Textbook Notes #2 PDF

Chapter #7 Trauma : & Dissociation This chapter discusses trauma and its potential effects. While not everyone suffers long-term from trauma, as many people are resilient, trauma can still lead to serious difficulties. The chapte...

Chapter #7 Trauma : & Dissociation This chapter discusses trauma and its potential effects. While not everyone suffers long-term from trauma, as many people are resilient, trauma can still lead to serious difficulties. The chapter focuses on two main groups of disorders: 1. **Trauma- and stressor-related disorders**: These involve conditions where trauma or significant stressors are central to the diagnosis. 2. **Dissociative disorders**: These are often observed following trauma and involve disruptions in awareness, self, memory, or perception. Dissociation can be a component of post-traumatic stress disorder (PTSD), showing the close connection between these two disorder categories. The DSM-5 highlights this link by positioning these disorders near each other in its classification system. Trauma & Stressor Related Disorders The DSM-5 introduced a new category called **trauma- and stressor-related disorders** for conditions arising after stressful or traumatic events. This category includes: - **Attachment disorders** in children, linked to inadequate or abusive caregiving. - **Adjustment disorders**, involving prolonged anxiety or depression after a stressful event. - **Trauma reactions** like post-traumatic stress disorder (PTSD) and acute stress disorder. Researchers reclassified these disorders because they didn’t align well with anxiety disorders, as once thought. Unlike anxiety disorders, trauma- and stressor-related disorders share an immediate triggering event and can involve a broader range of emotions—including fear, anxiety, rage, horror, guilt, and shame—especially in cases like PTSD. Post traumatic Stress Disorder Traumatic events can have severe and long-lasting emotional consequences. Perhaps the most notorious traumatic event is war, but severe emotional reactions also occur after physical assaults (particularly sexual assaults), car accidents, natural catastrophes, or the sudden death of a loved one. The emotional disorder that sometimes follows a trauma is known as post-traumatic stress disorder (PTSD). Clinical Description ### Diagnostic Criteria for PTSD According to the DSM-5-TR, PTSD develops after exposure to a traumatic event where the person either: 1. **Trauma Exposure**: The individual must have been exposed to actual or threatened death, serious injury, or sexual violence through: - Directly experiencing the traumatic event. - Witnessing the event happen to others. - Learning that a close family member or friend experienced such an event. - Repeated exposure to details of trauma (e.g., first responders). 2. **Intrusion Symptoms** (at least one required): Recurrent, involuntary, and distressing memories, dreams, flashbacks, or psychological/physiological distress when exposed to reminders of the trauma. 3. **Avoidance** (at least one required): Persistent efforts to avoid distressing memories, thoughts, feelings, or external reminders associated with the trauma. 4. **Negative Changes in Cognition and Mood** (at least two required): - Inability to recall key details of the trauma. - Negative beliefs or expectations about oneself, others, or the world. - Distorted blame of self or others for the event. - Persistent negative emotions (e.g., fear, horror, guilt). - Diminished interest in significant activities. - Detachment from others and inability to experience positive emotions. 5. **Arousal and Reactivity Changes** (at least two required): - Irritable behavior or angry outbursts. - Reckless or self-destructive behavior. - Hypervigilance. - Exaggerated startle response. - Concentration issues. - Sleep disturbances. 6. **Duration**: Symptoms must persist for more than one month. 7. **Impairment**: Symptoms cause significant distress or impair functioning in social, occupational, or other important areas. 8. **Exclusions**: Symptoms cannot be attributed to substance use or another medical condition. ### Specifiers - **With Dissociative Symptoms**: Includes depersonalization (feeling detached from oneself) or derealization (feeling that surroundings are unreal). - **With Delayed Expression**: Full criteria are not met until at least six months after the trauma. symptoms PTSD is characterized by several core symptoms: 1. **Intrusive Re-experiencing**: Survivors may experience flashbacks, nightmares, or distressing memories of the event. 2. **Avoidance**: Survivors often avoid trauma reminders, whether through avoiding places, people, or feelings associated with the trauma. 3. **Negative Cognitions and Mood**: Feelings of numbness, detachment, guilt, and negative beliefs about self or the world often develop. 4. **Altered Arousal and Reactivity**: Common symptoms include hypervigilance, irritability, sleep problems, and reckless behavior. Historical and Cultural Cases: PTSD was officially named in DSM-III in 1980, but similar symptoms have been documented throughout history, such as Samuel Pepys' account of the Great Fire of London. Additionally, a Canadian study on the Swissair Flight 111 crash showed how community members exposed to traumatic recovery efforts reported persistent symptoms of PTSD. PTSD in Children; PTSD can develop in young children, as illustrated by a case study of a traumatic dog attack on a child and her siblings. Symptoms in children may include developmental regression (e.g., bedwetting, fear of medical procedures), seperation anxiety and exaggerated memories of the trauma, sometimes incorporating fantastical elements like superheroes. Acute Stress Disorder (ASD): The DSM-IV introduced Acute Stress Disorder (ASD) to diagnose those with intense trauma responses within the first month post-trauma. ASD shares symptoms with PTSD but emphasizes the immediacy of the reaction. Around 50% of those with ASD go on to develop PTSD, though some people who later develop PTSD do not meet ASD criteria initially. ASD’s inclusion allows for early treatment, which is especially beneficial for individuals with severe initial reactions to trauma. Statistics Prevalence rates of PTSD vary significantly across different traumatic events and populations. While some studies report low PTSD rates in those exposed to extensive trauma (e.g., British citizens enduring WWII air raids), other studies show high rates among survivors of interpersonal violence like rape and assault. For instance, Kilpatrick et al. (1985) found that 19% of rape survivors attempted suicide and 44% reported suicidal thoughts. Resnick et al. (1993) also found that 32% of rape survivors and 18% of women who experienced various traumas developed PTSD. Research suggests that close proximity to trauma increases PTSD risk. For example, Vietnam War veterans’ PTSD rates were correlated with combat exposure, and Hurricane Katrina survivors faced elevated PTSD rates linked to their direct exposure to danger. After 9/11, proximity to Ground Zero was strongly associated with PTSD in adults and children alike, with higher rates of PTSD among those closer to the World Trade Center. Additionally, individual differences such as resiliency, coping skills, trauma exposure levels, early adversity, and mental health history affect susceptibility to PTSD. In Canada, PTSD rates vary by group: in 2012, 1.7% of Canadians over age 15 were diagnosed with PTSD, with higher rates among Canadian Armed Forces members (5.3%) who had been deployed in Afghanistan. There is limited research on PTSD among Indigenous populations, but studies acknowledge the compounded impact of colonial trauma and residential schools. Overall, while direct trauma exposure is a key factor, the development and persistence of PTSD are complex, influenced by both personal and contextual factors. Causes The etiology of PTSD is complex, involving a mix of trauma exposure and personal vulnerabilities across biological, psychological, and social dimensions. Exposure to trauma is a primary factor, yet not all individuals exposed to similar events develop PTSD. Key influences include: 1. **Trauma Severity and Proximity**: More intense or prolonged exposure, such as combat, assault, or disaster recovery work, increases PTSD risk. For instance, 67% of Vietnam War POWs developed PTSD, and children with severe burns had symptoms proportionate to the injury's severity. However, not everyone in high-trauma settings develops the disorder, pointing to additional factors. 2. **Biological Vulnerabilities**: Genetics play a role, though not as a direct cause. A family history of anxiety can increase PTSD susceptibility, as shown in twin studies where identical twins (who share more genetic material) are more likely to both develop PTSD than fraternal twins if one twin is affected. Some genetic traits also influence individuals' likelihood of experiencing certain traumas, likely by affecting personality characteristics that lead to risky environments. 3. **Psychological Vulnerabilities**: Personal traits, like anxiety sensitivity or a heightened fear of losing control, can increase PTSD risk. Individuals from unstable family backgrounds may see the world as dangerous and are more susceptible to PTSD following trauma. PTSD severity is also linked to a pre- existing tendency to perceive stress as uncontrollable. 4. **Social Support and Coping**: Strong social networks can buffer against PTSD. During Hurricane Andrew, children with family and peer support showed fewer symptoms, while isolated Canadians during COVID-19 reported higher PTSD rates. Supportive relationships reduce physiological stress responses, such as cortisol secretion, which may otherwise increase PTSD susceptibility. 5. **Neurological Impacts**: Trauma-related changes in brain regions, particularly the hippocampus, affect stress regulation and memory, and may drive chronic arousal in PTSD. Brain changes have been noted in trauma-exposed veterans, abuse survivors, and firefighters, potentially affecting treatment outcomes. (hpa axis heightened as well) 6. **Conditioned Responses and Learning**: PTSD may involve "conditioned" alarm responses where reminders of trauma (e.g., a certain place) trigger fear or anxiety, a mechanism similar to that seen in panic disorder. Unlike panic attacks (which are false alarms), these learned responses in PTSD are tied to real trauma and often involve anxiety about potential flashbacks. Overall, PTSD is influenced by a combination of exposure, vulnerability, and support. A biopsychosocial model captures these layers, as biological predispositions, individual traits, and social factors intersect to determine PTSD risk and symptom severity. Treatment Psychological treatment for PTSD focuses on re-exposing individuals to their trauma in a controlled, therapeutic setting to help them process the event and develop coping strategies. **Imaginal exposure** is a common technique where patients create a narrative of the trauma and repeatedly confront it in therapy. A newer adaptation involves combining exposure therapy with sleep, as research suggests that sleep aids in the extinction of traumatic memories. **Cognitive therapy** is often used alongside exposure to address negative beliefs, such as self-blame or guilt. **Preventive interventions** immediately after trauma, such as structured cognitive therapy, have been effective in reducing PTSD onset. For instance, early cognitive therapy after car accidents significantly reduced PTSD rates compared to minimal intervention. However, brief single-session debriefing may harm some individuals by intensifying distress. Specific approaches vary: Marcie, a young trauma survivor, was exposed gradually to anxiety-inducing situations with family support, aiding her recovery. **Constructivist-narrative therapy**, introduced by Meichenbaum, helps patients reinterpret their trauma story, fostering resilience. Additionally, **Eye Movement Desensitization and Reprocessing (EMDR)**, where patients follow finger movements while recalling trauma, has shown some efficacy, though traditional exposure therapy often proves more effective for reducing avoidance behaviors. Medications like SSRIs can also support PTSD treatment by alleviating anxiety and panic symptoms, although they are typically adjuncts to therapeutic approaches. Overall, tailored exposure-based therapies, sometimes enhanced by medication or immediate cognitive interventions, remain the core psychological treatments for PTSD. Other Trauma & Stress Related Disorders Grief, adjustment, and attachment disorders are all responses to various forms of stress and trauma, yet they manifest uniquely and have specific diagnostic criteria. **Prolonged Grief Disorder (PGD)** is diagnosed when intense grief does not diminish and instead intensifies over time. PGD, as defined in the DSM-5-TR, affects about 10% of adults experiencing grief, often following the loss of a close loved one. The key diagnostic criteria include: 1 Duration of Symptoms: Symptoms must persist for at least 12 months in adults and 6 months in children after the loss. 2 Core Symptoms: Individuals must experience one or both of: ◦ Intense yearning or longing for the deceased. ◦ Preoccupation with thoughts or memories of the deceased (for children, this may focus on how the person died). 