4th edition as of August 2026

 

Module Overview

In Module 4, we will discuss matters related to mood disorders to include their clinical presentation, epidemiology, comorbidity, etiology, and treatment options. Our discussion will cover major depressive disorder, persistent depressive disorder (formerly dysthymia), bipolar I disorder, bipolar II disorder, and cyclothymic disorder. We will also cover major depressive, manic, and hypomanic episodes. Be sure you refer Modules 1-3 for explanations of key terms (Module 1), an overview of the various models to explain psychopathology (Module 2), and descriptions of several therapies (Module 3). Note that this module will cover two chapters from the DSM 5-TR; namely, Bipolar and Related Disorders and Depressive Disorders.

 

Module Outline

• 4.1. Clinical Presentation – Depressive Disorders
• 4.2. Clinical Presentation – Bipolar and Related Disorders
• 4.3. Epidemiology
• 4.4. Comorbidity
• 4.5. Etiology
• 4.6. Treatment

 

Module Learning Outcomes

• Describe how depressive disorders present.
• Describe how bipolar and related disorders present.
• Describe the epidemiology of mood disorders.
• Describe comorbidity in relation to mood disorders.
• Describe the etiology of mood disorders.
• Describe treatment options for mood disorders.

 

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4.1. Clinical Presentation – Depressive Disorders

 

Section Learning Objectives

• Distinguish the two distinct groups of mood disorders.
• Identify and describe the two types of depressive disorders.
• Classify symptoms of depression.
• Describe premenstrual dysphoric disorder.

 

4.1.1. Distinguishing Mood Disorders

Within mood disorders are two distinct groups—individuals with depressive disorders and individuals with bipolar disorders. The key difference between the two mood disorder groups is episodes of mania/hypomania. More specifically, in bipolar I disorder, the individual experiences a manic episode that “may have been preceded by and may be followed by hypomanic or major depressive episodes” (APA, 2022, pg. 139) whereas for bipolar II disorder, the individual has experienced in the past or is currently experiencing a hypomanic episode and has experienced in the past or is currently experiencing a major depressive episode. In contrast, individuals presenting with a depressive disorder have never experienced a manic or hypomanic episode.  

 

4.1.2. Types of Depressive Disorders

The two most common types of depressive disorders are major depressive disorder (MDD) and persistent depressive disorder (PDD). Persistent depressive disorder, which in the DSM-5 now includes the diagnostic categories of dysthymia and chronic major depression, is a continuous and chronic form of depression. While the symptoms of PDD are very similar to MDD, they are usually less acute, as symptoms tend to ebb and flow over a long period (i.e., more than two years). Major depressive disorder, on the other hand, has discrete episodes lasting at least two weeks in which there are substantial changes in affect, cognition, and neurovegetative functions (APA, 2022, pg. 177).

It should be noted that after a careful review of the literature, premenstrual dysphoric disorder, was moved from “Criteria Sets and Axes Provided for Future Study” in the DSM-IV to Section II of DSM-5 as the disorder was confirmed as a “specific and treatment-responsive form of depressive disorder that begins sometime following ovulation and remits within a few days of menses and has a marked impact on functioning” (APA, 2022, pg. 177).

 

 

           4.1.4.3. Premenstrual dysphoric disorder. In terms of premenstrual dysphoric disorder, the DSM-5-TR states in the majority of menstrual cycles, at least five symptoms must be present in the final week before the onset of menses, begin improving with a few days after menses begins, and disappear or become negligible in the week postmenses. Individuals diagnosed with premenstrual dysphoric disorder must have one or more of the following: increased mood swings, irritability or anger, depressed mood, or anxiety/tension. Additionally, they must have one or more of the following to reach a total of five symptoms: anhedonia, difficulty concentrating, lethargy, changes in appetite, hypersomnia or insomnia, feelings of being overwhelmed or out of control, and/or experience breast tenderness or swelling. The symptoms lead to issues at work or school (i.e., decreased productivity and efficiency), within relationships (i.e., discord in the intimate partner relationship or with children, friends, or other family members), and with usual social activities (i.e., avoidance of the activities).

 

 

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4.2. Clinical Presentation – Bipolar and Related Disorders

 

Section Learning Objectives

• Distinguish the forms bipolar disorder takes.
• Contrast a manic episode with a hypomanic episode.
• Define cyclothymic disorder.

 

4.2.1. Distinguishing Bipolar I and II Disorders

According to the DSM-5-TR (APA, 2022), there are two types of bipolar disorder- bipolar I and bipolar II. A diagnosis of bipolar I disorder is made when there is at least one manic episode. This manic episode can be preceded by and/or followed by a hypomanic or major depressive episode, however, diagnostic criteria for a manic episode is the only criteria that needs to be met for a bipolar I diagnosis. A diagnosis of bipolar II Disorder is made when there is a current or history of a hypomanic episode and a current or past major depressive episode. Descriptions of both manic and hypomanic episodes follow below.

