Psychological Perspectives on Mood Disorders

Learning Objectives

  • Describe and compare viewpoints from the major psychological perspectives related to mood disorders
  • Describe biological and genetic explanations for mood disorders

Biological Theories on Mood Disorders

Mood disorders have been shown to have a strong genetic and biological basis. Relatives of those with major depressive disorder have double the risk of developing major depressive disorder, whereas relatives of patients with bipolar disorder have over nine times the risk (Merikangas et al., 2011). The rate of concordance for major depressive disorder is higher among identical twins than fraternal twins (50% vs. 38%, respectively), as is that of bipolar disorder (67% versus 16%, respectively), suggesting that genetic factors play a stronger role in bipolar disorder than in major depressive disorder (Merikangas et al. 2011). People with mood disorders often have imbalances in certain neurotransmitters, particularly norepinephrine and serotonin (Thase, 2009). Specific neurotransmitters are important regulators of the bodily functions that are disrupted in mood disorders, including appetite, sex drive, sleep, arousal, and mood. Medications that are used to treat major depressive disorder typically boost serotonin and norepinephrine activity, whereas lithium—used in the treatment of bipolar disorder—blocks norepinephrine activity at the synapses.
An illustration shows the synaptic space between two neurons with neurotransmitters being released into the synapse and attaching to receptors.

Figure 1. Many medications designed to treat mood disorders work by altering neurotransmitter activity in the neural synapse.

Depression is linked to abnormal activity in several regions of the brain (Fitzgerald, Laird, Maller, & Daskalakis, 2008), including those important in assessing the emotional significance of stimuli and experiencing emotions (amygdala) and in regulating and controlling emotions (like the prefrontal cortex, or PFC) (LeMoult, Castonguay, Joormann, & McAleavey, 2013). Depressed individuals show elevated amygdala activity (Drevets, Bogers, & Raichle, 2002), especially when presented with negative emotional stimuli, such as photos of sad faces (Surguladze et al., 2005). Interestingly, heightened amygdala activation to negative emotional stimuli among depressed persons occurs even when stimuli are presented outside of conscious awareness (Victor, Furey, Fromm, Öhman, & Drevets, 2010), and it persists even after the negative emotional stimuli are no longer present (Siegle, Thompson, Carter, Steinhauer, & Thase, 2007). Additionally, depressed individuals exhibit less activation in the prefrontal, particularly on the left side (Davidson, Pizzagalli, & Nitschke, 2009). Because the prefrontal cortex (PFC) can dampen amygdala activation, thereby enabling one to suppress negative emotions (Phan et al., 2005), decreased activation in certain regions of the prefrontal cortex (PFC) may inhibit its ability to override negative emotions that might then lead to more negative mood states (Davidson et al., 2009). These findings suggest that depressed persons are more prone to react to emotionally negative stimuli, yet have greater difficulty controlling these reactions.

A photograph shows a sad-looking dog.

Figure 2. Depressed individuals react to negative emotional stimuli, such as sad faces, with greater amygdala activation than do non-depressed individuals. (credit: Ian Munroe)

Since the 1950s, researchers have noted that depressed individuals have abnormal levels of cortisol, a stress hormone released into the blood by the neuroendocrine system during times of stress (Mackin & Young, 2004). When cortisol is released, the body initiates a fight-or-flight response in reaction to a threat or danger. Many people with depression show elevated cortisol levels (Holsboer & Ising, 2010), especially those reporting a history of early life trauma such as the loss of a parent or abuse during childhood (Baes, Tofoli, Martins, & Juruena, 2012). Such findings raise the question of whether high cortisol levels are a cause or a consequence of depression. High levels of cortisol are a risk factor for future depression (Halligan, Herbert, Goodyer, & Murray, 2007), and cortisol activates activity in the amygdala while deactivating activity in the PFC (McEwen, 2005)—both brain disturbances are connected to depression. Thus, high cortisol levels may have a causal effect on depression, as well as on its brain function abnormalities (van Praag, 2005). Also, because stress results in increased cortisol release (Michaud, Matheson, Kelly, Anisman, 2008), it is equally reasonable to assume that stress may precipitate depression.