3 Additional Symptoms: At least three of the following must be present most days for a month: ◦ Identity Disruption (feeling as though a part of oneself has died). ◦ Marked disbelief about the death. ◦ Avoidance of reminders of the deceased. ◦ Intense emotional pain (e.g., anger, sorrow, bitterness). ◦ Difficulty reintegrating into life (e.g., trouble engaging with others or planning for the future). ◦ Emotional numbness, feeling life is meaningless, or intense loneliness. The symptoms must cause significant impairment in daily functioning and exceed expected social, cultural, or religious norms for grief. PGD is considered a traumatic- and stressor-related disorder, with new treatments adapted from PTSD therapies focusing on managing prolonged grief. The COVID-19 pandemic has heightened instances of PGD as traditional grief rituals were disrupted. PGD is now treated with methods similar to PTSD therapy, adjusted for grief **Adjustment Disorders** involve anxious or depressive reactions to stressful, non-traumatic life events that impair daily functioning, though less severely than disorders like PTSD. Common in adolescents, these reactions can persist and become chronic if stressors remain. Adjustment disorders have been understudied due to their previous use as a general category for stress-related anxiety or depression that doesn’t fit other specific disorders. **Attachment Disorders** occur in children who fail to form normal attachments due to inadequate or abusive caregiving. The DSM-5-TR categorizes these as either **Reactive Attachment Disorder (RAD)**, where the child is emotionally withdrawn and unresponsive to caregivers, or **Disinhibited Social Engagement Disorder (DSED)**, where the child displays inappropriate openness with strangers. Both disorders stem from early-life stress, such as neglect or frequent changes in primary caregivers. These disorders highlight varied responses to loss, stress, and inadequate caregiving, with PGD reflecting grief-related distress, adjustment disorders showing responses to life stress, and attachment disorders emerging from early deprivation. Dissociative Disorders Dissociative experiences involve detachment from oneself or one's surroundings, often experienced as a temporary alteration in consciousness or identity. While mild dissociative sensations like feeling "unreal" or as if in a dream state are common, particularly under stress or fatigue, some individuals experience intense dissociative episodes that impair their ability to function and even cause memory loss or identity shifts. These conditions, known as **dissociative disorders**, occur when disconnections in perception, memory, or self-awareness become extreme. ### Types of Dissociative Experiences: 1. **Depersonalization**: An individual feels detached from their own reality, as though observing themselves from the outside. This can lead to a disturbing sense of unreality about one’s own body or actions. 2. **Derealization**: The external world feels unreal or distorted, with objects or people appearing altered in shape, size, or lifelessness, as if they were mechanical. Such dissociative episodes are thought to be coping mechanisms that arise in response to severe stress or trauma. These experiences can lead to a disintegrated sense of self, where individuals may struggle to recall events, know their location, or even retain their own identity. In extreme cases, individuals might even assume a completely new identity with distinct memories, traits, and sometimes physical responses, like developing new allergies. Cultural and social factors play a significant role in how dissociative disorders manifest. Even in severe cases, symptoms often conform to culturally understood expressions of identity and memory, reflecting society's influence on how dissociation is experienced and interpreted. Depersonalization & Derialization Disorder **Depersonalization-Derealization Disorder (DPDR)** is a rare dissociative disorder where individuals experience persistent or recurrent feelings of detachment from their own thoughts, body, or surroundings. These symptoms can be extremely distressing and interfere significantly with daily life, as people may feel as if they are outside observers of their own actions, similar to being in a dream. Importantly, however, individuals with DPDR maintain an understanding that their experiences are not real in the way psychosis might cause someone to believe them. This retention of "reality testing" distinguishes DPDR from conditions like schizophrenia. ### DSM-5-TR Criteria for Depersonalization-Derealization Disorder: 1. **Persistent or Recurrent Experiences of Depersonalization, Derealization, or Both**: - **Depersonalization**: A sense of detachment from oneself, such as feeling like an observer of one’s own thoughts or body, perceiving altered sensations, a distorted sense of time, or a numbness in emotions or physical sensations. - **Derealization**: A detachment from surroundings, where the external world seems unreal, dreamlike, foggy, or visually distorted. 2. **Intact Reality Testing**: The individual is aware that the experience of detachment is not an accurate representation of reality. 3. **Clinically Significant Distress or Impairment**: The symptoms lead to distress or difficulty in social, work, or other critical life areas. 4. **Not Caused by Substance Use or Medical Condition**: The disturbance cannot be attributed to drugs, medications, or medical conditions such as seizures. such as seizures. 5. **Not Better Explained by Another Mental Disorder**: Symptoms are not due to other mental health disorders, such as schizophrenia, major depressive disorder, PTSD, or other dissociative conditions. ### Prevalence and Demographics: - DPDR is rare in the general population, with rates estimated between 0.8% and 2.8% (Johnson et al., 2006; Spiegel et al., 2011). However, a meta-analysis found that as many as 11.4% of college students could meet criteria based on self-reported symptoms, though these numbers may be inflated due to reliance on self-report (Kate et al., 2020). - Onset often follows traumatic or highly stressful events, including abuse or significant life changes, and tends to appear in adolescence, with a typical age of onset around 16 (Simeon et al., 1997). ### Cognitive and Neurobiological Aspects: Studies show that individuals with DPDR have specific cognitive and perceptual difficulties: - **Cognitive Deficits**: People with DPDR tend to struggle with attention, short-term memory, and spatial reasoning. They may experience "tunnel vision" or perceive objects in a flattened, two-dimensional way, and report an “empty mind” (Guralnick et al., 2000). - **Emotional Blunting**: Emotional responses are often blunted, as observed in reduced skin conductance responses, indicating a dampened physiological reaction to emotional stimuli (Sierra et al., 2002). - **Brain and HPA Axis Dysregulation**: Studies reveal altered brain functioning in areas involved with perception and emotion regulation, as well as irregularities in the hypothalamic-pituitary-adrenal (HPA) axis, which is responsible for stress response (Simeon, 2009; Simeon et al., 2001; Spiegel et al., 2013). ### Treatment: Treatment for DPDR remains limited and under-researched. An evaluation of the medication Prozac did not find it effective compared with placebo, and psychotherapeutic approaches specifically tailored to DPDR are still lacking robust evidence. Dissociative Amnesia **Dissociative Amnesia** is a dissociative disorder characterized by the inability to recall important autobiographical information, typically of a traumatic or stressful nature. The disorder manifests in several distinct patterns, with memory loss ranging from specific events to an entire personal history, known as **generalized amnesia**. #### DSM-5-TR Diagnostic Criteria for Dissociative Amnesia (Table 7.4): 1. **Inability to Recall Important Autobiographical Information**: This memory loss is usually related to trauma or stress and goes beyond typical forgetfulness. - **Localized or Selective Amnesia**: Most commonly, individuals fail to recall specific traumatic events. - **Generalized Amnesia**: In rarer cases, individuals lose memory for their entire identity and life history. 2. **Significant Distress or Impairment**: The memory loss significantly disrupts social, occupational, or other essential areas of daily functioning. 3. **Not Due to Substance Use or Medical Conditions**: The memory disturbance cannot be attributed to substance use, medication effects, or other medical conditions, such as seizures or head injury. 4. **Not Explained by Other Mental Disorders**: The amnesia is not better accounted for by other disorders, such as dissociative identity disorder or PTSD. **Specifier**: **Dissociative Fugue** — A subtype involving purposeful travel or bewildered wandering, coupled with amnesia for one’s identity or critical autobiographical information. ### Cultural Variants of Dissociative Amnesia In some cultures, dissociative states may take unique forms: - **Amok**: Seen in some Southeast Asian cultures, "running amok" involves a dissociative state marked by violent outbursts, often followed by memory loss.(more common in men) - **Trance and Possession States**: In cultural contexts where trance states are accepted, such as Indian, Nigerian (vinvusa), and Thai (phiipob) cultural practices, these states are not viewed as pathological unless they are disruptive. ### Prevalence and Onset Dissociative amnesia typically begins in adolescence or adulthood, rarely appearing after age 50. Studies estimate its prevalence to range from 1.8% to 7.3%, making it the most common dissociative disorder【Spiegel et al., 2011】. It can persist across a person’s lifespan, especially if triggered by repeated trauma.  Chapter #8 : Mood 1. **Normal Sadness vs. Clinical Depression** - Normal sadness is temporary and often linked to specific situations. - Clinical depression is intense, persistent, and disrupts daily life. 2. **Katie’s Depression** - Katie, a shy 16-year-old, had few social interactions due to social anxiety. - Her isolation led to a deep, consuming depression, which she described as falling into a dark hole. - Symptoms included crying for hours, distorted self-perception, anger, and frustration. 3. **Coping Attempts** - Katie began drinking alcohol, initially approved by her parents, as prescribed medications were ineffective. - Her drinking escalated to dependency, becoming a way to numb emotional pain. 4. **Suicidal Thoughts and Actions** - Katie had thoughts of suicide since age 13 but hid them after seeing her parents’ emotional reaction. - At 16, she attempted suicide after a disagreement with her mother. She drank heavily, cut her wrist, and calmly sought help when the attempt failed. - Despite promising her father not to try again, Katie’s preoccupation with death persisted. 