic factors, although influential, are not 2000). The BAS is believed to react to rewards or the cessation as decisive as they are in bipolar disorder, with heritability of punishments by activating emotions such as hope or hap- estimates approximating 35% (Sullivan, Neale, & Kendler, 2000). piness that encourage approach behaviours (Gray, 1991; Gray, Furthermore, relatives of MOD probands are at somewhat 1990). Mania may reflect extremely high levels of BAS. Research increased risk for MOD; however, this risk is less than the risk suggests that high BAS sensitivity follows the differential expo- among relatives of bipolar probands (Andreasen et al., 1987). sure hypothesis, which is the notion that high BAS individuals Linkage analysis, which focuses on identifying the chro- seek out rewarding stimuli more often in order to experience mosomes involved, has also been applied to mood disorders. stronger affect (Gable, Reis, & Elliot, 2000). In a widely reported study of the Old Order Amish, Egeland and 218 CH APTER 8 Mood Disorders and Sui cide her colleagues (1987) found evidence favouring the hypothe- non-depressed children homozygous for the 5-HTTLPR short sis that bipolar disorder results from a dominant gene on the allele demonstrated greater negative processing on a self- 11th chromosome. However, attempts to replicate the Egeland referential encoding task after a negative mood induction than study as well as other apparently successful linkage studies children with other genotypes. have had mixed success (e.g., Smyth et al., 1996). Research on linkage has broadened to focus on other genes on other chro- mosomes. Muller et al. (2006) from the University of Toronto Neurochemistry, Neuroimaging, and reported that within bipolar disorder, variation in the brain- Mood Disorders derived neurotrophic factor (BDNF) gene appears to predict risk for developing rapid cycling. However, subsequent research, Researchers have sought to understand the role played by across various ethnicities, has been inconsistent regarding neurotransmitters in mood disorders. The most-studied neu- the relationship between BDNF and bipolar disorder (Wang, rotransmitters have been norepinephrine, serotonin, and Li, Gao, & Fang, 2014). Genome-wide association studies are dopamine. The original theory posited that low levels of nor- aimed at identifying the specific genes involved; however, for epinephrine and dopamine led to depression and high levels depression, these studies have generally not yielded significant led to mania. The serotonin theory suggests that serotonin, a findings (i.e., there has been little success in identifying specific neurotransmitter presumed to play a role in the regulation of genes; Ripke et al., 2013). norepinephrine, also produces depression and mania. How- Some people seem to be genetically predisposed to the ever, the weight of the evidence does not completely support onset of MOD when confronted with a series of adverse life the notion that levels of neurotransmitters are critical in the events. The pioneering work by Caspi et al. (2003) suggested mood disorders. that people who possess one or two copies of the short variant of The actions of drugs that were used to treat depression pro- the 5-HTTLPR (serotonin transporter) gene, which is involved vided the clues on which the theories are based. In the 1950s, two in modulating serotonin levels, experienced higher levels of groups of drugs, tricyclics and monoamine oxidase inhibitors, depression and suicidality following a recent stressful event were found effective in relieving depression. Tricyclic drugs (a gene-environment interaction). Wilhelm et al. (2006) also (e.g., imipramine, or Tofranil) are a group of antidepressant reported that the serotonin transporter gene-linked promoter medications so named because their molecular structure is region (5-HTTLPR) is a significant predictor of first major characterized by three fused rings. They prevent some of the depression onset following multiple adverse events. These reuptake of norepinephrine, serotonin, and/ or dopamine by the findings were initially supported by other studies, but more presynaptic neuron after it has fired, leaving more of the neu- recently there have been conflicting results (Smoller, 2016}. rotransmitter in the synapse so that transmission of the next Kaufman et al. (2006) reported that in abused children, depres- nerve impulse is made easier (see Figure 8.3). Monoamine sion severity was predicted in part by an interaction of the oxidase (MAO) inhibitors (e.g., tranylcypromine, or Parnate) 5-HTTPLR (short allele) with the brain-derived neurotrophic are antidepressants that keep the enzyme monoamine oxidase factor (Val/Met) genotype, especially in children receiving low from deactivating neurotransmitters, thus increasing the levels social support (a gene-gene interaction}. of serotonin, norepinephrine, and/or dopamine in the synapse. Many studies that have investigated gene- environment This action produces the same facilitating effect described for interactions in the etiology