Diathesis-Stress Model and Major Depressive Disorders

Indeed, it has long been believed that stressful life events can trigger depression, and research has consistently supported this conclusion (Mazure, 1998). Stressful life events include significant losses, such as the death of a loved one; divorce or separation; and serious health and money problems; life events such as these often precede the onset of depressive episodes (Brown & Harris, 1989). In particular, exit events—instances in which an important person departs (e.g., a death, divorce or separation, or a family member leaving home)—often occur prior to an episode (Paykel, 2003). Exit events are especially likely to trigger depression if these happenings occur in a way that humiliates or devalues the individual. For example, people who experience the breakup of a relationship initiated by the other person develop major depressive disorder at a rate more than two times that of people who experience the death of a loved one (Kendler, Hettema, Butera, Gardner, & Prescott, 2003).

Pie chart showing the interplay between biological, social/cultural, and psychological forces. Depression, biological is 40%, and psychological and social/cultural make up 30% each.

Figure 3. Depression is influenced by biological, psychological, and social/cultural factors, though research indicates that there are strong genetic and biological ties to depression.

Likewise, individuals who are exposed to traumatic stress during childhood—such as separation from a parent, family turmoil, and maltreatment (physical or sexual abuse)—are at a heightened risk of developing depression at any point in their lives (Kessler, 1997). A recent review of 16 studies involving over 23,000 subjects concluded that those who experience childhood maltreatment are more than two times as likely to develop recurring and persistent depression (Nanni, Uher, & Danese, 2012).

Of course, not everyone who experiences stressful life events or childhood adversities succumbs to depression—indeed, most do not. Clearly, a diathesis-stress interpretation of major depressive disorder, in which certain predispositions or vulnerability factors influence one’s reaction to stress, would seem logical. If so, what might such predispositions be? Caspi et al. (2003) suggested that an alteration in a specific gene that regulates serotonin (the 5-HTTLPR gene) might be one culprit. Caspi et al. found that people who experienced several stressful life events were significantly more likely to experience episodes of major depression if they carried one or two short versions of this gene than if they carried two long versions. Individuals who carried one or two short versions of the 5-HTTLPR gene were unlikely to experience an episode, however, if they had experienced few or no stressful life events. Numerous studies have replicated these findings, including studies of people who experienced maltreatment during childhood (Goodman & Brand, 2009). In a recent investigation conducted in the United Kingdom (Brown & Harris, 2013), researchers found that childhood maltreatment before age nine elevated the risk of chronic adult depression (a depression episode lasting for at least 12 months) among those individuals having one (LS) or two (SS) short versions of the 5-HTTLPR gene. Childhood maltreatment did not increase the risk for chronic depression for those have two long (LL) versions of this gene. Thus, genetic vulnerability may be one mechanism through which stress potentially leads to depression.

A bar graph has an x-axis labeled “version of 5-HTTLPR gene” and a y-axis labeled “percent of chronic depression in adulthood.” Data compares the type of gene combination and whether childhood maltreatment occurred prior to age 9. People with no childhood maltreatment prior to age 9 have a percentage of chronic depression of approximately 23% with the long-long gene, 19% with the long-short gene, and 20% with the short-short gene. People with childhood maltreatment prior to age 9 have a percentage of chronic depression of approximately 22% with the long-long gene, 53% with the long-short gene, and 71% with the short-short gene.

Figure 4. A study on gene-environment interaction in people experiencing chronic depression in adulthood suggests a much higher incidence in individuals with a short version of the gene in combination with childhood maltreatment (Brown & Harris, 2013).

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Cognitive Theories of Depression

Cognitive theories of depression take the view that depression is triggered by negative thoughts, interpretations, self-evaluations, and expectations (Joormann, 2009). These diathesis-stress models propose that depression is triggered by a “cognitive vulnerability” (negative and maladaptive thinking) and by precipitating stressful life events (Gotlib & Joormann, 2010).

Beck's triad wiith negative views about the world, negative views about oneself, and negative views about the future all interacting.

Figure 5. Beck’s cognitive triad assumes a pattern of negative thinking. For example, the self may think, “I’m worthless and ugly” or “I wish I was different,” leading to beliefs from the world that “no one values me” or “people ignore me all the time,” which may lead to thinking about the future as “I’m hopeless because things will never change” or “things can only get worse!”