5. **Key Differences from Normal Sadness** - Katie’s depression was severe, lasting years, and significantly impaired her daily life. - Her condition included hopelessness, distorted thoughts, and physical symptoms like dependence on alcohol. - Unlike normal sadness, her depression led to a suicide attempt and ongoing thoughts of death. An overview of depression and mania Mood disorders, historically known as "depressive disorders" or "affective disorders," are characterized by severe deviations in mood and classified in the DSM-5-TR into two categories: depressive disorders and bipolar and related disorders. The most severe form of depression, a major depressive episode (MDE), is defined as an extremely depressed mood lasting at least two weeks. According to the DSM-5-TR, an MDE is diagnosed if five or more of the following symptoms are present during the same two-week period, representing a change from previous functioning: (1) depressed mood most of the day, nearly every day, (2) markedly diminished interest or pleasure in almost all activities, (3) significant weight change or appetite disturbance, (4) insomnia or hypersomnia, (5) psychomotor agitation or retardation, (6) fatigue or loss of energy, (7) feelings of worthlessness or excessive guilt, (8) diminished ability to concentrate or indecisiveness, and (9) recurrent thoughts of death or suicidal ideation. At least one symptom must be depressed mood or loss of interest/pleasure. These symptoms must cause significant distress or impairment and not be attributable to a substance or medical condition. If untreated, MDEs typically last four to nine months, with key features including somatic symptoms, behavioral shutdown, and emotional detachment. Mania, the second fundamental state in mood disorders, involves a distinct period of abnormally and persistently elevated, expansive, or irritable mood and increased activity or energy, lasting at least one week (or less if hospitalization is required). The DSM-5-TR defines a manic episode as meeting this criterion along with three or more of the following symptoms (four if the mood is only irritable): (1) inflated self-esteem or grandiosity, (2) decreased need for sleep, (3) more talkative than usual or pressure to keep talking, (4) flight of ideas or racing thoughts, (5) distractibility, (6) increased goal-directed activity or psychomotor agitation, and (7) excessive involvement in activities with high potential for painful consequences (e.g., reckless spending or risky sexual behavior). These symptoms must cause marked impairment in functioning or require hospitalization and must not be attributable to a substance or medical condition. Manic episodes can last three to four months untreated and often include irritability or anxiety. The DSM-5-TR also describes hypomanic episodes, which are less severe versions of mania. Hypomanic episodes last at least four days, involve similar symptoms as manic episodes, and are noticeable to others but do not cause significant impairment in functioning or require hospitalization. The distinction between major depressive episodes, manic episodes, and hypomanic episodes is critical for diagnosing mood disorders such as major depressive disorder and bipolar disorder. The structure of mood disorders Unipolar mood disorders occur when individuals experience either depression or mania, remaining at one "pole" of the depression-mania continuum. Unipolar mania, where only manic episodes are present, is rare and often progresses to include depressive episodes. More commonly, someone alternating between depression and mania is diagnosed with a bipolar mood disorder, indicating movement between both poles. However, depression and mania are not always opposite; they can overlap, leading to "mixed features," where symptoms of both occur simultaneously. For instance, individuals may experience manic symptoms like racing thoughts or agitation while feeling anxious or depressed. Manic episodes with dysphoric (anxious or depressive) features are more common than previously thought, with studies showing high prevalence rates of mixed episodes among those hospitalized for mania. For example, one study found that 30% of patients with acute mania had mixed episodes, while two- thirds of those with bipolar depression exhibited manic symptoms like distractibility or agitation. These individuals often experience greater impairment than those with purely depressive or manic symptoms. Furthermore, unipolar mania typically evolves into depression over time, supporting models that conceptualize bipolar disorder as a progressive condition with early mild symptoms and later chronic episodes. The DSM-5-TR uses "mixed features" to describe episodes combining symptoms of opposite polarities, specifying whether the predominant episode is depressive or manic. For individuals with bipolar disorder, the "predominant polarity" refers to the dominant type of episode (manic or depressive) across their lifetime. Studies suggest that most individuals with bipolar disorder do not show a predominant polarity, while smaller percentages are primarily manic or depressive. Tracking the course of mood episodes is critical for accurate diagnosis and treatment. Clinicians assess whether episodes recur, the extent of recovery between episodes (full or partial remission), and whether depressive episodes alternate with manic or hypomanic ones. This information helps differentiate between mood disorders and guides clinical decisions. Depressive Disorders - Clinical Description ### Clinical Description of Depressive Disorders #### **Major Depressive Disorder (MDD)** Major depressive disorder (MDD) is characterized by a severely depressed mood and related symptoms such as feelings of worthlessness, difficulty concentrating, fatigue, sleep disturbances, and recurrent thoughts of death. To meet the DSM-5-TR criteria for MDD, an individual must experience at least five symptoms of depression, including either a depressed mood or loss of interest/pleasure, for at least two weeks. Additionally, no history of manic or hypomanic episodes should be present. A single episode of major depression is rare, as most individuals experience recurrent episodes. If two or more major depressive episodes occur, separated by at least two months of remission, the diagnosis is classified as **MDD, Recurrent**. This recurrent pattern is significant for predicting future episodes and treatment strategies. For example, as many as 85% of individuals with a single episode eventually experience additional episodes. The average number of lifetime episodes ranges from four to seven, with each episode lasting approximately four to five months. Katie, for instance, experienced recurring depressive episodes marked by severe symptoms, cycling in and out of depression. Her diagnosis would be **MDD, Recurrent**. #### **Persistent Depressive Disorder (PDD)** Persistent depressive disorder (PDD), formerly known as dysthymia, involves chronic depression lasting at least two years (one year for children/adolescents), during which individuals experience a depressed mood most of the time. While fewer symptoms are required than for MDD (at least two symptoms from the DSM-5-TR criteria), the chronicity of PDD makes it more severe. Individuals with PDD often present with comorbid mental disorders, slower treatment responses, and higher relapse rates. During the two-year period, individuals cannot be symptom-free for more than two months at a time, and symptoms may include low energy, low self-esteem, feelings of hopelessness, poor concentration, and appetite or sleep disturbances. A key distinction is that individuals may have persistent symptoms of PDD with intermittent major depressive episodes, a condition referred to as **double depression**. Double depression involves periods of chronic mild depression (PDD) punctuated by severe episodes of MDD. This pattern often results in a more challenging course of treatment. For example, Jack’s case illustrates **PDD with intermittent major depressive episodes**, as his baseline of persistent depression was occasionally interrupted by full major depressive episodes. ### DSM-5-TR Specifiers for Depressive Disorders To refine diagnoses, clinicians use specifiers to describe additional features of depressive episodes, including severity (mild, moderate, severe) and specific symptoms: 1. **Psychotic Features** - Hallucinations or delusions may accompany depressive episodes. These are classified as mood-congruent (e.g., delusions of guilt or worthlessness) or mood-incongruent (e.g., delusions of grandeur). Psychotic depression is associated with greater severity and poorer treatment outcomes. 2. **Peripartum Onset** - This specifier applies to depressive or manic episodes occurring during pregnancy or within six months postpartum. Peripartum depression affects up to 19% of women, often involving severe symptoms like suicidal ideation. Treatment typically includes cognitive-behavioral or interpersonal therapy. 3. **Seasonal Pattern** - Depressive episodes occurring in specific seasons, often winter, are classified as **seasonal affective disorder (SAD)**. Individuals with SAD often experience hypersomnia, increased appetite, and weight gain. This pattern must persist for at least two years without nonseasonal episodes. ### Additional Notes on Depression Depressive disorders are distinguished by their course, chronicity, and symptom severity. For instance, MDD is episodic but severe, while PDD is chronic and persistent. Diagnoses may overlap, such as in double depression, which combines chronicity with episodic severity. Specifiers allow clinicians to personalize treatment and understand prognosis better, acknowledging the unique presentation of each depressive disorder. Onset & Duration 1. **Age of Onset:** - For **major depressive disorder**, the mean age of onset is 25 years in community samples not receiving treatment and 29 years for patients in treatment. - The average age of onset appears to be decreasing over time. 2. **Duration of Depressive Episodes:** - MDD episodes vary in length, lasting from two weeks to several years. - The average duration of the **first untreated episode** is 2–9 months. - **Probability of remission** within one year is high, even for severe cases (approaching 90%). However, about 38% of patients with episodes lasting five years or longer eventually recover. - Residual symptoms after partial recovery increase the likelihood of future episodes with incomplete recovery, emphasizing the need for prolonged treatment in such cases. 3. **Persistent Depressive Disorder:** - PDD can last **20–30 years or more**, although its median duration is reported as five years in adults and four years in children. - Recovery is possible—74% of adults in a study recovered at some point. However, 71% of those who recovered relapsed within the study's 10-year follow-up period. - Compared to MDD, PDD is more chronic, with patients spending **60% of a 10-year period** meeting criteria for a mood disorder (versus 21% in MDD). - PDD with less severe symptoms is associated with a **higher risk of suicide attempts** than episodic major depressive disorder. 