of MOD have focused on a sin- tricyclics, compensating for the abnormally low levels of these gle candidate gene; however, many genes are known to be neurotransmitters in depressed people. These drug actions involved in the development of MOD, making it polygenic suggest that depression and mania are related to seroto- (Smoller, 2016). As such, Mullins and colleagues (2016) exam- nin, norepinephrine, and dopamine. Newer antidepres- ined the gene-environment interaction for MOD, specifically sant drugs, called e 1 1e serotonin ·eu ke ' nhibitors looking at polygenic risk interacting with stressful life events R s1 (e.g., fluoxetine, or Prozac), act more selectively than or childhood trauma. The polygenic risk score did not inter- older ones, specifically inhibiting the reuptake of serotonin. act with stressful life events, but did interact with a history of Because these drugs are presumed effective in treating MOD, a childhood trauma. Surprisingly the interaction was opposite to stronger link has been apparently shown between low levels of what was expected: lower polygenic risk interacted with more serotonin and depression. severe childhood trauma in predicting MOD status. Childhood It now appears that the explanation of why these drugs trauma is a known significant risk factor for depression and it work is not as straightforward as it first seemed. The thera- may be more strongly related to depression among people with peutic effects of tricyclics and MAO inhibitors do not depend lower genetic risk, although this requires replication. They con- solely on an increase in levels of neurotransmitters. The ear- cluded by emphasizing the importance of examining multiple lier findings were correct- tricyclics and MAO inhibitors do risk factors, both genetic and environmental, to understand the indeed increase levels of norepinephrine, serotonin, and/or complex etiology of MOD, and doing so with larger samples. dopamine when they are first taken-but after several days the Accumulating evidence also suggests that a genetic pre- neurotransmitters return to their earlier levels. This informa- disposition is related to biases in information processing (see tion is crucial because it does not fit with data on how much Beck, 2008). For example, Hayden et al. (2008) found that t ime must pass before antidepressants become effective. Both  8 3 Biological Theories of Mood Disorders 219 (a) Presynaptic neuron majority of neurons that use serotonin are found in the intes- tines and norepinephrine is also an important neurotrans- mitter in the peripheral nervous system. Further, despite the fact that some people showed the expected levels of neuro- transmitters in connection with their depression or mania, the expected high or low metabolites were not found consist- ently. Thus, many people with depression or mania did not have disturbances in absolute levels of neurotransmitters (e.g., Placidi et al., 2001). It would seem, then, that a simple change in the level of Norepinephrine norepinephrine or serotonin or dopamine is not a sufficient or serotonin or serotonin explanation for why people become depressed and/or manic. release re-uptake What is the impact of these findings? Researchers then focused on the postsynaptic effects of antidepressants and developed theories of depression that implicate postsynaptic mecha- nisms. One line of research examined whether antidepressants Postsynaptic neuron alter the chemical messengers that a postsynaptic receptor sends into the postsynaptic neuron (Duman, Heninger, & Nes- tler, 1997}. If receptors are overly sensitive they should respond (b) Presynaptic neuron to very small amounts of a neurotransmitter in the synaptic Researchers have focused primarily on dopamine and ser- otonin in this line of research. For example, drugs that increase dopamine levels have triggered manic behaviour in people with bipolar disorder, suggesting the possibility that dopamine receptors are overly sensitive (Anand et al., 2000}. Delgado et al. (1990) used a special diet to reduce the level of serotonin in depressed people in remission by lower- ing the level of its precursor, tryptophan. They found that 67% of clients experienced a return of their symptoms. A gradual remission followed when clients resumed their normal diet. Another study used this same tryptophan-depletion strategy in normal participants who had either a positive or a negative family history of depression. Again, as predicted by the low- serotonin theory, those with a positive family history experi- enced an increase in depressed mood (Benkelfat et al., 1994). Postsynaptic neuron Beck (2008} reviewed several studies that he interpreted as showing linkages between cognitive vulnerability and genetic O@l;lj;ii (a) When a neuron releases norepinephrine or serotonin vulnerability expressed as a hyperreactive serotonergic system from its endings, a pump-like reuptake mechanism Immediately begins (a neurochemical vulnerability). to recapture some of the neurotransmitter molecules before they are Fakhoury (2015) recently summarized