Perhaps the most well-known cognitive theory of depression was developed in the 1960s by psychiatrist Aaron Beck, based on clinical observations and supported by research (Beck, 2008). Beck theorized that depression-prone people possess depressive schemas, or mental predispositions to think about most things in a negative way (Beck, 1976). Depressive schemas contain themes of loss, failure, rejection, worthlessness, and inadequacy, and may develop early in childhood in response to adverse experiences, then remain dormant until they are activated by stressful or negative life events. Depressive schemas prompt dysfunctional and pessimistic thoughts about the self, the world, and the future.

Beck believed that this dysfunctional style of thinking is maintained by cognitive biases, or errors in how we process information about ourselves, which lead us to focus on negative aspects of experiences, interpret things negatively, and block positive memories (Beck, 2008). A person whose depressive schema consists of a theme of rejection might be overly attentive to social cues of rejection (more likely to notice another’s frown), and he might interpret this cue as a sign of rejection and automatically remember past incidents of rejection.

Longitudinal studies have supported Beck’s theory, in showing that a pre-existing tendency to engage in this negative, self-defeating style of thinking—when combined with life stress—over time predicts the onset of depression (Dozois & Beck, 2008). Cognitive therapies for depression, aimed at changing a depressed person’s negative thinking, were developed as an expansion of this theory (Beck, 1976).

Cognitive Therapy in Action

Having made a mistake at work, a man may believe, “I’m useless and can’t do anything right at work.” He may then focus on the mistake (which he takes as evidence that his belief is true), and his thoughts about being “useless” are likely to lead to negative emotions (frustration, sadness, and hopelessness). Given these thoughts and feelings, he may then begin to avoid challenges at work, which is behavior that could provide even more evidence for him that his belief is true. As a result, any adaptive response and further constructive consequences become unlikely, and he may focus even more on any mistakes he may make, which serve to reinforce the original belief of being “useless.” In therapy, this example could be identified as a self-fulfilling prophecy or “problem cycle,” and the efforts of the therapist and patient would be directed at working together to explore and shift this cycle.

People who are working with a cognitive therapist often practice the use of more flexible ways to think and respond, learning to ask themselves whether their thoughts are completely true and whether those thoughts are helping them to meet their goals. Thoughts that do not meet this description may then be shifted to something more accurate or helpful, leading to more positive emotion, more desirable behavior, and movement toward the person’s goals. Cognitive therapy takes a skill-building approach, where the therapist helps the person to learn and practice these skills independently, eventually “becoming their own therapist.”

Another cognitive theory of depression, hopelessness theory, postulates that a particular style of negative thinking leads to a sense of hopelessness, which then leads to depression (Abramson, Metalsky, & Alloy, 1989). According to this theory, hopelessness is an expectation that unpleasant outcomes will occur or that desired outcomes will not occur, and there is nothing one can do to prevent such outcomes. A key assumption of this theory is that hopelessness stems from a tendency to perceive negative life events as having stable (“It’s never going to change”), global (“It’s going to affect my whole life”) causes, in contrast to unstable (“It’s fixable”), and specific (“It applies only to this particular situation”) causes, especially if these negative life events occur in important life realms, such as relationships, academic achievement, and the like.

Suppose a student who wishes to go to law school does poorly on an admissions test. If the student infers negative life events as having stable and global causes, she may believe that her poor performance has a stable and global cause (“I lack intelligence, and it’s going to prevent me from ever finding a meaningful career”), as opposed to an unstable and specific cause (“I was sick the day of the exam, so my low score was a fluke”). Hopelessness theory predicts that people who exhibit this cognitive style in response to undesirable life events will view such events as having negative implications for their future and self-worth, thereby increasing the likelihood of hopelessness—the primary cause of depression (Abramson et al., 1989). One study testing hopelessness theory measured the tendency to make negative inferences for bad life effects in participants who were experiencing uncontrollable stressors. Over the ensuing six months, those individuals with scores reflecting high cognitive vulnerability were seven times more likely to develop depression compared to those with lower scores (Kleim, Gonzalo, & Ehlers, 2011).