4. **Children and Adolescents:** - Persistent mild depressive symptoms are less common in children (0.07%) than in adults (3–6%). However, these symptoms tend to remain stable in childhood, with **76% developing major depressive disorder** later in life. - The course of depression in children is generally shorter, with a median duration of four years. From Greeif To depression Grief is a natural response to the loss of a loved one, often accompanied by symptoms such as depression, anxiety, emotional numbness, and denial, especially when the death is unexpected. In severe cases, individuals may experience a major depressive episode with symptoms like psychosis, suicidal thoughts, severe weight loss, or an inability to function. Cultural and religious rituals, such as funerals, provide support and help individuals process their loss. Typically, grief progresses from acute grief, which resolves within several months, to integrated grief, where the individual acknowledges the finality of the loss, adjusts to life without the deceased, and incorporates positive, bittersweet memories. Integrated grief may resurface during anniversaries, holidays, or other meaningful occasions, which is a normal and healthy response. However, if grief persists beyond six months to a year, it may become prolonged grief disorder. This condition involves increased suicidal ideation focused on reuniting with the deceased, difficulty imagining a future without them, and rigid emotional responses. While prolonged grief is more likely in those with a history of depression, it can also occur in individuals without prior mental health issues. Grieving is essential for emotional processing, and professionals view the absence of grief as a cause for concern. Premenstral Dysphoric Disorder Premenstrual Dysphoric Disorder (PMDD) affects a small percentage of women (2–5%) who experience severe emotional and physical symptoms during the premenstrual phase of their menstrual cycle. These symptoms differ significantly from the premenstrual symptoms (PMS) experienced by 20–40% of women, which are less severe and do not impair functioning. While PMDD has faced criticism for potentially stigmatizing women by medicalizing normal menstrual symptoms, research supports that PMDD represents a distinct mood disorder. It is characterized by a combination of emotional distress, mood swings, anxiety, and physical discomfort that can be incapacitating. Establishing PMDD as a diagnosis aims to help affected women receive appropriate treatment to manage their symptoms and improve their quality of life. #### DSM-5 Diagnostic Criteria for PMDD PMDD symptoms must occur in most menstrual cycles, starting in the week before menses, improving within a few days after the onset of menses, and becoming minimal or absent in the week post-menses. The diagnosis requires at least **five symptoms**, with **at least one** from the core emotional symptoms. ##### **Core Emotional Symptoms (Criterion B)** 1. Marked affective lability (e.g., mood swings, feeling suddenly sad or tearful, or increased sensitivity to rejection). 2. Marked irritability or anger or increased interpersonal conflicts. 3. Marked depressed mood, feelings of hopelessness, or self-deprecating thoughts. 4. Marked anxiety, tension, and/or feelings of being keyed up or on edge. ##### **Additional Symptoms (Criterion C)** To meet diagnostic criteria, symptoms from this list are added to those in Criterion B to reach a total of at least five: 1. Decreased interest in usual activities (e.g., work, school, friends, hobbies). 2. Subjective difficulty concentrating. 3. Lethargy, fatigue, or marked lack of energy. 4. Marked changes in appetite (e.g., overeating or specific food cravings). 5. Hypersomnia or insomnia. 6. A sense of being overwhelmed or out of control. 7. Physical symptoms such as breast tenderness or swelling, joint or muscle pain, a sensation of bloating, or weight gain. ##### **Other Diagnostic Criteria** - Symptoms must cause significant distress or interfere with social, occupational, or other areas of functioning. - They cannot be explained by the exacerbation of another disorder (e.g., major depressive disorder or panic disorder). - Prospective daily ratings of symptoms are required for at least two symptomatic cycles, though a provisional diagnosis can be made earlier. - Symptoms are not attributable to the physiological effects of substances or another medical condition. Dysruptive Mood Dysregulation Disorder Over the past decades, the diagnosis of bipolar disorder in children and adolescents has increased significantly, but many of these cases involve children whose symptoms do not meet the criteria for classic bipolar disorder. These children often display chronic irritability, anger, aggression, hyperarousal, and frequent temper tantrums without evidence of mania, a hallmark of bipolar disorder. Research suggests that these symptoms increase the risk of future depressive and anxiety disorders rather than bipolar disorder and are not linked to a familial history of bipolar disorder. This pattern led to concerns that these children were being misdiagnosed with bipolar disorder or conduct disorder, exposing them to unnecessary treatments with severe side effects. Instead, their condition is now recognized as **Disruptive Mood Dysregulation Disorder (DMDD)**. DMDD is characterized by persistent irritability and difficulty regulating emotions, leading to substantial personal and family suffering. It is distinct from conditions like ADHD or conduct disorder because of the intense negative affect driving the irritability and mood dysregulation. The new diagnosis aims to provide a more accurate classification and guide appropriate treatment. Children diagnosed with DMDD are at an increased risk for developing mood and anxiety disorders later in life, as well as other adverse outcomes. Ongoing research is focusing on developing effective psychological treatments for this challenging condition, with promising approaches being adapted from therapies for severe emotional dysregulation in children. #### DSM-5 Diagnostic Criteria for DMDD 1. **Temper Outbursts**: Severe and recurrent temper outbursts that are verbal (e.g., rages) and/or behavioral (e.g., physical aggression), grossly out of proportion in intensity or duration to the situation. 2. **Inconsistency with Developmental Level**: The outbursts are not appropriate for the child’s developmental stage. 3. **Frequency**: Outbursts occur, on average, three or more times per week. 4. **Persistent Irritability or Anger**: Between outbursts, the child’s mood is persistently irritable or angry most of the day, nearly every day, as observed by others. 5. **Duration**: Criteria A–D have been present for 12 or more months, without a symptom-free period of 3 or more consecutive months. 6. **Settings**: Symptoms are present in at least two of three settings (home, school, or with peers) and severe in at least one. 7. **Age Restrictions**: Diagnosis must be made between ages 6 and 18, with symptom onset before age 10. 8. **Exclusion of Mania or Hypomania**: There has never been a period of more than one day during which full criteria for mania or hypomania were met. 9. **Exclusion of Other Disorders**: Symptoms do not occur exclusively during major depressive disorder episodes and are not better explained by autism spec disorder, PTSD, separation anxiety disorder, or persistent depressive disorder. 10. **Not Due to Substances or Medical Conditions**: Symptoms are not attributable to substance use or medical/neurological conditions. Bipolar Disorders Bipolar disorders, initially termed "manic-depressive illness" by Emil Kraepelin, are characterized by alternating manic episodes and major depressive episodes. These mood swings create an emotional roller coaster, with individuals experiencing periods of extreme elation and deep despair. Bipolar disorders share similarities with depressive disorders but involve mood changes that can vary in intensity. For instance, a manic episode may occur once or multiple times in an individual’s life. The case of **Jalah**, a woman with bipolar II disorder, illustrates these dynamics. Jalah exhibited frequent hypomanic episodes, marked by elevated mood, decreased need for sleep, and distractibility. During these episodes, she was energetic and socially engaging, although her speech was rapid and uninterruptible. However, she also experienced severe depressive episodes, during which she was immobile and unable to care for herself or her family. These fluctuations caused significant disruptions in her family life, especially for her son Mike, who struggled with obsessive-compulsive disorder (OCD). Despite treatment for Mike's condition, it was only after distancing himself from Jalah that his symptoms improved. Tragically, Jalah later took her own life, a common but devastating outcome for many with bipolar disorder. In **bipolar II disorder**, individuals experience major depressive episodes and hypomanic episodes (less severe than full mania). Hypomanic episodes are characterized by elevated mood and increased activity but do not cause significant impairment or require hospitalization. In contrast, **bipolar I disorder** is diagnosed when a person experiences at least one full manic episode, which is more severe and can result in hospitalization. The case of **Billy**, who had a full manic episode, demonstrates the extremes of manic behavior. Billy exhibited grandiosity, impulsive spending, and reckless decisions, believing that he could become the best at everything, such as Ping-Pong and setting up a sound studio. His behavior reflected the typical denial seen in manic episodes, where individuals feel no need for help and may even stop taking medication to experience the high again. Billy’s actions were extreme and ultimately led to his hospitalization. Bipolar disorder can be incredibly disruptive to an individual’s life and relationships, with some individuals being at risk for dangerous consequences, including suicide. Treatment for bipolar disorder typically includes medication and therapy to help manage mood swings and minimize the impact of both manic and depressive episodes. **Cyclothymic disorder** is a milder but chronic form of bipolar disorder characterized by long-term alternation between hypomanic symptoms (mild mood elevation) and depressive symptoms that do not meet the criteria for full manic or major depressive episodes. This condition lasts for at least two years (one year for children and adolescents), with the person experiencing mood swings for more than half of that time, and periods of neutral mood lasting no more than two months. Although the symptoms are not severe enough to require hospitalization, they can still interfere with daily functioning. Cyclothymic disorder is often seen as persistent moodiness and poses an increased risk for developing more severe forms of bipolar disorder, such as bipolar I or II. **DSM-5 Criteria for Cyclothymic Disorder**: - Numerous periods with hypomanic symptoms and depressive symptoms lasting at least 2 years (1 year for children/adolescents). - Symptoms must be present for at least half of the time, with no symptom-free periods lasting more than two months. - No major depressive, manic, or hypomanic episodes have occurred. - Symptoms cause significant distress or impairment in important areas of life. **Specifiers for Bipolar Disorders**: Bipolar disorders can also include various specifiers to describe additional features, such as: - **Catatonic features**: Rare in manic episodes but can occur. - **Psychotic features**: Delusions of grandeur may appear during manic episodes. - **Mixed features**: Episodes that involve symptoms of both depression and mania. - **Anxious distress**: Increased anxiety during mood episodes. - **Seasonal pattern**: Depressive episodes in winter and manic episodes in summer. - **Peripartum onset**: Episodes triggered around childbirth. **Rapid-Cycling Specifier**: A unique specifier for bipolar I and II disorders, **rapid cycling** involves four or more manic or depressive episodes within a year. It is linked to more severe episodes, a higher risk of suicide attempts, and reduced treatment efficacy. Rapid cycling is more common in females and tends to worsen over time, sometimes transitioning directly between manic and depressive states, referred to as **rapid mood switching**. This form of cycling is often resistant to treatment, especially when antidepressants are used, as they may trigger more frequent mood switches. However, rapid cycling does not typically persist long-term, with most patients returning to a non-rapid-cycling pattern within two years. **Ultra-Rapid and Ultra-Ultra-Rapid Cycling**: These rare forms of rapid cycling involve mood swings that last only days to weeks, or even within a 24-hour period, showing potential links to circadian rhythms. Onset & Duration Bipolar disorders typically begin earlier than major depressive disorder, with **bipolar I** starting between **ages 15-18** and **bipolar II** between **ages 19-22**, though both can appear in childhood. These disorders tend to develop suddenly, unlike the gradual onset of depression, and approximately **one-third** of cases start in adolescence, often preceded by mild mood fluctuations or cyclothymia. Around **10-25%** of individuals with **bipolar II** eventually develop **bipolar I**. Emerging research suggests that bipolar disorder and unipolar depression may exist on a spectrum, with many individuals with depression experiencing manic symptoms. Bipolar disorder usually appears before age 40 and is chronic, with alternating **manic** and **depressive episodes**. Without early intervention, it carries a high risk of suicide, with factors such as male sex, family history, and social isolation contributing to this risk. Early treatment can reduce mortality rates. **Cyclothymic disorder**, a milder and chronic form of bipolar disorder, typically begins in **adolescence** and may evolve into full bipolar disorder in **one-third to one-half** of cases. Often misidentified as moodiness or hyperactivity, cyclothymia can present with either depressive, hypomanic, or mixed symptoms.  