the research on the received by the postsynaptic (receptor) neuron. (b) Tricyclic drugs block this reuptake process, enabling more norepinephrine or serotonin to role of neurotransmitters in depressive disorders: "the mech- reach, and thus fire, the post-synaptic (receptor) neuron. Serotonin anisms underlying their mode of action are still not very well reuptake inhibitors act more selectively on serotonin. Adapted from characterized" (p. 174). Snyder (1996, p. 106). Both structural and functional activation brain-imaging studies have been conducted in research on mood disorders tricyclics and MAO inhibitors take from 7 to 14 days to relieve in an attempt to determine how depression relates to brain depression, but by that time, the neurotransmitter level has activity (see Davidson et al., 2002; Wise et al., 2014 for reviews). already returned to its previous state. The amygdala, hippocampus, prefrontal cortex, and the ante- Another approach to further evaluate the theories rior cingulate are the main brain structures implicated in MOD involved measuring metabolites of these neurotransmitters, and bipolar disorder. For example, many findings have tied the by-products of the breakdown of serotonin, norepineph- amygdala hyperactivity to depression. This hyperactivity in rine, and/or dopamine found in urine, blood serum, and the short 5-HTTLPR variant carriers is related to increased sensi- cerebrospinal fluid. The problem with such measurements tivity to negative stimuli (see Munafo, Brown, & Hariri, 2008). is that they are not direct reflections of levels of neurotrans- Further, Siegle et al. (2007) reported that almost all depressed mitters in the brain; metabolites measured in this way could people have reduced prefrontal function. Beck (2008) suggests reflect neurotransmitters anywhere in the body. Indeed, the that a hyperactive amygdala in combination with hypoactive 220 CHAPTER 8 Mood Disorders and Suicide prefrontal regions is related to diminished cognitive appraisal however, others remain skeptical (e.g., Gold, 2009; Paris, 2009). and depression and represents a neurophysiological correla te Moncrieff (2007b) summarized the skeptics' position as follows: of cognitive bias. Ravindran and Kennedy (2007a) summarized several "If I experience an adverse event, I will feel sad, major neuroimaging studies and among the conclusions were and if this emotion is strong enough, there are that structural imaging studies show that recurrent depres- likely to be associated biochemical changes- but sion and long-duration untreated depression are related to it is the event that has made me sad, not the decreased hippocampal volume and neurocognitive impair- chemical fluctuations. They are best viewed as an ment. However, quantitative meta-analyses of imaging studies accompaniment, or a biological correlation, of the in depression have found considerable heterogeneity in the emotional state." (p.100) results of resting studies and serotonin reuptake inhibitor anti- It will be a task of future research to resolve this issue. depressant treatment (e.g., Fitzgerald et al., 2006). Margaret McKinnon and her colleagues at McMaster University (2009) conducted a meta-analysis of 32 MRI studies of hippocampal The Neuroendocrine System volume in people with MDD. It was concluded that hippocam- pal volume reductions occur among people whose duration of The hypothalamic-pituitary-adrenocortical (HPA) axis may MDD was longer than two years or who had multiple episodes, also play a role in depression (see Figure 9.6 in Chapter 9). The suggesting that the reductions occur affer onset of MDD. limbic area of the brain is closely linked to emotion and also In a major breakthrough study, Jeffrey Meyer and col- affects the hypothalamus. The hypothalamus in turn controls leagues (2006) from the Centre for Addiction and Mental Health various endocrine glands and thus the levels of hormones they attempted to determine whether MAO-A levels in the brain are secrete. Hormones secreted by the hypothalamus also affect elevated during untreated depression. Monoamine oxidase A the pituitary gland and the hormones it produces. Because of (MAO-A) is an enzyme that metabolizes monoamines such as its relevance to the so-called vegetative symptoms of depres- serotonin, norepinephrine, and dopamine. The study com- sion, such as disturbances in appetite and sleep, the HPA axis is pared healthy and depressed people with MDD who had been thought to be overactive in depression. medication-free for at least five months. MAO-A was elevated Various findings support this proposition. Levels of cortisol by almost 35% throughout the brain during major depression. (an adrenocortical hormone) are high in depressed people, Meyer et al. (2006) concluded that "elevated MAO-A density perhaps because of oversecretion of thyrotropin-releasing is the primary monoamine-lowering process during major hormone by the hypothalamus (Garbutt et al., 1994). The excess depression" (p. 1209). Follow-up research in Toronto estab- secretion of cortisol in depressed persons also