Chapter 8 Flashcards

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An OVerVIew Of DePreSSIOn AnD MAnIA

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The disorders described in this chapter used to be categorized under several different general labels, such as “depressive disor- ders,” “affective disorders,” or even “depressive neuroses.” Tradi- tionally, these problems have been grouped under the heading mood disorders because they are characterized by severe devia- tions in mood. In DSM-5, these various mood disorders are grouped in two adjacent chapters: depressive disorders, and bipo- lar and related disorders.
The fundamental experiences of depression and mania contrib- ute, either singly or together, to all the mood disorders. We describe each state and discuss its contributions to the various mood disorders. Then we briefly describe the additional defining criteria, features, or symptoms that define the specific disorders.
The most commonly diagnosed and most severe depression is called a major depressive episode. DSM-5 criteria, items A to C listed under major depressive disorder (see DSM Table 8.1), describe it as an extremely depressed mood state that lasts at least two weeks and includes cognitive symptoms (such as feel- ings of worthlessness and indecisiveness) and disturbed physical functions (such as altered sleeping patterns, significant changes in appetite and weight, or a very notable loss of energy) to the point that even the slightest activity or movement requires an overwhelming effort. The episode is typically accompanied by a marked general loss of interest and of the ability to experience any pleasure from life, including interactions with family or friends and accomplishments at work or at school. (The inability to experience pleasure is termed anhedonia.) Although all symp- toms are important, evidence suggests that the most central indi- cators of a full major depressive episode are the physical changes (sometimes called somatic or vegetative symptoms) (Bech, 2009; Buchwald & Rudick-Davis, 1993; Keller et al., 1995; Kessler & Wang, 2009), along with the behavioural and emotional shut- down, as reflected by low behavioural activation (Dimidjian et al., 2011). The average duration of such an episode if untreated is approximately nine months (Eaton et al., 1997; Tollefson, 1993).

The second fundamental state in mood disorders is abnormally exaggerated elation, joy, or euphoria. In mania, individuals find extreme pleasure in every activity; in fact, some patients compare their daily experience of mania with a continuous orgasm. They become extraordinarily active (hyperac- tive), requiring very little sleep, and may develop grandiose plans, believing they can accomplish anything they desire. The DSM-5 highlights this feature by adding “persistently increased goal- directed activity or energy” to the “A” criterion (see DSM Table 8.2; American Psychiatric Association, 2013). Speech is typically very rapid and may become incoherent, because the individual is attempting to express so many exciting ideas at once; this feature is typically
referred to as flight of ideas.
The DSM-5 criteria for a manic
episode require a duration of only one week, less if the episode is severe enough to require hospitalization. Hospitalization could occur, for example, if the individual was engaging in a self-destructive buying spree, charging thousands of dollars in the expectation of making a million dollars the next day. Irritability is often part of a manic episode, usually near the end. Paradoxically, being anxious or depressed is also commonly part of mania, as described later. The average duration of an untreated manic episode is two to six months (Angst, 2009; Solomon et al., 2010).
The DSM-5 also defines a hypomanic episode, a less severe version of a manic episode that does not cause marked impairment in social or occupational functioning and need last only four days rather than a full week. (Hypo means “below”; thus, the episode is below the level of a manic episode.) A hypomanic episode is not in itself necessarily problematic, but it does contribute to the defi- nition of several mood disorders.

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2
Q

The STruCTure Of MOOD DISOrDerS

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Individuals who experience either depression or mania are said to have a unipolar mood disorder, because their mood remains at one “pole” of the depression-mania continuum. Mania by itself (unipolar mania) probably does occur but seems to be rare, because most people with a unipolar mood disorder eventually develop depression. Manic episodes alone may be somewhat more frequent in adolescents, however. Someone who alternates between depression and mania is said to have a bipolar mood disorder, travelling from one pole of the depression–elation continuum to the other and back again. This label is somewhat misleading, however, because depression and elation may not exactly be at opposite ends of the same mood state; in fact, though related, they are often relatively independent. An individual can experience manic symptoms but feel somewhat depressed or anxious at the same time or be depressed with a few symptoms of mania. This episode is characterized as having mixed features. Manic episodes are characterized by dysphoric (anxious or depressive) features more commonly than was thought, and dysphoria can be severe (Cassidy et al., 2008; Swann et al., 2013). In one study, 30 percent of 1090 patients hospitalized for acute mania had mixed episodes (Hantouche et al., 2006). In another carefully constructed study of more than 4000 patients, as many as two-thirds of patients with bipolar depressed episodes also had manic symptoms, most often racing thoughts (flight of ideas), distractibility, and agitation. These patients were also more severely impaired than those without concurrent depression and manic symptoms (Goldberg et al., 2009; Swann et al., 2013). The rare individual who suffers from manic episodes alone can be expected to become depressed later. In general, newer models view bipolar disorder as an evolving condition, proceeding through different at-risk stages with mild symptoms early in the disease progressing to a later chronic disorder (Frank et al., 2015; Kupfer et al., 2015). In the DSM-5, the term “mixed features” requires specifying whether a predominantly manic or predomi- nantly depressive episode is present, and then noting if enough symptoms of the opposite polarity are present to meet the mixed features criteria.
It is important to determine the course or temporal patterning of the depressive or manic episodes. For example, do they tend to recur? If they do, does the patient recover fully for at least two months between episodes (termed “full remission”) or only partially recover retaining some symptoms (“partial remission”)? Do the depressive episodes alternate with manic or hypomanic episodes or not? All these patterns for mood disorders are impor- tant to note, since they contribute to decisions on which diagnosis is appropriate.
The importance of temporal course (patterns of recurrence and remittance) makes the goals of treating mood disorders somewhat different from those for other psychological disorders. Clinicians want to do everything possible to relieve people like Katie of their current depressive episode, but an equally important goal is to prevent future episodes—in other words, to help people like Katie stay well for a longer period.

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3
Q

CliniCal DesCription - DePreSSIVe DISOrDerS

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The most easily recognized mood disorder is major depressive disorder, defined by the presence of depression and the absence of manic, or hypomanic, episodes before or during the episode (see DSM Table 8.1). We now know that an occurrence of just one isolated depressive episode in a lifetime is rare (Angst, 2009; Eaton et al., 2008; Kessler & Wang, 2009).
If two or more major depressive episodes occurred and were separated by at least two months during which the individual was not depressed, the major depressive disorder is noted as being recurrent. Recurrence is very important in predicting the future course of the disorder and in choosing appropriate treatments. Individuals with recurrent major depression usually have a family history of depression, unlike people who experience single episodes. As many as 85 percent of single-episode cases later experience a second episode (Angst, 2009; Eaton et al., 2008; Judd, 2000; Souery et al., 2012), based on follow-ups as long as 23 years (Eaton et al., 2008). In the first year following an episode, the risk of recurrence is 20 percent, but it rises as high as 40 percent in the second year (Boland & Keller, 2009). Because of this finding and others reviewed later, clinical scientists have recently concluded that unipolar depression is often a chronic condition that waxes and wanes over time but seldom disappears (Judd, 2012). The median lifetime number of major depressive episodes is four to seven; in one large sample, 25 percent experi- enced six or more episodes (Angst, 2009; Kessler & Wang, 2009). The median duration of recurrent major depressive episodes is four to five months (Boland & Keller, 2009; Kessler et al., 2003), somewhat shorter than the average length of the first episode.
On the basis of these criteria, how would you diagnose Katie? Katie experienced severely depressed mood, feelings of worth- lessness, difficulty concentrating, recurrent thoughts of death, sleep difficulties, and loss of energy. She clearly met the criteria for major depressive disorder, recurrent. Katie’s depressive episodes were quite severe when they occurred, but she tended to cycle in and out of them.
Persistent depressive disorder (dysthymia) shares many of the symptoms of major depressive disorder but differs in its course. There may be fewer symptoms (as few as two; see DSM Table 8.3) but depression remains relatively unchanged over long periods, sometimes 20 or 30 years or more (Angst, 2009; Cristancho et al., 2012; Klein, 2008; Klein et al., 2000, 2006; Murphy & Byrne, 2012).
Persistent depressive disorder is defined as depressed mood that continues at least two years, during which the patient cannot be symptom free for more than two months at a time even though they may not experience all of the symptoms of a major depres- sive episode. It identifies patients who were formerly diagnosed with dysthymic disorder and other depressive disorders (Rhebergen & Graham, 2014). Persistent depressive disorder differs from a major depressive disorder in the number of symp- toms required, but mostly in the chronicity. It is considered more severe, since patients with persistent depression present with higher rates of comorbidity with other mental disorders, are less responsive to treatment, and show a slower rate of improvement over time. In a 10-year prospective follow-up study, Klein and colleagues (2006) suggest that chronicity (versus nonchronicity) is the most important distinction in diagnosing depression independent of whether the symptom presentation meets criteria for a major depressive disorder (as just noted), because these two groups (chronic and nonchronic) seem different not only in course over time but also in family history and cognitive style. About 20 percent of patients with a major depressive episode report chronicity of this episode for at least two years, thereby meeting criteria for persistent depressive disorder (Klein, 2010).Also, 22 percent of people suffering from persistent depres- sion with fewer symptoms (specified as “with pure dysthymic syndrome”) eventually experienced a major depressive episode (Klein et al., 2006). These individuals, who suffer from both major depression episodes and persistent depression with fewer symptoms, are said to have double depression. Typically, a few depressive symptoms develop first, perhaps at an early age, and then one or more major depressive episodes occur later, only to revert to the underlying pattern of depression once the major depressive episode has run its course (Boland & Keller, 2009; Klein et al., 2006; Rubio et al., 2011). Identifying this particu- lar pattern is important because it is associated with higher severity and a problematic future course (Boland & Keller, 2009; Klein et al., 2006). For example, Klein et al. (2006) found that the relapse rate of depression among people meeting criteria for DSM-IV dysthymia was 71 percent. Consider the case of Jack.
Persistent depressive disorder is further specified depending on whether or not a major depressive episode is part of the picture. Thus, one might meet criteria for the disorder “with pure dysthymic syndrome,” meaning one has not met criteria for a major depressive episode in at least the preceding two years, “with persistent major depressive episode,” indicating the pres- ence of a major depressive episode over at least a two-year period, or “with intermittent major depressive episodes,” which is the double depression that Jack suffered from. In these cases, it is important to note whether or not the patient is currently in a major depressive episode. For both major depressive disorder and persistent depressive disorder, a depiction of the various course configurations of depression can be seen in ■ Figure 8.1.

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4
Q

Additional Defining Criteria for Depressive Disorders

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Look again at DSM Table 8.1 on the diagnostic criteria for major depressive disorder; notice the section at the bottom that asks the clinician to specify the features of the latest depressive episode. These instructions are here because these symptoms, or specifiers, may or may not accompany a depressive disorder; when they do, they are often helpful in determining the most effective treatment or likely course.
In addition to rating the severity of the episode as mild, moder- ate, or severe, clinicians use eight basic specifiers to describe depressive disorders. These are (1) with psychotic features (mood- congruent or mood-incongruent), (2) with anxious distress (mild to severe), (3) with mixed features, (4) with melancholic features, (5) with atypical features, (6) with catatonic features, (7) with peripartum onset, and (8) with seasonal pattern. Some of these specifiers apply only to major depressive disorder. Others apply to both major depressive disorder and persistent depressive disor- der. Three are described briefly below.
Psychotic features specifiers. Some individuals in the midst of a major depressive (or manic) episode may experience psychotic symptoms, specifically hallucinations (seeing or hearing things that aren’t there) and delusions (strongly held but inaccurate beliefs) (Rothschild, 2013). Patients may also have somatic (physical) delusions, believing, for example, that their bodies are rotting internally and deteriorating into nothingness. Some may hear voices telling them how evil and sinful they are (auditory hallucinations). Such hallucinations and delusions are called mood congruent, because they seem directly related to the depres- sion. On rare occasions, depressed individuals might have other types of hallucinations or delusions such as delusions of grandeur (believing, for example, they are supernatural or supremely gifted) that do not seem consistent with the depressed mood. This is a mood-incongruent hallucination or delusion. Although quite rare, this condition signifies a serious type of depressive episode that may progress to schizophrenia (or may be a symptom of schizophrenia to begin with). Delusions of grandeur accompany- ing a manic episode are mood congruent. Conditions in which psychotic symptoms accompany depressive episodes are rela- tively rare, occurring in 5 to 20 percent of identified cases of depression (Flores & Schatzberg, 2006; Ohayon & Schatzberg, 2002). Psychotic features in general are associated with a poor response to treatment, greater impairment, and fewer weeks with minimal symptoms, compared with nonpsychotic depressed patients over a 10-year period (Busatto, 2013; Flint et al., 2006).
Peripartum onset specifier. Peri means “surrounding”—in this case, the period of time just before and just after giving birth. This specifier can apply to both major depressive and manic episodes. Between 13 and 19 percent of all women giving birth (one in eight) meet criteria for a diagnosis of depression, referred to as peripartum depression. In one study, 7 percent met criteria for a full major depressive episode (Gavin et al., 2005). Typically, a somewhat higher incidence of depression is found postpartum (after the birth) than during pregnancy itself (Viguera et al.,
2011). In another recent important study, 14 percent of 10000 women who gave birth screened positively for depression and fully 19 percent of those depressed new mothers had serious thoughts of harming themselves (Wisner et al., 2013). During the peripartum period (pregnancy and the six-month period immedi- ately following childbirth), early recognition of possible psychotic depressive (or manic) episodes is important, because in a few tragic cases a mother in the midst of an episode has killed her newborn child (Purdy & Frank, 1993; Sit et al., 2006). Fathers don’t entirely escape the emotional consequences of birth. Ramchandani and colleagues (2005) followed 11833 mothers and 8431 fathers for eight weeks after the birth of their child. Of the mothers, 10 percent showed a marked increase in depressive symptoms on a rating scale, but so did 4 percent of the fathers. If you extend the period from the first trimester to one year after birth, the rate of depression is approximately 10 percent for fathers and as high as 40 percent for mothers. And depression in fathers was associated with adverse emotional and behavioural outcomes in children 3.5 years later (Paulson & Bazemore, 2010).
More minor reactions in adjustment to childbirth—called the “baby blues”—typically last a few days and occur in 40 to 80 percent of women between one and five days after delivery. During this period, new mothers may be tearful and have some temporary mood swings, but these are normal responses to the stresses of childbirth and disappear quickly; the peripartum onset specifier does not apply to them (O’Hara & McCabe, 2013; Wisner et al., 2010). However, in peripartum depression, most people, including the new mother herself, have difficulty under- standing why she is depressed, because they assume this is a joyous time. Many people forget that extreme stress can be brought on by physical exhaustion, new schedules, adjustment to nursing, sleep deprivation, and other changes that follow the birth. There is also some evidence that women with a history of peripartum depression meeting full criteria for an episode of major depression may be affected differently by the rapid decline in reproductive hormones that occurs after delivery (Wisner et al., 2002; Workman et al., 2012) or may have elevated corticotrophin- releasing hormone in the placenta (Meltzer-Brody et al., 2011; Yim et al., 2009) and that these factors may contribute to peripar- tum depression. But these findings need replication, because all women experience very substantial shifts in hormone levels after delivery, but only some develop a depressive disorder. Nor is there strong evidence that hormonal levels are significantly different in peripartum depressed and nondepressed women (Workman et al., 2012). A close examination of women with peripartum depression revealed no essential differences between the characteristics of this mood disorder and others (O’Hara & McCabe, 2013; Wisner et al., 2002). Therefore, peripartum depression did not require a separate category in the DSM-5 and is simply a specifier for a depressive disorder. (Approaches to treatment for peripartum depression do not differ from those for non-peripartum depression.)
Seasonal pattern specifier. This temporal specifier applies to recurrent major depressive disorder (and also to bipolar disor- ders). It accompanies episodes that occur during certain seasons (e.g., winter depression). The most usual pattern is a depressive episode that begins in the late fall and ends with the beginning of spring. (In bipolar disorder, individuals may become depressed during the winter and manic during the summer.) These episodes must have occurred for at least two years with no evidence of nonseasonal major depressive episodes occurring during that period of time. This condition is called seasonal affective disorder (SAD).
Although some studies have reported seasonal cycling of manic episodes, the overwhelming majority of seasonal mood disorders involve winter depression, which has been estimated to affect as many as 3 percent of North Americans (Lam et al., 2006; Levitt & Boyle, 2002). But fully 15 to 25 percent of the popula- tion might have some vulnerability to seasonal cycling of mood that does not reach criteria for a disorder (Kessler & Wang, 2009; Sohn & Lam, 2005). Unlike more severe melancholic types of depression, people with winter depressions tend toward excessive sleep (rather than decreased sleep) and increased appetite and weight gain (rather than decreased appetite and weight loss), symptoms shared with atypical depressive episodes. Although SAD seems a bit different from other major depressive episodes, family studies have not yet revealed any significant differences that would suggest winter depressions are a separate type (Lam & Lavitan, 2000).

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5
Q

onset anD Duration - depressive disorders

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The mean age of onset for major depressive disorder is 25 years in community samples who are not in treatment (Burke et al., 1990) and 29 years for patients who are in treatment (Judd et al., 1998a), but the average age of onset seems to be decreasing (Kessler et al., 2003; Weissman et al., 1991). In fact, the preva- lence of major depression increases dramatically during the adolescent years (e.g., Offord et al., 1987), particularly in adoles- cent girls (Georgiades et al., 2006; see also review in Santor & Kusumakar, 2001). In 1989, a survey of people in five different American cities (Klerman & Weissman, 1989; Wickramaratne et al., 1989) revealed a greatly increased risk of developing depression in younger people. Among those born before 1905, only 1 percent had developed depression by age 75; of those born since 1955, 6 percent had become depressed by age 24. A later study based on very similar surveys conducted in Canada, Puerto Rico, Italy, Germany, France, Taiwan, Lebanon, and New Zealand suggests that this trend toward developing depression at increas- ingly earlier ages is occurring worldwide (Cross-National Collaborative Group, 1992).

As we noted previously, the length of depressive episodes is variable, with some lasting as little as two weeks; in more severe cases, an episode might last for several years, with the average duration of the first episode being two to nine months if untreated (Angst, 2009; Boland & Keller, 2009). Although nine months is a long time to suffer with a severe depressive episode, evidence indicates that even in the most severe cases, the probability of remission of the episode within one year approaches 90 percent (Kessler & Wang, 2009). In those severe cases in which the episode lasts five years or longer, 38 percent can be expected to eventually recover (Mueller et al., 1996). Occasionally, however, episodes may not entirely clear up, leaving some residual symp- toms. In this case, the likelihood of a subsequent episode with another incomplete recovery is much higher (Boland & Keller, 2009; Judd, 2012). Awareness of this increased likelihood is important to treatment planning, because treatment should be continued much longer in these cases.
Investigators have found a lower (0.07 percent) prevalence of persistent mild depressive symptoms in children compared with adults (3 to 6 percent) (Klein et al., 2000), but symptoms tend to be stable throughout childhood (Garber, Gallerani, & Frankel, 2009). Kovacs, Akiskal, Gatsonis, and Parrone (1994) found that 76 percent of a sample of children with persistent mild depressive symptoms later developed major depressive disorder.
Persistent depressive disorder may last 20 to 30 years or more, although a preliminary study reported a median duration of approximately five years in adults (Klein et al., 2006) and four years in children (Kovacs et al., 1994). Klein and colleagues (2006) conducted a 10-year follow-up of 97 adults with DSM-IV dysthymia and found that 74 percent had recovered at some point, but 71 percent of those had relapsed. The whole sample of 97 patients spent approximately 60 percent of the 10-year follow- up period meeting full criteria for a mood disorder. This compares with 21 percent of a group of patients with major depressive disorder also followed for 10 years. Even worse, patients with persistent depressive disorder with less severe depressive symp- toms (dysthymia) were more likely to attempt suicide than a comparison group with (nonpersistent) episodes of major depres- sive disorder during a five-year period.