Prevalance of Mood Disorders In the 2019 Canadian Community Health Survey, about 9% of Canadians aged 12 and older reported having a mood disorder, such as depression, bipolar disorder, or persistent depressive disorder, with women being more likely to report these disorders than men. Worldwide, approximately 16% of people will experience major depressive disorder (MDD) in their lifetime, and around 6% will have it in the past year. In Canada, the annual prevalence of MDD is about 4.7-4.8%, with lifetime rates around 12%, consistent over time. Among working-age Canadians, 5.4% experience MDD annually, with rates doubling for unemployed individuals. For bipolar disorder, the lifetime prevalence is 2.4%, with 1.5% experiencing it in the past year. Bipolar disorder has a high suicide risk, with 6-7% of those affected dying by suicide, and suicide rates being significantly higher than in major depressive disorder. Lifespan Developmental Influences on Mood Disorder ↳ In children and adolescents Mood disorders can manifest in childhood and adolescence, challenging the assumption that they only arise from accumulated life experiences. Infants, particularly those of depressed mothers, can display depressive behaviors, suggesting that genetic and early environmental factors may contribute. While mood disorders in children are less common than in adults, the prevalence of depression rises significantly in adolescence, with rates often higher than those in adults. In young children, persistent depressive disorder is more prevalent, whereas in adolescents, major depressive disorder becomes more common, particularly among females. Mania in children is often characterized by irritability and emotional swings, which may be mistaken for hyperactivity or ADHD. Bipolar disorder is rare in childhood but becomes more prevalent in adolescence. Children with mood disorders may be misdiagnosed with conduct disorder or ADHD, but treating the underlying depression can resolve these symptoms. Adolescents with mood disorders face serious long-term consequences, including ongoing psychosocial impairments and increased risk for recurring depressive episodes into adulthood. In older adts Depression in older adults, especially those living in nursing homes, is common, with studies suggesting that 18 to 20 percent of nursing home residents experience major depressive episodes. Late-onset depression, which typically appears after the age of 60, is often chronic and associated with sleep disturbances, illness anxiety, and agitation. Diagnosing depression in older adults can be challenging due to overlapping symptoms of physical illness or dementia, leading to missed diagnoses. While the overall prevalence of major depressive disorder in older adults is similar to that in the general population, milder symptoms may be more common due to illness or physical decline. The gender imbalance seen in depression in younger populations disappears after age 65, with both men and women experiencing similar rates of depression. Depression in older adults is also strongly influenced by race and ethnicity, with ethnic minorities having a higher risk of symptoms like anhedonia and sadness. Anxiety disorders, particularly generalized anxiety and panic disorder, often co-occur with depression in older adults, complicating the diagnosis and worsening the severity of depression. Additionally, depression can exacerbate physical health issues, doubling the risk of death for older adults who have had a heart attack or stroke. Across cultures Cultural factors significantly influence how mood disorders, such as depression and anxiety, are experienced and expressed. In many cultures, especially those with a strong focus on individualism, people may describe their emotional distress in terms of personal feelings, such as saying "I feel blue" or "I am depressed." In contrast, in more collectivist societies, individuals may express their depression in terms of the group, such as stating, "Our life has lost its meaning." Despite these cultural differences, somatic symptoms like weakness, tiredness, and physical pain are commonly associated with mood disorders across cultures. Studies that use standardized diagnostic criteria, such as the DSM, help facilitate cross-cultural comparisons of mood disorders. One such study, the International Consortium of Psychiatric Epidemiology, revealed notable variations in depression prevalence across countries, with the U.S. having the highest rate (17%) and Japan the lowest (3%). In Canada, the prevalence was moderate (8%). Indigenous populations in North America face significantly higher rates of mood disorders, including major depression, often due to historical and ongoing social and economic stress. Research on Indigenous communities, such as First Nations and Inuit, shows much higher rates of mood disorders compared to the general population, with First Nations off-reserve and Métis populations experiencing 12% prevalence. These findings underline the severe impact of chronic life stress and cultural marginalization on mental health within these communities. Among the creative Research into the longstanding belief that "genius is allied with madness" suggests a possible connection between bipolar disorder and creativity. Historical examples include composers like Handel, who wrote *The Messiah* during a manic episode, and Rossini, who composed *The Barber of Seville* in a period of hypomania. Additionally, about 20% of 20th-century poets featured in *The New Oxford Book of American Verse*—a collection of highly distinguished poets—exhibited bipolar disorder, far exceeding the population prevalence of less than 1%. Manic episodes, characterized by heightened energy, rapid thinking, and elevated moods, are thought to foster creativity, as supported by recent studies showing creativity is specifically linked to manic states rather than depressive ones. The relationship between creativity and bipolar disorder may stem from shared genetic vulnerabilities or the impact of moderate symptoms that enhance creative thinking. For example, a study comparing bipolar patients with those having other mental health disorders found that moderately ill bipolar patients were more creative than severely ill ones, suggesting that creativity peaks at moderate levels of illness but declines with severe symptoms. While these findings are intriguing, they remain speculative and require further investigation.  causes of Mood Disorders ↳ Biological Dimensions #### **Familial and Genetic Influences** - **Family Studies**: Mood disorders are 2-3 times more likely in first-degree relatives of individuals with mood disorders. Severe, recurrent, or early-onset depression in the proband correlates with higher rates in relatives. - **Twin Studies**: Depression is moderately heritable (37%), with most variance attributed to nonshared environmental factors. Bipolar disorder has higher genetic contributions, and the genetics of mania appear distinct from depression. - **Sex Differences**: Women show higher heritability for depression (36-44%) than men (18-24%), with environmental factors playing a larger role in men. - **Joint Heritability**: Mood disorders (depression and bipolar) share genetic links with anxiety, schizophrenia, and ADHD but are distinct from neurological disorders. Genetic predisposition may reflect a general vulnerability to emotional disorders (e.g., neuroticism). #### **Neurotransmitter Systems** - **Serotonin**: Low serotonin levels, combined with dysregulated norepinephrine and dopamine, are implicated in mood disorders. The **permissive hypothesis** suggests that low serotonin destabilizes other neurotransmitter systems, contributing to mood dysregulation. - **Dopamine**: Associated with manic episodes and psychotic features in depression. Chronic stress reduces dopamine, potentially leading to depression. #### **Endocrine System** - **HPA Axis**: Elevated cortisol levels are common in depression, correlating with life stress. The dexamethasone suppression test initially suggested a biological marker for depression but lacked specificity, as anxiety disorders show similar patterns. - **Neurohormones**: Emerging research highlights the role of neurohormones and gut microbiota in mood regulation, opening avenues for dietary and biological interventions. #### **Sleep and Circadian Rhythms** - **Sleep Disturbances**: - Depressed individuals show quicker REM onset, more intense REM activity, and reduced slow-wave sleep. - Insomnia is a risk factor for depression and relapse, especially in older adults. - Bipolar disorder shows severe sleep disruptions, including hypersomnia and bidirectional links between mood and sleep. - **Circadian Rhythms**: - Disruptions in circadian rhythms (e.g., melatonin delays) are linked to depression severity and are potential targets for **chronotherapies**. - Seasonal Affective Disorder (SAD) and circadian disorganization further underline the importance of biological rhythms. - **Sleep and Treatment**: - Addressing sleep problems enhances depression treatment outcomes. - Sleep deprivation temporarily improves mood in some cases but is not a sustainable treatment. Additional studies of brain structure and function Research using EEG and neuroimaging has revealed key differences in brain activity associated with mood disorders. Depression is linked to greater right- sided anterior activation, reduced left-sided activation, and lower alpha wave activity, which may represent a biological vulnerability. This pattern is also observed in the offspring of depressed individuals. Conversely, bipolar disorder is associated with elevated left-frontal activity, which may predict the onset of bipolar I. Additional findings show reduced activity in the prefrontal cortex and hippocampus, and increased activity in the anterior cingulate cortex and amygdala in depression, correlating with goal inhibition and other depressive traits. These neural patterns may serve as markers for risk and diagnosis, though further research is needed to confirm whether they precede or result from mood disorders. Psychological Dimensions Stressful life events are significant contributors to the onset of depression, interacting with genetic and psychological vulnerabilities, as described by the diathesis–stress model. While many individuals report major life changes, such as job loss or divorce, as precursors to depression, the impact of such events depends on their context and meaning to the individual. For instance, losing a job may be less distressing for someone with financial support or alternative goals, but devastating for someone struggling to meet basic needs. How individuals interpret these events also plays a critical role in their psychological impact. Research during the COVID-19 pandemic highlights the importance of stressors like financial instability and loneliness in increasing depressive symptoms. A Canadian survey found that 32% of individuals struggling financially screened positive for major depressive disorder, compared to 12% of those without financial issues. Younger individuals and women were particularly affected, with studies estimating that one in four youths globally experienced clinically significant depressive symptoms during the pandemic. These findings underscore the importance of studying stressful events prospectively, as retrospective accounts may be biased by current moods, which can distort memory. The relationship between stress and depression is complex. While stressful events strongly predict the onset of depression, this link is often mediated by genetic predispositions. For example, individuals with genetically influenced personality traits might place themselves in high-stress environments, leading to depression. Stress