 

 

 

4.2.2. Manic and Hypomanic Episodes

           4.2.2.1. Manic episode. The key feature of a manic episode is a specific period in which an individual reports abnormal, persistent, or expansive irritable mood for nearly all day, every day, for at least one week (APA, 2022). Additionally, the individual will display increased activity or energy during this same time.  With regards to mood, an individual in a manic episode will appear excessively happy, often engaging haphazardly in sexual or interpersonal interactions. They also display rapid shifts in mood, also known as mood lability, ranging from happy, neutral, to irritable. At least three of the symptoms described below (four if the mood is only irritable) must be present and represent a noticeable change in the individual’s typical behavior.

Inflated self-esteem or grandiosity (Criterion B1) is present during a manic episode. Occasionally these inflated self-esteem levels can appear delusional. For example, individuals may believe they are friends with a celebrity, do not need to abide by laws, or even perceive themselves as God. They also engage in multiple overlapping new projects (Criteria B6 and 7), often initiated with no prior knowledge about the topic, and engaged in at unusual hours of the day.

Despite the increased activity level, individuals experiencing a manic episode also require a decreased need for sleep (Criterion B2), sleeping as little as a few hours a night yet still feeling rested. Reduced need for sleep may also be a precursor to a manic episode, suggesting that a manic episode is to begin imminently. It is not uncommon for those experiencing a manic episode to be more talkative than usual. It can be difficult to follow their conversation due to the quick pace of their talking, as well as tangential storytelling.  Additionally, they can be difficult to interrupt in conversation, often disregarding the reciprocal nature of communication (Criterion B3). If the individual is more irritable than expansive, speech can become hostile and they engage in tirades, particularly if they are interrupted or not allowed to engage in an activity they are seeking out (APA, 2022).

Based on their speech pattern, it should not be a surprise that racing thoughts and flights of ideas (Criterion B4) also present during manic episodes. Because of these rapid thoughts, speech may become disorganized or incoherent. Finally, individuals experiencing a manic episode are distractable (Criterion B5).

           4.2.2.2. Hypomanic episode. As mentioned above, for a bipolar II diagnosis, an individual must report symptoms consistent with a major depressive episode and at least one hypomanic episode. An individual with bipolar II disorder must not have a history of a manic episode—if there is a history of mania, the diagnosis will be diagnosed with bipolar I. A hypomanic episode is like a manic episode in that the individual will experience abnormally and persistently elevated, expansive, or irritable mood and energy levels, however, the behaviors are not as extreme as in mania. Additionally, behaviors consistent with a hypomanic episode must be present for at least four days, compared to the one week in a manic episode.

 

 

4.2.3. Cyclothymic Disorder

Notably, there is a subclass of individuals who experience numerous periods with hypomanic symptoms that do not meet the criteria for a hypomanic episode and mild depressive symptoms (i.e., do not fully meet criteria for a major depressive episode). These individuals are diagnosed with cyclothymic disorder (APA, 2022). Presentation of these symptoms occur for two or more years and are typically interrupted by periods of normal mood not lasting more than two months at a time. The symptoms cause clinically significant distress or impairment in important areas of functioning, such as social and occupational. While only a small percentage of the population develops cyclothymic disorder, it can eventually progress into bipolar I or bipolar II disorder (Zeschel et al., 2015).

 

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4.3. Epidemiology

 

Section Learning Objectives

• Describe the epidemiology of depressive disorders.
• Describe the epidemiology of bipolar disorders.
• Describe the epidemiology of suicidality.

 

4.3.1. Depressive Disorders

According to the DSM-5-TR (APA, 2022), the 12-month prevalence rate for major depressive disorder is approximately 7% within the United States. NIMH (National Institutes of Mental Health, 2021) report that an estimated 21.0 million adults in the United States had at least one major depressive episode and that this number represented 8.3% of all U.S. adults. As well, more females (10.3%) compared to males (6.2%), individuals aged 18-25 (18.6%), and people who report having multiple (two or more) races (13.9%) have MDD.

Recall that DSM-5 persistent depressive disorder is a blend of DSM-IV dysthymic disorder and chronic major depressive disorder. The prevalence rate for DSM-IV dysthymic disorder is much lower than MDD, with a 0.5% rate among adults in the United States, while DSM-IV chronic major depressive disorder is 1.5% (APA, 2022). NIMH says that an estimated 1.5% of U.S. adults had persistent depressive disorder in the past year and is higher for females (1.9%) than for males (1.0%). They further report that an estimated 2.5% of U.S. adults will experience persistent depressive disorder at some time in their lives.

 

4.3.2. Bipolar Disorders

The 12-month prevalence of bipolar I disorder in the United States is 1.5% and did not differ statistically between men and women. In contrast, bipolar II disorder has a prevalence rate of 0.8% in the United States and 0.3% internationally (APA, 2022) and some clinical samples suggest it is more common in women, with approximately 80-90% of individuals with rapid-cycling episodes being women (Bauer & Pfenning, 2005). Childbirth may be a specific trigger for a hypomanic episode, occurring in 10-20% of women in nonclinical settings and most often in the early postpartum period.  NIMH reports that an estimated 2.8% of U.S. adults had bipolar disorder in the past year and was similar for males (2.9%) and females (2.8%). An estimated 4.4% of U.S. adults experience bipolar disorder at some time in their lives (NIMH, 2026).