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6
Q

From GrieF to Depression

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At the beginning of the chapter, we asked if you had ever felt down or depressed. Almost everyone has. But if someone you love has died—particularly if the death was unexpected and the person was a member of your immediate family—you may, after your initial reaction to the trauma, have experienced a number of depressive symptoms, as well as anxiety, emotional numb- ness, and denial (Kendler et al., 2008; Shear, 2012; Shear et al., 2011; Simon, 2012). Sometimes individuals experience very severe symptoms requiring immediate treatment such as a full major depressive episode, perhaps with psychotic features, suicidal ideation, or severe weight loss and so little energy that the individual cannot function (Maciejewski et al., 2007). We must confront death and process it emotionally. All religions and cultures have rituals, such as funerals and burial ceremonies, to help us work through our losses with the support and love of our relatives and friends. Usually, the natural grieving process resolves within the first several months, although some people grieve for a year or longer (Currier et al., 2008; Maciejew- ski et al., 2007). The acute grief most of us feel eventually evolves into what is called integrated grief, in which the final- ity of death and its consequences are acknowledged and the individual adjusts to the loss. New, bittersweet, but mostly posi- tive memories of the deceased person that are no longer domi- nating or interfering with functioning are then incorporated into memory (Shear et al., 2011).
Integrated grief often recurs at significant anniversaries, such as the birthday of the loved one, holidays, and other meaningful occasions, including the anniversary of the death. This is all a very normal and positive reaction. In fact, mental health profes- sionals are concerned when someone does not grieve after a death, because grieving is our natural way of confronting and handling loss.
When grief lasts beyond the typical time, mental health professionals become concerned (Neimeyer & Currier, 2009). After six months to a year or so, the chance of recovering from severe grief without treatment is considerably reduced and, for approximately 7 percent of bereaved individuals (Kersting et al., 2011; Shear et al., 2011), a normal process becomes a disorder. At this stage, suicidal thoughts increase substantially and focus mostly on joining the beloved deceased (Stroebe et al., 2005).

The ability to imagine events in the future is generally impaired, because it is difficult to think of a future without the deceased (MacCallum & Bryant, 2011; Robinaugh & McNally, 2013). Individuals also have difficulty regulating their own emotions, which tend to become rigid and inflexible (Gupta & Bonanno, 2011). Many of the psychological and social factors related to mood disorders in general, including a history of past depressive episodes, also predict the development of what is called the syndrome of complicated grief, although this reaction can develop without a preexisting depressed state (Bonanno et al., 2004).
A longitudinal study by a group including researchers at the University of British Columbia (Bonanno et al., 2002) showed that pre-loss dependency was predictive of a pathological grief reaction following the loss of a spouse. Particularly prominent symptoms of a pathological grief reaction include intrusive memories and distressingly strong yearnings for the loved one and avoiding people or places that are reminders of the loved one. In cases of complicated grief, the rituals intended to help us face and accept death were ineffective. As with victims who have post-traumatic stress, one therapeutic approach is to help griev- ing individuals re-experience the trauma under close supervision (Shear, 2010). Usually the grieving person is encouraged to talk about the loved one, the death, and the meaning of the loss while experiencing all the associated emotions, until he or she can come to terms with reality. This would include finding some meaning in the traumatic loss, incorporating positive emotions associated with memories of the relationship into the intense negative emotions connected with the loss, and arriving at the position that the person can cope with the pain and life will go on, thereby achieving a state of integrated grief (Bonanno & Kaltman, 1999).
Some researchers have cautioned against treating pathological grief reaction and depression in the same manner. For example, at the University of British Columbia, John Ogrodniczuk and his colleagues (2003) showed that dimensions of pathological grief could be distinguished from dimensions of depression among close to 400 psychiatric outpatients who had experienced one or more significant losses. And it was the grief dimensions that showed the most improvement in group therapy specifically designed to treat pathological grief reaction.

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7
Q

other Depressive DisorDers

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Premenstrual dysphoric disorder (PMDD) and disruptive mood dysregulation disorder, both depressive disorders, were added to the DSM-5.

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8
Q

Premenstrual Dysphoric Disorder (PMDD)

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The history of the development of PMDD over the last several decades as a diagnosis was described in some detail in Chapter 3. Clinicians identified a small group of women, from 2 to 5 percent, who experienced severe and sometimes incapaci- tating emotional reactions during the premenstrual time (Epperson et al., 2012). But strong objections to making this condition an official diagnosis were based on concerns that women who were experiencing a very normal monthly physio- logical cycle, as part of being female, would now be classified as having a disorder, which would be very stigmatizing. It has now been clearly established that this small group of women differs in a number of ways from the 20 to 40 percent of women who experience uncomfortable premenstrual symptoms (PMS) that, nevertheless, are not associated with impairment of functioning. Criteria defining PMDD are presented in DSM Table 8.4. As you can see, a combination of physical symptoms, severe mood swings, and anxiety is associated with incapacitation during this time (Hartlage et al., 2012). All the evidence indicates that PMDD is best considered a disorder of mood as opposed to a physical disorder (such as an endocrine disorder), and, as pointed out in Chapter 3, the creation of this diagnostic category should greatly help the thousands of women coping with this disorder receive the treatment they need to relieve their suffering and improve their functioning.

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9
Q

Disruptive Mood Dysregulation Disorder

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Children and adolescents have been diagnosed with bipolar disorder at greatly increasing rates over the last several years. In fact, from 1995 to 2005 the diagnosis of bipolar disorder in children increased 40-fold overall and has quadrupled in U.S. community hospitals (up to 40 percent) (Leibenluft & Rich, 2008; Moreno et al., 2007). Why the increase? Many clinicians are now using much broader diagnostic criteria that would not correspond to current definitions of bipolar I or bipolar II disor- der but rather fall under the relatively vague category of bipolar disorder not otherwise specified, and include children with chronic irritability, anger, aggression, hyperarousal, and frequent temper tantrums that are not limited to an occasional episode (as might be the case if the child were cycling into a manic episode since irritability sometimes accompanies discrete manic episodes).
But the most important observation is that these children show no evidence of periods of elevated mood (mania), which has been a requirement for a diagnosis of bipolar disorder (Leibenluft, 2011). Additional research demonstrated that these children with chronic and severe irritability and difficulty regulating their emotions resulting in frequent temper tantrums are at increased risk for additional depressive and anxiety disorders rather than manic episodes, and that there is no evidence of excessive rates of bipolar disorder in their families, which would expect if this condition were truly bipolar disorder. It was also recognized that this severe irritability is more common than bipolar disorder but has not been well studied (Brotman et al., 2006). This irritability is associated with substantial suffering in the children them- selves, reflecting as it does chronically high rates of negative affect and marked disruption of family life. Although these broader definitions of symptoms do display some similarities with more classic bipolar disorder symptoms (Biederman et al., 2000, 2005), the danger is that these children are being misdiag- nosed when they might better meet criteria for more classic diagnostic categories, such as attention-deficit/hyperactivity disorder (ADHD) or conduct disorder (see Chapter 15). In that case, the very potent drug treatments for bipolar disorder with substantial side effects would pose more risks for these children than they would benefits. But these cases also differ from more typical conduct or ADHD conditions as well, since it is the intense negative affect that seems to be driving the irritability and marked inability to regulate mood. In view of the distinctive features of this condition reviewed above, it seemed very impor- tant to better describe these children up to 12 years of age as suffering from a diagnosis termed disruptive mood dysregulation disorder rather than have them continue to be mistakenly diag- nosed with bipolar disorder or perhaps conduct disorder (Roy et al., 2014). Criteria for this new disorder are presented in DSM Table 8.5. In one case seen at our clinic, a nine-year-old girl we will call Betsy was brought in by her father for evaluation for severe anxiety. The father described a situation in which Betsy, a very bright child from an upper middle class family who had done well in school, was continually irritable and increasingly unable to get along at home, engaging in intense arguments, particularly with her mother, at the slightest provocation. Her mood would then deteriorate into a full-blown aggressive temper tantrum, and she would run to her room and on occasion begin throwing things. She began refusing to eat meals with the family, since bitter argu- ments would often arise, and it just became easier to allow her to eat in her room. Since nothing else seemed to work to calm her down, her father resorted to something he used to do when she was a baby—take her for a long ride in the family car. After a while Betsy would begin to relax, but during one long ride she turned to her father and said, “Daddy, please help me feel better because if I keep feeling like this I just want to die.”
Adults with a history of disruptive mood dysregulation disorder are at increased risk for developing mood and anxiety disorders, as well as many other adverse health outcomes (Copeland et al., 2014). Therefore, a very important objective for the immediate future will be developing and evaluating both psychological and drug treatments for this difficult condition. For example, it is very possible that new psychological treatments under development for severe emotional dysregulation in children may be useful with this condition (Ehrenreich et al., 2009).

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10
Q

BIPOLAr DISOrDerS
CliniCal DesCription

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The key identifying feature of bipolar disorders is the tendency of manic episodes to alternate with major depressive episodes in an unending roller coaster ride from the peaks of elation to the depths of despair. Beyond that, bipolar disorders are parallel in many ways to depressive disorders. For example, a manic episode might occur only once or repeatedly. Consider the case of Jane.
Jane had bipolar II disorder, in which major depressive episodes alternate with hypomanic episodes rather than full manic episodes (see DSM Table 8.6). As we noted earlier, hypo- manic episodes are less severe. Although she was noticeably “up,” Jane functioned pretty well while in this mood state. The criteria for bipolar I disorder are the same, except the individual experi- ences a full manic episode. As in the criteria set for major depres- sive disorder, for the manic episodes to be considered separate, they must have a symptom-free period of at least two months between them. Otherwise, one episode is seen as a continuation of the last.

The case of Billy illustrates a full manic episode. This indi- vidual was first encountered when he was admitted to a hospital. During manic or hypomanic phases, patients often deny they have a problem, which was characteristic of Billy. Even after spending inordinate amounts of money or making foolish busi- ness decisions, these individuals, particularly if they are in the midst of a full manic episode, are so wrapped up in their enthusiasm and expansive- ness that their behaviour seems perfectly reasonable to them. The high during a manic state is so pleasurable, people may stop taking their medication during periods of distress or discouragement in an attempt to bring on a manic state once again; this is a serious challenge to professionals.

A milder but more chronic version of bipolar disorder is called cyclothymic disorder (Akiskal, 2009; Parker et al., 2012). Cyclothymic disorder is a chronic alternation of mood elevation and depression that does not reach the severity of manic or major depressive episodes (see DSM Table 8.7).
- individuals tend to be in one mood state or the other for many years with relatively few periods of neutral (or euthymic) mood. This pattern must last for at least two years (one year for children and adolescents) to
meet criteria for the disorder. Individuals with cyclothymic disorder alternate between the kinds of mild depressive symp- toms Jack experienced during his dysthymic states and the sorts of hypomanic episodes Jane experienced. In neither case was the behaviour severe enough to require hospitalization or immediate intervention. Much of the time, such individuals are just considered moody. However, the chronically fluctuating mood states are, by definition, substantial enough to interfere with functioning. Furthermore, people with cyclothymia should be treated because of their increased risk of developing the more severe bipolar I or bipolar II disorder (Akiskal, 2009; Goodwin & Jamison, 2007; Otto & Applebaum, 2011; Parker et al., 2012).

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11
Q

Additional Defining Criteria for Bipolar Disorders

A

For depressive disorders, we discussed additional defining crite- ria that may or may not accompany a mood disorder and noted that it was important to identify these specifiers or symptoms to plan the most effective treatment. All these specifiers apply to bipolar disorders (see DSM Table 8.4). Specifically, the cata- tonic features specifier applies mostly to major depressive episodes although rarely may apply to a manic episode. The psychotic features specifier may apply to manic episodes, during which it is common to have delusions of grandeur. The anxious distress specifier is also present in bipolar disorders, as it is in depressive disorders. New to the DSM-5 is the “mixed features” specifier, which, as in depressive disorders, is meant to
describe the major depressive or manic episode that has some symptoms from the opposite polarity; for example, a depressive episode with some manic symptoms. The seasonal pattern specifier may also apply to bipolar disorders. In the usual presentation, individuals may become depressed during the winter and manic during the summer. Finally, manic episodes may occur surrounding, but mostly after, childbirth in the peri- partum period.

Just as for depression, it is important to determine whether a patient suffering from a manic episode has had episodes of major depression or mania in the past, as well as whether the individual has fully recovered between past episodes. Just as it is important to determine if persistent depressive disorder preceded a major depressive episode, it is also important to determine whether cyclothymia preceded the onset of bipolar disorder. This is because the presence of cyclothymia predicts a decreased chance for a full inter-episode recovery (Akiskal, 2009).

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12
Q

Rapid-Cycling Specifier

A

One specifier is unique to bipolar I and II disorders: rapid-cycling specifier. Some people move quickly in and out of depressive or manic episodes. An individual with bipolar disorder who experi- ences at least four manic or depressive episodes within a year is considered to have a rapid-cycling pattern, which appears to be a severe variety of bipolar disorder that does not respond well to standard treatments (Angst, 2009; Kupka et al., 2005; Schneck et al., 2004, 2008). Coryell and colleagues (2003) demonstrated a higher probability of suicide attempts and more severe episodes of depression in 89 patients with a rapid-cycling pattern compared with a non-rapid-cycling group. Kupka and colleagues (2005) and Nierenberg and colleagues (2010) also found these patients’ symptoms were more severe on a number of measures. Some evidence indicates that alternative drug treatment, such as anti- convulsants and mood stabilizers, rather than antidepressants, may be more effective with this group of patients (Kilzieh & Akiskal, 1999).
Approximately 20 to 50 percent of bipolar patients experience rapid cycling. From 60 to 90 percent are female, a higher rate than in other variations of bipolar disorder (e.g., Altshuler et al., 2010; Coryell et al., 2003; Kupka et al., 2005; Schneck et al., 2004), and this finding is consistent across 10 studies (Kilzieh & Akiskal, 1999). In most cases, rapid cycling tends to increase in frequency over time and can reach severe states in which patients cycle between mania and depression without any break. When this direct transition from one mood state to another happens, it is referred to as rapid switching or rapid mood switching and is a particularly treatment-resistant form of the disorder (MacKinnon et al., 2003; Maj et al., 2002). Interestingly, one precipitant of rapid cycling may be taking antidepressant medication, which is prescribed for some individuals with bipolar disorder, because the frequency of rapid cycling is considerably higher among those taking antidepres- sants compared with those who are not taking them (Schneck et al., 2008). Fortu- nately, rapid cycling does not seem to be permanent, because only 3 to 5 percent of patients continue with rapid cycling across a five-year period (Coryell et al., 1992; Schneck et al., 2008), with 80 percent returning to a non–rapid-cycling pattern within two years (Coryell et al., 2003). There are also cases of ultra-rapid cycle lengths that only last for days to weeks and ultra-ultra-rapid cycling in cases where cycle lengths are less than 24 hours
(Wilk & Hegerl, 2010). In ultra-ultra-rapid cycling, switches into depression occurred at night and switches into mania occurred at daytime, suggesting a link to circadian aspects.

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13
Q

onset anD Duration

A

The average age of onset for bipolar I disorder is 18, and for bipolar II disorder it is 22, although cases of both can begin in childhood (Angst, 2009; Judd et al., 2003; Merikangas & Pato, 2009). This is somewhat younger than the average age of onset for major depres- sive disorder, and bipolar disorders begin more acutely; that is, they develop more suddenly (Angst & Sellaro, 2000; Johnson, Turkheimer, et al., 2009). About one-third of the cases of bipolar disorder begin in adolescence (Taylor & Abrams, 1981), and the onset is often preceded by minor oscillations in mood or mild cyclo- thymic mood swings (Goodwin & Jamison, 2007; Merikangas et al., 2007). Only 10 to 13 percent of bipolar II disorder cases progress to full bipolar I syndrome (Coryell et al., 1995; Depression Guideline Panel, 1993). The distinction between unipolar and bipolar mood disorder also seems well defined because only 5 percent of a large group of 381 patients with unipolar depression experienced a manic episode during a 10-year follow-up period (Coryell et al., 1995), although Angst and Sellaro (2000), in reviewing some older studies, estimated the rate of individuals with depression later experiencing mania at closer to 25 percent. In any case, if these disorders were more closely related, we would expect to see more individuals moving from one to the other.
It is relatively rare for someone to develop bipolar disorder after the age of 40. Once it does appear, the course is chronic; that is, mania and depression alternate indefinitely. Therapy usually involves managing the disorder with ongoing drug regimens that prevent recurrence of episodes. Suicide is an all-too-common consequence of bipolar disorder, usually occurring during depres- sive episodes, as it did in the case of Jane (Angst, 2009; Valtonen et al., 2007). A large Swedish study showed that, on average, people with bipolar disorder died eight to nine years earlier of various medical diseases and suicide than did the general population (Crump et al., 2013). When patients receive treatment early, however, the mortality rate was comparable to that of the general population. Bipolar disorder is associated with a high risk of suicide attempts and suicide death, the latter being associated with male sex and having a first-degree relative who committed suicide (Schaffer et al., 2015). The risk of suicide is not limited to Western countries but occurs in countries around the world (Meri- kangas et al., 2011).
In typical cases, cyclothymia is chronic and lifelong. In about one-third to one-half of patients, cyclothymic mood swings develop into full-blown bipolar disorder (Kochman et al., 2005; Parker et al., 2012). In one sample of cyclothymic patients, 60 percent were female, and the age of onset was often during the teenage years or before, with some data suggesting the most common age of onset to be 12 to 14 years (Goodwin & Jamison, 2007). The disorder is often not recognized, and sufferers are thought to be high-strung, explosive, moody, or hyperactive (Akiskal, 2009; Goodwin & Jamison, 2007). One subtype of cyclothymia is based on the predominance of mild depressive symptoms, one on the predominance of hypomanic symptoms, and another on an equal distribution of both.

