4.5: Mood Disorders - Etiology

Learning Objectives

• Describe the biological causes of mood disorders.
• Describe the cognitive causes of mood disorders.
• Describe the behavioral causes of mood disorders.
• Describe the sociocultural causes of mood disorders.

Biological

Research throughout the years continues to provide evidence that depressive disorders have some biological cause. While it does not explain every depressive case, it is safe to say that some individuals may at least have a predisposition to developing a depressive disorder. Among the biological factors are genetic factors, biochemical factors, and brain structure.

4.5.1.1. Genetics. Like with any disorder, researchers often explore the prevalence rate of depressive disorders among family members to determine if there is some genetic component, whether it be a direct link or a predisposition. If there is a genetic predisposition to developing depressive disorders, one would expect a higher rate of depression within families than that of the general population. Research supports this with regards to depressive disorders as there is nearly a 30% increase in relatives diagnosed with depression compared to 10% of the general population (Levinson & Nichols, 2014). Similarly, there is an elevated prevalence among first-degree relatives for both Bipolar I and Bipolar II disorders as well.

Another way to study the genetic component of a disorder is via twin studies. One would expect identical twins to have a higher rate of the disorder as opposed to fraternal twins, as identical twins share the same genetic make-up, whereas fraternal twins only share roughly 50%, similar to that of siblings. A large-scale study found that if one identical twin was diagnosed with depression, there was a 46% chance their identical twin was diagnosed with depression. In contrast, the rate of a depression diagnosis in fraternal twins was only 20%. Despite the fraternal twin rate still being higher than that of a first-degree relative, this study provided enough evidence that there is a strong genetic link in the development of depression (McGuffin et al., 1996).

More recently, scientists have been studying depression at a molecular level, exploring possibilities of gene abnormalities as a cause for developing a depressive disorder. While much of the research is speculation due to sampling issues and low power, there is some evidence that depression may be tied to the 5-HTT gene on chromosome 17, as this is responsible for the activity of serotonin (Jansen et al., 2016).

Bipolar disorders share a similar genetic predisposition to that of major depressive disorder. Twin studies within bipolar disorder yielded concordance rates for identical twins at as high as 72%, yet the range for fraternal twins, siblings, and other close relatives ranged from 5-15%. It is important to note that both percentages are significantly higher than that of the general population, suggesting a strong genetic component within bipolar disorder (Edvardsen et al., 2008). The DSM-5-TR more recently reports heritability estimates around 90% in some twin studies and the risk of bipolar disorder being around 1% in the general population compared to 5-10% in a first-degree relative (APA, 2022).

4.5.1.2. Biochemical. As you will read in the treatment section, there is strong evidence of a biochemical deficit in depression and bipolar disorders. More specifically, low activity levels of norepinephrine and serotonin, have long been documented as contributing factors to developing depressive disorders. This relationship was discovered accidentally in the 1950s when MAOIs were given to tuberculosis patients, and miraculously, their depressive moods were also improved. Soon thereafter, medical providers found that medications used to treat high blood pressure by causing a reduction in norepinephrine also caused depression in their patients (Ayd, 1956).

While these initial findings were premature in the identification of how neurotransmitters affected the development of depressive features, they did provide insight as to what neurotransmitters were involved in this system. Researchers are still trying to determine exact pathways; however, it does appear that both norepinephrine and serotonin are involved in the development of symptoms, whether it be between the interaction between them, or their interaction on other neurotransmitters (Ding et al., 2014).

Due to the close nature of depression and bipolar disorder, researchers initially believed that both norepinephrine and serotonin were implicated in the development of bipolar disorder; however, the idea was that there was a drastic increase in serotonin during mania episodes. Unfortunately, research supports the opposite. It is believed that low levels of serotonin and high levels of norepinephrine may explain mania episodes (Soreff & McInnes, 2014). Despite these findings, additional research within this area is needed to conclusively determine what is responsible for the manic episodes within bipolar disorder.