 

4.3.3. Suicidality

Individuals with a depressive disorder have a 17-fold increased risk for suicide over the age- and sex-adjusted general population rate. Features associated with an increased risk for death by suicide include anhedonia, living alone, being single, disconnecting socially, having access to a firearm, early life adversity, sleep disturbance, feelings of hopelessness, and problems with decision making. Women attempt suicide at a higher rate though men are more likely to complete suicide. Finally, the premenstrual phase is considered a risk period for suicide by some (APA, 2022).

In terms of bipolar disorders, the lifetime risk of suicide is estimated to be 20- to 30- fold greater than in the general population and 5-6% of individuals with bipolar disorder die by suicide. Like depressive disorders, women attempt suicide at a higher rate though lethal suicide is more common in men with bipolar disorder. About 1/3 of individuals with bipolar II disorder report a lifetime history of suicide attempt, which is similar in bipolar I disorder, though lethality of attempts is higher in individuals with bipolar II (APA, 2022).

 

 

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4.4. Comorbidity

 

Section Learning Objectives

• Describe the comorbidity of depressive disorders.
• Describe the comorbidity of bipolar disorders.

 

4.4.1. Depressive Disorders

Studies exploring depression symptoms among the general population show a substantial pattern of comorbidity between depression and other mental disorders, particularly substance use disorders (Kessler, Berglund, et al., 2003). Nearly three-fourths of participants with lifetime MDD in a large-scale research study also met the criteria for at least one other DSM disorder (Kessler, Berglund, et al., 2003). MDD has been found to co-occur with substance-related disorders, panic disorder, generalized anxiety disorder, PTSD, OCD, anorexia, bulimia, and borderline personality disorder. Gender differences do exist within comorbidities such that women report comorbid anxiety disorders, bulimia, and somatoform disorders while men report comorbid alcohol and substance abuse. In contrast, those with PDD are at higher risk for psychiatric comorbidity in general and for anxiety disorders, substance use disorders, and personality disorders in particular (APA, 2022).

Given the extent of comorbidity among individuals with MDD, researchers have tried to identify which disorder precipitated the other. The majority of studies found that most depression cases occur secondary to another mental health disorder, meaning that the onset of depression is a direct result of the onset of another disorder (Gotlib & Hammen, 2009).

 

4.4.2. Bipolar Disorders

Those with bipolar I disorder typically have a history of three or more mental disorders. The most frequent comorbid disorders include anxiety disorders, alcohol use disorder, other substance use disorder, and ADHD, along with borderline, schizotypal, and antisocial personality disorder.

Bipolar II disorder is more often than not associated with one or more comorbid mental disorders, with anxiety disorders being the most common (38% with social anxiety, 36% with specific phobia, and 30% having generalized anxiety). As with bipolar I, substance use disorders are common with alcohol use (42%) leading the way, followed by cannabis use (20%). Premenstrual syndrome and premenstrual dysphoric disorder are common in women with bipolar II disorder especially (APA, 2022).

Finally, cyclothymic disorder has been found to be comorbid with substance-related disorders and sleep disorders.

 

 

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4.5. Etiology

 

Section 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.

 

4.5.1. 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. As 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.

Twin and family studies suggest that unique life experiences and environmental factors play a significant role in the development of major depression. Because stressful or difficult life events are strongly linked to the onset of a major depressive episode, research suggests that epigenetics—the changes that affect how genes are turned on or off—may help explain how these experiences influence depression risk. Therefore, while we know that heritability estimates for major depression are roughly 35% and nearly 45% for early-onset major depression, the combination of genetic predisposition to major depression combined with environmental stress may better explain the increased risk of developing depression throughout one’s lifespan (Sullivan, Neale & Kendler, 2000).

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. Family studies show that people with a close family member who have bipolar disorder, are more likely to develop a mood disorder themselves. It is estimated that 8.7% of first-degree relatives of individuals with bipolar disorder will also develop bipolar disorder and 14.1% will develop major depression (Fabbri, 2020). These findings suggest that having a family history of bipolar disorder increases the risk of both bipolar disorder and major depression.

Although bipolar disorder is not a monogenic trait, twin studies among bipolar disorder individuals estimated a heritability rate between 60 and 85% (Fabbri, 2020). Adoption studies have also been used to examine the biological versus environmental differences in the rate of disorders. Specific to bipolar disorder, a higher rate of a depressive disorder was found in biological parents (30%) compared to adoptive parents (12%) suggesting a strong genetic influence within depressive disorders in general (Smoller & Finn, 2003).

            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).

Early research examining neurotransmitters and depression focused primarily on serotonin and norepinephrine, leading researchers to believe that deficiencies in these chemicals were responsible for depressive symptoms. Although these studies advanced our understanding of the biological basis of depression, current research suggests that the relationship is far more complex than originally believed. More specifically, depression appears to involve interactions among multiple neurotransmitter systems—including serotonin, norepinephrine, and dopamine—as well as changes in brain circuitry, neuroplasticity, genetics, stress hormones, and environmental influences. Researchers continue to investigate how these biological systems work together to contribute to the development of depression (Jauhar et al., 2023).