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14
Q

PreVALenCe Of MOOD DISOrDerS

A

In the 2017 Canadian Community Health Survey (CCHS), about 2.6 million Canadians, 8.6 percent of the population 12 years of age or older, reported that they have a mood disorder, such as depression, bipolar disorder, mania, or dysthymia (Statistics Canada, 2018). Half of this group reported that they also have been diagnosed with an anxiety disorder.
With regard to depression specifically, the best estimates of the worldwide prevalence suggest that approximately 16 percent of the population experience major depressive disorder over a life- time, and approximately 6 percent have experienced a major depressive disorder in the last year (Hasin et al., 2005; Kessler et al., 2003; Kessler, Chiu, et al., 2005). Two community studies conducted in large urban centres, one in Toronto by De Marco (2000) and a second in Calgary by Patten (2000), show similar one-year prevalence rates for major depression, 10.4 and 11 percent, respectively. However, estimates of the Canadian population based on two cycles of the CCHS (2002 and 2012) were lower, documenting annual prevalence for major depression to be 4.7 and 4.8 percent and estimating the lifetime prevalence at 12.2 and 11.3 percent (Patten et al., 2016; Pearson et al., 2013).
As Roger Bland, a leading psychiatric epidemiologist from the University of Alberta, has pointed out, different research methods may account for the differing rates of prevalence (Bland, 1997). Scott Patten at the University of Calgary concurred (Patten, 2000) but also provided another explanation for different prevalence rates: prevalence rates for depression in Canada appear to be decreasing, suggesting progress in public health efforts toward combating depression in our country (Patten, 2002). Patten’s more recent work with the 2002 and 2012 CCHS found support for an increase in the proportion of Canadians receiving treatment for major depression—however, the evidence did not support a reduction in the annual prevalence rate of major depression as it remained essentially the same, about 5 percent, over the 10-year period (Patten, 2016).
Women are about twice as likely to have mood disorders as men. For example, in the 2012 CCHS, the annual prevalence of major depressive episode for women was 5.8 percent and for men was 3.6 percent (Pearson et al., 2012; see ■ Figure 8.2). In fact, women were more likely to have a major depressive episode than men in all age groups except those 65 years and older. Bipolar disorders are distributed approximately equally across gender (Merikangas & Pato, 2009).

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15
Q

LIfeSPAn DeVeLOPMenTAL InfLuenCeS On MOOD DISOrDerS

A

The prevalence of mood disorders varies with age, and age and development also affect many of the characteristics of mood disorders. We review and highlight these developmental characteristics—first for children and adolescents, and then for older adults.

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16
Q

Mood disorders - in ChilDren anD aDolesCents

A

You might assume that depression requires some experience with life, that an accumulation of negative events or disappointments might create pessimism, which then leads to depression. Like many reasonable assumptions in psychopathology, this one is not uniformly correct. There is some evidence that three-month-old babies can show signs of depression. Infants of depressed mothers display marked depressive behaviours (sad faces, slow movement, lack of responsiveness), even when interacting with a nonde- pressed adult (Garber et al., 2009; Guedeney, 2007). Whether this behaviour or temperament is caused by a genetic tendency inher- ited from the mother, the result of early interaction patterns with a depressed mother or primary caregiver, or a combination is not yet clear.
Most investigators agree that mood disorders are fundamentally similar in children and in adults (Brent & Birmaher, 2009; Garber et al., 2009; Weiss & Garber, 2003). Therefore, no “childhood” mood disorders in the DSM-5 are specific to a developmental stage, with the exception of disruptive mood dysregulation disor- der, which can be diagnosed only up to 12 years of age. This is unlike the anxiety disorders in which a number of conditions occur only early in development. It seems clear, however, that the look of depression changes with age. For example, children under three years of age might manifest depression by their facial expressions, as well as by their eating and sleeping. In the extreme, this could develop into disruptive mood dysregulation disorder. In children between the ages of 9 and 12, many of these features would not occur. Psychologist Ian Gotlib, formerly of the University of West- ern Ontario, has shown that adolescents who are forced to limit their activities because of illness or injury are at high risk for depression (Lewinsohn et al., 1997).
Estimates on the prevalence of mood disorders in children and adolescents vary widely, although more sophisticated studies are beginning to appear. The general conclusion is that depressive disorders occur less frequently in children than in adults but rise dramatically in adolescence, when, if anything, depression is more frequent than in adults (Kashani et al., 1987; Kessler et al., 2012; Petersen et al., 1993; Rohde et al., 2013). In their study of major depressive disorder, Patten and his colleagues found evidence of a decline in annual prevalence rates from adolescence to adulthood. The 2002 and the 2012 cycles of the CCHS targeted Canadians 15 years of age or older and Patten and his colleagues (2006, 2015) found the highest annual prevalence rates occurred in the youngest age group and that there was a tendency for the rates to decline with age. The 2012 CCHS data have also been used to document this decline for annual rates of major depressive episode (Pearson et al., 2013; see ■ Figure 8.2).
Furthermore, some evidence indicates that, in young children, dysthymia is more prevalent than major depressive disorder, but this ratio reverses in adolescence. Like adults, adolescents experi- ence major depressive disorder more frequently than dysthymia (Kashani et al., 1983; Kashani et al., 1987). Major depressive disorder in adolescents is also largely a female disorder (Santor & Kusumakar, 2001), as it is in adults, although this is not true for more mild depression. Only among the adolescents referred to treatment does the gender imbalance exist (Compas et al., 1997), though why more girls reach a more severe state requiring referral to treatment is not clear.
As far as mania is concerned, children under the age of nine seem to present with more irritability and emotional swings as compared with classic manic states, and they are often mistaken as being hyperactive. In addition, their symptoms are more chronic in that they are always present rather than episodic as in adults (Biederman et al., 2000). This presentation seems to continue through adolescence (Faraone et al., 1997), although adolescents may appear more typically manic. Bipolar disorder seems to be rare in childhood, although case studies of children as young as four years of age displaying bipolar symptoms have been reported (Poznanski et al., 1984), and the diagnosis may be mistaken for conduct disorder or ADHD. However, the preva- lence of bipolar disorder rises substantially in adolescence, which is not surprising in that many adults with bipolar disorder report a first onset during the teen years (Keller & Wunder, 1990). “Emotional swing,” or oscillating manic states that are less distinct than in adults, may also be characteristic of children, as are brief or rapid-cycling manic episodes lasting only part of a day (Youngstrom, 2009).
One developmental difference between children and adoles- cents compared with adults concerns patterns of comorbidity. For example, childhood depression (and mania) is often associated with and sometimes misdiagnosed as ADHD or, more often, conduct disorder in which aggression and even destructive behav- iour are common (Fields & Fristad, 2009; Garber et al., 2009). Conduct disorder and depression often co-occur in bipolar disor- der. But, once again, many of these children might now meet the criteria for disruptive mood dysregulation disorder, which would better account for this comorbidity. In any case, successful treat- ment of the underlying depression (or spontaneous recovery) may resolve the associated ADHD or conduct disorder in these patients. Adolescents with bipolar disorder may also become aggressive, impulsive, sexually provocative, and accident prone (Carlson, 1990; Keller & Wunder, 1990).
Whatever the presentation, mood disorders in children and adolescents are very serious because of their likely consequences. In an important prospective study, conducted as part of the Ontario Child Health Study, Fleming, Boyle, and Offord (1993) followed 652 adolescents with either a major depressive disorder or a conduct disorder for four years. These adolescents largely continued to experience serious problems and markedly impaired functioning. Lewinsohn, Rhode, Seeley, Klein, and Gotlib (2000) also followed 274 adolescents with major depressive disorder into adulthood and identified several risk factors for additional depres- sive episodes as adults. Prominent among these were conflicts with parents, being female, and a higher proportion of family members experiencing depressive episodes. Their more recent longitudinal work shows that young adults who had experienced an episode of major depressive disorder in adolescence exhibited a very pervasive pattern of psychosocial impairments in areas such as interpersonal functioning, quality of life, and occupa- tional performance. Reduced life satisfaction in young adulthood was uniquely associated with a history of major depressive disor- der, rather than with a history of other mental disorders, in adoles- cence. These findings underline the seriousness of adolescent depression, in terms of negative consequences continuing into adulthood.

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17
Q

Mood disorders - older adults

A

Only recently have we seriously considered the problem of depression in older adults (Wittchen, 2012). A Canadian study by Dalhousie University researcher Kenneth Rockwood and colleagues estimated that 18 to 20 percent of nursing home residents may experience major depressive episodes (Rockwood et al., 1991; see also Katz et al., 1989), which are likely to be chronic if they appear first after the age of 60 (Rapp et al., 1991). Late-onset depressions are associated with marked sleep difficul- ties, illness anxiety disorders, and agitation. It can be difficult to diagnose depression in seniors because the presentation of mood disorders is often complicated by the presence of medical illnesses or symptoms of dementia (e.g., Blazer, 1989; Small, 1991). That is, seniors who become physically ill or begin to show signs of dementia might become depressed about it, but the signs of depression would be attributed to the illness or dementia and thus missed. Nevertheless, the overall prevalence of major depressive disorder is the same or slightly lower in the older adults as in the general population (Patten et al., 2006; Weissman et al., 1991), perhaps because stressful life events that trigger major depressive episodes decrease with age. But, as noted by Ian Gotlib, milder symptoms that do not meet the criteria for major depressive disorder may be more common among seniors (Gotlib & Nolan, 2000), perhaps because of illness and infirmity (Roberts et al., 1997).
Anxiety disorders frequently accompany depression in seniors (in about a third of cases), particularly generalized anxiety disor- der and panic disorder (Lenze et al., 2000), and when they do, patients are more severely depressed. In the DSM-5, as described earlier, clinicians now must specify the presence and severity of anxiety when diagnosing a mood disorder because of the implica- tions for severity and course of the mood disorder, as well as for treatment. Depression can also contribute to physical disease in seniors (Whooley & Wong, 2013). In fact, being depressed doubles the risk of death in older adults who have suffered a heart attack or stroke (Schulz et al., 2002).
The earlier gender imbalance in depression disappears after the age of 65. In early childhood, boys are more likely to be depressed than girls, but an overwhelming surge of depression in adolescent girls produces an imbalance in the sex ratio (Santor & Kusumakar, 2001) that is maintained until old age, when just as many women are depressed, but increasing numbers of men are also affected (Wallace & O’Hara, 1992). From the perspective of the lifespan, this is the first time since early childhood that the sex ratio for depression is balanced.

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18
Q

Mood disorders - across cultures

A

We noted the strong tendency of anxiety to take very physical or somatic forms in some cultures; instead of talking about fear, panic, or general anxiety, many people describe stomachaches, chest pains or heart distress, and headaches. Much the same tendency exists across cultures for mood disorders (Kim & Lopez, 2014), which is not surprising, given the close relation- ship of anxiety and depression (Kessler & Bromet, 2013). Feelings of weakness or tiredness particularly characterize depression that is accompanied by mental or physical slowing or retardation.
Although somatic symptoms that characterize mood disorders seem roughly equivalent across cultures, it is difficult to compare subjective feelings. The way people think of depression may be influenced by the cultural view of the individual and the role of the individual in society (Kleinman, 2004; Ryder et al., 2008). For example, in societies that focus on the individual instead of the group, it is common to hear statements such as “I feel blue,” or “I am depressed.” In cultures where the individual is tightly integrated into the larger group, however, someone might say, “Our life has lost its meaning,” referring to the group in which the individual resides (Manson & Good, 1993). Despite these influ- ences, it is generally agreed that to study the nature and preva- lence of mood disorders (or any other psychological disorder) in other cultures is first to determine their prevalence by using stan- dardized criteria (Neighbors et al., 1989). The DSM criteria are increasingly used, along with semistructured interviews in which the same questions are asked, with some allowances for different words that might be specific to a culture or subculture.
One such study is the International Consortium of Psychiatric Epidemiology study, which used the same structured interview and diagnostic criteria in ten countries, including Canada (Andrade et al., 2003). The Canadian data were collected by a team led by David Offord of the Chedoke-McMaster Hospital in Hamilton, Ontario. As shown in ■ Figure 8.3, the highest rates of major depressive episode were observed in the U.S. sample (17 percent prevalence), and the lowest in the Japanese sample (3 percent prevalence). Compared with the prevalence rates in the other countries, the rates in the Canadian sample were moder- ate (8 percent prevalence).
As noted by Laurence Kirmayer (Kirmayer et al., 2000; Kirmayer, Simpson, & Cargo, 2003), the appalling social and economic conditions faced by many groups of Indigenous Peoples in North America, as well as their long history of cultural oppression and marginalization, fulfill all the require- ments for chronic major life stress, which is strongly related to the onset of mood disorders, particularly major depressive disorder. Kinzie, Leung, Boehnlein, and Matsunaga (1992) used a structured interview to determine the percentage of adult members of a First Nations reserve who met the criteria for mood disorders. The lifetime prevalence for any mood disorder was 19 percent in men, 37 percent in women, and 28 percent overall, approximately four times as high as in the general popu- lation. Examined by disorder, almost all the increase is accounted for by greatly elevated rates of major depression. A study of mental health services use among the Cree of James Bay, Québec, indicated that depression was the most common psychi- atric illness, occurring in 16 percent of the 242 Cree people who were receiving treatment by nursing or other medical profes- sionals in the region (Lavallee et al., 1991). Similar findings emerged in a study conducted in a Canadian Arctic Inuit community of about 1100 people (Haggarty et al., 2000): This study revealed an estimated rate of past-week depression of 26 percent—a rate that is much higher than that seen in the general population.
More recently, and using data from the CCHS, Statistics Canada (2016a) documented the four-year prevalence rates (2011–2014) of mood disorders (i.e., depression, bipolar disorder, mania, or dysthymia) by Aboriginal identity among Canadians 12 years of age or older. The estimates were higher among the First Nations population living off-reserve (12 percent) and Métis (12.6 percent) than among the non-Aboriginal identity population (7.2 percent). In all groups, the rates for women were higher than for men. It is important to remember that the CCHS excludes persons living on reserves and other settlements in the provinces. The First Nations Regional Health Survey provided estimates for mood disorders among First Nations living on reserve (First Nations Information Governance Centre, 2018a, 2018b). Estimates based on data collected during 2015–2016 were that 7.8 percent of adults and 6.6 percent of First Nations youth had been diagnosed with a mood disorder during this period, lower rates than those found in the First Nations off-reserve population from the CCHS.

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19
Q

Mood disorders - amonG the Creative

A

Is there truth in the enduring belief that “genius is allied with madness”? Several researchers have attempted to find out. The results are surprising. Handel wrote The Messiah in only three weeks, apparently during a manic episode, and Rossini composed The Barber of Seville in only 13 days during a likely period of hypomania (Endler, 1990). Table 8.1 lists a group of famous poets, many of whom won the coveted Pulitzer Prize. All almost certainly had bipolar disorder. Many committed suicide. These eight poets are among the 36 born in the 20th century who are represented in The New Oxford Book of American Verse, a collec- tion reserved for the most distinguished poets. It is certainly striking that about 20 percent of these 36 poets exhibited bipolar disorders, given the population prevalence of slightly less than 1 percent.
Many composers, artists, and writers, whether suspected of mood disorders or not, speak of periods of inspiration when thought processes quicken, moods lift, and new associations are generated. Perhaps something inherent in manic states fosters creativity, and recent studies confirm that creativity is specifically associated with manic episodes and not depressive states
(Soeiro-de-Souza et al., 2011). But, as noted by the late Norman Endler (1990), “It is one thing to have the high degree of energy that exists in a manic state; it is another thing to channel it in a direction that creates new works and accomplishes effective tasks” (p. 19). It is also possible that the genetic vulnerability to mood disorders is independently accompanied by a predisposi- tion to creativity. In other words, the genetic patterns associated with bipolar disorder may also carry the spark of creativity. Yet another possibility is suggested by the work of Ghadirian, Gregoire, and Kosmidis (2001), Montréal researchers who conducted a scientific study into the relationship of bipolar disor- der to creativity. They compared a group of 20 patients with bipolar disorder to a group of 24 patients with other mental health disorders on measures of creativity. While the bipolar patients were not any more creative than the patients with other disorders, the researchers did find that moderately ill patients were signifi- cantly more creative than severely ill patients. These findings suggest that creativity may peak at a stage of the illness where symptoms are moderate but that creativity may actually decline as symptoms become progressively worse. These various possibili- ties are little more than speculations at present, but the study of creativity and leadership, so highly valued in all cultures, may well be enhanced by a deeper understanding of psychological disorders.

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20
Q

CAuSeS Of MOOD DISOrDerS

A

In Chapter 2, we described equifinality as the same end product resulting from possibly different causes. Just as a fever may have many causes, depression may also have a number of causes. For example, a depressive disorder that arises in winter has a different precipitant than a severe depression following a death, even though the episodes might look quite similar. Nevertheless, psychopathologists are identifying biological, psychological, and social factors that seem strongly implicated in the etiology of mood disorders, whatever the precipitating factor. An integrative theory of the etiology of mood disorders considers the interaction of biological, psychological, and social dimensions and also notes the very strong relationship between anxiety and depression.

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21
Q

Familial and Genetic Influences

A

In family studies, we look at the prevalence of a given disorder in the first-degree relatives of an individual known to have the disor- der (the proband). We have found that, despite wide variability, the rate in relatives of probands with mood disorders is consistently about two to three times that in relatives of people who don’t have mood disorders (Klein et al., 2002; Lau & Eley, 2010; Levinson, 2009). Increasing severity, recurrence of major depression, and earlier age of onset in the proband is associated with the highest rates of depression in relatives (Kendler et al., 2007; Klein et al., 2002; Weissman et al., 2005).
The best evidence that genes have something to do with mood disorders comes from twin studies, in which we examine the frequency with which identical twins (with identical genes) have the disorder, compared with fraternal twins, who share only 50 percent of their genes (as do all first-degree relatives). If a genetic contribution exists, the disorder should be present in identical twins to a much greater extent than in fraternal twins. Several twin studies, including those by Randy Katz and colleagues, suggest that the mood disorders are heritable (e.g., Hodgson & McGuffin, 2013; McGuffin et al., 2003). In a large meta-analysis of twin studies, Sullivan et al. (2000) estimated the heritability of depression to be 37 percent. Shared environmental factors have little influence, whereas 63 percent of the variance in depression can be attributed to nonshared environmental factors.
Two reports have appeared suggesting sex differences in genetic vulnerability to depression. Bierut et al. (1999) studied 2662 twin pairs in the Australian twin registry and found the characteristically higher rate of depressive disorders in women. Estimates of heritability in women ranged from 36 to 44 percent, consistent with other studies. But estimates for men were lower and ranged from 18 to 24 percent. These results agree for the most part with an important study of men in North America by Lyons et al. (1998). The authors conclude that environmental events play a larger role in causing depression in men than in women.
Note that bipolar disorder confers an increased risk of devel- oping some mood disorder but not necessarily bipolar disorder. This conclusion supports the notion that bipolar disorder may simply be a more severe variant of mood disorders rather than a fundamentally different disorder. Then again, of identical twins concordant for a mood disorder, 80 percent are also concordant for polarity. This finding suggests that these disorders may be inherited separately and may therefore be separate disorders after all (Nurnberger, 2012; Nurnberger & Gershon, 1992). A twin study drew similar conclusions and noted that most of the genetic variance in vulnerability to bipolar disorder is specific to the bipo- lar syndrome (McGuffin et al., 2003).
McGuffin and colleagues (2003) concluded that both points are partially correct. They found that the genetic contributions to depression in both disorders are the same or similar but that the genetics of mania are distinct from depression. Thus, individuals with bipolar disorder are genetically susceptible to depression and independently genetically susceptible to mania. This hypoth- esis still requires further confirmation.
Although research continues to raise questions about the rela- tive contributions of psychosocial and genetic factors to mood disorders, overwhelming evidence suggests that such disorders are familial and almost certainly reflect at least a small underlying genetic vulnerability, particularly for women. As with other psychological disorders, it seems unlikely that we will find any single dominant gene that is responsible, although occasional reports appear to that effect.
In conclusion, the best estimates of genetic contributions to depression fall in the range of approximately 40 percent for women, but seem to be significantly less for men. Genetic contribu- tions to bipolar disorder seem to be somewhat higher. Behavioural geneticists break down environmental factors into events shared by twins (experiencing the same upbringing in the same house, and perhaps, experiencing the same stressful events) and events that are not shared. What part of our experience causes depression? Wide agreement exists that it is the unique nonshared events, rather than what is shared, that interact with biological vulnerability to cause depression (Bierut et al., 1999; Plomin et al., 1997).