4.5.1.3. Endocrine system. As you may know, the endocrine system is a collection of glands responsible for regulating hormones, metabolism, growth and development, sleep, and mood, among other things. Some research has implicated hormones, particularly cortisol, a hormone released as a stress response, in the development of depression (Owens et al., 2014). Additionally, melatonin, a hormone released when it is dark outside to assist with the transition to sleep, may also be related to depressive symptoms, particularly during the winter months.

4.5.1.4. Brain anatomy. Seeing as neurotransmitters have been implicated in the development of depressive disorders, it should not be a surprise that various brain structures have also been identified as contributors to mood disorders. While exact anatomy and pathways are yet to be determined, research studies implicate the prefrontal cortex, the hippocampus, and the amygdala. More specifically, drastic changes in blood flow throughout the prefrontal cortex have been linked with depressive symptoms. Similarly, a smaller hippocampus, and consequently, fewer neurons, has also been linked to depressive symptoms. Finally, heightened activity and blood flow in the amygdala, the brain area responsible for our fight or flight response, is also consistently found in individuals with depressive symptoms.

Abnormalities in several brain structures have also been identified in individuals with bipolar disorder; however, what or why these structures are abnormal has yet to be determined. Researchers continue to focus on areas of the basal ganglia and cerebellum, which appear to be much smaller in individuals with bipolar disorder compared to the general public. Additionally, there appears to be a decrease in brain activity in regions associated with regulating emotions, as well as an increase in brain activity among structures related to emotional responsiveness (Houenou et al., 2011). Additional research is still needed to determine precisely how each of these brain structures may be implicated in the development of bipolar disorder.

Cognitive

The cognitive model, arguably the most conclusive model with regards to depressive disorders, focuses on the negative thoughts and perceptions of an individual. One theory often equated with the cognitive model of depression is learned helplessness. Coined by Martin Seligman (1975), learned helplessness was developed based on his laboratory experiment involving dogs. In this study, Seligman restrained dogs in an apparatus and routinely shocked them regardless of their behavior. The following day, the dogs were placed in a similar apparatus; however, this time they were not restrained and there was a small barrier placed between the “shock” floor and the “safe” floor. What Seligman observed was that despite the opportunity to escape the shock, the dogs flurried for a bit, and then ultimately laid down and whimpered while being shocked.

Based on this study, Seligman concluded that the animals essentially learned that they were unable to avoid the shock the day prior, and therefore, learned that they were helpless in preventing the shocks. When they were placed in a similar environment but had the opportunity to escape the shock, their learned helplessness carried over, and they continued to believe they were unable to escape the shock.

This study has been linked to humans through research on attributional style (Nolen-Hoeksema, Girgus & Seligman, 1992). There are two types of attributional styles—positive and negative. A negative attributional style focuses on the internal, stable, and global influence of daily lives, whereas a positive attributional style focuses on the external, unstable, and specific influence of the environment. Research has found that individuals with a negative attributional style are more likely to experience depression. This is likely due to their negative interpretation of daily events. For example, if something bad were to happen to them, they would conclude that it is their fault (internal), bad things always happen to them (stable), and bad things happen all day to them. Unfortunately, this maladaptive thinking style often takes over an individual’s daily view, thus making them more vulnerable to depression.

In addition to attributional style, Aaron Beck also attributed negative thinking as a precursor to depressive disorders (Beck, 2002, 1991, 1967). Often viewed as the grandfather of Cognitive-Behavioral Therapy, Beck went on to coin the terms—maladaptive attitudes, cognitive triad, errors in thinking, and automatic thoughts—all of which combine to explain the cognitive model of depressive disorders.

Maladaptive attitudes, or negative attitudes about oneself, others, and the world around them are often present in those with depressive symptoms. These attitudes are inaccurate and often global. For example, “If I fail my exam, the world will know I’m stupid.” Will the entire world really know you failed your exam? Not likely. Because you fail the exam, are you stupid? No. Individuals with depressive symptoms often develop these maladaptive attitudes regarding everything in their life, indirectly isolating themselves from others. The cognitive triad also plays into the maladaptive attitudes in that the individual interprets these negative thoughts about their experiences, themselves, and their futures.