can also affect bipolar disorder, triggering early episodes of mania or depression and, over time, contributing to a self-perpetuating cycle. Additionally, stress can prevent recovery and predict relapse in both unipolar and bipolar disorders. The learned helplessness theory proposed by Seligman emphasizes how individuals who perceive a lack of control over stressors may develop anxiety and, eventually, depression. This process involves three depressive attributional styles: internal (blaming oneself), stable (believing future events will also be one’s fault), and global (generalizing blame across various situations). While early life stress does not initially predict depressive symptoms, it can foster negative attributional styles that increase vulnerability to future episodes. This process often overlaps with anxiety disorders, as both involve a sense of uncontrollability. Aaron Beck's cognitive theory focuses on how individuals with depression interpret events negatively, often engaging in cognitive errors like **arbitrary inference** (focusing on the negative aspects of a situation) and **overgeneralization** (extrapolating one negative event to broader failures). Beck identified a "cognitive triad" of negative views about the self, the world, and the future. Deeply ingrained negative schemas, such as self-blame or negative self-evaluation, can persist from childhood, making individuals more susceptible to depressive episodes. Canadian researchers have further validated Beck’s theory. Studies show that cognitive biases, such as interconnected negative thought patterns, remain stable in individuals prone to depression. Negative schemas become activated by stress, leading to negative interpretations and depressive episodes. Prospective studies demonstrate that these biases are stronger during active depression but persist as vulnerabilities even after recovery. Both Beck’s cognitive theory and Seligman’s learned helplessness theory highlight the role of pessimistic explanatory styles in depression. These styles often predate depressive episodes, making them important targets for intervention. Together, these theories form the foundation of cognitive therapy, which aims to identify and correct negative thought patterns and has become one of the most effective treatments for depression. Social & Cultural Dimensions #### **Marital Relationships and Depression** Interpersonal stress, particularly marital dissatisfaction, has a profound impact on depression and bipolar disorder. Studies reveal that marital splits can drastically increase the risk of severe depression, especially for men. For instance, Bruce and Kim (1992) found that 21% of women and 17% of men who experienced a marital split reported severe depression. Among those without prior histories of depression, men had a significantly higher likelihood (14%) of developing depression following a split than women (5%). This suggests that men may be particularly vulnerable to their first depressive episode after marital separation. Additionally, ongoing depression in one partner can erode marital relationships, as the negativity, pessimism, and irritability associated with depression strain the partnership. Such dynamics can result in arguments, emotional withdrawal, or eventual separation. Notably, the direction of causality differs by gender: men are more likely to withdraw from relationships due to depression, whereas relational problems are more likely to lead to depression in women. Addressing marital conflicts alongside mood disorders in therapy is therefore critical to improving outcomes and preventing relapse. For individuals with bipolar disorder, marriage presents unique challenges. They are less likely to marry and more likely to divorce, but those in stable marriages often have better prognoses, as supportive spouses can assist with treatment adherence and medication management. #### **Gender and Mood Disorders** The gender disparity in mood disorders is striking. While bipolar disorder occurs equally among men and women, nearly 70% of individuals with major depressive disorder or persistent depressive disorder are women. This gender imbalance is consistent across cultures and may stem from various sociocultural factors. One explanation is the culturally driven perception of uncontrollability in women. Traditional gender roles often encourage women to be passive and dependent, fostering feelings of helplessness that heighten vulnerability to depression and anxiety. Parenting styles that reinforce these roles—such as overprotectiveness—may further increase susceptibility. Women’s emphasis on intimate relationships may also contribute. Disruptions in relationships, combined with difficulty coping, are more damaging to women than men. Moreover, women tend to ruminate on their problems, which can exacerbate depression. In contrast, men are more likely to distract themselves through activity, a behavior often incorporated into depression therapies. Economic factors also play a role. Single mothers and women living in poverty are at a significantly higher risk of depression, particularly when compared to married women employed full-time. Abuse histories, particularly early sexual abuse, are another key factor, as women are disproportionately affected by these experiences, which increase the likelihood of both depression and comorbid anxiety. #### **Social Support and Mental Health** Social support is a critical determinant of mental health, influencing both the onset and recovery of depressive episodes. Individuals living alone face an 80% higher risk of depression compared to those who live with others. The presence of a confidant can significantly buffer the effects of life stress, as demonstrated by studies showing that women with strong social connections are far less likely to develop depression after major stressors than those without such support. Social support not only prevents depression but also aids in recovery. For instance, postpartum depression studies show that partner support significantly reduces depressive symptoms in women. Similarly, a supportive network accelerates recovery from depressive episodes in individuals with bipolar disorder, although it has less impact on manic episodes. An integrative #### **Biological Vulnerability** Theory A shared genetic predisposition often underlies depression and anxiety, manifesting as an overactive neurobiological response to stress. This vulnerability is linked to genetic variations, such as in the serotonin transporter gene, which affect how individuals respond to stressful life events. This predisposition is not specific to depression or anxiety but reflects a general tendency toward emotional disorders. Women appear to have a stronger biological vulnerability to depression than men, which may help explain the gender disparity in mood disorders. Stress hormones, like cortisol, and neurotransmitters, including serotonin and norepinephrine, play a significant role in the development of depression by affecting brain regions involved in emotional regulation, such as the hippocampus. Chronic stress may lead to long-term structural changes in the brain, disrupting emotional regulation and increasing susceptibility to recurrent mood episodes. #### **Psychological Vulnerabilities** Psychological vulnerabilities are equally critical, often rooted in early life experiences. These vulnerabilities manifest as negative thinking patterns, feelings of helplessness, and a lack of confidence in coping with challenges. Adverse childhood experiences, such as neglect or having a caregiver with psychological disorders, can shape these vulnerabilities. For instance, children of depressed mothers may develop a less positive self-concept and a tendency to process information negatively, making them more susceptible to depression later in life. When psychological vulnerabilities are triggered by stress, individuals may experience a "giving-up" process, where they feel hopeless and unable to manage life's difficulties. #### **Stress and Mood Disorders** Stressful life events are pivotal in triggering the onset of mood disorders, particularly the first episode. In vulnerable individuals, stress activates stress hormones, which can disrupt neurotransmitter systems and even turn on certain genes, leading to structural and chemical brain changes. Chronic stress may cause atrophy in the hippocampus, impairing its ability to regulate emotions and contributing to mood disorders. Stress can also disrupt circadian rhythms, which are crucial for mood stability. These disruptions may explain the episodic nature of mood disorders, particularly the cycling characteristic of bipolar disorder. #### **The Role of Social and Cultural Factors** Interpersonal relationships, gender, and cultural influences can either protect against or exacerbate the effects of stress. Strong social support systems and healthy relationships can buffer individuals from the full impact of stress, reducing the likelihood of developing mood disorders. Conversely, poor relationships or lack of social support can increase vulnerability. #### **The Diathesis-Stress Model** The integrative theory aligns closely with the **diathesis-stress model**, which posits that mood disorders arise from the interaction of underlying vulnerabilities (diathesis) and environmental stressors. For example, a person with a genetic predisposition to depression may only develop the disorder after experiencing significant stress, such as a relationship breakup or job loss. While this model explains many aspects of mood disorders, it does not account for their varied presentations. Why does one person develop unipolar depression while another develops bipolar disorder or an anxiety disorder? Specific psychosocial factors, such as early learning experiences and personality traits, likely influence the outcome. These interactions add complexity and diversity to the presentation of emotional disorders. The development of mood disorders is shaped by the dynamic interaction of biological vulnerabilities, psychological traits, and social factors. Understanding these connections helps clinicians identify risk factors, tailor interventions, and support recovery. This integrative perspective underscores the importance of addressing all aspects of a person’s life—biological, psychological, and social—to effectively manage and treat mood disorders. Medications There are three primary types of antidepressant medications used to treat depressive disorders: tricyclic antidepressants (TCAs), monoamine oxidase (MAO) inhibitors, and selective serotonin reuptake inhibitors (SSRIs). Tricyclic antidepressants, such as imipramine (Tofranil) and amitriptyline (Elavil), work by blocking the reuptake of neurotransmitters like norepinephrine and serotonin, allowing them to accumulate in the synapse. This process, which takes 2–8 weeks to become effective, down-regulates neurotransmitter activity. While TCAs alleviate depression in approximately 50% of patients and up to 70% of those who complete treatment, their side effects—blurred vision, dry mouth, constipation, weight gain, sexual dysfunction, and cardiac risks—lead many to discontinue use. Additionally, TCAs can be lethal in overdose, posing a danger to suicidal patients. MAO inhibitors, on the other hand, work by preventing the breakdown of neurotransmitters such as norepinephrine and serotonin. Although they are as effective as TCAs and have fewer side effects, they are used less frequently due to serious dietary and drug interactions that can cause severe hypertensive episodes or death. These inhibitors are typically reserved for patients who do not respond to other treatments. SSRIs, such as fluoxetine (Prozac), are often the first choice for treating depression. They specifically block the presynaptic reuptake of serotonin, increasing its levels temporarily. SSRIs are as effective as TCAs but are better tolerated, with fewer bothersome side effects, though sexual dysfunction, agitation, and insomnia are common complaints. Despite early concerns about Prozac leading to suicidal tendencies, these risks are no greater than with other antidepressants. Newer antidepressants like venlafaxine and nefazodone offer alternative options. Venlafaxine reduces cardiovascular side