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22
Q

Joint Heritability of Anxiety and Depression

A

Although most studies have looked at specific disorders in isola- tion, a growing trend is to examine the heritability of related groups of disorders. Evidence supports the supposition of a close relationship among depression, anxiety, and panic. For example, data from family studies indicate that the more signs and symp- toms of anxiety and depression a given patient has, the greater the rate of anxiety or depression or both in first-degree relatives and children (e.g., Hammen et al., 1990). In several important reports from a major set of data on more than 2000 female twins, Kendler and his colleagues (Kendler et al., 1987, 1992b, 1995) also found that the same genetic factors contribute to both anxiety and depression. Social and psychological explanations seemed to account for the factors that differentiate anxiety from depression. These findings suggest, once again, that the biological vulnerabil- ity for mood disorders may not be specific to that disorder but may reflect a more general predisposition to anxiety or mood disorders, or, more likely to a basic temperament underlying all emotional disorders, such as neuroticism. The specific form of the disorder would be determined by unique psychological, social, or additional biological factors (Kilpatrick et al., 2007; Rutter, 2010; Slavich & Irwin, 2014).

23
Q

Neurotransmitter Systems

A

Mood disorders have been the subject of more intense neurobio- logical study than almost any other area of psychopathology, with the possible exception of schizophrenia. New findings describing the relationship of specific neurotransmitters to mood disorders appear almost monthly and are punctuated by occasional reports of so-called breakthroughs. In this difficult area, most break- throughs prove to be illusory, but false starts provide us with an ever-deeper understanding of the enormous complexity of the neurobiological underpinnings of mood disorders.
In Chapter 2, we observed that we now know that neurotrans- mitter systems have many subtypes and interact in many complex ways, with one another and with neuromodulators (products of the endocrine system). Research implicates low levels of sero- tonin in the etiology of mood disorders (Berney et al., 2006; Rosa-Neto et al., 2004; Sokolov & Kutcher, 2001) but only in relation to other neurotransmitters, including norepinephrine and dopamine (e.g., Goodwin & Jamison, 1990; Spoont, 1992). Remember that the apparent primary function of serotonin is to regulate our emotional reactions. For example, we are more impulsive, and our moods swing more widely, when our levels of serotonin are low, possibly because one of the functions of sero- tonin is to regulate systems involving norepinephrine and dopa- mine (Mandell & Knapp, 1979). According to the permissive hypothesis, when serotonin levels are low, other neurotransmitters are permitted to range more widely, become dysregulated, and contribute to mood irregularities, including depression. Current
thinking is that the balance of the various neurotransmitters and their subtypes is more important than the absolute level of any one neurotransmitter (Carver et al., 2009; Whisman et al., 2011; Yatham et al., 2012).
In the context of this delicate balance, there is continued inter- est in the role of dopamine, particularly in relationship to manic episodes, atypical depression, or depression with psychotic features (Dunlop & Nemeroff, 2007; Garlow & Nemeroff, 2003; Thase, 2009). For example, the dopamine agonist L-dopa seems to produce hypomania in bipolar patients (see, for instance, Van Praag & Korf, 1975), along with other dopamine agonists (Silver- stone, 1985). Chronic stress also reduces dopamine levels and produces depressive-like behaviour (Thase, 2009). But, as with other research in this area, it is quite difficult to pin down any relationships with certainty.

24
Q

The Endocrine System

A

Investigators became interested in the endocrine system when they noticed that patients with diseases affecting this system sometimes became depressed. For example, hypothyroidism, or Cushing’s disease, affects the adrenal cortex. This disease leads to excessive secretion of cortisol and, often, to depression (and anxiety).
In Chapter 2, and again in Chapter 5 on anxiety disorders, we discussed the brain circuit called the HPA axis. This axis begins in the hypothalamus and runs through the pituitary gland, which coordinates the endocrine system (see Figure 2.9). One of the glands influenced by the pituitary is the cortical section of the adrenal gland. The adrenal gland produces the stress hormone cortisol, which is called a stress hormone because it is elevated during stressful life events. For now, it is enough to know that cortisol levels are elevated in depressed patients, a finding that makes sense considering the relationship between depression and severe life stress (Bradley et al., 2008; Thase, 2009).
This connection led to the development of what was thought to be a biological test for depression, the dexamethasone suppres- sion test. Dexamethasone suppresses cortisol secretion in normal subjects. However, when dexamethasone was given to depressed patients, much less suppression was noticed, and what did occur didn’t last very long (Carroll et al., 1968; Carroll et al., 1980). Approximately 50 percent of depressed patients show this reduced suppression, particularly if their depression is severe (Rush et al., 1997). The thinking was that in depressed patients, the adrenal cortex secreted too much cortisol. This oversecretion of cortisol was thought to overwhelm the suppressive effects of dexametha- sone in depressed people. This theory was heralded as very important, because it promised the first biological laboratory test for a psychological disorder. However, later research demon- strated that individuals with other disorders, particularly anxiety disorders, also demonstrate this nonsuppression effect (Feinberg & Carroll, 1984; Goodwin & Jamison, 2007). This finding obvi- ously casts doubt on the usefulness of a test to diagnose depres- sion. Thus, as with early theories about single neurotransmitters, our understanding of the role of cortisol in producing depression has proven overly simplistic.
Researchers nevertheless remain very interested in the rela- tionship of cortisol to depression. Recent research in this area has taken some exciting new turns. Investigators have discovered that neurotransmitter activity in the hypothalamus regulates the release of hormones that affect the HPA axis. Neurohormones are an increasingly important focus of study in psychopathology (e.g., Hammen & Keenan-Miller, 2013; Ladd et al., 1996). We have literally thousands of neurohormones. Determining their effects on the central nervous system and sorting out their relationship to the various neurotransmitter systems is likely to be a very complex task indeed.

25
Q

Sleep and Circadian Rhythms

A

We have known for several years that sleep disturbances are a hallmark of most mood disorders. Most important, in people who are depressed, there is a significantly shorter period after falling asleep before rapid eye movement (REM) sleep begins. As you may remember from your introductory psychology or biology course, there are two major stages of sleep: REM sleep and non-REM sleep (see Chapter 10). When we first fall asleep, we go through several substages of progressively deeper sleep during which we achieve most of our rest. After about 90 minutes, we begin to experience REM sleep, when the brain arouses, and we begin to dream. Our eyes move rapidly back and forth under our eyelids, hence the name rapid eye movement sleep. As the night goes on, we have increasing amounts of REM sleep. In addition to entering REM sleep more quickly, depressed patients experience REM activity that is more intense, and the stages of deepest sleep, called slow wave sleep, don’t occur until later, if at all (Jindal et al., 2002; Kupfer, 1995; Thase, 2009). It seems that some sleep characteristics occur only while we are depressed and not at other times (Riemann et al., 2001; Rush et al., 1986). But other evidence suggests that, at least in more severe cases with recurrent depression, disturbances in sleep continuity, as well as reduction of deep sleep, may be present even when the individual is not depressed (Kupfer, 1995; Thase, 2009). In addition, unusually short and long sleep durations were associated with an increased risk for depression in adults (Zhai et al., 2015).
There are indications that the nature of sleep and circadian disturbances linked to depression differs across the lifespan, illus- trating once again the importance of developmental stage. The increase in REM and reduction in slow wave sleep seem to be less pronounced in depressed children than in adults, perhaps because children are very deep sleepers (Brent & Birmaher, 2009; Garber et al., 2009). Depression is more often accompanied by prominent delays in the sleep-wake cycle in younger individuals, while the sleep-wake cycle of older individuals with depression seems to have a lower amplitude, suggestive of a weaker circadian signal (Robillard et al., 2014). Insomnia, frequently experienced by older adults, is a risk factor for both the onset and persistence of depression (Fiske et al., 2009; Perlis et al., 2006; Talbot et al., 2012). In an interesting study, researchers found that treating insomnia directly in those patients who have both insomnia and depression may enhance the effects of treatment for depression (Manber et al., 2008).
Sleep disturbances also occur in bipolar patients, where they are particularly severe and are characterized not only by decreased REM latency but also by severe insomnia and hypersomnia (excessive sleep) (Goodwin & Jamison, 2007; Harvey, 2008; Harvey et al., 2009). Talbot and colleagues (2012) studied the relationship between sleep and mood in patients with bipolar disorder who were not currently in a depressed or manic state (inter-episode), compared with a group of patients experiencing insomnia. Both the bipolar and insomnia patients had greater sleep disturbance compared with a healthy control group. But the investigators discovered that the relationship between sleep and mood was bidirectional in both groups. That is, negative mood predicted sleep disruptions and sleep disruptions subsequently resulted in negative mood. Treating the insomnia of patients with bipolar I between episodes with CBT has been shown to reduce the risk of relapse and improve sleep, mood, and functioning (Harvey et al., 2015).
Increasing evidence suggests that some of the sleep distur- bances previously reported in depression studies may not be specific to depression, highlighting considerable overlaps across multiple psychological disorders (Baglioni et al., 2016; Benca et al., 1992; Robillard et al., 2015). While these sleep disturbances may cut across different diagnoses, perhaps the most important thing is that treating sleep disruptions directly might positively affect mood not only in people insomnia but also in people with depression and other psychological disorders.
Another interesting finding is that depriving depressed patients of sleep, particularly during the second half of the night, causes temporary improvement in their condition (Giedke & Schwarzler, 2002; Thase, 2009), particularly for patients with bipolar disorder in a depressive state (Harvey, 2008; Johnson et al., 2009), although the depression returns when the patients start sleeping normally again. In any case, because sleep patterns reflect a biological rhythm, there may be a relationship among SAD, sleep disturbances in depressed patients, and a more general disturbance in biological rhythms (Soreca et al., 2009). This would not be surprising if it were true, because most mammals are exquisitely sensitive to day length at the latitudes at which they live, and this internal clock controls eating, sleeping, and weight changes. Thus, substantial disrup- tion in circadian rhythm might be particularly problematic for some vulnerable individuals (Moore, 1999; Sohn & Lam, 2005; Soreca et al., 2009). For instance, mood disorders have been linked with significant abnormalities in circadian rhythms, such as delays in the timing of the soporific hormone melatonin (Crasson et al., 2004; Nair et al., 1984; Robillard et al., 2013). Considerable subgroups of people with depression show major temporal disorganization of circadian rhythms, a factor linked to worse depression severity (Emens et al., 2009; Hasler et al., 2010; Robillard et al., 2018). As such, similar to sleep disrup- tions, abnormalities in biological rhythms are thought to contribute to the pathophysiology of depression (Germain & Kupfer, 2008; Zaki et al., 2018). These types of circadian
disruptions linked to mood disorders are well amenable to chro- notherapies, or treatments directly targeting the realignment of the biological clock (Benedetti, 2012; Hickie et al., 2013; Robillard et al., 2018).
Finally, abnormal sleep profiles and, specifically, disturbances in REM sleep and poor sleep quality predict a somewhat poorer response to psychological treatment (Buysse et al., 1999; Thase, 2009; Thase et al., 1996), further supporting the potential useful- ness of treating disrupted sleep directly.

26
Q

aDDitional stuDies oF Brain struCture anD FunCtion

A

Measuring electrical activity in the brain with electroencephalo- gram (EEG) was described in Chapter 3, where we also described a type of brain wave activity, alpha waves, that indicate calm, positive feelings. In the 1990s, Davidson (1993) and Heller and Nitschke (1997) demonstrated that depressed individuals exhibit greater right-sided anterior activation of their brains, particularly in the prefrontal cortex (and less left-sided activation and, corre- spondingly, less alpha wave activity) than nondepressed individu- als (Davidson et al., 2002). Furthermore, right-sided anterior activation was also found in patients who are no longer depressed (Gotlib et al., 1998; Tomarken & Keener, 1998), suggesting this brain function might also exist before the individual becomes depressed and represent a vulnerability to depression. Follow-up studies showed that adolescent offspring of depressed mothers tend to show this pattern, compared with offspring of nonde- pressed mothers (Tomarken et al., 2004), also suggesting that this type of brain functioning could become an indicator of a biologi- cal vulnerability to depression (Gotlib & Abramson, 1999). In contrast, one recent study suggests that bipolar spectrum patients (individuals with subthreshold swings in mood) show elevated rather than diminished relative left-frontal EEG activity and that this brain activity predicts the onset of a full bipolar I disorder (Nusslock et al., 2012). In addition to studying the prefrontal cortex and hippocampus, neuroscientists are also studying the anterior cingulate cortex and the amygdala for clues to under- standing brain function in depression and finding that some areas are less active, and other areas more active, in people with depres- sion than in normal subjects, confirming the EEG studies just mentioned (Davidson et al., 2009). These areas of the brain are all interconnected and seem to be associated with increased inhibi- tion and with deficits in pursuing desired goals, which happen to be characteristics of depression. Scientists hope that further study of these brain circuits will lead to a deeper understanding of the origins of differences in depressed individuals, and whether these differences precede depression and may contribute to causing depression, as some studies suggest, or are simply a consequence of being depressed.

27
Q

Stressful Life Events

A

In reviewing the genetic contribution to the causes of depression, we noted that fully 60 to 80 percent of the causes of depression could be attributed to psychological experiences. Furthermore, most of those experiences are unique to the individual. Stress and trauma are among the most striking unique contributions to the etiology of all psychological disorders. This is reflected through- out psychopathology and is evident in the wide adoption of the diathesis–stress model of psychopathology presented in Chapter 2 (and referred to throughout this book), which describes possible genetic and psychological vulnerabilities. But in seeking what activates this vulnerability (diathesis), we usually look for a stressful or traumatic life event.
You would think it would be sufficient to ask people whether anything major had happened in their lives before they devel- oped depression or some other psychological disorder. Most people do report losing a job, getting divorced, having a child, or graduating from school and starting a career. But, as with most issues in the study of psychopathology, the significance of a major event is not easily discovered (Carter & Garber, 2011; Hammen, 2005; Hammen & Keenan-Miller, 2013), so most investigators have stopped simply asking patients whether something bad (or good) happened, and they have begun to look at the context of the event and the meaning it has for the individual.
For example, losing a job is stressful for most people, but it is far more difficult for some than others. A few people might even see it as a blessing. If you were laid off as a manager in a large corporation because of a restructuring, but your partner is the president of another corporation and makes more than enough money to support the family, it might not be so bad. Furthermore, if you are an aspiring writer or artist who has not had time to pursue your art, becoming jobless might be the opportunity you have been waiting for, particularly if your part- ner has been telling you for years to devote yourself to your creative pursuits.
Now consider losing your job if you are a single mother of two young children living from day to day and, because of a recent dentist’s bill, you have to choose between paying the electric bill or buying enough food. The stressful life event is the same, but the context is very different and transforms the significance of the event substantially. To complicate the scenario further, think for a minute about how such a woman might react to losing her job. One woman might well decide she is a total failure and thus becomes unable to carry on and provide for her children. Another woman might realize the job loss was not her fault at all and take advantage of a job-training program while scraping by somehow.

Thus, both the context of the life event and its meaning are important.
It is difficult to study life events, and psychologists are actively developing new methods to do so (e.g., Hammen, 2005; Monroe & Roberts, 1990; Monroe et al., 2009). One crucial issue is the bias inherent in remembering events. If you ask people who are currently depressed what happened when they first became depressed more than five years ago, you will probably get answers different from answers they would give if they were not currently depressed. Because current moods distort memories, many investigators have concluded that the only useful way to study stressful life events is to follow people prospectively, to determine more accurately the precise nature of events and their relation to subsequent problems.
In any case, in summarizing a large amount of research, it is clear that stressful life events are strongly related to the onset of mood disorders (Grant et al., 2004; Hammen, 2005; Kendler & Gardner, 2010; Monroe & Reid, 2009; Monroe et al., 2009). Measuring the context of events and their impact in a random sample of the population, several studies have found a marked relationship between severe and, in some cases, traumatic life events and the onset of depression (Brown, 1989; Brown et al., 1994; Kendler et al., 1999a; Mazure, 1998). Severe events precede nearly all types of depression (Brown et al., 1994). Major life stress is a somewhat stronger predictor for initial episodes of depression compared with recurrent episodes (e.g., Lewinsohn et al., 1999). In addition, for people with recurrent depression, the clear occurrence of a severe life stress before or early in the latest episode predicts a much poorer response to treatment and a longer time before remission (Monroe et al., 1992, 2009), as well as a greater likelihood of recurrence (Monroe et al., 1996, 2009). Again, the context and meaning are probably more important than the exact nature of the event itself. The work of Canadian researchers Williams, Connolly, and Segal (2001) similarly suggests that romantic relationships play a key role in vulnerabil- ity to depression in adolescent girls.
Despite this strong relationship, scientists are discovering that the link between stressful events and depression is not straightfor- ward. Remember in Chapter 2 where we noted that our genetic endowment might actually increase the probability that we will experience stressful life events? We referred to this as the gene– environment correlation model (Kendler, 2011; Kendler et al., 2011). One example would be people who tend to seek out diffi- cult relationships because of genetically based personality char- acteristics that then lead to depression. Another example would be people who display problematic social behaviours, such as complaining too often about personal difficulties to others, which may result in interpersonal rejection. Rejection in turn serves as a trigger for a depressive episode (Vaerum & McCabe, 2001; Wiebe & McCabe, 2002). Kendler et al. (1999a) reported that about one- third of the association between stressful life events and depres- sion is not the usual arrangement of stress triggering depression, but rather individuals vulnerable to depression who are placing themselves in high-risk stressful environments.
The relationship of stressful events to the onset of episodes in bipolar disorder is also strong (Goodwin & Jamison, 1990; Johnson & Roberts, 1995). Several issues may be particularly relevant to the etiology of bipolar disorders, however (Goodwin & Ghaemi, 1998). First, stressful life events seem to trigger early mania (Alloy et al., 2012) and depression, but as the disorder progresses these episodes seem to develop lives of their own. In other words, once the cycle begins, a process takes over and ensures the disorder will continue (e.g., Post, 1992; Post et al., 1989). Second, some of the precipitants of manic episodes seem to be related to loss of sleep, as in the postpartum period (Goodwin & Jamison, 1990), or as a result of jet lag, that is, disturbed circadian rhythms (Alloy et al., 2015). In most cases of bipolar disorder, nevertheless, stressful life events are implicated not only in provoking relapse but also in preventing recovery (Johnson & Miller, 1997).
Finally, although almost everyone who becomes depressed has experienced a significant stressful event, most people who experi- ence such events do not become depressed. Although the data are not yet as precise as we would like, somewhere between 20 and 50 percent of individuals who experience severe events become depressed. Thus, between 50 and 80 percent of individuals do not develop depression or, presumably, any other psychological disorder. Once again, data strongly support the interaction of stressful life events with some kind of vulnerability, either genetic, psychological, or, more likely, a combination of the two influences (Haeffel & Hames, 2014).
Given a genetic vulnerability (diathesis) and a severe life event (stress), what happens then? Research has isolated a number of psychological and biological processes. To illustrate one, let’s return to Katie. Her life event was attending a new school.