causes enlarge- lished that elevated MAO-A density is found in postpartum ment of their adrenal glands (Rubin et al., 1995). These high mothers during the period that is typically associated with the levels of cortisol have even led to the development of a biolog- postpartum blues (Sacher et al., 2010). Further, Meyer's team ical test for depression: the dexamethasone suppression test. has confirmed the elevated MAO-A density in a sample of 15 Dexamethasone suppresses cortisol secretion, but when given women with postpartum depression who were compared with dexamethasone during an overnight test, some depressed peo- 21 cont rol participants (Sacher et al., 2011). ple, especially those with delusional depression, do not experi- Results also vary for neuroimaging studies for bipolar dis- ence cortisol suppression (Nelson & Davis, 1997). It is believed order. "Neurobiological mechanisms of bipolar disorder (BD) that the failure of dexamethasone to suppress cortisol reflects are still unclear and subject to debate" (Houenou, Perlini, & overactivity in the HPA axis of clients. The failure to show sup- Brambilla, 2015, p. 117). Houenou and colleagues (2015) outline pression ceases when the depressive episode ends, suggesting several reasons for the inconsistent findings across studies: such failure is a non-specific response to stress. (1) small sample sizes, leading to difficulties replicating results; Gotlib and his colleagues {2008) reported that carriers of (2) different equipment (e.g., MRI scanners) used across stud- the short 5-HTTLPR show elevated cortisol response, cognitive ies; and (3) different patient characteristics (e.g., ages of onset, biases, and amygdala activation during a mood repair proce- suicide attempt status). They suggest using large samples and dure. These and other converging findings led Beck {2008) to focusing on specific characteristics of bipolar disorder, rather suggest the following pathway to depression: stress leads to than the whole disorder. For example, a neuroimaging study distorted appraisal leads to engagement of the HPA axis leads could focus on emotional reactivity, which is a core feature to cortisol leads to depressive symptoms. of bipolar disorder but is also present in other disorders (e.g., Finally, a review of research on the neuropsychology of borderline personality disorder). Emotional reactivity could be depression led the authors to conclude that there is solid evi- assessed dimensionally {i.e., on a scale, rather than as an "all- dence implicating both the right and left hemispheres in the or-none" diagnosis) and a possible correlation with a neuroim- experience of depression {Shena!, Harrison, & Demaree, 2003). aging variable would be examined. However, the depression itself may vary. Right hemisphere dys- Should we assume that any biochemical, structural, or function involves symptoms of indifference or flat affect, while functional irregularities associated with depression mean that left hemisphere dysfunction involves more overt symptoms of they play a causal role? Many experts believe that they do; agitation and sadness.  8.4 Therapies for Mood Disorders 221 Summary of Main Biological Hypotheses TABLE 8.2 About Major Depression and Bipolar Disorder - - - - - - - Genetic diathesis Major depression Genetic diathesis, low serotonin or serotonin-receptor dysfunction, high levels of cortisol. Reactive amygdala Bipolar disorder Genetic diathesis, low serotonin or low norepinephrlne in depressed phase, high norepinephrine in manic phase. Cognitive biases Exaggeration of stressful events All these data lend some support to theories that mood disorders have biological causes. (See Table 8.2 for a summary I of major biological positions.) Does this mean that psycho- '... - - -., Activation of hypothalamic- pituitafy-adrenal axis logical theories are irrelevant or useless? Not in the least. To assert that behavioural disorders have a basis in biological pro- Dominance of limbic cesses is to state the obvious. No psychogenic theorist would activity over deny that behaviour is mediated by some bodily changes. The p111frontal function biological and psychological theories may well be describing the same phenomena, but in different terms (such as learned helplessness vs. low serotonin). They should be thought of as * Deficient reappraisal of negative cognitions complementary, not incompatible. i Depressive symptoms Deconstructing Depression? Beck (2008) interpreted research comparing components of the cognitive model of depression with neurophysiological studies H@ll;IJ:li A developmental model of depression based on and proposed that it is possible to present a "pragmatic formu- anomalous genes Beck, A. T. (2008). The evolution of the cognitive lation of the interaction of the two levels" (p. 974). A summary model of depression and its neurobiological correlates. American of his "deconstructing" of the phenomenon of depression is Journal of Psychiatry, 165, 969-977. Reproduced with permission from The American Journal of Psychiatry. (Copyright 2008) American presented in Figure 8.4. He proposed a hypothetical pathway Psychiatric Association. that begins with a genetic vulnerability (probably the 5-HTTLPR polymorphism), which leads to excessive amygdala reactivity. 