effects compared to TCAs, while nefazodone improves sleep efficiency. Both are roughly as effective as older antidepressants but come with unique side effect profiles. St. John’s wort, a natural herb popular in Europe and North America, has shown promise in mild depression but is less effective for severe cases. Its unregulated status and potential for drug interactions, such as with antidepressants and HIV medications, make it a less reliable option. Emerging treatments like ketamine and psychedelics are being explored for their rapid effects, particularly for treatment-resistant depression and suicidal ideation. Lithium carbonate, a mood-stabilizing drug, is a common treatment for bipolar disorder, reducing manic symptoms in about 50% of patients. Lithium is more effective than anticonvulsants like valproate in preventing suicide but comes with significant side effects, including weight gain, thyroid dysfunction, and toxicity risks, requiring careful monitoring. Many patients struggle with compliance due to the appeal of manic episodes, increasing the risk of relapse. For both depression and bipolar disorder, long-term treatment is crucial. Antidepressants should be continued for 6–12 months after remission to prevent relapse. However, up to 50% of patients do not respond to medication, and many who do are left with residual symptoms. Special populations, including children, seniors, and pregnant women, require careful consideration due to heightened risks, such as cardiac side effects, memory impairment, and fetal harm. Despite limitations, antidepressants and mood stabilizers remain vital in managing mood disorders, and ongoing research into new treatments offers hope for more effective and tolerable therapies. Electroconvulsive Therapy and Transcranial Magnetic Stimulation For individuals who do not respond to medication or in cases of severe depression, clinicians may consider electroconvulsive therapy (ECT), one of the most controversial treatments for psychological disorders. Although it was historically misused, modern ECT is significantly improved and is considered safe and effective for severe depression unresponsive to other treatments. During ECT, patients are anesthetized to minimize discomfort and given muscle relaxants to prevent injuries from convulsions. A brief electric shock, lasting less than a second, induces a seizure that typically lasts a few minutes. Treatments are administered every other day for 6–10 sessions or until the patient's mood improves. Common side effects include short-term memory loss and confusion, which usually resolve within two weeks, though some individuals may experience long-term memory issues. Studies show that approximately 50% of patients with medication-resistant severe depression benefit from ECT, but continued therapy is essential as relapse rates can reach 60%. The exact mechanism by which ECT works remains unclear, but evidence suggests it may increase serotonin levels, block hormones, and promote neurogenesis in the hippocampus. Despite its efficacy, ECT’s controversial history led to a decline in its use during the 1970s and 1980s. Comparatively, transcranial magnetic stimulation (TMS), a newer technique, uses a magnetic coil placed on the head to generate localized electromagnetic pulses, altering brain activity. TMS does not require anesthesia, and its primary side effect is headaches. While TMS has shown promise in treating depression, clinical trials indicate that ECT is more effective, especially for treatment-resistant depression with psychotic features. Other non-drug approaches for treatment-resistant depression are also being explored. Vagus nerve stimulation involves implanting a device in the neck to stimulate the vagus nerve, influencing neurotransmitter production in the brainstem and limbic system. However, evidence for its effectiveness is weak, and its usage remains limited. Another experimental method, deep brain stimulation, involves surgically implanting electrodes in the limbic system, connected to a pacemaker-like device. While initial results have shown promise for severe depression, further research is needed to establish its efficacy. Psychosocial Treatments ### **Cognitive Therapy** Aaron T. Beck, the founder of cognitive therapy, emphasized the role of negative thought patterns in the development of depression. Cognitive therapy focuses on identifying and altering maladaptive thought processes, which are often automatic and unnoticed by individuals. Patients are taught to recognize these "depressive errors" and replace them with more realistic and less distressing thoughts. In therapy, underlying cognitive schemas—deep- seated ways of viewing the world—are also addressed. Through collaboration between therapist and client, these schemas are examined and reframed. For instance, in a dialogue between Beck and a client named Irene, the therapist helped her identify feelings of hopelessness about her future and explore her automatic negative thoughts. Between sessions, clients log their thoughts and engage in "behavioral experiments" to test their assumptions, such as participating in social or professional activities they might otherwise avoid. **Related Approaches:** - **Cognitive-Behavioral Analysis System of Psychotherapy (CBASP):** Designed for chronic depression, CBASP integrates cognitive, behavioral, and interpersonal strategies with a focus on problem-solving. - **Mindfulness-Based Cognitive Therapy (MBCT):** Combining mindfulness and cognitive techniques, MBCT is effective in preventing relapse, particularly in patients with recurrent depression. - **Behavioral Activation Therapy:** Focused on increasing activities and reducing avoidance, this approach has been shown to improve mood and self- concept, sometimes as effectively as cognitive therapy. Additionally, **exercise programs** have proven beneficial. For example, regular aerobic exercise has been found to be as effective as antidepressants in reducing depressive symptoms and is particularly effective in preventing relapse when continued over time. Research suggests that exercise may promote neurogenesis in the hippocampus, enhancing resilience to depression. ### **Interpersonal Psychotherapy (IPT)** IPT, developed by Myrna Weissman and Gerald Klerman, emphasizes the role of interpersonal relationships in the development and maintenance of depression. The therapy is structured, typically lasting 15–20 sessions, and focuses on resolving current interpersonal challenges. The therapist and patient collaborate to address four common areas of interpersonal difficulty: 1. **Role disputes** (e.g., conflicts in relationships). 2. **Role transitions** (e.g., adapting to life changes). 3. **Grief and loss** (e.g., mourning the death of a loved one). 4. **Interpersonal skill deficits** (e.g., difficulty forming or maintaining relationships). For instance, in addressing a marital conflict, the therapist works to identify the stage of the dispute (e.g., negotiation, impasse, or resolution) and then develops strategies to help resolve it. **Effectiveness:** Studies comparing IPT, cognitive therapy, and antidepressants suggest all three approaches are equally effective in treating major and persistent depressive disorders, with approximately 50–70% of patients showing significant improvement. IPT has also been successfully adapted for adolescents, showing high rates of symptom reduction in studies. ### **Prevention of Depression** Efforts to prevent depression focus on teaching social, cognitive, and problem-solving skills to at-risk groups. For example: - Programs targeting families with a depressed parent have shown sustained improvements in family functioning. - Cognitive and social problem-solving interventions for children and adolescents have reduced depressive symptoms and even prevented severe episodes. - University students at risk for depression due to pessimistic cognitive styles benefited from structured cognitive therapy sessions, with effects lasting up to three years. These findings suggest that early intervention and skill-building can effectively “immunize” individuals against depression, offering long-term protection against mood disorders. Combined Treatment A key question in treating depression is whether combining psychosocial treatments with medication is more effective than either treatment alone. In a study by Keller and colleagues (2000) on chronic depression, patients who received combined treatment (antidepressants and CBT) showed a 73% remission or satisfactory response rate, compared to 48% for those receiving either treatment alone. While this suggests a benefit to combined treatment, the study's limitations, such as not including a placebo control for CBT, mean further research is needed. Similarly, for children and adolescents, combining fluoxetine with CBT was more effective than CBT alone. However, given the cost of combined treatments, experts often recommend a sequential approach, starting with one treatment and switching if necessary. Preventing Relapse Given the high recurrence rate in depression, maintenance treatments are crucial for preventing relapse. Jarrett and colleagues (2013) compared the effectiveness of CBT, an SSRI (fluoxetine), and a placebo in preventing relapse after initial CBT treatment for recurrent major depressive disorder. The study found that both CBT and fluoxetine equally prevented relapse, significantly more than the placebo, with no difference in relapse rates between the two active treatments. Mindfulness-based cognitive therapy (MBCT) has also been shown to prevent relapse. It helps patients with a history of recurrent depression disengage from negative thinking by teaching mindfulness meditation. A randomized control study by Teasdale et al. (2000) demonstrated that MBCT significantly reduced the risk of relapse over a 60-week period in patients who had recovered from depression. MBCT helps patients change their relationship with negative thoughts, distancing themselves from them and reducing their impact on mood. Psychosocial Treatments for Bipolar Disorder Bipolar disorder is typically treated with medication, particularly lithium, but psychosocial interventions are also important to address interpersonal and practical problems and to ensure medication compliance. For example, interpersonal and social rhythm therapy (IPSRT), developed by Ellen Frank, helps regulate patients' daily routines, such as sleep and eating, to prevent mood episodes and manage stress. Research shows that IPSRT improves long-term outcomes for patients with bipolar disorder. Family-focused therapy is another approach that has proven effective in reducing relapse, especially when family members learn to understand symptoms and develop better communication and coping skills. Studies show that combining family therapy with medication results in lower relapse rates compared to other treatments. Additionally, cognitive-behavioral therapy (CBT) has shown benefits, particularly for patients with rapid cycling bipolar disorder.A case study of a woman named Katie illustrates the challenges of living with a mental health disorder and the importance of adequate treatment. Katie, who had experienced multiple episodes of depression and suicide attempts, struggled with anxiety, depression, and substance abuse. Despite these challenges, she found purpose through education and later pursued a Ph.D. in psychology. Through therapy, Katie learned to manage her emotional swings, accept her flaws, and develop strategies for achieving her goals. Her resilience and perseverance enabled her to overcome many obstacles and ultimately find fulfillment, illustrating the potential for recovery even in the face of significant psychological challenges. Hi Nado &  Chapter #12-substance use & Impulse control According to the 2012 Canadian Community Health Survey, 3.8% of Canadians experienced a substance use disorder in the past year, with 1.2% having both a substance use disorder and a mood or anxiety disorder. Certain groups, such as First Nations people, are disproportionately affected, with significantly higher hospitalization rates for substance-related disorders compared to non-Indigenous Canadians. This chapter examines substance- related and addictive disorders, including gambling