A third cognitive theory of depression focuses on how people’s thoughts about their distressed moods—depressed symptoms in particular—can increase the risk and duration of depression. This theory, which focuses on rumination in the development of depression, was first described in the late 1980s to explain the higher rates of depression in women than in men (Nolen-Hoeksema, 1987). Rumination is the repetitive and passive focus on the fact that one is depressed and dwelling on depressed symptoms, rather than distracting oneself from the symptoms or attempting to address them in an active, problem-solving manner (Nolen-Hoeksema, 1991). When people ruminate, they have thoughts such as “Why am I so unmotivated? I just can’t get going. I’m never going to get my work done feeling this way” (Nolen-Hoeksema & Hilt, 2009, p. 393). Women are more likely than men to ruminate when they are sad or depressed (Butler & Nolen-Hoeksema, 1994), and the tendency to ruminate is associated with increases in depression symptoms (Nolen-Hoeksema, Larson, & Grayson, 1999), heightened risk of major depressive episodes (Abela & Hankin, 2011), and chronicity of such episodes (Robinson & Alloy, 2003).

The Sociocultural Perspective

Depression is more prevalent in women than in men in individualist and collective cultures. Some have hypothesized that this is due to their inferior positions in the culture, in which they may experience domestic violence, poverty, and inequality that can greatly contribute to depression. Moreover, research conducted in the United States, Chile, and Spain found that cultural differences on the expectations of individuals based on gender varied across cultures and that resulted in different levels of depression across individuals. Changes in gender roles across countries and cultures in this study served to explain varying levels of stress and responsibility that changed on the basis of gender. These ever-changing expectations and these additional responsibilities on the basis of gender increased levels of depression.

The differences in gender roles within a community also impact one’s level of depression. According to Wichstrøm (1999), women tend to ruminate more and therefore symptoms of depression can be accentuated. Since women are encouraged to talk about and share their feelings, they can get caught talking about and staying in a negative state. On the other hand, boys are taught not to discuss their feelings with others, which then diminishes or even gets rid of rumination entirely. The way one is socialized to deal with their negative emotions will vary across cultures and may lead to different outcomes.

In many other non-Western societies, a stigma is associated with mental disorders despite the high prevalence of depression and anxiety. Many Easterners believe that symptoms of depression and anxiety are simply a part of life and do not require medical attention. Also, individuals from collective societies tend to be extremely careful in maintaining their reputations, and mental distress is usually interpreted as a weak faith in God and/or a weak self. Therefore, they do not seek treatment for their symptoms in order to avoid shame and gossip. This stigma stems in part from the limited knowledge many Easterners have about depression and anxiety. Multiple studies reveal that the majority of Easterners do not know the names of mental illnesses. Instead, they describe their symptoms through a series of physical complaints.

Considering the stigma associated with mental illness in the Arab culture, it is not surprising that many Easterners express depression and anxiety through somatic complaints. This is especially true with Eastern women, who may feel symptoms of depression as a result of inequality but are taught not to express personal feelings. Instead, they complain of headaches, numbness, breathlessness, and chest pains to receive some form of medical attention. Somatization is also common among individuals with little knowledge of mental health who have no linguistic way to express their symptoms.

The causes of depression and anxiety in Arabs and Arab Americans are a combination of biological factors and psychological and social factors that are greatly influenced by the Arab culture and immigration. Research indicates that biological markers of depression are consistent between Arab and Western populations, as are many psychological factors.

Arabs who seek psychological help are more confident about the effectiveness of medication over therapy. But since many Arabs either refuse to meet with mental health professionals or do not have any knowledge of them, traditional treatment methods are still commonly used. Islamic therapy, for example, involves Quran recitation by an imam to repel moral deviance from the soul of the individual. The imam may also suggest old Islamic remedies, such as ice baths and herbal antidotes. Using Islam to simply cope with psychological distress is a more widely used method of treatment that is supported by research. A study completed on depressed Pakistani patients also reported that the participants believed that medicine could rid them of their symptoms but had little to no knowledge of psychotherapy.[1]

Latino adolescents tend to have higher levels of symptoms of depression than some of their Caucasian and African-American peers. An explanation for this difference is the increase in cultural stressors that in turn add to this form of cultural disparity. Although the cultural stressors have not yet been identified, the correlation between them and symptoms of and the prevalence of depression is still significant. Within communities, discrimination on the basis of race and ethnicity is also a strong contributor to the elevated number of depressive symptoms among Latino youth.