Early theories of bipolar disorder suggested that mania resulted from increased serotonin activity and depression from decreased monoamine activity. More recent research, however, has found that no single neurotransmitter can fully explain the disorder. Instead, bipolar disorder appears to involve dysregulation across several neurotransmitter systems, including dopamine, norepinephrine, and serotonin, as well as abnormalities in neural networks responsible for emotion regulation. Additional research suggests that increased dopaminergic and noradrenergic activity may contribute to manic symptoms, while disruptions in serotonin function may play a role across both depressive and manic phases. Given the biological complexity of bipolar disorder, researchers continue to investigate the precise mechanisms underlying mood episodes (Pardossi et al., 2025).

            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. Individuals with depression often show reduced activity and altered connectivity with the prefrontal cortex, a region involved in decision making, attention, and emotion regulation. Additionally, studies have found reduced hippocampus volume, particularly in individuals with recurrent or chronic depression. In contrast, the amygdala, which is involved in processing emotional information, has shown increased activity in response to negative emotional stimuli (Lalousis et al., 2023; Mohammadi et al., 2023).

Abnormalities in several brain structures have also been identified in individuals with bipolar disorder. Current studies suggest that bipolar disorder is characterized by altered communication within emotion regulation networks rather than abnormalities within a specific brain structure. Imaging studies identified differences in activity within the prefrontal cortex, anterior cingulate cortex, amygdala, hippocampus and other limbic structures depending on whether the individual is experiencing mania, depression, or stable mood. Imaging studies have also identified changes in frontal, temporal, and subcortical brain regions, although it is unclear whether these changes represent a risk factor for the disorder, consequences of repeated mood episodes, or both. Researchers continue to explore these various brain regions and how they contribute to the onset, progression and treatment of bipolar disorder (Schumer et al., 2023; Abe et al., 2023).

 

4.5.2. 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.

Building on Seligman’s theory of learned helplessness, researchers proposed the learned helplessness model into the hopelessness theory of depression, which emphasizes the importance of how people explain the causes of negative life events (Liu, 2015). This theory suggests that an individual’s attributional style—the way an individual interprets an event—can influence the development of depressive symptoms.  More specifically, and individual with a negative attributional style focuses on the internal, stable, and global influence of daily lives, whereas individuals with a positive attributional style focuses on the external, unstable, and specific influence of the environment.

Research consistently demonstrates that individuals with a negative attributional style are at an increased risk of developing depression, particularly when they experience repeated, significant life events. Interpreting these events as personal, permanent, and widespread can contribute to feelings of hopelessness, making it more difficult for the individual to believe that future circumstances can improve (Peterson & Seligman, 2026). It is important to note that although a negative attributional style does not guarantee that someone will develop depression, it does represent an important cognitive distortion that can interact with other biological, psychological, and social risk factors.

In addition to attributional style, researchers have identified rumination—the tendency to repeatedly think about one’s negative emotions, the causes of those emotions, and the possible consequences without actively working toward a solution—as an important cognitive process associated with depression. Rather than helping solve problems, rumination often keeps individuals focused on their distress, making it more difficult to move forward. Research has consistently shown that individuals who engage in higher levels of rumination are more likely to develop depressive symptoms, experience more severe episodes of depression, and remain depressed for longer periods of time (Cano-Lopez et al., 2020; Ciobotaru et al., 2024; Rickerby et al., 2024). Furthermore, rumination may also increase the risk of future depressive episodes because it strengthens negative thinking patterns and makes it more difficult to regulate emotions.

While attributional style and rumination help explain why some individuals are vulnerable to depression and focus on negative experiences, Aaron Beck’s cognitive theory describes specific thought patterns that contribute to the development and maintenance of depressive symptoms.  Often viewed as one of the founders of Cognitive-Behavioral Therapy, Beck proposed that depression is characterized by persistent maladaptive thoughts, as well as predictable errors in thinking that reinforce these beliefs (Beck, 2024).

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 described several common cognitive distortions—catastrophizing, overgeneralization, black-and-white thinking to name a few—that contribute to negative emotions and depression (see the end of the module). 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 rapid, involuntary, 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. Decades of research continues to support cognitive models of depression, demonstrating that negative thinking patterns, dysfunctional beliefs, and maladaptive cognitive schemas contribute to the onset and maintenance of depressive symptoms (Tsolakis, 2025, Faith et al., 2022). These findings provide the theoretical basis for cognitive-behavioral interventions, which remain among the most well-supported psychological treatments for depression (Section 4.5).

 

4.5.3. Behavioral

The behavioral model proposes that depression develops and is maintained when individuals experience a reduction in positive reinforcement from their environment. Positive reinforcement—the rewarding experiences that increase the likelihood of engaging in a behavior again—come from many aspects of life including work, school, relationships, family, or even the environment in general. When rewarding experiences become less frequent or more difficult to obtain, individuals gradually withdraw from activities they once found enjoyable or meaningful (Gautam et al., 2020).