disorder, as well as impulse-control disorders, such as the inability to resist aggressive impulses, stealing, or setting fires. These disorders, often misunderstood as issues of willpower, have profound effects on individuals and society. Perspectives on Substance - Related & Addictive Disorders Substance-related and addictive disorders have significant global consequences, affecting lives, finances, and emotional well-being. While society often associates these issues with lack of willpower, they are complex and involve various levels of substance use, intoxication, and dependence. The DSM-5-TR classifies these disorders into substance use disorders, which involve continued use despite severe consequences, and substance-induced disorders, such as intoxication or withdrawal. Substances, including legal ones like alcohol, nicotine, and caffeine, alter mood and behavior and can lead to addiction. Legal substances often cause more health problems and fatalities than illegal drugs, underscoring the need for prevention efforts, particularly against smoking - due to its high addictive potential and harmful health effects. The story of Danny, a man whose polysubstance use escalated into deception, financial irresponsibility, and legal troubles, highlights the lifelong challenges of substance-related disorders. Despite early experimentation similar to his peers, Danny's drug use became increasingly problematic, leading to strained family relationships, unemployment, and criminal activity. Cases like Danny's illustrate the importance of understanding the causes and treatments of these disorders. levels of Involvement ### Substance Use, Intoxication, and Use Disorders Substance use involves the moderate ingestion of psychoactive substances, such as coffee, alcohol, or tobacco, without impairing daily functioning. Intoxication refers to the physiological and behavioral reactions to substances, such as impaired judgment and motor skills, influenced by the drug type, dose, and individual biology. ### Substance Use Disorder (SUD) SUD is not defined by the quantity of substance used but by the degree of interference with a person’s life. The DSM-5-TR diagnoses SUD based on at least two symptoms within a year, such as educational or occupational disruptions, risky behaviors (e.g., driving under the influence), or drug-seeking behaviors. Severity ranges from mild (2–3 symptoms) to severe (6 or more symptoms). Symptoms may include: - **Physiological dependence**: Tolerance (needing more of a substance for the same effect) and withdrawal (negative physical effects when the substance is absent). - **Psychological dependence**: Drug-seeking behaviors and inability to resist relapse after abstinence. Notably, physiological dependence can occur without misuse, as seen in cancer patients using morphine for pain management. ### Addiction and Individual Variation Addiction is often equated with severe SUD, though its exact definition remains debated. While some people can use substances like alcohol or even illicit drugs occasionally without developing problems, others may quickly develop dependence. Predicting who will misuse substances remains challenging. Substance use and its effects vary by individual biology, environmental factors, and the type of substance, which will be explored further in biological and psychosocial theories later in the chapter. Diagnostic Issues The classification of substance use disorders has evolved significantly. Early editions of the DSM categorized alcoholism and drug misuse as sociopathic personality disturbances, reflecting a view that these issues were signs of moral weakness rather than standalone disorders. This changed with the DSM-III in 1980, which recognized substance use disorders as complex conditions influenced by biological and psychological factors. In the DSM-5, the term *substance use disorders* includes 11 symptoms ranging from mild (e.g., neglecting major responsibilities) to severe (e.g., abandoning important activities due to substance use). Notably, the DSM-5 replaced the symptom related to legal issues with one addressing cravings. For severe cases, such as Danny’s cocaine use disorder, multiple symptoms like tolerance, failed attempts to quit, and life disruptions are present. Substance use disorders often co-occur with other psychiatric disorders, such as depression, anxiety, and gambling addiction. This comorbidity may arise from chance, substance-induced psychiatric symptoms (e.g., intoxication or withdrawal effects), or mental health disorders leading to substance use (e.g., self-medicating for anxiety). The DSM-5-TR provides guidelines to differentiate between substance-induced symptoms and independent mental health conditions. For instance, depression during withdrawal is not diagnosed as a mood disorder unless it predates substance use or persists beyond six weeks after stopping. Substances are classified into five categories: **depressants** (e.g., alcohol, barbiturates), which induce sedation and relaxation; **stimulants** (e.g., cocaine, nicotine), which enhance alertness and mood; **opioids** (e.g., heroin, morphine), which provide pain relief and euphoria; **hallucinogens** (e.g., LSD, cannabis), which alter perception; and **other drugs** (e.g., inhalants, steroids), which have diverse psychoactive effects. These categories highlight the broad range of substances that can impact the brain and behavior. Depressants Depressants are substances that decrease central nervous system activity, promoting relaxation and reducing physiological arousal. This category includes alcohol and drugs prescribed for insomnia or anxiety, such as sedatives, hypnotics, and anxiolytics. These substances are highly associated with tolerance and withdrawal symptoms. Alcohol, the most commonly used depressant, can lead to alcohol use disorder, characterized by a pattern of problematic alcohol use that impairs daily functioning. According to the DSM-5-TR, a diagnosis requires at least two of 11 criteria within a 12-month period. Symptoms range from consuming more alcohol than intended, unsuccessful attempts to reduce intake, and neglect of responsibilities, to experiencing cravings, tolerance, or withdrawal. Severity is categorized as mild (2–3 symptoms), moderate (4–5 symptoms), or severe (6 or more symptoms). Alcohol-related Disorders Danny’s substance use began with drinking beer socially, a common teenage activity. Alcohol has a long history of use, with evidence of wine and beer production dating back 7,000 years. It was widely consumed in Europe and brought to North America by settlers, introducing it to Indigenous populations. Alcohol was not a problem for Indigenous peoples until settlers introduced brandy and rum, leading to widespread intoxication and government regulation. The Temperance Movement promoted moderate drinking while condemning heavy use, paving the way for Prohibition in the U.S., which reduced overall alcohol consumption but increased organized crime. Alcohol’s effects start with initial stimulation, reducing inhibitions and creating a sense of well-being, though it is ultimately a depressant. Continued drinking impairs motor skills, judgment, and sensory abilities, making activities like driving dangerous. Alcohol interacts with several neurotransmitter systems, such as GABA (reducing anxiety), glutamate (causing blackouts), and serotonin (triggering cravings). It also stimulates the dopamine reward system, contributing to its addictive nature. Long-term heavy use leads to withdrawal symptoms, including nausea, hallucinations, and delirium tremens (DTs), and can cause liver disease, pancreatitis, cardiovascular disorders, and brain damage. Disorders like Wernicke-Korsakoff syndrome and alcohol-related dementia are severe consequences of chronic drinking. Although moderate drinking was once thought to protect against cognitive decline, recent studies refute this. Alcohol’s effects extend to prenatal development, with fetal alcohol spectrum disorders (FASD) causing growth, cognitive, and behavioral issues. Canada’s low-risk drinking guidelines recommend minimal alcohol use to avoid health risks. Despite these guidelines, surveys reveal heavy drinking is common among Canadians, particularly men, students, and Indigenous communities facing systemic challenges. Alcohol misuse often progresses, with early drinking predicting later dependence. Chronic alcohol use follows a pattern of worsening consequences, including blackouts, health issues, and social problems. Alcohol is also linked to violent behavior, influenced by factors like impulsivity and impaired judgment. Finally, chronic heavy drinking can result in serious social and personal harm, highlighting the need for education and intervention. Sedative -Hypnotic and anxiolytic-related Disorders , Depressants, including sedative, hypnotic, and anxiolytic drugs, such as barbiturates and benzodiazepines, act on the GABA neurotransmitter system to produce calming, sleep-inducing, and anxiety-reducing effects. Barbiturates (e.g., Amytal, Seconal, Nembutal), introduced in the 1880s, were widely prescribed for sleep but became heavily misused by the 1950s, with high overdose risk, especially when combined with alcohol. Benzodiazepines (e.g., Valium, Xanax, Ativan), introduced in the 1960s, were initially seen as safer but carry significant risks of dependence, especially when used for anxiety or sleep disorders, as demonstrated by Susan’s case. Susan escalated her Diazepam use to 12 times the prescribed dose, experienced severe withdrawal symptoms, and required hospitalization. This highlights the addictive potential of benzodiazepines, despite their perceived safety compared to barbiturates. Misuse of benzodiazepines like Rohypnol ("roofies") has also been linked to incidents such as drug-facilitated assaults. Clinically, these drugs can cause tolerance, withdrawal, and effects similar to alcohol intoxication, including slurred speech and impaired motor skills. Overdose risks increase when combined with alcohol, with notable fatalities including Marilyn Monroe and Heath Ledger. DSM-5-TR criteria for sedative-, hypnotic-, or anxiolytic-related disorders include patterns of misuse, withdrawal, and significant impairment, emphasizing the need for cautious prescribing. Although benzodiazepine use in Canada has declined slightly, misuse remains prevalent, with 12% of Canadians reporting sedative use annually, highlighting ongoing concerns about their safety and addictive potential. Stimulants Stimulants, the most commonly consumed psychoactive drugs in Canada, include caffeine, nicotine, amphetamines, and cocaine. These substances increase alertness and energy, contrasting with depressants. Stimulants have a long history of use, with the amphetamine compound Ma-huang (ephedra) used in traditional Chinese medicine for over 5000 years. Although marketed in North America as a dietary and weight-loss aid, Ma-huang was banned due to links to severe health risks, including elevated blood pressure and deaths, highlighting the dangers of natural compounds. The DSM-5-TR defines stimulant use disorder by patterns of amphetamine-type, cocaine, or other stimulant use that lead to significant impairment or distress, characterized by symptoms such as increased tolerance, withdrawal, craving, and failure to meet responsibilities. Severity ranges from mild (2–3 symptoms) to severe (6+ symptoms). Proper medical supervision is crucial to differentiate therapeutic use from problematic abuse. Stimulant Related Disorder Amphetamines are synthetic stimulants that at low doses induce euphoria, energy, and reduced fatigue but often lead to a crash characterized by depression and exhaustion. First synthesized in 1887, amphetamines were initially used for asthma treatment and as decongestants, later gaining popularity among individuals seeking weight loss or increased wakefulness, such as truck drivers and students. However, amphetamines carry significant risks, including impaired judgment, as seen in a U.S. military incident involving amphetamines that resulted in friendly fire deaths. Amphetamines, including drugs like Ritalin, are also prescribed for conditions like narcolepsy and ADHD but are widely misused for their stimulant effects. Chronic use can result in tolerance,