The Psychodynamic Perspective

According to the psychodynamic model, depression is caused by unresolved unconscious conflict or repressed anger towards others. A person may be so plagued with inner conflict, anxiety, and guilt that they are unable to perceive reality clearly or meet the ordinary demands of the environment in which they live.

The Humanistic Perspective

Humanistic psychology includes several approaches to counseling and therapy. Among the earliest approaches, we find the developmental theory of Abraham Maslow, emphasizing a hierarchy of needs and motivations; the existential psychology of Rollo May acknowledging human choice and the tragic aspects of human existence; and the person-centered or client-centered therapy of Carl Rogers, which is centered on the client’s capacity for self-direction and understanding of their own development. Client-centered therapy is non-directive; the therapist listens to the client without judgment, allowing the client to come to insights by themselves. The therapist should ensure that all of the client’s feelings are being considered and that the therapist has a firm grasp on the concerns of the client while ensuring that there is an air of acceptance and warmth. A client-centered therapist engages in active listening during therapy sessions.

Existential psychotherapies, an application of humanistic psychology, apply existential philosophy, which emphasizes the idea that humans have the freedom to make sense of their lives. They are free to define themselves and do whatever it is they want to do. This is a type of humanistic therapy that forces the client to explore the meaning of their life, as well as its purpose. There is a conflict between having freedoms and having limitations. Examples of limitations include genetics, culture, and many other factors. Existential therapy involves trying to resolve this conflict.

The Behavioral Perspective

Behavioral theories of depression emphasize the role maladaptive actions play in the onset and maintenance of depression. These theories stem from work concerning the principles of learning and conditioning from the early to mid-1900s. Ivan Pavlov and B. F. Skinner are often credited with the establishment of behavioral psychology with their research on classical conditioning and operant conditioning, respectively. Collectively, their research established that certain behaviors could be learned or unlearned, and these theories have been applied in a variety of contexts, including abnormal psychology. Theories specifically applied to depression emphasize the reactions individuals have to their environment and how they develop adaptive or maladaptive coping strategies. Beck’s cognitive theory of depression (mentioned above) originally began as cognitive-specific therapy and as a response to psychodynamic and behavioral therapies of the time but has since evolved to include and incorporate behavioral aspects, hence the more current umbrella term of cognitive behavioral therapy. CBT focuses on challenging and changing unhelpful cognitive distortions (e.g., thoughts, beliefs, and attitudes) and behaviors, improving emotional regulation, and the development of personal coping strategies that target solving current problems. Originally, it was designed to treat depression, but its uses have been expanded to include the treatment of a number of mental health conditions, including anxiety. CBT includes a number of cognitive or behavior psychotherapies that treat defined psychopathologies using evidence-based techniques and strategies. Cognitive-based therapies include, but are not limited to, rational emotive therapy (REBT), cognitive therapy, acceptance and commitment therapy, dialectical behavior therapy, reality therapy/choice theory, cognitive processing therapy, EMDR, and multimodal therapy. All of these therapies are a blending of cognitive- and behavior-based elements, and they are popular choices in treating depression.

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cognitive behavioral therapy: a therapy focused on challenging and changing unhelpful cognitive distortions and behaviors, improving emotional regulation, and developing personal coping strategies that target solving current problems

diathesis-stress model: theory in which certain predispositions or vulnerability factors influence one’s reaction to stress

hopelessness theory: cognitive theory of depression proposing that a style of thinking that perceives negative life events as having stable and global causes leads to a sense of hopelessness and then to depression

  1. Ahmed, Sawssan R.; Kia-Keating, Maryam; Tsai, Katherine H. (2 February 2011). "A structural model of racial discrimination, acculturative stress, and cultural resources among Arab American adolescents". American Journal of Community Psychology. 48 (3–4): 181–192. doi:10.1007/s10464-011-9424-3. PMID 21287262.