28
Q

Learned Helplessness

A

As discussed in Chapter 2, Martin E. P. Seligman discovered that dogs and rats have an emotional reaction to events over which they have no control. If rats receive occasional shocks, they can function reasonably well, if they can cope with the shocks by doing something to avoid them, such as pressing a lever. But if they learn that nothing they do helps them avoid the shocks, they eventually become very helpless, give up, and manifest an animal equivalent of depression (Seligman, 1975).
Do humans react the same way? Seligman suggests we seem to, but only under one important condition: People become anxious and depressed when they make an attribution that they have no control over the stress in their lives (Abramson et al., 1978; Miller & Norman, 1979). These findings evolved into an important model called the learned helplessness theory of depression. Often overlooked is Seligman’s point that anxiety is the first response to a stressful situation. Depression may follow marked hopelessness about coping with the difficult life events. The depressive attributional style is (1) internal, in that the indi- vidual attributes negative events to personal failings (“It is all my fault”), (2) stable, in that, even after a particular negative event passes, the attribution that “additional bad things will always be my fault” remains, and (3) global, in that the attribu- tions extend across a wide variety of issues. Research continues on this interesting concept, but you can see how it applies to Katie. Early in her difficulties with attending school, she began to believe events were totally out of her control and that she was unable even to begin to cope. More important, in her eyes the bad situation was all her fault: “I blamed myself for my lack of control.” A downward spiral into a major depressive episode followed.
But a major question remains: Is learned helplessness a cause of depression or a correlated side effect of becoming depressed? If it were a cause, learned helplessness would have to exist before the depressive episode. Results from a classic five-year longitudi- nal study in children may shed some light on this issue. Nolen- Hoeksema, Girgus, and Seligman (1992) reported that negative attributional style did not predict later symptoms of depression in young children; rather, stressful life events seemed to be the major precipitant of symptoms. As children under stress grew older, however, they tended to develop more negative cognitive styles, which did tend to predict symptoms of depression in reaction to additional negative events. Nolen-Hoeksema and colleagues speculate that meaningful negative events early in childhood may give rise to negative attributional styles in a developmental fash- ion, making these children more vulnerable to future depressive episodes when stressful events occur.
This thinking recalls the types of psychological vulnerabilities theorized to contribute to the development of anxiety disorders. That is, in a person who has a nonspecific genetic vulnerability to either anxiety or depression, stressful life events activate a psychological sense that life events are uncontrollable (Barlow, 2002; Chorpita & Barlow, 1998). Evidence suggests that negative attributional styles are not specific to depression but characterize anxiety patients as well (Barlow, 2002; Heimberg et al., 1989). This overlap may indicate that a psychological (cognitive) vulner- ability is no more specific for mood disorders than is genetic vulnerability. Both types of vulnerabilities may underlie numer- ous disorders.
Abramson, Metalsky, and Alloy (1989) revised the learned helplessness theory to de-emphasize specific attributions and highlight the development of a sense of hopelessness as a crucial cause of many forms of depression. Attributions are important only to the extent that they contribute to a sense of hopelessness. This fits well with recent thinking on crucial differences between anxiety and depression. Both anxious and depressed individuals feel helpless and believe they lack control, but only in depression do they give up and become hopeless about ever regaining control (Alloy & Abramson, 2006).
Evidence from the work of Ian Gotlib and his colleagues indi- cates that a pessimistic style of attributing negative events to our own character flaws results in hopelessness (Gotlib & Abramson, 1999). This style may predate and therefore, in a sense, contrib- ute to anxious or depressive episodes that follow negative or stressful events. In fact, a longitudinal study by McGill Univer- sity psychologist John Abela and psychology student Sabina Sarin (2002) followed children in Grade 7 for 10 weeks, obtain- ing information on their initial attributional styles, negative life events, and later symptoms of depression. This study obtained results supporting the hopelessness theory of depression, as has more recent work by this same research group (e.g., Abela et al., 2006).

29
Q

Negative Cognitive Styles

A

In 1967, Aaron T. Beck (1967, 1976) suggested that depression may result from a tendency to interpret everyday events in a nega- tive way. According to Beck, people with depression make the worst of everything; for them, the smallest setbacks are major catastrophes. In his extensive clinical work, Beck observed that all his depressed patients thought this way, and he began classify- ing the types of cognitive errors that characterized this style. From the long list he compiled, two representative examples are arbitrary inference and overgeneralization. Arbitrary inference is evident when a depressed individual emphasizes the negative rather than the positive aspects of a situation. A teacher may assume he is a terrible instructor because two students in his class fell asleep. He fails to consider other reasons they might be sleep- ing (up all night partying) and infers that his teaching style is at fault. As an example of overgeneralization, when your professor makes one critical remark on your paper, you then assume you will fail the class, despite a long string of very positive comments and good grades on other papers. You are overgeneralizing from one small remark. According to Beck, people who are depressed think like this all the time. They make cognitive errors in thinking negatively about themselves, their immediate world, and their future, three areas that together are called the cognitive triad (see ■ Figure 8.4).
In addition, Beck theorized, after a series of negative events in childhood, individuals may develop a deep-seated negative schema, an enduring negative cognitive belief system about some aspect of life (Dozois et al., 2006; Young et al., 2014). In a self-
blame schema, individuals feel personally responsible for every bad thing that happens. With a negative self-evaluation schema, they believe they can never do anything correctly. In Beck’s view, these cognitive errors and schemas are automatic—that is, not
necessarily conscious. Indeed, an individual might not even be aware of thinking negatively and illogically. Thus, very minor negative events can lead to a major depressive episode.
A variety of evidence supports a cognitive theory of emotional disorders in general and depression in particular (Gotlib et al., 2014; Hammen & Keenan-Miller, 2013; Ingram et al., 2006; Mazure et al., 2000), and Canadian researchers have been at the forefront of developments in testing Beck’s cognitive theory of depression (Rector et al., 1998). The thinking of depressed indi- viduals is consistently more negative than that of nondepressed individuals (Dobson & Shaw, 1987; Gotlib & Abramson, 1999; Gotlib et al., 2014; Zuroff et al., 1999) in each dimension of the cognitive triad—the self, the world, and the future (e.g., Bradley & Mathews, 1988; Gotlib
et al., 2014; Segal et al., 1988).

Research by Nicholas Kuiper and his colleagues at the University of Western Ontario has focused on the self-component of Beck’s cognitive triad. For exam- ple, Derry and Kuiper (1981) asked depressed and nondepressed individuals to complete a “self-referent encoding task” in which they rated a series of traits as to whether or not each described them. The depressed group viewed traits with depres- sive content (e.g., stupid, boring) as being significantly more applicable to themselves than did nondepressed participants. Conversely, the depressed group viewed traits with nondepressive content (e.g., nice, attractive) as being significantly less applica- ble to themselves. Keith Dobson and Brian Shaw (1987) repli- cated this finding and took it a step further by showing that when depressed patients were in remission (i.e., no longer actively depressed), their self-descriptiveness ratings of depressive content traits were no different from those made by a nondepressed comparison group. Brinker, Harris, Guyitt, and Dozois (2006) took this research yet another step further by having participants complete the self-referent encoding task and subsequently asking them to indicate how important it was for them to possess or fail to exhibit each trait. They found that the greater the importance of positive traits that an individual believed he or she lacks, the higher the person’s level of depression. For example, if a person believed it was very important to be nice but also felt that she was not a nice person, then she was at higher risk for depressed mood. Conversely, the more important the negative traits a person believed he or she is free of, the lower the person’s level of depression. For example, if a person believed it was very impor- tant not to be boring and also felt that he was not a boring person, then he was at lower risk for depressed mood.
Much of the recent work in this area has focused on whether these cognitive biases are stable features of the individual or whether they instead shift with a depressed person’s mood state. Some interesting work by David Dozois at the University of Western Ontario and Keith Dobson at the University of Calgary demonstrates that the answer to this question is complex. These authors followed 45 depressed patients over six months. Participants completed tests of information processing (e.g., the self-referent encoding task described earlier) and tests of cogni- tive organization, which allowed the researchers to determine how closely related certain topics were to one another in a given person. Each test was completed twice, once when all participants were depressed and again six months later, when half of the participants had recovered from their depression. Only those who had recovered from their depression showed less negative cogni- tive biases on the two information-processing tasks at the six-month follow-up than they had when they were actively depressed. In contrast, these same individuals showed a high level of interconnectedness of negative material at both testing times on the tests of cognitive organization. These results are consistent with Beck’s theoretical predictions that underlying negative sche- mas are stable in individuals prone to depression and that these schemas become activated by negative events, in turn triggering negative information-processing biases (Dozois & Dobson, 2001). Dozois and Dobson have continued to use these tests of cognitive organization with clinically depressed research partici- pants. Their more recent work has shown that higher levels of interconnectedness of negative material and lower levels of inter- connectedness of positive material are associated with recurrent depression (Dozois & Dobson, 2003).
The implications of Beck’s theory are very important. By recognizing cognitive errors and the underlying schemas, we can correct them and potentially alleviate depression and related emotional disorders. In developing ways to do this, Beck became the father of cognitive therapy, one of the most important devel- opments in psychotherapy in the past 50 years.

30
Q

Cognitive Vulnerability for Depression: An Integration

A

Seligman and Abramson, on the one hand, and Beck, on the other, developed their theories independently, and good evidence indi- cates their models are independent, in that some people may have a negative outlook (dysfunctional attitudes), whereas others may explain things negatively (hopeless attributes). Nevertheless, the basic premises overlap a great deal and considerable evidence suggests that depression is always associated with pessimistic explanatory style and negative cognitions. Evidence also exists that cognitive vulnerabilities predispose some people to view events in a very negative way, putting them at risk for depression (e.g., Abela et al., 2011; Alloy et al., 2012; Ingram et al., 2006; Reilly-Harrington et al., 1999).

31
Q

Marital Relations

A

Depression and bipolar disorder are strongly influenced by inter- personal stress (Sheets & Craighead, 2014; Vrshek-Schallhorn et al., 2015), and especially marital dissatisfaction, as disruptions in relationships often lead to depression (Davila et al., 2009). Bruce and Kim (1992) collected data on 695 women and 530 men and then interviewed them again up to one year later. During this period some participants separated from or divorced their spouses, though the majority reported stable marriages. Approximately 21 percent of the women who reported a marital split during the study experienced severe depression, a rate three times that for women who remained married. Nearly 17 percent of the men who reported a marital split developed severe depression, a rate nine times that for men who remained married. When the researchers considered only those participants with no history of severe depression, however, 14 percent of the men who separated or divorced during the period experienced severe depression, as did approximately 5 percent of the women. In other words, only the men faced a heightened risk of developing a mood disorder for the first time immediately following a marital split.
Another finding with considerable support is that depression, particularly if it continues, may lead to substantial deterioration in marital relationships (Beach et al., 1990, 2009; Davila et al., 2009; Uebelacker & Whisman, 2006). It is not hard to figure out why. Being around someone who is continually negative, ill tempered, and pessimistic becomes tiring after a while. Because emotions are contagious, the spouse probably begins to feel bad also. These kinds of interactions precipitate arguments or, worse, make the nondepressed spouse want to leave (Joiner & Timmons, 2009; Whisman et al., 2006).
But conflict within a marriage seems to have different effects on men and women. Depression seems to cause men to withdraw or otherwise disrupt the relationship. For women, in contrast, it is problems in the relationship that most often cause depression. Thus, for both men and women, depression and problems in mari- tal relations are associated, but the causal direction is different (Fincham et al., 1997), a result also found by Spangler, Simons, Monroe, and Thase (1996). Given these factors, Beach, Jones, and Franklin (2009) suggest that therapists treat disturbed marital relationships at the same time as the mood disorder to ensure the highest level of success for the patient and the best chance of preventing future relapses. Individuals with bipolar disorder are less likely to be married at all and more likely to get divorced if they do marry, although those who stay married have a somewhat better prognosis, perhaps because their spouses are helpful in regulating their treatments and keeping them on medications (Davila et al., 2009).

32
Q

Mood Disorders in Women

A

There is a fairly dramatic gender imbalance in mood disorders (Bland, 1997). Although bipolar disorder is evenly divided between men and women, almost 70 percent of the individuals with major depressive disorder and persistent depressive disorder are women (Nolen-Hoeksema, 1987; Kessler, 2006; Kessler & Bromet, 2013). What is particularly striking is that, even though overall rates of disorder may vary from country to country, this gender imbalance is constant around the world (Andrade et al., 2003; Kessler & Bromet, 2013; Seedat et al., 2009; Weissman & Olfson, 1995). For example, according to the 2017 CCHS, 6.4 percent of Canadian men and 10.7 percent of Canadian women 12 years of age or older report they are currently diag- nosed with a mood disorder such as depression, bipolar disorder, mania, or dysthymia (Statistics Canada, 2018). Often overlooked is the similar ratio for most anxiety disorders, particularly panic disorder and generalized anxiety disorder. Women represent an even greater proportion of specific phobias, as we noted in Chapter 2. What could account for this?
It may be that gender differences in the development of emotional disorders are strongly influenced by perceptions of uncontrollability. If you feel a sense of mastery over your life and the difficult events we all encounter, you might experience occa- sional stress, but you will not feel the helplessness central to anxiety and mood disorders. The source of these differences is cultural, in the sex roles assigned to men and women in our soci- ety. Boys and men are strongly encouraged to be independent, masterful, and assertive; girls and women, by contrast, are expected to be more passive, to be sensitive to other people, and, perhaps, to rely on others more than males do. Although these stereotypes are slowly changing, they still describe current sex roles, to a large extent. But this culturally induced dependence and passivity may well put women at severe risk for emotional disorders by increasing their feelings of uncontrollability and helplessness. Evidence has accumulated that parenting styles encouraging stereotypic gender roles are implicated in the devel- opment of early psychological vulnerability to later depression or anxiety (Chorpita & Barlow, 1998; Suárez et al., 2009), specifi- cally, a smothering overprotective style that prevents the child from developing initiative.
The value women place on intimate relationships may also put them at risk. Disruptions in such relationships, combined with an inability to cope with the disruptions, may be far more damaging to women than to men (Kendler & Gardner, 2014; Nolen- Hoeksema & Hilt, 2009). Cyranowski and associates (2000) note that the tendency for adolescent girls to express aggression by rejecting other girls, combined with a greater sensitivity to rejec- tion, may precipitate more depressive episodes in these adoles- cent girls compared with boys. Kendler, Myers, and Prescott (2005) also observed that women tend to have larger and more intimate social networks than men and that emotionally support- ive groups of friends protect against depression.
Another potentially important gender difference is that women tend to ruminate more than men about their situation and blame themselves for being depressed (Nolen-Hoeksema, 1990, 2000b; Nolan-Hoeksema et al., 2008). This response style predicted the later development of depression when under stress (Abela & Hankin, 2011). Men tend to ignore their feelings, perhaps engag- ing in activity to take their minds off them (Addis, 2008). This male behaviour may be therapeutic because activating people (getting them busy doing something) is a common element of successful therapy for depression (Dimidjian et al., 2014; Jacobson et al., 2001).
Another issue to consider is that the majority of the people living in poverty in North America are women and children. Women, particularly single mothers, have a difficult time enter- ing the workplace. Therefore, the meaning of conflict in a rela- tionship is greater for women than for men, who are likely to respond more to problems at work. Data from the Canadian National Population Health Survey indicate that rates of depres- sion are 2.5 times as high in single women with a child under five years old as among married mothers (Cairney et al., 1999; see also Bulloch et al., 2009). In fact, married women employed full- time outside the home report levels of depression no greater than those of employed married men. Single, divorced, and widowed women experience significantly more depression than men in the same categories (Weissman & Klerman, 1977). These results do not necessarily mean that people should get a job to avoid becom- ing depressed. Indeed, for a man or woman, feeling mastery, control, and value in the strongly socially supported role of homemaker and parent should be associated with low rates of depression. Moreover, findings from the Canadian National Population Health Survey show that work stress can be associ- ated with depression in both men and women. It is just that gender may alter the type of work stress that is most strongly associated with depression (i.e., psychological demands predict depression in men whereas physical demands do so in women; Wang & Patten, 2001). In another study with the same survey, job insecurity was associated with depression in men but not in women (Wang et al., 2002).
A further possible contributing factor to the higher rates of depression in women pertains to a particular type of stressor— specifically, abuse histories. A study by Robert Levitan and his colleagues at the University of Toronto indicated that a history of abuse in childhood was a risk factor for depression (Levitan et al., 1998). A later study by this same research group noted a particularly strong association between early sexual abuse and comorbid depression and anxiety (Levitan et al., 2003). Another Toronto study by Sahay, Piran, and Maddocks (2000) examined the prevalence of sexual victimization in 60 female patients with depression. An alarming 65 percent reported sexual violation in childhood, adolescence, or adulthood. These studies are certainly suggestive of the possibility that the higher rates of abuse expe- riences may help explain women’s greater susceptibility to depression.

33
Q

Social Support

A

To take one example, the risk of depression for people who live alone is almost 80 percent higher than for people who live with others (Pulkki-Råback et al., 2012). In an early landmark study, Brown and Harris (1978) first suggested the important role of social support in the onset of depression. In a study of a large number of women who had experienced a serious life stress, they discovered that only 10 percent of the women who had a friend in whom they could confide became depressed, compared with 37 percent of the women who did not have a close supportive rela- tionship. Later prospective studies have also confirmed the impor- tance of social support (or lack of it) in predicting the onset of depressive symptoms at a later time (Cutrona, 1984; Joiner, 1997). Other studies have established the importance of social support in speeding recovery from depressive episodes (Johnson et al., 2008, 2009; Keitner et al., 1995; Sherbourne et al., 1995).
A Canadian randomized control study by Misri, Kostaras, Fox, and Kostaras (2000) examined the effects of partner support on the treatment of women with postpartum depression. Relative to other treated patients, women who received the treatment involving partner support showed a significant decrease in their symptoms of depression, attesting to the importance of social support in recovery aurora Photos/alamy Stock Photo
from postpartum depression. Johnson, Winett, Meyer, Greenhouse, and Miller (1999) examined the effects of social support in speeding recovery from both manic and depres- sive episodes in patients with bipolar disorder, and they came up with a surprising finding: A socially supportive network of friends and family helped speed recovery from depres- sive episodes but not from manic episodes. This finding highlights the uniquely differ- ent quality of manic episodes. These and related findings on the importance of social support have led to an exciting
new psychosocial therapeutic approach for emotional disor- ders called interpersonal psychotherapy, which we discuss later in this chapter.