Cognitive distortions, also known as errors in thinking, are a key component in Beck’s cognitive theory. Beck identified 15 errors in thinking that are most common in individuals with depression (see the end of the module). Among the most common are catastrophizing, jumping to conclusions, and overgeneralization. I always like to use my dad (first author’s dad) as an example for overgeneralization. Whenever we go to the grocery store, he always comments about how whatever line he chooses, at every store, it is always the slowest line. Does this happen every time he is at the store? I’m doubtful, but his error in thinking leads to him believing this is true.

Finally, automatic thoughts, or the constant stream of negative thoughts, also leads to symptoms of depression as individuals begin to feel as though they are inadequate or helpless in a given situation. While some cognitions are manipulated and interpreted negatively, Beck stated that there is another set of negative thoughts that occur automatically. Research studies have continually supported Beck’s maladaptive thoughts, attitudes, and errors in thinking as fundamental issues in those with depressive disorders (Lai et al., 2014; Possel & Black, 2014). Furthermore, as you will see in the treatment section (Section 4.5), cognitive strategies are among the most effective forms of treatment for depressive disorders.

Behavioral

The behavioral model explains depression as a result of a change in the number of rewards and punishments one receives throughout their life. This change can come from work, intimate relationships, family, or even the environment in general. Among the most influential in the field of depression is Peter Lewinsohn. He stated depression occurred in most people due to reduced positive rewards in their life. Because they were not positively rewarded, their constructive behaviors occurred more infrequently until they stop engaging in the behavior completely (Lewinsohn et al., 1990; 1984). An example of this is a student who keeps receiving bad grades on their exam despite studying for hours. Over time, the individual will reduce the amount of time they are studying, thus continuing to earn poor grades.

Sociocultural

In the sociocultural theory, the role of family and one’s social environment play a substantial role in the development of depressive disorders. There are two sociocultural views: the family-social perspective and the multi-cultural perspective.

4.5.4.1. Family-social perspective. Similar to that of the behavioral theory, the family-social perspective of depression suggests that depression is related to the unavailability of social support. This is often supported by research studies that show separated and divorced individuals are three times more likely to experience depressive symptoms than those that are married or even widowed (Schultz, 2007). While many factors lead a couple to separate or end their marriage, some relationships end due to a spouse’s mental health issues, particularly depressive symptoms. Depressive symptoms have been positively related to increased interpersonal conflicts, reduced communication, and intimacy issues, all of which are often reported in causal factors leading to a divorce (Najman et al., 2014).

The family-social perspective can also be viewed oppositely, with stress and marital discord leading to increased rates of depression in one or both spouses (Nezlek et al., 2000). While some research indicates that having children provides a positive influence in one’s life, it can also lead to stress both within the individual, as well as between partners due to division of work and discipline differences. Studies have shown that women who had three or more young children, and also lacked a close confidante and outside employment, were more likely than other mothers to become depressed (Brown, 2002).

4.5.4.2. Multi-cultural perspective. While depression is experienced across the entire world, one’s cultural background may influence what symptoms of depression are presented. Common depressive symptoms such as feeling sad, lack of energy, anhedonia, difficulty concentrating, and thoughts of suicide are a hallmark in most societies; other symptoms may be more specific to one’s nationality. More specifically, individuals from non-Western countries (China and other Asian countries) often focus on the physical symptoms of depression—tiredness, weakness, sleep issues—and less of an emphasis on the cognitive symptoms.

Within the United States, many researchers have explored potential differences across ethnic or racial groups in both rates of depression, as well as presenting symptoms of those diagnosed with depression. These studies continually fail to identify any significant differences between ethnic and racial groups; however, one major study has identified a difference in the rate of recurrence of depression in Hispanic and African Americans (Gonzalez et al., 2010). While the exact reason for this is unclear, researchers propose a lack of treatment opportunities as a possible explanation. According to Gonzalez and colleagues (2010), approximately 54% of depressed white Americans seek out treatment, compared to the 34% and 40% Hispanic and African Americans, respectively. The fact that there is a large discrepancy in the use of treatment between white Americans and minority Americans suggests that these individuals are not receiving the effective treatment necessary to resolve the disorder, thus leaving them more vulnerable for repeated depressive episodes.