'Multiple interactions are not shown. Genetic pathways leading to reduced prefrontal activity have not been determined as yet. Increased Heightened limbic reactivity to stressful events causes deploy- limbic activity overrides prefrontal control. ment of increased attentional resources to these emotional events, which is manifested in negative attentional bias and recall (cognitive reactivity). Selective focus on the "negative" results in cognitive distortions (e.g., overgeneralization) and formation of dysfunctional attitudes (e.g., "I must be perfect"). s.4 Therapies for Mood Frequent occurrences of negative interpretations shape the content of schemas (e.g., worthless). At the same time, the negative interpretations affect the HPA axis and set in motion Disorders a cycle involving the overreactive serotonergic system, which "The burden (of depression) persists because leads to depression. individuals do not seek treatment for their Beck (2008) notes that his formulation is tentative and depression when they relapse and effective subject to further research. There are methodological pit- proactive treatment is not always provided when falls in analyses of gene-environment analyses, including the they do seek it." 5-HTTLPR gene, and some aspects of his cognitive theory are speculative. - Gavin Andrews, 2008, p. 420 Further, the model's biological component undoubtedly involves complex circuits in multiple brain regions (see May- Most episodes of depression lift after a few months, although berg, 2006). A series of multiple wave prospective studies the time may seem immeasurably longer to the depressed starting in early childhood will be necessary to address various individual and to those close to him or her. That most depres- problems and questions and investigate the causal sequence. sions are self-limiting is fortunate. However, depression is too 222 CHAP TER 8 Mood Dis orders a nd Suicid e widespread and too incapacitating, both to the depressed a more contemporary meta-analytic review (Leichsenring, person and to those around him or her, simply to wait for the 2001) concluded that short-term psychodynamic treatment disorder to go away untreated. Bouts of depression tend to and cognitive-behavioural therapy (CBT) are equally effective recur, and suicide is a risk. Thus, it is important to treat MDD, as in alleviating depression, it was acknowledged that this con - well as bipolar disorder. Current therapies are both psychologi- clusion must remain tentative because of the relatively small cal and biological; singly or in combination, they are somewhat number of studies conducted. A more recent "mega-analysis" effective. However, it should be noted that an examination of based on three randomized clinical trials (de Maat et al., 2008) health service delivery in British Columbia determined that in concluded that a short psychodynamic supportive psycho- 2000-01, 92% of people who received a diagnosis of depression therapy was as effective as antidepressants for people with mild were treated by a primary care physician alone; i.e., no psychi- to moderate MDD. Combined therapy was superior to phar- atric services were provided (Bilsker, Goldner, & Jones, 2007). As macotherapy alone. noted by Andrews (2008), many depressed people do not have Findings from a well-known large-scale study (Elkin et al., their disorder identified and are thus not given proactive care. 1989) suggest that a form of psychodynamic therapy that con- However, the clinical course of MDD is highly variable. Patten, centrates on present-day interactions between the depressed Bilsker, and Goldner (2008) argued that a sizeable proportion person and the social environment- Klerman and Weissman's of people who meet criteria for MDD might not require the interpersonal therapy (IPT) (Klerman et al., 1984)-is effective intensive treatment emphasized by current Canadian practice for alleviating unipolar depression, as well as for maintaining guidelines and they eschewed "a one-size-fits-all" approach. treatment gains (Frank et al., 1990). The core of the therapy They suggested that strategies such as watchful waiting, self- is to help depressed people examine the ways in which their guided management, and stepped care (see Chapter 17) could be current interpersonal behaviour might interfere with obtaining included in a spectrum of primary care services for the subset pleasure from relationships. For example, the clients might be of people with mild MOD. taught how to improve communication with others to meet their own needs better and to have more satisfying social inter- actions and support. This psychodynamic therapy is not as Psychological Therapies much intrapsychic as it is interperson al. It emphasizes better understanding of the Interpersonal problems assumed to give "It is probably fair to say that we have a great rise to depress