34
Q

an inteGrative theory

A

How do we put all this together? Depression and anxiety may often share a common, genetically determined biological vulner- ability (Barlow, 2002) that can be described as an overactive neurobiological response to stressful life events. One genetic pattern implicated in this vulnerability is in the serotonin trans- porter gene-linked polymorphic region, which was described in Chapter 2. Once again, this vulnerability is simply a general tendency to develop depression (or anxiety) rather than a specific vulnerability for depression or anxiety itself. This biological vulnerability to develop depression seems stronger for women than for men (Bierut et al., 1999). To understand the causes of depression, we must look at psychological vulnerabilities as well as life experiences that interact with genetic vulnerabilities.
People who develop mood disorders also possess a psychologi- cal vulnerability experienced as feelings of inadequacy for coping with the difficulties confronting them. As with anxiety, we may develop this sense of control in childhood (Barlow, 2002; Chorpita & Barlow, 1998). It may range on a continuum from total confi- dence to a complete inability to cope. When vulnerabilities are triggered, the giving-up process seems crucial to the development of depression (Alloy et al., 2000; Alloy & Abramson, 2006). A variety of evidence indicates that these attitudes and attributions correlate rather strongly with such biochemical markers of stress and depression as by-products of norepinephrine (Samson et al., 1992) and hemispheric lateral asymmetry (Davidson 1993; Heller & Nitschke, 1997).
The causes of this psychological vulnerability can be traced to adverse experiences in childhood or exposure to caregivers with psychopathology perhaps years before the onset of mood disor- ders. For example, Taylor and Ingram (1999) demonstrated that children of depressed mothers possess a less positive self-concept and more negative information processing if one probes for this vulnerability. This enduring psychological vulnerability intensi- fies the biochemical and cognitive response to stress later in life (Nolen-Hoeksema, 2000a).
Good evidence suggests that stressful life events trigger the onset of depression in most cases, particularly initial episodes (Jenness et al., 2011). How do these factors interact? The best current thinking is that stressful life events in vulnerable individu- als activate stress hormones, which, in turn, have wide-ranging effects on neurotransmitter systems, particularly those involving serotonin, norepinephrine, and the corticotropin-releasing factor system. Evidence also indicates that activation of stress hormones over the long term may actually turn on certain genes, producing long-term structural and chemical changes in the brain. For example, processes triggered by long-term stress may lead to atrophy of neurons in the hippocampus that help regulate emotions. Such structural change might permanently affect the regulation of neurotransmitter activity. The extended effects of stress may also disrupt the circadian rhythms in certain individu- als, who then become susceptible to the recurrent episodic cycling that seems so uniquely characteristic of the mood disor- ders (Moore, 1999; Post, 1992).
As noted earlier, triggering stressful life events also activate a dormant psychological vulnerability characterized by negative thinking and a sense of helplessness and hopelessness. What we have so far is a possible mechanism for the diathesis–stress model. Finally, it seems clear that such factors as interpersonal relationships or our gender may protect us from the effects of stress and therefore from developing mood disorders. Alterna- tively, these factors may at least determine whether we quickly recover from these disorders.
In summary, biological, psychological, and social factors all influence the development of mood disorders, as depicted in ■ Figure 8.5. This model does not account for the varied presentation of mood disorders—unipolar, bipolar, and so on. In other words, why would someone with an underlying genetic vulnerability who experiences a stressful life event develop a bipolar disorder rather than a unipolar disorder or, for that matter, an anxiety disorder? As with the anxiety disorders and other stress disorders, specific psychosocial circumstances, such as early learning experiences, may interact with specific genetic vulnera- bilities and personality characteristics to produce the rich variety of emotional disorders. Only time will tell.

35
Q

TreATMenT

A

We have learned a great deal about the neurobiology of mood disorders during the past several years. Findings on the complex interplay of neurochemicals are beginning to shed light on the nature of mood disorders. As we have noted, the principal effect of medications is to alter levels of these neurotransmitters and other related neurochemicals. Other biological treatments, such as electroconvulsive therapy (ECT), dramatically affect brain chemistry. A more interesting development, however, alluded to throughout this book, is that powerful psychological treatments also alter brain chemistry. Despite these advances, most cases of depression go untreated because neither health-care professionals nor patients recognize and correctly identify or diagnose depres- sion. Similarly, many professionals and patients are unaware of the existence of successful treatments (Delano-Wood & Abeles, 2005; Hirschfeld et al., 1997). For this reason, it is important to learn about treatments for depression.

36
Q

meDiCations

A

Three basic types of antidepressant medications are used to treat depressive disorders: tricyclic antidepressants, monoamine oxidase (MAO) inhibitors, and the newer selective-serotonin reuptake inhibitors (SSRIs).
Tricyclic antidepressants are widely used treatments for depression. The best-known variants are probably imipramine (Tofranil) and amitriptyline (Elavil). It is not yet clear how these drugs work, but initially, at least, they block the reuptake of certain neurotransmitters, allowing them to pool in the synapse and, as the theory goes, desensitize or down regulate the trans- mission of that particular neurotransmitter (so less of the neuro- chemical is transmitted). Tricyclic antidepressants seem to have their greatest effect by down regulating norepinephrine, although other neurotransmitter systems, particularly serotonin, are also affected. This process then has a complex effect on both presyn- aptic and postsynaptic regulation of neurotransmitters activity. This process takes a while to work, often between two and eight weeks. During this time, many patients feel a bit worse and develop side effects such as blurred vision, dry mouth, constipa- tion, difficulty urinating, drowsiness, weight gain (at least six kilograms), and, sometimes, sexual dysfunction. For this reason, as many as 40 percent of these patients stop taking the drug, thinking that the cure is worse than the disease. Nevertheless, with careful management, many side effects disappear. Tricy- clics alleviate depression in approximately 50 percent of patients, compared with approximately 25 to 30 percent of patients taking placebo pills, based on a summary analysis of more than 100 studies (American Psychiatric Association, 2000a; Depression Guideline Panel, 1993). If dropouts are excluded and only those who complete treatment are counted, success rates increase to between 60 and 70 percent (American Psychiatric Association 2010), but one thorough meta-analysis indicated that antidepressants were relatively ineffective for mild to moderate depression compared with placebo. Only in severely depressed patients is there a clear advantage for taking an antidepressant compared with placebo (Fournier et al., 2010). Another issue clinicians must consider is the potential cardiac side effect of the tricyclic antidepressants (Tingelstad, 1991). In fact, tricyclics are lethal if taken in excessive doses; therefore, they must be prescribed with great caution to patients with suicidal tendencies.
MAO inhibitors work very differently; as their name suggests, they block the enzyme monoamine oxidase that breaks down such neurotransmitters as norepinephrine and serotonin. The result is roughly equivalent to the effect of the tricyclics. Because they are not broken down, the neurotransmitters pool in the synapse, ulti- mately leading to a down regulation or desensitization. The MAO inhibitors seem to be as effective as the tricyclics (American Psychiatric Association, 2010), with somewhat fewer side effects. But MAO inhibitors are used far less often because of two poten- tially serious consequences: Consuming foods and beverages containing tyramine, such as cheese, red wine, or beer, can lead to severe hypertensive episodes and, occasionally, death. In addi- tion, many other drugs that people take daily, such as cold medi- cations, are dangerous and even fatal in interaction with an MAO inhibitor. For this reason, MAO inhibitors are usually prescribed only when tricyclics are not effective.
The class of drugs currently considered the first choice in drug treatment for depression seems to have a specific effect on the serotonin neurotransmitter system (although such drugs affect other systems to some extent). These SSRIs specifically block the presynaptic reuptake of serotonin. This temporarily increases levels of serotonin at the receptor site, but again the precise long- term mechanism of action is unknown (Gitlin, 2009; Thase & Denko, 2008). Perhaps the best-known drug in this class is fluox- etine (Prozac). Like many other medications, Prozac was initially hailed as a breakthrough drug; it even made the cover of Newsweek (March 26, 1990). Then reports began to appear that it might lead to suicidal preoccupation, paranoid reactions, and, occasionally, violence (e.g., Mandalos & Szarek, 1990; Teicher et al., 1990). Prozac went from being a wonder drug in the eyes of the press to a potential menace to modern society. Of course, neither conclusion was true. More recent findings indicate that the risks of suicide with this drug are no greater than with any other antidepressant, and the effectiveness is about the same (Fava & Rosenbaum, 1991). However, Prozac has its own set of side effects, the most prominent of which are physical agitation, sexual dysfunction or low desire (which is very prevalent, occur- ring in 50 to 75 percent of cases), insomnia, and gastrointestinal upset. But these side effects, on the whole, seem to bother most patients less than the side effects associated with tricyclic antide- pressants, with the possible exception of the sexual dysfunction. Studies suggest similar effectiveness of SSRIs and tricyclics with dysthymia (Lapierre, 1994).

Two newer antidepressants seem to have somewhat different mechanisms of neurobiological action. Venlafaxine is related to tricyclic antidepressants but acts in a slightly different manner, reducing some of the associated side effects and the risk of damage to the cardiovascular system. Other typical side effects remain, including nausea and sexual dysfunction. Nefazodone is closely related to the SSRIs but seems to improve sleep effi- ciency instead of disrupting sleep. Both drugs are roughly comparable in effectiveness to older antidepressants (American Psychiatric Association, 2000b; Preskorn, 1995; Thase & Kupfer, 1996).
Finally, there has been a great deal of interest in the antidepres- sant properties of the natural herb St. John’s wort (Hypericum). St. John’s wort is very popular in Europe, and it began catching on in Canada and the United States around 1995 (Canterbury Farms, 1997). While uncontrolled trials suggest benefits for those who complete treatment (e.g., Simeon et al., 2005), a large North American study showed no specific effectiveness for the herb compared with placebo treatments or other medications (Hyperi- cum Depression Trial Study Group, 2002). The latter controlled trial has been criticized because it included only severely depressed patients, and St. John’s wort might work better with people who are only mildly depressed. Furthermore, it is significant that even the active antidepressant drug did no better than placebo in this study, although this finding is not uncommon, since many studies on the effects of drugs on depression do not show differences between drug and placebo. In any case, St. John’s wort is available at many health food stores and nutritional supplement stores, but there is no guarantee that any given brand of St. John’s wort contains the appropriate ingredients, since this herb is not regu- lated by any government agency. Moreover, Health Canada issued a letter to Canadian physicians, pharmacists, and alternative medi- cine practitioners warning them about the possibility of negative drug interactions with St. John’s wort (e.g., with drug treatments for HIV, immunosuppressant drugs taken by transplant patients, antidepressants, and oral contraceptives; Health Canada, 2000a). For example, there have been case reports of grogginess, weak- ness, and lethargy resulting from the combination of St. John’s wort and prescribed antidepressants, such as paroxetine (Vermani et al., 2005).

Current studies indicate that drug treatments effective with adults are not necessarily effective with children (American Psychiatric Association, 2010b). Sudden deaths of children under 14 who were taking tricyclic antidepressants have been reported, particularly during exercise, as in routine school athletic competition (Tingelstad, 1991). Cardiac side effects have been implicated in these deaths. Traditional antidepres- sant drug treatments are usually effective with seniors, but administering them takes considerable skill because older people may experience a variety of side effects not experi- enced by younger adults, including memory impairment and physical agitation (Deptula & Pomara, 1990; Marcopulos & Graves, 1990).
Clinicians and researchers have concluded that recovery from depression, although important, may not be the most important therapeutic outcome (Frank et al., 1990; Prien & Kupfer, 1986). The large majority of people eventually recover from a major depressive episode, some rather quickly. A more important goal is often to delay the next depressive episode or even prevent it entirely (Thase, 1990; Thase & Kupfer, 1996). This prevention is particularly important for patients who retain some symptoms of depression or have a past history of chronic depression or multiple depressive episodes (Forand & DeRubeis, 2013; Hammen & Keenan-Miller, 2013). Because all these factors put people at risk for relapse, it is recommended that drug treatment go well beyond the termination of a depres- sive episode, continuing perhaps 6 to 12 months after the episode is over, or even longer (American Psychiatric Associa- tion, 2010). The drug is then gradually withdrawn over a period of weeks or months.
Antidepressant medications have relieved severe depression and undoubtedly prevented suicide in many patients around the world, particularly in cases of more severe depression. Although these medications are readily available, many people refuse or are not eligible to take them. Some are wary of long-term side effects. Women of childbearing age must protect themselves against the possibility of conceiving while taking antidepres- sants, because they can damage the fetus. In one recent study of all births over a 10-year period in Denmark, infants of mothers who were taking SSRIs during pregnancy, but not other antide- pressants, had an almost twofold increased risk of having a low Apgar score—a measure of infant health immediately after birth that predicts IQ scores, performance in school, and neuro- logical disability, including cerebral palsy, epilepsy, and cognitive impairment lasting for many years after birth (Jensen et al., 2013). In addition, 40 to 50 percent of patients do not respond to these drugs, and a substantial number of the remainder are left with residual symptoms. A review of the literature by Michael Bagby and his colleagues at the University of Toronto indicates that response to antidepressant medications appears to be better in those with high social support and worse in those with co-occurring anxiety disorders (Bagby, Ryder, & Cristi, 2002).

37
Q

Lithium

A

Another type of antidepressant drug, lithium carbonate, is a common salt widely available in the natural environment (Alda, 2015). It is found in our drinking water in amounts too small to have any effect. The side effects of therapeutic doses of lithium, however, are potentially more serious than the side effects of other antidepressants. Dosage has to be very carefully regulated to prevent toxicity (poisoning) and lowered thyroid functioning, which might intensify the lack of energy associated with depres- sion. Substantial weight gain is also common. Lithium, however, has one major advantage that distinguishes it from other antide- pressants: It is often effective in preventing and treating manic episodes. For this reason it is most often referred to as a mood- stabilizing drug. Because tricyclic antidepressants can induce manic episodes, even in individuals without preexisting bipolar disorder (Goodwin & Ghaemi, 1998; Goodwin & Jamison, 2007), lithium is a treatment of choice for bipolar disorder, as outlined in the Canadian Network for Mood and Anxiety Treatment guide- lines (Yatham et al., 2013). Other pharmacological treatments for acute bipolar depression include antidepressants, anticonvulsants, and antipsychotics (Vazques et al., 2015).
We are not sure how lithium works (Alda, 2015; Nivoli et al., 2010). It may limit the availability of dopamine and norepineph- rine, but it may have more important effects on some of the neurohormones in the endocrine system, particularly those that influence the production and availability of sodium and potas- sium, electrolytes found in body fluids (Goodwin & Jamison, 1990). Results indicate that 50 percent of bipolar patients respond well to lithium initially, with at least a 50 percent reduction in manic symptoms (Goodwin & Jamison, 2007). Thus, although effective, lithium provides many people with inadequate thera- peutic benefit. Patients who don’t respond to lithium can take other drugs with antimanic properties, including anticonvulsants, such as carbamazepine and valproate (Divalproex), as well as calcium channel blockers such as verapamil (Keck & McElroy, 2002; Sachs & Rush, 2003; Thase & Denko, 2008). Valproate has recently overtaken lithium as the most commonly prescribed mood stabilizer for bipolar disorder (Thase & Denko, 2008) and is equally effective, even for patients with rapid-cycling symp- toms (Calabrese et al., 2005). But newer studies show that these drugs have one distinct disadvantage: They are less effective than lithium in preventing suicide (Thase & Denko, 2008; Tondo et al., 1997). Goodwin and colleagues (2003) reviewed records of more than 20 000 patients taking either lithium or valproate and found the rate of completed suicides was 2.7 times as high in people taking valproate as in people taking lithium. Thus, lithium remains the preferred drug for bipolar disorder, although other mood-stabilizing drugs are often combined with therapeutic doses of lithium (Dunlop et al., 2013; Goodwin & Jamison, 2007; Nierenberg et al., 2013). This finding on the importance of mood- stabilizing drugs was confirmed in a large trial that demonstrated no advantage to adding a traditional antidepressant drug, such as an SSRI, to a mood stabilizer, such as lithium (Sachs et al., 2007).
For those patients who do respond to lithium, studies follow- ing patients for up to five years report that approximately 70 percent relapse, even if they continue to take lithium (Frank et al., 1999; Hammen & Keenan-Miller, 2013). Nevertheless, for almost anyone with recurrent manic episodes, maintenance on lithium or a related drug is recommended to prevent relapse (Yatham et al., 2013).
Another problem with drug treatment of bipolar disorder is that people usually like the euphoric or high feeling that mania produces and they often stop taking lithium to maintain or regain the state; that is, they do not comply with the medication regimen. Because the evidence now clearly indicates that individuals who stop their medication are at considerable risk for relapse, other treatment methods, usually psychological in nature, are used to increase compliance.

38
Q

eleCtroConvulsive therapy anD transCranial maGnetiC stimulation

A

When someone does not respond to medication (or in an extremely severe case), clinicians may consider a more dramatic treatment, electroconvulsive therapy (ECT), the most contro- versial treatment for psychological disorders after psychosurgery. In Chapter 1, we described how ECT was used in the early 20th century. Despite many unfortunate abuses along the way, ECT is considerably changed today. It is now a safe and reason- ably effective treatment for those cases of severe depression that do not improve with other treatments (American Psychiatric Association, 2010; Gitlin, 2009; Kellner et al., 2012; National Institute of Mental Health, 2003).
In current administrations, patients are anaesthetized to reduce discomfort and given muscle-relaxing drugs to prevent bone breakage from convulsions during seizures. Electric shock is administered directly through the brain for less than a second, producing a seizure and a series of brief convulsions that usually lasts for several minutes. In current practice, treatments are administered once every other day for a total of six to ten treat- ments (fewer if the patient’s mood returns to normal). Side effects are generally limited to short-term memory loss and confusion that disappear after a week or two, although some patients may have long-term memory problems. For severely depressed inpa- tients with psychotic features, controlled studies indicate that approximately 50 percent of those not responding to medication will benefit. Continued treatment with medication or psycho- therapy is then necessary because the relapse rate approaches 60 percent (American Psychiatric Association, 2010a; Gitlin, 2009). For example, Sackeim and colleagues (2001) treated 84 patients with ECT and then randomly assigned them to follow- up placebo or one of several antidepressant drug treatments. All patients assigned to placebo relapsed within six months compared to 40 to 60 percent on medication. Thus, follow-up treatment with antidepressant drugs or psychological treatments is necessary, but relapse is still high. Nevertheless, it may not be in the best interest of psychotically depressed and acutely suicidal inpatients to wait three to six weeks to determine whether a drug or psychological treatment is working; in these cases, immediate ECT may be appropriate.
We do not really know why ECT works. Repeated seizures induce massive functional and perhaps structural changes in the brain, which seems to be therapeutic. There is some evidence that ECT increases levels of serotonin, blocks stress hormones, and promotes neurogenesis in the hippocampus. Because of thecontroversial nature of this treatment, its use declined consider- ably during the 1970s and 1980s (American Psychiatric Associa- tion, 2001; De Raedt et al., 2015).
Recently, another method for altering electrical activity in the brain by setting up a strong magnetic field has been introduced. This procedure is called transcranial magnetic stimulation (TMS), and it works by placing a magnetic coil over the individual’s head to generate a precisely localized electromagnetic pulse. Anaesthe- sia is not required, and side effects are usually limited to head- aches. Initial reports, as with most new procedures, showed promise in treating depression (George et al., 2013), and recent observations and reviews have confirmed that TMS can be effec- tive (De Raedt et al., 2015; Mantovani et al., 2012; Schutter, 2009). But results from several important clinical trials with severe or treatment-resistant psychotic depression reported ECT to be clearly more effective than TMS (Eranti et al., 2007). It may be that TMS is more comparable to antidepressant medication than to ECT, and one study reported a slight advantage for combining TMS and medication compared to using either treat- ment alone (Brunoni et al., 2013; Gitlin, 2009).
Several other nondrug approaches for treatment-resistant depression are in development. Vagus nerve stimulation involves implanting a pacemaker-like device that generates pulses to the vagus nerve in the neck, which, in turn, is thought to influence neurotransmitter production in the brain stem and limbic system (Gitlin, 2009; Marangell et al., 2002). Sufficient evidence has accumulated, but results are generally weak and it has been little used. Deep brain stimulation has been used with a few severely depressed patients. In this procedure, electrodes are surgically implanted in the limbic system (the emotional brain). These elec- trodes are also connected to a pacemaker-like device (Mayberg et al., 2005). Initial results show some promise in treatment- resistant patients, but time will tell if this is a useful treatment (Kennedy et al., 2011; Lozano et al., 2012).

39
Q

psyChosoCial treatments

A

Of the effective psychosocial treatments now available for depres- sive disorders, two major approaches are most effective. The first is cognitive behavioural; Aaron T. Beck, the founder of cognitive therapy, is most closely associated with this approach. The second approach, interpersonal psychotherapy, was developed by Myrna Weissman and Gerald Klerman.