One of the earliest and most influential behavioral theories of depression was developed by Peter Lewinsohn, who proposed that depression results, in part, from a decrease in response-contingent positive reinforcement (Lewinsohn et al., 1990; 1984). As rewarding experiences decline, individuals often become less motivated to participate in daily activities. This withdrawal further reduces opportunities for positive experiences, creating a self-perpetuating cycle in which depressive symptoms continue or worsen.  An example of this is a student who is well prepared but repeatedly performs poorly on exams. After repeated disappointing experiences, the student may begin to believe that studying is not worthwhile and gradually spend less time preparing for future exams. As these study habits decline, academic performance may worsen, reinforcing feelings of discouragement and hopelessness.

 

4.5.4. 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 the behavioral theory, the family-social perspective of depression emphasizes the role of an individual’s social environment, particularly the availability and quality of social support. According to this perspective, depression is influenced not only by internal psychological processes but also by interpersonal relationships and social experiences. Supportive relationships can serve as protective factors against depression, whereas social isolation, loneliness, interpersonal conflict, and stressful relationships can increase the likelihood of depressive symptoms.

Research consistently demonstrates that individuals with limited social support or strained relationships are at a greater risk for depression. With that said, it is important to remember that the relationship between depression and social functioning appears to be bidirectional. Therefore, a lack of meaningful social connections can contribute to the development and maintenance of depression, while depressive symptoms can also make it more difficult for individuals to maintain relationships due to withdrawal, irritability, and decreased emotional availability (Faronbi et al., 2025; Santini et al., 2020; Wang et al., 2023).

Relationship difficulties, including marital conflict and divorce, have also been associated with increased risk for depression, although relationship quality may be more important than relationship status alone. Individuals in supportive, stable relationships often experience better mental health outcomes than individuals experiencing conflict, poor communication, or low emotional support in relationships (Whisman & Uebelacker, 2009; Braithwaite & Holt-Lunstad, 2017).

Family stressors can also influence depression risk. While strong family relationships can provide emotional support and protection, caregiving responsibilities, parenting demands, financial pressures and disagreement on household responsibilities can increase stress. In fact, research has shown that parenting stress and reduced social support are associated with greater depressive symptoms among parents, particularly when individuals lack opportunities for personal support or meaningful connections (Nomaguchi & Milkie, 2020).

            4.5.4.2. Multi-cultural perspective. While depression is experienced across the entire world, cultural beliefs and values can influence how symptoms are experienced, interpreted, and expressed. While common depressive symptoms such as feeling sad, lack of energy, anhedonia, difficulty concentrating, and thoughts of suicide are recognized across cultures, the way these symptoms are described may differ by individuals. Research suggests that people from some cultural backgrounds may emphasize physical symptoms of depression—tiredness, weakness, sleep issues—whereas others may describe their experiences primarily in emotional or cognitive symptoms. It is important to note that these differences do not suggest that depression is fundamentally different; they reflect differences in how cultural norms regarding emotional distress is understood and communicated (APA, 2022).

Within the United States, research has found that depression affects individuals from all racial and ethnic backgrounds; however, the differences in access to mental health services, quality of care, and treatment outcomes also impacts these statistics. More specifically, individuals of historically marginalized racial and ethnic communities are less likely to receive mental health treatment and are more likely to experience barriers to care, thus contributing to delayed diagnosis, greater symptom severity, and in increased likelihood that depression becomes chronic or recurrent (Bailey et al, 2019). According to Williams and colleagues (2007), prevalence rates for major depressive disorder among Caucasians was 17.9% as opposed to African Americans, whose prevalence estimate was only 10.4%. However, statistics related to the chronicity of disease was higher for African Americans (56%) than Caucasians (38.6%). Furthermore, fewer than half the African American participants sought treatment for their depression, despite labeling their symptoms as severe. These findings highlight the importance in reducing disparities in mental health care to increase the likelihood that individuals receive effective, evidence-based treatment.

            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. Although research does not support the idea that diagnostic bias alone explains gender differences in depression, evidence suggests that traditional masculine norms may influence how men recognize, express, and seek treatment for depression. As a result, depression in men may sometimes go unrecognized or be expressed differently than the symptoms typically emphasized in diagnostic criteria (Rice et al., 2022).

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. Traditional gender roles often encourage women to prioritize relationships and caregiving responsibilities, whereas men are more frequently encouraged to value independence, emotional restraint, and achievement. These expectations may influence coping styles, stress exposure, and willingness to seek help for mental health concerns.

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 (Zou et al., 2025) Several studies have supported this theory and shown that rumination of negative thoughts is positively related to an increase in depression symptoms (Rickerby et al., 2024).

Current research suggests that no single biological, psychological, or social factor fully explains why depression is more common among women. Researchers believe that gender differences result from the interaction of a combination of biological, psychological, and social and environmental influences. This biopsychosocial perspective remains the dominant explanation for gender differences in depression.

 

 

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4.6. Treatment of Mood Disorders

 

Section Learning Objectives

• Describe treatment options for depressive disorders.
• Describe treatment options for bipolar disorders.
• Determine the efficacy of treatment options for depressive disorders.
• Determine the efficacy of treatment options for bipolar disorders.