4.5.4.3. Gender differences. As previously discussed, there is a significant difference between gender and rates of depression, with women twice as likely to experience an episode of depression than men (Schuch et al., 2014). There are a few speculations as to why there is such an imbalance in the rate of depression across genders.

The first theory, artifact theory, suggests that the difference between genders is due to clinician or diagnostic systems being more sensitive to diagnosing women with depression than men. While women are often thought to be more “emotional,” easily expressing their feelings and more willing to discuss their symptoms with clinicians and physicians, men often withhold their symptoms or will present with more traditionally “masculine” symptoms of anger or aggression. While this theory is a possible explanation for the gender differences in the rate of depression, research has failed to support this theory, suggesting that men and women are equally likely to seek out treatment and discuss their depressive symptoms (McSweeney, 2004; Rieker & Bird, 2005).

The second theory, hormone theory, suggests that variations in hormone levels trigger depression in women more than men (Graziottin & Serafini, 2009). While there is biological evidence supporting the changes in hormone levels during various phases of the menstrual cycle and their impact on women’s ability to integrate and process emotional information, research fails to support this theory as the reason for higher rates of depression in women (Whiffen & Demidenko, 2006).

The third theory, life stress theory, suggests that women are more likely to experience chronic stressors than men, thus accounting for their higher rate of depression (Astbury, 2010). Women face increased risk for poverty, lower employment opportunities, discrimination, and poorer quality of housing than men, all of which are strong predictors of depressive symptoms (Garcia-Toro et al., 2013).

The fourth theory, gender roles theory, suggests that social and or psychological factors related to traditional gender roles also influence the rate of depression in women. For example, men are often encouraged to develop personal autonomy, seek out activities that interest them, and display achievement-oriented goals; women are encouraged to empathize and care for others, often fostering an interdependent functioning, which may cause women to value the opinion of others more highly than their male counterparts do.

The final theory, rumination theory, suggests that women are more likely than men to ruminate, or intently focus, on their depressive symptoms, thus making them more vulnerable to developing depression at a clinical level (Nolen-Hoeksema, 2012). Several studies have supported this theory and shown that rumination of negative thoughts is positively related to an increase in depression symptoms (Hankin, 2009).

While many theories try to explain the gender discrepancy in depressive episodes, no single theory has produced enough evidence to fully explain why women experience depression more than men. Due to the lack of evidence, gender differences in depression remains one of the most researched topics within the subject of depression, while simultaneously being the least understood phenomena within clinical psychology.

Key Takeaways

You should have learned the following in this section:

• In terms of biological explanations for depressive disorders, there is evidence that rates of depression are higher among identical twins (the same is true for bipolar disorders), that the 5-HTT gene on chromosome 17 may be involved in depressive disorders, that norepinephrine and serotonin affect depressive (both being low) and bipolar disorders (low serotonin and high norepinephrine), the hormones cortisol and melatonin affect depression, and several brain structures are implicated in depression (prefrontal cortex, hippocampus, and amygdala) and bipolar disorder (basal ganglia and cerebellum).
• In terms of cognitive explanations, learned helplessness, attributional style, and maladaptive attitudes to include the cognitive triad, errors in thinking, and automatic thoughts, help to explain depressive disorders.
• Behavioral explanations center on changes in the rewards and punishments received throughout life.
• Sociocultural explanations include the family-social perspective and multi-cultural perspective.
• Women are twice as likely to experience depression and this could be due to women being more likely to be diagnosed than men (called the artifact theory), variations in hormone levels in women (hormone theory), women being more likely to experience chronic stressors (life stress theory), the fostering of an interdependent functioning in women (gender roles theory), and that women are more likely to intently focus on their symptoms (rumination theory).

Review Questions

1. How do twin studies explain the biological causes of mood disorders?
2. What brain structures are implicated in the development of mood disorders? Discuss their role.
3. What is learned helplessness? How has this concept been used to study the development and maintenance of mood disorders?
4. What is the cognitive triad?
5. What are common cognitive distortions observed in individuals with mood disorders?
6. What are the identified theories that are used to explain the gender differences in mood disorder development?