40
Q

Cognitive Therapy

A

Beck’s cognitive therapy grew directly out of his observations of the role of deep-seated negative thinking in generating depression (Beck, 1967, 1976; Clark et al., 1999; Young et al., 2014). Univer- sity of New Brunswick Emeritus Professor David A. Clark described the approach as follows. First, clients are taught to examine carefully their thought processes while they are depressed and to recognize “depressive” errors in thinking. This task is not always easy, because many thoughts are automatic and beyond clients’ awareness. Negative thinking seems natural to them. Clients are taught that errors in thinking can directly cause depression. Treatment involves correcting cognitive errors and substituting less depressing and (perhaps) more realistic thoughts and appraisals. Later in therapy, underlying negative cognitive schemas (characteristic ways of viewing the world) that trigger specific cognitive errors are targeted, not only in the clinic but also as part of the client’s daily life. The therapist purposefully takes a Socratic approach, making it clear that therapist and client are working as a team to uncover faulty thinking patterns and the underlying schemas from which they are generated. Therapists must be skillful and highly trained (see Clark et al., 1999). What follows is an example of an actual interaction between Beck and a client named Irene.

Between sessions, clients are instructed to monitor and log their thought processes carefully, particularly during situations in which they might feel depressed. They also attempt to change their behaviour by carrying out specific activities assigned as homework, such as tasks in which clients can test their faulty thinking. For example, a client who has to participate in an upcoming meeting might think, “If I go to that meeting, I’ll just make a fool of myself and all my colleagues will think I’m stupid.” The therapist might instruct the client to go to the meet- ing, predict ahead of time the reaction of her colleagues, and then see what really happens. This part of treatment is called a behav- ioural experiment because the client makes a hypothesis about what’s going to happen (usually a depressing outcome) and then, most often, discovers it is incorrect (“My colleagues congratu- lated me on my presentation”). The therapist typically schedules other activities to reactivate depressed patients who have given up most activities.

41
Q

Interpersonal Psychotherapy

A

We have seen that major disruptions in our interpersonal relation- ships are an important category of stresses that can trigger mood disorders (Joiner & Timmons, 2009; Kendler et al., 2003). In addi- tion, people with few, if any, important social relationships seem at risk for developing and sustaining mood disorders (Beach et al., 2009). Interpersonal psychotherapy (IPT) focuses on resolving problems in existing relationships and learning to form important new interpersonal relationships (Bleiberg & Markowitz, 2014; Gillies, 2001; Klerman et al., 1984; Weissman, 1995).
Therapist Laurie Gillies of the Ontario Institute for Studies in Education and the University of Toronto has described the approach as follows. Like cognitive-behavioural approaches, IPT is highly structured and seldom takes longer than 15 to 20 sessions, usually scheduled once a week (Cuijpers et al., 2011). After identifying life stressors that seem to precipitate the depression, the therapist and patient work collaboratively on the patient’s current interpersonal problems. Typically, these include one or more of four interpersonal issues: (1) dealing with inter- personal role disputes, such as marital conflict; (2) adjusting to the loss of a relationship, such as grief over the death of a loved one; (3) acquiring new relationships, such as getting married or establishing professional relationships; and (4) identifying and correcting deficits in social skills that prevent the person from initiating or maintaining important relationships (Gillies, 2001).
To take a common example, the therapist’s first job is to iden- tify and define an interpersonal dispute (Bleiberg & Markowitz, 2014; Weissman, 1995), perhaps with someone who expects her spouse to support her but has had to take an outside job to help pay bills. The spouse might expect her to share equally in generat- ing income. If this dispute seems to be associated with the onset of depressive symptoms and to result in a continuing series of arguments and disagreements without resolution, it would become the focus for IPT.
After helping identify the dispute, the next step is to bring it to a resolution. First, the therapist helps the patient determine the stage of the dispute.
1. Negotiation stage: Both partners are aware it is a dispute, and they are trying to renegotiate it.
2. Impasse stage: The dispute smoulders beneath the surface and results in low-level resentment, but no attempts are made to resolve it.
3. Resolution stage: The partners are taking some action, such as divorce or separation.
The therapist works with the patient to define the dispute clearly for both parties and develop specific strategies for resolv- ing it.
Studies comparing the results of cognitive therapy and IPT with those of tricyclic antidepressants and other control condi- tions have found that psychosocial approaches and medication are equally effective, and all treatments are more effective than placebo conditions, brief psychodynamic treatments, or other appropriate control conditions for both major depressive disorder and persistent depressive disorder (Hollon, 2011; Hollon & Dimidjian, 2009; Miller, Norman, & Keitner, 1989; Paykel & Scott, 2009; Schulberg et al., 1996). Depending on how success is defined, approximately 50 to 70 percent or more of people benefit from treatment to a significant extent, compared with approximately 30 percent in placebo or control conditions.
Research by Darcy Santor and Vivek Kusumakar at Dalhousie University evaluated the effectiveness of IPT in depressed adoles- cents. Twenty-five adolescents (mean age of 16 years) received 12 weeks of IPT. The majority of teens improved substantially on both self-ratings and clinician ratings of depression symptoms. Depending on the criteria used, 80 to 84 percent of the teens were no longer showing meaningful levels of depressive symptoms by therapy completion. The study suggests that IPT may be effective for treating moderate to severe depression in adolescents, although this needs to be demonstrated in a randomized control study before we can be sure that the changes were actually due to the therapy (Santor & Kusumakar, 2001).

In view of the seriousness of mood disorders in children and adolescents, work has begun on preventing these disorders in these age groups (Muñoz et al., 2010, 2012). Most researchers focus on instilling in children social and problem-solving skills that are adequate to prevent the kinds of social stress so often associated with depression. In fact, Sanders and colleagues (1992) and Dadds, Sanders, Morrison, and Rebgetz (1992) determined that disordered communication and prob- lem-solving skills, particularly within the family, are charac- teristic of depressed children and a natural target for treatment. Beardslee et al. (1997) have observed sustained effects from a preventive program directed at families with children between the ages of 8 and 15 in which one parent had experienced a recent episode of depression. Eighteen months after participat- ing in six to ten family sessions, these families were doing substantially better on most measures than the control families.
In another preventive effort, Gilham, Reivich, Jaycox, and Seligman (1995) taught cognitive and social problem-solving techniques to 69 children in Grades 5 and 6 who were at risk for depression. Compared with children in a matched no-treatment control group, the prevention group reported fewer depressive symptoms during the two years they were followed. More importantly, moderate to severe symptoms were reduced by half and the positive effects of this program increased during the period of follow-up. In a replication, Seligman, Schulman, DeRubeis, and Hollon (1999) conducted a similar course for university students who were at risk for depression based on a pessimistic cognitive style. After three years, students taking the eight-session program experienced less anxiety and depression than a control group receiving the assessments only. This suggests that it might be possible to psychologically “immunize” children and adolescents against depression by teaching appropriate cognitive and social skills before they enter puberty.

42
Q

ComBineD treatments

A

A few studies have tested the very important question of whether combining psychosocial treatments with medication is effective in treating depression (e.g., Beck et al., 1985; Blackburn & Moore, 1997; Hollon et al., 1992; Miller, Norman, Keitner, Bishop, & Down, 1989). With one exception, the results thus far do not strongly suggest any immediate advantage of combined treatment over separate drug or psychosocial treatment. The exception to this finding is a very large study reported by Keller et al. (2000) on the treatment of chronic major depression that was conducted at 12 different clinics. In this, the largest study ever conducted on the treatment of depression, 681 patients were assigned to receive either antidepressant medication (nefazo- done), a cognitive-behavioural therapy constructed specifically for chronically depressed patients, or the combination of the two treatments.
Forty-eight percent of patients receiving each of the individ- ual treatments either were remitted or responded in a clinically satisfactory way, compared with 73 percent of the patients receiving combined treatment. Because this study was conducted with only a subset of depressed patients, those with chronic depression, the findings would need to be replicated before we could say combined treatment was useful for depression generally. In addition, because the study did not include a condi- tion in which the cognitive-behavioural treatment was combined with placebo, we cannot rule out the fact that the enhanced effec- tiveness of the combined treatment was due to placebo factors. A review by Zindel Segal and his colleagues at the Centre for Addiction and Mental Health in Toronto suggests that combined treatment is generally just as effective as separate drug or psychosocial therapies in the treatment of depression. However, when the depression is severe, combined drug and psychosocial treatments appear to have some additional benefits over either treatment administered separately (Segal, Vincent, & Levitt, 2002).
Drugs and CBT seem to operate in different ways, but it remains uncertain which is more effective. It might just be that the most effective treatment depends on the individual, but we know little about these patient characteristics that could be used to personalize therapies. Until we develop such methods, studies continue to compare groups of individuals who share the same diagnosis. Moreover, it is possible that medication, when it works, does so more quickly than psychological treatments for the most part, which in turn have the advantage of increasing the patient’s long-range social functioning (particularly in the case of IPT) and protecting against relapse or recurrence (particu- larly cognitive-behavioural therapy). Combining treatments, therefore, might take advantage of the drugs’ rapid action and the psychosocial protection against recurrence or relapse, thereby allowing eventual discontinuation of the medications.

43
Q

preventinG relapse

A

Given the high rate of recurrence in depression, it is not surprising that well over 50 percent of patients on antidepressant medication relapse if their medication is stopped within four months after their last depressive episode (Thase, 1990). Therefore, one impor- tant question has to do with maintenance treatment to prevent relapse or recurrence over the long term.
In several studies, cognitive therapy reduced rates of subse- quent relapse in depressed patients by more than 50 percent over groups treated with antidepressant medication (see, e.g., Hollon et al., 2005, 2006; Teasdale et al., 2000). Jarrett and colleagues (2013) compared CBT, an SSRI (fluoxetine), and a pill placebo as a relapse prevention strategy for people with recurrent major depressive disorder. The study first treated everybody with CBT and then randomized people to receive either continued CBT, the SSRI, or the placebo for eight months. Then, treatment was stopped and patients were followed up for two years to examine relapse rates. The study showed that, overall, both CBT and the SSRI prevented relapse equally well and more so than the placebo. Relapse rates after having received CBT and fluoxetine did not differ.
Zindel Segal and his colleagues collaborated with researchers in the United Kingdom on a variant of traditional cognitive ther- apy that is specifically designed to prevent depressive relapse. This new therapy is called mindfulness-based cognitive therapy (Segal, Williams, & Teasdale, 2002). It is a group therapy designed to teach recovered depressed patients to disengage from he kinds of negative thinking that can precipitate a relapse to depression. More specifically, they are trained in mindfulness meditation to help them become more aware of their thoughts and feelings and to view their thoughts as mental events rather than as accurate reflections of reality. In a recent randomized control study, 145 patients recovered from depression were assigned to receive either mind- fulness-based cognitive therapy or treatment as usual, and relapse of major depression was assessed over a 60-week period.

44
Q

psyChosoCial treatments For Bipolar DisorDer

A

Although medication, particularly lithium, is the preferred treat- ment for bipolar disorder, most clinicians emphasize the need for psychosocial intervention to manage interpersonal and practical problems, such as marital and job difficulties, that result from the disorder (Clarkin et al., 1988). Until recently, the principal objec- tive of psychosocial intervention was to increase compliance with medication regimens, such as lithium (Cochran, 1984). We noted before that the “pleasures” of a manic state make refusal to take lithium a major therapeutic obstacle. Giving up drugs between episodes or skipping dosages during an episode significantly undermines treatment. Therefore, a careful integration of psycho- social and lithium treatments is very important (Goodwin & Jamison, 2007). For example, Clarkin, Carpenter, Hull, Wilner, and Glick (1998) evaluated the advantages of adding a psycho- logical treatment to medication in inpatients and found it improved adherence to medication for all patients and resulted in better overall outcomes for the most severe patients compared with medication alone.
More recently, psychological treatments have also been directed at psychosocial aspects of bipolar disorder. Ellen Frank and her colleagues developed a psychological treatment that regulates circa- dian rhythms by helping patients regulate their eating and sleep cycles and other daily schedules and cope more effectively with stressful life events, particularly interpersonal issues (Frank et al., 1997, 1999, 2005). In an evaluation of this approach, called interper- sonal and social rhythm therapy (IPSRT), patients receiving IPSRT lasted longer without a new manic or depressive episode compared with patients undergoing standard, intensive clinical management. Initial results with adolescents are also promising (Hlastala et al., 2010).
David Miklowitz and his colleagues found that family tension is associated with relapse in bipolar disorder. Preliminary studies indicate that treatments directed at helping families understand symptoms and develop new coping skills and communication stylesdochangecommunicationstyles(Simoneauetal.,1999) and prevent relapse (Miklowitz, 2014). Miklowitz, George, Richards, Simoneau, and Suddath (2003) demonstrated that their family-focused treatment combined with medication results in significantly less relapse one year following initiation of treat- ment than occurs in patients receiving crisis management and medication over the same period. Specifically, only 35 percent of patients receiving family therapy plus medication relapsed, compared with 54 percent in the comparison group. Similarly, family therapy patients averaged over a year and a half (73.5 weeks) before relapsing, significantly longer than the compari- son group.

Rea, Tompson, and Miklowitz (2003) compared this approach to an individualized psychotherapy in which patients received the same number of sessions over the same period and continued to find an advantage for the family therapy after two years. Reilly- Harrington et al. (2007) found some evidence that CBT is effec- tive for bipolar patients with rapid cycling. In view of the relative ineffectiveness of antidepressant medication for the depressive stage of bipolar disorder reviewed above, Miklowitz et al. (2007) reported an important study showing that up to 30 sessions of an intensive psychological treatment was significantly more effec- tive than the customary best treatment in promoting recovery from bipolar depression and remaining well. A more recent trial compared the effects after one year of four months of family- focused therapy and an educational control condition on prevent- ing mood symptoms in youths who are at high risk for developing bipolar disorder based on their family history and environment (Miklowitz et al., 2013). The study showed that participants who received the family-focused therapy had a more rapid recovery from their initial mood symptoms and were more often in remis- sion one year following treatment than those in the education control condition. The specificity of this effect on bipolar depres- sion, which is the most common stage of bipolar disorder, combined with the lack of effectiveness of antidepressants, suggest that these procedures will provide an important contribu- tion to the comprehensive treatment of bipolar disorder.
Let us now return to Katie who, you will remember, had made a serious suicide attempt in the midst of a major depressive episode.

45
Q

SuICIDe

A

Most days we are confronted with news about the war on cancer or the frantic race to find a cure for AIDS. We also hear never-ending admonitions to improve our diet and to exercise more to prevent heart disease. But another cause of death is as frightening and dangerous as these medical conditions—the decision to kill oneself, made by about 800 000 people per year worldwide (World Health Organization, 2014). Suicide mortality rates are given per 100 000 people, and in 2016 the World Health Organization (2019) esti- mated the global suicide rate to be 10.5 per 100 000 people. The global rate has declined since 2000, but not in all regions or countries; some have seen dramatic increases in their suicide mortality rate (World Health Organization [WHO], 2014). Canada is one of the fortunate countries witnessing a decline; the suicide rate dropped from 14.4 per 100 00 people in 1979 to 10.4 per 100 000 in 2012 (Skinner et al., 2016). However, it is important to recognize that most epidemiologists agree that the actual number of suicides is higher than official statistics suggest. Many of these unreported suicides occur when people purposefully drive off a bridge or a cliff (Blumenthal, 1990).
Regardless of age, in every country around the world except China, men are more likely to commit suicide than women. Although it was previously thought that men were at least three times as likely to commit suicide as women, recent work by the WHO (2014) demonstrated that this is likely a phenomenon specific to high-income countries. In high-income countries, the ratio of male-to-female suicides was 3.5, compared to a ratio of 1.6 in middle- and low-income countries. The Public Health Agency of Canada (PHAC, 2018), in a high-income country, esti- mated that Canadian men committed suicide at rates 3.3 times that of Canadian women. ■ Figure 8.7 displays the suicide rates for Canadian men and women across time. It clearly illustrates this gender difference as well as the general decline in suicide rates over time, although it appears that the rates continue to decline for men but not women (Skinner et al., 2016)
This gender difference seems to be related in part to the types of suicide attempts made by men and women. Men generally choose far more violent methods, such as guns and hanging; women tend to rely on less violent options, such as drug overdose (Buda & Tsuang, 1990; Callanan & Davis, 2012; Nock et al., 2011). A Canadian study provides further support for gender differences in method of suicide (Skinner et al., 2016). Although suffocation accounted for the majority of suicide deaths for both men and women (48 and 44 percent, respectively), it was esti- mated that in 2012 firearms accounted for 18 percent of suicide deaths for men but only 2 percent of women, whereas poisoning accounted for 40 percent of suicide deaths for women but only 18 percent of men. In China, and uniquely in China, more women commit suicide than do men, particularly in rural settings (Nock et al., 2008; Sun, 2011; Wu, 2009). What accounts for this rever- sal? Chinese scientists agree that China’s suicide rates are due to an absence of stigma. In fact, suicide, particularly among women, is often portrayed in classical Chinese literature as a reasonable solution to problems. A rural Chinese woman’s family is her entire world, and suicide is an honourable solution if the family collapses.
Globally, the suicide mortality rate is lowest among young people 15 years of age or younger and highest among those 70 years of age and older. However, as with gender differences, age differences are affected by a country’s income (WHO, 2014). For example, young adults and older women have higher suicide mortality rates in lower- and middle-income countries than inhigh-income countries. Middle-aged men have higher suicide mortality rates in higher-income countries than in low- and middle-income countries. Canadian studies have provided
evidence for low suicide rates among young people under the age of 15, as well as a peak in suicide rates among middle-aged men (PHAC, 2018; Skinner et al., 2016).
In Canada, suicide is the second-leading cause of death, after accidents (Navaneelan, 2012). However, this ranking changes as Canadians age. Suicide is the second-leading cause of death for Canadians between 15 and 34 years of age (accounting for 28 percent of deaths for those 15 to 19 years of age, 23 percent for those 20 to 24 years, and 20 percent of those 25 to 34 years). Suicide drops to the third-leading cause of death among 35- to 44-year-olds and to the fourth-leading cause among 45- to 54-year-olds (accounting for 14 and 7 percent of deaths, respec- tively) as other causes of death, such as cancer and circulatory problems, become more prominent (Skinner et al., 2016). For teenagers in the United States, suicide is the third-leading cause of death, behind motor vehicle accidents and homicide (Centers for Disease Control and Prevention [CDC], 2010b). Suicide rates are also a concern among seniors, often connected to the growing incidence of medical illness in our oldest citizens and to their increasing loss of social support. As we have noted, a strong rela- tionship exists between illness or infirmity and hopelessness or depression (Brown et al., 2000). Suicide is not attempted only by adolescents and adults: Rosenthal and Rosenthal (1984) described 16 children aged two to five years who had attempted suicide at least once, many injuring themselves severely.
In addition to completed suicides, two other important indi- ces of suicidal behaviour are suicidal attempts (the person survives) and suicidal ideation (thinking seriously about suicide). Although males commit suicide more often than females in most of the world (e.g., CDC, 2013), females attempt suicide more often (Berman & Jobes, 1991). The high incidence of suicidal attempts among women may reflect the fact that more women than men are depressed and that depression is strongly related to suicide attempts (Frances et al., 1986). Some estimates place the ratio of attempted to completed suicides at 50 or more to one (Garfield & Zigler, 1993). In addition, results from another study (Kovacs et al., 1993) suggest that among adoles- cents, the ratio of thoughts about suicide to attempts is between three to one and six to one. In other words, between 16 and 30 percent of adolescents in this study who had thought about killing themselves actually attempted it. “Thoughts” in this context does not refer to a fleeting philosophical type of consid-
eration but rather to a serious contemplation of the act. The first step down the dangerous road to suicide is seriously thinking about it (Mishara, 1999).