 

4.6.1. Depressive Disorders

Given that Major Depressive Disorder is among the most frequent and debilitating psychiatric disorders, it should not be surprising that the research on this disorder is quite extensive. Among its treatment options, the most efficacious ones include antidepressant medications, Cognitive-Behavioral Therapy (CBT; Beck et al., 1979), Behavioral Activation (BA; Jacobson et al., 2001), and Interpersonal Therapy (IPT; Klerman et al., 1984). Although CBT is the most widely known and used treatment for Major Depressive Disorder, there is minimal evidence to support one treatment modality over the other; treatment is generally dictated by therapist competence, availability, and patient preference (Craighhead & Dunlop, 2014).

            4.6.1.1. Psychopharmacology – Antidepressant medications. Antidepressants are often the most common first-line attempt at treatment for MDD for a few reasons. Oftentimes an individual will present with symptoms to their primary caregiver (a medical doctor) who will prescribe them some line of antidepressant medication. Medication is often seen as an “easier” treatment for depression as the individual can take the medication at their home, rather than attending weekly therapy sessions; however, this also leaves room for adherence issues as a large percentage of individuals fail to take prescription medication as indicated by their physician. Given the biological functions of neurotransmitters and their involvement in maintaining depressive symptoms, it makes sense that this is an effective type of treatment.

Within antidepressant medications, there are a few different classes, each categorized by their structural or functional relationships. Most recent evidence suggests that most second-generation antidepressants (SSRIs, SNRIs and atypical antidepressants) have similar overall efficacy, however, they differ in side effects and tolerability. Medication selection is very individualized based on symptoms, previous treatment response, comorbid functioning, drug interactions and side-effects (APA, 2019).

            4.6.1.2. Psychopharmacology – Selective serotonin reuptake inhibitors (SSRIs). SSRIs are among the most common medications used to treat depression due to their relatively benign side effects. Additionally, the required dose to reach therapeutic levels is low compared to the other medication options.  Possible side effects from SSRIs include but are not limited to nausea, insomnia, and reduced sex drive.

SSRIs selectively block serotonin reuptake, increasing serotonin availability in the synapse. While this is the general mechanism through which all SSRI’s work, there are minor biological differences among different types of medications within the SSRI family. These small differences are beneficial to patients in that there are a few treatment options to maximize medication benefits and minimize side effects (APA, 2019).

            4.6.1.3. Psychopharmacology – Tricyclic antidepressants. Although originally developed to treat schizophrenia, tricyclic antidepressants were adapted to treat depression after failing to manage symptoms of schizophrenia (Kuhn, 1958). The term tricyclic came from the molecular shape of the structure: three rings.

Tricyclic antidepressants are like SSRIs in that they work by affecting brain chemistry, altering the number of neurotransmitters available for neurons. More specifically, they block the absorption or reuptake of serotonin and norepinephrine, thus increasing their availability for postsynaptic neurons. While effective, tricyclic antidepressants have been increasingly replaced by SSRIs due to their reduced side effects. However, tricyclic antidepressants have been shown to be more effective in treating depressive symptoms in individuals who have not been able to achieve symptom reduction via other pharmacological approaches (APA, 2019).

While the majority of the side effects are minimal – dry mouth, blurry vision, constipation, others can be serious such as sexual dysfunction, tachycardia, cognitive and/or memory impairment. Due to the potential impact on the heart, tricyclic antidepressants should not be used in cardiac patients as they may exacerbate cardiac arrhythmias (Roose & Spatz, 1999).

            4.6.1.4. Psychopharmacology – Monoamine oxidase inhibitors (MAOIs).  The use of MAOIs as a treatment for depression began serendipitously as patients in the early 1950s reported reduced depression symptoms while on the medication to treat tuberculosis. Research studies confirmed that MAOIs were effective in treating depression in adults outside the treatment of tuberculosis. Although still prescribed, they are not typically first-line medications due to their safety concerns with hypertensive crises. Because of this, individuals on MAOIs have strict diet restrictions to reduce their risk of hypertensive crises (Chamberlain & Baldwin, 2021).

How do MAOIs work? In basic terms, monoamine oxidase is released in the brain to remove excess neurotransmitters norepinephrine, serotonin, and dopamine. MAOIs essentially prevent the monoamine oxidase (hence the name monoamine oxidase inhibitors) from removing these neurotransmitters, thus resulting in an increase in these brain chemicals (Shulman, Herman & Walker, 2013). As previously discussed, norepinephrine, serotonin, and dopamine are all involved in the biological mechanisms of maintaining depressive symptoms.

While these drugs are effective, they come with serious side effects. In addition to the hypertensive episodes, they can also cause nausea, headaches, drowsiness, involuntary muscle jerks, reduced sexual desire, weight gain, etc. (APA, 2019). Despite these side effects, studies have shown that individuals prescribed MAOIs for depression have a treatment response rate of 74% (Birkenhager & Heijnen, 2024). Overall, despite their effectiveness, MAOIs are likely the best treatment for late-stage, treatment-resistant depression patients who have exhausted other treatment options (Van den Eynde, 2022).

It should be noted that occasionally, antipsychotic medications are used for individuals with MDD; however, these are limited to individuals presenting with psychotic features.

            4.6.1.5. Psychopharmacology- Ketamine and Esketamine. In recent years, researchers have explored newer medications for individuals with depression who do not respond to traditional antidepressants. One of the most promising developments has been the use of ketamine for individuals whose symptoms have not improved after trying multiple standard treatments.