In a study of university students (whose rate of suicide is about half that of the general population), approximately 12 percent had thoughts about suicide during the past 12 months (Wilcox et al., 2010). Only a minority of these students with thoughts of suicide (perhaps around 10 percent) attempt to kill themselves, and only a few succeed (Schwartz, 2011). Nevertheless, given the enormity of the problem, suicidal thoughts are taken very seriously by mental health professionals.
In Canada, the suicide rate and the rate of suicidal attempts vary widely across the provinces and territories (Skinner et al., 2016). For example, the highest rates of suicide occurred in the territories (Nunavut at 64 per 100 000 people, Yukon at 18.7 per 100 000, and the Northwest Territories at 18.4 per 100 000), and Newfoundland and Labrador and Ontario having two of the lowest rates (7.8 per 100 000 and 8.5 per 100 000, respectively). The alarmingly high suicide rates in Nunavut highlight concerns about suicide among Canadian Inuit. While recognizing that previous research has found that suicide rates can vary dramati- cally across First Nations and Inuit communities (e.g., Chandler & Lalonde, 1998), PHAC (2018) documented that areas with high concentrations of Indigenous Peoples had suicide rates several times as high as areas with low concentrations of Indige- nous Peoples. This difference in rates was much higher in areas where Inuit were the predominant group. The rate was 6.5 times as high for areas with a high concentration of Inuit compared to only 3.7 and 2.7 as high for areas with high concentrations of First Nations and Métis, respectively. Men in all groups had higher suicide rates than women—the suicide rate among male Inuit was five times that of female Inuit (118.2 per 100 000 compared to 24.5 per 100 000).
Boothroyd, Kirmayer, Spreng, Malus, and Hodgins (2001) studied cases of completed suicides in Nunavik from 1982 to 1996 to identify risk factors. Most cases were young males, ages 15 to 24, who usually committed suicide by hanging or gunshot. Psychiatric problems, such as depression, personality disorder, and drug abuse, were very common in these cases. A study of all suicides by Inuit that occurred between 2003 and 2006 found differences between these individuals and community-matched comparison persons who did not commit suicide (Chachamovich et al., 2015). Similar to findings in the previous study, Inuit who committed suicide were more likely to have been affected by depression or a personality disorder and be dependent on alcohol or cannabis. They also were more likely to have experienced abuse during childhood and to have family histories that included depression and suicide. As we describe in a later section, these factors are typically related to suicide in studies of the general population. The authors also noted a high prevalence of mental health problems among the community-comparison persons who did not commit suicide and called for improved access to mental health services for Inuit.
A study of suicidal ideation (thinking seriously about suicide) found similar patterns of results when comparing the population of non-Indigenous adults living in the Canadian provinces with adult Indigenous Peoples (Statistic Canada, 2016b). Data from the 2012 Canadian Community Health Survey-Mental Health Survey (CCHS-MH) and the 2012 Aboriginal Peoples Survey demonstrated that a greater propor- tion of off-reserve First Nations (21 percent), Métis (18 percent), and Inuit (22 percent) had seriously thought about suicide in their lifetime compared to the non-Indigenous Canadian popu- lation (12 percent). These surveys do not cover First Nations living on reserve, but a separate study indicated 16 percent of adult First Nations living on reserve had considered suicide in their lifetime (First Nations Information Governance Centre [FNIGC], 2018b). In keeping with the findings discussed earlier regarding suicide attempts, for all groups in these studies, a greater proportion of women than men had seriously considered suicide in their lifetime.
The impact of residential schools on suicide ideation was examined for First Nations living on reserve (FNIGC, 2018a). The study examined four groups: First Nations not affected by residential schools, those who had at least one grandparent who attended, those with at least one parent who attended, and survivors (15 percent of First Nations had personally attended residential school). The proportion of adults who had seriously considered suicide in their lifetime varied considerably across the groups. Among adults, the proportion considering suicide in their lifetime was lowest among those not affected by resi- dential schools (8.7 percent) and highest among those with at least one parent who had attended (21.6 percent). Survivors (16.6 percent) and those with at least one grandparent who attended (18.7 percent) also had higher proportions of those who seriously considered suicide compared with those not affected by residential schools.

46
Q

Causes of suicide

A

The great sociologist Émile Durkheim (1951) defined several suicide types, based on the social or cultural conditions in which they occurred. One type is “formalized” suicides that were approved of, such as the ancient custom of hara-kiri in Japan, in which an individual who brought dishonour to himself or his family was expected to impale himself on a sword. Durkheim referred to this as altruistic suicide. Durkheim also recognized the loss of social supports as an important provocation for suicide; he called this egoistic suicide. (Seniors who kill them- selves after losing touch with their friends or family fit into this category.) Magne-Ingvar, Ojehagen, and Traskman-Bendz (1992) found that only 13 percent of 75 individuals who had seriously attempted suicide had an adequate social network of friends and relationships. Similarly, a recent study found that suicide attempters perceived themselves to have lower social support than did those who did not attempt suicide (Riihimaki et al., 2013). Anomic suicides are the result of marked disrup- tions, such as the sudden loss of a high-prestige job. (Anomie is feeling lost and confused.) Finally, fatalistic suicides result from a loss of control over our own destiny. The mass suicide of 39 Heaven’s Gate cult members is an example of this type, because the lives of those people were largely in the hands of Marshall Applewhite, a supreme and charismatic leader.
Durkheim’s work was important in alerting us to the social contribution to suicide. Freud (1917, 1957) believed that suicide (and depression, to some extent) indicated unconscious hostility directed inward to the self rather than outward to the person or situation causing the anger. Indeed, suicide victims often seem to be psychologically punishing others who may have rejected them or caused some other personal hurt. Current thinking considers social and psychological factors but also highlights the potential importance of biological contributions.

47
Q

risk FaCtors of suicide

A

Edward Shneidman pioneered the study of risk factors for suicide (Shneidman, 1989; Shneidman et al., 1970). Among the methods he and others have used to study those conditions and events that make a person vulnerable is psychological autopsy. The psycho- logical profile of the person who committed suicide is recon- structed through extensive interviews with friends and family members who are likely to know what the individual was thinking and doing in the period before death. This and other methods have allowed researchers to identify a number of risk factors for suicide.

48
Q

Family History

A

If a family member committed suicide, the risk increases that someone else in the family will also (Brent et al., 2014; Mann et al., 2005). In fact, among depressed patients, the strongest predictor of suicidal behaviour was having a family history of suicide (Hantouche et al., 2010). This may not be surprising, because so many people who kill themselves are depressed, and depression runs in families. Nevertheless, the question remains: Are people who kill themselves simply adopting a familiar solu- tion or does an inherited trait, such as impulsivity, account for increased suicidal behaviour in families? The possibility that something is inherited is supported by several adoption studies. One found an increased rate of suicide in the biological relatives of adopted individuals who had committed suicide, compared with a group of adoptees who had not committed suicide (Nock et al., 2011). Also, reviewing studies of adopted children and their biological and adopted families, Brent and Mann (2005) found that adopted individuals’ suicidal behaviour was predicted only by suicidal behaviour in their biological relatives. In a small study of people whose twins had committed suicide, 10 out of 26 surviving monozygotic co-twins, and none of nine surviving dizy- gotic co-twins had themselves attempted suicide (Roy et al., 1995). This finding suggests some biological (genetic) contribu- tion to suicide, even if it is relatively small.

49
Q

Neurobiology

A

A variety of evidence suggests that low levels of serotonin may be associated with suicide and with violent suicide attempts (Cremniter et al., 1999; Pompili et al., 2010; Winchel et al., 1990). As we have noted, extremely low levels of serotonin are associated with impulsivity, instability, and the tendency to overreact to situa- tions (Spoont, 1992). It is very possible then that low levels of serotonin may contribute to creating a vulnerability to act impul- sively. This impulsiveness may include suicide, which is sometimes a very impulsive act. Studies by Brent and colleagues (2002) and Mann and colleagues (2005) suggest that transmission of vulnera- bilities for a mood disorder, including the trait of impulsivity, may mediate family transmission of suicide attempts.

50
Q

Existing Psychological Disorders

A

More than 90 percent of people who kill themselves have a psychological disorder (Conwell et al., 1996; Orbach, 1997). Suicide is often associated with mood disorders and for good reason. As many as 60 percent of suicides (75 percent of adoles- cent suicides) are associated with an existing mood disorder (Brent & Kolko, 1990; Frances et al., 1986). Lewinsohn, Rohde, and Seeley (1993) concluded that, in adolescents, suicidal behav- iour is in large part an expression of severe depression. But many people with mood disorders do not attempt suicide. Analyses of the 2012 CCHS-MH revealed that only 6.6 percent of those Cana- dians 15 years of age or older with major depressive disorder attempted suicide in the past year compared to less than 1 percent of those without major depressive disorder (Patten et al., 2015). Conversely, some people who attempt suicide do not have mood disorders. Looking more closely at the relationship of mood disorder and suicide, some investigators have isolated hopeless- ness, a specific component of depression, as strongly predictive of suicide (Beck, 1986; Kazdin, 1983). Hopelessness also predicts suicide among individuals whose primary mental health problem is not depression (David Klonsky et al., 2012; Simpson et al., 2011).
Alcohol use and abuse are associated with approximately 25 to 50 percent of suicides and are particularly evident in suicide among college students (Lamis et al., 2010) and adolescents (Berman, 2009; Hawton et al., 2003; Pompili et al., 2012). Brent and colleagues (1988) found that about one-third of adolescents who commit suicide were intoxicated when they died and that many more might have been under the influence of drugs. Combi- nations of disorders, such as substance abuse and mood disorders in adults or mood disorders and conduct disorder in children and adolescents, seem to create a stronger vulnerability than any one disorder alone (Conwell et al., 1996; Nock, Hwang, et al., 2010; Woods et al., 1997). Woods and colleagues found that substance abuse combined with other risk-taking behaviours, such as getting into fights, carrying a gun, or smoking, were predictive of teenage suicide, possibly reflecting impulsivity in these troubled adoles- cents. A closely related trait termed sensation-seeking predicts teenage suicidal behaviour as well—beyond its relationship with depression and substance use (Ortin et al., 2012). Past suicide attempts are another strong risk factor and must be taken seri- ously (Berman, 2009). Cooper and colleagues (2005) followed for up to four years almost 8000 individuals who were treated in the emergency room for deliberate self-harm. Sixty of these people later killed themselves, which equates to 30 times the rate for the general population.
A disorder characterized more by impulsivity than depression is borderline personality disorder (see Chapter 13). Frances and Blumenthal (1989) suggest that these individuals, known for making manipulative and impulsive suicidal gestures without necessarily wanting to destroy themselves, sometimes kill them- selves by mistake in as many as 10 percent of the cases. The combination of borderline personality disorder and depression is particularly deadly (Soloff et al., 2000)

51
Q

Stressful Life Events

A

Perhaps the most important risk factor for suicide is a severe, stressful event experienced as shameful or humiliating, such as a failure (real or imagined) in school or at work, an unexpected arrest, or rejection by a loved one (Conwell et al., 2002; Joiner & Rudd, 2000). Physical and sexual abuse are also important sources of stress (Kirmayer et al., 1996; Wagner, 1997). New evidence now confirms that the stress and disruption of natural disasters increase the likelihood of suicide (Krug et al., 1998) particularly in the case of extreme catastrophes, like massive earthquakes (Matsubayashi et al., 2012). Based on data from 337 countries experiencing natural disasters in the 1980s, Krug and colleagues (1998) concluded that the rates of suicide increased 14 percent in the four years after severe floods, 31 percent in the two years after hurricanes, and 63 percent in the first year after an earthquake. Given preexisting vulnerabilities—including psycho- logical disorders, traits of impulsiveness, and lack of social support—a stressful event can often put a person over the edge. An integrated model of the causes of suicidal behaviour is presented in ■ Figure 8.8.

52
Q

is suiCiDe ContaGious?

A

We hear all too often of the suicide of a teenager or celebrity. Most people react with sadness and curiosity. Some people react by attempting suicide themselves, often by the same method they have just heard about. Gould (1990) reported an increase in suicides during the nine days after widespread publicity about a suicide, and a recent review found a positive relationship between suicidal behaviour and exposure to media coverage related to suicide (Sisask & Varnik, 2012). Clusters of suicides (several people copying one person) seem to predominate among teenagers, with as many as 5 percent of all teenage suicides reflecting an imitation (Gould, 1990; Gould et al., 2003).
Why would anyone want to copy a suicide? First, suicides are often romanticized in the media: An attractive young person under unbearable pressure commits suicide and becomes a martyr to friends and peers by getting even with the (adult) world for creating such a difficult situation. Media accounts often describe in detail the methods used in the suicide, thereby providing a guide to potential victims. Little is reported about the paralysis, brain damage, and other tragic consequences of the incomplete or failed suicide or about the fact that suicide is almost always associated with a severe psychological disorder. More important, even less is said about the futility of this method of solving problems (Gould, 1990; O’Carroll, 1990). To prevent these tragedies, the media should not inadvertently glorify suicides in any way, and mental health professionals must inter- vene immediately in schools and other locations with people who might be depressed or otherwise vulnerable to the contagion of suicide (Boyce, 2011). But it isn’t clear that suicide is really contagious in the infectious disease sense. Rather, the stress of a friend’s suicide or some other major stress may affect several individuals who are vulnerable because of existing psychological disorders (Blasco-Fontecilla, 2012; Joiner, 1999). Nevertheless, effective intervention is essential.

53
Q

treatment for suicide

A

Despite the identification of important risk factors, predicting suicide is still an uncertain art. Individuals with very few precipi- tating factors unexpectedly kill themselves, and many who live with seemingly insurmountable stress and illness and have little social support or guidance somehow survive and overcome their difficulties.
Mental health professionals are very thoroughly trained in assessing for possible suicidal ideation (Fowler, 2012; Joiner et al., 2007). Others might be reluctant to ask leading questions for fear of putting the idea in someone’s head. We know, however, that it is far more important to check for these ideas than to do nothing, because the risk of inspiring suicidal thoughts is very small and the risk of leaving them undiscovered is enormous (Berman, 2009). Gould and colleagues (2005) found that more than 1000 high school students who were asked about suicidal thoughts or behaviours during a screening program showed no risk of increased suicidal thoughts compared with a second group of 1000 students who had the screening program without the questions about suicide. Therefore, if there is any indication whatsoever that someone is suicidal, the mental health professional will inquire, “Has there been any time recently when you’ve had some thoughts about hurting yourself or possibly killing yourself?”

The mental health professional will also check whether any of the risk factors are present that might indicate a high probability of suicide. For example, does a person who is thinking of suicide have a detailed plan or just a vague fantasy? If a plan is discov- ered that includes a specific time, place, and method, the risk is obviously high. Does the detailed plan include putting all personal affairs in order, giving away possessions, and other final acts? If so, the risk is higher still. What specific method is the person considering? Generally, the more violent the method (guns, hang- ing, poison, and so on), the greater the risk it will be used. Does the person really understand what might actually happen? Many people do not understand the effects of the pills on which they might overdose. Finally, has the person taken any precautions against being discovered? If so, the risk is extreme (American Psychiatric Association, 2003).
If a risk is present, clinicians attempt to get the individual to agree to or perhaps even sign a “no-suicide contract.” Usually, this includes a promise not to do anything remotely connected with suicide without contacting the mental health professional first. Although signing a contract will not prevent a suicide attempt in someone who is determined, if the person at risk refuses a contract (or the clinician has serious doubts about the patient’s sincerity) and the suicidal risk is judged to be high, immediate hospitalization is indicated, even against the will of the patient. Whether the person is hospitalized or not, treatment aimed at resolving underlying life stressors and treating existing psychological disorders should be initiated immediately.
In view of the public health consequences of suicide, many programs have been implemented to reduce the rates of suicide both in Canada and in other parts of the world. They include curriculum-based programs in which teams of professionals go into schools or other organizations to educate people about suicide and provide information on handling life stress. The United Kingdom targeted reducing suicide rates by 15 percent, and policymakers and mental health professionals are determin- ing the best methods for achieving this goal (Lewis, Hawton, & Jones, 1997). More than 200 suicide prevention and crisis centres across Canada provide 24-hour phone service to people in crisis, including those considering suicide (Dyck & White, 1998). Some findings are encouraging, such as a study showing that suicide rates declined in the years following the establish- ment of suicide prevention centres in several cities (Lester, 1991). Unfortunately, however, most research indicates that such educational and crisis phone line programs are not effective (Garfield & Zigler, 1993; Shaffer et al., 1991). As Garfield and Zigler point out, hotline volunteers must be backed up by compe- tent mental health professionals who can identify potentially serious risks.
More helpful are programs targeted to at-risk individuals, including adolescents in schools where a student has commit- ted suicide. The Institute of Medicine (2002) recommends making services available immediately to friends and relatives of victims. In a study following a suicide in a high school, Brent and colleagues (1989) identified 16 students as strongly at risk and referred them for treatment. Another important step is limiting access to lethal weapons for anyone at risk for suicide.
Specific treatments for people at risk have also been devel- oped. Suicide prevention programs for older adults, for example, tend to focus on decreasing risk factors (e.g., treating depression) rather than shoring up protective factors like familial support, and could be improved by greater involvement of individuals’ social networks (Lapierre et al., 2011). Other interventions target specific mental health problems associated with suicide. For instance, Marsha Linehan and her colleagues (e.g., Linehan & Kehrer, 1993) developed a noteworthy treatment for borderline personality disorder that addresses the impulsive suicidal behav- iour associated with this condition.
Emphasizing protective factors, such as culture and commu- nity, is likely critical to the success of programs developed for Indigenous Peoples in Canada. One study documented that among First Nations adults living on reserve and in northern communities, those who had never made a suicidal attempt reported higher levels of community wellness than those who had made a suicidal attempt (FNIGC, 2018b). First Nations emphasize the interconnections between mental wellness and factors such as language, land, family, and environment, and have embedded them in the First Nations Mental Wellness Continuum, a model to support First Nations mental health initiatives (Assembly of First Nations & Health Canada, 2015). Concerns about suicide rates among Inuit youth prompted the development of an intervention program for youth that was based on Inuit and community perspectives on health (Healey et al., 2016). The resulting camp program emphasized Inuit identity and cultural skill building, and early evaluations have documented its success in promoting wellness among the participants.
Empirical research indicates that cognitive-behavioural inter- ventions can help decrease suicide risk. For example, in an impor- tant study, David Rudd and colleagues developed a brief psychological treatment targeting young adults who were at risk for suicide due to the presence of suicidal ideation accompanied by previous suicidal attempts or mood or substance use disorders (Rudd et al., 1996). Patients were assessed up to two years following treatment, and results indicated reductions in suicidal ideation and behaviour, as well as marked improvement in prob- lem-solving ability. This program has now been expanded into the first psychological treatment for suicidal behaviour with empiri- cal support for its efficacy (Rudd et al., 2001). The quest will go on to determine more effective and efficient ways of preventing one of the most serious consequences of any psychological disorder.