Unlike traditional antidepressant medications, ketamine works through different brain systems involving glutamate, a neurotransmitter involved in communication between brain cells. The effect on glutamate helps produce antidepressant effects much quicker than traditional medications. In fact, some individuals report improvement in depressive symptoms within hours or days after receiving ketamine, whereas many traditional antidepressants may take several weeks to produce noticeable effects (Jelen & Stone, 2021; Nikolin et al., 2023).

In 2019, the FDA approved esketamine, a form of ketamine, as a treatment for adults with treatment-resistant depression. Esketamine is administered as a nasal spray under medical supervision due to potential severe side-effects. Although both ketamine and esketamine provide a new option for individuals with severe or treatment-resistant depression, they are not considered first-line treatments for most people with depression (Vasiliu, 2023; Daly et al., 2018). Researchers continue to study the effects of ketamine on depression including how long the benefits last, how often treatments should be given, and which individuals are most likely to benefit.

            4.6.1.6. Psychotherapy – Cognitive behavioral therapy (CBT). CBT is one of the most widely researched and commonly used psychological treatments for depression and many other mental health disorders. Developed primarily by Aaron Beck’s work in the 1960s, CBT based on the idea that psychological distress is influenced by the interaction of the cognitive triangle— cognitions (thoughts), behaviors, and emotions. Beck believed that individuals experiencing depression often develop negative interpretations of themselves, their experiences, and their future, which can contribute to and maintain depressive symptoms.

A central component of CBT is the idea that thoughts, emotions, and behaviors are interconnected. Therefore, CBT aims to improve emotions in depressed patients by changing both cognitions (thoughts) and behaviors, which in return enhances mood. Common cognitive interventions with CBT include thought monitoring and recording, identifying cognitive errors, examining evidence supporting/negating cognitions, and creating rational alternatives to maladaptive thought patterns. Behavioral interventions of CBT include activity planning, pleasant event scheduling, task assignments, and coping-skills training.

CBT generally follows four phases of treatment:

• Phase 1: Increasing pleasurable activities. Similar to behavioral activation (see below), the clinician encourages the patient to identify and engage in activities that are pleasurable to the individual. The clinician can help the patient to select the activity, as well as help them plan when they will engage in that activity.
• Phase 2: Challenging automatic thoughts. During this stage, the clinician provides psychoeducation about the negative automatic thoughts that can maintain depressive symptoms. The patient will learn to identify these thoughts on their own during the week and maintain a thought journal of these cognitions to review with the clinician in session.
• Phase 3: Identifying negative thoughts. Once the individual is consistently able to identify these negative thoughts on a daily basis, the clinician can help the patient identify how these thoughts are maintaining their depressive symptoms. It is at this point that the patient begins to have direct insight as to how their cognitions contribute to their disorder.
• Phase 4: Changing thoughts. The final stage of treatment involves challenging the negative thoughts the patient has been identifying in the last two phases of treatment and replacing them with positive thoughts.

Research consistently demonstrates that CBT is an effective treatment for major depressive disorder. Meta-analyses indicate that CBT produces significant reductions in depressive symptoms and has effects comparable to antidepressant medication for many individuals, especially those with mild to moderate depression (Cuijpers et al., 2025). Furthermore, CBT skills may provide lasting benefits because individuals learn strategies they can continue using after treatment ends, potentially reducing the risk of relapsing.

            4.6.1.7. Psychotherapy – Behavioral activation (BA). BA is a therapeutic approach for depression that is based on the behavioral model of psychopathology. Similar to the behavioral component of CBT, BA focuses on the relationship between behavior, environment reinforcement, and mood. The primary goal of BA is to help individuals increase participation in meaningful and rewarding activities while reducing patterns of avoidance and withdrawal that often maintain depressive symptoms.

Founded by Ferster (1973), as well as Lewinsohn and colleagues (Lewinsohn, 1974; Lewinsohn, Biglan, & Zeiss, 1976), who proposed that depression develops, in part, when individuals experience a reduction in positive reinforcement from their environment. Modern BA expands on these early behavioral theories by emphasizing the role of avoidance behaviors in maintaining depression. When individuals experience depression, they may withdraw from relationships, activities, or responsibilities as it provides temporary relief from distress.

During BA, the clinician and patient work together to identify activities that promote pleasure, accomplishment and connection, such as scheduling social interactions, engaging in hobbies or exercise, identifying work related goals, or even daily responsibilities. Rather than waiting for motivation or improved mood to engage in these activities, individuals learn to act and schedule the behaviors to help improve mood overtime. It is important that the therapist work with the individual to monitor their activities, identify barriers to engagement, and develop problem-solving strategies.

Research has consistently demonstrated that BA is an effective treatment for major depressive disorder, with meta-analyses indicating that BA produces significant reduction in depressive symptoms and is comparable in effectiveness to CBT (Cuijpers et al., 2023; Cuijpers et al., 2020). Similar to CBT, because BA focuses on practical skills that can be applied outside of therapy, it may also help in long-term reduction of depressive symptoms.

            4.6.1.8. Psychotherapy – Interpersonal therapy (IPT). IPT was developed by Klerman, Weissman, and colleagues in the 1970s as a treatment arm for a pharmacotherapy study of depression (Weissman, 1995). The treatment was created based on data from post-World War II individuals who expressed a substantial impact on their psychosocial life events. Klerman and colleagues noticed a significant relationship between the development of depression and complicated bereavement, role disputes, role transitions, and interpersonal deficits in these individuals (Weissman, 1995). The idea behind IPT is that depressive episodes compromise interpersonal functioning, which makes it difficult to manage stressful life events. The basic mechanism of IPT is to establish effective strategies to manage interpersonal issues, which in return, will ameliorate depressive symptoms.

There are two main principles of IPT. First, depression is a common medical illness with a complex and multi-determined etiology. Since depression is a medical illness, it is also treatable and not the patient’s fault. Second, depression is connected to a current or recent life event. The goal of IPT is to identify the interpersonal problem that is related to the depressive symptoms and solve this crisis so the patient can improve their life situation while relieving depressive symptoms (Weissman, 2020).

            4.6.1.9. Multimodal treatment. While both pharmacological and psychological treatment alone is very effective in treating depression, a combination of the two treatments may offer additional benefits, particularly in the maintenance of wellness. Additionally, multimodal treatment options may be helpful for individuals who have not achieved wellness in a single modality.

Multimodal treatments can be offered in three different ways: concurrently, sequentially, or within a stepped manner (McGorry et al., 2010). With a stepped manner treatment, pharmacological therapy is often used initially to treat depressive symptoms. Once the patient reports some relief in symptoms, the psychosocial treatment is added to address the remaining symptoms. While all three methods are effective in managing depressive symptoms, matching patients to their treatment preferences may produce better outcomes than clinician-driven treatment decisions.

 

4.6.2. Bipolar Disorder

            4.6.2.1. Psychopharmacology. Unlike treatment for MDD, treatment for bipolar disorder requires careful consideration of both depressive and manic symptoms, as well as prevention of future mood episodes. Because antidepressant medications can increase the risk of triggering mania or hypomania in some individuals, current treatment guidelines generally recommend mood stabilizers or certain second-generation antipsychotic medications as first-line treatments for bipolar disorder (Nierenberg et al., 2023).

Lithium remains one of the most well-established treatments for bipolar disorder. Research has demonstrated that lithium is effective for treating acute manic episodes and preventing future mood episodes, including both manic and depressive recurrences (Verdolini et al., 2021). Additionally, lithium has been associated with reduced suicide risk among individuals with bipolar disorder.

Other mood-stabilizing medications, including Depakote, may also be used depending on an individual’s symptoms and treatment needs. Treatment decisions are individualized because medications differ in effectiveness, side effects, and risks for specific populations.

Although antidepressants may be helpful for some individuals with bipolar depression, they are generally not recommended as a standalone treatment for bipolar disorder. When used, antidepressants are often prescribed in combination with a mood stabilizer or another medication that reduces the risk of mood switching. Research has shown that antidepressant response varies considerably among individuals with bipolar disorder, highlighting the importance of careful monitoring during treatment (Nierenberg et al., 2023; Verdolini et al., 2021).

            4.6.2.2. Psychological treatment. Although psychopharmacology is the first and most widely used treatment for bipolar disorders, occasionally psychological interventions are also paired with medication as psychotherapy alone is not a sufficient treatment option. Majority of psychological interventions are aimed at medication adherence, as many bipolar patients stop taking their mood stabilizers when they “feel better” (Advokat et al., 2014). Social skills training and problem-solving skills are also helpful techniques to address in the therapeutic setting as individuals with bipolar disorder often struggle in this area.

 

4.6.3. Outcome of Treatment

            4.6.3.1. Depressive treatment. As we have discussed, major depressive disorder has a variety of treatment options, all found to be efficacious. However, research suggests that while psychopharmacological interventions are more effective in rapidly reducing symptoms, psychotherapy, or even a combined treatment approach, are more effective in establishing long-term relief of symptoms.

Rates of relapse for major depressive disorder are often associated with individuals whose onset was at a younger age (particularly adolescents), those who have already experienced multiple major depressive episodes, and those with more severe symptomology, especially those presenting with severe suicidal ideation and psychotic features (APA, 2022).

            4.6.3.2. Bipolar treatment. Lithium and other mood stabilizers are very effective in managing symptoms of patients with bipolar disorder. Unfortunately, it is the adherence to the medication regimen that is often the issue with these patients. Bipolar patients often desire the euphoric highs that are associated with manic and hypomanic episodes, leading them to forgo their medication. A combination of psychopharmacology and psychotherapy aimed at increasing the rate of adherence to medical treatment may be the most effective treatment option for bipolar I and II disorder.

 

 

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Module Recap

That concludes our discussion of mood disorders. You should now have a good understanding of the two major types of mood disorders – depressive and bipolar disorders. Be sure you are clear on what makes them different from one another in terms of their clinical presentation, epidemiology, comorbidity, and etiology. This will help you with understanding treatment options and their efficacy.

 

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End Module 4

4th edition as of August 2026